Amal Mattu’s ECG Case of the Week – May 17, 2021

Key Teaching Points

Atrial flutter with 2:1 conduction

Most missed atrial tachyarrhythmia, always be wary of atrial flutter!

Consider flutter with 2:1 conduction when ventricular rate is 150 ± 20 bpm
2 atrial beats for every QRS
- Look in all leads for atrial activity, especially lead V1
- Saw tooth pattern, flipping the ECG upside down and paying attention to all 12 leads will help you identify subtle flutter waves which may be inverted
- When dealing with questionable flutter waves, use calipers and map them out
  - Artifact does not map out, consider flutter when atrial beats map out around 300 bpm
Flutter waves often confuse the computer and may result in misdiagnosis of ACS and mimic STEMI

Wellens syndrome and “pseudo-Wellens” waves

Wellens syndrome is the result of critical stenosis of the LAD manifesting in the characteristic ECG patterns (biphasic Wellens T waves). It is a pre-infarction state, that tends to progress to large anterior MI with poor morbidity and mortality when not recognized early and treated appropriately
Beware Wellens syndrome but also watch out for normal variants and “pseudo-Wellens waves” that can result in false positive cath lab activation
- Normal variant ST elevation and T wave inversions may mimic Wellens waves and STEMI.
- Be careful when diagnosing Wellens syndrome in patients with high voltage QRS complexes or features more suggestive of a normal variant:
  - Young males, especially athletes
  - Typically, African-Caribbean decent
    - Less common in Caucasians
  - Concave upward ST segment elevation, followed by a sharp drop into biphasic T waves, often with notch or “fishhook” appearance at the J-point
  - ST segment elevation in this pattern will mimic 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

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

ECG findings in Hypothermia

Onset of ECG findings can vary, but resolve with warming:

Early sinus tachycardia
Shivering artifact
Bradycardia: sinus, junctional rhythms, slow atrial fibrillation
J-waves/Osborn waves (positive deflections at the J-point)
- “Classic” textbook finding, but not sensitive
- Can cause pseudo-ST segment elevation or depression
Prolongation of all intervals
- Long QT due to lengthening of the ST segment
Ventricular fibrillation
Asystole

DDx of Rightward Axis Deviation

Acute pulmonary hypertension (e.g., PE)
Chronic pulmonary hypertension (g., COPD)
Right ventricular hypertrophy
Hyperkalemia
Na⁺channel blocker toxicity
Left posterior fascicular block
Old lateral MI (from Q-waves in lead I)
Ventricular ectopy
Lead misplacement / dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Left anterior vs. posterior fascicular block

AV dissociation without complete heart block

Complete heart block should have a completely regular escape rhythm
- If there is evidence of irregularity, some of the beats are likely getting conducted, hence, not a complete heart block

Key Teaching Points

DDx of Rightward Axis Deviation

Acute pulmonary hypertension (e.g., PE)
Chronic pulmonary hypertension (g., COPD)
Right ventricular hypertrophy
Hyperkalemia
Na⁺channel blocker toxicity
Left posterior fascicular block
Old lateral MI (from Q-waves in lead I)
Ventricular ectopy
Lead misplacement / dextrocardia
Normal variant in young kids & thin adults with horizontally positioned hearts

Left anterior vs. posterior fascicular block

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

Take-home Points:

Right bundle branch block (RBBB) can mimic ST segment elevation
- Pay attention to the QRS duration before judging where the J-point is
Learn the differential diagnosis for right axis deviation!

Key Teaching Points

Take home Points

Isorhythmic AV dissociation
- Atrial rate and ventricular rate are approximately the same
- Can occur with complete heart block (escape rhythm will be regular) or with occasional conduction/capture beats (these QRS complexes appear early)

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!

March 16, 2015

Case Interpretation

Rhythm – Sinus rhythm with blocked (non-conducted) PAC’s

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

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

Take home Points

Complete heart block should have a completely regular escape rhythm
- If there is evidence of irregularity, some of the beats are likely getting conducted, hence this is not complete heart

Key Teaching Points

Normal Right Bundle Branch Block (RBBB)

Leads V₁-V₂ can have mild discordant 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:

In a typical RBBB, leads V₁-V₂ can have mild discordant ST-segment depression, which is a normal finding
RBBB should have no ST-segment elevation in any lead
Beware STEMI’s in RBBB…often missed by the computer and the clinician
Don’t trust the computer to make the diagnoses when the STE is subtle
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

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

Take home Points

Ventricular tachycardia should have a heart rate > 120-130 bpm
- Should be regular in rhythm
- QRS is usually < 200 ms wide
Really REALLY wide complex tachycardia (RRWCT) = strongly consider toxicologic or metabolic conditions (especially hyperkalemia) FIRST!
- Na⁺ channel blockers can kill! Use of typical ACLS antiarrhythmics in patients with sodium channel blockade can be deadly!
- Consider empiric treatment with calcium and sodium bicarbonate, can be lifesaving
Hyperkalemia is the GREAT IMITATOR in electrocardiography!

Key Teaching Points

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion in setting of LBBB/paced rhythms
The original criteria are reviewed 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 (most specific in pacers)

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

Sgarbossa criteria can and should be applied to paced ECG’s (high specificity)

A. Concordant STE in any lead

B. Concordant STD in V1, V2, or V3

C. Discordant STE > 5 mm in any lead

- - Watch for new literature upcoming on using the revised criteria C for patients with paced rhythms

References:

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
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

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

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion in setting of LBBB/paced rhythms
The original criteria are reviewed 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 (most specific in pacers)

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

Sgarbossa criteria can and should be applied to paced ECG’s (high specificity)

A. Concordant STE in any lead

B. Concordant STD in V1, V2, or V3

C. STE > 25% of the size of the S-wave

References:

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
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.

Key Teaching Points

Take Home Points

Acute reperfusion therapy is indicated in patients with signs and symptoms consistent with ACS AND the following ECG findings:

What about new LBBB?
- Removed from ACC/AHA guidelines in 2013
What about hyperacute T-waves?
- No strict definition, lots of false-positive and false-negative “hyperacute T-waves”
- Pick this up based on “intractable ischemia” or with serial ECG’s (evolving changes)
What about Wellens’ syndrome?
- Asymptomatic – non-emergent cath

Key Teaching Points

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

Take home Points

Consider BRASH syndrome in bradycardic patients on AV nodal blockers
Treat hyperkalemia as usual, serum potassium levels may only be mildly elevated, and the ECG may not show classic findings of hyperkalemia
Treat shock aggressively
Remove and treat the underlying cause

Key Teaching Points

The many causes of ST-segment elevation

Acute myocardial injury (acute coronary occlusion or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Early Repolarization
Myo/pericarditis
Vasospasm
Ventricular aneurysm
LBBB/pacemaker
Pulmonary embolism
LVH/high left ventricular voltage (WPW, athlete’s heart, etc.)
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Post-cardioversion (stunning)
Hyperkalemia
Hypothermia
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Causes of Rightward Axis Deviation

Acute pulmonary HTN – Acute (PE) & chronic lung disease (COPD)Ventricular ectopy
Hyperkalemia
Na⁺channel blocker toxicity
Right ventricular hypertrophy
Left posterior fascicular block
Old 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 (which usually does not produce rightward axis)

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

Final take-home points:

ST-segment elevation has many causes
Right axis deviation has many causes
PE’s commonly mimic ACS on ECG
Large PE’s can often mimic STEMI with ST-segment elevation (especially in rightward leads). Pay attention to the axis!
STEMI’s don’t tend to produce a rightward axis
Rightward axis in apparent “STEMI”? Pay attention to the axis and consider large PE!

Key Teaching Points

Differential diagnosis for right axis deviation

Ventricular beats/ectopy
Right ventricular hypertrophy
Left posterior fascicular block
Pulmonary hypertension (acute and chronic, e.g. PE)
Old lateral MI (Q-waves)
Na⁺ channel blocker toxicity
Hyperkalemia
Misplaced leads
Situs inversus
Newborns/infants

Causes of widening of the QRS-complex

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

Differential diagnosis for long QTc

Hypokalemia, Hypomagnesemia, Hypocalcemia
Hypothermia
Na⁺channel blocking drugs
Elevated ICP
Congenital

Take-home points

TCA/sodium-channel blocker effects on ECG

Tachycardia, typically wide-complex
Rightward axis
- Large S wave in lateral leads
- Tall R in aVR producing ST segment elevation
- Tall R wave in V₁, pseudo-Brugada pattern
Prolonged QT interval
Use a step-by-step approach to ECG interpretation, and use your DDx’s

Key Teaching Points

Differential diagnosis for large T-waves

Hyperkalemia
Acute ischemia (“hyperacute T-waves”)
High voltage, LVH

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

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.

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

Causes of prolonged QT-interval summary

Prolonged QT due to abnormal/prolonged T –waves

Hypokalemia
Hypomagnesemia
Medications
Misc: Elevated ICP, Cardiac ischemia, Congenital

Prolonged QT due to prolonged ST-segment

Hypocalcemia
Hypothermia

Take-home points:

If the long QTc is specifically due to a long ST segment, think of
- Hypothermia
- Hypocalcemia
Hyperkalemia is often associated with a long QT due to hypocalcemia

Key Teaching Points

Take-home points:

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

Key Teaching Points

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)

Take-home Points:

Don’t trust the computer!
Narrow complex regular tachycardia DDx
- Sinus tachycardia
- SVT
- Atrial flutter with 2:1 conduction
When the ventricular rate is 150 ± 20, assume atrial flutter
The Bix rule, described by cardiologist Harold Bix, states that if a T-wave is located halfway between two QRS complexes, there is a good chance that P-waves are also buried inside the QRS complexes, think atrial flutter!

Reference:

Nikolić G. The Bix rule. Heart Lung 2008;37(4):321–2. PMID: 18620109.

