Amal Mattu’s ECG Case of the Week – May 23, 2016

Key Teaching Points

Low Voltage Definition

Sensitive Definition
- QRS amplitudes in leads I+II+III < 15 mm
- Or QRS amplitudes in leads V₁+V₂+V₃ < 30 mm
Specific Definition
- QRS amplitudes in limb leads all < 5 mm
- Or QRS amplitude in all precordial leads < 10 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Differential for Non-conducted P-waves (P:QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes
- P-waves are irregular, non-conducted P-waves come early
2^nd degree AV Block: Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
2^nd degree AV Block: Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Narrow vs. wide complex QRS in setting of complete heart block

Narrow complexes usually are junctional escape rhythms and generally have a better prognosis when compared to wide complex QRS rhythms
- Ventricular rate < 40 = Junctional bradycardia
- Ventricular rate 40-60 = Junctional escape rhythm
- Ventricular rate > 60-110 = Accelerated junctional rhythm
- Ventricular rate >110 = Junctional tachycardia
Wide complexes are usually ventricular escape rhythms and generally have a worse prognosis when compared to narrow complex QRS rhythms

Take home Points

Don’t trust your ECG computer interpretation! It will fool you
No P-waves? Think junctional (narrow) vs. ventricular (wide) escape rhythms
Electrocardiographic polyuria (more p-waves than QRS complexes)? Look at what the atrium and ventricle are doing and what their relationship is, the answer is in the PR-interval
Low voltage + bradycardia? Think hypothyroidism
Non-sustained VT = VT that lasts less than 30 seconds, look for an underlying cause, consider treatment with beta blockers
ST-segment depression is common in SVT, not significant if it resolves after conversion

Key Teaching Points

Post “seizure” & syncope ECG

When the history and physical exam do not suggest a diagnosis, always think of the following differentials when interpreting the ECG of patients with syncope or new-onset seizures:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy (HCM)
Brugada pattern
Arrhythmogenic RV dysplasia

ECG findings in severe hypokalemia

U-waves (can be very large)
Prolonged QT-interval (T-wave/U-wave fusion)
Flattening of the T-waves, then ST-segment downsloping/depression
Biphasic T-waves that deflect down before going up “reverse Wellens’ waves” a.k.a. “NikEleKam T waves” are caused by severe hypokalemia that prolongs the QT interval because of large U-waves.
ST-segment elevation in aVR
PVC’s, ventricular dysrhythmias

Key Teaching Points

Review Key Teaching Points

The 5 Step Approach to ECG Interpretation

Rate and Rhythm
Axis
Intervals
Enlargement
Ischemia/Infarction (ST-segments, Q-waves, T-waves, R-wave progression)

Find a method and master it!
Run through the differentials when you encounter abnormalities!

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (TCA’s/Na⁺channel blockers, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressure
Congenital

Quick Evaluation of the QT-interval

T-waves should end before the midpoint of the R-R interval.
Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance!

Causes of prolonged QT-interval summary

Prolonged QT due to prolonged T –waves
- Hypokalemia
- Hypomagnesemia
- Medications
- Misc: Elevated ICP, Cardiac ischemia, Congenital
Prolonged QT due to prolonged ST-segment
- Hypocalcemia
- Hypothermia

Poor R-wave Progression Differential

Defined as a < 3 mm R-wave by lead V3

- Prior anteroseptal MI
- LVH
- LAFB
- LBBB
- Lead misplacement
- Normal variant

Low Voltage Definition

Sensitive Definition
- QRS amplitudes in leads I+II+III < 15 mm
- Or QRS amplitudes in leads V₁+V₂+V₃ < 30 mm
Specific Definition
- QRS amplitudes in limb leads all < 5 mm
- Or QRS amplitude in all precordial leads < 10 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Key Teaching Points

Digoxin

Can cause dysrhythmias, due to increased automaticity and decreased AV conduction
- “Digoxin effect”
  - Downsloping ST-segment depression with a characteristic sagging appearance (a.k.a Salvador Dali moustache appearance)
  - Note the presence of digoxin effect on the ECG is not a marker of digoxin toxicity, but merely indicates that the patient is taking digoxin
- Digoxin toxicity
  - Classic dysrhythmia is a combination of a supraventricular tachycardia (due to increased automaticity) with a slow ventricular response (due to decreased AV conduction)
  - Atrial fibrillation with “regularized” ventricular response (complete heart block and a junctional or ventricular escape rhythm)
  - Atrial flutter, or atrial tachycardia with slow conduction is another possible presentation
  - Most common arrhythmia associated with digoxin toxicity is PVC’s

Key Teaching Points

Rate: ~ 79 ventricular
Rhythm: Normal sinus rhythm
Axis: Normal
Intervals: PR & QRS are normal, QTc is short
Enlargement: None
ST segments / T waves: ST-segment elevation in V1/V2

Key Teaching Points

Systematic approach to ECGs

Rate & Rhythm
Axis
Intervals
Enlargement
Ischemic/infarction

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypotermia
Post-cardioversion (stunning)
Tako tsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take home points

Hypercalcemia can mimic STEMI by shortening the QT
DDx of short QTc
- Hypercalcemia
- Digoxin
- Congenital Short QT syndrome
For detailed review of Hypercalcemia & Short QT intervals check out this previous case: Feb 2, 2015

References

Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838

Key Teaching Points

Normal Sinus Rhythm

Upright P waves in all limb leads (except aVR)
PR-interval > 120 ms
Otherwise considered an “ectopic atrial rhythm” or junctional rhythm (short PR-interval)

History is still the key predictor of ACS!

Clinical factors that INCREASE the likelihood of ACS:

Chest pain (CP) that radiates to bilateral > right >> left
CP with diaphoresis
CP with vomiting
CP that worsens with exertion

Bonus Pearl: CP patients who have RE²D flags (Radiation, Exertion, Emesis, Diaphoresis) are high risk for ACS.

Clinical factors that DECREASE the likelihood of ACS:

CP that is pleuritic
CP that is sharp and stabbing
CP that is reproducible with palpation
CP that is positional

ECG Pearls:

Reciprocal changes can precede STE
Reciprocal changes in aVL can be the first sign of inferior STEMI
Inferior MI? Consider RV extension
- Get right sided leads
- Aggressively give IVF, monitor lung sounds
- Avoid preload reduction (Nitrates)

References:

Body R, Carley S, Wibberley C, et al. The value of symptoms and signs in the emergent diagnosis of acute coronary syndromes. Resuscitation. 2010;81(3):281–286. PMID: 20036454
Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623–2629. PMID: 16304077
Panju AA, Hemmelgarn BR, Guyatt GH, et al. The rational clinical examination. Is this patient having a myocardial infarction? JAMA. 1998;280(14):1256–1263. PMID: 9786377

Key Teaching Points

Quick Evaluation of the QT-interval

T-waves should end before the midpoint of the R-R interval.

Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance.

Differential for Prolonged QT

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Medications (many)
Congenital

ECG Findings in Severe Hypokalemia

Prolonged QT-interval
U-waves (Can be very large)
Flattening of T waves then ST segment down-sloping/depression
Nikelekam T waves, formerly known as “reverse Wellens’ waves”
Ventricular ectopy

Key Teaching Points

Differential for Non-conducted P-waves (P:QRS > 1)

Blocked Premature Atrial Complexes

P-waves are irregular, the non-conducted P-waves come early

Mobitz I (Wenckebach)

P-waves are regular (P-P interval is constant)
Progressive PR-interval lengthening before a non conducted beat

Mobitz II

P-waves are regular (P-P interval is constant)
Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening

AV Dissociation, 3^rd degree AV Block

P-waves are regular (P-P interval is constant)
PR-interval is randomly changing

ECG Bonus Pearl:

3-step approach to diagnosing AV Blocks

Find out what the atrium is doing
Find out what the ventricle is doing
Figure out the relationship between the atrium and ventricle (PR-interval)

The answer usually lies in the PR-interval!

Key Teaching Points

Case Interpretation

Case 1 – Rate and Rhythm – Sinus tachycardia ~145 bpm (atrial), Mobitz I with 7:6 AV conduction, Ventricular Rate ~125

Case 2 – Rate and Rhythm – Sinus tachycardia ~100 bpm (atrial), Mobitz II conduction (advanced AV Block), Ventricular Rate ~ 40-45

Differential for Non-conducted P-waves (P:QRS > 1)

Blocked Premature Atrial Complexes

P-waves are irregular, the non-conducted P-waves come early

Mobitz I (Wenckebach)

P-waves are regular (P-P interval is constant)
Progressive PR-interval lengthening before a non conducted beat

Mobitz II

P-waves are regular (P-P interval is constant)
Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening

AV Dissociation, 3^rd degree AV Block

P-waves are regular (P-P interval is constant)
PR-interval is randomly changing

ECG Bonus Pearl:

3-step approach to diagnosing AV Blocks

Find out what the atrium is doing
Find out what the ventricle is doing
Figure out the relationship between the atrium and ventricle (PR-interval)

The answer usually lies in the PR-interval!

Key Teaching Points

Rhythm – Sinus tachycardia, complete heart block, junctional escape rhythm at rate of ~ 40

3-step approach to diagnosing AV Blocks

Find out what the atrium is doing
Find out what the ventricle is doing
Figure out the relationship between the atrium and ventricle (PR-interval)

The answer usually lies in the PR-interval!

Differential for Non-conducted P-waves (P:QRS > 1)

Blocked Premature Atrial Complexes
- P-waves are irregular, the non-conducted P-waves come early
- Usually a benign cause (mild electrolyte abnormalities)
- May mimic Mobitz II, often misdiagnosed by the ECG machine
Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non conducted beat
Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Before diagnosing Mobitz blocks, be certain that the P-P interval is REGULAR, an irregular P-P interval may be simply caused by non-conducted PAC’s.

Key Teaching Points

The 5 Step Approach to ECG Interpretation

Rate and Rhythm – Normal sinus rhythm with a ventricular rate of ~ 60
Axis – Left axis deviation from LAFB
Intervals – Wide QRS ~ 220 ms from RBBB
Enlargement – None
Ischemia/Infarction – Pseudo STE and ST deviation in setting of BBB

Run through the differentials when you encounter abnormalities!

Key Teaching Points

Differential diagnosis of leftward axis

Left ventricular hypertrophy (LVH)
Left bundle branch block (LBBB)
Paced rhythm
Ventricular beats/ectopy
Pre-excitation (e.g. WPW)
Inferior MI (from Q-waves)
Left anterior fascicular block (LAFB
Hyperkalemia
Normal Variant

Causes of QRS Prolongation

Bundle branch blocks (LBBB or RBBB)
Paced beats
Pre-excitation (e.g. WPW)
Ventricular ectopy
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)

Take home point:

Beware of pseudo- ST deviation in patients with BBB. Measure our the QRS duration and make sure you are not confusing the QRS with the ST-segment!

ECG Bonus Pearl: Fascicular blocks

Type of Fascicular Block	LAFB	LPFB
Axis	Left Axis Deviation	Right Axis Deviation
Leads I & aVL
Lead II

Bifascicular Block

Conduction abnormality where two of the three main fascicles of the His/Purkinje system are blocked

- Usually a RBBB + LAFB
- Or RBBB + LPFB

Trifascicular Block

1st degree AV Block + RBBB + LAFB
Or 1st degree AV Block + RBBB + LPFB

Class IIB Indications

Pacemakers and AMI
- Paced rhythms cause ST-segment & T wave changes that can make identification of acute MI difficult
- As in in LBBB, paced rhythms are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
- ST–segment deviations that are concordant(in same direction) to the QRS complex or excessively discordant are abnormal
- Sgarbossa Criteria
  - Sgarbossa criteria can be used to help diagnose AMI in setting of paced rhythms
  - The criteria are reviewed below:

Concordant STE ≥ 1mm (in any lead)
Concordant STD ≥ 1mm in V1, V2, or V3
Discordant STE ≥ 5mm (most specific)

Take-home Points:

Sgarbossa criteria appear to predict acute MI in patients with pacemakers. The criteria have low sensitivity but are very specific. Criteria C (excessively discordant ST-segment elevation) seem to be most specific in patients with pacemakers.

Reference

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing.Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802
Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576
Maloy KR, Bhat R, Davis J, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers.West J Emerg Med. 2010;11(4):354–357. PMID: 21079708

de Winter T-waves

1-3 mm ST-depression at the J-point in the mid precordial leads, leading into tall symmetric T-waves
- High risk of acute anterior MI
- Suggestive of an acute proximal LAD occlusion (contrast to sub-acute occlusion of Wellens syndrome), or less commonly a 1^st diagonal or left circumflex occlusion
- Although no ST-elevation, may be an unstable lesion for which urgent cath should be “strongly considered”
- Get serial ECG’s while the patient is having pain, may progress to STEMI
- Have high concern for potential decompensation and treat aggressively

References:

de Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008 Nov 6;359(19):2071-3. PMID:18987380
Verouden NJ, Koch KT, Peters RJ, et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. 2009;95(20):1701–6. PMID: 19620137
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec;160(6):995-1003. PMID:21146650
Stankovic I, Ilic I, Panic M, et al. The absence of the ST-segment elevation in acute coronary artery thrombosis: what does not fit, the patient or the explanation? J Electrocardiol. 2011; 44(1):7–10. PMID: 20591442
Birnbaum I, Birnbaum Y. High-risk ECG patterns in ACS—need for guideline revision. J Electrocardiol. 2013;46(6):535–9. PMID: 23863685
Goebel M, Bledsoe J, Orford JL, et al. A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr. Am J Emerg Med. 2014;32(3):287.e5–8. PMID: 24176590

ST-segment elevation in aVR with ST-segment depression in multiple other leads

Reflects global subendocardial ischemia of the left ventricle, often associated with proximal lesions or multi-vessel disease
STE in aVR (> 1-1.5 mm) Differential
- LMCA stenosis
- Proximal LAD
- Triple vessel disease
- Any cause of severe generalized global ischemia
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Massive PE, etc.

Take-home points:

Must be used in the correct patient with signs and symptoms of ACS! These patients typically have active anginal symptoms and look sick
Watch out for normal variants such as LBBB, severe LVH, or SVT
Literature is increasingly supportive of incorporating this into cath lab activation criteria

Reference:

Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74. PMID: 17098112
Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiology. 2008 Nov-Dec;41(6):626-9. PMID: 18790498
Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol. 2009 Mar 17;53(11):1007. PMID: 19281933
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID:21146650
Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. 2010 Mar-Apr;43(2):93, 97-98. PMID: 19913800
Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500. PMID: 21184992
Taglieri, N., Marzocchi, A., Saia, F., et al. Short- and Long-Term Prognostic Significance of ST-Segment Elevation in Lead aVR in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome. Am J Cardiol. 2011; 108(1), 21–28. PMID: 21529728
Kosuge M, Uchida K, Imoto K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2015 Jun 16;65(23):2570-1. PMID: 26065996

Final Class IIB Take-home points

Use Sgarbossa criteria to diagnose acute MI in patients with pacemakers
Beware de Winter T-waves
In the right patient, beware STE in lead aVR!

Share the literature and be an advocate for your patients!

Class IIA Indications

Criteria in LBBB
- New LBBB is out!
  - A new or presumed new LBBB used to be a STEMI equivalent. In the past few years, increasing literature has suggested that a new LBBB does NOT predict a high likelihood of AMI/acute thrombosis.
  - The most recent STEMI Guidelines state that new or presumed new LBBB is no longer an indication for emergent CLA/lytics!Reference:O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. JAC 2013;61(4):e78–e140. PMID: 23256914.

Left Bundle Branch Block Basics
- LBBB’s cause ST-segment & T wave changes that can make the identification of acute MI difficult
- Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
- ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal
- Suspected ACS and new or old LBBB with hemodynamic/electrical instability or acute heart failure should go to the cath lab emergentlyReferenceNeeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96–105. PMID: 22766335.

Sgarbossa Criteria
- Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
- Meeting the criteria in a single lead can be specific for AMI
- The criteria are reviewed below

Concordant STE ≥ 1mm (in any lead) = Most specific for MI

Concordant STD ≥ 1mm in V1, V2, or V3 = Specific for MI

Discordant STE ≥ 5mm = Less specific for MI

A revised Sgarbossa C rule has been proposed (not yet validated) to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥5 mm) with a proportional criterion (ST-segment to S-wave ratio ≤-0.25). This is consistent with the electrophysiological principle that repolarization voltages should be proportional to depolarization voltages.
- References:
- Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.
- Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal. 2013;166(3):409–413. PMID: 24016487.
- Kontos MC, Aziz HA, Chau VQ, et al. Outcomes in patients with chronicity of left bundle-branch block with possible acute myocardial infarction. American Heart Journal 2011;161(4):698–704. PMID: 21473968.
- Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol 2011;107(8):1111–6. PMID: 21296327.
- Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27(8):916–21. PMID: 19857407.

Class I Indications

Classic STEMI – Use the J-point to determine the magnitude of ST-segment elevation relative to the isoelectric TP segment.
- J-point elevation in 2 contiguous leads > 1 mm is required in all leads (except V₂/V₃)
- Leads V₂ and V₃limits are age and sex dependent
  1. In males < 40 years old, J-point elevation of as much as 2.5 mm in V₂ and V₃ can be a normal finding, but decreases with age
    - Cutoff = ≥ 2.5 mm in V₂ and V₃in men < 40 years
  2. In males ≥ 40 years old, J-point elevation as much as 2 mm in V₂ and V₃ can be a normal finding
    - Cutoff = ≥ 2 mm in V₂ and V₃in men ≥ 40 years
  3. J-point elevation in women is less than in men, elevation as much as 1.5 mm in V₂ and V₃ can be a normal finding.
  4. Cutoff = ≥ 1.5 mm in V₂ and V₃in women
    
    Pearl: Lesser degrees of ST displacement DO NOT exclude ischemia or evolving MI. A single ECG may miss dynamic changes, so do serial ECGs when in doubt!Reference:Thygesen K, Alpert JS, Jaffe AS, et al. Third Universal Definition of Myocardial Infarction. J Am Coll Cardiol 2012;60(16):1581–98. PMID: 22958960
Posterior STEMI (“inferolateral”) – the most common type of missed STEMI!
- 4-10% of STEMI’s are isolated Posterior MI’s
- Often misdiagnosed as just ischemia or NSTEMI
- Only 30% are revascularized within 90 mins
- Usually associated with inferior or lateral MI due to RCA or circumflex occlusion
- Pearl: Even 0.5 mm of STE on posterior lead ECGs is diagnosticDifferential for ST-depression in anteroseptal leads
- Posterior STEMI
  - Mirror image of septal STEMI in leads V₁-V₃
  - Large R waves (instead of Q waves)
  - ST-depression (instead of STE)
  - Upright T waves in V₁-V₃ (instead of inversions)
- Anteroseptal ischemia
- Miscellaneous
  1. RBBB
  2. Hypokalemia, etc
    
    References:Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes among patients with an isolated posterior myocardial infarction: insights from the National Cardiovascular Data Registry (NCDR). American Heart Journal 2014;167(3):350–4. PMID: 24576519Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. Journal of Electrocardiology 2014;47(4):448–58. PMID: 24792903.Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among patients with acute myocardial infarction. Journal of Electrocardiology 2013;46(6):653–9. PMID: 23890685.Waldo SW, Armstrong EJ, Kulkarni A, et al. Clinical characteristics and reperfusion times among patients with an isolated posterior myocardial infarction. J Invasive Cardiol 2013;25(8):371-5. PMID: 23913600.

Post-arrest STEMI/NSTEMI
- STEMI patients post-arrest should go to the cath lab (Class IB in national guidelines)
- STEMI patients post-arrest who remain comatose should go to the cath lab unless they have multiple unfavorable resuscitation features (Rab T, et al.)
- NSTE-ACS patients post-arrest who remain comatose should be assessed for unfavorable resuscitation features. Immediate consultation with cardiology and intensive care is recommended (Rab T, et al.)References:O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. JAC 2013;61(4):e78–e140. PMID: 23256914.Rab T, Kern KB, Tamis-Holland JE, et al. Cardiac Arrest: A Treatment Algorithm for Emergent Invasive Cardiac Procedures in the Resuscitated Comatose Patient. J Am Coll Cardiol 2015;66(1):62–73. PMID: 26139060.

4. Non-STE ACS (Class IA in national guidelines)

Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that develop hemodynamic or electrical instability (VT or VF arrest)
Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that have intractable ischemia
Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that develop acute decompensating heart failureReference:Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64(24):e139–228. PMID: 25260718.

Key Teaching Points

- Atrial fibrillation is commonly misdiagnosed
- Atrial fibrillation should cause an irregularly irregular rhythm
- Lead II is not 100% reliable for P-waves, look at all 12 leads and make sure to scrutinize lead V1 (closest to the sinus node) for P-waves
- If the rhythm is regularly irregular and you have grouped or “clumped” beats, consider PAC’s and second degree AV blocks (Mobitz I and Mobitz II)

Take-home points:

Both physicians and ECG machines tend to over-call atrial fibrillation. This leads to patients being anticoagulated inappropriately and can cause bad outcomes! If the rhythm is regularly irregular it is not atrial fibrillation, consider PAC’s and 2^nd degree AV blocks.

Key Teaching Points

Subtle early signs of ischemia

Reciprocal changes (e.g. aVL, V₂)
“Checkmark sign”
- QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
Hyperacute T-waves
- Straightening of the upslope of the T-waves
- Excessively large T-waves (especially when larger than QRS)
New upright T-wave in V₁ (loss of precordial T-wave balance)

Take-home Points:

Don’t settle for a single ECG when patients have ongoing or changing concerning pain!
Serial ECGs can save lives!

Key Teaching Points

Differential for Prolonged QT-Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
Medications/Drugs (Na⁺ channel blockers, methadone, & many others)
Elevated intracranial pressures
ACS / cardiac ischemia
Congenital

ECG findings in severe hypokalemia

U-waves (can be very large, lead to “camel hump T-waves”)
Prolonged QTc interval (due to T wave/U wave fusion)
Flattened/inverted T waves, ST-segment downsloping/depression
Biphasic T-waves that deflect down before going up “reverse Wellens’ waves” a.k.a. “NikEleKam T waves”
ST-segment elevation in aVR
PVC’s, ventricular dysrhythmias
Pseudo-ischemic patterns

Key Teaching Points

Ashman Phenomenon

Aberrantly conducted beats usually seen in atrial fibrillation that are often mistaken for ventricular tachycardia and PVCs
- This aberrant ventricular conduction is due a change in heart rate and QRS cycle length (follows a long-short cycle)
- Refractory period of the ventricle is related to the heart rate and the duration of the preceding R-R interval
- When the atrial impulse arrives during the refractory period it causes aberrant conduction
- Typically conducted in a RBBB morphology (right bundle branch has a longer refractory period than the left)
- Benign condition, important to differentiate from non-sustained ventricular tachycardia & PVC’s
- Treatment: rate control and treatment of the underlying condition

Takehome Points

Ashman phenomenon
- Aberrant ventricular conduction that follows a long-short cycle in atrial fibrillation and other atrial tachycardias
- Often occurs in groups and is commonly mistaken for non-sustained ventricular tachycardia or PVC’s
- Typically conducted in a RBBB morphology (right bundle branch has a longer refractory period than the left)
- Benign ECG manifestation of the underlying condition

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take-home points

Hyperkalemia frequently mimics ventricular tachycardia
Ventricular tachycardia should have a heart rate > 120-130 bpm
Ventricular tachycardia QRS is usually < 200 ms
Too slow or too wide? Consider tox or metabolic causes and consider empiric treatment with Ca²⁺and/or bicarb
Any dysrhythmia in a patient with ESRD is related to K⁺until proven otherwise
- If patient just completed HD, think hypokalemia
- All others, think hyperkalemia

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take-home points

Hyperkalemia can do just about anything it wants to the ECG!

Key Teaching Points

ECG findings in Pericarditis vs. STEMI

Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that stronglysuggest STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
Horizontal or convex upward ST-segment morphology
STE in lead III > the STE in lead II
Q-waves that youknow are new (be cautious it they are old)
R-T sign or “checkmark sign”

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis (only after step 1):

Pronounced PR-segment depression in multiple leads
Friction rub

When in doubt…do serial ECGs and consider CATH!

Key Teaching Points

Take-home Points

A normal ECG (or two) does not rule out ACS
A normal troponin (or two) does not rule out ACS
If troponin is rising, get another one!
Troponin negative ACS still exists!
ACS is diagnosed on history, ECG, and troponin (not just troponin)

Chest pain + (vomiting, radiation of pain, diaphoresis, or exertional worsening) is predictive of ACS

Key Teaching Points

If you did not see the Brugada Syndrome Part I, please review the March 26, 2018 case

The Brugada Syndrome Part II

Genetic condition associated with arrhythmia and sudden cardiac death
Generally considered a hereditary disease
Described in 1992 by Pedro and Josep Brugada
- Initially described in 1988 by Nava, with the first complete description in 1989 by Martini, Nava, et al. (PMID: 2589161)
Individuals thought to be usually healthy with structurally normal hearts
- Increasing literature demonstrates that there may actually be structural abnormalities that are technically difficult to diagnose
First onset of symptoms (VT, VF, syncope, sudden death) ~ 40 yo.
- 41 ± 15 years on average for VF episodes
- Arrhythmias reported from 2-84 years
- A reported cause of SIDS or sudden cardiac death in young children
Mortality ~ 10% per year if not treated with internal cardioverter-defibrillator (ICD)
- New data showing VF episodes and mortality rates are probably lower, mainly with Type I (coved) patterns
- Antidysrhythmic medications have no effect on prognosis
Arrhythmic events happen at rest or sleep (esp. 12am-6am)
Vagal tone and fever increase VF episodes
Atrial fibrillation can occur (11-14%), SVT less commonly

The Brugada Pattern: ECG findings

V1 & V2
- RBBB or IRBBB pattern
- ST-segment elevation – 2 types
  - “Coved-type” (most common)
  - “Saddle-type”
- Moving the V1-V2 leads one interspace higher may increase the abnormality
- ECG findings can come and go
  - More commonly present around the time of the arrhythmia
  - Fever/hot ambient temperature can bring out the ECG findings

The Brugada Syndrome: Diagnosis

Diagnosis requires 2 parts (ECG findings + clinical findings)
- Typical ECG abnormalities reviewed above (esp. coved type)
- Clinical characteristics, 1 of the following:
  - History of VT/VF
  - FHx of sudden cardiac death
  - FHx of coved-type ECG
  - Agonal respirations during sleep
  - Inducible VT/VF during EP study

Take-home points:

Consider Brugada syndrome in any patient presenting after syncope
ECG: (I)RBBB + STE in V1-V2 (coved STE most concerning)
Discuss/refer to electrophysiologist
Remember that fever and sodium channel blockers can bring out the Brugada pattern

References

Martini B, Nava A, Thiene G, et al. Ventricular fibrillation without apparent heart disease: description of six cases. Am Heart J. 1989 Dec;118(6):1203-9. PMID: 2589161.

Key Teaching Points

Subtle early signs of ischemia

Hyperacute T-waves
- Straightening of the upslope of the T-waves
- Excessively large T-waves (especially when larger than QRS)
- Beware of T-waves that are larger than the entire QRS complex
Reciprocal changes (e.g. aVL, V₂)
“Checkmark sign”
- QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
New upright T-wave in V₁(loss of precordial T-wave balance)

Riley, et al. Am Heart J 2013. PMID: 23237133

41,560 patients from a STEMI database
- 36,994 patients had initial ECG with STEMI
- 4566 patients (11%) were diagnosed with STEMI on follow-up ECG (initial ECG was non-diagnostic)
  - 72% had STEMI in ECG within 90 mins
- No difference in characteristics between groups

Millard, et al. Ann Noninvasive Electrocardiol 2017. PMID: 28044391

334 patients diagnosed with STEMI
- 85% diagnosed in first ECG
- 15% were diagnosed on subsequent ECG
- Prior literature: up to 20% of STEMI’s are diagnosed on a repeat ECG

Take-home points:

Get serial ECG’s in suspected ACS!

For persistent ischemic signs and symptoms
When the pain or status of the patient changes
Guidelines recommend every 15-30 mins
STEMI doesn’t always “show itself” on the first ECG

Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. American Heart Journal 2013;165(1):50–6. PMID: 23237133
Millard MA, Nagarajan V, Kohan LC, et al. Initial electrocardiogram as determinant of hospital course in ST elevation myocardial infarction. Ann Noninvasive Electrocardiol 2017;22(4). PMID: 28044391

Key Teaching Points

Left Bundle Branch Block

LBBB causes ST-segment & T wave changes that can make the identification of acute MI more challenging
Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex.This is normal & referred to as the “Rule of Appropriate Discordance”
ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal

Sgarbossa Criteria

Sgarbossa and now the modified Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
Meeting the criteria in a single lead can be specific for AMI
The criteria are reviewed below
A revised Sgarbossa C rule has been proposed to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥ 5 mm) with a proportional criterion (ST-segment to S-wave ratio ≥ 25%) and has been found to be superior to the original criteria for identifying acute coronary occlusion in LBBB.

Take-home Points:

LBBB does not obviate the ability to diagnose acute coronary occlusion
- Sgarbossa criteria A, B, and revised C are very specific
- Increasing literature supports these as “STEMI equivalents” including the recent ESC guidelines published in 2017

References:

Sgarbossa EB, Pinski SL, Barbagelata A, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. GUSTO-1 (Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries) Investigators. N Engl J Med 1996;334(8):481–7.PMID: 8559200.
Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013;166(3):409–413. PMID: 24016487.
Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.
Mayers H, Limakakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170:1255-1264. PMID:26678648.
Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2017;39(2):119–77.PMID: 28886621.

