Syncope

Key Teaching Points

Really Wide Complex Tachycardia (RWCT = QRS > 200 ms)

Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause RWCT’s that mimic Ventricular Tachycardia
Look closely at V₁ and all other leads for subtle P-waves suggesting sinus tachycardia with aberrant conduction rather than a ventricular origin
Consider empiric treatment with calcium and bicarb before ACLS antiarrhythmics (amiodarone, lidocaine, procainamide) which can kill these patients!

Take home Points

Ventricular tachycardia is a regular wide complex rhythm (QRS > 120 ms, but not too wide (< 200 ms)) with heart rate > 120-130 bpm
Really wide complex tachycardias (RWCT) have QRS complexes that are > 200 ms, which should caution you to strongly consider toxicologic or metabolic conditions first! (Especially hyperkalemia & Na⁺ channel blocker toxicity)
- Na⁺ channel blockers can kill these patients! Use of typical ACLS antiarrhythmics in patients with sodium channel blockade and hyperkalemia can be deadly!
- Empiric treatment with calcium and sodium bicarbonate prior to diagnosing ventricular tachycardia in patients with RWCTs can be lifesaving
Hyperkalemia is the great imitator in electrocardiography!

Key Teaching Points

DDx of ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g., Epinephrine administration, 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

DDx of Short QTc Interval

Hypercalcemia
Digoxin
Congenital short QT syndrome

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

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)
- Can cause pseudo-ST segment elevation or depression
Prolongation of all intervals
- Long QT due to lengthening of the ST segment
Ventricular fibrillation
Asystole

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 generally ~ (220 bpm – Age)
- Maximum sinus rate can sometimes exceed this in cases of thyrotoxicosis, sympathomimetic toxicity, well-conditioned athletes, etc.

Supraventricular Tachycardia (SVT)

No distinct P-waves. May be hidden or may follow the QRS complex (“retrograde atrial activity”)
Different types (AVNRT, AVRT, atrial tachycardia, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign if 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
The 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)

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

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

Key Teaching Points

Post-seizure ECG’s

Always think of the following differentials when interpreting the ECG of patients with new onset or unexplained seizures:

Direct or indirect signs of arrhythmia

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

Electrolyte abnormalities
Intracranial abnormalities, etc.

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

Key Teaching Points

Cardiac Risk Factors

HEART score risk factors
- Hypertension
- Hypercholesterolemia
- Diabetes
- Obesity (BMI > 30)
- Current tobacco smoking (or quit < 3 months ago)
- Family history of early CAD (1^st degree relative)
Additional risk factors to consider
- Chronic cocaine use
- SLE, other inflammatory disorders to lesser extent
- Chronic kidney disease
- HIV
- Chronic alcoholism (recent data)
- Female-specific risk factors (recent data)

Cardiovascular effects of marijuana

Increased heart rate, postural hypotension, elevation in SBP and DBP
- Can increase the risk of AMI and CVA
8x increased risk of AMI in the first hour after smoking marijuana (Mittleman, et al.)
3x increased risk of mortality in patients with CAD who use marijuana > 1x/week (Mukamal, et al.)
Cannabis users had 43% increased odds of myocardial injury, association stronger among patients with history of HTN (Skipina, et al.)

Take-home Points

Regular marijuana appears to be associated with increased risk of early AMI, especially in patients with underlying CAD
- Increasing literature suggests cardiovascular dangers
- More research pending…stay tuned!
Acute MI can and does occur in young patients!

References:

Skipina TM, Upadhya B, Soliman EZ. Cannabis Use and Electrocardiographic Myocardial Injury. AmJ Cardiol 2021 Jul 15;151:. PMID: 30447899.
Rezkalla S, Kloner R. Cardiovascular effects of marijuana. Trends Cardiovasc Med 2019 Oct;29(7):403-407. PMID: 30447899.
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, et al. 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:155(3), 465-470. PMID: 18294478.

Key Teaching Points

Differential Dx for Wide Complex Tachycardia

Regular rhythm
- Monomorphic Ventricular Tachycardia (VT)
  - Most common form of sustained VT
  - HR usually > 120-130 bpm
  - Wide QRS complexes (>120 ms), that should not be too wide (< 200 ms) in the absence of concurrent toxicologic or metabolic derangement
  - QRS complexes have same general appearance in monomorphic VT, as opposed to polymorphic VT (PMVT) where there is constant beat to beat variation in QRS morphology
  - Rhythm typically regular or almost regular, if obviously irregular consider atrial fibrillation with aberrant conduction & PMVT
  - May self-terminate, termed “sustained” if lasts > 30s
  - The sinus node continues to initiate atrial contraction independent of ventricular activity (AV dissociation) and may produce a capture beat or fusion beats. However, P waves may be difficult to detect or distinguish from artifact
- SVT with aberrant conduction (BBB, WPW)
  - No clear P-waves, mimics VT
  - If previous ECGs show known BBB in sinus rhythm identical with that during the tachycardia, may be SVT
  - Safest to consider WCTs of uncertain origin as VT unless good evidence suggests a supraventricular origin, as the ECG cannot reliably distinguish them
- Accelerated Idioventricular Rhythm (AIVR)
  - Ventricular rhythm with rate of 100-120 bpm, may mimic VT
  - Transient and suggestive of reperfusion, avoid antiarrhythmics
- Sinus tachycardia with Hyperkalemia
  - Look carefully for P-QRS complexes and peaked T waves
  - As hyperkalemia worsens, PR-interval prolongation and loss of P-waves may occur (sino-ventricular rhythm), mimicking VT
  - Really wide QRS complexes (> 200 ms) may be present, always consider hyperkalemia when the QRS complexes appear wider than typical VT
- Sinus tachycardia with Na⁺ channel blocker toxicity
  - Look carefully for P-QRS complexes, right axis deviation, and a terminal R wave in aVR
  - Severe toxicity may result in really wide QRS complexes (> 200 ms), always consider hyperkalemia & Na⁺channel blocker toxicity when the QRS seems too wide
- Irregular rhythm
  - Polymorphic Ventricular Tachycardia
    - Very rapid heart rate
    - QRS complexes that vary in amplitude, axis, and duration
    - Cardiac axis rotates over 5-20 beats from one direction to another
    - Termed “Torsades de pointes” when associated with a prolonged QT interval in sinus rhythm
  - Atrial fibrillation with WPW
    - Irregularly irregular with very rapid heart rates up to 250-300 in some portions
    - Wide QRS complexes have marked variation in shape and morphology
    - Avoid all AV nodal blocking medications
  - Atrial fibrillation with aberrant conduction (BBB)
    - Always consider WPW when rate is very rapid
    - AV node protects the ventricles from very rapid atrial activity in patients without an accessory pathway
  - Hyperkalemia
    - Look carefully for P-QRS complexes and peaked T waves
    - As hyperkalemia worsens, PR-interval prolongation and loss of P-waves may occur (sino-ventricular rhythm), mimicking VT
    - Really wide QRS complexes (> 200 ms) may be present, always consider hyperkalemia when the QRS complexes appear wider than typical VT
  - Na⁺ channel blocker toxicity
    - Look carefully for P-QRS complexes, right axis deviation, and a terminal R wave in aVR
    - Severe toxicity may result in a really wide QRS complexes (> 200 ms), always consider hyperkalemia & Na⁺channel blocker toxicity when the QRS seems too wide

Take-home Points

Toxicological and metabolic disturbances like hyperkalemia and Na⁺ channel blocker toxicities can cause regular and irregular wide complex tachycardias that mimic ventricular tachycardia
Lidocaine, amiodarone, and procainamide all have Na⁺ channel blocking properties that can worsen toxicities
Consider empiric treatment with calcium and bicarb before ACLS antiarrhythmics which can kill these patients!
Always consider sodium channel blocker toxicity when the diagnosis is unclear, and don’t forget about empiric treatment with bicarb!!!

Key Teaching Points

ECG Potpourri Case Pearls

Case 1

Wellens’ syndrome is the result of critical stenosis of the LAD manifesting in the characteristic ECG patterns (Wellens’ 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
See prior episodes for more examples: May 17, 2021 & Feb 5, 2018

Case 2

ECG findings in Pulmonary Embolism

Sinus Tachycardia (only seen in ~30% of patients with PE)
Atrial and ventricular dysrhythmias
Signs of right heart strain
- Rightward axis (look for large S wave in lead I)
- New RBBB or incomplete RBBB
- New T-wave inversions (especially in anteroseptal +/- inferior leads)
- ST-segment elevations or depressions
  - ST-elevation in rightward leads (V₁, V₂, aVR, III)

Case 3 & 4

Co, et al. J Emerg Med 2017 (PMID: 27742402) – identified the most common ECG changes in patients with known PE when comparing their ECGs with previous ECGs

T wave inversion ~ 34%
T wave flattening ~ 30%
Sinus tachycardia ~ 27%
Rightward axis ~ 11%
ST segment changes ~ 9%
S1Q3T3 ~ 4%

Case 5

Electrical alternans is a broad term that describes beat to beat variation in amplitude or axis of QRS complexes. It is an ECG sign suggestive of tamponade or large pericardial effusion but can be seen in other conditions such as SVT with an accessory pathway. Electrical alternans is distinct from the more gradual variation in QRS amplitude demonstrated in this case, which is due to respiratory variation in a tachypneic patient as the heart position and proximity to the ECG leads changes with inspiration and exhalation.

Case 6 & 7

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 (Tachy-, Brady-, AV-blocks)
WPW/Pre-excitation syndromes (may be intermittent!)
Long & Short QT syndromes
Hypertrophic cardiomyopathy
Brugada syndrome
Arrhythmogenic RV dysplasia
Atrial septal defect

Case 8

Sinus tachycardia has one P wave for every QRS. P waves in sinus rhythm should be upright in limb leads (I, II, III, aVF), inverted in aVR, and biphasic in V1. The rhythm in this case is atrial tachycardia with 2:1 conduction, with P waves buried in T waves.

Case 9

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)

Electrical alternans is a late finding that is only present in < 30% of patients with tamponade. Always consider pericardial effusions in patients with low voltage (especially if new) and tachycardia

Key Teaching Points

ST-segment Elevation Differential Dx

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

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

Differential diagnosis for wide QRS

Ventricular beats/ectopy
Paced beats
Bundle branch block (LBBB, RBBB, etc.)
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)

Hyperkalemic Paralysis aka 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 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
May mimic acute Guillain-Barré syndrome and other demyelinating polyneuropathic based on nerve conduction studies
Clinically, can produce ascending areflexic paresis/paralysis
Resolves rapidly (within days) of treating hyperkalemia

Take-home Points

Hyperkalemia is the great imitator!
- Can produce profound muscle weakness and depressed reflexes, mimicking spinal cord syndrome, stroke, GBS
  - Primary or secondary hyperkalemic paralysis syndromes
- Responds rapidly to potassium correction
Get the ECG early in patients with acute neurological abnormalities!