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
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 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, 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)

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
Especially useful when deciding between ventricular tachycardia vs. SVT or atrial flutter with aberrant conduction
How to obtain a Lewis lead:
- Move the right arm electrode to the manubrium (below suprasternal notch)
- Move left arm electrode to right fifth intracoastal space next to sternum
- Move left leg electrode to 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

5-Step Approach to ECG Interpretation

Rate & Rhythm
Axis
Intervals
Enlargement
Ischemic/infarction

Differential diagnoses for rightward axis

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

Differential diagnoses for wide QRS complexes

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

Differential diagnoses for long QTc intervals

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Na⁺channel blocking drugs (e.g. TCA’s)
Medications
Congenital

Differential diagnoses for tall R-waves in V₁

Ventricular beats/ectopy
Right ventricular hypertrophy
Acute RV strain (PE)
Incomplete/Complete RBBB
Na⁺ channelopathies (e.g TCA, hyperkalemia)
Posterior MI
WPW
Hypertrophic cardiomyopathy
Dextrocardia, situs inversus
Misplaced precordial lead

Differential diagnoses for ST-segment elevation

Acute myocardial injury (acute coronary occlusion or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Early Repolarization
Myo/pericarditis
Vasospasm
Ventricular aneurysm
LBBB/pacemaker
Pulmonary embolism
LVH/high left ventricular voltage (WPW, athlete’s heart, etc.)
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Post-cardioversion (stunning)
Hyperkalemia
Hypothermia
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take-home Points:

Be systematic and use a step-by-step approach to ECG interpretation every time!
Use differentials for the abnormal findings.

Key Teaching Points

Differential diagnoses for rightward axis

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

Take-home Points:

PE and hyperkalemia can cause ST segment elevation
Especially in the rightward leads (V1, aVR, ± V2, III)

Key Teaching Points

Differential diagnoses for ST-segment elevation

Acute myocardial injury (acute coronary occlusion or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Early Repolarization
Myo/pericarditis
Vasospasm
Ventricular aneurysm
LBBB/pacemaker
Pulmonary embolism
LVH/high left ventricular voltage (WPW, athlete’s heart, etc.)
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Post-cardioversion (stunning)
Hyperkalemia
Hypothermia
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Differential diagnoses for long QTc intervals

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Na⁺channel blocking drugs (e.g. TCA’s)
Medications
Congenital

Differential diagnoses 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

Brain-Heart Interaction (ECG abnormalities)

Described at least since the 1950’s
Can occur with any brain problems
- 42% of patients with brainstem tumors & 56% of patients with intracerebral tumors
  - Rudehill, et al. 1987
- 71% of patients with SAH & 57% of patients with intracerebral hemorrhage
  - Gibson, et al. 2012
- Documented with ischemic strokes
Theories
- Altered autonomic tone
- Vagal response
- Sympathetic surge producing electrical problems and/or myocardial injury
ECG
- Large T wave inversions, especially in the anterolateral leads
  - “Cerebral T waves”, “rollercoaster T waves”
- Prolonged QTc (most common)
- U-waves
- ST elevation or depression mimicking STEMI
- Tachy- or bradydysrhythmias

Take-home Points:

Brain problems often produce ECG abnormalities
- Prolonged QTc
- Large T wave inversions
- ST changes that mimic ACS
- Dysrhythmias

References:

Rudehill A, Olsson GL, Sundvist K, et al. ECG abnormalities in patients with subarachnoid haemorrhage and intracranial tumors. J Neruol Neurosurg Psychiatry. 1987. Oct;50(10):1375-81. PMID: 3681317

Key Teaching Points

Precordial T-waves

The normal ECG has a flat or inverted T-wave in lead V₁
- An upright T-wave in V₁ (TV₁) should be considered possibly abnormal
  - Marriott: If the TV₁ large (TV₁ > TV₆), it is particularly abnormal
  - “Loss of precordial T-wave balance”
  - Suggests underlying CAD
  - Suggests acute ischemia if new (new upright T wave in V_1,NUTV₁)
- New tall T-wave in V₁ (NTTV₁)
  - A type of hyperacute T-wave
  - This finding may precede other expected ischemic ECG changes
  - Worry about this in patients with active symptoms
  - Get serial ECGs
  - Beware for normal variants
    - Precordial lead reversals
    - LBBB
    - LVH
    - High left ventricular voltages

Take-home Points:

Beware the upright T-wave in V₁ in patients with active symptoms
- Especially if new (NUTV₁)
- Especially if TV₁ > TV₆
  - “Loss of precordial T-wave balance” (Marriott)
- Suggests underlying CAD or acute ischemia
- Get repeat ECG’s

Key Teaching Points

Artifact:

Artifact is not uncommon and can be misdiagnosed as polymorphic ventricular tachycardia (PVT), torsades, or ventricular fibrillation (VF)
- Always correlate with clinical condition
- PVT, torsades, and VF patients are usually sick!
If patient is stable, look at every lead for evidence of regular organized activity buried within artifact!
If unstable/unconscious, check pulse and don’t delay shock

Take-home Points:

Artifact is common
Bad artifact can often mimic ventricular tachydysrhythmias, especially PVT, VF
If you have time, look carefully at the full rhythm strip or 12-lead
Organized beats cannot exist within PVT, VF

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 40-120: Accelerated ventricular escape rhythm (accelerated idioventricular rhythm, AIVR)
Ventricular rate > 120: 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 of an occluded coronary vessel in AMI (spontaneous or s/p thrombolytics)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, post-arrest rhythms
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Tends to be transient. Treatment is to simply observe!

Take-home Points:

Ventricular tachycardia: HR > 120
- If rate < 120 consider, don’t treat as ventricular tachycardia; consider the mimics instead
  - Accelerated idioventricular rhythm (AIVR)
  - Hyperkalemia
  - Sodium channel blocker toxicity
- Ventricular antiarrhythmics can kill!
- Post-reperfusion AIVR is GOOD!
- Suggests successful reperfusion
- Treatment: observe!
Post-lytic reperfusion: what you want to see
- Resolution of symptoms
- Resolution of ST-segment elevation
- Reperfusion arrhythmia (AIVR)
- T-wave inversions

References:

Szerlip M, Anwaruddin S, Aronow HD, et al. Considerations for cardiac catheterization laboratory procedures during the COVID-19 pandemic perspectives from the Society for Cardiovascular Angiography and Interventions Emerging Leader Mentorship (SCAI ELM) Members and Graduates. Catheter Cardiovasc Interv.2020 Mar 25. [Epub ahead of print]. PMID: 32212409.

Key Teaching Points

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

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion in setting of LBBB/paced rhythms
The original criteria are reviewed 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 (most specific in pacers)

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.

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.

Take home Points

Sgarbossa criteria can and should be applied to LBBB ECG’s (high specificity)
- Concordant STE in any lead
- Concordant STD in V1, V2, or V3
- STE > 25% of the size of the S-wave

References:

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
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.

Key Teaching Points

COVID and the Heart

Cardiovascular manifestations of COVID-19 are complex with patients presenting with AMI, myocarditis mimicking STEMI, stress cardiomyopathy, non-ischemic cardiomyopathy, coronary spasms, and other nonspecific myocardial injury.
The prevalence of COVID-19 disease in the US population remains unclear with risk of asymptomatic spread.
Early experiences with COVID-19 in China suggested that a fibrinolysis-based strategy may useful to avoid unnecessary exposure to staff when rapid testing for SARS-CoV-2 infection is not available or reliable.
If using thrombolytics for AMI, the following are indicators of reperfusion that you should evaluate for at 90 minutes:
- Resolution of symptoms
- 70% resolution of STE in the lead with maximal STE
- Reperfusion dysrhythmias
- T-wave inversions
Persistent ischemia despite lytic use is an indication for rescue PCI

SCAI/ACC/ACEP Consensus Statement on Management of AMI During the Pandemic

Key points
- Acknowledge that STEMI mimics may be more common with COVID-19
- If significant uncertainty exists, consider ECHO or POCUS
- If no ECHO, default should be cath rather than lytics
  - Lytics may cause harm without benefit if it is a mimic
  - Lytics fail in up to 50% of STEMI cases, and persistent STE or ischemia requires rescue PCI
- Transfer patients: primary PCI if possible but consider lytics before transfer if you expect a delay
- Support consultation with cardiology for joint decision-making
- Assume every patient is potentially COVID-19 positive and use appropriate PPE in all cases

Take home Points

ST segment elevation in the COVID-19 era can be true STEMI or myocarditis
- Best choice for STEMI remains primary PCI (standard of care) at PCI capable hospitals when it can be provided in a timely fashion with PPE
- When in doubt consider ECHO or primary PCI

References:

Madjid M, Safavi-Naeini, Solomon SD, et al. Potential Effects of Coronaviruses on the Cardiovascular System: A Review. JAMA Cardiol. 2020 [Epub ahead of print]. PMID: 32219363
Zeng J, Huang J, Pan L. How to balance acute myocardial infarction and COVID-19: the protocols from Sichuan Provincial People’s Hospital.Intensive Care Med. 2020 [Epub ahead of print]. PMID: 32162032
Mahmud E, Dauerman HL, Welt FG, et al. (including Mattu A!). Management of Acute Myocardial Infarction During the COVID-19 Pandemic. J Am Coll Cardiol. 2020 [Epub ahead of print]. PMID: 32330544

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 40-120: Accelerated ventricular escape rhythm (accelerated idioventricular rhythm (AIVR))
- Ventricular rate > 120: Ventricular tachycardia (VT)
  - 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 of an occluded coronary vessel in AMI (s/p thrombolytics or spontaneously)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, post-arrest rhythms
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Tends to be transient. Treatment is to simply observe!

Take-home Points:

Ventricular tachycardia: Consider with heart rates > 120
- If heart rate is < think of VT mimics instead
  - Accelerated idioventricular rhythm (AIVR)
  - Hyperkalemia
  - Sodium channel blocker toxicity
- Ventricular antiarrhythmics can kill!
- Post-reperfusion AIVR is GOOD!
- Suggests successful reperfusion, may occur with reperfusion treatment or spontaneously
- Treatment: observe!