Key Teaching Points

ST-segment elevation in aVR with ST-segment depression in multiple other leads

Reflects global subendocardial ischemia of the left ventricle, often associated with proximal lesions or multi-vessel disease
Patients are actively having symptoms and typically look sick
STE in aVR (>1-1.5 mm) differential diagnosis
- Sick ACS patients
  - LMCA stenosis
  - Proximal LAD
  - Triple vessel disease
- Any cause of severe generalized global ischemia (non-ACS sick patients)
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Massive PE, etc.
  - Na⁺channel blocker toxicity
  - Hyperkalemia, hypokalemia
- Normal variants
  - SVT’s, rapid atrial fibrillation
  - LBBB
  - LVH with strain pattern (severe HTN)

References:

Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2017;39(2):119–77.PMID: 28886621
Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol2018;72(18):2231–64.PMID: 30153967

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Reference:

Durfey N, et al. Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events? WJEM 2017. PMID:28874951

188 patients with K⁺≥ 6.5 mEq/L
15% developed adverse effects within 6 hours (e.g. symptomatic dysrhythmia, arrest, death)
Correlated short term adverse events with presenting ECG findings
100% of short-term adverse events were preceded by ECG abnormalities…but abnormal or peaked T-waves did not correlate!
Highest correlation with
- Bradycardia (HR < 50) – RR 12.29
- Junctional rhythm – RR 7.46
- Widened QRS (> 100 ms) – RR 4.74

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement (tip: lead aVR and V6 should have different QRS vectors)/ Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Take-home Points:

In patients with symptoms of an acute coronary syndrome, ST depression in multiple leads + ST elevation in aVR is concerning for left main coronary artery occlusion vs. triple vessel disease vs. proximal LAD occlusion
Hyperkalemia often produces bradycardia, and T-waves alone are not reliable in prediction of short-term adverse events
When the QRS vector in V6 and aVR are in the same direction, think of lead misplacement

Key Teaching Points

Take-home Points:

S1Q3T3 is not sensitive or specific for pulmonary embolism
V1 is the best lead to look for atrial activity and diagnose rhythm abnormalities
“Checkmark sign”- QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology, concerning for ACS
Narrow complex regular tachycardia differential
- Sinus tachycardia
- SVT (ST depression and rate related changes do not correlate with CAD)
- Atrial flutter (always consider when rate is 150 ±20)

Rapid atrial tachydysrhythmias often produce ST segment elevation in aVR but do not correlate with CAD

Key Teaching Points

Lewis Lead

First described by Sir Thomas Lewis in 1931
Also called the “S5 lead”
Modified ECG lead used to augment the analysis of atrial activity when it is not obvious on standard ECG
- Move the right arm electrode to the manubrium (below suprasternal notch)
- Move left arm electrode to the right fifth intracostal space next to the sternum
- Move the left leg electrode to the right lower costal margin
- Lewis lead is then read on lead I (but look everywhere for atrial activity!)

Take-home Points:

V1 is the best lead to look for atrial activity and diagnose rhythm abnormalities
When uncertain about atrial activity, obtain a “Lewis Lead”
- Especially useful when deciding between ventricular tachycardia vs. SVT or atrial flutter with aberrant conduction

Key Teaching Points

Brugada syndrome

Hereditary sodium channelopathy associated with arrhythmia and sudden cardiac death
First onset of symptoms (VT, VF, syncope, sudden death) ~ 40 Y.O.
- 41±15 years on average for VF episodes
- Arrhythmias reported from 2-84 years
- A reported cause of SIDS or sudden cardiac death in young children
Mortality ~ 10% per year if not treated with internal cardioverter-defibrillator (ICD)
- New data showing VF episodes and mortality rates are probably lower, mainly with Type I (coved) patterns
- Antidysrhythmic medications have no effect on prognosis
Vagal tone and fever increase VF episodes

The Brugada Pattern: ECG findings

V₁& V₂
- RBBB or IRBBB pattern
- ST-segment elevation – 2 types

“Coved-type” (most common)
“Saddle-type”

Moving the V1-V2 leads one interspace higher may increase the abnormality
ECG findings can come and go
- More commonly present around the time of the arrhythmia
- Fever/hot ambient temperature can bring out the ECG findings

The Brugada Syndrome: Diagnosis

Diagnosis requires 2 parts (ECG findings + clinical findings)
1. Typical ECG abnormalities reviewed above (esp. coved type)
2. Clinical characteristics, 1 of the following:
  - History of VT/VF
  - FHx of sudden cardiac death
  - FHx of coved-type ECG
  - Agonal respirations during sleep
  - Inducible VT/VF during EP study

Take-home Points:

Be thorough in evaluating an ECG
- Look closely at all 12 leads!
- Sometimes the answer is in the “quiet” complexes
- If there are different morphologies on the ECG, look at all of the morphologies!
- Don’t give sodium channel blockers to patients with Brugada syndrome (or hyperkalemia). Typical sodium channel blockers (lidocaine, amiodarone, procainamide) could be dangerous!

Key Teaching Points

T-waves should end before the midpoint of the R-R interval.
Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance.

Differential for Prolonged QT (Greatest concern when QTc > 500ms)

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Medications (many, including methadone)
Congenital

ECG Findings in Severe Hypokalemia

Prolonged QTc interval (due to T-U wave fusion)
U-waves (can be very large, “camel hump T-waves”)
Flattening of T waves then ST segment down-sloping/depression
“Nikelekam T waves”, also known as “reverse Wellens’ waves”
ST segment elevation in aVR
PVC’s, ventricular dysrhythmias
Pseudo-ischemic patterns

Take-home points:

Triad of long QT interval, PVC’s, & ST segment depression is concerning for hypokalemia
The biphasic T waves associated with hypokalemia go down first then up, as opposed to Wellens’ waves associated with ACS

Key Teaching Points

Pericardial effusion

Classic teaching

- Electrical alternans
  - Present in <30% of patients
- Tachycardia
  - May be blunted in patients taking cardiac medications
- Low voltage
- Cardiomegaly in CXR
  - Sensitive but not specific

Low Voltage Definition

Sensitive Definition
- QRS amplitudes in leads I+II+III < 15 mm
- Or QRS amplitudes in leads V₁+V₂+V₃ < 30 mm
Specific Definition
- QRS amplitudes in limb leads all < 5 mm
- Or QRS amplitude in all precordial leads < 10 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloidosis, Sarcoidosis, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Take home Points

Always consider pericardial effusions in patients with low voltage and tachycardia
Electrical alternans is “classic” …so don’t rely on it!
Avoid anticoagulants until pericardial effusion is ruled out
Low QRS Voltage DDx
- Conduction blockage: pericardial/pleural effusion, COPD, obesity
- Low power: Severe hypothyroidism, infiltrative disease, severe cardiomyopathy

Key Teaching Points

Differential for Non-conducted P-waves (P:QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes
- P-waves are irregular, the non-conducted P-waves come early
Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Fascicular Block Definitions

Left anterior fascicular block (LAFB)

Leftward axis
qR in I and aVL
rS in III
QRS may be normal or slightly prolonged
Poor R-wave progression is common
No other clear reasons for leftward axis

Left posterior fascicular block (LPFB)

Rightward axis
rS in I and aVL
qR in III
QRS may be normal or slightly prolonged
Rarely a normal variant
- Left posterior fascicle receives blood supply from both left and right coronary arteries
- Almost always occurs in presence of CAD: if acute MI, there is usually multivessel disease, extensive infarct and poor prognosis
No other clear reasons for rightward axis

Bifascicular Block

Conduction abnormality where two of the three main fascicles of the His/Purkinje system are blocked
- Usually a RBBB + LAFB
- Or RBBB + LPFB

Trifascicular Block

Any AV Block (especially 2^nd degree or 3^rd degree) + RBBB + LAFB
Or any AV block (especially 2^nd degree or 3^rd degree) + RBBB + LPFB
Or any AV block (especially 2^nd degree or 3^rd degree) + LBBB

Take Home Points:

When you see electrocardiographic polyuria…map out the P-waves and look closely at the PR-interval

Blocked PAC’s = P-waves irregular, non-conducted P-wave comes early
Mobitz I = P-waves are regular, PR-interval increasing before dropped beat
Mobitz II = P-waves regular, some fail to conduct without PR-interval lengthening
AVD, 3^rd degree AVB = P-waves regular, PR-interval randomly changing
The answer lies in the PR-interval!

Key Teaching Points

Differential for Non-conducted P-waves (P:QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes
- P-waves are irregular, the non-conducted P-waves come early
Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Narrow vs. wide complex QRS in setting of complete heart block

Narrow complexes usually are junctional escape rhythms and generally have a better prognosis when compared to wide complex QRS rhythms
Wide complexes usually are ventricular escape rhythms and generally have a worse prognosis when compared to narrow complex QRS rhythms

Take Home Points:

When you see electrocardiographic polyuria…map out the P-waves and look closely at the PR-interval

Blocked PAC’s = P-waves irregular, non-conducted P-wave comes early
Mobitz I = P-waves are regular, PR-interval increasing before dropped beat
Mobitz II = P-waves regular, some fail to conduct without PR-interval lengthening
AVD, 3^rd degree AVB = P-waves regular, PR-interval randomly changing
The answer lies in the PR-interval!

Key Teaching Points

Case 1 Pearls

Clues to RV Infarction on the 12-lead ECG

In the presence of an inferior STEMI…
- ST-segment depression in lead V2 with
  - ST-segment elevation in lead V1 OR
  - Isoelectric ST-segment in lead V1
- STE in lead III >>> II
- When in doubt, just get right-sided leads!
1/3 of inferior STEMI’s will extend to the right ventricle
- These patients will be very preload dependent
- Preload reducing meds (like nitroglycerin) can cause significant hypotension and should be avoided
- If the lung are clear, treat with IVF and not vasopressors

Case 2 Pearls

Left Bundle Branch Block

LBBB causes ST-segment & T wave changes that can make the identification of acute MI more challenging
Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal

Sgarbossa Criteria

Sgarbossa and now the modified Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
Meeting the criteria in a single lead can be specific for AMI
The criteria are reviewed below

A revised Sgarbossa C rule has been proposed (recently validated) to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥ 5 mm) with a proportional criterion (ST-segment to S-wave ratio ≥ 25%) and has been found to be superior to the original criteria for identifying acute coronary occlusion in LBBB.

Case 3 Pearls

When the history and physical exam do not suggest a diagnosis, always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy (HCM)
Brugada syndrome
Arrhythmogenic RV dysplasia

Case 4 Pearls

New T-wave inversion in aVL may be a reciprocal change

Reciprocal changes can precede ST-elevation (STE) in MI
New TWI in aVL can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Key Teaching Points

The 3 Causes of Narrow-Complex & Regular Tachycardia

Sinus Tachycardia

One P-wave for every QRS
Upright P-waves in limb leads (I, II, III, aVF), & inverted P-wave in aVR
Maximum sinus node rate is ~ (220 bpm – age)

Supraventricular Tachycardia (SVT)

No distinct P-waves. May be hidden or may follow the QRS complex (“retrograde atrial activity”)
Different types (AV Nodal re-entry, Non-paroxysmal junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment depression that is typically benign if it resolves when sinus rhythm is restored
Beware of STEMI when there is ST-segment elevation is SVT (except in aVR, normal variant)
SVT can also cause electrical alternans that disappears when sinus rhythm is restored

Atrial flutter with 2:1 Conduction

2 atrial beats for every QRS
Saw tooth pattern, flipping the ECG upside down and paying attention to all 12 leads will help you identify subtle flutter waves
Most commonly missed atrial tachycardia
Always consider when rate is 150 +/- 20 bpm

To differentiate…always look at what the atrium is doing

(V1 typically best lead to look for atrial activity)

Some causes of ST-elevation in aVR (“global cardiac ischemia”)

Left main coronary artery insufficiency
Proximal left anterior descending artery insufficiency
Triple vessel disease
Supraventricular Tachycardia
Left bundle branch block (LBBB)
LVH and severe hypertension
Hypokalemia
Hyperkalemia
Severe anemia
Thoracic aortic dissection
Large pulmonary embolism

Case 2 Pearl

Differential for Non-conducted P-waves (P:QRS > 1)

Blocked Premature Atrial Complexes
- P-waves are irregular, non-conducted P-waves come early
2^nd degree AV Block: Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
2^nd degree AV Block: Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Case 3 Pearl

Characteristics of a normal sinus rhythm

Regular rhythm at rate of 60-100 bpm in adults
Only one normal P-wave for each QRS complex
Normal P-wave axis: upright P-waves in leads I, II, III, & aVF, inverted in aVR
PR-interval remains constant

Key Teaching Points

Causes of Widening of the QRS-complex

Bundle branch blocks (LBBB or RBBB)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)
Paced beats
Pre-excitation (e.g. WPW)
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Ventricular ectopy

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults

Na⁺channel blocker toxicity

Tachycardia
Tall R wave in aVR
Rightward axis
QRS-interval widening

Take Home Points:

When interpreting ECG’s…
- Use a systematic step-by-step approach
- Know your differential diagnosis!
Right axis deviation + wide-complex QRS + Prolonged QTc = Think about Na⁺channel blocker toxicity!
Ventricular tachycardia has rates > 120 bpm. Consider toxicological and metabolic causes when dealing with a wide complex tachycardia with rates < 120 bpm
Wide complex tachycardia: When in doubt about a diagnosis, consider empiric treatment of hyperkalemia & Na⁺ channel blocker toxicity with sodium bicarbonate and calcium

Key Teaching Points

Differential diagnosis for regular wide complex tachycardia (RWCT)

Ventricular Tachycardia (VT)
- Rate usually > 120-130 bpm, and not too wide (QRS < 200 ms)
SVT with aberrant conduction
- No clear P-waves, consider VT
Sinus Tachycardia with aberrant conduction (e.g. BBB, WPW)
- Look carefully for P-QRS complexes in all leads
Massive STEMI
- Look carefully for P-QRS complexes, confirm that QRS is wide in all leads
- Rightward axis weighs against STEMI
Hyperkalemia
- Look carefully for P-QRS complexes, often really wide (QRS > 200 ms)
- May have Brugada patterns in aVR and V₁
Sinus tachycardia with Na⁺channel blocker toxicity
- Look carefully for P-QRS complexes, often really wide (QRS > 200 ms)
- May have Brugada patterns in aVR and V₁

Differential diagnosis for regular really wide complex tachycardia (RRWCT)

Regular really wide QRS complexes > 200 ms = RRWCT
Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause RRWCT’s that mimic Ventricular Tachycardia
Lidocaine, amiodarone, and procainamide all have Na⁺ channel blocking properties and can worsen toxicities
Consider empiric treatment with calcium and bicarb before antiarrhythmics which can kill these patients!

Take Home Points:

Hyperkalemia is the great imitator. It does what it wants to the ECG!
Don’t trust your ECG machine or monitor interpretation. It will fool you!
Always consider hyperkalemia and Na⁺ channel blocker toxicity in your differential for RRWCT and consider empiric treatment with calcium and bicarb

Key Teaching Points

Differential Diagnosis for Prolonged QTc Interval

Elevated intracranial pressure
- “Rollercoaster T-waves” a.k.a. “Cerebral T-waves”
  - Giant, wide based, deeply inverted T-waves
- Can present with dysrhythmias (fast or slow)
- Typically produce ST-segment abnormalities
Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (TCA’s/Na⁺channel blockers, & many others)
Hypothermia
ACS / cardiac ischemia
Congenital

Differential Diagnosis for T-wave inversions

Coronary artery disease (Wellens, ischemia, reperfusion)
Neurological causes (elevated intracranial pressure)
Pulmonary causes (PE, pneumothorax, pulmonary hypertension, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia (V₁-V₃)
Brugada syndrome (V₁-V₂)
Wide QRS complexes (BBB’s. PVC’s, Paced rhythms, WPW)
High left ventricular voltage, LVH with strain pattern
Pericarditis, myocarditis
Hyperkalemia
Normal finding in V₁, aVR, and lead III

Key Teaching Points

New T-wave inversion or ST-segment down sloping in aVL may be an early reciprocal change that precedes inferior STEMI

Reciprocal changes can precede ST-elevation (STE) in MI
ST-segment down sloping in aVL and straightening of the ST-segment in the inferior leads can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Key Teaching Points

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take home points:

Hypercalcemia can mimic STEMI by shortening the QT-interval
DDx of short QTc
1. Hypercalcemia
2. Digoxin
3. Congenital short QT syndrome

References

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838
Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Key Teaching Points

2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes (Class IA)

An urgent/immediate invasive strategy (within 2 hours) is indicated for non-STE-ACS patients that:

have refractory angina
develop hemodynamic or electrical instability
develop acute decompensating heart failure

Take-home Points:

The ECG is not perfect for detecting acute coronary occlusions and need for emergent cath lab activation. ST-elevation is not always present and symptoms concerning for ongoing ischemia matter!
If initial ECG in not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs (15-30 min intervals during the first hour) should be performed to detect ischemic changes
It is reasonable to get supplemental leads (right sided and posterior leads) in patients whose initial ECG is not diagnostic and suspicion for ACS is high
Immediate invasive strategies are indicated for non-STE ACS patients that have refractory ischemia, develop hemodynamic or electrical instability, or develop acute decompensating heart failure

Reference:

Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64(24):e139–228. PMID: 25260718.

Key Teaching Points

Take-home Points:

Hyperacute T-waves are early ECG signs of cardiac ischemia and may precede ST-segment elevation or Q waves
Beware of hyperacute T-waves
- T-waves that are too large (compared to the size of the QRS complex)
- T-waves that are too straight (e.g. “R-T sign” or lack of ST-segment, R-wave shoots straight into the T-wave)
- When you notice early markers of cardiac ischemia or non-specific ECG abnormalities in patients who you are concerned for ACS…get serial ECG’s!

Key Teaching Points

New T-wave inversion or ST-segment down sloping in aVL may be an early reciprocal change that precedes inferior STEMI

Reciprocal changes can precede ST-elevation (STE) in MI
ST-segment down sloping in aVL and straightening of the ST-segment in the inferior leads can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Key Teaching Points

Post-syncope ECG

When the history and physical exam do not suggest a diagnosis, always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy (HCM)
Brugada pattern
Arrhythmogenic RV dysplasia

Differential Diagnosis for T-wave inversions

Coronary artery disease (Wellens, ischemia, reperfusion)
Neurological causes (elevated intracranial pressure)
Pulmonary causes (PE, pneumothorax, pulmonary hypertension, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Wide QRS complexes (BBB’s. PVC’s, Paced rhythms, WPW)
High left ventricular voltage, LVH with strain pattern
Pericarditis, myocarditis
Hyperkalemia
Normal finding in V₁, aVR, and lead III

Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Inherited progressive cardiomyopathy characterized by ventricular arrhythmias and increased risk of sudden cardiac death, especially in young individuals and athletes
Not common, but increased prevalence in certain populations/regions

- General population; 1/1,000-1/10,000
- Italy 40/10,000: Most common cause of sudden cardiac death in young population
Familial
- Autosomal dominant trait with variable penetrance
  - 50% chance of inheriting the gene defect
  - Men > Woman
Pathogenesis
- Progressive replacement of the RV myocardium by fibrofatty tissue
- Causes interference with electrical impulse conduction
- CAN also occur in LV posterolateral subepicardium, RV more common
Clinical
- Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  - 22% of cases of SCD among athletes in N. Italy
  - 4% of cases of SCD in US (HCM #1)
- Often have family history of premature sudden death in family members < 35 years of age
- Usually manifests in patients between second to fifth decades of life
- Symptoms included palpitations, lightheadedness, syncope, and sudden death
Diagnosis
- ECG (imperfect)
  - Leads V1-V3
    - Epsilon waves (most specific, but seen in < 1/3 of patients)
    - TWIs (most sensitive, seen in > 80% of patients)
    - Slight prolongation of QRS
  - LBBB type VT (~90%) or PVCs (many)
- ECHO
- MRI
- MDCT
- Endomyocardial biopsy
Management
- Send to electrophysiologist
- Active ventricular dysrhythmias
  - Stable: beta blockers, Class III antiarrhythmics
  - ICD placement for patients with cardiac arrest, syncope, VT

Take home Points

When history and physical exam do not give you a diagnosis in syncope, don’t forget the no-brainers (dysrhythmias), interval abnormalities (i.e. WPW, prolonged QT) and genetic causes (HCM, Brugada, ARVC)!
Arrhythmogenic right ventricular dysplasia/cardiomyopathy: Have heightened concern if…
Young patients, especially males
Family history of early sudden death
Many PVC’s
LBBB-type Ventricular Tachycardia
Epsilon waves with TWI’s in V₁-V₃

References:

Basso C, Corrado D, Marcus FI, Nava A, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet 2009;373(9671):1289–300.PMID: 19362677
Orgeron GM, Crosson JE. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Cardiol Young 2017;27(S1):S57–S61. PMID: 28084951
Diez D, Brugada J. Diagnosis and Management of Arrhythmogenic Right Ventricular Dysplasia: An article from the E-Journal of the ESC Council for Cardiology Practice, European Society of Cardiology 2008 [Full text].

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take home Points

~ 2% of ED patients have cardiac arrest post-intubation
Regular wide complex tachycardia (RWCT) after succinylcholine? Assume hyperkalemia until proven otherwise
RWCT with ventricular rate <120-130 bpm, or a regular really wide complex tachycardia (RRWCT)? Assume hyperkalemia until proven otherwise
Beware of succinylcholine and hyperkalemia in patients with motor neuron disease and treat empirically with calcium and bicarb!

References:

Martyn JAJ, Richtsfeld M. Succinylcholine-induced hyperkalemia in acquired pathologic states: etiologic factors and molecular mechanisms. Anesthesiology 2006;104(1):158–69. PMID: 16394702

Key Teaching Points

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Intracranial hemorrhage (ICH) & cardiac arrest

ICH can cause cardiac arrest
PEA and asystole are the most common initial rhythms and VFib arrest is rare
History of headaches that preceded arrest is helpful
Have a low threshold for CT brain before cath lab activation (and anticoagulation) when suspected
ICH causes several ECG abnormalities
- Giant, wide based, deeply inverted T-waves
- “Rollercoaster T-waves” a.k.a. “Cerebral T-waves”
- Prolonged QT intervals
- Dysrhythmias (fast or slow)
- ST-segment abnormalities
- Premature ventricular contractions

Take home Points

Consider intracranial hemorrhage in patients with cardiac arrest, especially with:
- History of recent headaches
- PEA or asystole as the initial rhythm
Intracranial hemorrhage can produce several different ECG abnormalities, especially ischemic findings
- Always obtain a thorough and complete history!

References:

Chatterjee S. ECG Changes in Subarachnoid Haemorrhage: A Synopsis. Neth Heart J 2011;19(1):31–4. PMID: 22020856
Hubner P, Meron G, Kürkciyan I, et al. Neurologic causes of cardiac arrest and outcomes. Journal of Emergency Medicine 2014;47(6):660–7. PMID: 25304078

Key Teaching Points

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take home points:

Hypercalcemia can mimic STEMI by shortening the QT-interval
DDx of short QTc
1. Hypercalcemia
2. Digoxin
3. Congenital short QT syndrome

References

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838
Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Key Teaching Points

2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes (Class IA)

An urgent/immediate invasive strategy (within 2 hours) is indicated for non-STE-ACS patients that:

have refractory angina
develop hemodynamic or electrical instability
develop acute decompensating heart failure

Take-home Points:

The ECG is not perfect for detecting acute coronary occlusions and need for emergent cath lab activation. ST-elevation is not always present and symptoms concerning for ongoing ischemia matter!
If initial ECG in not diagnostic but the patient remains symptomatic and there is high clinical suspicion for ACS, serial ECGs (15-30 min intervals during the first hour) should be performed to detect ischemic changes
It is reasonable to get supplemental leads (right sided and posterior leads) in patients whose initial ECG is not diagnostic and suspicion for ACS is high
Immediate invasive strategies are indicated for non-STE ACS patients that have refractory ischemia, develop hemodynamic or electrical instability, or develop acute decompensating heart failure

Reference:

Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64(24):e139–228. PMID: 25260718.

Key Teaching Points

Take-home Points:

Hyperacute T-waves are early ECG signs of cardiac ischemia and may precede ST-segment elevation or Q waves
Beware of hyperacute T-waves
- T-waves that are too large (compared to the size of the QRS complex)
- T-waves that are too straight (e.g. “R-T sign” or lack of ST-segment, R-wave shoots straight into the T-wave)
- When you notice early markers of cardiac ischemia or non-specific ECG abnormalities in patients who you are concerned for ACS…get serial ECG’s!

Key Teaching Points

New T-wave inversion or ST-segment down sloping in aVL may be an early reciprocal change that precedes inferior STEMI

Reciprocal changes can precede ST-elevation (STE) in MI
ST-segment down sloping in aVL and straightening of the ST-segment in the inferior leads can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Key Teaching Points

Post-syncope ECG

When the history and physical exam do not suggest a diagnosis, always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy (HCM)
Brugada pattern
Arrhythmogenic RV dysplasia

Differential Diagnosis for T-wave inversions

Coronary artery disease (Wellens, ischemia, reperfusion)
Neurological causes (elevated intracranial pressure)
Pulmonary causes (PE, pneumothorax, pulmonary hypertension, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Wide QRS complexes (BBB’s. PVC’s, Paced rhythms, WPW)
High left ventricular voltage, LVH with strain pattern
Pericarditis, myocarditis
Hyperkalemia
Normal finding in V₁, aVR, and lead III

Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy

Inherited progressive cardiomyopathy characterized by ventricular arrhythmias and increased risk of sudden cardiac death, especially in young individuals and athletes
Not common, but increased prevalence in certain populations/regions

- General population; 1/1,000-1/10,000
- Italy 40/10,000: Most common cause of sudden cardiac death in young population
Familial
- Autosomal dominant trait with variable penetrance
  - 50% chance of inheriting the gene defect
  - Men > Woman
Pathogenesis
- Progressive replacement of the RV myocardium by fibrofatty tissue
- Causes interference with electrical impulse conduction
- CAN also occur in LV posterolateral subepicardium, RV more common
Clinical
- Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  - 22% of cases of SCD among athletes in N. Italy
  - 4% of cases of SCD in US (HCM #1)
- Often have family history of premature sudden death in family members < 35 years of age
- Usually manifests in patients between second to fifth decades of life
- Symptoms included palpitations, lightheadedness, syncope, and sudden death
Diagnosis
- ECG (imperfect)
  - Leads V1-V3
    - Epsilon waves (most specific, but seen in < 1/3 of patients)
    - TWIs (most sensitive, seen in > 80% of patients)
    - Slight prolongation of QRS
  - LBBB type VT (~90%) or PVCs (many)
- ECHO
- MRI
- MDCT
- Endomyocardial biopsy
Management
- Send to electrophysiologist
- Active ventricular dysrhythmias
  - Stable: beta blockers, Class III antiarrhythmics
  - ICD placement for patients with cardiac arrest, syncope, VT

Take home Points

When history and physical exam do not give you a diagnosis in syncope, don’t forget the no-brainers (dysrhythmias), interval abnormalities (i.e. WPW, prolonged QT) and genetic causes (HCM, Brugada, ARVC)!
Arrhythmogenic right ventricular dysplasia/cardiomyopathy: Have heightened concern if…
Young patients, especially males
Family history of early sudden death
Many PVC’s
LBBB-type Ventricular Tachycardia
Epsilon waves with TWI’s in V₁-V₃

References:

Basso C, Corrado D, Marcus FI, Nava A, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet 2009;373(9671):1289–300.PMID: 19362677
Orgeron GM, Crosson JE. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Cardiol Young 2017;27(S1):S57–S61. PMID: 28084951
Diez D, Brugada J. Diagnosis and Management of Arrhythmogenic Right Ventricular Dysplasia: An article from the E-Journal of the ESC Council for Cardiology Practice, European Society of Cardiology 2008 [Full text].

Key Teaching Points

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Intracranial hemorrhage (ICH) & cardiac arrest

ICH can cause cardiac arrest
PEA and asystole are the most common initial rhythms and VFib arrest is rare
History of headaches that preceded arrest is helpful
Have a low threshold for CT brain before cath lab activation (and anticoagulation) when suspected
ICH causes several ECG abnormalities
- Giant, wide based, deeply inverted T-waves
- “Rollercoaster T-waves” a.k.a. “Cerebral T-waves”
- Prolonged QT intervals
- Dysrhythmias (fast or slow)
- ST-segment abnormalities
- Premature ventricular contractions

Take home Points

Consider intracranial hemorrhage in patients with cardiac arrest, especially with:
- History of recent headaches
- PEA or asystole as the initial rhythm
Intracranial hemorrhage can produce several different ECG abnormalities, especially ischemic findings
- Always obtain a thorough and complete history!

References:

Chatterjee S. ECG Changes in Subarachnoid Haemorrhage: A Synopsis. Neth Heart J 2011;19(1):31–4. PMID: 22020856
Hubner P, Meron G, Kürkciyan I, et al. Neurologic causes of cardiac arrest and outcomes. Journal of Emergency Medicine 2014;47(6):660–7. PMID: 25304078

Key Teaching Points

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Causes of Widening of the QRS-complex

Bundle branch blocks (LBBB or RBBB)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)
Paced beats
Pre-excitation (e.g. WPW)
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Ventricular ectopy

Take home Points

Wide complex tachycardia: ventricular tachycardia mimics

Ventricular tachycardia has a heart rate that is fast (usually > 120-130 bpm), and not too wide (QRS < 200 ms)
Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause regular really wide complex tachycardia (RRWCT = QRS > 200 ms) and mild tachycardia (HR < 120-130) that may mimic ventricular tachycardia
When in doubt about the diagnosis, consider empiric treatment with calcium and sodium bicarbonate before antiarrhythmics which can kill these patients!

Key Teaching Points

Differential for ST-segment elevation in aVR (with multilead ST-depression)

Acute coronary syndromes
- Left main coronary artery insufficiency
- Proximal left anterior descending artery insufficiency
- Triple vessel disease
Other causes of global cardiac ischemia
- Thoracic aortic dissection
- Large pulmonary embolism
- Severe anemia
- Post-arrest (within 15 mins of epinephrine or defibrillation)
Miscellaneous causes
- Supraventricular Tachycardia (esp. AVRT)
- Left bundle branch block (LBBB) & paced rhythms
- LVH with strain (from severe hypertension)
- Severe hypokalemia
- Na⁺channel blockade (TCA toxicities, hyperkalemia, Brugada, etc.)

Take-home Points:

Hypokalemia can produce ischemic appearing ECGs with ST-segment depressions and ST-segment elevation in aVR
ECG Findings in severe hypokalemia
- U-waves (can be very large)
- Prolonged QT-interval (due to T-U wave fusion)
- Flattening of T waves then ST segment down-sloping/depression
- Biphasic T-waves that deflect down before going up “reverse Wellens’ waves”, a.k.a “NikEleKam T waves”
- Ventricular ectopy – PVC’s and ventricular dysrhythmias!

References:

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. J Am Coll Cardiol. 2013;61(4):e78–e140. PMID: 23256914.

Key Teaching Points

Differential for ST-segment elevation in aVR (with multilead ST-depression)

Acute coronary syndromes
- Left main coronary artery insufficiency
- Proximal left anterior descending artery insufficiency
- Triple vessel disease
Other causes of global cardiac ischemia
- Thoracic aortic dissection
- Large pulmonary embolism
- Severe anemia
- Post-arrest (within 15 mins of epinephrine or defibrillation)
Miscellaneous causes
- Supraventricular Tachycardia (esp. AVRT)
- Left bundle branch block (LBBB) & paced rhythms
- LVH with strain (from severe hypertension)
- Severe hypokalemia
- Na⁺channel blockade (TCA toxicities, hyperkalemia, Brugada, etc.)