References:

Nauman M, Reiners K, Schalke B, et al. Hyperkalemia mimicking acute Guillain-Barré syndrome. J Neurol Neurosurg Psychiatry. 1994 Nov;57(11):1436-7. PMID: 7964831
Naik KR, Saroja AO, Khanpet MS. Reversible electrophysiological abnormalities in acute secondary hyperkalemic paralysis. Ann Indian Acad Neurol. 2012 Oct;15(4):339-43. PMID: 23349611
Tariq W, Ahmad A. Two cases of hyperkalemia presenting as acute demyelinating polyneuropathy: clinical and electrophysiological reversibility with in 72 hours with potassium correction.PJNS. 2016;11(2): Article 8. Link
Gard SK, Saxena S, Juneja D, et al. Hyperkalemia: A rare cause of acute flaccid quadriparesis. Indian J Crit Care Med. 2014 Jan;18(1):46-8.PMID: 24550615
D’Ercole M, Cipriani L, Picciotto, et al. Hyperkalemia-induced acute flaccid paralysis: a case report. G Ital Nefrol. 2021 Apr 14;38(2):2021-vol2.PMID: 33852225

Key Teaching Points

Differential Dx for long QT interval (greatest concern when QTc > 500ms)

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Medications (i.e., sodium channel blocking drugs)
Congenital

Causes of prolonged QT-interval summary

Prolonged QT due to abnormal/prolonged T –waves

Hypokalemia
Hypomagnesemia
Medications (i.e., sodium channel blocking drugs)
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:

Episodes of intermittent wide complex tachycardia especially when intermixed with narrow complex tachycardia, make it difficult to differentiate between intermittent runs of non-sustained VT vs. aberrant conduction
- Look closely at the morphology of the wide QRS complexes to help make the distinction (RBBB pattern in V1 is suggestive of aberrant conduction)
- Determine if the rate of the wide QRS complex rhythm is the same as the rate of the narrow QRS complex rhythm (suggests the same underlying rhythm)
- When in doubt, consider using beta blockers (when BP can tolerate it)

Key Teaching Points

The ECG in left ventricular hypertrophy (LVH)

Patients with hypertension and various other valvular disorders (i.e., aortic stenosis) may develop left ventricular hypertrophy which can cause ECG abnormalities that mimic cardiac ischemia
LVH leads to prolonged depolarization (increased R wave peak time) and delayed repolarization (ST & T wave abnormalities) in the lateral leads
There are numerous ECG voltage criteria that are specific for the diagnosis of LVH, however they are insensitive (~50%) and some patients with LVH may have relatively normal ECGs
Voltage criteria alone are not diagnostic of LVH and must be accompanied by non-voltage criteria
Gold standard diagnostic tests for LVH include echocardiography and cardiac MRI

ECG findings of LVH

LVH results in high voltage R waves in the left sided leads (I, aVL, V4-V6) and high voltage S waves in the right sided leads (III, aVR, V1-V3)
Voltage criteria
- Limb leads
  - Lead I (R wave) + lead III (S wave) > 25 mm
  - aVL (R wave) > 11 mm
  - aVF (R wave) > 20 mm
  - aVR (S wave) > 14 mm
- Precordial Leads
  - V4, V5, or V6 (R wave) > 26 mm
  - V5 or V6 (R wave) + V1 (S wave) > 35 mm
  - Highest voltage precordial R wave + highest precordial S wave > 45 mm
- Non-voltage criteria
  - R wave peak time > 50 ms in V5 or V6
  - Strain pattern: repolarization abnormalities resulting in ST segment depression & T wave inversion in left sided leads. Presence of a strain pattern will increase specificity
    - ST depression and asymmetric T wave inversions (in leads I, aVL, V4-V6 [+/- II & aVF])
    - Appropriately discordant ST segment elevation in leads V1-V3 (and often aVR)
    - QRS widening (non-specific IVCD)

LVH with strain pattern & cardiac ischemia

ST segment changes may lack sensitivity and specificity for coronary occlusion, and diagnostic uncertainty is especially exacerbated in patients with underlying LVH
Nothing has been adequately validated to help differentiate the two with certainty

If voltage criteria for LVH are not present, it is best to assume ischemia
LVH has asymmetric T wave inversions while ischemic T wave inversions tend to be symmetrical
Horizontal ST segment depression favors ischemia
Horizontal ST segment elevation (checkmark sign) favors ischemia
When in doubt, get serial ECGs and compare to old ECGs to look for evolving changes

Diagnosing STEMI in patients with LVH with strain pattern

LVH may mimic anterior coronary occlusion and is known to be a common cause of “false-positive” cath lab activations
Like the anterior ST segment elevation seen in LBBB, it is thought that ST segment elevation that exceeds 25% of the preceding QRS is excessively discordant for LVH, and this may be a useful method for identifying occlusion
Armstrong et al. proposed the following algorithm to help identify STEMI in patients with LVH:
- Of note, this study is from 2012 and has yet to be validated. It is a difficult topic to study because cases of LAD occlusion where there is also high voltage in V1-V4 are scarce, and the criteria may ultimately prove to be insensitive
- While this algorithm may be helpful in some cases, this topic certainly requires further study.
When in doubt, serial ECGs and early cardiology consultation is encouraged
The best way to learn how to diagnose anterior STEMI in patients with LVH with strain pattern is to study lots of cases until you can recognize the subtleties of both patterns

Take-home points

LVH with strain pattern often mimics anterior STEMI
There is no perfect way to determine if patients with LVH with strain pattern also have anterior coronary occlusion/STEMI or ischemia
- Symmetrical T wave inversions, horizontal morphology of ST segment deviation, and excessively discordant ST segment elevation suggest occlusion or ischemia. However, no specific criteria or algorithm is adequately validated or proven to be sufficiently reliable to date
It is important to know the ECG criteria for LVH and become comfortable with identifying strain pattern
When in doubt, get serial ECGs looking for dynamic changes in patients with symptoms concerning for ACS
Lastly…practice, practice, practice – ECG pattern recognition takes time!

Reference:

Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. Am J Cardiol. 2012;110(7):977-983. PMID: 22738872

Key Teaching Points

The ECG in left ventricular hypertrophy (LVH)

Patients with hypertension and various other valvular disorders (i.e., aortic stenosis) may develop left ventricular hypertrophy which can cause ECG abnormalities that mimic cardiac ischemia
LVH leads to prolonged depolarization (increased R wave peak time) and delayed repolarization (ST & T wave abnormalities) in the lateral leads
There are numerous ECG voltage criteria that are specific for the diagnosis of LVH, however they are insensitive (~50%) and some patients with LVH may have relatively normal ECGs
Voltage criteria alone are not diagnostic of LVH and must be accompanied by non-voltage criteria
Gold standard diagnostic tests for LVH include echocardiography and cardiac MRI

ECG findings of LVH

LVH results in high voltage R waves in the left sided leads (I, aVL, V4-V6) and high voltage S waves in the right sided leads (III, aVR, V1-V3)
Voltage criteria
- Limb leads
  - Lead I (R wave) + lead III (S wave) > 25 mm
  - aVL (R wave) > 11 mm
  - aVF (R wave) > 20 mm
  - aVR (S wave) > 14 mm
- Precordial Leads
  - V4, V5, or V6 (R wave) > 26 mm
  - V5 or V6 (R wave) + V1 (S wave) > 35 mm
  - Highest voltage precordial R wave + highest precordial S wave > 45 mm
- Non-voltage criteria
  - R wave peak time > 50 ms in V5 or V6
  - Strain pattern: repolarization abnormalities resulting in ST segment depression & T wave inversion in left sided leads. Presence of a strain pattern will increase specificity
    - ST depression and asymmetric T wave inversions (in leads I, aVL, V4-V6 [+/- II & aVF])
    - Appropriately discordant ST segment elevation in leads V1-V3 (and often aVR)
    - QRS widening (non-specific IVCD)

LVH with strain pattern & cardiac ischemia

ST segment changes may lack sensitivity and specificity for coronary occlusion, and diagnostic uncertainty is especially exacerbated in patients with underlying LVH
Nothing has been adequately validated to help differentiate the two with certainty

If voltage criteria for LVH are not present, it is best to assume ischemia
LVH has asymmetric T wave inversions while ischemic T wave inversions tend to be symmetrical
Horizontal ST segment depression favors ischemia
Horizontal ST segment elevation (checkmark sign) favors ischemia
When in doubt, get serial ECGs and compare to old ECGs to look for evolving changes

Diagnosing STEMI in patients with LVH with strain pattern

LVH may mimic anterior coronary occlusion and is known to be a common cause of “false-positive” cath lab activations
Like the anterior ST segment elevation seen in LBBB, it is thought that ST segment elevation that exceeds 25% of the preceding QRS is excessively discordant for LVH, and this may be a useful method for identifying occlusion
Armstrong et al. proposed the following algorithm to help identify STEMI in patients with LVH:
- Of note, this study is from 2012 and has yet to be validated. It is a difficult topic to study because cases of LAD occlusion where there is also high voltage in V1-V4 are scarce, and the criteria may ultimately prove to be insensitive
- While this algorithm may be helpful in some cases, this topic certainly requires further study.
When in doubt, serial ECGs and early cardiology consultation is encouraged
The best way to learn how to diagnose anterior STEMI in patients with LVH with strain pattern is to study lots of cases until you can recognize the subtleties of both patterns

Take-home points

LVH with strain pattern often mimics anterior STEMI
There is no perfect way to determine if patients with LVH with strain pattern also have anterior coronary occlusion/STEMI or ischemia
- Symmetrical T wave inversions, horizontal morphology of ST segment deviation, and excessively discordant ST segment elevation suggest occlusion or ischemia. However, no specific criteria or algorithm is adequately validated or proven to be sufficiently reliable to date
It is important to know the ECG criteria for LVH and become comfortable with identifying strain pattern
When in doubt, get serial ECGs looking for dynamic changes in patients with symptoms concerning for ACS
Lastly…practice, practice, practice – ECG pattern recognition takes time!

Reference:

Armstrong EJ, Kulkarni AR, Bhave PD, et al. Electrocardiographic criteria for ST-elevation myocardial infarction in patients with left ventricular hypertrophy. Am J Cardiol. 2012;110(7):977-983. PMID: 22738872

Key Teaching Points

Differential Dx for Regular Wide Complex Tachycardias

Monomorphic Ventricular Tachycardia (VT)
- Most common form of sustained VT
- HR usually > 120-130 bpm
- Wide QRS complexes (>120 ms), that should not be too wide (< 200 ms) in the absence of concurrent toxicologic or metabolic derangement
- QRS complexes have same general appearance in monomorphic VT, as opposed to polymorphic VT (PMVT) where there is constant beat to beat variation in QRS morphology
- Rhythm typically regular or “almost regular”, if obviously irregular consider atrial fibrillation with aberrant conduction & PMVT
- May self-terminate, termed “sustained” if lasts > 30s
- The sinus node continues to initiate atrial contraction independent of ventricular activity (AV dissociation) and may produce a capture beat or fusion beats. However, P waves may be difficult to detect or distinguish from artifact
SVT with aberrant conduction (BBB, WPW, etc.)
- No clear P-waves, mimics VT
- If previous ECGs show known BBB in sinus rhythm identical with that during the tachycardia, may be SVT
- Safest to consider WCTs of uncertain origin as VT unless good evidence suggests a supraventricular origin, as the ECG cannot reliably distinguish them
Atrial flutter with aberrant conduction (BBB, WPW, etc.)
- Look for atrial activity: “spikey or pokey” T waves or deformed T waves suggestive of buried flutter waves
- 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!
- Consider Lewis lead ECG to better assess atrial activity when not clear on standard ECG
Accelerated Idioventricular Rhythm (AIVR)
- Ventricular rhythm with rate of 100-120 bpm, may mimic VT
- Transient and suggestive of reperfusion, avoid antiarrhythmics as they may be harmful
Sinus tachycardia with aberrant conduction (BBB, WPW, etc.)
- Look carefully in all leads for P-QRS complexes
Sinus tachycardia with Hyperkalemia
- As hyperkalemia worsens, PR-interval prolongation and loss of P-waves may occur (sino-ventricular rhythm), mimicking VT
- Look carefully for P-QRS complexes and peaked T waves
- Really wide QRS complexes (> 200 ms) may be present, always consider hyperkalemia when the QRS complexes appear wider than typical VT
Sinus tachycardia with Na⁺ channel blocker toxicity
- Look carefully for P-QRS complexes, right axis deviation, and a terminal R wave in aVR
- Severe toxicity may result in really wide QRS complexes (> 200 ms), always consider hyperkalemia & Na⁺ channel blocker toxicity when the QRS seems too wide