Key Teaching Points

3 types of Ventricular Tachycardia (VT)

Monomorphic VT
Usually associated with scar from prior MI or other structural abnormalities
Can sometimes be associated with ACS (rarely)
Can also be caused by electrolyte abnormalities
- Sedation and shock are the treatment of choice
  - Medications: procainamide >> amiodarone, lidocaine
  - Once converted to sinus rhythm, consider beta blockers
  - Look for and treat the underlying cause
- 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.
    - Note: 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 (should be strongly considered)
  - Sustained VT
    - Rate > 120-130
    - Lasts at least 30 seconds or produces hemodynamic instability
      - Treatment with meds or shock
        
        Search for and treat underlying cause
        
        Shock, procainamide, amiodarone, or lidocaine; then beta blockers after conversion
      - Generic polymorphic VT
      - Normal QTc
      - Usually associated with ACS
        
        Brugada syndrome and other miscellaneous causes should also be considered (look closely at post-cardioversion ECG)
      - Patients usually are unstable
      - If persistent, proceed with shock, then…
        
        Treat for ACS/cardiac ischemia, consider beta blockers >> amiodarone
        
        Brugada, refer to electrophysiologist for AICD. If refractory, consider quinidine or isoproterenol
      - Torsades de pointes (type of polymorphic VT)
      - Defined by prolonged QTc (major risk when QTc is greater than 500 ms)
      - Note: diagnosis is NOT based on morphology, rather the QTc
      - Usually are unstable, proceed with shock if persistent
        
        Magnesium IV push if shocks don’t work, followed by infusion
      - If intermittent…
        
        Magnesium slow IVP followed by infusion
        
        Overdrive pacing (shortens the QTc)
        
        Electrically pace at 100-120 bpm
        
        Chemically pace with isoproterenol, dopamine, or epinephrine
        
        After conversion…
        
        Magnesium infusion until underlying cause is identified and corrected
        
        Hypomagnesemia, hypokalemia, hypocalcemia
        
        Hypothermia
        
        Medication effects
        
        Elevated ICP
        
        Congenital
        
        AVOID procainamide or amiodarone! (QT prolonging effects)
        
        AVOID beta blockers (slowing rate, increases QT)

Take-home Points:

3 type of ventricular tachycardia with different causes and different treatments!
- Monomorphic VT
  - only rarely associated with ACS
  - if sustained, shock > procainamide, amiodarone, lidocaine
- Generic polymorphic VT
  - Usually associated with ACS
  - Normal QTc
  - Usually unstable, shock
- Torsades de pointes polymorphic VT
  - Defined by prolonged QTc
  - If persistent, shock, magnesium IV push
  - If intermittent, magnesium, overdrive pacing (electrically or chemically)
Always look for and treat the underlying cause, inspect the post conversion ECG carefully

Key Teaching Points

How reliable are reciprocal changes in STEMI?

Anterior STEMI – reciprocal changes seen in ~ only 70%
- ~30% or more will NOT have reciprocal changes
Inferior STEMI – nearly 100% (aVL)
- Occlusion of dominant left circumflex artery may result in absence of reciprocal changes

Reference:

Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. 6^th Edition. Amazon link.

Take-home Points:

Don’t use the computer ECG interpretation. It will fool you!
Don’t rely on reciprocal changes, especially in anterior STEMI’s

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)

Take home Points

When the ECG looks complicated, be systematic and break it down!
- Start with the intrinsic beats
- Follow a stepwise approach
- Do your differentials whenever you encounter an abnormality

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 abrupt changes in rhythm
Bradycardic rhythms (wide or narrow) are very common in cases of hyperkalemia
Atropine, pacers, and vasopressors are unreliable in treating these bradycardias. ACLS often does not work!

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 abrupt changes in rhythm
Really REALLY wide complex tachycardia (RRWCT) = strongly consider tox. or metabolic conditions (especially hyperkalemia) until proven otherwise!
- Consider empiric treatment with calcium and sodium bicarbonate, can be life-saving
- Use of typical ACLS antiarrhythmics in patients with sodium channel blockade can be deadly!
Ventricular tachycardia should have a heart rate > 120-130 bpm
Ventricular tachycardia QRS is usually < 200 ms

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 appear to predict acute MI in patients with pacemakers
ST depression in the right precordial leads? Consider posterior STEMI and get posterior leads

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
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

Causes of widening of the QRS-complex

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

Differential diagnosis for right axis deviation

Ventricular beats/ectopy
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 tall R-wave in V₁

Ventricular beats/ectopy
Incomplete/Complete RBBB
Na⁺channelopathies (e.g TCA, hyperkalemia)
Posterior MI
Right ventricular hypertrophy (RVH- e.g. COPD, Pulmonary HTN, muscular dystrophy, etc.)
Acute RV strain (PE)
Hypertrophic cardiomyopathy
Dextrocardia, situs inversus
Misplaced precordial lead

Take-home points

TCA effects on ECG

Tachycardia, typically wide-complex
Rightward shift of axis
- Large S wave in lateral leads
- Tall R in aVR producing ST segment elevation
- Tall R wave in V₁, pseudo-Brugada pattern
Prolonged QT interval

“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. Am J Cardiol 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

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^nddegree AV Block: Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
2^nddegree 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^rddegree AV Block (complete heart block)
- P-waves are regular (P-P interval is constant), QRS also occur regularly
- PR-interval is randomly changing
- No apparent communication between atrium and ventricle
Isorhythmic AV Dissociation + 3^rddegree AV Block (complete heart block)
- Atrial rate and ventricular rate are approximately the same

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^nddegree AV Block: Mobitz I (Wenckebach)
- P-waves are regular (P-P interval is constant)
- Progressive PR-interval lengthening before a non-conducted beat
2^nddegree 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^rddegree AV Block (complete heart block)
- P-waves are regular (P-P interval is constant), QRS’s also occur regularly
- PR-interval is randomly changing
- No apparent communication between atrium and ventricle
Isorhythmic AV Dissociation + 3^rddegree AV Block (complete heart block)
- Atrial rate and ventricular rate are approximately the same

Take-home points

AV Dissociation ¹ Complete heart block
Patients with complete heart block have AV dissociation, but patients with AV dissociation do not always have complete heart block

Key Teaching Points

Poor R-wave Progression Differential

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

The “7 L’s”
- Prior anteroseptal MI (LAD)
- LVH
- LAFB
- LBBB/Pacers
- Lead misplacement
- Low voltage
- Long life (older age)
- Normal variant

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

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

Take-home points

If the long QTc is specifically due to a long ST segment, think of hypocalcemia & hypothermia!

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 in patients with symptoms of cardiac ischemia
Patients are actively having symptoms and typically look sick
STE in aVR can also be associated with many different conditions, not just ACS!

STE in aVR (>1-1.5 mm) differential diagnosis

Sick ACS patients (signs and symptoms of acute cardiac ischemia)
- LMCA stenosis/occlusion
- Proximal LAD
- Triple vessel disease
Any cause of severe generalized global ischemia (Other sick non-ACS patients)
- Severe anemia (e.g. GI Bleeding)
- Type A dissection
- Massive PE
- Na⁺channel blocker toxicity (TCA, Hyperkalemia, Brugada, etc.)
- Severe hypokalemia
- Early post-arrest (within 15 mins of epinephrine or defibrillation)
Normal variants
- LVH with strain pattern (severe HTN)
- SVT’s (esp. AVRT), rapid atrial fibrillation
- LBBB, pacemakers

Take-home points

The history matters when dealing with your DDx of ST-segment elevation in aVR, because it is associated with many different conditions!
STE in aVR (>1-1.5 mm) differential diagnosis
- Sick ACS patients (signs and symptoms of acute cardiac ischemia)
  - LMCA stenosis/occlusion
  - Proximal LAD
  - Triple vessel disease
- Any cause of severe generalized global ischemia (Other sick non-ACS patients)
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Massive PE
  - Na⁺channel blocker toxicity (TCA, Hyperkalemia, Brugada, etc.)
  - Severe hypokalemia
  - Early post-arrest (within 15 mins of epinephrine or defibrillation)
- Normal variants
  - LVH with strain pattern (severe HTN)
  - SVT’s (esp. AVRT), rapid atrial fibrillation
  - LBBB, pacemakers

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

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 in patients with symptoms of cardiac ischemia
Patients are actively having symptoms and typically look sick
STE in aVR can also be associated with many different conditions, not just ACS!

STE in aVR (>1-1.5 mm) differential diagnosis

Sick ACS patients (signs and symptoms of acute cardiac ischemia)
- LMCA stenosis/occlusion
- Proximal LAD
- Triple vessel disease
Any cause of severe generalized global ischemia (Other sick non-ACS patients)
- Severe anemia (e.g. GI Bleeding)
- Type A dissection
- Massive PE
- Na⁺channel blocker toxicity (TCA, Hyperkalemia, Brugada, etc.)
- Severe hypokalemia
- Early post-arrest (within 15 mins of epinephrine or defibrillation)
Normal variants
- LVH with strain pattern (severe HTN)
- SVT’s (esp. AVRT), rapid atrial fibrillation
- LBBB, pacemakers

ECG Findings in Severe Hypokalemia

Remember that hypokalemia can mimic cardiac ischemia!
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

The history matters when dealing with your DDx of ST-segment elevation in aVR, because it is associated with many different conditions!
STE in aVR (>1-1.5 mm) differential diagnosis
- Sick ACS patients (signs and symptoms of acute cardiac ischemia)
  - LMCA stenosis/occlusion
  - Proximal LAD
  - Triple vessel disease
- Any cause of severe generalized global ischemia (Other sick non-ACS patients)
  - Severe anemia (e.g. GI Bleeding)
  - Type A dissection
  - Massive PE
  - Na⁺channel blocker toxicity (TCA, Hyperkalemia, Brugada, etc.)
  - Severe hypokalemia
  - Early post-arrest (within 15 mins of epinephrine or defibrillation)
- Normal variants
  - LVH with strain pattern (severe HTN)
  - SVT’s (esp. AVRT), rapid atrial fibrillation
  - LBBB, pacemakers
- Remember that hypokalemia can mimic cardiac ischemia!

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

Key Teaching Points

DDx of Rightward Axis Deviation

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

DDxof ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take-home points

Beware hyperkalemia!
- The most rapid killer in DKA, do an ECG
- ST-segment elevation is common in V1-V2, aVR
- Often has a rightward axis (rare in STEMI)
- Can produce a Brugada pattern

Key Teaching Points

DDx of Short QTc Interval

Hypercalcemia
Digoxin
Congenital short QT syndrome

DDxof ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

Take-home points

Hypercalcemia shortens the QTc (via shortening the ST-segment)
- QRS complex fuses with the T-wave, and can look like a STEMI
DDx of short QTc: hypercalcemia, digoxin, congenital short QT syndrome
Don’t forget that there is a long differential for causes of ST-segment elevation, not just STEMI!