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
Atrial and ventricular dysrhythmias
Signs of right heart strain

- Rightward axis (look for large S wave in lead I)
- New RBBB or incomplete RBBB
- New T-wave inversions (especially in anteroseptal +/- inferior leads)
- ST-segment elevations or depressions
  - ST-elevation in rightward leads (V₁, V₂, aVR, III)

Key Teaching Points

Question 1. List up to 16 causes of ST-segment elevation (1 point for every 3 you list; bonus point for all 16; max 6 points).

16 causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
Hyperkalemia
LBBB/pacemaker
LVH/high left ventricular voltage
Pulmonary embolism
Brugada syndrome & mimics
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Question 2. Name 6 causes of ST-segment elevation in lead aVR that are NOT related to an acute coronary occlusion (i.e. not left main, triple vessel, or proximal LAD artery disease). (max 3 points)

Differential for ST-segment elevation in aVR (with multilead ST-depression)

Acute coronary syndromes
- Left main coronary artery insufficiency
- Proximal left anterior descending artery insufficiency
- Triple vessel disease
Other causes of global cardiac ischemia
- Thoracic aortic dissection
- Large pulmonary embolism
- Severe anemia
- Post-arrest (within 15 mins of epinephrine or defibrillation)
Miscellaneous causes
- Supraventricular Tachycardia (esp. AVRT)
- Left bundle branch block (LBBB) & paced rhythms
- LVH with strain (from severe hypertension)
- Severe hypokalemia
- Na⁺channel blockade (TCA toxicities, hyperkalemia, Brugada, etc.)

Question 3. Name 4 ECG signs of right heart strain that might be found on the ECG of a patient with massive PE. Note that sinus tachycardia is too nonspecific…don’t bother listing that! (max 2 points)

ECG findings in Pulmonary Embolism

Sinus Tachycardia
Atrial and ventricular dysrhythmias
Signs of right heart strain

- Rightward axis (look for large S wave in lead I)
- New RBBB or incomplete RBBB
- New T-wave inversions (especially in anteroseptal +/- inferior leads)
- ST-segment elevations or depressions
  - ST-elevation in rightward leads (V₁, V₂, aVR, III)

Question 4. Name causes for a rightward axis (1 point for every 3 you list; max 3 points)

Causes of Rightward Axis Deviation

Ventricular ectopy (VT)
Right ventricular hypertrophy
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Left posterior fascicular block
Hyperkalemia
Na⁺channel blocker toxicity
Lateral MI (from Q-waves in lead I)
Dextrocardia (situs inversus)
Lead misplacement
Newborn/infants

Question 5. A 38-year-old man presents with sharp chest pain and the ECG below is obtained. In deciding between STEMI vs. pericarditis, name 2 findings which strongly favor the correct diagnosis over the other. (2 points)

ECG findings in Pericarditis vs. STEMI

Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that strongly favor STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
Horizontal or convex upward ST-segment morphology
STE in lead III > the STE in lead II
R-T sign or “checkmark sign”
Q-waves that youknow are new (be cautious it they are old)

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis (only after step 1):

Pronounced PR-segment depression in multiple leads
Spodick sign (TP segment downsloping) – may be useful after considering all the other factors above, but be wary as new research suggests it may be seen in both STEMI and pericarditis. Not sensitive or specific!

When in doubt…do serial ECGs and consider CATH!

Question 6. A 45-year-old woman presents feeling weak, with the ECG shown below. What is the diagnosis? (1 point) Name 4 typical ECG findings associated with the diagnosis. (2 points)

ECG findings in severe hypokalemia

U-waves (can be very large)
Prolonged QT-interval (T-wave/U-wave fusion)
Flattening of the T-waves, then ST-segment downsloping/depression
Biphasic T-waves that deflect down before going up “reverse Wellens’ waves” a.k.a. “NikEleKam T waves” are caused by severe hypokalemia that prolongs the QT interval because of large U-waves.
ST-segment elevation in aVR
PVC’s, ventricular dysrhythmias

Key Teaching Points

Question 7. A 62-year-old male with history of CAD presents with palpitations. BP is 115/60. He has no pain, minimal dyspnea, clear lungs, and normal mental status. Electrolytes are normal. What is the ECG diagnosis? (1 point) What is the DRUG of choice? (1 point)

Ventricular Tachycardia (VT)

Sustained VT
- Rate > 120-130
- Lasts at least 30 seconds or produces hemodynamic instability
- Treatment with meds or shock
Non-sustained VT (Correct Answer)
- Rate > 120-130
- Lasts < 30 seconds, no associated hemodynamic instability
- Key to treatment is to look for and treat underlying cause
  - Cardiac ischemic, hypoxia, electrolyte abnormalities, PE, etc.
  - Cardiac ischemia may induce sustained or non-sustained monomorphic VT in the presence of a myocardial scar
  - Empiric antiarrhythmic therapies are probably not indicated. No antiarrhythmic drug is suitable for primary prevention of cardiac death except for beta blockers

Question 8. A 37-year-old man presents with chest pain and the ECG below. What is the diagnosis (2 points)

Large pulmonary embolism! There is right axis deviation, sinus tachycardia, ST-segment elevation in aVR, and T-wave inversions in anterior and inferior leads. Pay attention to axis, as right axis deviation can help distinguish massive PE from STEMI.

Question 9. A 31-year-old male presents after a near-syncopal episode. His ECG is shown below. What is the diagnosis (1 point) What is the diagnostic test of choice (1 point) The patient insists on being discharged but will follow up with cardiology in 3 days. What is the optimal outpatient management until follow up? (1 point)

Hypertrophic obstructive cardiomyopathy (HOCM)

ECG abnormalities present in 85-93%
- Deep narrow “dagger like” Q-waves in inferior, lateral leads
- High left ventricular voltages
- Left atrial enlargement is most common
- Tall R wave in V1 (mimics posterior MI)
Definitive diagnosis – Doppler ECHO
- Can also help to assess severity of obstruction at rest and with provocative maneuvers
Treatment
- Beta blockers and minimization of exertion

Question 10. A 54-year-old man presents with chest pain and the ECG noted below. What is the full ECG diagnosis? (2 points)

Sinus rhythm with inferior and right ventricular STEMI

Question 11. A 50-year-old woman presents with mild dyspnea. Nurses noted ~ 10 seconds of an unusual rhythm disturbance on the monitor and they obtained a 12-lead ECG off the monitor, noted below. What is the diagnosis? (1 point) What would be the treatment if this finding persisted? (1 point)

Artifact, no treatment necessary.

Question 12. A 58-year-old man presents with chest pain and the ECG noted below. What is the full ECG diagnosis? (3 points)

Sinus Tachycardia with Mobitz I AV conduction, inferior and posterior STEMI

Question 13. A 64-year-old male presents with palpitations and lightheadedness. ECG is below. What is the optimal treatment? (2 points)

Treatment for hyperkalemia. The QRS is too wide and ventricular rate too slow to be ventricular tachycardia.

Question 14. A 65-year-old woman presents after a syncopal episode. with palpitations and lightheadedness. ECG is below. What is the optimal treatment? (2 points)

Sinus tachycardia with complete heart block and junctional escape rhythm, left posterior fascicular block with inferior-lateral ischemia.

Key Teaching Points

Causes of Rightward Axis Deviation

Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Causes of Rightward Axis + ST-segment elevation mimicking STEMI (usually does not produce rightward axis)

Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI, STE common in V₁-V₂, aVR)
Pseudo Brugada syndrome pattern
Sine wave morphology

ECG findings in PE associated with hemodynamic instability and increased morbidity and mortality (not specific for PE)

TWIs in right precordial leads
ST-segment elevation and depression
- Especially STE in aVR, V₁-V₂
Tachycardia (sinus, afib/flutter)
Signs of right heart strain (RAD, tall R wave in V₁)

Final take-home points:

Large PE’s and hyperkalemia can often mimic STEMI with ST-segment elevation (especially in rightward leads)
STEMI’s don’t tend to produce a rightward axis
Rightward axis in apparent “STEMI”? Pay attention to the axis and consider large PE and hyperkalemia!

References:

Shopp JD, Stewart LK, Emmett TW, Kline JA. Findings From 12-lead Electrocardiography That Predict Circulatory Shock from Pulmonary Embolism: Systematic Review and Meta-analysis. Acad Emerg Med 2015;22(10):1127–37. PMID:26394330

Dibgy,GC, Kulka P, Zhan ZQ, et al. The value of electrocardiographic abnormalities in the prognosis of pulmonary embolism: a consensus paper. Ann Noninvasive Electrocardiol 2015. May;20(3):207-23. PMID:25994548

Kukla P, McIntyre WF, Fijorek K, et al. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med 2014;32(6):507–10. PMID:24602894

Zhan Z-Q, Wang C-Q, Nikus KC, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51.PMID:24750207

Abarca E, Baddi A, Manrique R. ECG manifestations in submassive and massive pulmonary embolism. Report of 4 cases and review of literature. Journal of Electrocardiology 2014;47(1):75–9. PMID:23890684

Key Teaching Points

Differential for Left Axis Deviation

Left bundle branch block
Paced rhythm
Pre-excitation (e.g. WPW)
Prior Inferior MI (from Q-waves)
Left anterior fascicular block
Left ventricular hypertrophy
Hyperkalemia
Normal Variant (may be seen in elderly patients)

Left anterior fascicular block (LAFB)

Leftward axis
qR in I and aVL
rS in III
QRS may be normal or slightly prolonged
Poor R-wave progression is common
No other reasons for leftward axis

Type of Fascicular Block	LAFB	LPFB
Axis	Left Axis Deviation	Right Axis Deviation
Leads I & aVL
Lead III

Take-home points:

The ECG must always be interpreted in the context of clinical presentation
History and physical exam still matter

Key Teaching Points

Wellens’ Syndrome

Pattern of T-wave abnormality in mid precordial leads (V₂-V₃, +/- V₄)
No loss of R-waves in precordial leads
Highly specific for critical obstruction of the proximal LAD
High risk for extensive anterior wall MI and death

- 2 types

- Type 1 – Deeply symmetric TWI
- Type 2 – Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”). Often misdiagnosed as “non-specific T-wave pattern” or “normal”.

ST changes are often absent and patient can be in a chest pain free state!
Cardiac biomarkers often initially normal
Best to diagnose in absence of high voltage
Not currently a guideline indication for cath or lytics (especially when pain free without STE) but…
Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous and precipitate acute MI.
Patients will have anterior wall MI unless they get early PCI. 75% developed acute MI within weeks when only medically managed.
Get serial ECG’s, as some of these do evolve into STEMI in the ED
Watch carefully for Wellens’ as some of your consultants may not know about this.

Take home Points

Beware Wellens’ syndrome & Wellens’ waves

Predicts critical occlusion in LAD, usually proximal
Your ECG machine (and consultants) often don’t know about this
Low threshold for serial ECG’s especially if symptoms change, may evolve into a STEMI
Beware stress testing! May be hazardous and precipitate MI

References:

De Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 1892 Apr;103(4 Pt 2):730-6. PMID: 6121481

Key Teaching Points

Does Gastro-Esophageal Reflux Provoke the Myocardial Ischemia in Patients with CAD?

Background: prior studies have shown
- 47% of patients with acute MI report an increase in belching symptoms
- 20% of patients with ACS describe “burning” or “indigestion”
- 7-15% of patients report improvement/resolution of symptoms with antacids
- 8% of patients report onset of ACS symptoms with eating
- GERD occurs more commonly in patients with CAD
Dobrzycki S, Int J Cardiol 2005
- 50 patients with angiographically proven CAD underwent simultaneous 24-hour ECG and esophageal pH monitoring to correlate episodes of GERD with ischemia
- Results:
  - 21% of episodes of cardiac ischemia were associated with episodes of reflux
  - GERD patients had more frequent episodes of ST-depression
  - GERD patients had more prolonged episodes of cardiac ischemia
  - PPI’s reduced reflux and ischemic episodes
- Conclusion:
  - GERD is common in patients with CAD and may provokes or worsen cardiac ischemia
    - PPI therapy that restores esophageal pH may reduce myocardial ischemia, possibly due to elimination of acid-derived esophago-cardiac reflex compromising coronary perfusion (phenomenon known as “linked angina”)
    - First described in 1962!

Take home Points

Before you ever diagnose a chest pain patient with reflux…think twice!
Both GERD and CAD can cause chest pain and frequently co-exist
GERD is common and may also be a risk factor for extra-esophageal complications
Beware Wellens’ syndrome & Wellens’ waves
- Predicts critical occlusion in LAD, usually proximal
- Your ECG machine (and consultants) often don’t know about this
- Low threshold for serial ECG’s especially if symptoms change, may evolve into a STEMI

Key Teaching Points

LVH with repolarization abnormality (“strain”)

ECG criteria for LVH tend to be very specific, but not sensitive (~50%)
Gold standard is generally LV mass on echocardiography or cardiac MR
- ECG LVH Criteria:
  - R in V₅ or V₆ + S in V₁ > 35 mm
  - Max R + max S in precordial leads > 45 mm
  - R in aVL > 11 mm
  - R in I > 15 mm or 20 mm (varies)
  - And other criteria exist…
  - Under age 50 these voltage criteria may be normal variants (“high left ventricular voltage” – Dr. Edward Chung)
  - Repolarization abnormalities increases the specificity
    - ST depression in any of: I, aVL, V₄-V₆ [+/- II & aVF]
    - Inverted T-waves in same leads (asymmetric)
    - STE in V1-V3 [and often aVR]
    - QRS widening (non-specific IVCD)

LVH with strain vs. Cardiac Ischemia

Nothing has been adequately validated to use with complete certainty
- If voltage criteria for LVH not present, assume ischemia
- LVH has asymmetric TWI’s, ischemic TWI’s tend to be symmetric
- Horizontal ST depression favors ischemia
When in doubt, get serial and old ECG’s to look for evolving changes

Take home Points

No good way of distinguishing between ischemia vs. LVH with strain
- TWI symmetry? Horizontal ST-segments? Excessively discordant ST-elevation? Nothing is adequately validated and reliable
Know and look for LVH criteria
Get serial and old ECG’s when in doubt!
Practice, practice, practice ECG’s – pattern recognition takes time

Key Teaching Points

Monomorphic Ventricular Rhythm Nomenclature

Rate 20-40 = ventricular escape rhythm (idioventricular rhythm)
Rate 40-120 = accelerated ventricular rhythm (AIVR)
Rate > 120-130 = ventricular tachycardia
Rate > 250 = ventricular flutter
Disorganized, pulseless = ventricular fibrillation

Ventricular Tachycardia Pearls

Following characteristic aid in the identification of VT:
Very broad QRS complexes (>160 ms)
Extreme right axis deviation (“northwest axis”, a.k.a “axis in no mans land”) – QRS is positive in aVR and negative in I + aVF
Josephson’s sign – Notching near the nadir of the S-wave, finding increases likelihood of VT
Steeple sign – Wide RS wave in V₁ seen in RBBB pattern VT. RSR’ complexes with a taller left rabbit ear also increase likelihood of VT. This contrasts with RBBB, where the right rabbit ear is taller
QS wave in V₆ – entirely negative (QS) complexes with no RS complexes seen
Initial R wave in aVR – large dominant R wave in aVR increases likelihood of VT
Too much to remember? Regular wide complex tachycardia? When in doubt, just call it ventricular tachycardia?

Take home Points

Don’t trust your ECG computer interpretation! It will fool you
Don’t be misled by PVC’s, don’t stop looking for other abnormalities or you may miss a STEMI!
Large S wave in lead I? Consider deadly causes of right axis deviation like hyperkalemia and Na⁺ channel blocker toxicities
Regular wide complex tachycardia? Assume ventricular tachycardia
Regular REALLY wide complex tachycardia? Assume toxicologic and metabolic derangements

Key Teaching Points

Take home Points

Beware the “checkmark sign”
- QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- May signal early ischemic change
When in doubt…
- Get old ECG’s for comparison
- Get serial ECG’s

Key Teaching Points

Take home Points

What do you do when ST-segment elevation in STEMI resolved before cath lab activation (spontaneously or with medical treatment?

Ownbey M. Prehospital Emerg Care, 2014. PMID: 24400994
- Evaluated cases of prehospital ECG’s with presumed STEMI
- Compared patients with resolved ST-elevation vs. unresolved ST-elevation on first ECG in hospital
  - 22% of cases had resolution of ST-elevation by arrival
  - Occlusions > 95% at cath in patient with resolved ST-elevation vs. unresolved ST-elevation: 65% vs. 85% (not statistically different)
  - Occlusions ³ 50% at cath: 94% vs. 97%
- Cath lab activation is probably warranted, even if the ST-segment elevation has resolved

Reference:

Ownbey M, Suffoletto B, Frisch A, et al. Prevalence and interventional outcomes of patients with resolution of ST-segment elevation between prehospital and inhospital ECG. Prehosp Emerg Care, 2014 Apr-Jun;18(2):174-9. PMID: 24400994

Key Teaching Points

Take home Points

Don’t be fooled by…
- Pseudo ST-segment deviation in the setting of BBB’s (especially common in aVR), the BBB and wide QRS may be mistaken for ST-segment deviation
- Pseudo-narrow QRS complexes in the setting of ventricular tachycardia
Don’t rely on a single lead or rhythm strips to assess intervals or ST-segment deviation
- Rhythm strips will often mislead you!
- Get a 12- lead and look in ALL leads for clues

Key Teaching Points

Differential for Prolonged QT-Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
Medications/Drugs (Na⁺ channel blockers, methadone, & many others)
Elevated intracranial pressures
ACS / cardiac ischemia
Congenital

Take home Points

Assume electrolyte abnormalities in patients on diuretics
Be careful of QT-prolonging meds in these patients or any patient that appears dehydrated
QTc > 500ms places patients at significant risk for torsades
Treatment: Shock, Mg²⁺bolus and infusion, overdrive pacing
Avoid Class I antiarrhythmic medications (including amiodarone), which can prolong the QT further!

Key Teaching Points

New T-wave inversion or ST-segment down sloping in aVL or V₂ may be an early reciprocal change that precedes inferior STEMI

Reciprocal changes can precede ST-elevation (STE) in MI
ST-segment down sloping in aVL and straightening of the ST-segment in the inferior leads can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Take home Points

Signs of early ischemia
- Straightening of the initial part of the T-wave
- Reciprocal ST changes (focus on aVL and V₂ in inferior STEMI)
Sign of underlying coronary artery disease
- Biphasic T-waves in inferior leads
Serial ECG’s are key!
- Repeat ECG’s when in doubt or when there is a change in symptoms

Key Teaching Points

Differential for Non-conducted P-waves (P:QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes
- P-waves are irregular, non-conducted P-waves come early
2^nd degree AV Block: Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
2^nd degree AV Block: Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Take home Points

Pokey T-waves? Consider hidden P-waves, and map them out!
ECG polyuria? (Too many P-waves for every QRS) Look at the PR-interval
- Constant PR – Mobitz II (unless it’s 2^nd degree AVB with 2:1)
- Ratio of P:QRS ³ 3:1? Called “advanced AVB” or “high grade AVB”
- Mobitz II is unlikely to respond to pressors or atropine
  - Need trans-cutaneous or trans-venous pacing (likely a permanent pacemaker)

Key Teaching Points

Low Voltage Definition

Sensitive Definition
- QRS amplitudes in leads I+II+III < 15 mm
- Or QRS amplitudes in leads V₁+V₂+V₃ < 30 mm
Specific Definition
- QRS amplitudes in limb leads all < 5 mm
- Or QRS amplitude in all precordial leads < 10 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Take home Points

Pulmonary embolism and large pericardial effusions can often present similarly!
- Both have similar patient risk factors
- Both may present with: dyspnea, tachypnea, tachycardia, JVD, and hypotension when severe
- Don’t forget about pericardial effusion in the differential diagnosis for patients with dyspnea and clear lungs!
(Large) Pericardial effusion triad is not always present
- Low voltage (best to compare to prior ECGs)
- Tachycardia (medications may blunt a tachycardic response)
- Electrical alternans (present in < 1/3 of cases)
- When in doubt…do the bedside echo looking for an effusion!

Key Teaching Points

Causes of Widening of the QRS-complex

Bundle branch blocks (LBBB or RBBB)
Paced beats
Ventricular ectopy
Pre-excitation (e.g. WPW)
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)

Wolff-Parkinson-White Syndrome with Atrial Fibrillation

Very rapid irregularly irregular tachycardia (rates may approach 300 beats/min) with wide QRS complexes that vary in morphology
Often misdiagnosed as SVT, VT or atrial fibrillation with BBB
Misdiagnosis and treatment with AVN blockers can be deadly!
Treat with procainamide, flecainide (?), or preferably electrical cardioversion
Key Point: Avoid all AV Nodal blockers
Adenosine
Beta-blockers
Calcium channel blockers
Digoxin
Amiodarone

Take Home Points:

WPW + Atrial Fibrillation

Irregularly irregular tachycardia
Complexes vary in shape and width
May approach 250-300 bpm or higher
Avoid all AV nodal blockers…including Amiodarone!
- Use Procainamide, Flecainide (?),or electrical cardioversion
- Pitfall: Treatment with Amiodarone results in patient decompensation (see references)

References:

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745
Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399
Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217
Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602
Tijunelis MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. 2005 Jul;7(4), 262–265. PMID: 17355684
Badshah A, Mirza B, Janjua M, et al. Amiodarone-induced torsade de pointes in a patient with wolff-Parkinson-White syndrome. Hellenic J Cardiol 2009;50(3):224–6. PMID: 19465366
Nebojša M, DRAGAN S,Nebojša A, et al. Lethal outcome after intravenous administration of amiodarone in patient with atrial fibrillation and ventricular preexcitation. J Cardiovasc Electrophysiol 2011;22(9):1077–8. PMID: 21332863
Writing Committee Members. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. JAC 2014;64(21):2246–80. PMID: 24682347
Marriott, Advanced concepts in Arrhythmias, Mosby 1998. Amazon Link

Key Teaching Points

de Winter T-waves

1-3 mm ST-depression at the J-point in the mid precordial leads, leading into tall symmetric T-waves
High risk of acute anterior MI
Suggestive of an acute proximal LAD occlusion (contrast to sub-acute occlusion of Wellens syndrome), or less commonly a 1^st diagonal or left circumflex occlusion
Although no ST-elevation, may be an unstable lesion for which urgent cath should be “strongly considered”
Have high concern for decompensation and treat aggressively
Increasing push to consider this a STEMI equivalent, we now have cases of de Winter T’s progressing to STEMI within ED time frame
Get serial ECG’s while the patient is having pain, may progress to STEMI

Take Home Points:

De Winter T-waves

Although no ST-segment elevation, high concern for decompensation
Unstable proximal LAD stenosis
Recommendations
- Currently – monitor closely, serial ECG’s
- Future? – STEMI equivalent

References:

de Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008 Nov 6;359(19):2071-3. PMID:18987380
Birnbaum I, Birnbaum Y. High-risk ECG patterns in ACS—need for guideline revision. J Electrocardiol 2013;46(6):535–9. PMID: 23863685
Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr. Am J Emerg Med 2014;32(3):287.e5–8. PMID: 24176590
Verouden NJ, Koch KT, Peters RJ, et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart 2009;95(20):1701–6. PMID: 19620137
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec;160(6):995-1003. PMID:
21146650Stankovic I, Ilic I, Panic M, et al. The absence of the ST-segment elevation in acute coronary artery thrombosis: what does not fit, the patient or the explanation? J Electrocardiol 2011;44(1):7–10. PMID: 20591442

Key Teaching Points

aVR – The forgotten 12^th lead

STE in aVR in the patient with other ischemic findings on ECG is bad!
Reflects global subendocardial ischemia of the left ventricle, often associated with proximal lesions or multi-vessel disease
STE in aVR (> 1-1.5 mm) Differential
- LMCA stenosis
- Proximal LAD
- Triple vessel disease
- Any cause of severe generalized global ischemia
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Early post-arrest (within 15 mins of epi or defibrillation)
  - Massive PE, etc.
- Patients with acute coronary occlusions typically will have active symptoms and look sick!
- Estimated 70% mortality without immediate PCI
- Medical therapy (including lytics) does not improve mortality
- Emergency PCI may decrease mortality to 40%
- Time delay to PCI is the only predictor of survival

DDx for ST-segment elevation in aVR (with multilead ST-depression) “global cardiac ischemia”

Acute coronary syndromes
- Left main coronary artery insufficiency
- Proximal left anterior descending artery insufficiency
- Triple vessel disease
Other causes of global cardiac ischemia
- Thoracic aortic dissection
- Large pulmonary embolism
- Severe anemia
- Post-arrest (within 15 mins of epinephrine or defibrillation)
Miscellaneous causes
- Supraventricular Tachycardia (esp. AVRT)
- Left bundle branch block (LBBB) & paced rhythms
- LVH with strain (from severe hypertension)
- Severe hypokalemia
- Na⁺channel blockade (TCA toxicity, hyperkalemia, Brugada, etc.)

Take-home points:

Important points about STE in aVR

Patients are actively having ACS symptoms and typically look sick
STE > 1-1.5mm
- Indicative of severe generalized ischemia
  - In ACS: LMCA, triple vessel disease, proximal LAD
  - Increasing support to incorporate this into cath lab activation criteria
- Always consider other causes aside from ACS!

Reference:

Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74. PMID: 17098112
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID:21146650
Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiology. 2008 Nov-Dec;41(6):626-9. PMID: 18790498
Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500. PMID: 21184992
Taglieri, N., Marzocchi, A., Saia, F., et al. Short- and Long-Term Prognostic Significance of ST-Segment Elevation in Lead aVR in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome. Am J Cardiol. 2011; 108(1), 21–28. PMID: 21529728
Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. 2010 Mar-Apr;43(2):93, 97-98. PMID: 19913800
Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol. 2009 Mar 17;53(11):1007. PMID: 19281933
Kosuge M, Uchida K, Imoto K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2015 Jun 16;65(23):2570-1. PMID: 26065996

Key Teaching Points

aVR – The forgotten 12^th lead

STE in aVR in the patient with other ischemic findings on ECG is bad!
Reflects global subendocardial ischemia of the left ventricle, often associated with proximal lesions or multi-vessel disease
STE in aVR (> 1-1.5 mm) Differential
- LMCA stenosis
- Proximal LAD
- Triple vessel disease
- Any cause of severe generalized global ischemia
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Early post-arrest (within 15 mins of epi or defibrillation)
  - Massive PE, etc.
- Patients with acute coronary occlusions typically will have active symptoms and look sick!
- Estimated 70% mortality without immediate PCI
- Medical therapy (including lytics) does not improve mortality
- Emergency PCI may decrease mortality to 40%
- Time delay to PCI is the only predictor of survival

DDx for ST-segment elevation in aVR (with multilead ST-depression) “global cardiac ischemia”

Acute coronary syndromes
- Left main coronary artery insufficiency
- Proximal left anterior descending artery insufficiency
- Triple vessel disease
Other causes of global cardiac ischemia
- Thoracic aortic dissection
- Large pulmonary embolism
- Severe anemia
- Post-arrest (within 15 mins of epinephrine or defibrillation)
Miscellaneous causes
- Supraventricular Tachycardia (esp. AVRT)
- Left bundle branch block (LBBB) & paced rhythms
- LVH with strain (from severe hypertension)
- Severe hypokalemia
- Na⁺channel blockade (TCA toxicity, hyperkalemia, Brugada, etc.)

Take-home points:

Important points about STE in aVR

Patients are actively having ACS symptoms and typically look sick
STE > 1-1.5mm
- Indicative of severe generalized ischemia
  - In ACS: LMCA, triple vessel disease, proximal LAD
  - Increasing support to incorporate this into cath lab activation criteria
- Always consider other causes aside from ACS!

Reference:

Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74. PMID: 17098112
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003. PMID:21146650
Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiology. 2008 Nov-Dec;41(6):626-9. PMID: 18790498
Kosuge M, Ebina T, Hibi K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500. PMID: 21184992
Taglieri, N., Marzocchi, A., Saia, F., et al. Short- and Long-Term Prognostic Significance of ST-Segment Elevation in Lead aVR in Patients With Non–ST-Segment Elevation Acute Coronary Syndrome. Am J Cardiol. 2011; 108(1), 21–28. PMID: 21529728
Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. 2010 Mar-Apr;43(2):93, 97-98. PMID: 19913800
Wagner GS, Macfarlane P, Wellens H, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: Part VI: acute ischemia/infarction: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. J Am Coll Cardiol. 2009 Mar 17;53(11):1007. PMID: 19281933
Kosuge M, Uchida K, Imoto K, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2015 Jun 16;65(23):2570-1. PMID: 26065996

Key Teaching Points

Riley, et al. Am Heart J 2013. PMID: 23237133

41,560 patients from a STEMI database
- 36,994 patients had initial ECG with STEMI
- 4566 patients (11%) were diagnosed with STEMI on follow-up ECG (initial ECG was non-diagnostic)
  - 72% had STEMI in ECG within 90 mins
- No difference in characteristics between groups

Take-home points:

Get serial ECG’s in suspected ACS!

For persistent ischemic signs and symptoms
When the pain or status of the patient changes
Guidelines recommend every 15-30 mins
STEMI doesn’t always “show itself” on the first ECG

Subtle early signs of ischemia

Reciprocal changes (e.g. aVL, V₂)
“Checkmark sign”
Hyperacute T-waves
- Straightening of the upslope of the T-waves
- Excessively large T-waves
New upright T-wave in V₁ (loss of precordial T-wave balance)

When you seen any of these…one ECG begets another!

Reference:

Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. American Heart Journal 2013;165(1):50–6. PMID: 23237133

Key Teaching Points

Schläpfer, et al. J Am Coll Cardiol 2017. PMID: 28838369

There is no international accepted standard for computer interpretations
- Small but significant differences exist between manufacturers and their algorithms
- Algorithms are programed by humans…and humans sometimes disagree
Direct comparative evaluations of the various commercially available computer-interpreted electrocardiogram programs have never been performed
- Reluctance on the part of the manufacturers
“Computer-based analysis of the ECG may lead to erroneous diagnosis with useless, inappropriate, or even dangerous care of the patient”
“It has been roughly estimated that these misdiagnoses may account for up to 10,000 adverse effects or avoidable deaths worldwide annually” – Mele, et al. J Healthc Risk Manag 2008

Take-home points:

Computer interpreted electrocardiograms are unreliable and may miss or misdiagnose life threatening diagnoses such as STEMI and arrhythmias. This results in unacceptably high adverse event rates and avoidable deaths.
Just because electrocardiography is a basic skill in medicine, doesn’t mean that our skills should be basic.
You must strive for expertise in electrocardiography!