Take-home points

Regular wide complex tachycardias
- DDx: VT, SVT or atrial flutter with aberrant conduction (including WPW), AIVR, Sinus tachycardia with aberrant conduction, hyperkalemia, sodium channel blocker toxicity
- If unstable: shock!
- If stable: VT vs SVT? Best to assume VT, but…
  - Look for atrial activity: “spikes or pokey” T waves, deformed T waves, Bix rule, or other signs of AV dissociation
  - Don’t forget about Lewis lead ECG to better assess atrial activity when not clear on standard ECG

Reference:

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

Key Teaching Points

Take-home points

Don’t trust the computer ECG interpretation!
When you have a 12-lead…look carefully in all 12 leads!
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
- Sometimes the answer is in the “quiet” or less exciting complexes

Key Teaching Points

Ashman Phenomenon

Ashman phenomenon is an intraventricular conduction abnormality caused by a change in the heart rate. Aberrantly conducted beats (usually seen in atrial fibrillation) are often mistaken for PVCs or ventricular tachycardia, causing diagnostic confusion. Ashman phenomenon is an ECG finding that is usually linked to benign conduction irregularity, but it is an important finding to be aware of to avoid misdiagnosis

First reported in 1947 by Gouaux and Ashman, they showed that the earlier in the cardiac cycle a premature atrial contraction (PAC) occurs, and the longer the preceding cycle is, the more likely that PAC conduction will deviate from the normal pathway and be conducted with aberration
Ashman phenomenon can occur in any supraventricular rhythm (most commonly atrial fibrillation, but may even occur in sinus rhythm occasionally)
Physiological aberrancy of ventricular conduction is due to a change in the QRS cycle length
- Typically follows a long-short cycle, and is especially likely to occur with a short-long-short cycle
The refractory period of the ventricle is proportional to the heart rate and the duration of the preceding R-R interval
- Shorter R-R intervals are associated with a shorter duration action potential and vice versa
- With longer R-R intervals the refractory period is longer, and if a short R-R interval follows, the beat that terminates the cycle is likely to be conducted aberrantly
Aberrant conduction results when a supraventricular impulse reaches the His-Purkinje system while one of its branches is still in the relative or absolute refractory period
- Typically conducted with a RBBB morphology (right bundle branch has a longer refractory period than the left), may have LBBB morphology as well but seen less frequently
- When the aberrancy occurs in groups, it can resemble non-sustained ventricular tachycardia
Fisch Criteria for diagnosing Ashman phenomenon:
- A relatively long cycle immediately ahead of the cycle terminated by the aberrant QRS complex
- RBBB from aberrancy with a normal orientation of the initial QRS vector: concealed propagation of aberration is possible, such that it is possible to have a series of wide QRS supraventricular beats
- Irregular coupling of aberrant QRS complexes
- Absence of a full compensatory pause, as full compensatory pauses favor a ventricular origin.
Treatment
- No treatment needed for isolated complexes
- Rate control and treatment of the underlying condition may be necessary

Take home points

Ashman phenomenon

Aberrant ventricular conduction that follows a long-short cycle in atrial fibrillation and other supraventricular arrhythmias
Often occurs in groups and may be 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 that usually responds to rate control

References:

Grigg WS, Nagalli S. Ashman phenomenon.StatPearls [Internet]. 2020 Sept 21. Full Text
Gouaux JL, Ashman R. Auricular fibrillation with aberration stimulating ventricular paroxysmal tachycardia.Am Heart J. 1947. 34:366. PMID: 20262631
Fisch C. Electrocardiography of arrhythmias: from deductive analysis to laboratory confirmation–twenty-five years of progress. J Am Coll Cardiol. 1983 Jan. 1(1):306-16. PMID: 6826940

Key Teaching Points

Wolff-Parkinson-White (WPW) Syndrome

Ventricular pre-excitation caused by the presence of a congenital accessory pathway in patients with symptomatic arrhythmias
Prevalence of the WPW pattern (ECG abnormality in asymptomatic patients) ~ 0.1-0.3% of the general population, and ~ 10-100X’s more common than WPW syndrome
Classic ECG triad: Short PR interval (< 120 ms), widened QRS interval (> 120 ms), delta wave (slurring and slow rise of the initial upstroke of the QRS)
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!
Modified conduction through the accessory pathway will cause abnormal ventricular depolarization and result in secondary ST segment and T wave abnormalities
WPW pattern can be subtle, transient, or intermittent!

WPW Syndrome with SVT

Narrow complex rhythm (orthodromic AVRT) – looks like other types of paroxysmal SVT, treat like usual SVT
Wide complex rhythm (antidromic AVRT) – looks like ventricular tachycardia, treat like ventricular tachycardia

WPW Syndrome with Atrial Fibrillation

Very rapid irregularly irregular tachycardia (rates may approach 250-300 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. 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:

RBBB: STEMI is commonly missed, beware!
- ANY ST segment elevation is abnormal
- Your ECG computer interpretation will commonly miss these

References:

Birnbaum Y, Nikus K, Atar D, Jneid H. Is RBBB the new LBBB? Are we going to repeat the same mistakes? J Electrocardiol. 2021 Mar-Apr;65:34-36.PMID: 33477070
Figueroa-Triana JF, Mora-Pabón G, Quitian-Moreno J, et al. Acute myocardial infarction with right bundle branch block at presentation: Prevalence and mortality. J Electrocardiol. 2021 May-Jun;66:38-42. PMID: 33770645
Farinha JM, Parreira L, Marinheiro R, et al. Right bundle brunch block in patients with acute myocardial infarction is associated with a higher in-hospital arrhythmic risk and mortality, and a worse prognosis after discharge. J Electrocardiol. 2021 Jan-Feb;64:3-8. PMID: 33242763

Key Teaching Points

Left Bundle Branch Block Basics

In the absence of acute ischemia, patients with LBBB patterns have ST-segment deviation opposite to the direction of the QRS (discordant ST deviation), that is proportional to the voltage of the corresponding QRS complex. This is normal, expected, and referred to as the “rule of appropriate discordance”
These expected ECG abnormalities in patients with LBBB patterns can make the identification of acute MI in patients with symptoms of acute ischemia difficult
LBBB in patients with ischemic symptoms were traditionally considered a STEMI equivalent, however evidence suggested that this was a major cause of false positive cath lab activation. Hence, LBBB is no longer considered diagnostic of acute MI in isolation (removed from 2013 AHA STEMI criteria guidelines)
However, ST-segment deviations that are concordant(in same direction) or excessively discordant to the QRS complex are abnormal and suggestive of acute MI
Patients with LBBB and acute MI are at high risk and delays in reperfusion therapy may lead to bad outcomes
Despite traditional teaching that suggests that you cannot reliably diagnose MI in patients with LBBB, acute coronary occlusion can in fact be detected using the ECG criteria described below

Sgarbossa & Modified Sgarbossa Criteria

Sgarbossa & modified Sgarbossa criteria can be used to help diagnose acute coronary occlusion with good specificity in the setting of LBBB

The original criteria presented by Sgarbossa et al. (1996) are summarized below:

A. Concordant ST elevation ≥ 1 mm (in any lead) = most specific for MI in LBBB
B. Concordant ST depression ≥ 1 mm in V₁, V₂, or V₃ = specific for MI
C. Discordant ST elevation ≥ 5 mm = less specific for MI in LBBB

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

Take home Points

Diagnosing occlusion MI in the presence of LBBB

Acute coronary occlusion CAN be detected on the ECGs of patients with left bundle branch blocks with high specificity
Look for Sgarbossa & Modified Sgarbossa criteria in patients with LBBBs whenever there is concern for acute MI
- Concordant ST segment elevation ≥ 1 mm in any lead
- Concordant ST segment depression ≥ 1 mm in V1, V2, V3
- Excessively discordant STE (STE/S wave ratio > 25%)

References:

Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing.Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802
Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576
Maloy KR, Bhat R, Davis J, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers.West J Emerg Med. 2010;11(4):354–357. PMID: 21079708
Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607
Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal.2013;166(3):409–413. PMID: 24016487
Pendell Meyers H, Limkakeng AT, Jaffa EJ, et al. Validation of the modified Sgarbossa criteria for acute coronary occlusion in the setting of left bundle branch block: A retrospective case-control study. Am Heart J. 2015;170(6):1255-1264. PMID: 26678648
Cravens MG, Ali SF, Gibbs MA, Littmann L. Real-time validation of the Sgarbossa and modified Sgarbossa criteria in intermittent left bundle branch block. J Electrocardiol. 2020 Nov-Dec;63:24-27. Epub 2020 Sep 30. PMID: 33045460
Borovac JA, Orsolic A, Miric D, Glavas D. The use of Smith-modified Sgarbossa criteria to diagnose an extensive anterior acute myocardial infarction in a patient presenting with a left bundle branch block. J Electrocardiol. 2021 Jan-Feb;64:80-84. Epub 2020 Dec 13. PMID: 33359958.
Lai YC, Chen YH, Wu KH, Chen YC. Validation of the diagnosis and triage algorithm for acute myocardial infarction in the setting of left bundle branch block. Am J Emerg Med. 2020 Dec;38(12):2614-2619. Epub 2020 Mar 19. PMID: 32245703.
Birnbaum Y, Ye Y, Smith SW, Jneid H. Rapid Diagnosis of STEMI Equivalent in Patients With Left Bundle‐Branch Block: Is It Feasible? J Am Heart Assoc. 2021;10(18):1-4. PMID: 34514811

Key Teaching Points

Last week we reviewed how to diagnose acute coronary occlusion in patients with LBBB, this week we will focus on how you can diagnose occlusion MI in patients with paced rhythms. To review last week’s video and written summary click here!

Ventricular Paced Rhythm Basics

Paced rhythms cause ST-segment & T wave changes that can make identification of acute MI more challenging than patients with native cardiac conduction
In the absence of acute ischemia, patients with both right ventricular paced rhythms and LBBB patterns have ST-segment deviation opposite to the direction of the QRS complex (discordant ST deviation) that is proportional to the voltage of the corresponding QRS complex. This is normal, expected, and referred to as the “rule of appropriate discordance”
The rule of appropriate discordance applies to both LBBB and paced rhythms, as conduction patterns are similar. One distinction is that in paced rhythms the QRS axis in leads V4-V6 points down, as opposed to up in LBBB.
ST-segment deviations that are concordant(in same direction) or excessively discordant to the QRS complex are abnormal and suggestive of acute MI
Patients with paced rhythms and acute occlusion MI are at high risk and delays in reperfusion therapy may lead to worse outcomes
Despite traditional teaching that suggests that you cannot reliably diagnose MI in patients with paced rhythms, acute coronary occlusion can in fact be detected using the ECG criteria described below

Ventricular Paced Rhythm and Acute Coronary Occlusion MI

Sgarbossa and the more recently validated Modified Sgarbossa Criteria (MSC) can be used to help diagnose acute coronary occlusion with high specificity in the setting of paced rhythms. The modified criteria have been shown to be more sensitive than the original criteria (Dodd et al., PMID: 34172301):

The MSC were found to have high sensitivity (86%) and specificity (84-96%) for diagnosing acute coronary occlusion. See publication for more details and how they used different control groups.
The 2017 ESC STEMI guidelines include original Sgarbossa criteria as an indication for emergent cath lab activation, and we hope the next US guidelines will include these validated criteria to improve the accuracy of diagnosis in this population of patients

Take home Points

Diagnosing occlusion MI in the presence ventricular paced rhythms

Acute coronary occlusion CAN be detected on the ECGs of patients with ventricular paced rhythms with high specificity
Modified Sgarbossa Criteria is more sensitive than the original Sgarbossa criteria in patients with paced rhythms whenever there is concern for acute MI
Look closely for the following in patients with paced rhythm and concern for ACS:
- Concordant ST segment elevation > 1 mm in any lead
- Concordant ST segment depression > 1 mm in any of V1-V6
- Excessively discordant STE (STE/S wave ratio > 25%) in any lead