Key Teaching Points

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

DDx of tall R-wave in V₁

Ventricular beats/ectopy
Right ventricular hypertrophy
Acute RV strain (PE)
Incomplete/Complete RBBB
Na⁺ channelopathies (e.g TCA, hyperkalemia)
Posterior MI
WPW
Hypertrophic cardiomyopathy
Dextrocardia, situs inversus
Misplaced precordial lead

Take-home points Dextrocardia ECG

Right axis deviation with inverted P waves
Tall R wave in V₁
Loss of (or very small) R-waves across the precordium
Repeat the ECG with precordial and limb leads reversed for more accurate interpretation

Key Teaching Points

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

Blocked Premature Atrial Complexes
- P waves are irregularin 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 pause before the next normal sinus beat
2^nddegree 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
2^nddegree 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^nddegree 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^nddegree 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 ³3:1)
  - In contrast to 3^rddegree (complete) heart block, some P waves continue to be conducted to the ventricle
- 3^rddegree AV Block (Complete Heart Block) + AV dissociation
  - P-P intervals and QRS complex intervals are regular but occur independent of each other
  - No apparent communication between atrium and ventricle
  - PR-interval is randomly changing
- 3^rddegree 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 (P: QRS > 1)…

Look at the PR interval to decide if it is…
- Mobitz I = PR lengthens before a lonely P-wave
- Mobitz II = PR constant with lonely P-waves
- Complete heart block (AVD) = PR randomly changes

Key Teaching Points

Wolff-Parkinson-White Syndrome

Ventricular pre-excitation syndrome
Affects 0.1 – 0.3% of population
Classic ECG triad: Short PR, delta waves, wide QRS complex
Delta waves may be very subtle or absent in some leads
Short PR interval is your major clue…always check intervals!
Pseudo-infarction patterns are common with WPW
- Pseudo-inferior MI
- Pseudo-posterior MI
Can produce SVT or atrial fibrillation
Can’t miss cause of…
- Syncope
- Aborted sudden cardiac arrest
- “New-onset seizure”
- Palpitations

Take-home points

Don’t hesitate to get ECGs on young patients!
If there is an ECG abnormality you want followed up, send the ECG with the patient!
WPW canbe intermittent
WPW can be subtle!
Always scrutinize the entireECG

Key Teaching Points

Wolff-Parkinson-White Syndrome

Ventricular pre-excitation syndrome
Affects 0.1 – 0.3% of population
Classic ECG triad: Short PR, delta waves, wide QRS complex
Delta waves may be very subtle or absent in some leads
Short PR interval is your major clue…always check intervals!
Pseudo-infarction patterns are common with WPW
- Pseudo-inferior MI
- Pseudo-posterior MI
Can produce SVT or atrial fibrillation
Can’t miss cause of…
- Syncope
- Aborted sudden cardiac arrest
- “New-onset seizure”
- Palpitations
Can be intermittent!

Take-home points

Don’t hesitate to get ECGs on young patients!
If there is an ECG abnormality you want followed up, send the ECG with the patient!
WPW canbe intermittent
WPW can be subtle!
Always scrutinize the entireECG
WPW with SVT
- Narrow (orthodromic) – Looks like SVT, treat it like usual SVT
- Wide (antidromic) – Looks like ventricular tachycardia, treat it like ventricular tachycardia

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

Take Home Points:

Atrial Fibrillation with WPW

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

Key Teaching Points

Beware of computer interpreted “normal” ECG’s!

Hughes, et al. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med 2017. PMID: 27519772

Do physicians need to review triage ECGs that are interpreted by the computer as “normal”?
- 855 ECGs reviewed, of those 222 were read as “normal ECG”
- ECGs were over-read by cardiologists and emergency physicians
- How often did the over-read of the “normal ECG” alter triage care?
  - In only 1/222 cases was triage care altered (patient brought back immediately for care)
    - Had STE in aVR, STD in II, TWI in III
  - “Normal ECG” had a 99% NPV for clinical significance (95% CI 97-99%)
- Author conclusion: “ECGs identified at triage by the computer as “normal” are unlikely to have clinical significance that will change triage care. Eliminating physician review of the triage ECGs with a computer interpretation of normal may be a safe way to improve patient care by decreasing physician interruptions.”
  - However, this study is under powered to make this conclusion!
    - Only 222 “normal ECGs”
    - If you see 11 normal ECGs/shift, you will see 220 normal ECGs after 20 shifts
    - Is it okay for you to miss 1 clinically significant ECG case every 20 shifts?

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:

Don’t trust the computer interpretation, even when it is “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
T wave inversion in aVL in a symptomatic patient can be an early predictor of inferior 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

Syncope ECG’s

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)

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)
Juvenile T-wave 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

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)
Juvenile T-wave pattern

Persistent juvenile T-wave pattern

Edward Chung, MD
- A normal variant pattern
- T wave abnormalities in leads V₁-V₃(up to V₄-V₆in some cases)
  - T wave inversions or biphasic T-waves
  - Not symmetric or deep
  - < 3 mm deep
- Healthy children and young adults
- Women > > men
- Usually women < 40-45 years old
- DDx: ischemia, PE, ARVD

Take home Points

Persistent juvenile T-wave pattern

A normal variant pattern
T wave abnormalities in leads V₁-V₃(up to V₄-V₆in some cases)
- T wave inversions or biphasic T-waves
- Not symmetric or deep
- < 3 mm deep
Healthy children and young adults
Women > > men
Usually women < 40-45 years old
DDx: ischemia, PE, ARVD

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

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

Blocked Premature Atrial Complexes
- P waves are irregularin 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 pause before the next normal sinus beat
- Commonly misdiagnosed as Mobitz II
2^nddegree 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
2^nddegree 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^nddegree 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^nddegree 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 ³3:1)
  - In contrast to 3^rddegree (complete) heart block, some P waves continue to be conducted to the ventricle
- 3^rddegree AV Block (Complete Heart Block) + AV dissociation
  - P-P intervals and QRS complex intervals are regular but occur independent of each other
  - No apparent communication between atrium and ventricle
  - PR-interval is randomly changing
- 3^rddegree AV Block (Complete Heart Block) + Isorhythmic AV dissociation
  - CHB where atrial rate and ventricular rate are approximately the same

Take-home points

When things look complicated, break down the ECG into parts, then interpret
Whenever you see pauses, look for premature complexes
Before you ever diagnose Mobitz, make sure the P-P intervals are constant
If the lonely P comes early, it’s most likely a blocked PAC

Key Teaching Points

Normal Right Bundle Branch Block (RBBB)

Leads V₁-V₃can have mild discordant 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:

In a typical RBBB, leads V₁-V₃can have mild discordant ST-segment depression, which is a normal finding
RBBB should have no ST-segment elevation
Beware STEMI’s in RBBB…often missed by the computer and the clinician
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

ECG findings in Hypothermia

Bradycardia
- Sinus bradycardia, junctional rhythms, slow atrial fibrillation
J-waves (Osborn waves)
- Positive deflections at the J-point
- Can cause pseudo ST-segment elevation appearance
Prolongation of all intervals
Tremor artifact from shivering
Ventricular arrhythmias
Asystole
Patients don’t always present classically!
Onset of ECG findings can vary, but resolve with warming

Take-home Points

Don’t skip the basics, even when the diagnosis seems obvious
Bradycardias that don’t respond reliably to ACLS
- Massive MI
- Tox (BB, CCB, etc…)
- Hyperkalemia
- Hypothermia

Key Teaching Points

Take-home Points

ECG computers tend to be particularly poor at detecting early signs of ischemia
2 types of hyperacute T waves to look for:
- Look for straightening of the initial part of the T-wave (doesn’t have to be tall)
- Look for disproportionately large T-waves in comparison to the QRS complexes
Don’t expect the computer to diagnose these
When in doubt or when symptoms are changing, get serial ECGs!

Key Teaching Points

Hyperkalemic Periodic Paralysis a.k.a Impressive Syndrome

Affects humans (1 in 200K) and horses (1 in 50 quarter horses)
- Can be traced to a single ancestor, a stallion named “Impressive”
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

Why should you get an early ECG in patients presenting with neurological complaints?
- Electrolytes
- Cardiac ischemia
- Dysrhythmias and markers of dysrhythmias (e.g. long QT, WPW, etc.)

Key Teaching Points

Poor R-wave Progression (PRWP) Differential

Defined as a R-wave < 3 mm by lead V3
8 L’s of PRWP

- Left bundle branch block
- Left ventricular hypertrophy
- Left anterior fascicular block
- Low voltage
- LAD (Prior anteroseptal MI)
- Long life (elderly)
- Lungs (COPD)
- Lead misplacement

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)

Pericardial effusion

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

Take home Points

Always consider pericardial effusions in patients with low voltage and tachycardia
- Especially if new low voltage
- Electrical alternans is “classic” …so don’t rely on it! (Seen in <1/3 of cases)
Avoid anticoagulants/lytics until pericardial effusion is ruled out
Large pericardial effusions often are misdiagnosed as ACS

Key Teaching Points

Early Repolarization vs. STEMI

Both can have concave ST segment morphology
Convex and horizontal ST segment morphology is seen in STEMI and not early repolarization
- J (junction) point = is present in all ECGs and occurs at the junction of the QRS complex to the ST segment
- The J point marks the end of the QRS complex and is often situated above the baseline, particularly in healthy young males
Terminal QRS distortion is defined as the absence of both an S wave and J wave in either lead V₂ or V₃
- S wave = any deflection at the end of the R wave that dipped below the level of the PQ junction
- J wave = any positive deflection (notching or slurring) above the level of the ST segment at the J point.
  - Distinct from the J point and classically seen in early repolarization and hypothermia.
- Terminal QRS distortion is highly specific to STEMI (left anterior descending artery occlusion.
- Absence of terminal QRS distortion does not rule out STEMI or early repolarization.
- Early repolarization has consistent characteristics in lead V₂ and V₃that allow it to be distinguished from terminal QRS distortion.
  - When J waves are present in early repolarization, S waves are significantly diminished and often absent in the same lead
  - Conversely, the absence of J waves in early repolarization correlated with high S wave amplitudes within the same lead

Take-home Points:

When debating between STEMI vs. early repolarization, look for terminal QRS distortion
In order to diagnose benign early repolarization, you must have either an S-wave or J-wave in both V₂ and V₃
Absence of either an S-wave or J-wave in either V₂ or V₃ is called “terminal QRS distortion”
Terminal QRS distortion is highly specific to STEMI
If V₂ has neither an S-wave nor a J-wave, it cannot be early repolarization
If V₃ has neither an S-wave nor a J-wave, it cannot be early repolarization
Absence of terminal QRS distortion can be either STEMI or early repolarization
Other helpful features seen with early repolarization:
- No reciprocal ST depression (aside from V₁ & aVR)
- ST elevation should always be concave upwards
- ST elevation in lead II should be greater than the degree of ST elevation in lead III
- Height of ST:T in V₆should be < 0.25
- Serial ECGs should not show evolving changes