Reference:

Schläpfer J, Wellens HJ. Computer-Interpreted Electrocardiograms: Benefits and Limitations. J Am Coll Cardiol 2017;70(9):1183–92. PMID: 28838369
de Champlain F, Boothroyd LJ, Vadeboncoeur A, et al. Computerized interpretation of the prehospital electrocardiogram: predictive value for ST segment elevation myocardial infarction and impact on-scene time. CJEM 2014;16(2):94-105. PMID: 24626114
Min MK, Ryu JH, Kim YI, et al. Does cardiac catheterization laboratory activation by electrocardiography machine auto-interpretation reduce door-to-balloon time? Am J Emerg Med 2014;32(11):1305–10. PMID:
25249338Willems JL, Abreu-Lima C, Arnaud P, et al. The diagnostic performance of computer programs for the interpretation of electrocardiograms. N Engl J Med 1991;325(25):1767–73. PMID: 1834940

Key Teaching Points

Poor R-wave Progression Differential

Defined as a < 3 mm R-wave by lead V₃

Prior anteroseptal MI
LVH
LAFB
LBBB
Low voltage
Older age
Lead misplacement
Normal variant

Clues to RV Infarction on the 12-lead ECG

1/3 of inferior STEMI’s will extend to the right ventricle
- These patients will be very preload dependent
- Preload reducing meds (like nitroglycerin) can cause significant hypotension and should be avoided
- If the lungs are clear, treat with IVF, not vasopressors
In the presence of an inferior STEMI…
- ST-segment depression in lead V2 with
  - ST-segment elevation in lead V1 OR
  - Isoelectric ST-segment in lead V1
- STE in lead III >>> II
Or when in doubt, just get right-sided leads!

Narrow-Complex & Regular Tachycardia Differential

1. Sinus Tachycardia

One P-wave for every QRS
Upright P-waves in limb leads (I, II, III, aVF), & inverted P-wave in aVR
Maximum sinus node rate is ~ (220 bpm – age)

2. Supraventricular Tachycardia (SVT)

No distinct P-waves. May be hidden or may follow the QRS complex (“retrograde atrial activity”)
Different types (AV Nodal re-entry, Non-paroxysmal junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign as long as it goes away when sinus rhythm is restored
SVT can also cause electrical alternans that disappears when sinus rhythm is restored

3. Atrial flutter with 2:1 Conduction

2 atrial beats for every QRS
Saw tooth pattern, flipping the ECG upside down and paying attention to all 12 leads will help you identify subtle flutter waves
Most commonly missed atrial tachycardia
Always consider when rate is 150 +/- 20 bpm

To differentiate…always look at what the atrium is doing (V1 typically best lead to look for atrial activity)

Narrow Complex & Irregular Tachycardia Differential

Atrial fibrillation
Atrial flutter with variable conduction
Multifocal atrial tachycardia (3 different p-wave morphologies)

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Regular Really Wide Complex Tachycardia (RRWCT)

Regular Really wide QRS complexes > 200 ms = RRWCT
Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause RRWCT’s that mimic Ventricular Tachycadia
Look at V₁ and all other leads for subtle P-waves
Consider empiric treatment with calcium and bicarb before antiarrhythmics which can kill these patients!
In sick patients with hyperglycemia, consider DKA! The fastest killer in DKA is hyperkalemia…so make sure to get an ECG early.

Key Teaching Points

Post-syncope ECG

When the history and physical exam do not suggest a diagnosis, always think of the following differentials when interpreting the ECG of patients with syncope or new-onset seizures:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy (HCM)
Brugada pattern
Arrhythmogenic RV dysplasia

Differential Diagnosis for T-wave inversions

Coronary artery disease (Wellens, ischemia, reperfusion)
Neurological causes (elevated intracranial pressure)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Wide QRS complexes (BBB’s. PVC’s, Paced rhythms, WPW)
High left ventricular voltage, LVH with strain pattern
Pericarditis, myocarditis
Hyperkalemia, hypokalemia
Juvenile T-wave pattern
Mitral valve prolapse
Normal finding in V₁, aVR, and lead III

Arrhythmogenic Right Ventricular Cardiomyopathy

Inherited progressive cardiomyopathy characterized by ventricular arrhythmias and increased risk of sudden cardiac death, especially in young individuals and athletes
Not common, but increased prevalence in certain populations/regions
- General population; 1/1,000-1/10,000
- Italy 40/10,000: Most common cause of sudden cardiac death in young population
- Newfoundland?
Familial
- Autosomal dominant trait with variable penetrance
  - 50% chance of inheriting the gene defect
  - Men > Woman
Pathogenesis
- Progressive replacement of the RV myocardium by fibrofatty tissue
- Causes interference with electrical impulse conduction
- CAN also occur in left ventricle posterolateral subepicardium
Clinical
- Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  - 22% of cases of SCD among athletes in N. Italy
  - 4% of cases of SCD in US (HCM #1)
- Often have family history of premature sudden death in family members < 35 years of age
- Usually manifests in patients between second to fifth decades of life
- Symptoms included palpitations, lightheadedness, syncope, and sudden death
Diagnosis
- ECG (imperfect)
  - Leads V₁-V₃
    - Epsilon waves (most specific, but seen in < 1/3 of patients)
    - TWIs (most sensitive, seen in > 80% of patients)
    - Slight prolongation of QRS
  - LBBB type VT (~90%) or PVCs (many)
- ECHO
- MRI
- MDCT
- Endomyocardial biopsy
Management
- Send to electrophysiologist
- Active ventricular dysrhythmias
  - Stable: beta blockers, Class III antiarrhythmics
  - ICD placement for patients with cardiac arrest, syncope, VT

Take home Points

When history and physical exam do not give you a diagnosis in syncope, don’t forget the no-brainers (dysrhythmias), interval abnormalities (i.e. WPW, prolonged QT) and genetic causes (HCM, Brugada, ARVC)!
ARVC: Have heightened concern if…

Young patients, especially males
Family history of early sudden death
Many PVC’s
LBBB-type Ventricular Tachycardia
Epsilon waves with TWI’s in V₁-V₃

References:

Basso C, Corrado D, Marcus FI, Nava A, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet 2009;373(9671):1289–300. PMID: 19362677
Orgeron GM, Crosson JE. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Cardiol Young 2017;27(S1): S57–S61. PMID: 28084951
Diez D, Brugada J. Diagnosis and Management of Arrhythmogenic Right Ventricular Dysplasia: An article from the E-Journal of the ESC Council for Cardiology Practice, European Society of Cardiology 2008.

Key Teaching Points

Hyperkalemia

Durfey N, et al. Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events? WJEM 2017. PMID: 28874951

188 patients with K⁺≥ 6.5 mEq/L
15% developed adverse effects within 6 hours (e.g. symptomatic dysrhythmia, arrest, death)
Correlated short term adverse events with presenting ECG findings
100% of short-term adverse events were preceded by ECG abnormalities…but abnormal or peaked T-waves did not correlate!
Highest correlation with
- Bradycardia (HR < 50) – RR 12.29
- Junctional rhythm – RR 7.46
- Widened QRS (> 100 ms) – RR 4.74

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Reference:

Durfey N, Lehnhof B, Bergeson A, et al. Severe Hyperkalemia: Can the Electrocardiogram Risk Stratify for Short-term Adverse Events? West J Emerg Med 2017;18(5):963–71. PMID: 28874951

Key Teaching Points

Always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV cardiomyopathy

Hypertrophic Cardiomyopathy

Many other names
- IHSS, ASH, HOCM
Characteristic anatomic abnormalities
- Hypertrophied, non-dilated LV (normal CXR)
- Thickening usually prominent in the septum (Doppler ECHO)
Epidemiology
- Familial incidence in 55% of cases
- Average age at diagnosis is 30-40
- Men:Women ~ 3:2
- 1/500 in general population
- Most common cause of death in the US
- Mortality ~3.5% per year
Pathophysiology (theories)
- Inherited abnormality in myocardial response to adrenergic stimulation
- Abnormal diastolic function
- Subaortic obstruction to cardiac outflow
Clinical features
- Syncope, chest pain, palpitations, dyspnea, sudden death
  - Often associated with exertion (not always!)
  - Attributable to dysrhythmias or sudden drops in cardiac output
- Systolic murmur at apex or LLSB
  - Increases with valsalva, standing
  - Decreases with trendelenburg, squatting
- ECG abnormalities present in 85-93%
  - High left ventricular voltages (most common)
  - Tall R wave in V1 (mimics posterior MI)
  - Deep narrow Q waves in inferior, lateral leads
- Definitive diagnosis – Doppler ECHO
  - Can also help to assess severity of obstruction at rest and with provocative maneuvers
Treatment
- Beta blockers, calcium channel blockers
- Amiodarone for ventricular dysrhythmias

Take-home point:

Hypertrophic cardiomyopathy is a common cause of sudden cardiac death in young males. Look for high voltage and deep narrow Q-waves. Diagnostic test is a dopple echocardiogram!

Key Teaching Points

Can’t miss differential diagnosis for chest pain

Acute coronary syndromes
Aortic dissection
Pulmonary embolism
Pericarditis/pericardial effusion
Esophageal rupture
Tension pneumothorax

Can’t miss differential diagnosis for dyspnea (with clear lungs)

Acute coronary syndromes
Pulmonary embolism
Pericardial effusion
Severe anemia
Metabolic acidosis
Tension pneumothorax

Differential diagnosis for right axis deviation

Right ventricular hypertrophy
Left posterior fascicular block
Pulmonary hypertension (acute and chronic)
Old lateral MI (Q-waves)
Na⁺ channel blocker toxicity
Misplaced leads
Situs inversus
Newborns/infants

Differential diagnosis for low voltage QRS

Pericardial effusion
Pleural effusion
Obesity
COPD
Infiltrative disease
End-stage cardiomyopathy
Myxedema

Take-home point:

S_IQ_IIIT_III is not pathognomonic for PE!
PE and pericardial effusions clinically present similarly
Don’t ignore low voltage! When in doubt, do a bedside echocardiogram
Remember your differentials

Key Teaching Points

ECG findings in Hypothermia

Onset of ECG findings can vary, but resolve with warming
- J-waves (Osborn waves – positive deflections at the J-point)
- Sinus bradycardia, junctional rhythms
- Prolongation of all intervals
- Slow atrial fibrillation
- Tremor artifact
- ST-segment elevation or depression
- Ventricular fibrillation
- Asystole

Key Teaching Points

Is this Reflux???

Be careful when diagnosing reflux esophagitis in patients with chest pain or possible ACS
Patients with proven ACS may present with the following:
- “Burning pain/indigestion” in 20%
- Upper abdominal pain in 20%
- Relief with antacids in 15%
- Pain starts while eating in 8%
- Increased with belching in 47%
- GERD often co-exists with CAD!

Take home points

Beware reflux symptoms!
- ACS commonly presents with reflux-like symptoms
Straightening of the initial portion of the T-wave is often a sign of early ischemia
- Watch out for horizontal morphology of ST-segments and get serial ECGs when in doubt
ST-segment depression in V1-V3?
- Repeat an ECG with posterior leads to evaluate for isolated posterior STEMI

Key Teaching Points

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
New RBBB or incomplete RBBB
Superventricular tachydysrhythmias
Ventricular dysrhythmias
ST-segment elevations or depressions
New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

ECG findings in PE associated with hemodynamic instability and increased morbidity and mortality (not necessarily specific for PE):

TWIs in right precordial leads
ST elevation and depression
- Especially STE in aVR, V1-V2
Tachycardia (sinus, afib/flutter)
Signs of right heart strain (RAD, tall R wave in V1)

Take home Points

PE’s mimics ACS!
- Make sure to consider PE in cases of acute onset chest pain and pay close attention to new TWI’s, ST-segment changes, or ventricular dysrhythmias.
- Consider empiric treatment with heparin in cases when most likely differential includes ACS vs. PE
PE’s can also cause low-grade fever, don’t be fooled in just calling it a pneumonia!
PE findings associated with/predictive of hemodynamic instability
Ischemic findings
Tachycardia (sinus, afib)
Signs of right heart strain (RAD, tall R wave in V1)

References:

Shopp JD, Stewart LK, Emmett TW, Kline JA. Findings From 12-lead Electrocardiography That Predict Circulatory Shock From Pulmonary Embolism: Systematic Review and Meta-analysis. Acad Emerg Med 2015;22(10):1127–37. PMID: 26394330

Dibgy,GC, Kulka P, Zhan ZQ, et al. The value of electrocardiographic abnormalities in the prognosis of pulmonary embolism: a consensus paper. Ann Noninvasive Electrocardiol 2015. May;20(3):207-23. PMID: 25994548

Kukla P, McIntyre WF, Fijorek K, et al. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med 2014;32(6):507–10. PMID: 24602894

Zhan Z-Q, Wang C-Q, Nikus KC, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51.PMID: 24750207

Abarca E, Baddi A, Manrique R. ECG manifestations in submassive and massive pulmonary embolism. Report of 4 cases and review of literature. Journal of Electrocardiology 2014;47(1):75–9. PMID: 23890684

Key Teaching Points

ECG findings in Hypothermia

ST-segment elevation or depression
Tremor artifact
J-waves (Osborn waves – positive deflections at the J-point)
Sinus bradycardia, junctional rhythms
Prolongation of all intervals
Slow irregular atrial fibrillation
Ventricular fibrillation
Asystole

Key Teaching Points

Take home points

Beware of straightening of the initial part of the T-wave

- This is often an early finding in acute ischemia
- When in doubt get serial ECGs to evaluate for dynamic changes that could help you diagnose an early STEMI!

Key Teaching Points

Narrow-Complex & Regular Tachycardia Differential

Sinus Tachycardia

One P-wave for every QRS
Upright P-waves in limb leads (I, II, III, aVF), & inverted P-wave in aVR

Supraventricular Tachycardia (SVT)

No distinct P-waves. May be hidden or may follow the QRS complex (“retrograde atrial activity”)
Different types (AV Nodal re-entry, Non-paroxysmal junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign as long as it goes away when sinus rhythm is restored
SVT can also cause electrical alternans that disappears when sinus rhythm is restored

Atrial flutter with 2:1 Conduction

2 atrial beats for every QRS
Saw tooth pattern
Always consider when rate is 150 +/- 20

To differentiate…always look at what the atrium is doing.

Take home points:

SVT’s

ST-segment depression in inferior and lateral leads is common
STE in aVR is common
These are typically not associated with coronary lesions (as long as they resolve after cardioversion)

Wolff-Parkinson-White Syndrome

Ventricular pre-excitation syndrome
Affects 0.1 – 0.3% of population
Classic triad: Short PR, delta waves, wide QRS complex
Delta waves may be very subtle or absent in some leads
Short PR is your major clue…always check intervals!
Pseudo-infarction patterns are common
Pseudo-inferior MI
Pseudo-posterior MI

WPW with SVT

Narrow (orthodromic) – Treat like SVT
Wide (antidromic) – Treat like Ventricular Tachycardia

Key Teaching Points

Check out last week’s case that covers WPW with orthodromic and antidromic SVT here: February 22, 2016 Case of the Week

Wolff-Parkinson-White Syndrome with Atrial Fibrillation

Very rapid irregularly irregular tachycardia (rates may approach 300 beats/min) with wide QRS complexes that vary in morphology
Often misdiagnosed as SVT, VT or atrial fibrillation with BBB
Misdiagnosis and treatment with AVN blockers can be deadly!
Treat with procainamide, flecainide (?), or preferably cardioversion
Key Point: Avoid all AV Nodal blockers
Adenosine
Beta-blockers
Calcium channel blockers
Digoxin
Amiodarone

Pitfall: Treatment with Amiodarone results in patient decompensation (see references)

Take Home Points:

WPW + Atrial Fibrillation

Irregularly irregular tachycardia
Complexes vary in shape and width
May approach 250-300 bpm or higher
Avoid all AV nodal blockers… including amiodarone!
Use procainamide, flecainide (?),or cardioversion

References:

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745
Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399
Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217
Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602
Tijunelis MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. 2005 Jul;7(4), 262–265. PMID: 17355684
Badshah A, Mirza B, Janjua M, et al. Amiodarone-induced torsade de pointes in a patient with wolff-Parkinson-White syndrome. Hellenic J Cardiol 2009;50(3):224–6. PMID: 19465366
Nebojša M, DRAGAN S,Nebojša A, et al. Lethal outcome after intravenous administration of amiodarone in patient with atrial fibrillation and ventricular preexcitation. J Cardiovasc Electrophysiol 2011;22(9):1077–8. PMID: 21332863
Writing Committee Members. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. JAC 2014;64(21):2246–80. PMID: 24682347
Marriott, Advanced concepts in Arrhythmias, Mosby 1998. Amazon Link

Key Teaching Points

Take Home Points:

Hyperacute T-waves

This is often an early finding in ischemia

Look for straightening of the initial part of the T-wave
- Check out this previous case from Feb 15,2016 on this topic
Look for disproportionately large T-waves in comparison to the QRS complexes

When in doubt get serial ECGs to evaluate for dynamic changes that could help you diagnose an early STEMI!

Key Teaching Points

Take Home Points:

Don’t jump to conclusions! Be systematic.

Systematic approach to ECGs

Rate & Rhythm
Axis
Intervals (PR, QRS, QT)
Enlargement (atrial, ventricular)
Ischemic/infarction (Q’s, T’s, ST-segments)

Differential for Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Differential for QRS Prolongation

Bundle branch blocks (LBBB or RBBB)
Paced beats
Pre-excitation (e.g. WPW)
Ventricular ectopy
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

Na⁺channel blocker toxicity

Tachycardia
Tall R wave in aVR
Rightward axis
QRS-interval widening
QT interval prolongation

Take Home Points:

ECG’s can be very helpful in patients with seizures
When interpreting ECG’s…
- Use a systematic step-by-step approach
- Know your differential diagnosis!
- Right axis deviation, wide-complex QRS, Prolonged QTc = Think Na⁺channel blocker toxicity!

Key Teaching Points

Ventricular Tachycardia (VT)

Sustained VT
- Rate > 120-130
- Lasts at least 30 seconds or produces hemodynamic instability
- Treatment with meds or shock
Non-sustained VT
- Rate > 120-130
- Lasts < 30 seconds, no associated hemodynamic instability
- Key to treatment is to look for and treat underlying cause
  - Cardiac ischemic, hypoxia, electrolyte abnormalities, PE, etc.
  - Cardiac ischemia may induce sustained or non-sustained monomorphic VT in the presence of a myocardial scar
  - Empiric antiarrhythmic therapies are probably not indicated. No antiarrhythmic drug is suitable for primary prevention of cardiac death with the exception of beta blockers

References:

1. Katritsis DG, Zareba W, Camm AJ. Nonsustained ventricular tachycardia. J Am Coll Cardiol 2012;60(20):1993–2004. PMID: 23983773

2. Foley P, Kalra P, Andrews N. Amiodardone—avoid the danger of torsade de pointes. Resuscitation. 2008;76(1):137-41. PMID: 17716804

Key Teaching Points

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

Himalayan T-waves

Very tall, broad-based T-waves
Market prolongation of QTc
ST-segment elevation
May have camel hump due to large U-waves
Commonly caused by hypokalemia
Congenital long QT syndrome with deafness (Jervell-Lange-Nielsen syndrome)
Association with syncope & seizures (due to torsades)

Take Home Points:

Tall broad T-waves ± U waves, prolonged QTc, STE
Think of hypokalemia & congenital long QT syndromes
Beware of torsades!

Key Teaching Points

Atrial Septal Defect (ASD)

Causes intra-atrial shunting that contributes to cryptogenic strokes
Often diagnosed and corrected in childhood
- If uncorrected, patients typically do well in early adulthood, but may become symptomatic in their 40’s
- Signs and symptoms include: Dyspnea on exertion, heart failure, palpitations, syncope, pulmonary hypertension, atrial dysrhythmias, strokes
Typical ECG Abnormalities
- 1^st degree AV Block
- Atrial dysrhythmias
- Incomplete right bundle branch block
- Right axis deviation as pulmonary hypertension develops
- Crochetage (notching) pattern in inferior leads is very specific and correlates with shunt severity!

Take Home Points:

Crochetage pattern
- Notching of the R wave in the inferior limb leads that is suggestive of ASD or PFO (patent foramen ovale)
- Consider in young patients with dyspnea on exertion or stroke like symptoms
- Definitive diagnosis can be made with echocardiography

Reference

Heller J, Hagège AA, Besse B, et al. “Crochetage” (notch) on R wave in inferior limb leads: a new independent electrocardiographic sign of atrial septal defect. JAC 1996;27(4):877–82. PMID: 8613618

Key Teaching Points

Want to learn about low risk chest pain?

Check out the recent lectures from the University of Maryland Emergency Cardiology Symposium here: Livestream Lectures & check out the #UMESC16 tweets.

Uncomplicated Right Bundle Branch Block

Wide QRS
Tall R wave in V1 (qR or rsR’)
Wide S-wave in leads I and V6
Common to gave some STD and TWI in V1-3, which is normal
Any ST-segment elevation in setting of RBBB is abnormal!

Take Home Points:

Any STE in RBBB is abnormal
The computer’s ECG interpretation is not to be trusted!

Key Teaching Points

Want to learn about low risk chest pain?

Check out the recent lectures from the University of Maryland Emergency Cardiology Symposium here: Livestream Lectures & check out the #UMESC16 tweets.

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take Home Points:

Beware! Hyperkalemia is “the great imitator in ECG’s”
Serum K⁺ levels don’t always correlate with expected ECG findings
Really wide complex VT? Think of tox & metabolic causes
Slow VT (rate <120-130)? Think of tox & metabolic causes
Hyperkalemia can also mimic STEMI
- Think of hyperkalemia when QRS is very wide or a rightward axis is present

Key Teaching Points

Differential diagnosis for regular wide complex tachycardia

Ventricular tachycardia
Sinus tachycardia with aberrant conduction
Supraventricular tachycardia with aberrant conduction
Atrial flutter with 2:1 conduction with aberrant conduction

Take Home Points:

Pay attention to the T-waves!
- Abnormal morphology? Consider buried p-waves!
- When in doubt, map it out!
- Best lead to look for p-waves is V1

Key Teaching Points

ECG 1 Answer

Multifocal atrial tachycardia with voltage criteria for LVH. Treat the underlying condition!

Differential Diagnosis for Narrow Complex Irregular Tachycardia

Atrial fibrillation
Atrial flutter with variable conduction
Multifocal atrial tachycardia (3 different p-wave morphologies)

ECG 2 Answer

Sinus tachycardia with complete heart block and a junctional escape rhythm. There is evidence of inferior STEMI with probable posterior extension.

Pearl: Remember that sinus rhythm should have upright p-waves in the limb leads (inverted in aVR)

ECG 3 Answer

Atrial fibrillation with complete heart block and a junctional escape rhythm. The ECG suggests digoxin toxicity. There are also biphasic T-waves that deflect down before going up “reverse Wellens’ waves” a.k.a. “NikEleKam T waves” caused by U-waves and a prolonged QT interval that is consistent with severe hypokalemia

ECG 4 Answer

Calcium & Bicarb!

This is a regular really wide complex tachycardia that is too slow to be ventricular tachycardia. You should think of toxicological and metabolic causes. Treat empirically with Calcium & Bicarb when in doubt!

Case 5 Answer

Early inferior wall STEMI

New T-wave inversion in aVL may be an early reciprocal change

Reciprocal changes can precede ST-elevation (STE) in MI
New TWI in aVL can be the first sign of an inferior STEMI
Also watch out for hyperdynamic t-waves and downsloping ST-segments which suggest other early reciprocal changes
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECGs

Case 6 Answer

Artifact. There are intrinsic beats that can be mapped out. Correlate clinically!

Key Teaching Points

ECG 7 Answer

Hypertrophic obstructive cardiomyopathy (HOCM)

ECG abnormalities present in 85-93%
- High left ventricular voltages
- Left atrial enlargement is most common
- Tall R wave in V1 (mimics posterior MI)
- Deep narrow Q waves in inferior, lateral leads
Definitive diagnosis – Doppler ECHO
- Can also help to assess severity of obstruction at rest and with provocative maneuvers
Treatment
- Beta blockers, calcium channel blockers
- Amiodarone for ventricular dysrhythmias

For more on HOCM, review the case from November 16, 2015.

ECG 8 Answer

Impressive Syndrome, treat for hyperkalemia!

Hyperkalemic Periodic Paralysis (HYPP) a.k.a Impressive Syndrome

Inherited autosomal dominant condition that affects Na⁺ channels in muscle tissues and affects the ability to regulate K⁺in the blood.
Produces significant muscle weakness and paralysis, can cause death because of diaphragmatic paralysis
Episodic, usually caused by medications, K⁺ rich foods, or significant stressors to the body

Take-home point:

Bizarre rhythm? Wide QRS? Think tox/metabolic & get your Calcium and Bicarb ready!

For more on this topic, review the case from December 28, 2015.

ECG 9 Answer

Sinus rhythm with junctional trigemeny, left axis deviation, and WPW

Differential Diagnosis for Short PR interval

Junctional rhythm
Pre-excitation syndromes
- WPW (Wolff-Parkinson-White syndrome)
- LGL (Lown-Ganong-Levine syndrome)
Normal variant (EAVNC – enhanced AV nodal conduction)

Differential diagnosis of leftward axis

Left ventricular hypertrophy (LVH)
Left bundle branch block (LBBB)
Paced rhythm
Ventricular beats/ectopy
Pre-excitation (e.g. WPW)
Inferior MI (from Q-waves)
Left anterior fascicular block (LAFB)
Hyperkalemia
Normal Variant

For more on WPW, review the case from February 22, 2016 & February 29, 2016.

ECG 10 Answer

TCA/ Na⁺channel blocker toxicity. Treat with Sodium Bicarbonate.

Na⁺channel blocker toxicity ECG

Tachycardia
Tall R wave in aVR
Rightward axis
QRS-interval widening

To learn more about Na⁺channel blocker toxicity review the case from March 14, 2016.

ECG 11 Answer

Calcium for Hyperkalemia

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Causes of Rightward Axis Deviation

Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Lead misplacement / Dextrocardia
Normal thin adults with horizontally positioned hearts

Pearl: When you see a wide QRS rhythm with a rightward axis, think of HYPERKALEMIA or other sodium channel blocker toxicities.

For more practice on this topic, review the case from Jan 12, 2015.

ECG 12 Answer

Hypokalemia causing Himalayan T-waves and a prolonged QT interval. Watch out for Torsades!

Himalayan T-waves

Very tall, broad-based T-waves
Market prolongation of QTc
ST-segment elevation
May have camel hump due to large U-waves

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

For more practice on this topic, review the case from March 28, 2016.

Key Teaching Points

Left anterior fascicular block (LAFB)

Leftward axis
qR in I and aVL
rS in III
QRS may be normal or slightly prolonged
Poor R-wave progression is common
No other reasons for leftward axis

Differential diagnosis for leftward axis

Left ventricular hypertrophy (LVH)
Left bundle branch block (LBBB)
Left anterior fascicular block (LAFB)
Paced rhythm
Ventricular beats/ectopy
Pre-excitation (e.g. WPW)
Inferior MI (from Q-waves)
Hyperkalemia
Normal Variant

Left posterior fascicular block (LPFB)

Rightward axis
- Rarely a normal variant
  - Left posterior fascicle receives blood supply from both left and right coronary arteries
  - Almost always occurs in presence of CAD: if acute MI, there is usually multivessel disease, extensive infarct and poor prognosis
- rS in I and aVL
- qR in III
- QRS may be normal or slightly prolonged
- No other reasons for rightward axis

Differential diagnosis for rightward axis

Right ventricular hypertrophy (RVH)
Left posterior fascicular block (LPFB)
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Type of Fascicular Block	LAFB	LPFB
Axis	Left Axis Deviation	Right Axis Deviation
Leads I & aVL
Lead III

Bonus Pearls:

Bifascicular Block

Conduction abnormality where two of the three main fascicles of the His/Purkinje system are blocked

- Usually a RBBB + LAFB
- Or RBBB + LPFB

Trifascicular Block

1st degree AV Block + RBBB + LAFB
Or 1st degree AV Block + RBBB + LPFB

References:

Chung EK. ECG Diagnosis: A Self-Assessment Workbook. Blackwell Science. 2000. Amazon Link.

Key Teaching Points

Diagnostic criteria for Acute Pericarditis

At least 2 of the following clinical criteria are required:
- Chest pain (typically sharp and pleuritic, improved by sitting up and leaning forward)
- Pericardial friction rub
- New or worsening pericardial effusion
- Suggestive ECG changes

ECG findings in Pericarditis vs. STEMI

Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that strongly favor STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
Horizontal or convex upward ST-segment morphology
STE in lead III > the STE in lead II
R-T sign or “checkmark sign”
Q-waves that youknow are new (be cautious if they are old)

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis (only after step 1):

Pronounced PR-segment depression in multiple leads
Spodick sign (TP segment downsloping) – may be useful after considering all the other factors above, but be wary as new research suggests it may be seen in both STEMI and pericarditis. Not sensitive or specific!

When in doubt…do serial ECGs and consider CATH!

Take home points:

PR depression is not specific for pericarditis!
Spodick sign is suggestive but not perfect!
Diagnose pericarditis only after you’ve ruled out STEMI on ECG & formal clinical criteria are met

References:

Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic Review. JAMA 2015;314(14):1498–506. PMID: 26461998

Key Teaching Points

Normal Right Bundle Branch Block (RBBB)

Leads V₁-V₃ can have mild ST-segment depression, which is a normal finding
The rest of the ST-segments should be isoelectric and any ST-segment elevation is ABNORMAL

Take home points:

RBBB should have no ST-segment elevation
Expect ST-depression in V₁ & V₂
Be wary of the intervals!

Look at all the leads and trace out where the QRS ends and where the J-point begins to evaluate for ST-segment deviations.