References:

Dodd KW, Zvosec DL, Hart MA, et al. Electrocardiographic Diagnosis of Acute Coronary Occlusion Myocardial Infarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria. Ann Emerg Med. 2021 Oct;78(4):517-529. PMID: 34172301
Sgarbossa EB. Recent advances in the electrocardiographic diagnosis of myocardial infarction: left bundle branch block and pacing.Pacing Clin Electrophysiol. 1996;19(9):1370–1379. PMID: 8880802
Sgarbossa EB, Pinski SL, Gates KB, et al. Early electrocardiographic diagnosis of acute myocardial infarction in the presence of ventricular paced rhythm. GUSTO-I investigators. Am J Cardiol. 1996;77(5):423–424. PMID: 8602576
Maloy KR, Bhat R, Davis J, et al. Sgarbossa Criteria are Highly Specific for Acute Myocardial Infarction with Pacemakers.West J Emerg Med. 2010;11(4):354–357. PMID: 21079708
Smith SW, Dodd KW, Henry TD, et al. Diagnosis of ST-Elevation Myocardial Infarction in the Presence of Left Bundle Branch Block With the ST-Elevation to S-Wave Ratio in a Modified Sgarbossa Rule. Ann Emerg Med. 2012;60(6):766–776. PMID: 22939607
Cai Q, Mehta N, Sgarbossa EB, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: From falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? American Heart Journal.2013;166(3):409–413. PMID: 24016487
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

Amiodarone

Amiodarone is categorized as a class III antiarrhythmic agent that prolongs phase 3 (repolarization phase) of the cardiac action potential. However, it also has numerous other effects, including actions that are like those of antiarrhythmic classes Ia, II, and IV
Vaughan Williams Classification
1. Sodium channel blockade
  - Prolongs refractoriness, slows intracardiac conduction
2. Beta blockade
  - Slows heart rate and AV nodal conduction

Potassium channel blockade
- Prolongs refractoriness

Calcium channel blockade
- Slows heart rate and AV nodal conduction

Wolff-Parkinson-White (WPW) Syndrome

Ventricular pre-excitation caused by the presence of a congenital accessory pathway in patients with symptomatic arrhythmias
Prevalence of the WPW pattern (ECG abnormality in asymptomatic patients) ~ 0.1-0.3% of the general population, and ~ 10-100X’s more common than WPW syndrome
Classic ECG triad: Short PR interval (< 120 ms), widened QRS interval (> 120 ms), delta wave (slurring and slow rise of the initial upstroke of the QRS)
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!
Modified conduction through the accessory pathway will cause abnormal ventricular depolarization and result in secondary ST segment and T wave abnormalities
WPW pattern can be subtle, transient, or intermittent!

WPW Syndrome with SVT

Narrow complex rhythm (orthodromic AVRT) – looks like other types of paroxysmal SVT, treat like usual SVT
Wide complex rhythm (antidromic AVRT) – looks like ventricular tachycardia, treat like ventricular tachycardia

WPW Syndrome with Atrial Fibrillation

Very rapid irregularly irregular tachycardia (rates may approach 250-300 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. 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

Treating dysrhythmias in pregnancy

Adenosine is generally regarded as safe for SVT
- May induce atrial fibrillation in 1-12% of cases depending on dosage
BBs and CCBs are generally regarded as safe
- Caveat: some literature suggests avoiding atenolol
Procainamide or lidocaine can be used for ventricular tachycardia
- Avoid amiodarone in all stages of pregnancy!
Electricity is generally regarded as safe at any stage of pregnancy
Use continuous cardiotocography (CTM) for fetal monitoring when possible

Take Home Points:

Treating dysrhythmias in pregnancy

Respect dysrhythmias, including SVT
No drug, including adenosine, is 100% safe or effective
- Can occasionally convert SVT to atrial fibrillation
- Be ready to shock!
Probably safe to use standard treatments, EXCEPT stay away from amiodarone!
Electricity is generally regarded as safe
Use continuous cardiotocography (CTM) for fetal monitoring when possible

References:

Ip JE, Cheung JW, Chung JH, et al. Adenosine-induced atrial fibrillation: insights into mechanism. Circ Arrhythm Electrophysiol. 2013 Jun;6(3):e34-7. PMID: 23778252
Chakraborty P, Subramanian A. An unusual complication of adenosine administration in supraventricular tachycardia. Indian Pacing Electrophysiol J. 2018 Jan-Feb;18(1):36-38. Epub 2017 Dec 26. PMID: 29287916

Key Teaching Points

Wolff-Parkinson-White (WPW) Syndrome

Ventricular pre-excitation caused by the presence of a congenital accessory pathway in patients with symptomatic arrhythmias
Prevalence of the WPW pattern (ECG abnormality in asymptomatic patients) ~ 0.1-0.3% of the general population, and ~ 10-100X’s more common than WPW syndrome
Classic ECG triad: Short PR interval (< 120 ms), widened QRS interval (> 120 ms), delta wave (slurring and slow rise of the initial upstroke of the QRS)
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!
Modified conduction through the accessory pathway will cause abnormal ventricular depolarization and result in secondary ST segment and T wave abnormalities
WPW pattern can be subtle, transient, or intermittent!

Take Home Points:

Always scrutinize the post cardioversion ECG, looking for underlying causes
When you see some complexes that look different, look closely at them!
WPW can be intermittent
- These patients tend to be lower risk but can still produce problems that need EP follow up

Key Teaching Points

Artifact

Artifact is common and frequently 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 unstable/unconscious, check pulse and don’t delay shock
- If patient is stable, look at all 12-leads or the entire rhythm strip for evidence of regular organized activity buried within artifact!
Syncope can be caused by transient malignant dysrhythmia
Syncope (with myoclonic jerks) can also cause a pseudo-malignant dysrhythmia (artifact)

Key Teaching Points

Differential diagnosis for regular wide complex tachycardias (RWCT)

Ventricular tachycardia (VT)
- Heart rate usually > 120-130 bpm
- Wide QRS complexes (>120 ms), that should not be too wide (< 200 ms) in the absence of concurrent toxicologic or metabolic derangement
SVT with aberrant conduction (e.g., BBB, WPW)
- No clear P-waves, mimics VT
- If previous ECGs show known BBB in sinus rhythm identical with that during the tachycardia, may be SVT
- Safest to consider WCTs of uncertain origin as VT unless good evidence suggests a supraventricular origin, as the ECG cannot reliably distinguish them
Massive STEMI
- Look carefully for P-QRS complexes
- Confirm that QRS is wide in all 12 leads, narrow complexes with massive ST segment elevation suggest STEMI
- Rightward axis weighs against STEMI
Accelerated Idioventricular Rhythm (AIVR)
- Ventricular rhythm with rate of 100-120 bpm, may mimic VT
- Transient and suggestive of reperfusion, avoid antiarrhythmics
Sinus tachycardia with aberrant conduction (e.g., BBB, WPW)
- Look carefully for P-QRS complexes in all leads
- Compare to prior ECGs, looking for history of aberrant conduction
Sinus tachycardia with hyperkalemia
- Look carefully for P-QRS complexes and other ECG evidence of hyperkalemia (peaked T waves)
- As hyperkalemia worsens, PR-interval prolongation and loss of P-waves may occur (sino-ventricular rhythm), mimicking VT
- Really wide QRS complexes (> 200 ms) may be present, always consider hyperkalemia when the QRS complexes appear wider than typical VT
Sinus tachycardia with Na⁺channel blocker toxicity
- Look carefully for P-QRS complexes, right axis deviation, and a terminal R wave in aVR
- Severe toxicity may result in really wide QRS complexes (> 200 ms), always consider hyperkalemia & Na⁺channel blocker toxicity when the QRS seems too wide

Take Home Points:

Massive ST segment elevation can mimic a wide complex QRS
- Easily misdiagnosed as VT or hyperkalemia
Look closely in all 12 leads to verify if the QRS is truly wide

Key Teaching Points

Take Home Points:

Acute coronary occlusion in RBBB: beware of even mild ST segment elevation in V1-V2
Acute coronary occlusion in LBBB: know the Sgarbossa criteria!
Pay attention to the PR intervals for the diagnosis of AV blocks

Key Teaching Points

EMS Cases Week – Key Points

Case #1

Narrow complex regular tachycardia DDx

Sinus tachycardia
Supraventricular tachycardia
Atrial flutter with 2:1 conduction

Max sinus heart rate = 220 – age

Case #2

Ventricular Rhythms

Wide QRS complex rhythm with no P-waves or no P-QRS association (look closely at lead V1)
Ventricular rate 20-40: ventricular escape rhythm (idioventricular rhythm)
Ventricular rate 40-120s: Accelerated ventricular escape rhythm (accelerated idioventricular rhythm, AIVR)
Ventricular rate > 120s-130s: Ventricular tachycardia
- Caveat: VT can have slower rates if patient is on an antiarrhythmic (e.g., oral flecainide or amiodarone)
- Other mimics of VT (rate often <120)
  - Hyperkalemia
  - Sodium channel blocker toxicity

AIVR

Accelerated idioventricular rhythm (AIVR) is a relatively benign reperfusion arrhythmia
Suggests successful reperfusion (partial or complete) of an occluded coronary vessel in AMI (spontaneous or s/p thrombolytics)
Other presentations: digoxin toxicity, severe electrolyte abnormalities, cardiac ischemia
May be seen during cardiac arrest resuscitation
Unlikely to cause hemodynamic instability
Suppression can cause instability, asystole
Tends to be transient. Treatment is to simply observe!

Case #3

ECG findings of hypothermia:

Bradycardia
- Junctional rhythms
- Slow afib
J-waves
Tremor artifact
Prolonged intervals
Vfib
Asystole

Case #4

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
- Patients are very preload dependent
- Preload reducing meds cause significant hypotension (i.e., NTG), avoid them!
- When lungs are clear, use IV fluids, not vasopressors
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

Case #5

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

Key Teaching Points

Differential for non-conducted P-waves (P: QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and ectopic with a different P wave morphology from normal sinus P waves
The non-conducted P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the single non-conducted P-wave
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P: QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with good prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take-home points:

Electrocardiographic polyuria? The answer lies in the PR interval!
- Mobitz I – Progressive PR interval lengthening prior to a non-conducted P wave
- Mobitz II – Constant PR interval that remains unchanged prior to a non-conducted P wave
- CHB – PR-interval is randomly changing with no apparent communication between atrium and ventricle

Key Teaching Points

Differential for non-conducted P-waves (P:QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and an ectopic P wave is present (different morphology, with abnormal P wave axis)
The non-conducted ectopic P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the single non-conducted P wave (two consecutive non-conducted P waves rules out Mobitz I)
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P:QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with better prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take-home points:

When you see electrocardiographic polyuria (P:QRS > 1)…map out the P waves and look at the PR interval!
- Blocked PACs – P waves are irregular in rhythm, non-conducted P waves come early
- Mobitz I – P waves are regular in rhythm, progressive PR interval lengthening prior to a non-conducted P wave
- Mobitz II – P waves are regular in rhythm, constant PR interval that remains unchanged prior to a non-conducted P wave
- CHB – P waves are regular in rhythm, PR-interval is randomly changing with no apparent communication between atrium and ventricle
- The answer lies in the PR segment!