Reference:

Lee DH, Walsh B, Smith SW. Terminal QRS distortion is present in anterior myocardial infarction but absent in early repolarization. Am J Emerg Med 2016;34(11):2182–5. PMID: 27658331

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
Bizarre 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:

Think of hyperkalemia in cases of strange or bizarre bradycardia or tachycardia!
- Hyperkalemia can produce abrupt changes in rhythm
- Bradycardic rhythms (wide or narrow) are common in cases of hyperkalemia
- Atropine, pacers, and vasopressors are unreliable in treating these bradycardias & ACLS often does not work!
- Hyperkalemia may also cause really wide complex tachycardias (RRWCT, QRS > 200 ms)
- Consider empiric treatment with calcium and sodium bicarbonate
STE in aVR is associated with many different conditions, not just ACS!
- ST segment elevation in aVR is common in atrial tachydysrhythmias
- STE seen in aVR in the setting of an atrial tachydysrhythmias is not concerning for ACS in isolation, unless it persists after cardioversion/rate control or is associated with other symptoms concerning for ACS
Sinus arrest ® sinoatrial node transiently ceases to generate electrical impulses and P waves disappear
- Be prepared to pace as these patients will go on to need transvenous or permanent pacemakers
Junctional rhythms commonly have retrograde P waves
- Ventricular rate < 40 – junctional bradycardia
- Ventricular rate 40-60 – junctional escape rhythm
- Ventricular rate > 60-100 – accelerated junctional rhythm
- Ventricular rate > 100 – junctional tachycardia (rare)
- Ventricular rate > 120 – AVNRT (most commonly) vs. junctional tachycardia (difficult to differentiate)
Regular wide complex tachycardia ® assume ventricular tachycardia (VT)!
- Ventricular rate > 200 does not rule out VT
- VT can occur in young patients
- VT can occur in patients without known structural heart disease
- VT can present with a stable blood pressure
- VT can convert with adenosine in some patients, this does not rule in SVT or rule out VT

Key Teaching Points

Take-home Points:

Reciprocal changes can precede ST segment elevation in MI
New T-wave inversions in lead aVL can be the first sign of an inferior STEMI
Always compare with old ECGs and correlate with the clinical presentation
Get serial ECGs in patients with concerning symptoms and a “non-diagnostic” initial ECG
Repeat ECGs when symptoms change significantly

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)

Pericardial effusion

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

Take home Points

Always consider pericardial effusions in patients with low voltage and tachycardia
- Especially if new low voltage
- Electrical alternans is “classic” …so don’t rely on it! (Seen in <1/3 of cases)
Avoid anticoagulants/lytics until pericardial effusion is ruled out
Large pericardial effusions often are misdiagnosed as ACS and PE

Key Teaching Points

ECG findings in patients on digoxin

“Digoxin effect”
- Downsloping ST-segment depression with a characteristic sagging appearance (a.k.a Salvador Dali moustache appearance)
- The presence of digoxin effect 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

Clues to digoxin toxicity
- Slow “regularized” atrial fibrillation
- Atrial flutter/atrial tachycardia with slow ventricular response
- Bidirectional VT
If a patient has ECG evidence of hyperkalemia and possibly digoxin toxicity, it appears to be safe to give calcium
- 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

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion in setting of LBBB/paced rhythms
The original criteria are reviewed below:

Concordant ST elevation ≥ 1 mm (in any lead) = Most specific for MI in LBBB
Concordant ST depression ≥ 1 mm in V₁, V₂, or V₃ = Specific for MI
Discordant ST elevation ≥ 5 mm = Less specific for MI in LBBB (most specific in pacers)

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

Be wary of relying on troponins, especially the first one!
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”

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
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
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

Poor R-wave Progression (PRWP) Differential
- Defined as a R-wave < 3 mm by lead V3
- 8 L’s of PRWP
- - Left bundle branch block
  - Left ventricular hypertrophy
  - Left anterior fascicular block
  - Low voltage
  - LAD (Prior anteroseptal MI)
  - Long life (elderly)
  - Lungs (COPD)
  - Lead misplacement
Take-home Points
- ECG computers tend to be particularly poor at detecting early signs of ischemia
- 2 types of hyperacute T waves to look for:
  - Look for straightening of the initial part of the T-wave (doesn’t have to be tall)
  - Look for disproportionately large T-waves in comparison to the QRS complexes
- Don’t expect the computer to diagnose these
- When in doubt or when symptoms are changing, get serial ECGs!

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 (Greatest concern when QTc > 500ms)

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

Causes of prolonged QT-interval summary

Prolonged QT due to abnormal/prolonged T –waves

Hypokalemia
Hypomagnesemia
Medications
Misc: Elevated ICP, Cardiac ischemia, Congenital

Prolonged QT due to prolonged ST-segment

Hypocalcemia
Hypothermia

Take-home points:

- Don’t trust the computer!
- When you have a 12-lead ECG…look in all 12 leads!

Key Teaching Points

Wolff-Parkinson-White Syndrome

Ventricular pre-excitation syndrome
Classic ECG triad: Short PR, delta waves, wide QRS complex
Delta waves may be very subtle or absent in some leads
Short PR interval is your major clue…always check intervals and look in all 12 leads!
Can be subtle and intermittent!

Take-home points:

WPW can be intermittent
Don’t trust the computer!
When you have a 12-lead ECG…look in all 12 leads!

Key Teaching Points

Causes of Rightward Axis Deviation

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

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

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

Causes of ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

ECG findings in PE associated with hemodynamic instability and increased morbidity and mortality

Note that these are not necessarily specific for PE
- TWIs in right precordial leads
- ST-segment elevation and depression
  - Especially STE in aVR, V₁-V₂, III
- Tachycardia (sinus, afib/flutter)
- Signs of right heart strain (rightward axis, tall R wave in V₁)

Final take-home points:

ECG findings for PE
- Sinus tachycardia
- Atrial/ventricular dysrhythmias
- Signs of right heart strain
  - Tall R wave in V₁
  - Rightward axis
  - TWIs (esp. anteroseptal +/- inferior leads)
  - ST changes, including STE in rightward leads
    - V₁, V₂, aVR, III
  - Large PE’s 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!

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

Causes of ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g. Epi, dissection, massive GI bleeding, etc.)
Vasospasm
Early Repolarization
Myo/pericarditis
Ventricular aneurysm
LVH/high left ventricular voltage
LBBB/pacemaker
Pulmonary embolism
Hyperkalemia
Na⁺channelopathy (e.g. Brugada syndrome & mimics, TCA’s, etc.)
Hypothermia
Post-cardioversion (stunning)
Takotsubo cardiomyopathy
Intracranial abnormalities
“Spiked Helmet” sign
Hypercalcemia

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
Bizarre 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

Causes of Rightward Axis Deviation

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

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

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

Final take-home points:

Beware hyperkalemia!!
- Peaked T’s
- Widening of QRS
- Prolonged PR
- Flattening and eventual loss of P’s
- Tachycardias
- Bradycardias, AV blocks and sinus pauses
- Pseudo-ACS, new BBB’s, ST changes
- Sine wave
STE common in V1-V2, and aVR in hyperkalemia
Large PE’s 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!

Key Teaching Points

Sgarbossa Criteria

Sgarbossa criteria can be used to help diagnose acute coronary occlusion in setting of LBBB/paced rhythms
The original criteria are reviewed 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 (most specific in pacers)

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/paced rhythms do not obviate the ability to diagnose acute coronary occlusion
- (Small) Studies indicate that Sgarbossa criteria can/should be used for pacers

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
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

ECG’s with lots of ectopy

Don’t get distracted, try to find the intrinsic beats first!
Be methodical and thorough in interpreting the ECG
Consider beta-blockers in patients with symptomatic PVC’s

Take home Points

If the patient is stable, interpret the ECG before jumping to treatment
Be thorough in interpreting the ECG
- If there are different morphologies on the ECG, look at all the morphologies!
- When there is a lot of ectopy, look for and interpret the intrinsic beats first

Links to referenced previous episodes:

ECGWeekly Case of the Week – October 7, 2019 – Pseudo-hypocalcemia

ECGWeekly Case of the Week – October 14, 2019 – Intermittent WPW

ECGWeekly Case of the Week – December 17, 2018 – Runs of NSVT

Key Teaching Points

Differential diagnosis for diffuse ST segment elevation

Large Acute MI

± reciprocal ST-segment depression with active symptoms
Evolving changes (especially with tx)

Acute Pericarditis

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

Vasospasm

No reciprocal ST-segment depression
May evolve with treatment

Ventricular aneurysm

No reciprocal ST-segment depression
+ Q-waves from previous MI

Early repolarization

No reciprocal ST-segment depression
No PR-segment depression
Fishhooks, J-waves

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)
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 (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!

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
- “Checkmark” sign and Spodick sign can be used AFTER the above
- PR depression and Spodick sign (T-P downsloping) are not specific to pericarditis

References:

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

The Brugada Syndrome

Genetic condition associated with arrhythmia (polymorphic VT) and sudden cardiac death that was originally described in adolescent males in southeast Asia
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
- Primarily an electrical problem (sodium channelopathy)
- 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)
- 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
- Positive family history in 20-30%
More common than you may realize!
- 4% of ALL sudden deaths
- 20% of sudden death in patients with structurally normal hearts
- A leading cause of death in patients < 40 years of age
- Prevalence in general population ~1/2000
- Identified in all ethnic groups, both males and females
Mortality
- Early data: ~ 10% per year if not treated with internal cardioverter-defibrillator (ICD, only effective treatment)
- New data showing VF episodes and mortality rates are probably lower, mainly with Type I (coved) pattern
- Isoproterenol and quinidine may decrease incidence
  - Quinidine not shown to improve outcomes and is not easily available
  - Isoproterenol may be helpful in arrhythmic storm
- Arrhythmic events happen at rest or sleep esp. 12am-6am (during increased vagal tone)
- Fever and hot ambient temperature bring out the ECG findings and PVT/VF episodes
  - Treat fevers aggressively
- Type Ia and Ic medications increase the ECG findings (questionable if increases arrhythmias)

The Brugada Pattern: ECG findings

V1 & V2
- RBBB or IRBBB pattern
- ST-segment elevation – 2 types
  - “Coved-type” (more sensitive and specific)
  - “Saddle-type”
  - Type 1 “coved-type” pattern is much more concerning, type 2 less worrisome in more recent literature
- 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 or the coved ECG finding 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), place leads V1-V2 1 interspace higher if any doubts
Remember that fever and sodium channel blockers can bring out the Brugada pattern and increase risk of PVT/VF
- Treat fevers aggressively!
Discuss/refer to electrophysiologist

References

Vohra J, Rajagopalan S, CSANZ Genetics Council Writing Group. Update on the Diagnosis and Management of Brugada Syndrome. Heart Lung Circ 2015;24(12):1141–8. PMID: 26412486.