Key Teaching Points

Age as a cardiac risk factor

Young patients do have MI’s
- 123,000 AMIs per year in patients 29-44 years old
- 5-10% of AMIs occur in patients < 45 years old
- Only a minority are related to cocaine use
In another study in patients 24-39 years old (n=1023) with chest pain
- 4% ruled in for ACS
- 2% had an adverse cardiac event (death, MI, need for PCI/CABG)

ECG Pearls: Pericarditis vs. STEMI

PR depression (and PR elevation in aVR) is not pathognomonic for pericarditis
ST depression outside aVR and V1 = STEMI
Other findings suggestive of ACS
- Disproportionate T wave size in comparison to QRS complex
- Straightening of initial potion of T-wave
- R-T sign or “checkmark sign”

Final take-home points:

CAD, ACS, & STEMI DOES occur in young patients!

We will continue to see an increase in MI’s in young patients
Focus on the presentation, not the age!

References

Marsan RJ, Shaver KJ, Sease KL, et al. Evaluation of a clinical decision rule for young adult patients with chest pain. Academic Emergency Medicine 2005;12(1):26–31. PMID: 15635134.

Key Teaching Points

Lumen stenosis doesn’t matter…It’s all about plaque vulnerability!

Plaque vulnerability based on 3 major factors

Fibrous cap
Lipid core
Inflammatory cells

Recent stress testing and catheterizations are not predictive of new plaque rupture!

Plaques grow into the vessel wall rather than into the lumen, and may appear patent in angiography despite significant coronary artery disease and false negative angiography
Small plaques may be more unstable and more prone to rupture
Infarct related arteries often have non-obstructing plaque, before rupture and MI
Angiography can not distinguish stable vs. unstable plaque composition, and give no information about the fibrous cap or lipid core

Final take-home points:

Nothing will risk stratify you to zero!
You can’t always rely on the recently negative stress test or “unremarkable” cath.
History of presenting illness is the most important information and should guide your management.

References:

Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 2013;368(21):2004–13. PMID: 23697515

Arbab-Zadeh A, Nakano M, Virmani R, et al. Acute coronary events. Circulation 2012;125(9):1147–56. PMID: 22392862

Fanaroff AC, Rymer JA, Goldstein SA, et al. Does This Patient With Chest Pain Have Acute Coronary Syndrome?: The Rational Clinical Examination Systematic Review. JAMA 2015;314(18):1955–65. PMID: 26547467

Virmani R, Burke AP, Farb A, et al. Pathology of the vulnerable plaque. J Am Coll Cardiol 2006;47(8 Suppl):C13–8. PMID: 16631505

Caussin C, Ohanessian A, Lancelin B, et al. Coronary plaque burden detected by multislice computed tomography after acute myocardial infarction with near-normal coronary arteries by angiography. AJC 2003;92(7):849–52. PMID: 14516892

Key Teaching Points

ECG Diagnosis of Ventricular Tachycardia (VT)

The ECG can NOT reliably distinguish between VT and supraventricular tachycardia with aberrant conduction (SVT-AC)
- The ECG is reliable at ruling in VT
- The ECG is unreliable at ruling out VT (i.e. at ruling in SVT with AC)
Algorithms created to distinguish VT vs. SVT-AC are far from perfect and difficult to use clinically. The references review the most popular ones in detail, but they all miss cases of VT. Here is a more simple method…

Mattu Algorithm for Wide Complex Tachycardias (WCTs)

Is the WCT clearly sinus tachycardia with aberrant conduction?
1. If yes – treat the underlying cause
2. If no – go to step 2
It’s Ventricular Tachycardia

Final take-home points:

Wide complex tachycardia? Call it VT!
The WCT rules and algorithms are far from perfect
More about WCTs next week…

References:

Jastrzebski M, Kulka P, Czarnecka D, et al. Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace 2012;14(8):1165-71. PMID:22333239

Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med 2013;20(11):1121–30. PMID: 24238314

Key Teaching Points

ECG Diagnosis of Ventricular Tachycardia (VT)

The ECG can NOT reliably distinguish between VT and supraventricular tachycardia with aberrant conduction (SVT-AC)
- The ECG is reliable at ruling in VT
- The ECG is unreliable at ruling out VT (i.e. at ruling in SVT with AC)
Algorithms created to distinguish VT vs. SVT-AC are far from perfect and difficult to use clinically. The references review the most popular ones in detail, but they all miss cases of VT. Here is a more simple method…

Mattu Algorithm for Wide Complex Tachycardias (WCTs)

Is the WCT clearly sinus tachycardia with aberrant conduction?
1. If yes – treat the underlying cause
2. If no – go to step 2
It’s Ventricular Tachycardia

What about an Adenosine diagnostic challenge?

Adenosine sensitive VT is not benign and many patients go on to have unstable VT even after conversion to sinus rhythm
Response to Adenosine does NOT rule out VT!

Final take-home points:

Wide complex tachycardia? Call it VT!
- Exception: if you have a baseline and the QRS complexes are the same during sinus rhythm
The WCT rules and algorithms are far from perfect
Adenosine is not a reliable diagnostic challenge!

References:

Marill KA, Wolfram S, Desouza IS, et al. Adenosine for wide-complex tachycardia: efficacy and safety. Crit Care Med 2009;37(9):2512-8. PMID:19623049

Jastrzebski M, Kulka P, Czarnecka D, et al. Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace 2012;14(8):1165-71. PMID:22333239

Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med 2013;20(11):1121–30. PMID: 24238314

Key Teaching Points

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
New RBBB or incomplete RBBB
Superventricular tachydysrhythmias
Ventricular dysrhythmias
ST-segment elevations or depressions
New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

Differential diagnosis for tall R-wave in V₁

Posterior MI
Incomplete/Complete RBBB
Right ventricular hypertrophy (RVH- e.g. COPD, Pulmonary HTN, muscular dystrophy, etc.)
Acute RV strain (PE)
Pre-excitation/WPW
Ventricular ectopy (VT)
Hyperkalemia
Hypertrophic cardiomyopathy
Lead misplacement

Differential diagnosis for rightward axis

Lateral MI (from Q-waves in lead I)
Left posterior fascicular block (LPFB)
Right ventricular hypertrophy (RVH- e.g. COPD, Pulmonary HTN, muscular dystrophy, etc.)
Acute RV strain (PE)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Lead misplacement / Dextrocardia

ECG findings in PE associated with hemodynamic instability and increased morbidity and mortality (not specific for PE):

TWIs in right precordial leads
ST-segment elevation and depression
- Especially STE in aVR, V₁-V₂
Tachycardia (sinus, afib/flutter)
Signs of right heart strain (RAD, tall R wave in V₁)

Final take-home points:

PE commonly mimics ACS (especially big PEs)
- Expect T-wave inversions and ST-segment changes
- STE in V₁-V₂ & aVR
Consider your ECG Differentials!
- Rightward axis is not typical for STEMI
- Consider PE & Hyperkalemia when dealing with STE & RAD

References:

Shopp JD, Stewart LK, Emmett TW, Kline JA. Findings From 12-lead Electrocardiography That Predict Circulatory Shock From Pulmonary Embolism: Systematic Review and Meta-analysis. Acad Emerg Med 2015;22(10):1127–37. PMID:26394330

Dibgy,GC, Kulka P, Zhan ZQ, et al. The value of electrocardiographic abnormalities in the prognosis of pulmonary embolism: a consensus paper. Ann Noninvasive Electrocardiol 2015. May;20(3):207-23. PMID:25994548

Kukla P, McIntyre WF, Fijorek K, et al. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med 2014;32(6):507–10. PMID:24602894

Zhan Z-Q, Wang C-Q, Nikus KC, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51.PMID:24750207

Abarca E, Baddi A, Manrique R. ECG manifestations in submassive and massive pulmonary embolism. Report of 4 cases and review of literature. Journal of Electrocardiology 2014;47(1):75–9. PMID:23890684

Key Teaching Points

Prehospital ECG Pearls

Consider PE & Hyperkalemia when dealing with ST–segment elevation & Right axis deviation (RAD). Both can mimic ACS, STEMI with RAD is atypical!
Consider posterior MI when there is ST-depression in anterior leads with tall R-waves and upright T-waves
Young people can still have MI’s and any STE in RBBB is abnormal!

Final take-home points:

Just because electrocardiography is a basic skill doesn’t mean that our skills should be basic

YOU must be the experts in electrocardiography!

Key Teaching Points

Systematic approach to ECGs

Rate & Rhythm
Axis
Intervals
Enlargement
Ischemic/infarction

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypotermia
Post-cardioversion (stunning)
Tako tsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take home points:

Hypercalcemia can mimic STEMI by shortening the QT
DDx of short QTc
1. Hypercalcemia
2. Digoxin
3. Congenital Short QT syndrome

References

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838

Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Key Teaching Points

Systematic approach to ECGs

Rate & Rhythm
Axis
Intervals
Enlargement
Ischemic/infarction

Causes of ST-segment Elevation

Acute myocardial injury (ACS or trauma)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Brugada syndrome & mimics
Hypotermia
Post-cardioversion (stunning)
Tako tsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take home points:

Hypercalcemia can mimic STEMI by shortening the QT
DDx of short QTc
1. Hypercalcemia
2. Digoxin
3. Congenital Short QT syndrome

References

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838

Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Key Teaching Points

Review Key Teaching Points (Red Box)

Quick Evaluation of the QT-interval

T-waves should end before the midpoint of the R-R interval.

Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance.

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressure
Congenital

Bonus Pearl

Prolongation of the ST-segment contributing to a prolonged QT interval is the hallmark ECG change in hypocalcemia. Only hypocalcemia and hypothermia produce these ECG changes, so when the temperature is normal…consider hypocalcemia!

Key Teaching Points

Left Bundle Branch Block

LBBB causes ST-segment & T wave changes that can make the identification of acute MI more challenging
Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal

Sgarbossa Criteria

Sgarbossa and now the modified Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
Meeting the criteria in a single lead can be specific for AMI
The criteria are reviewed below

Concordant STE ≥ 1mm (in any lead) = Most specific for MI
Concordant STD ≥ 1mm in V1, V2, or V3 = Specific for MI
Discordant STE ≥ 5mm = Less specific for MI

A revised Sgarbossa C rule has been proposed (recently validated) to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥ 5 mm) with a proportional criterion (ST-segment to S-wave ratio ≥ 25%) and has been found to be superior to the original criteria for identifying acute coronary occlusion in LBBB.

Take-home Points:

Despite cardiology literature supporting Sgarbossa concordance criteria, it is not clearly stated in AHA/ACC guidelines
Share the literature with your colleagues if they are unaware of it
Anticipate increasing literature supporting the modified Sgarbossa criteria

References:

Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013;166(3):409–413. PMID: 24016487.

Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96–105. PMID: 22766335.

Mayers H, Limakakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170:1255-1264. PMID:26678648

Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.
Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing. Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802.

Key Teaching Points

Pacemakers and AMI

Paced rhythms cause ST-segment & T wave changes that can make identification of acute MI difficult
As in in LBBB, paced rhythms are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST–segment deviations that are concordant(in same direction) to the QRS complex or excessively discordant are abnormal

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose AMI in setting of paced rhythms
The criteria are reviewed below:

A. Concordant STE ≥ 1mm (in any lead)

B. Concordant STD ≥ 1mm in V1, V2, or V3

C. Discordant STE ≥ 5mm (most specific)

Take-home Points:

Sgarbossa criteria appear to predict acute MI in patients with pacemakers. The criteria have low sensitivity but are very specific. Criteria C (excessively discordant ST-segment elevation) seem to be most specific in patients with pacemakers.
Anticipate increasing literature supporting the modified Sgarbossa criteria in paced rhythms (not yet published)
Despite cardiology literature supporting Sgarbossa concordance criteria, it is not clearly stated in AHA/ACC guidelines
Share the literature with your colleagues if they are unaware of it

References:

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing.Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802
Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576
Maloy KR, Bhat R, Davis J, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers. West J Emerg Med. 2010;11(4):354–357. PMID: 21079708

Key Teaching Points

Polymorphic Ventricular Tachycardia & Torsade de pointes vs. Artifact

Monomorphic VT is usually (not always) seen in patients with old MI’s and scarred myocardium
Typical polymorphic VT without a prolonged QT-interval is frequently associated with acute MI
Torsades is a type of polymorphic VT associated with a prolonged QT-interval after conversion of the rhythm
Torsades is typically treated with Magnesium to avoid any further prolongation of the QT-interval with anti-arrhythmic drugs
Artifact is not uncommon and can mimic polymorphic VT, look at all 12 leads!

Take home points

For suspected polymorphic VT or ventricular fibrillation, always consider the possibility of artifact
If unstable/unconscious, check pulse and don’t delay shock
If stable, look for regular beats that may be buried within artifact!

Key Teaching Points

Clues to RV Infarction on the 12-lead ECG

In the presence of an inferior STEMI…
- ST-segment depression in lead V2 with
  - ST-segment elevation in lead V1 OR
  - Isoelectric ST-segment in lead V1
- STE in lead III >>> II
Or when in doubt, just get right-sided leads!

Take home points

1/3 of inferior STEMI’s will extend to the right ventricle
- These patients will be very preload dependent
- Preload reducing meds (like nitroglycerin) can cause significant hypotension and should be avoided
- If the lungs are clear, treat with IVF, not vasopressors

Key Teaching Points

Differential for ST-depression in anteroseptal leads

Posterior STEMI
- Mirror image of septal STEMI in leads V₁-V₃
- Large R waves (instead of Q waves)
- ST-depression (instead of STE)
- Upright T waves in V₁-V₃ (instead of inversions)
Anteroseptal ischemia
Miscellaneous
- RBBB
- Hypokalemia, etc.

Posterior STEMI (“inferolateral”) – the most common type of missed STEMI!

Usually associated with inferior or lateral MI due to RCA or circumflex occlusion
4-5% of STEMI’s are isolated Posterior MI’s
Often misdiagnosed as just ischemia or NSTEMI
Only 30% are revascularized within 90 mins
Increased morbidity and mortality
Pearl: Even 0.5 mm of STE on posterior lead ECGs is diagnostic

Take-home Points:

Always consider posterior STEMI when patients have ST-segment depression in V1-V3
- Especially with upright T waves and tall R waves (late finding)
Have a low threshold for serial ECG’s in patients with ongoing or changing chest pain!

References:

Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes among patients with an isolated posterior myocardial infarction: insights from the National Cardiovascular Data Registry (NCDR). American Heart Journal. 2014;167(3):350–4. PMID: 24576519
Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. Journal of Electrocardiology. 2014;47(4):448–58. PMID: 24792903.
Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among patients with acute myocardial infarction. Journal of Electrocardiology. 2013;46(6):653–9. PMID: 23890685.
Waldo SW, Armstrong EJ, Kulkarni A, et al. Clinical characteristics and reperfusion times among patients with an isolated posterior myocardial infarction. J Invasive Cardiol. 2013;25(8):371-5. PMID: 23913600.

Key Teaching Points

ECG findings in TCA/Na⁺channel blocker toxicity

Tachycardia
Rightward axis
- Large S-waves in lateral leads
- Tall R-wave in aVR
- Tall R-wave in V1, pseudo-Brugada pattern
QRS-interval widening
Prolonged QT-interval

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Causes of QRS Prolongation

Bundle branch blocks (LBBB or RBBB)
Paced beats
Pre-excitation (e.g. WPW)
Ventricular ectopy
Metabolic (Hyperkalemia or severe acidosis)
Na⁺channel blocking drugs (e.g. TCA’s)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

Take-home Points:

Why get an ECG on a patient with seizure?
- Evidence of arrhythmia that may have caused syncope (mistaken as a seizure)
  - Especially with long QT-intervals
- Evidence of metabolic abnormality or drug toxicity
  - Especially TCA’s

Key Teaching Points

Non-STE ACS (Class IA in national guidelines)

Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that:
- Develop hemodynamic or electrical instability
- Have intractable ischemia
- Develop acute decompensating heart failure

Reference:

Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64(24):e139–228. PMID: 25260718.

Take-home Points:

Left circumflex lesions are the most common electrocardiographically silent vessel occlusion
Persistent ischemic symptoms despite maximal medical treatment mandate cath lab activation

Key Teaching Points

de Winter T-waves

1-3 mm ST-depression at the J-point in the mid precordial leads, leading into tall symmetric T-waves
High risk of acute anterior MI
Suggestive of an acute proximal LAD occlusion (contrast to sub-acute occlusion of Wellens syndrome), or less commonly a 1^st diagonal or left circumflex occlusion
Although no ST-elevation, may be an unstable lesion for which urgent cath should be “strongly considered”
Get serial ECG’s while the patient is having pain, may progress to STEMI
Have high concern for decompensation and treat aggressively
Increasing push to consider this a STEMI equivalent

References:

Birnbaum I, Birnbaum Y. High-risk ECG patterns in ACS—need for guideline revision. J Electrocardiol 2013;46(6):535–9. PMID: 23863685
Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr. Am J Emerg Med 2014;32(3):287.e5–8. PMID: 24176590
de Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008 Nov 6;359(19):2071-3. PMID:18987380
Verouden NJ, Koch KT, Peters RJ, et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart 2009;95(20):1701–6. PMID: 19620137
Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec;160(6):995-1003. PMID:21146650
Stankovic I, Ilic I, Panic M, et al. The absence of the ST-segment elevation in acute coronary artery thrombosis: what does not fit, the patient or the explanation? J Electrocardiol 2011;44(1):7–10. PMID: 20591442

Key Teaching Points

Differential for ST-depression in anteroseptal leads

Posterior STEMI
- Mirror image of septal STEMI in leads V₁-V₃
- Large R waves (instead of Q waves)
- ST-depression (instead of STE)
- Upright T waves in V₁-V₃ (instead of inversions)
Anteroseptal ischemia
Miscellaneous
- RBBB
- Hypokalemia, etc.

Posterior STEMI (“inferolateral”) – the most common type of missed STEMI!

Usually associated with inferior or lateral MI due to RCA or circumflex occlusion
4-5% of STEMI’s are isolated Posterior MI’s
Often misdiagnosed as just ischemia or NSTEMI
Only 30% are revascularized within 90 mins
Increased morbidity and mortality
Pearl: Even 0.5 mm of STE on posterior lead ECGs is diagnostic

Take-home Points:

Always consider posterior STEMI when patients have ST-segment depression in V1-V3
- Especially with upright T waves and tall R waves (late finding)
Have a low threshold for serial ECG’s in patients with ongoing or changing chest pain!

References:

Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes among patients with an isolated posterior myocardial infarction: insights from the National Cardiovascular Data Registry (NCDR). American Heart Journal. 2014;167(3):350–4. PMID: 24576519
Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. Journal of Electrocardiology. 2014;47(4):448–58. PMID: 24792903.
Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among patients with acute myocardial infarction. Journal of Electrocardiology. 2013;46(6):653–9. PMID: 23890685.
Waldo SW, Armstrong EJ, Kulkarni A, et al. Clinical characteristics and reperfusion times among patients with an isolated posterior myocardial infarction. J Invasive Cardiol. 2013;25(8):371-5. PMID: 23913600.

Key Teaching Points

Poor R-wave Progression Differential

Defined as a < 3 mm R-wave by lead V3

- Prior anteroseptal MI
- LVH
- High precordial electrode placement
- Normal variant

New T-wave inversion in aVL may be a reciprocal change

Reciprocal changes can precede ST-elevation (STE) in MI
New TWI in aVL can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECG’s!

Take-home Points:

Don’t trust the ECG computer interpretation!
Symptoms of ACS with new TWI is aVL is concerning for impending inferior STEMI
Beware of straightening of the T-wave upslope, morphology changes before STE develops
Worry about T-waves that are large or bigger that the size of the QRS complex, hyperacute T-waves may develop before STE
For persistent symptoms and concern for ACS, one ECG begets another. Get serial ECG’s!

Key Teaching Points

Differential Diagnosis for Diffuse ST-Elevation (STE)

Large Acute STEMI

Has reciprocal ST-segment depression
Straight, horizontal, convex or concave ST-segment morphology
STE in lead III > II
Evolving changes (especially with tx)

Benign Early repolarization

No reciprocal ST-segment depression
Concave ST-segment morphology
STE in lead II > III
No PR-segment depression
Fishhook j-point elevation

Pericarditis/Myocarditis

No reciprocal ST-segment depression
Concave ST-segment morphology
STE in lead II > III
PR-segment depression (not specific)
Spodick’s sign (not sensitive or specific)

Ventricular aneurysm

No reciprocal ST-segment depression
+ Q-waves

Vasospasm

No reciprocal ST-segment depression
May evolve with treatment

Acute Pericarditis vs. Benign Early Repolarization (BER)

Positional changes in pain suggests BER
“Fishhook” (J-wave) suggests BER
Height of ST segment elevation compared to height of T wave in lead V6 < 25% suggests BER
Compare with old ECG

Take-home Points:

Is “benign” early repolarization truly benign?
- Can be confusing and complicated
  - Variables:
    - Lateral vs. inferior lead involvement
    - STE vs. elevated J-waves vs. QRS slurring vs. J-waves without STE
  - The bottom line…patients with early repolarization are at slightly higher risk of arrhythmias and SCD over the course of many years
    - Risk varies depending on the type of pattern
    - Absolute risk difference is ~ 0.0007%/yr
  - “From a population perspective, early repolarization can properly be called a normal variant: – Patton, Circulation 2016
- Still can’t figure out what’s causing the STE? When in doubt, get serial ECG’s and get your cardiologist involved!

References:

Patton KK, Ellinor PT, Exekowitz M, et al. Electrocardiographic early repolarization: a scientific statement from the American Heart Association. Circulation 2016;133:1520-1529. PMID: 27067089
O’Neal WT, Wang YG, Wu HT, et.al. Electrocardiographic J wave and cardiovascular outcomes in the general population (from the Atherosclerosis Risk in Communities Study). Am J Cardiol 2016;118:811-815. PMID: 27596326

Key Teaching Points

ECG findings in Hypothermia
- J-waves (Osborn waves – positive deflections at the J-point)
- Sinus bradycardia, junctional rhythms
- Prolongation of all intervals
- Slow atrial fibrillation
- Tremor artifact
- ST-segment elevation or depression
- Ventricular fibrillation
- Asystole

Key Teaching Points

Take-home Points:
- Electricity is GREAT! But beware…
  - Large T-waves can fool the defibrillator machines into thinking they are QRS complexes
  - If the arrowheads during synchronized cardioversion are lining up on the T-waves, switch to a different lead to correct this or electricity will be delivered at the wrong time (during ventricular repolarization) and can put patients into v fib arrest!

Key Teaching Points

Wolff-Parkinson-White Syndrome with Atrial Fibrillation

Very rapid irregularly irregular tachycardia (rates may approach 300 beats/min) with wide QRS complexes that vary in morphology
Often misdiagnosed as SVT, VT or atrial fibrillation with BBB
Misdiagnosis and treatment with AVN blockers can be deadly!
Treat with procainamide, flecainide (?), or preferably electrical cardioversion
Key Point: Avoid all AV Nodal blockers
Adenosine
Beta-blockers
Calcium channel blockers
Digoxin
Amiodarone

Pitfall: Treatment with Amiodarone results in patient decompensation (see references)

Take Home Points:

WPW + Atrial Fibrillation

Irregularly irregular tachycardia
Complexes vary in shape and width
May approach 250-300 bpm or higher
Avoid all AV nodal blockers…including Amiodarone!
Use Procainamide, Flecainide (?),or electrical cardioversion

References:

Sheinman BD, Evans T. Acceleration of ventricular rate by fibrillation associated with the Wolff-Parkinson-White syndrome. Br Med J (Clin Res Ed). 1982 Oct 9; 285(6347), 999–1000. PMID: 6812745
Schützenberger W, Leisch F, Gmeiner R. Enhanced accessory pathway conduction following intravenous amiodarone in atrial fibrillation. A case report. Int J Cardiol. 1987 Jul;16(1):93-5. PMID: 3610399
Gaita F, Giustetto C, Riccardi R, et al. Wolff-Parkinson-White syndrome. Identification and management. Drugs. 1992 Feb;43(2):185-200. PMID: 1372217
Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am Heart J. 1996 Jun;131(6):1214-6. PMID: 8644602
Tijunelis MA, Herbert ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. 2005 Jul;7(4), 262–265. PMID: 17355684
Badshah A, Mirza B, Janjua M, et al. Amiodarone-induced torsade de pointes in a patient with wolff-Parkinson-White syndrome. Hellenic J Cardiol 2009;50(3):224–6. PMID: 19465366
Nebojša M, DRAGAN S,Nebojša A, et al. Lethal outcome after intravenous administration of amiodarone in patient with atrial fibrillation and ventricular preexcitation. J Cardiovasc Electrophysiol 2011;22(9):1077–8. PMID: 21332863
Writing Committee Members. 2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. JAC 2014;64(21):2246–80. PMID: 24682347
Marriott, Advanced concepts in Arrhythmias, Mosby 1998. Amazon Link

Key Teaching Points

Ventricular Tachycardia (VT)

Sustained VT
- Rate > 120-130
- Lasts at least 30 seconds or produces hemodynamic instability
- Treatment with antiarrhythmic medications or electrical cardioversion
Non-sustained VT
- Rate > 120-130
- Lasts < 30 seconds, no associated hemodynamic instability
- Key to treatment is to look for and treat underlying cause
  - Cardiac ischemic, hypoxia, electrolyte abnormalities, PE, etc.
  - Cardiac ischemia may induce sustained or non-sustained monomorphic VT in the presence of a myocardial scar
  - Empiric antiarrhythmic therapies are probably not indicated. No antiarrhythmic drug is suitable for primary prevention of cardiac death with the exception of beta blockers
  - Consider empiric beta-blockers & magnesium

Take Home Points:

Look in all of the leads for clues! Your answer may be seen in only a single lead
Massive ST-segment elevation can make the QRS complexes look wide and may mimic PVC’s or VT
Non-sustained VT
- Look for the underlying cause and treat
- Empiric beta blockers, +/- magnesium

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias
Bradydysrhythmias, advanced AV Blocks, and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Regular Really Wide Complex Tachycardia (RRWCT)

Regular Really wide QRS complexes > 200 ms = RRWCT
Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause RRWCT’s that mimic Ventricular Tachycadia (rate however is typically < 120 bpm)
Consider empiric treatment with calcium and bicarb before antiarrhythmics that can kill these patients!

Take Home Points:

Hyperkalemia is the great imitator. It does what it wants to the ECG!
Always consider hyperkalemia in your differential for bradycardias and AV blocks!

When ACLS isn’t working, think of toxicological and metabolic causes and consider empiric treatment with calcium and bicarb

Key Teaching Points

Quick Evaluation of the QT-interval

T-waves should end before the midpoint of the R-R interval.

Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance.

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressure
Congenital

Take Home Points:

ECG findings in severe hypokalemia
- “Prolonged QT-interval”
- U-waves (can be very large)
- Flattening of the T-waves, then ST-segment downsloping/depression
- Biphasic T-waves that deflect down before going up “reverse Wellens’ waves” a.k.a. “NikEleKam T waves” are caused by severe hypokalemia that prolongs the QT interval because of large U-waves.
- Ventricular ectopy!

Key Teaching Points

Quick Evaluation of the QT-interval

T-waves should end before the midpoint of the R-R interval.

Beware of a prolonged QT when the T-waves end after ½ the R-R wave distance.

Differential for Prolonged QTc Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, TCA’s, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressure
Congenital

Take Home Points:

Prolonged QT due to prolonged T –wave
- Hypokalemia
- Hypomagnesemia
- Medications
- Misc: Elevated ICP, Cardiac ischemia, Congenital

Prolonged QT due to prolonged ST-segment
- Hypocalcemia
- Hypothermia

Key Teaching Points

Differential for Fever & Altered Mental Status

Infection (especially intracranial)
Toxicological
- Sympathomimetic
- Anticholinergics
- Delirium tremens
- Aspirin toxicity
- PCP intoxication
- Neuroleptic malignant syndrome (NMS)
- Serotonin syndrome
- Malignant hyperthermia
Endocrine
- Adrenal crisis
- Pheochromocytoma
- Thyroid storm
Heat stroke
CVA that involves the hypothalamus

Differential for Widened QRS

Bundle branch blocks (LBBB or RBBB)
Paced beats
Pre-excitation (e.g. WPW)
Ventricular ectopy
Metabolic (Hyperkalemia or severe acidosis)
Na²⁺channel blocking drugs (e.g. TCA’s)
Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)

Differential for Rightward Axis Deviation

Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Lead misplacement / Dextrocardia
Normal thin adults with horizontally positioned hearts

Differential for Brugada pattern in V1

Brugada syndrome
Hyperkalemia
Na⁺ channel blocker toxicity

Key Teaching Points

Differential for Non-conducted P-waves (P:QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes
- P-waves are irregular, the non-conducted P-waves come early
Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
Mobitz II
- P-waves are regular (P-P interval is constant)
- Some impulses fail to conduct to the ventricles WITHOUT progressive PR-interval lengthening
AV Dissociation, 3^rd degree AV Block
- P-waves are regular (P-P interval is constant)
- PR-interval is randomly changing

Differential for Left Axis Deviation

Left bundle branch block
Paced rhythm
Pre-excitation (e.g. WPW)
Prior Inferior MI (from Q-waves)
Left anterior fascicular block
Left ventricular hypertrophy
Hyperkalemia
Normal Variant (may be seen in elderly patients)

Left anterior fascicular block (LAFB)

Leftward axis
qR in I and aVL
rS in III
QRS may be normal or slightly prolonged
Poor R-wave progression is common
No other reasons for leftward axis

Type of Block	Left Anterior Fascicular Block	Left Posterior Fascicular Block
Axis	Left Axis Deviation	Right Axis Deviation
Leads I & aVL
Lead III

Take Home Points:

When you see electrocardiographic polyuria…map out the P-waves and look closely at the PR-interval

Blocked PAC’s = P-waves irregular, non-conducted P-wave comes early
Mobitz I = P-waves are regular, PR-interval increasing before dropped beat
Mobitz II = P-waves regular, some fail to conduct without PR-interval lengthening
AVD, 3^rd degree AVB = P-waves regular, PR-interval randomly changing
The answer lies in the PR-interval!

Key Teaching Points

Beware Hyperkalemia!

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Pearl: When you see a wide QRS rhythm with a rightward axis, think HYPERKALEMIA or other sodium channel blocker toxicities.

Bonus Pearl: Massive STE can mimic wide QRS complexes (usually only in a few leads, but usually not with a rightward axis).