Key Teaching Points

Ventricular conduction in atrial flutter:

Atrial flutter is caused by an abnormal re-entrant rhythm typically in the right atrium that is propagated due to differences in the refractory periods of atrial tissue
Atrial flutter is a common rhythm abnormality and is frequently misdiagnosed when it results in atrial tachyarrhythmias
The atrial rate in flutter is typically around ~300 bpm and the sawtooth pattern of regular P wave activity is best seen in leads V1 & II
The impact and symptoms of atrial flutter depend on the ventricular heart rate, which is determined by AV conduction
Atrial flutter results in a regular rhythm when AV conduction is fixed (atrial flutter with 2:1 AV conduction, 3:1, 4:1, etc.). In these cases, the atrial rate is an exact multiple of the ventricular rate
Atrial flutter results in regularly or irregularly irregular rhythms when AV conduction is variable (e.g., varies from 2:1 to 3:1 to 4:1 and back)
When the atrial rate is not an exact multiple of the ventricular rate, AV dissociation and complete heart block should be considered
Ventricular escape rhythms can emanate from the left anterior/posterior fascicles, or the bundle branches themselves, not just the ventricular myocytes

Take-home points:

Atrial flutter or fibrillation with regular response: consider complete heart block when the atrial rate is not an exact multiple of the ventricular rate
Ventricular escape rhythms (20-40 bpm) may mimic junctional escape rhythms (40-60 bpm) with bundle branch blocks
- Pay attention to the ventricular rate
- Escape rhythms with ventricular rates of 20-40 bpm are likely ventricular in origin
Treatment for unstable rhythms is based on the ventricular rate!

Key Teaching Points

Take-home points:

Don’t mess with the T-waves!
- Be cautious when performing synchronized cardioversion to make sure the device is synchronized to the QRS complexes rather than T waves to avoid R on T phenomenon and development of ventricular fibrillation
“Seizures” can sometimes be due to dysrhythmias, get an ECG in every patient with new onset seizures to evaluate for a potential cardiac source of symptoms
Hyperkalemia can progress quickly
Hyperkalemia can produce brady and tachydysrhythmias

Reference:

Mattu A, Zira D, Tabas JA, Brady WJ. An Adverse Outcome With Cardioversion of a Wide-Complex Tachycardia. Ann Emerg Med. 2022 Feb;79(2):113-115. PMID: 35065739

Key Teaching Points

Hypercalcemia

Etiologies

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

ECG findings

Short QT interval (< 400 ms)
- DDx: hypercalcemia, digoxin toxicity, congenital short QT-syndrome
ST segment and T wave abnormalities

- Shortened ST segments
- ST segment elevation
- Will mimic ACS, differentiate by eliciting a good HPI and looking for short QT interval

Treatment

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

DDx of ST-segment elevation

Acute myocardial injury (ACO or trauma)
Global ischemia (e.g., Epinephrine administration, 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 (including hypercalcemia), not just STEMI!

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

Atrial flutter and atrial tachycardia:

Atrial flutter is a specific type of supraventricular tachycardia caused by an abnormal re-entrant circuit
The abnormal re-entry circuit is typically in the right atrium and propagated by differences in the refractory periods of atrial tissue
Atrial flutter is common and frequently misdiagnosed by the computer ECG interpretation
The atrial rate in flutter is typically around ~250-350 bpm, with a sawtooth pattern of regular flutter waves (F-waves) best seen in lead V1
- Flutter waves are also commonly seen in the inferior leads (II, III, aVF), however the counterclockwise flutter waves of typical flutter will result in inverted F-waves that may be difficult to identify. Flipping the ECG upside down will sometimes allow you identify the waves more accurately as they will appear upright
The atrial rate in atrial fibrillation is 400-600 bpm, with coarse or fine fibrillatory waves
The atrial rate in atrial tachycardia is > 100 bpm, with non-sinus P wave axis and morphologies that may be unifocal or multifocal in origin
The impact and symptoms of atrial flutter depend on the ventricular heart rate, which is determined by AV conduction
- Atrial flutter results in a regular rhythm when AV conduction is fixed (atrial flutter with 2:1 AV conduction, 3:1, 4:1, etc.). In these cases, the atrial rate is an exact multiple of the ventricular rate
- Atrial flutter results in regularly irregular or irregularly irregular rhythms when AV conduction is variable (e.g., varies from 2:1 to 3:1 to 4:1 and back)

Take-home points:

Be wary of atrial flutter!
Frequently missed diagnosis
- Bumps that map out with calipers? Worry about P waves/flutter. Artifact does not map out!
- Look in all leads for atrial activity, but especially lead V1!
- Ventricular rate ~ 150 bpm +/-? Look for atrial flutter!

Key Teaching Points

Atrial flutter and atrial tachycardia:

Atrial flutter is a specific type of supraventricular tachycardia caused by an abnormal re-entrant circuit
The abnormal re-entry circuit is typically in the right atrium and propagated by differences in the refractory periods of atrial tissue
Atrial flutter is common and frequently misdiagnosed by the computer ECG interpretation
The atrial rate in flutter is typically around ~250-350 bpm, with a sawtooth pattern of regular flutter waves (F-waves) best seen in lead V1
- Flutter waves are also commonly seen in the inferior leads (II, III, aVF), however the counterclockwise flutter waves of typical flutter will result in inverted F-waves that may be difficult to identify. Flipping the ECG upside down will sometimes allow you identify the waves more accurately as they will appear upright
The atrial rate in atrial fibrillation is 400-600 bpm, with coarse or fine fibrillatory waves
The atrial rate in atrial tachycardia is > 100 bpm, with non-sinus P wave axis and morphologies that may be unifocal or multifocal in origin
The impact and symptoms of atrial flutter depend on the ventricular heart rate, which is determined by AV conduction
- Atrial flutter results in a regular rhythm when AV conduction is fixed (atrial flutter with 2:1 AV conduction, 3:1, 4:1, etc.). In these cases, the atrial rate is an exact multiple of the ventricular rate
- Atrial flutter results in regularly irregular or irregularly irregular rhythms when AV conduction is variable (e.g., varies from 2:1 to 3:1 to 4:1 and back)

Take-home points:

Be wary of atrial flutter!
Frequently missed diagnosis
- Bumps that map out with calipers? You must worry about P waves/flutter. Artifact does not map out!
- Look in all leads for atrial activity, but especially lead V1!
- Ventricular rate ~ 150 bpm +/-? Look for atrial flutter!
- Flutter waves often confuse the computer and may result in misdiagnosis of ACS and mimic STEMI

Key Teaching Points

ECG Diagnosis of Ventricular Tachycardia (VT)

The ECG can NOT reliably distinguish between VT and supraventricular tachycardia with aberrant conduction (SVT-AC)
- The ECG and clinical factors are reliable at ruling in VT
- The ECG (including the published algorithms below) and clinical factors are unreliable at ruling out VT (i.e. at ruling in SVT with AC/BBB)
Algorithms created to distinguish VT vs. SVT-AC are far from perfect and difficult to use clinically. The references review the most popular ones in detail, but they all miss cases of VT.
- Best attempts at creating algorithms to distinguish SCT-AC vs. VT have failed:
  - Brugada algorithm
  - Bayesian algorithm
  - Griffith algorithm
  - Vereckei aVR algorithm
  - Lead II R-wave-peak-time algorithm (RWPT)
- Classic teaching:
  - “…assume WCT is VT until proven otherwise…”
  - “…when in doubt, assume and treat WCT as VT…”

Mattu Algorithm for Wide Complex Tachycardias (WCTs)

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

What about an Adenosine diagnostic challenge?

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

Take-home points:

The WCT rules and algorithms are far from perfect
If you see a regular wide complect tachycardia that is not clearly sinus tachycardia, just call it VT!
Young and otherwise healthy people CAN have VT!
VT can have ventricular rates > 160-180 bpm
Patients with multiple cardiac risk factors are far more likely to have VT rather than SVT-AC
Patients with CT can present hemodynamically stable
PVCs on other ECGs can be helpful and suggestive of ventricular ectopy when the morphology of the PVCs is similar when in a wide complex tachycardia

References:

McGill TD, Kashou AH, Deshmukh AJ, LoCoco S, May AM, DeSimone C V. Wide complex tachycardia differentiation: An examination of traditional and contemporary approaches. J Electrocardiol. 2020;60:203-208. PMID:32417627
Kashou AH, Noseworthy PA, DeSimone C V, Deshmukh AJ, Asirvatham SJ, May AM. Wide Complex Tachycardia Differentiation: A Reappraisal of the State-of-the-Art. J Am Heart Assoc. 2020;9(11):e016598. PMID:32427020
Jastrzebski M, Sasaki K, Kukla P, Fijorek K, Stec S, Czarnecka D. The ventricular tachycardia score: A novel approach to electrocardiographic diagnosis of ventricular tachycardia. Europace. 2016;18(4):578-584. PMID:25995387
Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med 2013;20(11):1121–30. PMID: 24238314
Jastrzebski M, Kulka P, Czarnecka D, et al. Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace 2012;14(8):1165-71. PMID:22333239
Marill KA, Wolfram S, Desouza IS, et al. Adenosine for wide-complex tachycardia: efficacy and safety. Crit Care Med 2009;37(9):2512-8. PMID:19623049

Key Teaching Points

Troponin testing in Supraventricular Tachycardia (SVT)

When studied, troponin levels were found to be measured frequently in patients with SVT (35-80% of cases)
30-35% of SVT cases are known to be associated with elevated troponin levels, typically caused by oxygen supply-demand mismatch
Troponin elevation has not been found to correlate with 30-day risk of adverse outcome or the presence of coronary artery disease
Troponin elevation is associated with significantly higher rate of hospital admissions and both invasive and non-invasive diagnostic investigations

Take-home points:

ST segment changes and troponin elevation are seen in a significant number of patients with paroxysmal supraventricular tachycardia
Routine troponin testing is associated with higher rates of hospital admission and downstream diagnostic investigations, but has not been found to correlate with presence of CAD or risk of short-term adverse outcomes
Recommendation: Make troponin testing decisions based on the clinical signs and symptoms following conversion to sinus rhythm

References:

Gabrielli M, Cucurachi R, Lamendola P, et al. Troponin testing in adult patients presenting to the emergency department for paroxysmal supraventricular tachycardia: a review. Cardiol Rev. 2022 Feb 7. Epub ahead of print. PMID: 35148534
Allen R, deSouza IS. Troponin Testing in Patients With Supraventricular Tachycardia-Are We Overtesting?: A Teachable Moment. JAMA Intern Med. 2021 Jun 1;181(6):842-843. PMID: 33779679
Foy A, Mandrola J. Updating Our Thinking on Troponin Use and Interpretation. JAMA Intern Med. 2021 Jun 1;181(6):843-844. PMID: 33779692

Key Teaching Points

Take-home points:

Emergency physicians get interrupted…a lot!
Review of ECGs are often a source of frequent interruptions
A computer interpretation of “normal” still requires you to review the ECG!
Computers tend to be particularly poor at detecting early signs of ischemia
- Early reciprocal changes in aVL
- Hyperacute T waves
When there are concerns, perform serial ECGs!

References:

Ioannides KLH, Brownstein DJ, Henreid AJ, et al. Quantifying Emergency Physician Interruptions due to Electrocardiogram Review. J Emerg Med. 2021 Apr;60(4):444-450. Epub 2021 Jan 5. PMID: 33414047
Winters LJ, Dhillon RK, Pannu GK, et al. Emergent cardiac outcomes in patients with normal electrocardiograms in the emergency department. Am J Emerg Med. 2022 Jan;51:384-387. Epub 2021 Nov 17. PMID: 34823195
Tabner A, Jones M, Fakis A, et al. Can an ECG performed during emergency department triage and interpreted as normal by computer analysis safely wait for clinician review until the time of patient assessment? A pilot study. J Electrocardiol. 2021 Sep-Oct;68:145-149. Epub 2021 Aug 19. PMID: 34450449
Hughes KE, Lewis SM, Katz L, Jones J. Safety of Computer Interpretation of Normal Triage Electrocardiograms. Acad Emerg Med. 2017 Jan;24(1):120-124. PMID: 27519772

Key Teaching Points

Take-home points:

Ectopic beats can sometimes be a distraction, but they can also sometimes give you the diagnosis! PVCs can sometimes show evidence of myocardial injury that may not be as evident in intrinsic beats.
Scrutinize the ECG and don’t rely on the computer interpretation. Be methodical & thorough in your interpretation.
“Feeling better” does not equal asymptomatic.