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.

Viskin S, Hochstadt A, Rosso R. Type-I Paradox of Brugada Syndrome. Journal of the American Heart Association 2018;7(10). PMID: 29748179.

Pieroni M, Notarstefano P, Bolognese L. Brugada Syndrome in the Young and in the Adult: A Tale of 2 Diseases? J Am Coll Cardiol 2019;73(14):1766–8. PMID: 30975292.

Ueoka A, Morita H, Watanabe A, et al. Prognostic Significance of the Sodium Channel Blocker Test in Patients with Brugada Syndrome. Journal of the American Heart Association 2018;7(10). PMID: 29748178.

Papadakis M, Papatheodorou E, Mellor G, et al. The Diagnostic Yield of Brugada Syndrome After Sudden Death with Normal Autopsy. J Am Coll Cardiol 2018;71(11):1204–14. PMID: 29544603.

Delise P, Allocca G, Sitta N, et al. Cardiac arrest and Brugada syndrome: Is drug-induced type 1 ECG pattern always a marker of low risk? International Journal of Cardiology 2018; 254:142–5. PMID: 29180267.

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Reciprocal changes (e.g. aVL, V₂)
  - Especially aVL when the RCA is involved
- 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!

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 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 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
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 independent 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

Be wary of diagnosing “atrial fibrillation”
- Mobitz I is often misdiagnosed as atrial fibrillation
- True atrial fibrillation is irregularly irregular
- Before you diagnose atrial fibrillation, take another look, especially looking for clumps of hidden P-waves
Always scrutinize lead V1 for P waves
Don’t trust the computer!

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 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 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 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

Be wary of diagnosing “atrial fibrillation”
- Mobitz I is often misdiagnosed as atrial fibrillation
- True atrial fibrillation is irregularly irregular
- Before you diagnose atrial fibrillation, take another look, especially looking for clumps of hidden P-waves
Always scrutinize lead V1 for P waves
Don’t trust the computer!

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 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 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 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

Be wary of diagnosing “atrial fibrillation”
- Mobitz I is often misdiagnosed as atrial fibrillation
- True atrial fibrillation is irregularly irregular
- Before you diagnose atrial fibrillation, take another look, especially looking for clumps of hidden P-wave

Key Teaching Points

T-wave alternans

Beat-to-beat variation in the size or shape of the T-wave
- Does not involve the P or QRS complex
- Associated with prolonged QT intervals
One of the strongest predictors of malignant ventricular dysrhythmias and sudden cardiac arrest

Take-home points

Respect the T-wave! Pay attention to its shape and height. Here is a list of several different conditions where the T-wave can help you figure out the diagnosis:
- Hyperacute T-waves
- deWinter T-waves
- T-wave inversions – ischemia, reperfusion, PE, ARVC, etc.
- Wellens and “pseudo-Wellens” T-waves
- “Pokey” T-waves, “camel-hump” T-waves, deformed T-waves (buried P-waves)
- Hyperkalemia peaked T-waves
- Hypokalemia “NikEleKam” T-waves
- “Himalayan” T-waves
- Cerebral “rollercoaster” T-waves
- T-wave alternans
T-wave alternans
- Beat-to-beat variation in the size or shape of the T-wave
- One of the strongest predictors of malignant ventricular dysrhythmias and sudden cardiac arrest!

References

Rajesekharan C, Vysakha KV, Karthik V, et al. T-wave alternans: a harbinger for malignant ventricular arrhythmias. BMJ Case Rep 2018 Jul 22. PMID: 30002155.

Key Teaching Points

Causes of Widening of the QRS-complex

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

Differential diagnosis for right axis deviation

Ventricular beats/ectopy
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 tall R-wave in V₁

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

Differential diagnosis 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

TCA effects on ECG

Tachycardia, typically wide-complex
Rightward shift of axis
- Large S wave in lateral leads
- Tall R in aVR producing ST segment elevation
- Tall R wave in V₁, pseudo-Bruygada pattern
Prolonged QT interval

Key Teaching Points

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

Plaque vulnerability based on 3 major factors
1. Fibrous cap
2. Lipid core
3. 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 on angiography despite significant coronary artery disease causing false negative angiography
● Small plaques may be more unstable and more prone to rupture, despite association with negative stress tests
● Infarct related arteries often have non-obstructing plaque, before rupture and MI
● Angiography can not distinguish stable vs. unstable plaque composition, and gives no information about the fibrous cap or lipid core
● Angiography can not identify “coronary artery remodeling”, which is a new concept in atherogenesis and identified on intravascular ultrasound studies and autopsy
● Angiography can not reliably identify recent plaque rupture (e.g. classic unstable angina, with plaque rupture without complete occlusion)

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

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

Funabashi N, Asano M, Komuro I. Non-calcified plaques of coronary arteries with obvious outward remodeling demonstrated by multislice computed tomography. International Journal of Cardiology 2006;109(2):264. PMID: 16644390

Walker J, Galuska M, Vega D. Coronary disease in emergency department chest pain patients with recent negative stress testing. West J Emerg Med 2010;11(4):384–8. PMID: 21079714

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.
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:

1. 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

2. 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

3. 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

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:

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
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. CJEM. 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

Key Teaching Points

Take-home points:

Get serial ECG’s in suspected ACS!

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

Subtle early signs of ischemia

Reciprocal changes (e.g. aVL, V₂)
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!

Key Teaching Points

Take-home points:

Wellens’ Syndrome:

Pattern of T-wave abnormality in mid precordial leads (V₂-V₃, +/-V₄)
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
When in doubt get serial ECG’s, some will evolve into STEMI!

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 or Caribbean descent
    - Less common in Caucasians
  - High Voltage QRS complexes
  - Biphasic T-waves, often with notch

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

Key Teaching Points

Take-home points:

Young people DO get acute coronary syndromes!
In patients with symptoms of ACS, a new T wave inversion in aVL can be an early sign of an impending inferior MI
Get serial ECG’s in suspected ACS!
- Guidelines recommend every 15-30 mins
- Repeat with persistent ischemic signs and symptoms
- STEMI doesn’t always “show itself” on the first ECG, ~15-20% of cases require a subsequent ECG to make the diagnosis!

References:

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

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)

Take-home points:

You can’t rule out PE based on a normal HR (or normal ECG)!
Massive pulmonary embolism can mimic acute coronary syndrome and cause ST-segment elevations in rightward leads

Key Teaching Points

Take-home points:

Get a repeat ECG when signs and symptoms change!
“Shark fin STEMI” ECG pattern
- Large usual ST-segment elevation that may mimic wide QRS, ventricular tachycardia, and hyperkalemia
- Seems to be a high-risk pattern that may come and go
  - Reflects large are of transmural infarction
  - Predicts cardiogenic shock and high in hospital mortality
  - As with all STEMI’s be aggressive…early mechanical support often needed for these patients

References:

Cipriani A, D’Amico G, Brunello G, et al. The electrocardiographic “triangular QRS-ST-T waveform” pattern in patients with ST-segment elevation myocardial infarction: Incidence, pathophysiology and clinical implications. Journal of Electrocardiology 2018;51(1):8–14. PMID: 28928045

Key Teaching Points

The many 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

Left ventricular aneurysm

Causes persistent ST elevation, > 2 weeks post MI
Most often seen in anterior MI, may also be inferior
Occurs due to scar formation and paradoxical wall movement
Causes
- Post MI
- Cardiomyopathy
- Cardiac infection
- Congenital
Clinical significance
- May cause cardiomyopathy/CHF
- Arrhythmogenic, may cause sudden cardiac death
- Potential for thrombus formation, risk of thromboembolic stroke

Take-home points:

Key causes of diffuse ST-segment elevation (especially on the boards)
- STEMI/Vasospasm
  - Signs and symptoms of ACS, evolving ECG changes, reciprocal changes, ± Q waves
- Pericarditis/Myocarditis
  - No Q waves, non-STEMI ST morphology, no reciprocal changes, PR segment depression
- Early repolarization
  - No Q waves, concave ST morphology with J-waves, no reciprocal changes
- Ventricular aneurysm
  - Has Q waves, no reciprocal changes, similar to old ECG
All that is ST elevation is not MI and pericarditis
If you cannot explain ST elevation clinically, consider STAT echo in the ED to evaluate for other causes
LV aneurysm causes persistent ST elevation due to wall motion defect
LV aneurysms are clinically important high risk for arrhythmia, thrombus formation

Key Teaching Points

Differential diagnosis for narrow complex irregular tachycardia

Atrial fibrillation
- No distinct regular atrial activity
Atrial flutter with variable conduction
- Regular atrial activity (F-waves) present
Multifocal atrial tachycardia
- P-waves present, but irregular and with 3 or more different P-wave morphologies

Multifocal atrial tachycardia

Most often associated with pulmonary disease (acute or chronic), hypoxia
Contributing factors
- Theophylline
- Hypomagnesemia
- Hypokalemia
Often associated with or leads to atrial fibrillation/flutter
No dominant atrial focus
- Irregularly irregular rhythm
- At least 3 morphologically distinct P’s
Variable PP, PR, and RR intervals
Some P-waves may be non-conducted
Aberrant conduction may be present
Rate can be 90-250 bpm (usually 100-150 bpm)
Treatment
- Cardioversion doesn’t help!
- Treat the underlying respiratory problem
  - Rhythm may persist for days
- Correct electrolyte abnormalities

Take-home points:

Multifocal atrial tachycardia
- Irregularly irregular
- At least 3 distinct P-wave morphologies
- Treat the underlying cause (hypoxia)
- Don’t shock!