Key Teaching Points

Age as a cardiac risk factor

Young patients do have MI’s
- 123,000 AMIs per year in patients 29-44 years old
- 5-10% of AMIs occur in patients < 45 years old
- Only a minority are related to cocaine use
Autopsy studies from Korean/Vietnam wars
1993 JACC study (n=111, average age 26 years old) showed evidence of atherosclerosis in 78%
- 20% had LAD or “significant” 2 and 3 vessel involvement
- 9% had > 75% narrowing in at least one vessel
In another study in patients 24-39 years old (n=1023) with chest pain
- 5.4% ruled in for ACS
- 2.2% had an adverse cardiac event (death, MI, need for PCI/CABG)

ECG Pearls: Pericarditis vs. STEMI

PR depression (and PR elevation in aVR) is not pathognomonic for pericarditis
ST depression outside aVR and V1 = STEMI
Other findings suggestive of ACS
- Disproportionate T wave size in comparison to QRS complex
- Straightening of initial potion of T-wave

Final take-home points:

CAD, ACS, & STEMI DOES occur in young patients

We will continue to see an increase in MI’s in young patients
Focus on the presentation, not the age!
4 greatest predictors of ACS in patients with chest pain:
- Vomiting
- Diaphoresis
- Radiation
- Pain worsening with exertion

References

Joseph A, Ackerman D, Talley JD, et al. Manifestations of coronary atherosclerosis in young trauma victims–an autopsy study. JAC 1993;22(2):459–67. PMID: 8335815

Marsan RJ, Shaver KJ, Sease KL, et al. Evaluation of a clinical decision rule for young adult patients with chest pain. Academic Emergency Medicine 2005;12(1):26–31. PMID: 15635134

Key Teaching Points

ECG Pearls: Acute Pericarditis vs. STEMI

ECG machine interpretation is not to be trusted!
Know the differences in ECG findings & use a stepwise approach

Look for the factors that rule in STEMI before thinking pericarditis!

Step 1. Factors that strongly favor STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
STE in lead III > STE in lead II
Horizontal or convex upward ST-segment morphology
- Additional factors that favor STEMI:
  - R-T sign or “checkmark sign”
  - Q-waves that you know are new

Step 2. Factors that suggest acute pericarditis:

Pronounced PR depression in multiple leads (transient)
Pericardial friction rub
Pericardial effusion
- Additional factor that favors pericarditis
  - Spodick sign (TP segment down-sloping)

Nothing is 100%

When in doubt…do serial ECGs, ECHO, and consider CATH!

Acute Pericarditis

80-90% are idiopathic (assumed viral)
- Remaining 10-20% usually post-cardiac injury
2/3 cases have pericardial effusions
Diagnosis requires at least 2 of the following:
- Typical chest pain
  - Pleuritic, positional pain
  - Relieved sitting forward
  - Radiates to the trapezius ridge (“virtually pathognomonic”)
- Typical ECG changes
  - Diffuse STE, PR depression may be the only ECG finding
- Pericardial friction rub
- Pericardial effusion
Labs are non-specific
Clinical signs & symptoms are often unreliable
Treatment
- Treat underlying cause (Cancer, TB, Renal failure, etc.)
- NSAIDs
  - Ibuprofen 600-800 mg q 6-8hrs, OR
  - Indomethacin 25-5 mg q 8 hrs, OR
  - Aspirin 2-4 g/day in divided doses
- Add Colchicine
  - Reduces duration of symptoms, recurrences, and rate of hospitalization
  - 0.5 mg BID if > 70 kg
  - 0.5 mg/day if ≤ 70 kg for 3 months
Disposition
- Low risk patients can be treated on outpatient basis with good follow up
  - No fever
  - Not immunosuppressed
  - Not caused by trauma
  - No evidence of myopericarditis (negative troponin)
  - No large pericardial effusions
  - Not anticoagulated

Final take-home points:

Just because electrocardiography is a basic skill in medicine, doesn’t mean that out skills should be basic.
Be the best in electrocardiography!

References

LeWinter MM. Clinical practice. Acute pericarditis. N Engl J Med 2014;371(25):2410–6.. PMID: 25517707

Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N Engl J Med 2013;369(16):1522–8. PMID: 23992557

Alabed S, Cabello JB, Irving GJ, Qintar M, Burls A. Colchicine for pericarditis. Cochrane Database Syst Rev 2014;8:CD010652. PMID: 25164988

Key Teaching Points

Hypercalcemia

Etiologies

“Pam P. Schmidt” Mnemonic
- P – Parathyroid hormone
- A – Addison’s disease
- M – Milk-alkali syndrome
- P – Paget’s disease
- S – Sarcoidosis
- C – Cancer
- H – Hyperthyroidism
- M – Multiple myeloma
- I – Immobilization
- D – Hypervitaminosis D
- T – Thiazide diuretics

Signs and symptoms

Typically manifest with Ca²⁺ levels > 12-14 mg/dL
“Stones, bones, groans, thrones, and psychiatric overtones”
- Stones – nephrolithiasis, ectopic calcification
- Bones – bone pain
- Groans – lethargy, fatigue, weakness, headache
- Thrones – polyuria, polydipsia, oliguria (later)
- Moans – ileus, abdominal pain, nausea and vomiting, pancreatitis
- Psychiatric overtones – confusion, depression, AMS
Watch for bradycardia and hypotension (volume depletion)
Bonus Pearl: hypercalcemia and hypermagnesemia cause HYPOreflexia, while hypocalcemia and hypomagnesemia produce HYPERrelexia!

ECG findings

Short QT interval
- DDx: hypercalcemia, digoxin toxicity, congenital short QT-syndrome
Prolonged PR interval
Bradycardia, AV blocks
QRS interval widening, bundle branch blocks
ST segment changes (can mimic ACS)
- Differentiate by eliciting a good HPI and looking for short QT interval

Treatment

IV fluid resuscitation is critical to acute treatment
Loop diuretics, after IVF
Supportive care, correct other electrolyte disturbances
Consider bisphosphonates, calcitonin in symptomatic patients

Final take-home points:

DDx for short QT intervals [~ QTc < 400 ms]
- Hypercalcemia
- Digoxin Toxicity
- Congenital short QT syndrome
Hypercalcemia
- Look for short QT intervals
- ST segment elevation that mimics ACS is not uncommon
- IV fluid hydration is the key treatment in the ED

References

Nishi SPE, Barbagelata NA, Atar S, et al. Hypercalcemia-induced ST-segment elevation mimicking acute myocardial infarction. Journal of Electrocardiology 2006;39(3):298–300. PMID: 16777515

Littmann L, Taylor L, Brearley WD. ST-segment elevation: a common finding in severe hypercalcemia. Journal of Electrocardiology 2007;40(1):60–2. PMID: 17027838

Key Teaching Points

Be very careful with using the ECG computer interpretations in making the diagnosis of STEMI
- Recent literature reports frequent false positive & false negative diagnoses
When in doubt, discuss with a colleague or cardiology
The TP-segment is often a better isoelectric segment than the PR-segment
- PR-segment down-slopping or depression can cause the ST-segments to look falsely elevated when they are not actually elevated in comparison to the TP-segment

ECG Bonus Pearls:

ECG manifestations of Acute MI (in absence of LVH and LBBB) are age and sex specific, and require different cut-off points.
Criteria for the ECG diagnosis of acute ischemia that may or may not lead to MI are detailed in an expert consensus document, “Third Universal Definition of MI” PMID: 22958960
- ST-segment elevation
  - Use the J point to determine the magnitude of ST-segment shift
  - New, or presumed new, J-point elevation in two contiguous leads > 0.1 mV is required in all leads other than V₂ and V₃
  - In males < 40 years old, J-point elevation of as much as 0.25 mV in V₂ and V₃ can be a normal finding, but decreases with age
    - Cutoff = ≥ 0.25 mV in V₂ and V₃in men < 40 years
  - In males ≥ 40 years old, J-point elevation as much as 0.2 mV in V₂ and V₃ can a normal finding
    - Cutoff = ≥ 0.2 mV in V₂ and V₃in men ≥ 40 years
  - J-point elevation in women is less than in men, elevation as much as 0.15 mV in V₂ and V₃ can be a normal finding.
    - Cutoff = ≥ 0.15 mV in V₂ and V₃in women
- Lesser degrees of ST displacement DO NOT exclude ischemia or evolving MI, since a single ECG may miss dynamic changes. So make sure to do serial ECGs when in doubt!

References:

de Champlain F, Boothroyd LJ, Vadeboncoeur A, et al. Computerized interpretation of the prehospital electrocardiogram: predictive value of ST segment elevation myocardial infarction and impact on on-scene time. CJEM 2014. Mar;16(2):94-105. PMID: 24626114

Min MK, Ryu JH, Kim YI, et al. Does cardiac catheterization laboratory activation by electrocardiography machine auto-interpretation reduce door-to-balloon time? Am J Emerg Med 2014;32(11):1305–10. PMID: 25249338

Thygesen K, Alpert JS, Jaffe AS, et al. Third Universal Definition of Myocardial Infarction. J Am Coll Cardiol 2012;60(16):1581–98. PMID: 22958960

Key Teaching Points

Differential Diagnosis for Rightward Axis
- Right ventricular hypertrophy
- Pulmonary hypertension (e.g. PE, COPD)
- Lateral MI (due to Q wave in I)
- Ventricular ectopy
- Dextrocardia
- Hyperkalemia
- Na⁺channel blocking drugs (e.g. TCA’s)
- Left posterior fascicular block
- Misplaced leads
- Normal in young kids
Causes of QRS Prolongation
- Bundle branch blocks (LBBB or RBBB)
- Paced beats
- Pre-excitation (e.g. WPW)
- Ventricular ectopy
- Metabolic (Hyperkalemia or severe acidosis)
- Na⁺channel blocking drugs (e.g. TCA’s)
- Non-specific intraventricular conduction delay (e.g. LVH, cardiomyopathy)
Na²⁺channel blocker toxicity
- Tachycardia
- Tall R wave in aVR
- Rightward axis
- QRS-interval widening
- Possible Brugada pattern
“The biggest reason we miss a diagnosis is that we make a diagnosis (and then stop looking)”

References:

Bebarta VS, Phillips S, Eberhardt A, et al. Incidence of Brugada electrocardiographic pattern and outcomes of these patients after intentional tricyclic antidepressant ingestion. AJC 2007;100(4):656–60. PMID: 17697824

Chan HY, Chan YC, Lau FL. Reversal of Brugada electrocardiographic pattern with sodium bicarbonate solution after amitriptyline overdose. Clin Toxicol (Phila) 2008;46(9):892–6. PMID: 18788005

Key Teaching Points

Dysrhythmias can produce syncope or seizure-like activity so make sure to get an ECG!

Always think of the following differential when interpreting the ECG of patients with syncope or “new onset seizures”:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV dysplasia

Differential for Prolonged QT

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications (Type Ia & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

Remember to check electrolytes and medications!

Key Teaching Points

Inverted U-waves

Usually occurs in lateral leads
Associated with LAD or LMCA disease
May occur during pain or painless state
Should not be ignored!

References:

Marriott HJL. Emergency Electrocardiography. 1997. Amazon Link.

Sovari AA, Farokhi F, Kocheril AG. Inverted U wave, a specific electrocardiographic sign of cardiac ischemia. American Journal of Emergency Medicine 2007;25(2):235–7. PMID: 17276833

Gerson MC, McHenry PL. Resting U wave inversion as a marker of stenosis of the left anterior descending coronary artery. The American Journal of Medicine 1980;69(4):545–50. PMID: 7424944

Key Teaching Points

Pericardial Effusion

Cardiomegaly
- CXR is sensitive but not specific
Electrical alternans
- Only present in <30 % of patients
Tachycardia
- May be blunted in patients taking cardiac medications
Low Voltage

Low Voltage Definition

- Specific Definition
  - QRS amplitudes in limb leads all < 5 mm OR in all chest leads < 10mm
- Sensitive Definition

QRS amplitudes in I+II+III < 15 mm OR V1+V2+V3 < 30 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

New Low Voltage ECG + Tachycardia = Pericardial effusion until proven otherwise!

Avoid anticoagulants until pericardial effusion is ruled out.

Key Teaching Points

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal in young kids & thin adults with horizontally positioned hearts

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
New RBBB or incomplete RBBB
Superventricular tachydysrhythmias
Ventricular dysrhythmias
ST-segment elevations or depressions
New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

References:

Kosuge M, Kimura K, Ishikawa T, et al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes on the basis of negative T waves. AJC 2007;99(6):817–21. PMID: 17350373

Witting MD, Mattu A, Rogers R, Halvorson C. Simultaneous T-wave inversions in anterior and inferior leads: an uncommon sign of pulmonary embolism. Journal of Emergency Medicine 2012;43(2):228–35. PMID: 22142671

Further Reading:

Kukla P, McIntyre WF, Fijorek K, et al. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med 2014;32(6):507–10. PMID: 24602894

Key Teaching Points

Pre-hospital ECG Case Pearls

Consider RV & isolated posterior MI. Get right-sided ECGs in patients with inferior MI’s, and posterior leads with ST-segment depression in the anterior precordial leads
Inferior Wall STEMI with ST-depression in V2, but not in V1 or V3, is predictive of RV infarction
Avoid nitrates in patients with RV infarction, as they are pre-load dependent
Patients with RBBB should have ST-segment depression in V1 & V2. STE in anteroseptal leads with RBBB is abnormal and concerning for STEMI!
Junctional rhythms and ventricular escape rhythms should be regular. Consider atrial fibrillation in patients with irregularly irregular rhythms
Prolonged QT specifically caused by a prolonged ST-segment is concerning for Hypocalcemia and Hypothermia
Normal sinus rhythm should have upright p-waves in the limb leads. Ectopic atrial rhythms have inverted p-waves in the limb leads
Narrow complex, regular tachycardia differential = Sinus tachycardia, SVT, Atrial flutter with 2:1 conduction
Consider Atrial flutter when the ventricular rate is 150 +/- 20. Turning the ECG upside down can help you identify flutter waves

Patients with ventricular tachycardia can be stable, careful calling it anything else and treat with procainamide or electrical cardioversion.

Key Teaching Points

Rhythm – Sinus bradycardia at a rate of ~ 57 bpm. Short PR interval.

[/fusion_modal]

[fusion_button link=”” color=”default” size=”” type=”” shape=”” target=”_self” title=”” gradient_colors=”|” gradient_hover_colors=”|” accent_color=”” accent_hover_color=”” bevel_color=”” border_width=”1px” shadow=”” icon=”” icon_position=”left” icon_divider=”yes” modal=”case2″ animation_type=”0″ animation_direction=”down” animation_speed=”0.1″ alignment=”left” class=”” id=””]Review Key Teaching Points[/fusion_button]

[fusion_modal name=”case2″ title=”Review Key Teaching Points” size=”large” background=”” border_color=”” show_footer=”yes” class=”” id=””]

Differential Diagnosis for Short PR interval

Junctional rhythm
Pre-excitation syndromes
- WPW (Wolff-Parkinson-White syndrome)
- LGL (Lown-Ganong-Levine syndrome)
Normal variant (EAVNC – enhanced AV nodal conduction)

LGL syndrome

Described in 1952 by Lown, Ganong, & Levine
Clinical syndrome associated with paroxysms of tachycardia and ECG findings (short PR interval and a normal QRS (No delta wave or QRS widening))
Originally thought to be associated with an alternative pathway for conduction and an increased risk of arrhythmias and sudden death
Recent literature has described several reasons for short PR intervals and raises doubts about the conferred risks of tachyarrhythmias & sudden death

Ablation procedures do not appear to be necessary, and there does not seen to be any clinical relevance.

Key Teaching Points

Large pericardial effusion or tamponade, suggested by tachycardia, low voltage QRS and electrical alternans

Low Voltage Definition

Specific Definition
- QRS amplitudes in limb leads all < 5 mm OR in all chest leads < 10mm
Sensitive Definition
- QRS amplitudes in I+II+III < 15 mm OR V1+V2+V3 < 30 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Pearls:

New low voltage ECG + Tachycardia = Pericardial effusion until proven otherwise! New low voltage ECG + Bradycardia = Myxedema until proven otherwise!

For more information about low voltage, review the case from April 6, 2015.

Key Teaching Points

Posterior MI’s are the most common type of missed STEMI!

4-10% of STEMI’s are isolated Posterior MI’s
Usually associated with inferior or lateral MI due to RCA or circumflex occlusion
Often misdiagnosed as just ischemia or Non-STE-ACS
Only 30% are revascularized within 90 minutes
Look for ST-depression in anteroseptal leads!

Differential for ST-depression in anteroseptal leads

Anteroseptal ischemia
Posterior STEMI
- Mirror image of septal STEMI in leads V1-V3
- Look for tall R waves, ST-depression, and upright T waves in V1-V3 on conventional 12 lead ECGs
- Even 0.5 mm of STE on posterior lead ECGs is diagnostic
Miscellaneous
- RBBB
- Hypokalemia
- Etc.

Take home Point:

ST-depression in the anteroseptal leads might represent posterior STEMI. Get posterior leads!

References:

Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes among patients with an isolated posterior myocardial infarction: insights from the National Cardiovascular Data Registry (NCDR). American Heart Journal 2014;167(3):350–4. PMID: 24576519

Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. Journal of Electrocardiology 2014;47(4):448–58. PMID: 24792903.

Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among patients with acute myocardial infarction. Journal of Electrocardiology 2013;46(6):653–9. PMID: 23890685.

Waldo SW, Armstrong EJ, Kulkarni A, et al. Clinical characteristics and reperfusion times among patients with an isolated posterior myocardial infarction. J Invasive Cardiol 2013;25(8):371-5. PMID: 23913600.

Key Teaching Points

LBBB and AMI

A new or presumed new LBBB used to be a STEMI equivalent. In the past few years, increasing literature has suggested that a new LBBB does NOT predict a high likelihood of AMI/acute thrombosis.

References:

Kontos MC, Aziz HA, Chau VQ, et al. Outcomes in patients with chronicity of left bundle-branch block with possible acute myocardial infarction. American Heart Journal 2011;161(4):698–704. PMID: 21473968.

Jain S, Ting HT, Bell M, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol 2011;107(8):1111–6. PMID: 21296327.

Chang AM, Shofer FS, Tabas JA, et al. Lack of association between left bundle-branch block and acute myocardial infarction in symptomatic ED patients. Am J Emerg Med 2009;27(8):916–21. PMID: 19857407.

The most recent STEMI Guidelines state that new or presumed new LBBB is no longer an indication for emergent CLA/lytics!

Reference:

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. JAC 2013;61(4):e78–e140. PMID: 23256914.

Left Bundle Branch Block

LBBB’s cause ST-segment & T wave changes that can make the identification of acute MI difficult
Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
Meeting the criteria in a single lead can be specific for AMI
The criteria are reviewed below

A revised Sgarbossa C rule has been proposed (not yet validated) to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥5 mm) with a proportional criterion (ST-segment to S-wave ratio ≤-0.25). This is consistent with the electrophysiological principle that repolarization voltages should be proportional to depolarization voltages.

Reference

Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.

Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96–105. PMID: 22766335.

Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal. 2013;166(3):409–413. PMID: 24016487.

Take-home Points:

Sgarbossa A –> concordant STE = AMI

Sgarbossa B –> concordant STD in V1, V2, or V3 = AMI

Revised Sgarbossa C –> discordant ST segment > 25% size of R or S wave = AMI (pending validation study)

Key Teaching Points

Pacemakers and AMI

Paced rhythms cause ST-segment & T wave changes that can make the identification of acute MI difficult
As in LBBB, paced rhythm are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST-segment deviations that are concordant (in same direction) to the QRS complex or excessively discordant are abnormal

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose AMI in setting of paced rhythms

The criteria are reviewed below

Concordant STE ≥ 1mm (in any lead)
Concordant STD ≥ 1mm in V1, V2, or V3
Discordant STE ≥ 5mm

Maloy, et al. WJEM 2010

Sgarbossa A: Not found in any patients
Sgarbossa B: sensitivity 19%, specificity 81%
Sgarbossa C: sensitivity 10%, specificity 99%

Take-home Points:

Sgarbossa criteria appear to predict acute MI in patients with pacemakers. Criteria C (excessively discordant ST-segment elevation) may be most specific.

Reference

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing. Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802.

Sgarbossa EB, Pinski SL, Gates KB, Wagner GS. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576.

Maloy KR, Bhat R, Davis J, Reed K, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers. West J Emerg Med. 2010;11(4):354–357. PMID: 21079708.

Key Teaching Points

Case 1: LBBB and AMI

Which patients with LBBB need emergent reperfusion therapy?

Sgarbossa A & concordant STE = AMI
Sgarbossa B & concordant STD in V1, V2, or V3 = AMI
Revised Sgarbossa C & discordant ST segment > 25% size of R or S wave = AMI (pending validation study)

For more on this, review the case from June 1^st, 2015

Case 2: Atrial Fibrillation with WPW

Very rapid, irregularly irregular tachycardia
Rates may approach 250-300 bpm or higher
Variable QRS-complex shape and width
Often misdiagnosed as SVT, VT, or A.fib with aberrancy
AV nodal blockers (BB/CCB’s, Digoxin, Amiodarone, etc.) can cause V.fib & death

Avoid all AV nodal blockers in Atrial fibrillation with WPW!

Case 3: Septal STEMI vs Hyperkalemia?

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI with focal STE!)
Pseudo Brugada syndrome pattern
Sine wave morphology

Beware…Hyperkalemia does whatever it wants to the ECG!

For more on hyperkalemia, review the case from Jan 12th, 2015

Case 4: Ventricular Tachycardia vs. AIVR

Accelerated idioventricular rhythm (AIVR) is a relatively benign reperfusion arrhythmia
It often occurs during reperfusion with thrombolytics after MI
True ventricular tachycardia typically has a rate > 120 bpm

Case 5: Syncope & Anteroseptal ST-segment Depression

Differential for ST-depression in anteroseptal leads

Anteroseptal ischemia
Posterior STEMI
- Mirror image of septal STEMI in leads V1-V3
- Look for tall R waves, ST-depression, and upright T waves in V1-V3 on conventional 12 lead ECGs
- Even 0.5 mm of STE on posterior lead ECGs is diagnostic
Miscellaneous
- RBBB
- Hypokalemia

ST-depression in the anteroseptal leads might represent posterior STEMI. Get posterior leads!

Case 6: Really Wide Complex Tachycardia

When the QRS complex is really wide (> 1 big box or 200 ms) think of tox. and metabolic etiologies (ex. hyperkalemia and severe acidosis)
Consider empiric treatment with Calcium & Sodium Bicarbonate!

For more about Na²⁺ channel blocker toxicity, review the case from Feb 23rd, 2015

Case 7: Bizarre Bradycardia

Remember that hyperkalemia can also cause bizzare bradycardias and AV blocks
When dealing with a bizarre rhythm that is not responding to ACLS therapy, consider empiric treatment for hyperkalemia!

Case 8: Low Voltage

Low Voltage Definition

Specific Definition
- QRS amplitudes in limb leads all < 5 mm OR in all chest leads < 10mm
Sensitive Definition
- QRS amplitudes in I+II+III < 15 mm OR V1+V2+V3 < 30 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

New low voltage ECG + Tachycardia = Pericardial effusion until proven otherwise!

Avoid anticoagulants until pericardial effusion is ruled out.

For more, review the case from April 6th, 2015

Key Teaching Points

de Winter T-waves

1-3 mm ST-depression at the J-point in the mid precordial leads, leading into tall symmetric T-waves

High risk for acute anterior MI
Suggestive of an acute proximal LAD occlusion (contrast to sub-acute occlusion of Wellens syndrome), or less commonly a 1^st diagonal or left circumflex occlusion
Although no ST-elevation, may represent an unstable lesion for which urgent cath should be “strongly considered”
Get serial ECG’s while the patient is having pain, may progress to STEMI
Have high concern for decompensation and treat aggressively

References:

de Winter RJ, Verouden NJ, Wellens HJ, et al. A new ECG sign of proximal LAD occlusion. N Engl J Med. 2008 Nov 6;359(19):2071-3. PMID:18987380

Verouden NJ, Koch KT, Peters RJ, et al. Persistent precordial “hyperacute” T-waves signify proximal left anterior descending artery occlusion. Heart 2009;95(20):1701–6. PMID: 19620137

Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing electrocardiogram interpretation and clinical decision-making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec;160(6):995-1003. PMID: 21146650

Stankovic I, Ilic I, Panic M, et al. The absence of the ST-segment elevation in acute coronary artery thrombosis: what does not fit, the patient or the explanation? J Electrocardiol 2011;44(1):7–10. PMID: 20591442

Goebel M, Bledsoe J, Orford JL, Mattu A, Brady WJ. A new ST-segment elevation myocardial infarction equivalent pattern? Prominent T wave and J-point depression in the precordial leads associated with ST-segment elevation in lead aVr. Am J Emerg Med 2014;32(3):287.e5–8. PMID: 24176590

Birnbaum I, Birnbaum Y. High-risk ECG patterns in ACS—need for guideline revision. J Electrocardiol 2013;46(6):535–9. PMID: 23863685

Key Teaching Points

Chest Pain History: Associated symptoms

Clinical factors that INCREASE the likelihood of ACS:

Chest pain (CP) that radiates to bilateral upper extremities > right >> left
CP with diaphoresis
CP with vomiting
CP that worsens with exertion

Clinical factors that DECREASE the likelihood of ACS:

CP that is pleuritic
CP that is sharp and stabbing
CP that is reproducible with palpation
CP that is positional

Pericarditis vs. STEMI

Clinical signs & symptoms may help, but are often unreliable!
STEMI’s DO occur in young patients
ECG machine interpretation is not to be trusted
Beware the oblique (straightening) ST-segment, which is an early marker of ischemia
Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that rule-in STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
Horizontal or convex upward ST-segment morphology
STE in lead III> the STE in lead II
R-T sign or “checkmark sign”
Q-waves that youknow are new

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis:

Pronounced PR depression in multiple leads
Pericardial friction rub
Pericardial effusion
Spodick sign – may be useful after considering all the other factors above, but be wary as new research suggests it may be seen in both STEMI and pericarditis

When in doubt…do serial ECGs and consider CATH!

Bonus Pearl: Expect to see ST-segment changes in the first 10-15 minutes in cardiac arrest patients that have received epinephrine or were defibrillated.

Key Teaching Points

Most Important Pearl:

Always look at all 12 leads & be systematic. When in doubt do serial ECG’s!

More Pearls:

Artifact is not uncommon!

Look at the patient:

If unstable, don’t hesitate to assume the worst
If stable, look for normal intrinsic beats that may be buried within artifact!

New T-wave inversion in aVL may be a reciprocal change

Early reciprocal changes can precede ST-elevation (STE) in MI
New TWI in aVL can be the first sign of an inferior STEMI
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECGs

Poor R-wave Progression

Defined as a < 3 mm R-wave by lead V3
Differential

- Prior anteroseptal MI
- LVH
- High precordial electrode placement
- Normal variant

Key Teaching Points

Differential Diagnosis for Diffuse ST-Elevation

Large Acute STEMI

Has reciprocal ST-segment depression
Evolving changes (especially with tx)

Pericarditis/Myocarditis

No reciprocal ST-segment depression
PR-segment depression (not specific)
Spodick’s sign (not sensitive or specific)

Ventricular aneurysm

No reciprocal ST-segment depression
+ Q-waves

Early repolarization

No reciprocal ST-segment depression
No PR-segment depression
Fishhook j-point elevation

Vasospasm

No reciprocal ST-segment depression
May evolve with treatment

Pericarditis vs. STEMI

Clinical signs & symptoms may help, but are often unreliable!
Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that strongly favor STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
Horizontal or convex upward ST-segment morphology
STE in lead III > the STE in lead II
R-T sign or “checkmark sign”
Q-waves that you know are new

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis:

Pronounced PR-segment depression in multiple leads
Pericardial friction rub
Pericardial effusion
Spodick sign (TP segment downsloping) – may be useful after considering all the other factors above, but be wary as new research suggests it may be seen in both STEMI and pericarditis

When in doubt…do serial ECGs and consider CATH!

Low Voltage Definition

- Specific Definition
  - QRS amplitudes in limb leads all < 5 mm OR in all chest leads < 10mm
- Sensitive Definition

QRS amplitudes in I+II+III < 15 mm OR V1+V2+V3 < 30 mm

Low Voltage QRS Differential

“Low Power”
- Myxedema (severe hypothyroidism)
- Infiltrative diseases (Amyloid, Sarcoid, etc.)
- End stage cardiomyopathy
Conduction blockage
- Fluid/Effusion (pericardial or pleural)
- Fat (obesity)
- Air (COPD)

Pericardial Effusion

Cardiomegaly
- CXR is sensitive but not specific
Electrical alternans
- Only present in <30 % of patients
Tachycardia
- May be blunted in patients taking cardiac medications
Low Voltage

New low voltage ECG + Tachycardia = Pericardial effusion until proven otherwise!

Avoid anticoagulants until pericardial effusion is ruled out.

Key Teaching Points

Ventricular Rhythms

Wide QRS complex rhythm
No P-waves or no P-QRS association
Rate = 20-40: Ventricular escape rhythm (idioventricular rhythm)
Rate = 40-120: Accelerated ventricular escape rhythm (accelerated idioventricular rhythm, AIVR)
Rate > 120: Ventricular tachycardia
- Caveat: VT can have slower rates if patient is on an antiarrhythmic (e.g oral Flecanide or Amiodarone)
- Other mimics of VT (rate often <120)
  - Hyperkalemia
  - Sodium channel blocker toxicity

AIVR

Suggests successful reperfusion of an occluded coronary vessel in AMI (spontaneous vs. s/p thrombolytics)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, post-arrest rhythms
Tends to be transient
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Treatment is to simply observe!

Take home points:

Ventricular tachycardia: HR > 120

If rate < 120, consider the mimics instead
- AIVR
  - Suggests successful reperfusion and is a good sign!
  - Treatment is to simply observe
- Hyperkalemia
- Sodium channel blocker toxicity

Ventricular antiarrhythmics can kill!

Key Teaching Points

Regular Really Wide Complex Tachycardia (RRWCT)

Regular really wide QRS-complexes > 200 ms = RRWCT
Toxicological and metabolic disturbances like Hyperkalemia and Na⁺ channel blocker toxicities can cause RRWCT’s that mimic Ventricular Tachycardia
Consider empiric treatment with calcium and bicarb before antiarrhythmics that can kill these patients!

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Pearl:

Patients with hyperkalemia may present with significant bradycardia (without peaked T-waves or widening of the QRS). The bradycardia may not respond to conventional ACLS therapies. Having a high degree of suspicion for hyperkalemia when faced with a bizzare rhythm will save lives!

Take home points:

Hyperkalemia is the great imitator! Have a high degree of clinical suspicion for the diagnosis to not be fooled
Always consider hyperkalemia when faced with bizarre rhythms and bradycardias that do not respond to ACLS therapies

When in doubt, treat empirically for hyperkalemia with calcium & bicarb!