Key Teaching Points

Posterior Occlusion MI

Posterior MI is usually associated with inferior MI due to RCA or circumflex occlusion, but ~10% of occlusion MIs are isolated posterior MIs that can be challenging to diagnose as they do not typically manifest any ST elevation
In fact, isolated posterior STEMI is the most common type of missed STEMI!
- Often misdiagnosed as just ischemia or “NSTEMI”
- Only ~30% are revascularized within 90 mins and patients are known to have increased morbidity and mortality compared to those with isolated inferior MIs
ECG findings: Ischemic ST segment depression maximal in leads V1-V4
- ST elevation is typically not seen on the standard 12-lead ECG in isolated posterior STEMI, but rather manifests as ST depression in the anterior leads (V1-V4)
- Posterior leads (V7-V9) may be obtained and are suggestive of STEMI when STE is ³5 mm in a single lead. However, these leads typically have low voltage and are insensitive.
- In patients with signs and symptoms concerning for an acute coronary syndrome, ischemic STD that is maximal in leads V1-V4 alone is strongly suggestive of occlusion MI, as opposed to STD of subendocardial ischemic which is maximal in V5-V6
  - Alternative non-ischemic causes of ST depression in V1-V4 should always be considered (RBBB, severe hypokalemia, RVH, etc.)
- STD maximal in V1-V4 (rather than V5-V6) was found to have 96% specificity for occlusion MI that required PCI in an emergency department cohort of patients deemed high risk for acute coronary syndrome (Meyers et al. 2021)

Take-home point:

In patients with signs and symptoms concerning for an acute coronary syndrome, ischemic ST segment depression maximal in leads V1-V4 without an alternative cause should be considered an occlusion MI until proven otherwise

Reference:

Meyers HP, Bracey A, Lee D, et al. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion Myocardial Infarction (Versus Nonocclusive Ischemia). J Am Heart Assoc. 2021 Dec 7;10(23):e022866. Epub 2021 Nov 15. PMID: 34775811

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

Anteroseptal ischemia
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada pattern
Right bundle branch block
Juvenile T-wave pattern

Take home Points:

Persistent juvenile T-wave pattern

A normal variant pattern
T wave abnormalities in leads V₁-V₃ (up to V₄-V₆ in some cases)
- T wave inversions or biphasic T-waves
- Not symmetric or deep
- < 3 mm deep
Seen in healthy children and young adults
Usually women < 40-45 years old
- Much more commonly seen in women vs. men
DDx: ischemia, PE, ARVD, Brugada, & RBBB

Key Teaching Points

Take-home Points

Look carefully at the morphology of ectopic beats as they can sometimes give you the diagnosis!
Scrutinize the ECG and don’t rely on the computer interpretation. Be methodical & thorough in your interpretation.
What should you do when ST segment elevation and symptoms in presumed STEMI resolves before cath lab activation?
- There is no definitive answer or agreement on the optimal timing of revascularization in this population. The referenced studies below had discrepant results, with one suggesting benefit to early cath and the other showing no significant difference in outcomes between immediate vs. delayed cath
- Consult your cardiologist early and discuss a patient specific plan

References:

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
Lemkes JS, Janssens GN, van der Hoeven NW, et al. Timing of revascularization in patients with transient ST-segment elevation myocardial infarction: a randomized clinical trial. Eur Heart J. 2019 Jan 14;40(3):283-291. PMID: 30371767

Key Teaching Points

Differential diagnoses for T wave inversions

Coronary artery disease (ischemia, reperfusion, Wellens waves)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Neurological causes (elevated intracranial pressure, hemorrhage, 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
Vasospasm (cocaine, amphetamines, etc.)
Hyperkalemia, hypokalemia
Juvenile T-wave pattern, normal finding in pediatric ECGs
Mitral valve prolapse
Normal finding in V₁, aVR, and lead III

Differential diagnoses for long QTc interval

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

Brain-Heart Interaction (ECG abnormalities)

Described at least since the 1950’s
Can occur with any significant 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
- Prolonged QTc (most common)
- Large T wave inversions, especially in the anterolateral leads
  - Also called “cerebral T waves” or “rollercoaster T waves”
- 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 (“rollercoaster T waves”)
- ST changes that mimic ACS
- Dysrhythmias
Clinical presentation matters!

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

Normal Right Bundle Branch Block (RBBB)

Leads V1-V3 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:

Right bundle branch blocks (RBBB) can be tricky!
In typical RBBB, leads V1-V3 can have mild discordant ST-segment depression which is a normal finding
RBBB should have no ST-segment elevation in any lead, any STE is abnormal and must be explained
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, especially STE in V1-V2 in with subtle anterior STEMI
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

Differential diagnoses for T wave inversions

Coronary artery disease (ischemia, reperfusion, Wellens waves)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Neurological causes (elevated intracranial pressure, hemorrhage, 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
Vasospasm (cocaine, amphetamines, etc.)
Hyperkalemia, hypokalemia
Juvenile T-wave pattern, normal finding in pediatric ECGs
Mitral valve prolapse
Normal finding in V₁, aVR, and lead III

Wellens’ waves (T wave inversion patterns associated with ACS)

Two distinct patterns of T wave abnormalities in the mid precordial leads (V₂-V₃, +/-V_4-6) that are highly specific for critical obstruction of the left anterior descending artery (LAD)
Reported by Wellens’ et al in 1982, the presence of these abnormal ECG patterns during a pain-free period in patients admitted with unstable angina was associated with very high risk for impending large anterior wall MI
Later prospective studies on patients with Wellens’ syndrome confirmed association of the findings with significant proximal LAD disease by coronary angiography

- Pattern A describes a biphasic T wave abnormality, initially positive with terminal negativity (~25% of cases)
  - Commonly misdiagnosed as “normal” or “non-specific T wave abnormality” in patients with atypical symptoms
  - Distinct from “reverse Wellens’ waves” associated with hypokalemia (biphasic T wave abnormality, initially negative with terminal positivity)
- Pattern B describes a deeply (> 2 mm) and symmetrically inverted T waves (~75% of cases)

Wellens’ waves typically evolve when serial ECGs are obtained and can help diagnose LAD related ACS

- During acute occlusion patients may have chest pain and diaphoresis with transient anterior ST elevation that may not be captured on the initial ECG
- During reperfusion (through spontaneous lysis or with medical treatment) chest pain and clinical symptoms may resolve while ST segment elevation improves, and T waves become biphasic or deeply inverted (like reperfusion s/p successful PCI)
- T waves may evolve from biphasic to deeply inverted if reperfusion is maintained, but lesions that cause these changes are considered unstable and can re-occlude at anytime
- During re-occlusion “pseudo-normalization” may occur, and previously biphasic or inverted T waves may become prominent and upright, a sign of evolving anterior occlusion MI

Wellens’ waves are specifically described as T wave abnormalities in the precordial leads, but similar changes can be seen in other coronary distributions during transient occlusion, reperfusion, and re-occlusion. The inciting event may be thrombus from acute plaque rupture, but has also been described in patients with vasospasm without CAD (sometimes in the setting of cocaine or amphetamine abuse)

As an isolated ECG finding, Wellens’ waves are not specific to ACS and false positives patterns that mimic ACS will diminish diagnostic accuracy (eg. benign T wave inversions which may also evolve, vasospasm, PE, RBBB, LVH, hypokalemia, CNS injury, stress cardiomyopathy, etc.)
Key Point: Wellens’ syndrome is a clinical diagnosis in patients with Wellens’ waves, and caution should be taken to obtain a thorough history and appreciate other potential reasons for Wellens’-like ECG patterns

Wellens’ Syndrome

A clinical syndrome in patients with a recent history of angina or concern for unstable angina/NSTE-ACS who have Wellens’ pattern ECG abnormalities described above, PLUS the following:
- Isoelectric or minimally elevated ST segments (no STEMI criteria)
- No precordial Q waves, with preserved precordial R wave progression (no old anterior infarct)
- Recent history of angina, with ECG pattern noted while chest pain free
- Normal or slightly elevated conventional troponin
Patients may present to the ED pain-free, comfortable, and have a normal physical exam. However, there are usually preceding symptoms concerning for ACS, or mild distress with diaphoresis
Wellens’ syndrome is not always an acute process, and can develop sub-acutely over days to weeks
Wellens’ syndrome exists on a spectrum of disease and biphasic T waves (pattern A) may evolve into deeply inverted T waves (pattern B) that may persist for hours or weeks, even when the patient is pain-free
Cardiac biomarkers may be falsely reassuring, and commonly within normal limits or only slightly elevated
While not currently a guideline indication for emergent cath or lytics (especially when pain free and without ST segment elevation), consider cardiology consultation when suspected
Medical management alone is usually ineffective and definitive treatment is procedural with PCI. Stress testing may be hazardous in the setting of an unstable lesion and may precipitate acute MI or sudden death
Best to diagnose in absence of high voltage, be cautious in making the diagnosis in the presence of large amplitude QRS complexes, and watch for normal variant T wave abnormalities
When in doubt get serial ECG’s, some will evolve into STEMI!

Take home Points

Wellens’ syndrome is the result of critical stenosis of the LAD manifesting in the characteristic ECG patterns (Wellens’ 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
This episode highlights several cases of normal variant ST elevation and T wave inversions that mimicked 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

Take home points

What is the most accurate isoelectric baseline (PR segment vs. TP segment) to assess the magnitude of ST segment deviation?

Many cardiologists who interpret stress tests have learned to use the PR segment, as the TP segment is not reliable when patients are tachycardic (TP segment shortened with tachycardia and difficult to visualize)
The PR segment can be affected by atrial abnormalities (e.g., pericarditis, atrial ischemia) that limit accuracy of this method
The TP segment can be affected by tachycardia. baseline artifact, U-waves, and down slopping TP segments (Spodick sign)
The fourth universal definition of MI document states: “The J-point (junction between QRS termination and ST-segment onset) is used to determine the magnitude of ST-segment shift with the onset of the QRS serving as a reference point. In patients with a stable baseline, the TP segment (isoelectric interval) is a more accurate method to assess the magnitude of ST-segment shift, and in distinguishing pericarditis (PT depression) from acute myocardial ischemia. Tachycardia and baseline shift are common in the acute setting and can make this determination difficult…”
Ultimately, you should use whichever is most flat/isoelectric with the least amount of artifact or baseline wander, but, if both look good…use the TP segment (especially in undifferentiated patients when pericarditis is considered)

Reference:

Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric. 6^th Amazon link.
Wagner GS, Strauss DG. Marriott’s Practical Electrocardiography, 12^th Edition, 2013. Amazon Link.
Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol 2018;72(18):2231–64. PMID: 30153967

Key Teaching Points

Left ventricular assist devices (LVADs)

Continuous flow device that provides mechanical circulatory support in patients with advanced left ventricular heart failure
3 main indications
- Bridge to recovery until native cardiac function improves
- Bridge to transplant until transplant obtainable
- Destination therapy (permanent placement in patients ineligible for transplant)
Obtain mean arterial pressure (MAP) using manual doppler measurement (goal 75-90 mmHg), typical flow should be ≥ 4 L/min
Critical device-related complications include:
- Pump or battery failure
- LVAD pump thrombosis
- Drive-line related infections
Dysrhythmias are common
- 30-50% of patients with LVADs have dysrhythmia, usually within 30 days of implantation
- May be asymptomatic, as LVADs maintain circulatory support despite heart rate or rhythm
Atrial dysrhythmias
- Prioritize beta-blockers for rate control, followed by digoxin, lastly amiodarone
- Use diltiazem cautiously given negative ionotropic effect
Ventricular dysrhythmias
- Often refractory to medical therapy
- Anti-dysrhythmics usually don’t work at terminating the dysrhythmia but may prevent long-term recurrence
  - Cardioversion is often necessary and compatible with LVADs if the pads are not placed directly over the pump
  - Amiodarone, lidocaine, or procainamide are second line therapies
  - Use maximum tolerated doses of beta blockers for medical therapy
- CPR/ACLS (advanced cardiac life support) is acceptable and encouraged when needed, but use signs of perfusion, MAP, and end-tidal CO₂ to guide resuscitation rather than the pulse vs. pulseless algorithm
  - End points of resuscitation is clinical signs of improvement
    - End-tidal CO2 in intubated patients ≥ 20 mmHg
    - And/or a MAP ≥ 50 mmHg

Take home points

Patients with LVADs are at high risk for dysrhythmias
Patients with LVADs can be minimally symptomatic with dysrhythmias…until things quickly go bad
Electricity typically is better than antiarrhythmic medications

Reference:

Gopalsami Anand. Left Ventricular Assist Devices (LVAD). In: Mattu A and Swadron S, ed. CorePendium. Burbank, CA: CorePendium, LLC. https://www.emrap.org/corependium/chapter/recS6rSMCMOtqKNe9/Left-Ventricular-Assist-Devices-LVAD#h.2wv9a9z2n011. Updated October 7, 2021. Accessed May 13, 2022.