Key Teaching Points

ACS in Young Patients

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 (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)

Take-home points:

Young people DO get ACS, MI’s and die
We will continue to see an increase in MI’s in young patients
Focus on the presentation, not the age!
You cannot rule out ACS based on absence of cardiac risk factors
When pain is persistent, get repeat ECGs
Pay attention to subtle ST or T-wave abnormalities on initial or serial ECGs!

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

Key Teaching Points

The Brugada Syndrome

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
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
Isoproterenol and quinidine may decrease incidence

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

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

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

Poor R-wave Progression Differential

Defined as a R-wave < 3 mm by lead V3
- Prior anteroseptal MI
- LVH
- LAFB
- LBBB
- Low voltage
- Lead misplacement
- Normal variant

Take-home Points:

PRWP: R in V3 < 3mm
- DDx: 6L’s
  - LAD (prior anteroseptal MI)
  - Lead misplacement
  - LVH
  - LAFB
  - LBBB
Low Voltage

Key Teaching Points

Differential diagnosis for new right axis deviation

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

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 specifically in leads V₁-V₃

Septal and/or anterior 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
Normal finding if isolated to V₁

Take-home Points:

Pulmonary embolism will try to fool you!
- Can be associated with URI symptoms
- Can be associated with low grade fever
- Patients are not always tachycardic (HR can vary)
When debating PE vs. ACS
- Abrupt onset favors PR
- Tachypnea with clear lungs favors PE
- Absence of evolving ECG changes favors PE
- New rightward axis favors PE
- TWI’s in inferior and anteroseptal leads favors PE
- Bedside ECHO can help!
- When there is significant doubt, give ASA, start heparin and go to cath!

Key Teaching Points

Atrial septal defect

Often diagnosed and corrected in childhood
If uncorrected, usually do well in early adulthood
By age 40, many patients begin developing symptoms
- Exertional dyspnea, heart failure
- Palpitations, syncope
- Pulmonary hypertension
- Right heart failure
- Atrial fibrillation and flutter
- Stroke – paradoxical emboli
Typical ECG abnormalities
- 1^st degree AV block
- Atrial dysrhythmias
- Incomplete right bundle branch block
- Right axis deviation if pulmonary hypertension develops
- Crochetage (notching) in inferior leads (very specific)
  - Correlates with shunt severity
  - Heller, JACC 1996 – 92% specific for ASD

Take-home Points:

- Crochetage pattern – notching in inferior leads suggestive of atrial septal defect or patent foramen ovale
- Consider in young patients with dyspnea on exertion, cerebrovascular accident, or syncope
- Dx: ECHO and referral for surgical repair

Key Teaching Points

Differential diagnosis for new right axis deviation

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

Differential diagnosis for new right axis deviation + STE

Acute pulmonary hypertension (e.g PE)
Left posterior fascicular block (if acute MI)
Hyperkalemia

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

Take-home Points:

Chest pain + ST segment elevation + rightward axis = commonly PE, but…
- STEMI can produce rightward axis if
  - Left posterior fascicular block is present
  - Marked reciprocal ST segment depression is present in lead I

Key Teaching Points

Precordial T-waves

The normal ECG has a flat or inverted T-wave in lead V₁
- In other patients, an upright T-wave in V₁ (TV₁) should be considered possibly abnormal
  - Marriott: If the TV₁ large (TV₁ > TV₆), it is particularly abnormal
  - “Loss of precordial T-wave balance”
  - Suggests underlying CAD
  - Suggests acute ischemia if new (New upright T-wave in V_1,NUTV₁)
- New tall T-wave in V₁ (NTTV₁)
  - This finding may precede other expected ischemic ECG changes
  - Worry about this in patients with active symptoms
  - Get serial ECGs
  - Beware for normal variants
    - Precordial lead reversals
    - LBBB
    - LVH
    - High left ventricular voltages

Take-home Points:

Beware the upright T-wave in V₁ in patients with active symptoms
- Especially if new (NUTV₁)
- Especially if TV₁ > TV₆
  - “Loss of precordial T-wave balance” (Marriott)
- Suggests underlying CAD or acute ischemia
- Get repeat ECG’s

Key Teaching Points

Narrow Complex & Irregular Tachycardia Differential

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

The most overdiagnosed tachydysrhythmia

Be wary of diagnosing “atrial fibrillation”
- Atrial fibrillation is commonly misdiagnosed (by the computer & providers)
- 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

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

Low QRS Voltage DDx
- Conduction blockage: pericardial/pleural effusion, COPD, obesity
- Low power: Severe hypothyroidism, infiltrative disease, sever cardiomyopathy
- Low voltage + tachycardia = Think pericardial effusion!

Key Teaching Points

Schläpfer, et al. Computer-Interpreted Electrocardiograms: Benefits and Limitations. J Am Coll Cardiol 2017. PMID: 28838369

There is no internationally accepted standard for computer ECG 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.

Hughes, et al. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med 2017. PMID: 27519772

Do physicians need to review triage ECGs that are interpreted by the computer as “normal”?
- 855 ECGs reviewed, of those 222 were read as “normal ECG”
- ECGs were over-read by cardiologists and emergency physicians
- How often did the over-read of the “normal ECG” alter triage care?
- Results:
  - In only 1/222 cases was triage care altered (patient brought back immediately for care)
    - Had STE in aVR, STD in II, TWI in III
    - Discharged for stress test next day
  - “Normal ECG” had a 99% NPV for clinical significance (95% CI 97-99%)
- Conclusion:
  - ECGs identified at triage by the computer as “normal” are unlikely to have clinical significance that will change triage care
  - “Eliminating physician review of the triage ECGs with a computer interpretation of normal may be a safe way to improve patient care by decreasing physician interruptions.”
  - However, the numbers…
    - Only 222 “normal ECGs”
    - If you see 11 normal ECGs/shift, you will see 220 normal ECGs after 20 shifts
    - Is it okay for you to miss 1 clinically significant ECG case every 20 shifts???

Take-home points:

A computer interpretation of “normal ECG” 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 and hyperacute T waves suggestive of early MI). 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
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

Key Teaching Points

Post-arrest survivors

Key point: post-arrest patients benefit from urgent cath unless there is an obvious non-cardiac cause
STEMI patients post-arrest should go to the cath lab (Class IB in national guidelines, 2013)
Non-STE ACS patients that develop hemodynamic or electrical instability (e.g. VT/VF arrest should have urgent cath (Class IA, 2014)
STEMI patients post-arrest who remain comatose should go to the cath lab unless they have multiple unfavorable resuscitation features (Rab et al., 2015)
NSTE-ACS patients post-arrest who remain comatose should be assessed for unfavorable resuscitation features and urgent cath should be considered. Immediate consultation with cardiology and intensive care is recommended (Rab et al., 2015)

Journal of the American College of Cardiology, 66 (2015) 62-73. doi:10.1016/j.jacc.2015.05.009

Take-home Points:

Post-arrest STEMI should have cath lab activation, with consideration of survival benefit/risk ratio, especially if multiple unfavorable resuscitation features are present
Post-arrest non-STE ACS should strongly consider cath lab activation after assessment for unfavorable resuscitation features, consult interventional cath.
ACS can occur in the presence of a NORMAL ECG!

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.
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.
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.
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: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 2018;39(2):119–77. PMID: 28886621.
Reynolds JC, Callaway CW, Khoudary El SR, et al. Coronary angiography predicts improved outcome following cardiac arrest: propensity-adjusted analysis. Journal of Intensive Care Medicine 2009;24(3):179–86. PMID: 19321536.
Ewy GA, Kern KB. Recent advances in cardiopulmonary resuscitation: cardiocerebral resuscitation. J Am Coll Cardiol 2009;53(2):149–57. PMID: 19130982
Dumas F, Cariou A, Manzo-Silberman S, et al. Immediate percutaneous coronary intervention is associated with better survival after out-of-hospital cardiac arrest: insights from the PROCAT (Parisian Region Out of hospital Cardiac ArresT) registry. Circ Cardiovasc Interv 2010;3(3):200–7. PMID: 20484098.
Radsel P, Knafelj R, Kocjancic S, Noc M. Angiographic characteristics of coronary disease and postresuscitation electrocardiograms in patients with aborted cardiac arrest outside a hospital. Am J Cardiol 2011;108(5):634–8. PMID: 21676367.
Aurore, A., Jabre, P., Liot, P., Margenet, A., Lecarpentier, E., & Combes, X. (n.d.). Predictive factors for positive coronary angiography in out-of-hospital cardiac arrest patients. European Journal of Emergency Medicine.,18(2), 73-76. PMID: 20664351.
Larsen JM, Ravkilde J. Acute coronary angiography in patients resuscitated from out-of-hospital cardiac arrest–a systematic review and meta-analysis. Resuscitation 2012;83(12):1427–33. PMID: 22960567.
Zanuttini D, Armellini I, Nucifora G, et al. Impact of emergency coronary angiography on in-hospital outcome of unconscious survivors after out-of-hospital cardiac arrest. Am J Cardiol 2012;110(12):1723–8. PMID: 22975468.
Chelly J, Mongardon N, Dumas F, et al. Benefit of an early and systematic imaging procedure after cardiac arrest: insights from the PROCAT (Parisian Region Out of Hospital Cardiac Arrest) registry. Resuscitation 2012;83(12):1444–50. PMID: 22922264.
Hollenbeck RD, McPherson JA, Mooney MR, et al. Early cardiac catheterization is associated with improved survival in comatose survivors of cardiac arrest without STEMI. Resuscitation 2014;85(1):88–95. PMID: 23927955.
Kim MJ, Ro YS, Shin SD, et al. Association of emergent and elective percutaneous coronary intervention with neurological outcome and survival after out-of-hospital cardiac arrest in patients with and without a history of heart disease. Resuscitation 2015; 97:115–21. PMID: 26384459.
Redfors B, Råmunddal T, Angerås O, et al. Angiographic findings and survival in patients undergoing coronary angiography due to sudden cardiac arrest in western Sweden. Resuscitation 2015; 90:13–20. PMID: 25698668.
Choudry, F., Weerackody, R., Timmis, A., et al. Importance of primary percutaneous coronary intervention for reducing mortality in ST-elevation myocardial infarction complicated by out of hospital cardiac arrest. European Heart Journal., 4(4), 378-385. PMID: 25326470.
Salam I, Hassager C, Thomsen JH, et al. Editor’s Choice-Is the pre-hospital ECG after out-of-hospital cardiac arrest accurate for the diagnosis of ST-elevation myocardial infarction? Eur Heart J Acute Cardiovasc Care 2016;5(4):317–26. PMID: 25943555.
Millin MG, Comer AC, Nable JV, et al. Patients without ST elevation after return of spontaneous circulation may benefit from emergent percutaneous intervention: A systematic review and meta-analysis. Resuscitation 2016; 108:54–60. PMID: 27640933.