Key Teaching Points

Typical ECG findings on the Pediatric ECG

Rightward axis (large R wave in V₁-V₂, small S wave in V₅-V₆) is due to RV predominance and normalizes as the left ventricle thickens.
Juvenile T-wave pattern (TWI in V₁-V₃ through age 8 is normal)
The PR & QRS intervals tend to be shorter (QRS <80 ms before age 3) and this is normal. Consider Ventricular Tachycardia when QRS is >90 ms in infants and small children!
Small narrow Q-waves in inferior and lateral leads (pseudo-infarction pattern, but benign). Pathologic Q-waves are 1 box (40ms) wide.

Persistent juvenile T-wave pattern

A normal variant pattern
Asymmetric T-wave inversions or biphasic T-waves in leads V₁-V₃ (up to V₄-V₆ in some cases)
T waves are NOT symmetric nor deep (<3 mm)
Found in healthy children and young adults
Women > men
Usually women < 40-45 years of age

Pearl: A prolonged QT interval in pediatric patients is ABNORMAL! The QTc for all patients under 16 years of age should be < 450 ms

Differential for Prolonged QT-interval caused by Prolonged T-wave’s

Hypokalemia & Hypomagnesemia
Acute coronary syndromes
Elevated intracranial pressures
Several drugs and medications
Congenital causes

What are the only 2 things that prolong the QT-interval specifically by stretching the ST-segment?

Hypocalcemia
Hypothermia

Take home points:

Typical ECG findings in young kids
- Rightward axis
- Tall R waves in the right precordial leads
- TWI’s in right precordial leads

Bonus:

For those who want more information about the normal interval limits for the pediatric ECG (and more), check out the following references with links to their free text articles:

Rijnbeek PR, Witsenburg M, Schrama E, et al. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001;22(8):702–11. PMID: 11286528
Dickinson DF. The normal ECG in childhood and adolescence. Heart 2005;91(12):1626–30. PMID: 16287757

Key Teaching Points

Typical ECG findings on the Pediatric ECG

Rightward axis (large R wave in V₁-V₂, small S wave in V₅-V₆) is due to RV predominance and normalizes as the left ventricle thickens.
Juvenile T-wave pattern (TWI in V₁-V₃ through age 8 is normal)
The PR & QRS intervals tend to be shorter (QRS <80 ms before age 3) and this is normal. Consider Ventricular Tachycardia when QRS is >90 ms in infants and small children!
Small narrow Q-waves in inferior and lateral leads (pseudo-infarction pattern, but benign). Pathologic Q-waves are 1 box (40ms) wide.

Persistent juvenile T-wave pattern

A normal variant pattern
Asymmetric T-wave inversions or biphasic T-waves in leads V₁-V₃ (up to V₄-V₆ in some cases)
T waves are NOT symmetric nor deep (<3 mm)
Found in healthy children and young adults
Incidence in women >>> men
Usually women < 40-45 years of age

DDx: Ischemic, PE, ARVD

Bonus:

For those who want more information about the normal interval limits for the pediatric ECG (and more), check out the following references with links to their free text articles:

Rijnbeek PR, Witsenburg M, Schrama E, et al. New normal limits for the paediatric electrocardiogram. Eur Heart J 2001;22(8):702–11. PMID: 11286528
Dickinson DF. The normal ECG in childhood and adolescence. Heart 2005;91(12):1626–30. PMID: 16287757

Key Teaching Points

Take home points:

Most Important Pearl:

Always look at all 12 leads & be systematic. When in doubt do serial ECG’s!

True VT/Polymorphic VT/Torsade de pointes vs. Artifact

Artifact is not uncommon!

Look at the patient:

If unstable, don’t hesitate to assume the worst
If stable, look for normal intrinsic beats that may be buried within artifact!

Key Teaching Points

Diagnostic considerations in syncope should always include:

Subarachnoid hemorrhage
Acute cardiac ischemia
Thoracic aortic dissection
Pulmonary Embolism
Ruptured AAA
Ruptured ectopic pregnancy

Causes of Rightward Axis Deviation

Right ventricular hypertrophy
Left posterior fascicular block
Lateral MI (from Q-waves in lead I)
Ventricular ectopy (VT)
Hyperkalemia
Na⁺channel blocker toxicity
Pulmonary HTN – Acute (PE) & chronic lung disease (COPD)
Lead misplacement / Dextrocardia
Normal in young kids & thin adults with horizontally positioned hearts

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
New RBBB or incomplete RBBB
Superventricular tachydysrhythmias
Ventricular dysrhythmias
ST-segment elevations or depressions
New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

Take home Points

PE can mimic ACS! Make sure to consider PE in cases of syncope and pay close attention to the axis and look for new TWI’s.

Key Teaching Points

Wellens’ Syndrome:

Pattern of T-wave abnormality in mid precordial leads (V₂-V₃, +/-V₄)
No loss of R-waves in precordial leads
Highly specific for critical obstruction of the proximal LAD
High risk for extensive anterior wall MI and death

- 2 types
- Type 1 – Deeply symmetric TWI
- Type 2 – Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).

ST-changes are often absent and patient can be chest pain free!
Cardiac biomarkers often initially normal
Best to diagnose in absence of high voltage
Not currently a guideline indication for cath or lytics (especially when pain free without STE)
Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
Do not diagnose in the presence of large amplitude QRS complexes
When in doubt get serial ECG’s, some will evolve into STEMI!

Take home Points

Beware Wellens’ syndrome & Wellens’ waves

Predicts critical occlusion in LAD, usually proximal
Your ECG machine and consultants often will not know about this
Have a low threshold for serial ECG’s, especially if symptoms change as it may evolve into a STEMI

References:

de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 1892 Apr;103(4 Pt 2):730-6. PMID: 6121481

Key Teaching Points

Take home Points

Beware Wellens’ syndrome & Wellens’ waves, but also watch out for normal variants!

Careful when diagnosing Wellens’ in patients with high voltage ECG’s
- “Pseudo-Wellens”
  - Young males, especially athletes
  - Typically African-Caribbean decent
  - Less common in Caucasians
  - High Voltage QRS complexes
  - Biphasic T-waves, often with notch

Make sure to check out last week’s case for a thorough review of true Wellens’ here. The following is a summary of last week’s content:

Wellens’ Syndrome:

Pattern of T-wave abnormality in mid precordial leads (V₂-V₃, +/-V₄)
No loss of R-waves in precordial leads
Highly specific for critical obstruction of the proximal LAD
High risk for extensive anterior wall MI and death
2 types
- Type 1 – Deeply symmetric TWI
- Type 2 – Biphasic T waves with terminal TWI. Goes up first, then down (often misdiagnosed as “normal” or “non-specific T-wave abnormality”).
- ST changes are often absent and patient can be chest pain free!
- Cardiac biomarkers often initially normal
- Best to diagnose in absence of high voltage
- Not currently a guideline indication for cath or lytics (especially when pain free without STE)
- Medical management usually ineffective and patients are best treated with PCI, treadmill stress testing may be hazardous.
- Do not diagnose in the presence of large amplitude QRS complexes
- When in doubt get serial ECG’s, some will evolve into STEMI!

References:

Wang K, Asinger RW, Marriott HJL. ST-segment elevation in conditions other than acute myocardial infarction. N Engl J Med 2003;349(22):2128–35. PMID: 14645641

Corrado D, Pelliccia A, Heidbuchel H, et al. Recommendations for interpretation of 12-lead electrocardiogram in the athlete. Eur. Heart J. 2010;31(2):243–59. PMID: 19933514

de Zwaan C, Bär FW, Wellens HJ. Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction. Am Heart J, 1892 Apr;103(4 Pt 2):730-6. PMID: 6121481

Key Teaching Points

Post-Arrest and Syncope ECG Differential

Ischemia
Dysrhythmias, AVB’s
Prolonged QT (and short QT, especially in pediatrics)
WPW/Pre-excitation
Hypertrophic Cardiomyopathy
Brugada pattern
Arrhythmogenic right ventricular dysplasia (ARVD)
Miscellaneous (PE, electrolytes, ICB, etc.)

Arrhythmogenic Right Ventricular Dysplasia (ARVD)

Not common except in certain populations/regions
- General population 1/1,000-1/10,000
- Italy 40/10,000: Most common cause of sudden cardiac death in young population
Familial
- Autosomal dominant trait with variable penetrance
  - 50% chance of inheriting the gene defect
    - Men> Woman
Pathogenesis
- Progressive replacement of the RV myocardium by fibrofatty tissue
- Causes interference with electrical impulse conduction
- CAN occur (>50% of cases) in LV posterolateral subepicardium
Clinical
- Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
- Often have family history of premature sudden death in family members < 35 years old
- Usually manifests in patients between puberty- 60 years of age
Diagnosis
- ECG (imperfect)
  - Leads V1-V3
    - Epsilon waves (most specific)
    - TWIs (most sensitive)
    - Slight prolongation of QRS
  - LBBB type VT or PVCs (many)
- ECHO
- MRI
- MDCT
- Endomyocardial biopsy
Management
- Send to electrophysiologist
- Active ventricular dysrhythmias
  - Stable: beta blockers, Class III antiarrhythmics
  - ICD placement for patients with cardiac arrest, syncope, VT

Take home Points

ARVD: Heightened Concern if

Young patients, especially males
Family history of early sudden death
Many PVC’s
LBBB-type Ventricular Tachycardia
Epsilon waves with TWI’s in V₁-V₃

References:

Basso C., et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet 2009;373(9671):1289–1300. PMID: 19362677

Diez D, Brugada J. Diagnosis and Management of Arrhythmogenic Right Ventricular Dysplasia: An article from the E-Journal of the ESC Council for Cardiology Practice, European Society of Cardiology 2008 [Full text].

Key Teaching Points

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only in 30-50%)
SIQIII or SIQIIITIII, a.k.a. Rightward Axis (not sensitive or specific)
New RBBB or incomplete RBBB
Superventricular tachydysrhythmias
Ventricular dysrhythmias
ST-segment elevations or depressions
New TWI’s, especially in anteroseptal +/- inferior leads = Acute Pulmonary Hypertension = PE until proven otherwise!

Take home Points

PE commonly mimics ACS! Make sure to consider PE in cases of acute onset chest pain and pay close attention to new TWI’s, ST-segment changes, or ventricular dysrhythmias.
Trust the ECG, but…you still need to do a history and physical exam!

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrrhythmias
Advanced AV Blocks and sinus pauses
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take home points:

Beware hyperkalemia! Hyperkalemia is the great imitator.
- Can mimic STEMI
- Can mimic Brugada appearance with ST-elevation in V₁-V₂

Key Teaching Points

Who Should Go To The Cath Lab Emergently?

Symptoms concerning for acute cardiac ischemia (CP or anginal equivalent)

+ STEMI ECG findings, or… “Sick” NSTE-ACS (unstable, acute heart failure, intractable ischemia)

Mattu Class I = Do the cath! (No argument, good literature/support)
Mattu Class II = I think you should do the cath… (Argument possible, good literature)
- IIA – send some papers with the patient
- IIB – send some papers and sign out!
Mattu Class III = Don’t cath.

Mattu Class I Indications

Classic STEMI – Use the J-point to determine the magnitude of ST-segment elevation relative to the isoelectric TP segment.
- J-point elevation in 2 contiguous leads > 1 mm is required in all leads (except V₂/V₃)
- Leads V₂ and V₃limits are age and sex dependent
  - In males < 40 years old, J-point elevation of as much as 2.5 mm in V₂ and V₃ can be a normal finding, but decreases with age
    - Cutoff = ≥ 2.5 mm in V₂ and V₃in men < 40 years
  - In males ≥ 40 years old, J-point elevation as much as 2 mm in V₂ and V₃ can be a normal finding
    - Cutoff = ≥ 2 mm in V₂ and V₃in men ≥ 40 years
  - J-point elevation in women is less than in men, elevation as much as 1.5 mm in V₂ and V₃ can be a normal finding.
    - Cutoff = ≥ 1.5 mm in V₂ and V₃in women
  - Pearl: Lesser degrees of ST displacement DO NOT exclude ischemia or evolving MI. A single ECG may miss dynamic changes, so do serial ECGs when in doubt!

Reference:

Thygesen K, Alpert JS, Jaffe AS, et al. Third Universal Definition of Myocardial Infarction. J Am Coll Cardiol 2012;60(16):1581–98. PMID: 22958960

Posterior STEMI (“inferolateral”) – the most common type of missed STEMI!
- 4-10% of STEMI’s are isolated Posterior MI’s
- Often misdiagnosed as just ischemia or NSTEMI
- Only 30% are revascularized within 90 mins
- Usually associated with inferior or lateral MI due to RCA or circumflex occlusion
- Pearl: Even 0.5 mm of STE on posterior lead ECGs is diagnostic

Differential for ST-depression in anteroseptal leads

Posterior STEMI
- Mirror image of septal STEMI in leads V₁-V₃
- Large R waves (instead of Q waves)
- ST-depression (instead of STE)
- Upright T waves in V₁-V₃ (instead of inversions)
Anteroseptal ischemia
Miscellaneous
- RBBB
- Hypokalemia, etc

References:

Waldo SW, Brenner DA, Li S, et al. Reperfusion times and in-hospital outcomes among patients with an isolated posterior myocardial infarction: insights from the National Cardiovascular Data Registry (NCDR). American Heart Journal 2014;167(3):350–4. PMID: 24576519

Ayer A, Terkelsen CJ. Difficult ECGs in STEMI: lessons learned from serial sampling of pre- and in-hospital ECGs. Journal of Electrocardiology 2014;47(4):448–58. PMID: 24792903.

Wei EY, Hira RS, Huang HD, et al. Pitfalls in diagnosing ST elevation among patients with acute myocardial infarction. Journal of Electrocardiology 2013;46(6):653–9. PMID: 23890685.

Waldo SW, Armstrong EJ, Kulkarni A, et al. Clinical characteristics and reperfusion times among patients with an isolated posterior myocardial infarction. J Invasive Cardiol 2013;25(8):371-5. PMID: 23913600.

Post-arrest STEMI/NSTEMI
- STEMI patients post-arrest should go to the cath lab (Class IB in national guidelines)
- STEMI patients post-arrest who remain comatose should go to the cath lab unless they have multiple unfavorable resuscitation features (Rab T, et al.)
- NSTE-ACS patients post-arrest who remain comatose should be assessed for unfavorable resuscitation features. Immediate consultation with cardiology and intensive care is recommended (Rab T, et al.)

References:

O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction. JAC 2013;61(4):e78–e140. PMID: 23256914.
Rab T, Kern KB, Tamis-Holland JE, et al. Cardiac Arrest: A Treatment Algorithm for Emergent Invasive Cardiac Procedures in the Resuscitated Comatose Patient. J Am Coll Cardiol 2015;66(1):62–73. PMID: 26139060.

4. Non-STE ACS (Class IA in national guidelines)

Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that develop hemodynamic or electrical instability (VT or VF arrest)
Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that have intractable ischemia
Urgent/immediate invasive strategy (within 2 hours) is indicated for NSTE-ACS patients that develop acute decompensating heart failure

Reference:

Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64(24):e139–228. PMID: 25260718.

Key Teaching Points

Who Should Go To The Cath Lab Emergently?

Symptoms concerning for acute cardiac ischemia (CP or anginal equivalent)

+

STEMI ECG findings, or… “Sick” NSTE-ACS (unstable, acute heart failure, intractable ischemia)

Mattu Class I = Do the cath! (No argument, good literature/support)
Mattu Class II = I think you should do the cath… (Argument possible, good literature)
- IIA – send some papers with the patient
- IIB – send some papers and sign out!
Mattu Class III = Don’t cath.

Key Teaching Points

Who Should Go To The Cath Lab Emergently?

Symptoms concerning for acute cardiac ischemia (CP or anginal equivalent)

+ STEMI ECG findings, or… “Sick” NSTE-ACS (unstable, acute heart failure, intractable ischemia)

Mattu Class I = Do the cath! (No argument, good literature/support)
Mattu Class II = I think you should do the cath… (Argument possible, good literature)
- IIA – send some papers with the patient
- IIB – send some papers and sign out!
Mattu Class III = Don’t cath.

Key Teaching Points

Always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV dysplasia

Hypertrophic Cardiomyopathy

Many other names
- IHSS, ASH, HOCM
Characteristic anatomic abnormalities
- Hypertrophied, non-dilated LV (normal CXR)
- Thickening usually prominent in the septum (Doppler ECHO)
Epidemiology
- Familial incidence in 55% of cases
- Average age at diagnosis is 30-40
- Male:female ~ 3:2
- 1/500 in general population
- Most common cause of sudden cardiac death in young adults in the US
- Mortality ~3.5% per year
Pathophysiology (theories)
- Inherited abnormality in myocardium’s response to adrenergic stimulation
- Abnormal diastolic function
- Subaortic obstruction to cardiac outflow
Clinical features
- Syncope, chest pain, palpitations, dyspnea, sudden death
  - Often associated with exertion (not always!)
  - Attributable to dysrhythmias or sudden drops in cardiac output
- Systolic murmur at apex or LLSB
  - Increases with valsalva, standing
  - Decreases with trendelenburg, squatting
- ECG abnormalities present in 85-93%
  - Left atrial enlargement is most common
  - High left ventricular voltage
  - Tall R wave in V1 (mimics posterior MI)
  - Deep narrow Q-waves in inferior, lateral leads
- Definitive diagnosis – Doppler ECHO
  - Can also help to assess severity of obstruction at rest and with provocative maneuvers
- Treatment
  - Beta blockers, calcium channel blockers
  - Amiodarone for ventricular dysrhythmias

Take-home points:

Hypertrophic cardiomyopathy is a common cause of sudden cardiac death in young males. Look for high voltage and deep narrow Q-waves.

Key Teaching Points

Always think of the following differentials when interpreting the ECG of patients with syncope:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV dysplasia

Take-home points:

Reciprocal changes can precede ST-segment elevation in STEMI. New TWI or ST-segment depression in aVL may predict an evolving inferior STEMI. Remember to always obtain serial ECGs in patients with ongoing or changing ischemic symptoms.

Key Teaching Points

Differential for Prolonged QT Interval

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Medications/Drugs (Type Ia, methadone, & many others)
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Congenital

Take-home points:

In patients with first time “seizures”, make sure to get an ECG and look for potential signs of dysrhythmia. Torsade de pointes may mimic seizure activity.

Key Teaching Points

Left Bundle Branch Block
- LBBB causes ST-segment & T wave changes that can make the identification of acute MI more challenging
- Patients with LBBB are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
- ST-segment deviations that are concordant(in same direction) to the QRS complex are abnormal
Sgarbossa Criteria
- Sgarbossa and now the modified Sgarbossa criteria can be used to help diagnose AMI in setting of LBBB
- Meeting the criteria in a single lead can be specific for AMI
- The criteria are reviewed below
Concordant STE ≥ 1mm (in any lead) = Most specific for MI

Concordant STD ≥ 1mm in V1, V2, or V3 = Specific for MI

Discordant STE ≥ 5mm = Less specific for MI
- A revised Sgarbossa C rule has been proposed (recently validated) to increase the diagnostic utility of the rule for STEMI. This revised rule replaces the absolute criterion (discordant STE ≥5 mm) with a proportional criterion (ST-segment to S-wave ratio ≤-0.25) and has been found to be superior to the original criteria for identifying acute coronary occlusion in LBBB.

Reference

Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal. 2013;166(3):409–413. PMID: 24016487.

Neeland IJ, Kontos MC, de Lemos JA. Evolving considerations in the management of patients with left bundle branch block and suspected myocardial infarction. J Am Coll Cardiol 2012;60(2):96–105. PMID: 22766335.

Mayers H, Limakakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. American Heart Journal. 2015;170:1255-1264. DOI: http://dx.doi.org/10.1016/j.ahj.2015.09.005

Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing. Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802.

Key Teaching Points

The spiked helmet sign

A dome and spike-patterned apparent ST-segment elevation, where the upward shift of the baseline starts before the onset of the QRS complex
The morphology of the complexes resemble the shape of a German military spiked helmet
Cause of the morphology is uncertain, but has been found to be associated with critical noncardiac illness and high risk of in-hospital death.
Limb leads: Acute rise in intrabdominal pressure
Precordial leads: Acute rise in intrathoracic pressure

References:

Littmann L, Monroe MH. The “spiked helmet” sign: a new electrocardiographic marker of critical illness and high risk of death. Mayo Clin Proc 2011. PMID: 22134944
Agarwal A, Janz TG, Garikipati NV. Spiked helmet sign: An under-recognized electrocardiogram finding in critically ill patients. Indian J Crit Care Med 2014;18(4):238–40. PMID: 24872654
Tomcsányi J, Frész T, Proctor P, Littmann L. Emergence and resolution of the electrocardiographic spiked helmet sign in acute noncardiac conditions. Am J Emerg Med 2015;33(1):127.e5–7. PMID: 25066910

Key Teaching Points

Hyperkalemic Periodic Paralysis (HYPP) a.k.a Impressive Syndrome

Affects humans (1 in 200K) and horses (1 in 50 quarter horses)
Inherited autosomal dominant condition that affects Na⁺ channels in muscle tissues and affects the ability to regulate K⁺in the blood.
Produces significant muscle weakness and paralysis, can cause death because of diaphragmatic paralysis
Episodic, usually caused by medications, K⁺ rich foods, or significant stressors to the body
Episodes are more common in infancy, and decrease by mid-adulthood

Take-home points:

Hyperkalemia is the syphilis of electrocardiography… “The great imitator”
Renal patients with systemic complaints should get an ECG and hyperkalemia should be considered
Hyperkalemia can also cause ST-segment elevation and mimic STEMI’s and is the most rapid killer in DKA
Bizarre rhythm? Wide QRS? Think tox/metabolic & get your Calcium and Bicarb ready!

Key Teaching Points

EMS Cases Week 2 of 2 – Key Points

Case #6

Subtle early signs of ischemia

Early ischemia is often associated with…
- Reciprocal changes (e.g. aVL, V₂)
  - Especially aVL when the RCA is involved in inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - Hyperacute T-waves
    - Straightening of the upslope of the T-waves
    - Disproportionately large T-waves (especially when larger than QRS)
  - “Checkmark sign”
    - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

Case #7

Narrow complex regular tachycardia DDx

Sinus tachycardia
Supraventricular tachycardia
Atrial flutter with 2:1 conduction

Case #8

Rate related ST-segment abnormalities

SVTs, and rapid atrial fibrillation/flutter often have rate related ST depression (or STE in aVR)
- No correlation with atherosclerotic disease if they resolve when rate is controlled

Case #9

Hyperkalemia:

Remember that hyperkalemia can produce ST-segment and mimic STEMI
RBBB’s typically produce ST-segment depression in V1-V2

Case #10

Differential for Non-conducted P-waves (P: QRS > 1, a.k.a “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
Clumped or grouped beats, regularly irregular rhythm
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction)
It is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
Two or more consecutive P waves are non-conducted (P: QRS ≥ 3:1)
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular but occur independently of each other
No apparent communication between atrium and ventricle
PR-interval is randomly changing

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Key Teaching Points

Differential diagnosis for T-wave inversions

Coronary artery disease (Wellens, ischemia, reperfusion)
Neurological causes (elevated intracranial pressure)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Post-tachycardia, post-shock, post-pacing (“cardiac memory”)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Wide QRS complexes (BBB’s. PVC’s, Paced rhythms, WPW)
High left ventricular voltage, LVH with strain pattern
Pericarditis, myocarditis
Hyperkalemia, hypokalemia
Juvenile T-wave pattern
Mitral valve prolapse
Normal finding in V₁, aVR, and lead III

Differential diagnosis for T-wave inversions in V1-V3

Coronary artery disease (ischemia)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Juvenile T-wave pattern

Always think of the following differentials when interpreting the ECG of patients with syncope when the history and physical exam are non-diagnostic:

Ischemia (Acute Coronary Syndrome, Cardiomyopathy, etc.)
Dysrhythmias (Tachycardia, Bradycardia, AV-blocks)
WPW/Pre-excitation syndromes
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV cardiomyopathy
Atrial septal defect (crochetage pattern)

Arrhythmogenic Right Ventricular Cardiomyopathy

Inherited progressive cardiomyopathy characterized by ventricular arrhythmias and increased risk of sudden cardiac death, especially in young individuals and athletes
Not common, but increased prevalence in certain populations/regions

- General population; 1/1,000-1/10,000
- Italy 40/10,000: Most common cause of sudden cardiac death in young population
Familial
- Autosomal dominant trait with variable penetrance
  - 50% chance of inheriting the gene defect
  - Men > Woman
Pathogenesis
- Progressive replacement of the RV myocardium by fibrofatty tissue
- Causes interference with electrical impulse conduction
- CAN also occur in left ventricle posterolateral subepicardium
Clinical
- Common cause of ventricular arrhythmias and sudden death in adolescents and young adults, athletes
  - 22% of cases of SCD among athletes in N. Italy
  - 4% of cases of SCD in US (HCM #1)
- Often have family history of premature sudden death in family members < 35 years of age
- Usually manifests in patients between second to fifth decades of life
- Symptoms included palpitations, lightheadedness, syncope, and sudden death
Diagnosis
- ECG (imperfect)
  - Leads V₁-V₃
    - Epsilon waves (most specific, but seen in < 1/3 of patients)
    - TWIs (most sensitive, seen in > 80% of patients)
    - Slight prolongation of QRS
  - LBBB type VT (~90%) or PVCs (many)
- ECHO
- MRI
- MDCT
- Endomyocardial biopsy
Management
- Send to electrophysiologist
- Active ventricular dysrhythmias
  - Stable: beta blockers, Class III antiarrhythmics
  - ICD placement for patients with cardiac arrest, syncope, VT

Take home Points

When history and physical exam do not give you a diagnosis in syncope, don’t forget the no-brainers (ischemia, dysrhythmias), interval abnormalities (i.e. WPW, long/short QT), genetic causes (HCM, Brugada), and the notches (ARVC, ASD)
ARVC: Have heightened concern in syncope if…
Young patients, especially males
Family history of early sudden death
Many PVC’s
LBBB-type Ventricular Tachycardia
Epsilon waves with TWI’s in V₁-V₃

References:

Basso C, Corrado D, Marcus FI, Nava A, et al. Arrhythmogenic right ventricular cardiomyopathy. Lancet 2009;373(9671):1289–300.PMID: 19362677
Orgeron GM, Crosson JE. Arrhythmogenic right ventricular dysplasia/cardiomyopathy. Cardiol Young 2017;27(S1): S57–S61. PMID: 28084951
Diez D, Brugada J. Diagnosis and Management of Arrhythmogenic Right Ventricular Dysplasia: An article from the E-Journal of the ESC Council for Cardiology Practice, European Society of Cardiology 2008.

Key Teaching Points

Take Home Points:

Don’t trust the computer interpretation, even when it reads “normal”
A computer interpretation of normal still requires you to review the ECG!
Computers tend to be particularly poor at detecting early signs of ischemia, e.g.:
- Early reciprocal changes in aVL
- Hyperacute T waves
PVC’s can sometimes reveal STEMI!
If the first ECG is non-diagnostic in a symptomatic patient, get a repeat ECG!

Reference:

Hughes KE, Lewis SM, Katz L, Jones J. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med 2017;24(1):120–4. PMID: 27519772.
Riley RF, Newby LK, Don CW, et al. Diagnostic time course, treatment, and in-hospital outcomes for patients with ST-segment elevation myocardial infarction presenting with nondiagnostic initial electrocardiogram: a report from the American Heart Association Mission: Lifeline program. American Heart Journal 2013;165(1):50–6. PMID: 23237133.
Millard MA, Nagarajan V, Kohan LC, et al. Initial electrocardiogram as determinant of hospital course in ST elevation myocardial infarction. Ann Noninvasive Electrocardiol 2017;22(4).PMID: 28044391.

Key Teaching Points

Differential diagnosis for diffuse ST segment elevation without reciprocal ST segment depression

Ventricular aneurysm
Benign early repolarization
Pericarditis
Myocarditis
STEMI

Take Home Points:

Don’t rule out STEMI based on age or absence of (known) medical history!

Key Teaching Points

Differential for Non-conducted P-waves (P: QRS > 1)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (has constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
Results in clumped or grouped beats, regularly irregular rhythm
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction)
It is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
Two or more consecutive P waves are non-conducted (P: QRS ³ 3:1)
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular but occur independently of each other
No apparent communication between atrium and ventricle
PR-interval is randomly changing

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take Home Points:

When you see clumped beats (grouped beats, regular irregularity), consider the following:
- Mobitz (I or II)
- Premature complexes
- Hyperkalemia
These rhythms are often misdiagnosed as:
- Atrial fibrillation
- Mobitz

Key Teaching Points

Atrioventricular (AV) Block Review Summary

1^st Degree AV Block

PR interval of greater than 200 ms without disruption of atrial to ventricular conduction (P:QRS = 1)
A benign finding associated with increased age
Patients are generally asymptomatic and without significant complication or need for treatment

Differential for Non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take Home Points:

When you see electrocardiographic polyuria…map the Ps and look at the PRs
- Blocked PACs = non-conducted Ps come early
- Mobitz I = Ps regular, PR increasing
- Mobitz II = Ps regular, PR unchanging
- AVD, 3^rd degree AVB = Ps regular, PR randomly changing
- When P:QRS conduction ratio is ³ 3:1= “Advanced AVB or high-grade AVB”
  - AV nodal vs. infranodal block is usually based on the QRS duration
- The answer lies in the PR segment

Key Teaching Points

Atrioventricular (AV) Block Review Summary

1^st Degree AV Block

PR interval of greater than 200 ms without disruption of atrial to ventricular conduction (P:QRS = 1)
A benign finding associated with increased age
Patients are generally asymptomatic and without significant complication or need for treatment

Differential for Non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take Home Points:

When you see electrocardiographic polyuria…map the Ps and look at the PRs
- Blocked PACs = non-conducted Ps come early
- Mobitz I = Ps regular, PR increasing
- Mobitz II = Ps regular, PR unchanging
- AVD, 3^rd degree AVB = Ps regular, PR randomly changing
- When P:QRS conduction ratio is ³ 3:1= “Advanced AVB or high-grade AVB”
  - AV nodal vs. infranodal block is usually based on the QRS duration
- The answer lies in the PR segment

Key Teaching Points

Atrioventricular (AV) Block Review Summary

1^st Degree AV Block

PR interval of greater than 200 ms without disruption of atrial to ventricular conduction (P:QRS = 1)
A benign finding associated with increased age
Patients are generally asymptomatic and without significant complication or need for treatment

Differential for Non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take Home Points:

When you see electrocardiographic polyuria…map the Ps and look at the PRs
- Blocked PACs = non-conducted Ps come early
- Mobitz I = Ps regular, PR increasing
- Mobitz II = Ps regular, PR unchanging
- AVD, 3^rd degree AVB = Ps regular, PR randomly changing
- When P:QRS conduction ratio is ³ 3:1= “Advanced AVB or high-grade AVB”
  - AV nodal vs. infranodal block is usually based on the QRS duration
- The answer lies in the PR segment!