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Hyperacute T-waves
  - Disproportionately large T-waves (especially when larger than QRS)
  - Straightening of the upslope of the T-waves
- “Checkmark or BAM sign”
  - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- Reciprocal changes (e.g., aVL, V₂)
  - Especially aVL when the RCA is involved in early inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

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

Bizarre Bradycardia

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

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 bradydysrhythmia, 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

Wellens Syndrome

A clinical syndrome in patients with a recent history of angina or concern for unstable angina/NSTE-ACS who have Wellens pattern ECG abnormalities, PLUS the following:
- Isoelectric or minimally elevated ST segments (no STEMI criteria)
- No precordial Q waves, with preserved precordial R wave progression (no old anterior infarct)
- Recent history of angina, with ECG pattern noted while chest pain free
- Normal or slightly elevated conventional troponin
Patients may present to the ED pain-free, comfortable, and have a normal physical exam. However, there are usually preceding symptoms concerning for ACS, or mild distress with diaphoresis
Wellens syndrome is not always an acute process, and can develop sub-acutely over days to weeks
Wellens syndrome exists on a spectrum of disease and biphasic T waves (pattern A) may evolve into deeply inverted T waves (pattern B) that may persist for hours or weeks, even when the patient is pain-free
Cardiac biomarkers may be falsely reassuring, and commonly within normal limits or only slightly elevated
While not currently a guideline indication for emergent cath or lytics (especially when pain free and without ST segment elevation), consider cardiology consultation when suspected
Medical management alone is usually ineffective and definitive treatment is procedural with PCI. Stress testing may be hazardous in the setting of an unstable lesion and may precipitate acute MI or sudden death
Best to diagnose in absence of high voltage, be cautious in making the diagnosis in the presence of large amplitude QRS complexes, and watch for normal variant T wave abnormalities
When in doubt get serial ECG’s, some will evolve into STEMI!

Take home points

Serial ECGs for ongoing chest pain concerning for ischemia is very important!
- New TWI in aVL may be a sign of early inferior STEMI
Remember the DDx of STE in aVR (listed above)
Strange or bizarre bradydysrhythmia not responding to ACLS? Consider hyperkalemia!
The most common cause of a pause is a preceding premature atrial contraction (PAC)
Wellens syndrome is concerning for proximal LAD occlusion

Key Teaching Points

ECG findings in patients on digoxin

“Digoxin effect”
- Down sloping ST-segment depression with a characteristic sagging appearance (a.k.a Salvador Dali moustache)
- The presence of digoxin effect pattern on the ECG is not a marker of supratherapeutic digoxin levels or toxicity, but merely suggests that the patient is taking digoxin
Digoxin toxicity
- Digoxin toxicity causes a multitude of dysrhythmias due to increased automaticity and decreased AV conduction
- Most common finding is frequent PVC’s
- Sinus bradycardia and AV blocks may be seen
- Slow “regularized” atrial fibrillation is a classic finding
  - Regularized due to complete heart block and junctional or ventricular escape rhythm
- Bidirectional VT (rare)

Bizarre Bradycardia

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

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 bradydysrhythmia, 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

Diagnosing occlusion MI in the presence of LBBB & RV paced rhythms

Acute coronary occlusion CAN be detected on the ECGs of patients with left bundle branch blocks and paced rhythms with high specificity
Look for Sgarbossa & Modified Sgarbossa criteria whenever there is concern for acute MI
- Concordant ST segment elevation ≥ 1 mm in any lead
- Concordant ST segment depression ≥ 1 mm in V1, V2, V3
- Excessively discordant STE (STE/S wave ratio > 25%)
For much more on Sgarbossa check out prior episodes here: LBBB & paced rhythms

Take home points

“Regularized atrial fibrillation”? Think about digoxin toxicity!
Strange or bizarre bradydysrhythmia not responding to ACLS? Consider hyperkalemia!
Know the Sgarbossa criteria for LBBB and paced rhythms

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Hyperacute T-waves
  - Disproportionately large T-waves (especially when larger than QRS)
  - Straightening of the upslope of the T-waves
- “Checkmark or BAM sign”
  - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- Reciprocal changes (e.g., aVL, V₂)
  - Especially aVL when the RCA is involved in early inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

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

Lumen stenosis doesn’t matter! It’s all about plaque vulnerability
- Plaque vulnerability is based on 3 major factors
  1. Fibrous cap
  2. Lipid core
  3. Inflammatory cells
- Plaques grow into the vessel wall rather than into the lumen
  - May appear patent on angiography despite significant coronary artery disease and may result in false negative angiography
  - Small plaques may be more unstable and more prone to rupture
  - Infarct related arteries often have non-obstructing plaque, before rupture and MI
  - Angiography cannot distinguish stable vs. unstable plaque composition, and give no information about the fibrous cap or lipid core
- Smaller plaques with thin-capped fibroatheromas may be more unstable and prone to rupture than thicker capped plaques. Both can evolve over time, and any observations of plaque stability represent a snapshot in time of a moving target
  - These smaller plaques can still rupture and cause complete occlusion and acute MI
  - Studies of infarct related arteries have shown that they often have non-obstructing plaques before rupture and MI
  - Smaller plaques are often associated with negative stress tests
    - A small study looking at the frequency of significant CAD in ED patients with chest pain and a recent negative or inconclusive stress test, showed that more than 20% of these patients were still found to have significant CAD (PMID: 21079714)

Take home points

T wave inversions in aVL can be the first finding of impending inferior STEMI
Note when ECGs are done with vs. without active symptoms
A recent negative stress test is not a guarantee of absence of CAD/ACS!
- Nothing will risk stratify you to zero!
- You can’t always rely in the recently negative stress test or “unremarkable” cath.
- History of presenting illness is the most important information and should guide your management.

References:

Libby P. Mechanisms of acute coronary syndromes and their implications for therapy. N Engl J Med 2013;368(21):2004–13. PMID: 23697515
Arbab-Zadeh A, Nakano M, Virmani R, et al. Acute coronary events. Circulation 2012;125(9):1147–56. PMID: 22392862
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
Walker J, Galuska M, Vega D. Coronary disease in emergency department chest pain patients with recent negative stress testing. West J Emerg Med. 2010 Sep;11(4):384-8. Erratum in: West J Emerg Med. 2018 Nov;19(6):1065. PMID: 21079714

Key Teaching Points

Subtle early signs of ischemia

Early ischemia is often associated with…
- Hyperacute T-waves
  - Disproportionately large T-waves (especially when larger than QRS)
  - Straightening of the upslope of the T-waves
- “Checkmark or BAM sign”
  - QRS complexes that lead straight into the T-wave with abnormal ST-segment morphology
- Reciprocal changes (e.g., aVL, V₂)
  - Especially aVL when the RCA is involved in early inferior STEMI
  - Anterior STEMI – reciprocal changes seen in ~ only 70%
    - Beware, ~30% or more will NOT have reciprocal changes
  - New upright T-wave in V₁ (loss of precordial T-wave balance)
- When in doubt, get repeat ECGs!

Take home points

Dyspnea is a common anginal equivalent
Get serial ECGs for ongoing symptoms of ACS
T wave inversion in aVL can be a sign of early inferior STEMI
- Computer ECG interpretations won’t pick this up!
de Winter T waves represent acutely unstable proximal LAD occlusion
- If cardiology declines, treat in the ED aggressively and monitor closely
- May evolve into STEMI within hours
Prior negative stress tests have less utility if the HPI is concerning
Concerning HPI + non-diagnostic ECG = get a repeat ECG
Wellens T waves represent proximal LAD occlusion

Key Teaching Points

Differential diagnoses for T wave inversions

Coronary artery disease (ischemia, reperfusion, Wellens waves)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Neurological causes (elevated intracranial pressure, hemorrhage, 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
Vasospasm (cocaine, amphetamines, etc.)
Hyperkalemia, hypokalemia
Juvenile T-wave pattern, normal finding in pediatric ECGs (V₁-V₃)
Mitral valve prolapse
Normal finding in V₁, aVR, and lead III

Differential diagnosis for T-wave inversions in V1-V3

Anteroseptal ischemia
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada pattern
Right bundle branch block
Juvenile T-wave pattern

Differential Dx for long QT interval (greatest concern when QTc > 500ms)

Electrolytes
- Hypokalemia
- Hypomagnesemia
- Hypocalcemia
Hypothermia
ACS / cardiac ischemia
Elevated intracranial pressures
Medications (i.e., sodium channel blocking drugs)
Congenital

Causes of prolonged QT-interval summary

Prolonged QT due to abnormal/prolonged T –waves

Hypokalemia
Hypomagnesemia
Medications (i.e., sodium channel blocking drugs)
Misc: Elevated ICP, Cardiac ischemia, Congenital

Prolonged QT due to prolonged ST-segment

Hypocalcemia
Hypothermia

Differential for non-conducted P-waves (P:QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and an ectopic P wave is present (different morphology, with abnormal P wave axis)
The non-conducted ectopic P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the single non-conducted P wave (two consecutive non-conducted P waves rules out Mobitz I)
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P:QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with better prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Key Teaching Points

Differential diagnosis for narrow complex irregular tachycardia

Atrial fibrillation
- No distinct regular atrial activity
- Fibrillatory waves usually coarse (bumpy with higher voltage) early on, then fine (lower voltage)
- Atrial rate > 350 bpm
Atrial flutter with variable conduction
- Regular atrial activity (F-waves) present
- Flutter waves may be mapped out with calipers
- Atrial rate = 250-350
Multifocal atrial tachycardia
- P-waves present, but irregular and with 3 or more different P-wave morphologies
- Variable PP, PR, and RR intervals

Differential diagnosis for short QTc interval

Hypercalcemia
Digoxin
Congenital short QT syndrome

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 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

Bifascicular & Trifascicular Blocks

Bifascicular Block

Conduction delay below the AV node where two of the three main fascicles of the His/Purkinje system are blocked
- RBBB + LAFB (resulting in left axis deviation) is most common (single coronary perfusion via LAD)
- RBBB + LPFB (resulting in right axis deviation) is a less common pattern (dual coronary perfusion via right and left circumflex arteries)
Associated with structural heart disease with fibrosis of conducting system
Risk of progression to complete heart block if the remaining fascicle is damaged, most concerning in symptomatic patients with syncope who may require hospitalization and consideration of pacemaker insertion
New onset Bifascicular block in patients with symptoms of ACS is highly associated with proximal LAD occlusion even in the absence of ST elevation