Key Teaching Points

Classic STEMI Criteria

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!

Cardiovascular effects of marijuana

Increased heart rate, postural hypotension, elevation in SBP and DBP
- Can increase the risk of AMI and CVA
4.8x increased risk of AMI in the first hour after smoking marijuana
3x increased risk of mortality in patients with CAD who use marijuana > 1x/week

Take-home Points

Don’t trust the computer ECG interpretation!
Pay attention to reciprocal changes
- They often precede ST-segment elevation
Marijuana appears to be associated with increased risk of early AMI, especially in patients with underlying CAD
- More research pending…stay tuned!

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
Kattoor A, Mehta JL. Expert Analysis: Marijuana and Coronary Heart Disease. J Am Coll Cardiol. Published online Sept 22, 2016. Link.
Mittleman MA, Lewis RA, Maclure M, Sherwood JB, Muller JE. Triggering myocardial infarction by marijuana. Circulation 2001;103(23):2805–9. PMID:11401936.
Mukamal, K., Maclure, M., Muller, J. et al. An exploratory prospective study of marijuana use and mortality following acute myocardial infarction. American Heart Journal : AHJ., 155(3), 465-470. PMID:18294478.

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 disproportionately 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

Take-home Points:

3 types of Ventricular Tachycardia (VT)

Monomorphic VT
- Usually associated with scar from prior MI or other anatomic pathology
- Can sometimes be associated with ACS
- Sedation and shock is the best treatment
  - Medications: procainamide >> amiodarone
  - Treat the underlying cause
Generic polymorphic VT (PVT)
- Normal QTc
- Usually associated with ACS
- Usually are unstable, proceed with shock
- Sedation and shock is the best treatment
  - Medications: amiodarone >> procainamide
  - Beta blockers after conversion are helpful
  - Treat for cardiac ischemia
Torsades de pointes (type of PVT)
- Defined by prolonged QTc
- Usually are unstable, proceed with shock
  - Medications: magnesium, isoproterenol
  - Overdrive pacing
  - Magnesium infusion after conversion
  - Look for and treat underlying cause

Key Teaching Points

Artifact

Artifact is not uncommon and can be misdiagnosed as polymorphic ventricular tachycardia (PVT), torsades, or ventricular fibrillation (VF)
- Always correlate with clinical condition
- PVT, torsades, and VF patients usually appear sick!
If patient is stable, look for evidence of regular organized activity buried within artifact!
If unstable/unconscious, check pulse and don’t delay shock

Key Teaching Points

Question 1. A 45-year-old man presents with chest pain and suddenly becomes unconscious during an ECG. What is the ECG diagnosis? If shocking the patient is not successful in converting the rhythm, what is the 2nd line therapy?

ECG Courtesy Dr. Ramon Estrella

Question 1 Answer

What is the ECG diagnosis? Inferior STEMI followed by polymorphic ventricular tachycardia
If shocking the patient does not work, what is the 2^nd line therapy? Amiodarone

Question 2. A 55-year-old woman with active chest pain has this ECG.

What is the key finding? What is the suspected diagnosis?

Question 2 Answer

What is the key finding? T-wave inversion in aVL
What is the suspected diagnosis? Early inferior STEMI

Question 3. A 65-year-old male presents with palpitations and a systolic blood pressure of 75. The following ECG is obtained.What is the best initial treatment?

Question 3 Answer

What is the best initial treatment? Multifocal atrial tachycardia, treat the underlying cause

Question 4. A 52-year-old man presents after a syncopal episode. What is the diagnosis? What are the two key diagnostic ECG findings in this condition? Indicate which one is more sensitive and which is more specific. (2 pts)

ECG Courtesy Dr. Cameron Earl

Question 4 Answer

What is the diagnosis? Arrhythmogenic right ventricular cardiomyopathy (ARVC)
What are the two key diagnostic ECG findings in this condition? Which is more sensitive, and which is more specific? Epsilon wave (specific), T wave inversions in V_1-3(sensitive)

Question 5. A 54-year-old male presents for chest pain. The following ECG was obtained during active pain. What is the key finding and what is the suspected diagnosis?

Question 5 Answer

What is the key finding and what is the suspected diagnosis? Loss of precordial T wave balance (or hyperacute T waves), suggestive of early anterior ischemia

Question 6. A 54-year-old man presents with chest pain and the ECG noted below.What is the FULL ECG diagnosis? (3 points)

Question 6 Answer

What is the full ECG diagnosis? Normal sinus rhythm with complete heart block, junctional escape rhythm, with inferior STEMI (possibly accompanied by RV/posterior MI)

Key Teaching Points

Question 7. A 39-year-old male presents after a syncopal episode. He is now asymptomatic, and this ECG was obtained. What is the diagnosis? What is the diagnostic test of choice?

ECG Courtesy Dr. Ben Smedley

Question 7 Answer

What is the diagnosis? Brugada syndrome
What is the diagnostic test of choice? Electrophysiology testing, or sodium channel blocker challenge

Question 8. A 31-year-old male presents with chest pain. He is now asymptomatic when this ECG is obtained.

What is the diagnosis? What is the demographic group in which this ECG is most typically found?

Question 8 Answer

What is the diagnosis? Benign early repolarization variant
What is the demographic group in which this ECG is most typically found? Young males of Afro-Caribbean descent

Question 9. A 46-year-old woman presents with active chest pain. The following ECG is obtained.

Question 9 Answer

What is the ECG diagnosis? Lead misplacement, leads V1 & V3 reversed

Question 10. A 35-year-old male presents with palpitations. The following ECG is obtained.

What is the diagnosis? What is the significance of the ST-segment changes? Name 5 other causes of STE in lead aVR (3 points)

Question 10 Answer

What is the ECG diagnosis? SVT
What is the significance of ST-segment abnormalities? None (if resolves after conversion)
Name 5 other causes of STE in lead aVR. LMCA/proximal LAD/triple vessel disease, thoracic aortic dissection, massive PE, severe anemia, sodium-channel blocker toxicity, hyperkalemia, hypokalemia, LBBB, severe LVH

Question 11. An 80-year-old woman presents after a syncopal episode. Her ECG is below.

What is the FULL ECG diagnosis? (3 points) Name 4 other causes of a tall R wave in lead V1 (2 points).

Question 11 Answer

What is the FULL ECG diagnosis? Normal sinus rhythm with Mobitz I conduction, RBBB, LAFB
Name 4 other causes of tall R wave in V1 (2pts) Hypertrophic cardiomyopathy, Right ventricular hypertrophy, right heart strain, WPW, hyperkalemia, Brugada, Sodium channel blocker toxicity, posterior MI, dextrocardia, misplaced leads, ventricular beats

Question 12. A 56-year-old male presents with ongoing chest pressure with diaphoresis and vomiting. The following ECG is obtained.

What is the probable diagnosis?

Question 12 Answer

What is the probable diagnosis? Posterior STEMI

Key Teaching Points

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)

Take-home Points:

Don’t trust the computer!
Narrow complex regular tachycardia DDx
- Sinus tachycardia
- SVT
- Atrial flutter with 2:1 conduction
When the ventricular rate is 150 ± 20, assume atrial flutter
The Bix rule, described by cardiologist Harold Bix, states that if a P-wave is located halfway between two QRS complexes, there is a good chance that P-waves are also buried inside the QRS complexes.

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

Poor R-wave Progression Differential

Defined as a R-wave < 3 mm by lead V3
- Prior anteroseptal MI
- LVH
- LAFB
- LBBB
- Low voltage
- Lead misplacement
- Normal variant

Take-home Points:

Respect lead aVL!
- New T wave inversion or ST-segment depression is a sign of possible early inferior MI, when in doubt get serial ECG’s
Closely look for ST-segment depression < 1mm (your ECG machine will call it “non-specific”)
- Can be ischemia or an early reciprocal change in STEMI
Straightening of the ST-segments is early ischemia until proven
- Reciprocal changes often precede ST-segment elevation
New right axis deviation with good chest pain HPI, must consider large PE
Some sick patients can have normal ECG’s

Key Teaching Points

ECG findings in Hypothermia

Onset of ECG findings can vary, but resolve with warming

Bradycardia
- Sinus bradycardia, junctional rhythms, slow atrial fibrillation
J-waves (Osborn waves)
- Positive deflections at the J-point
- Can cause pseudo ST-segment elevation appearance
Prolongation of all intervals
Tremor artifact from shivering
Ventricular fibrillation
Asystole

Ventricular Rhythms

Wide QRS complex rhythm
No P-waves or no P-QRS association (look closely at lead V1)
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 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 of an occluded coronary vessel in AMI (spontaneous or s/p thrombolytics)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, post-arrest rhythms
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Tends to be transient. Treatment is to simply observe!

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:

Hypothermia: bradycardia, prolongation of all intervals, J-waves (Osborn), slow atrial fibrillation
Always scrutinize lead V1 for P-waves!
Pay attention to the intervals
- Key to diagnosing WPW is the PR-interval
Scrutinize the ST-T morphologies
- See “checkmark sign”? Think ACS
- T-wave larger than the QRS? Think ACS
Don’t trust the computer!

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
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

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

Signs of right ventricular myocardial infarction

1/3 of inferior STEMI’s will extend to the right ventricle
It is important to distinguish RV MI clinically as it may change treatment
Clues to RV Infarction of the 12-lead ECG
- In the presence of an inferior STEMI…
  - ST depression in lead V2 with
    - ST elevation in lead V1 OR
    - Isoelectric ST segment in lead V1 & V3
  - ST elevation in III >>> II

Pearls with AV Blocks

Regularly irregular rhythms, think Mobitz vs. PACs
- If P waves are constant with a regular P-P interval = Mobitz
- If “lonely P wave” come early, with an irregular P-P interval = PAC
Complete heart block should have a regular escape rhythm
Use calipers!!!

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

Amal Mattu’s ECG Case of the Week – May 17, 2021

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