Key Teaching Points

Ventricular Rhythms

Wide QRS complex rhythm with no P-waves or no P-QRS association (look closely at lead V1)
Ventricular rate 20-40: ventricular escape rhythm (idioventricular rhythm)
Ventricular rate 40-120s: Accelerated ventricular escape rhythm (accelerated idioventricular rhythm, AIVR)
Ventricular rate > 120s-130s: Ventricular tachycardia
- Caveat: VT can have slower rates if patient is on an antiarrhythmic (e.g. oral flecainide or amiodarone)
- Other mimics of VT (rate often <120)
  - Hyperkalemia
  - Sodium channel blocker toxicity

AIVR

Accelerated idioventricular rhythm (AIVR) is a relatively benign reperfusion arrhythmia
Suggests successful reperfusion (partial or complete) of an occluded coronary vessel in AMI (spontaneous or s/p thrombolytics)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, cardiac ischemia
May be seen during cardiac arrest resuscitation
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Tends to be transient. Treatment is to simply observe!

Take-home Points:

Accelerated idioventricular rhythm (AIVR)
- Ventricular rhythm with rate 40-120s
- NOT a destabilizing rhythm
- Typically, transient and does not need treatment!
- Antiarrhythmics may kill the patient!
Ventricular tachycardia: HR > 120s-130s (exception: patients on antiarrhythmics or end stage cardiomyopathy)
- If rate < 120 consider, don’t treat as ventricular tachycardia; consider the mimics instead
  - Accelerated idioventricular rhythm (AIVR)
  - Hyperkalemia
  - Sodium channel blocker toxicity

References:

ECG Diagnosis: A Self-Assessment Workbook by Edward Chung. Amazon Link
Chou’s Electrocardiography in Clinical Practice. Amazon Link
Hurst’s The Heart, 14^th Edition. Amazon Link

Key Teaching Points

New T-wave inversion in aVL may be an early reciprocal change

Reciprocal changes can precede ST-elevation (STE) in MI
New TWI in aVL can be the first sign of an inferior STEMI
Also watch out for hyperdynamic t-waves and downsloping ST-segments which suggest other early reciprocal changes
Compare with old ECGs and correlate with the clinical presentation
When in doubt, get serial ECGs

Take-home Points:

T wave inversion in aVL during active symptoms of ischemia are concerning for early or evolving inferior STEMI
Disproportionately large T waves during active symptoms of ischemia are concerning for early ischemia
If symptoms are concerning and the initial ECG is nondiagnostic, get a repeat ECG!

Key Teaching Points

Pacemakers and AMI

Paced rhythms cause ST-segment & T wave changes that can make identification of acute MI difficult
As in in LBBB, paced rhythms are expected to have ST segment & T wave changes that are discordant to the direction of the QRS complex. This is normal & referred to as the “Rule of Appropriate Discordance”
ST–segment deviations that are concordant(in same direction) to the QRS complex or excessively discordant are abnormal
Sgarbossa Criteria
- Sgarbossa criteria can be used to help diagnose AMI in setting of paced rhythms
- The criteria are reviewed below:

Take home Points

Sgarbossa criteria can and should be applied to paced ECGs (high specificity)
Currently in the ESC STEMI guidelines
1. Concordant STE ≥ 1mm (in any lead)
2. Concordant STD ≥ 1mm in V1, V2, or V3
3. Discordant STE ≥ 5mm (most specific)
A revised Sgarbossa C criterion has been described for LBBB and is being researched for paced rhythms, we will discuss in a future episode as soon as it is published!

Key Teaching Points

QRS fragmentation (fQRS)

Additional notches/spikes within the QRS complex of at least 2 contiguous leads corresponding to a coronary artery territory
Abnormal myocardial activation and conduction delay thought to be due to myocardial scarring
Indicator of previous myocardial injury and predictor of future adverse cardiac events and mortality in various heart diseases

Take home Points

ST segment elevation in the presence of ST depression in other leads increases the specificity for the diagnosing STEMI
- Caveat: reciprocal depression is not a requirement for diagnosing STEMI!
An injury pattern can sometimes be seen in ectopic beats, so pay attention to premature complexes (look for abnormal concordant ST segment elevation or depression, or excessively discordant ST elevation)
QRS fragmentation
- Indicative of myocardial scar, underlying CAD
- Often predictor of future cardiac events

References:

Das MK, Saha C, El Masry H, et al. Fragmented QRS on a 12-lead ECG: A predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11):1385-1392. PMID: 17954396
Das MK, Saha C, El Masry H, et al. Fragmented QRS on a 12-lead ECG: A predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11):1385-1392. PMID: 20129288
Güngör B, Özcan KS, Karataş MB, et al. Prognostic Value of QRS Fragmentation in Patients with Acute Myocardial Infarction: A Meta-Analysis. Ann Noninvasive Electrocardiol. 2016;21(6):604-612. PMID: 27018003
Xia W, Feng XY. Fragmented QRS (fQRS) complex predicts adverse cardiac events of ST-segment elevation myocardial infarction patients undergoing percutaneous coronary intervention and thrombolysis. Med Sci Monit. 2018;24:4634-4640. PMID: 29974889
Seong CS, Gwag H Bin, Hwang JK, et al. Clinical significance of fragmented QRS complexes or J waves in patients with idiopathic ventricular arrhythmias. PLoS One. 2018;13(4):1-11. PMID: 29694354
Cetin MS, Ozcan Cetin EH, Arisoy F, et al. Fragmented QRS Complex Predicts In-Hospital Adverse Events and Long-Term Mortality in Patients with Acute Pulmonary Embolism. Ann Noninvasive Electrocardiol. 2016;21(5):470-478. PMID: 26701225
Qaddoura A, Digby GC, Kabali C, et al. Use of fragmented QRS in prognosticating clinical deterioration and mortality in pulmonary embolism: A meta-analysis. Ann Noninvasive Electrocardiol. 2018;23(5):1-7. PMID: 29676061
Rattanawong P, Riangwiwat T, Prasitlumkum N, et al. Baseline fragmented QRS increases the risk of major arrhythmic events in Brugada syndrome: Systematic review and meta-analysis. Ann Noninvasive Electrocardiol. 2018;23(2):1-8. PMID: 29030919
Temiz A, Gazi E, Altun B, et al. Fragmented QRS is associated with frequency of premature ventricular contractions in patients without overt cardiac disease. Anadolu Kardiyol Derg. 2015;15(6):456-462. PMID: 25430411
Zhang L, Liu L, Kowey P, Fontaine G. The Electrocardiographic Manifestations of Arrhythmogenic Right Ventricular Dysplasia. Curr Cardiol Rev. 2014;10(3):237-245. PMID: 24827798
Ogura S, Nakamura K, Morita H, et al. New Appearance of Fragmented QRS as a Predictor of Ventricular Arrhythmic Events in Patients With Hypertrophic Cardiomyopathy. Circ J. 2020;84(3):487-494. PMID: 32037379
Haukilahti MAE, Eranti A, Kenttä T, et al. QRS fragmentation patterns representing myocardial scar need to be separated from benign normal variants: Hypotheses and proposal for morphology based classification. Front Physiol. 2016;7(DEC):1-10. PMID: 28082919

Key Teaching Points

QRS fragmentation (fQRS)

Additional notches/spikes within the QRS complex of at least 2 contiguous leads corresponding to a coronary artery territory
Abnormal myocardial activation and conduction delay thought to be due to myocardial scarring
Indicator of previous myocardial injury and predictor of future adverse cardiac events and mortality in various heart diseases

Pseudonormalization of T waves

First described in the 1970s
Normalization of previously abnormal T-waves
At rest or during exercise testing, suggestive of reversible ischemia or coronary occlusion
May be an early or only marker of ischemia

Take home Points

QRS fragmentation

Indicative of myocardial scar, underlying CAD
Often predictor of future cardiac events

Pseudonormalization of T waves

Suggestive of ischemia
Beware of straightening of the upslope of the T-wave

Key Pearl: When the symptoms are concerning but the ECG is non-diagnostic, look at old ECGs and get a repeat ECG!

References:

Das MK, Saha C, El Masry H, et al. Fragmented QRS on a 12-lead ECG: A predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11):1385-1392. PMID: 17954396
Das MK, Saha C, El Masry H, et al. Fragmented QRS on a 12-lead ECG: A predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11):1385-1392. PMID: 20129288
Güngör B, Özcan KS, Karataş MB, et al. Prognostic Value of QRS Fragmentation in Patients with Acute Myocardial Infarction: A Meta-Analysis. Ann Noninvasive Electrocardiol. 2016;21(6):604-612. PMID: 27018003
Xia W, Feng XY. Fragmented QRS (fQRS) complex predicts adverse cardiac events of ST-segment elevation myocardial infarction patients undergoing percutaneous coronary intervention and thrombolysis. Med Sci Monit. 2018;24:4634-4640. PMID: 29974889
Seong CS, Gwag H Bin, Hwang JK, et al. Clinical significance of fragmented QRS complexes or J waves in patients with idiopathic ventricular arrhythmias. PLoS One. 2018;13(4):1-11. PMID: 29694354
Cetin MS, Ozcan Cetin EH, Arisoy F, et al. Fragmented QRS Complex Predicts In-Hospital Adverse Events and Long-Term Mortality in Patients with Acute Pulmonary Embolism. Ann Noninvasive Electrocardiol. 2016;21(5):470-478. PMID: 26701225
Qaddoura A, Digby GC, Kabali C, et al. Use of fragmented QRS in prognosticating clinical deterioration and mortality in pulmonary embolism: A meta-analysis. Ann Noninvasive Electrocardiol. 2018;23(5):1-7. PMID: 29676061
Rattanawong P, Riangwiwat T, Prasitlumkum N, et al. Baseline fragmented QRS increases the risk of major arrhythmic events in Brugada syndrome: Systematic review and meta-analysis. Ann Noninvasive Electrocardiol. 2018;23(2):1-8. PMID: 29030919
Temiz A, Gazi E, Altun B, et al. Fragmented QRS is associated with frequency of premature ventricular contractions in patients without overt cardiac disease. Anadolu Kardiyol Derg. 2015;15(6):456-462. PMID: 25430411
Zhang L, Liu L, Kowey P, Fontaine G. The Electrocardiographic Manifestations of Arrhythmogenic Right Ventricular Dysplasia. Curr Cardiol Rev. 2014;10(3):237-245. PMID: 24827798
Ogura S, Nakamura K, Morita H, et al. New Appearance of Fragmented QRS as a Predictor of Ventricular Arrhythmic Events in Patients With Hypertrophic Cardiomyopathy. Circ J. 2020;84(3):487-494. PMID: 32037379
Haukilahti MAE, Eranti A, Kenttä T, et al. QRS fragmentation patterns representing myocardial scar need to be separated from benign normal variants: Hypotheses and proposal for morphology based classification. Front Physiol. 2016;7(DEC):1-10. PMID: 28082919

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
ST-segment changes with (can mimic ACS)
Pseudo Brugada pattern
Sine wave morphology, asystole

ECG findings in patients on digoxin

“Digoxin effect”
- Downsloping ST-segment depression with a characteristic sagging appearance (a.k.a Salvador Dali moustache)
- The presence of digoxin effect pattern on the ECG is not a marker of supratherapeutic digoxin levels or toxicity, but merely suggests that the patient is taking digoxin
Digoxin toxicity
- Digoxin toxicity causes a multitude of dysrhythmias due to increased automaticity and decreased AV conduction
- Most common finding is frequent PVC’s
- Sinus bradycardia and AV blocks may be seen
- Slow “regularized” atrial fibrillation is a classic finding
  - Regularized due to complete heart block and junctional or ventricular escape rhythm
- Bidirectional VT (rare)

Take home Points

Bizarre bradydysrhythmias, think about hyperkalemia!
If a patient has ECG evidence of hyperkalemia and possibly digoxin toxicity, evidence does not support problems with calcium administration in patients on digoxin or with digoxin toxicity

References:

Levine M, Nikkanen H, Pallin DJ, et al. The effects of intravenous calcium in patients with digoxin toxicity. J Emerg Med 2011; 40:41-46. PMID:19201134

Key Teaching Points

Diffuse ST segment elevation DDx

Large Acute MI

± reciprocal ST-segment depression with active symptoms
Evolving changes (especially with treatment)

Acute Pericarditis

No reciprocal ST-segment depression
PR-segment depression (not specific)
Spodick’s sign (not sensitive or specific)

Early repolarization

No reciprocal ST-segment depression
No PR-segment depression
Fishhooks, J-waves

Vasospasm

No reciprocal ST-segment depression
May evolve with treatment

Ventricular aneurysm

No reciprocal ST-segment depression
+ Q-waves from previous MI

STEMI or Acute Pericarditis?

Distinction is often difficult
STEMI sometimes misdiagnosed as pericarditis
Pericarditis sometimes misdiagnosed as STEMI
- 15-20% of “inappropriate” referrals for PCI were due to pericarditis (Larson, JAMA 2017)

ECG findings in STEMI vs. Acute Pericarditis

Know the differences in ECG findings & use a stepwise approach

Step 1. Factors that strongly suggest STEMI:

Reciprocal ST depression in any leads (except aVR & V1)
STE in lead III > the STE in lead II
Horizontal or convex upward ST-segment morphology
R-T sign or “checkmark sign”
Q-waves that you know are new (be cautious it they are old)

Look for the factors that rule in STEMI before thinking pericarditis!

Step 2. Factors that suggest pericarditis (look for these only after looking for STEMI in step 1):

Pronounced PR-segment depression in multiple leads (only reliably seen in viral acute pericarditis, may be transient)
Pericardial friction rub
Spodick sign (may be suggestive of pericarditis if no signs of STEMI found)

When in doubt…do serial ECGs and consider CATH!

Highlights of new study on this topic: Evaluation of Spodick’s sign and other electrocardiographic findings as indicators of STEMI and pericarditis. J Emerg Med 2020. PMID: 32222321

Retrospective review of 165 cases of STEMI and 42 cases of acute pericarditis
Spodick’s sign occurred in 5% of patients with confirmed STEMI vs. 29% of patients with confirmed pericarditis
PR depression occurred in 12% of patients with confirmed STEMI
ECG findings that statistically distinguished STEMI from pericarditis are highlighted below and detailed in Table 2.
- ST segment depression (OR for STEMI = 31)
- ST segment elevation in III>II (OR for STEMI = 21)
- Horizontal or convex upward ST elevation (OR for STEMI = 6)
- Absence of PR depression (OR for STEMI = 12)
- R-T “checkmark” sign (OR for STEMI = 8)
- Absence of Spodick’s sign (OR for STEMI = 7)

Take home Points

STEMI vs. acute pericarditis
- Look first for factors that rule IN STEMI before you look at PR segments
  - ST depression (aside from aVR and V1)
  - STE III > II
  - Horizontal or convex upward STE
  - R-T sign (“Checkmark sign”)
- Looking for PR depression and Spodick sign should only be done AFTER the above
- PR depression and Spodick sign (T-P downsloping) are helpful…but not 100% specific to pericarditis!

References:

Witting MD, Hu KM, Westreich AA, Tewelde S, Farzad A, Mattu A. Evaluation of Spodick’s Sign and Other Electrocardiographic Findings as Indicators of STEMI and Pericarditis. J Emerg Med. 2020;58(4). PMID: 32222321
Larson DM, Menssen KM, Sharkey SW. “False-Positive” Cardiac Catheterization Laboratory Activation Among Patients with Suspected ST-Segment Elevation Myocardial Infarction. JAMA. 2007;298(23):2754-2760. PMID: 18165668
Chhabra L. Loss of a cardiology legend: A tribute to Professor David H. Spodick (1927-2019). J Electrocardiol. 2019 Sep-Oct;56:125-127. PMID: 31277841

Key Teaching Points

Left Bundle Branch Block Basics

LBBB ECG Criteria:
QRS > 120 ms (conventional criteria)
- QRS ≥ 130 ms; women, QRS ≥ 140 ms; men (strict criteria)
Leftward conduction delay (QS or rS in lead V1)
R wave peak time > 60 ms (late R or R’) in lead I, V5 or V6 with no Q waves in these leads
Mid-QRS notching/slurring in two of the following leads; I, aVL, V1, V2, V5 or V6 (strict criteria)
ST segments and T waves are usually discordant to the QRS complex
In the absence of acute ischemia, patients with LBBB patterns have ST-segment deviation opposite to the direction of the QRS (discordant ST deviation), that is proportional to the voltage of the corresponding QRS complex. This is normal & referred to as the “rule of appropriate discordance”
These expected ECG abnormalities in patients with LBBB patterns can make the identification of acute MI difficult in patients with symptoms of acute ischemia
LBBB in patients with ischemic symptoms were traditionally considered a STEMI equivalent, however evidence suggested that this was a major cause of false positive cath lab activation. Hence, LBBB is no longer considered diagnostic of acute MI in isolation (removed from 2013 AHA STEMI criteria guidelines)
However, ST-segment deviations that are concordant(in same direction) or excessively discordant to the QRS complex are abnormal and suggestive of acute MI
Patients with LBBB and acute MI are at high risk and delays in reperfusion therapy may lead to bad outcomes
Despite traditional teaching that suggests that you cannot reliably diagnose MI in patients with LBBB, acute coronary occlusion can in fact be detected using the ECG criteria described below

Sgarbossa Criteria, Modified Sgarbossa Criteria, and the BARCELONA Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion with good specificity in the setting of LBBB and ventricularly paced rhythms
Unlike ECGs without conduction disturbances, infarct localization or identification of the culprit coronary artery using the ECG in patients with a LBBB is inaccurate. The Sgarbossa criteria can help identify which patients should have emergent angiography to identify coronary occlusion and the culprit vessel.
The original criteria presented by Sgarbossa et al. (1996) are summarized below:

A. Concordant ST elevation ≥ 1 mm (in any lead) = Most specific for MI in LBBB

B. Concordant ST depression ≥ 1 mm in V₁, V₂, or V₃ = Specific for MI

C. Discordant ST elevation ≥ 5 mm = Less specific for MI in LBBB

A revised Sgarbossa C rule was proposed to increase the diagnostic utility of the rule for acute coronary occlusion
The revised rule replaces the absolute criterion (discordant STE ≥ 5 mm) with a proportional criterion (ST-segment elevation to S-wave depth (ST/S ratio) ≥ 25%) and has been found to be superior to the original criteria for identifying acute coronary occlusion in LBBB.
Although the Sgarbossa and Modified Sgarbossa criteria are very specific for acute MI, these criteria have low sensitivity
Di Marco et al. recently published a new Barcelona algorithm which reportedly has much greater sensitivity and comparable specificity for AMI in LBBB:
- Concordant ST deviation (≥ 1 mm) is abnormal in any lead (extends Sgarbossa rule of concordant ST depression in V1-V3 to any other lead)
- Discordant ST deviation (≥ 1 mm) in low voltage QRS complexes (maximal R or S wave is £ 6 mm)
- The BARCELONA algorithm reportedly attained the highest sensitivity and negative predictive values, while maintaining high specificity
- While the high sensitivity and specificity of the new Barcelona algorithm are promising, they still need external validation to see if the criteria perform as well after independent assessment

Take home Points

Diagnosing OMI (STEMI equivalent) in the presence of LBBB

Acute coronary occlusion CAN be detected on the ECG with good sensitivity
Know the Sgarbossa criteria, which can and should be applied to LBBB ECG’s where there is concern for acute MI (very specific)
1. Concordant STE ≥ 1 mm in any lead (most specific)
2. Concordant STD ≥ 1 mm in V1, V2, or V3 (very specific)
3. Excessively discordant STE ≥ 5 mm (less specific)
Smith et al. proposed a modified Sgarbossa C criterion that replaces the absolute measurement of STE ≥ 5 mm with a STE/S wave ratio > 25% (more specific than original Sgarbossa C)
Di Marco et al. recently published a new (BARCELONA) algorithm which reportedly has much greater sensitivity and comparable specificity for AMI in LBBB
- Concordant ST deviation ≥ 1 mm in any lead
- Discordant ST deviation ≥ 1 mm in any lead with a small QRS complex (maximal R or S wave is £ 6 mm)
We are awaiting further studies to externally validate modified Sgarbossa and Barcelona criteria

References:

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing.Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802.
Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576.
Maloy KR, Bhat R, Davis J, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers.West J Emerg Med. 2010;11(4):354–357. PMID: 21079708.
Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607.
Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal.2013;166(3):409–413. PMID: 24016487.
Pendell Meyers H, Limkakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-1264. PMID: 26678648.
Ibanez B, James S, Agewall S, et al. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J 2017;39(2):119–77. PMID: 28886621.
Di Marco A, Rodriguez M, Cinca J, et al. New Electrocardiographic Algorithm for the Diagnosis of Acute Myocardial Infarction in Patients with Left Bundle Branch Block. J Am Heart Assoc. 2020;9(14):e015573. PMID: 32627643.

Key Teaching Points

ECG Diagnosis of Ventricular Tachycardia (VT)

The ECG can NOT reliably distinguish between VT and supraventricular tachycardia with aberrant conduction (SVT-AC)
- The ECG and clinical factors are reliable at ruling in VT
- The ECG (including the published algorithms below) and clinical factors are unreliable at ruling out VT (i.e. at ruling in SVT with AC/BBB)
Algorithms created to distinguish VT vs. SVT-AC are far from perfect and difficult to use clinically. The references review the most popular ones in detail, but they all miss cases of VT.
- Best attempts at creating algorithms to distinguish SCT-AC vs. VT have failed:
  - Brugada algorithm
  - Bayesian algorithm
  - Griffith algorithm
  - Vereckei aVR algorithm
  - Lead II R-wave-peak-time algorithm (RWPT)
- Classic teaching:
  - “…assume WCT is VT until proven otherwise…”
  - “…when in doubt, assume and treat WCT as VT…”
- Here is a simpler method…

Mattu Algorithm for Wide Complex Tachycardias (WCTs)

Is the WCT clearly sinus tachycardia with aberrant conduction?
1. If yes – treat the underlying cause
2. If no – go to step 2
It’s Ventricular Tachycardia!

What about an Adenosine diagnostic challenge?

Adenosine sensitive VT is not benign, and many patients go on to have unstable VT even after conversion to sinus rhythm
Response to Adenosine does NOT rule out VT!

Take-home points:

Wide complex tachycardia? Call it VT!
The WCT rules and algorithms are far from perfect

References:

Jastrzebski M, Sasaki K, Kukla P, Fijorek K, Stec S, Czarnecka D. The ventricular tachycardia score: A novel approach to electrocardiographic diagnosis of ventricular tachycardia. Europace. 2016;18(4):578-584. PMID:25995387
McGill TD, Kashou AH, Deshmukh AJ, LoCoco S, May AM, DeSimone C V. Wide complex tachycardia differentiation: An examination of traditional and contemporary approaches. J Electrocardiol. 2020;60:203-208. PMID:32417627
Kashou AH, Noseworthy PA, DeSimone C V, Deshmukh AJ, Asirvatham SJ, May AM. Wide Complex Tachycardia Differentiation: A Reappraisal of the State-of-the-Art. J Am Heart Assoc. 2020;9(11):e016598. PMID:32427020
Jastrzebski M, Kulka P, Czarnecka D, et al. Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace 2012;14(8):1165-71. PMID:22333239
Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med 2013;20(11):1121–30. PMID: 24238314
Marill KA, Wolfram S, Desouza IS, et al. Adenosine for wide-complex tachycardia: efficacy and safety. Crit Care Med 2009;37(9):2512-8. PMID:19623049

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Hyperkalemia

Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: Can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med. 2017;18(5):963-971. PMID: 28874951

188 patients with K⁺≥ 6.5 mEq/L
15% developed adverse effects within 6 hours (e.g. symptomatic dysrhythmia, arrest, death)
Correlated short term adverse events with presenting ECG findings
100% of short-term adverse events were preceded by ECG abnormalities…but abnormal or peaked T-waves did not correlate!
Highest correlation with
- Bradycardia (HR < 50) – RR 12.29
- Junctional rhythm – RR 7.46
- Widened QRS (> 100 ms) – RR 4.74

Take-home Points:

Hyperkalemia does it all, and you’ve got to know what to look for!

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Reference:

Rafique Z, Aceves J, Espina I, Peacock F, Sheikh-Hamad D, Kuo D. Can physicians detect hyperkalemia based on the electrocardiogram? Am J Emerg Med. 2020;38(1):105-108. PMID: 31047740
Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: Can the electrocardiogram risk stratify for short-term adverse events? West J Emerg Med. 2017;18(5):963-971. PMID: 28874951

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Hyperacute T-waves
  - Disproportionately large T-waves (especially when larger than QRS)
  - Straightening of the upslope of the T-waves
- “Checkmark or BAM sign”
  - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- Reciprocal changes (e.g. aVL, V₂)
  - Especially aVL when the RCA is involved in inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

Take-home Points:

30% of anterior STEMIs have no reciprocal ST segment depression
- Computers will often diagnose these as pericarditis, early repolarization or normal
- Don’t rely on reciprocal changes, especially in anterior STEMI’s
Don’t trust the computer ECG interpretation, it will fool you!

Reference:
Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. 6^th Edition. Amazon link.

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Hyperacute T-waves
  - Disproportionately large T-waves (especially when larger than QRS)
  - Straightening of the upslope of the T-waves
- “Checkmark or BAM sign”
  - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- Reciprocal changes (e.g. aVL, V₂)
  - Especially aVL when the RCA is involved in inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

Take-home Points:

30% of anterior STEMIs have no reciprocal ST segment depression
- Computers will often diagnose these as pericarditis, early repolarization or normal
- Don’t rely on reciprocal changes, especially in anterior STEMI’s
Don’t trust the computer ECG interpretation, it will fool you!

Reference:
Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. 6^th Edition. Amazon link.

Key Teaching Points

Differential for Non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Bifascicular & Trifascicular Blocks

Bifascicular Block

Conduction abnormality where two of the three main fascicles of the His/Purkinje system are blocked

- Usually a RBBB + LAFB
- Or RBBB + LPFB

Trifascicular Block

Any AV Block (especially 2^nd degree or 3^rd degree) + RBBB + LAFB
Or any AV block (especially 2^nd degree or 3^rd degree) + RBBB + LPFB
Or any AV block (especially 2^nd degree or 3^rd degree) + LBBB

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Key Teaching Points

Differential for Non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only seen in ~30% of patients with PE)
Atrial and ventricular dysrhythmias
Signs of right heart strain

- Rightward axis (look for large S wave in lead I)
- New RBBB or incomplete RBBB
- New T-wave inversions (especially in anteroseptal +/- inferior leads)
- ST-segment elevations or depressions
  - ST-elevation in rightward leads (V₁, V₂, aVR, III)
Co, et al.. J Emerg Med 2017 (PMID: 27742402) – identified the most common ECG changes in patients with known PE when comparing their ECGs with previous ECGs
- T wave inversion ~ 34%
- T wave flattening ~ 30%
- Sinus tachycardia ~ 27%
- Rightward axis ~ 11%
- ST segment changes ~ 9%
- S1Q3T3 ~ 4%

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

BRASH syndrome

Bradycardia, Renal failure, AV nodal blocker, Shock, Hyperkalemia

An inciting event leads to renal failure and hyperkalemia. Hyperkalemia synergizes with AV nodal blocking medications that leads to the development of bradycardia and shock. Hypoperfusion causes worsening renal failure and hyperkalemia leading to a vicious cycle that can be deadly without aggressive treatment.
Goals in management
- Aggressive blood pressure support
- Treatment of hyperkalemia
- Remove/treat inciting event

LAFB vs. RAFB

Type of Fascicular Block	Left Anterior FB	Left Posterior FB
Axis	Left Axis Deviation	Right Axis Deviation
Leads I & aVL
Lead III

References:

Co I, Eilbert W, Chiganos T. New Electrocardiographic Changes in Patients Diagnosed with Pulmonary Embolism. J Emerg Med. 2017;52(3):280-285. PMID: 27742402
Shopp JD, Stewart LK, Emmett TW, Kline JA. Findings From 12-lead Electrocardiography That Predict Circulatory Shock From Pulmonary Embolism: Systematic Review and Meta-analysis. Acad Emerg Med 2015;22(10):1127–37. PMID: 26394330
Dibgy,GC, Kulka P, Zhan ZQ, et al. The value of electrocardiographic abnormalities in the prognosis of pulmonary embolism: a consensus paper. Ann Noninvasive Electrocardiol 2015. May;20(3):207-23. PMID: 25994548
Kukla P, McIntyre WF, Fijorek K, et al. Electrocardiographic abnormalities in patients with acute pulmonary embolism complicated by cardiogenic shock. Am J Emerg Med 2014;32(6):507–10. PMID: 24602894
Zhan Z-Q, Wang C-Q, Nikus KC, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51.PMID: 24750207

Abarca E, Baddi A, Manrique R. ECG manifestations in submassive and massive pulmonary embolism. Report of 4 cases and review of literature. Journal of Electrocardiology 2014;47(1):75–9. PMID: 23890684

Key Teaching Points

ECG findings in Hyperkalemia

Peaked T-waves (even when inverted)
Widening of the QRS (often marked)
Prolonged PR-interval
Flattening and eventual loss of P-waves
Tachydysrhythmias, pseudo ventricular tachycardia
Bizarre bradydysrhythmias, advanced AV Blocks and sinus pauses
Axis changes (especially RAD)
Fascicular & Bundle Branch Blocks
Pseudo ACS with ST-segment changes (can mimic STEMI)
Pseudo Brugada syndrome pattern
Sine wave morphology

Take-home Points

Hyperkalemia can produce STE
- Especially in the “rightward” leads (V1, V2, aVR, III)
- Often associated with right axis deviation
STEMI rarely produced right axis deviation

Amal Mattu’s ECG Case of the Week – May 23, 2016

Cases by Month

Cases by Type

Be the best at electrocardiography!

Key Teaching Points

Key Teaching Points

Key Teaching Points

Key Teaching Points

Key Teaching Points