Trifascicular Block

Conduction abnormality involving all three fascicles below the AV node (RBBB, LAFB, LPFB)

- 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

Key Teaching Points

Differential for non-conducted P-waves (P:QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and an ectopic P wave is present (different morphology, with abnormal P wave axis)
The non-conducted ectopic P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the single non-conducted P wave (two consecutive non-conducted P waves rules out Mobitz I)
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P:QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with better prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Differential diagnosis for T-wave inversions

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

Differential diagnosis for T-wave inversions in V1-V3

Coronary artery disease (ischemia)
Pulmonary causes (PE, pneumothorax, pulmonary HTN, pneumonia, hyperventilation, etc.)
Arrhythmogenic right ventricular dysplasia/cardiomyopathy (V₁-V₃)
Brugada syndrome (V₁-V₂)
Juvenile T-wave pattern

Always think of the following differentials when interpreting the ECG of patients with syncope when the history and physical exam are non-diagnostic:

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

Differential diagnosis for narrow complex irregular tachycardia

Atrial fibrillation

No distinct regular atrial activity
Fibrillatory waves usually coarse (bumpy with higher voltage) early on, then fine (lower voltage)
Atrial rate > 350 bpm
Commonly over diagnosed in patients with irregular rhythms from PACs

Atrial flutter with variable conduction

Regular atrial activity (F-waves) present
Flutter waves may be mapped out with calipers
Atrial rate = 250-350

Multifocal atrial tachycardia

P-waves present, but irregular and with 3 or more different P-wave morphologies
Variable PP, PR, and RR intervals

Differential diagnosis for 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 (AVRT AVNRT, junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign if 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 missed atrial tachyarrhythmia
Always consider when rate is 150 ± 20 bpm

Key Teaching Points

Differential for non-conducted P-waves (P:QRS > 1, “electrocardiographic polyuria”)

Blocked Premature Atrial Complexes

P waves are irregular in rhythm, and an ectopic P wave is present (different morphology, with abnormal P wave axis)
The non-conducted ectopic P wave comes early and there is a compensatory atrial pause before the next normal sinus beat
Commonly misdiagnosed as Mobitz II (which is distinguished by a constant P-P interval)

2^nd degree AV Block: Mobitz I (Wenckebach)

P waves are regular (P-P interval is constant)
Progressive PR interval lengthening prior to a non-conducted P wave
At least 2 consecutive P-QRS complexes that demonstrate the gradually increasing PR interval before the single non-conducted P wave (two consecutive non-conducted P waves rules out Mobitz I)
QRS complexes are usually narrow (block at level of AV node) unless there is also a bundle branch or fascicular block
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Commonly misdiagnosed as atrial fibrillation

2^nd degree AV Block: Mobitz II

P waves are regular (P-P interval is constant)
Constant PR interval that remains unchanged prior to a non-conducted P wave (e.g., 3:2 conduction, 4:3 conduction, etc.)
At least 2 consecutive P-QRS complexes that demonstrate the constant PR interval before the non-conducted P-wave
QRS complexes are usually wide (infranodal block)
Results in clumped or grouped beats and a regularly irregular ventricular rhythm when conduction is fixed (variable conduction ratios also possible)
Patients usually need permanent pacemaker

2^nd degree AV Block: 2:1 conduction

P waves are regular (P-P interval is constant)
Every other P wave is a non-conducted P wave (2:1 conduction), so you do not have 2 consecutive P-QRS complexes before the non-conducted P wave
Hence, it is difficult to differentiate Mobitz I vs. Mobitz II when 2:1 AV block is present
- With a standard ECG, there is limited opportunity to observe for the constant PR interval characteristic of Mobitz II
- Consider a long rhythm strip or repeat ECGs

2^nd degree AV Block: Advanced AV Block or “High-grade AV Block”

P waves are regular (P-P interval is constant)
More than 2 consecutive P waves are non-conducted (P:QRS ³ 3:1)
- Type I: block at level of AV node
- Type II: block is infranodal, suspected usually based on width of QRS, ~75-80% are Type II
- Most patients will require a pacemaker regardless of terminology
In contrast to 3^rd degree (complete) heart block, some P waves continue to be conducted to the ventricle

3^rd degree AV Block (Complete Heart Block) + AV dissociation

P-P intervals and QRS complex intervals are regular and constant but occur independently of each other
PR-interval is randomly changing
No apparent communication between atrium and ventricle (AV dissociation)
Narrow QRS = Junctional escape rhythms (ventricular rate ~40-60), usually vagal with better prognosis
Wide QRS = Ventricular escape rhythms (ventricular rate ~20-40), infranodal, more likely to need a permanent pacemaker

3^rd degree AV Block (Complete Heart Block) + Isorhythmic AV dissociation

CHB where atrial rate and ventricular rate are approximately the same

Take home points

When interpreting ECGs with complicated rhythms…
- Break it down into sections
- Use calipers and figure out what maps out
  - What is the atrium doing, what is the ventricle doing, and what is their relationship?
- Compare with old ECGs, and get serial ECGs

Key Teaching Points

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
- Patients are very preload dependent
- Preload reducing meds cause significant hypotension (i.e., NTG), avoid them!
- When lungs are clear, use IV fluids first line rather than vasopressors
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

Differential diagnosis for narrow complex irregular tachycardia

Atrial fibrillation

No distinct regular atrial activity
Fibrillatory waves usually coarse (bumpy with higher voltage) early on, then fine (lower voltage)
Atrial rate > 350 bpm
Commonly over diagnosed in patients with irregular rhythms from PACs

Atrial flutter with variable conduction

Regular atrial activity (F-waves) present
Flutter waves may be mapped out with calipers
Atrial rate = 250-350

Multifocal atrial tachycardia

P-waves present, but irregular and with 3 or more different P-wave morphologies
Variable PP, PR, and RR intervals

Differential diagnosis for 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 (AVRT AVNRT, junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign if 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 missed atrial tachyarrhythmia
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)

What is the most accurate isoelectric baseline (PR segment vs. TP segment) to assess the magnitude of ST segment deviation?

Many cardiologists who interpret stress tests have learned to use the PR segment, as the TP segment is not reliable when patients are tachycardic (TP segment shortened with tachycardia and difficult to visualize)
The PR segment can be affected by atrial abnormalities (e.g., pericarditis, atrial ischemia) that limit accuracy of this method
The TP segment can be affected by tachycardia. baseline artifact, U-waves, and down slopping TP segments (Spodick sign)
The fourth universal definition of MI document states: “The J-point (junction between QRS termination and ST-segment onset) is used to determine the magnitude of ST-segment shift with the onset of the QRS serving as a reference point. In patients with a stable baseline, the TP segment (isoelectric interval) is a more accurate method to assess the magnitude of ST-segment shift, and in distinguishing pericarditis (PT depression) from acute myocardial ischemia. Tachycardia and baseline shift are common in the acute setting and can make this determination difficult…”
Ultimately, you should use whichever is most flat/isoelectric with the least amount of artifact or baseline wander, but, if both look good…use the TP segment (especially in undifferentiated patients when pericarditis is considered)

Take home points

Junctional rhythms:
- Junctional escape rhythm (40 – 60 bpm)
- Accelerated junctional rhythm (60 – 100 bpm)
- Junctional tachycardia (> 100 bpm)
Acute inferior STEMI? Consider right ventricular MI as it will change management
SVT often has ST segment depression and ST elevation in aVR (these are normal related findings, that should resolve with cardioversion)
Ventricular rate 150 +/- 20? Suspect atrial flutter
- Look carefully for inverted P waves in the inferior leads, flipping the ECG upside down can help identify inverted P waves
Use the TP segment as the isoelectric baseline to assess for ST segment elevation

Key Teaching Points

Differential diagnosis for narrow complex irregular tachycardia

Atrial fibrillation

No distinct regular atrial activity
Fibrillatory waves usually coarse (bumpy with higher voltage) early on, then fine (lower voltage)
Atrial rate > 350 bpm
Commonly over diagnosed in patients with irregular rhythms from PACs

Atrial flutter with variable conduction

Regular atrial activity (F-waves) present
Flutter waves may be mapped out with calipers
Atrial rate = 250-350

Multifocal atrial tachycardia

P-waves present, but irregular and with 3 or more different P-wave morphologies
Variable PP, PR, and RR intervals

Differential diagnosis for 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 (AVRT AVNRT, junctional, etc.) but generally same treatment and management approach for emergency physicians
SVT can commonly cause rate dependent ST-segment changes that are benign if 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 missed atrial tachyarrhythmia
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)

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

Take home points

Pay attention to V1 for rhythm analysis
Hypothermia: slow atrial fibrillation, intraventricular conduction delays, J waves
Sinus beats: upright P waves in I, II, aVF, with inverted P waves in aVR
Patients with LVADs can have any rhythm, convert rhythms aggressively
Junctional rhythms:
- Junctional escape rhythm (40 – 60 bpm)
- Accelerated junctional rhythm (60 – 100 bpm)
- Junctional tachycardia (> 100 bpm)

Key Teaching Points

Polymorphic ventricular tachycardia (PVT)

Life threatening wide complex tachyarrhythmia with very rapid heart rate and variable QRS patterns (changing axis, amplitudes, and duration)
Will either terminate spontaneously (may result in syncope) or persist with risk of deterioration to ventricular fibrillation (resulting in cardiac arrest)
Two main types with similar ECG findings, it is important to differentiate the etiology and type as they respond to different forms of therapy. Medications that are life saving for one type may be contraindicated for others.
Diagnosis is NOT based on morphology during tachyarrhythmia, as it is difficult to differentiate pulseless generic PVT from torsades or ventricular fibrillation based on morphology alone. All forms of PVT may have a “twisting of the points” appearance in some leads. Important to scrutinize the QT interval before and after rhythm conversion.

Types of polymorphic ventricular tachycardia

Generic polymorphic VT (normal QTc)
- Causes
  - Usually associated with cardiac ischemic/ACS, also seen with Brugada syndrome and other miscellaneous reasons
  - In the absence of a Brugada pattern or other clear cause, consider and treat for cardiac ischemia until proven otherwise.
- Treatment
  - When persistent, patients are usually unstable. Proceed with sedation and defibrillation, then…
    - Treat for ACS and seek urgent revascularization when possible if an occlusion MI is thought to be the cause, consider beta blockers >> lidocaine and amiodarone
    - Cases of Brugada need consultation with electrophysiology, quinidine and isoproterenol are recommended for treatment of arrhythmic storms and to avoid recurrence

Torsades de pointes (type of PVT associated with long QT syndrome)
- At significant risk when QTc ³ 500 ms in sinus rhythm
- Note: Diagnosis is NOT based on morphology alone. All forms of PVT may have a “twisting of the points” appearance in some leads. Scrutinize the QT interval before and after rhythm conversion.
- Causes
  - Electrolytes: Hypomagnesemia, Hypokalemia, Hypocalcemia
  - Hypothermia
  - Medication and drug induced
  - Elevated intracranial pressure
  - Congenital long QT syndromes
- Treatment
  - Most episodes of torsades are self-limited. If persistent, defibrillate when unstable and give magnesium bolus if defibrillation is unsuccessful or to prevent recurrence
  - When intermittent, give magnesium slow IV push and infusion even when serum magnesium levels are normal (monitor for hypermagnesemia and toxicity during infusion)
  - Overdrive pacing (shortens the QTc) may be necessary
    - Electrically pace at 100-120 bpm
    - Chemically with isoproterenol, dopamine, or epinephrine
  - Avoid procainamide and amiodarone (will further prolong QTc)
  - Avoid beta blockers in acquired forms (will further prolong QTc)
  - Discontinue any QT prolonging medications and raise serum potassium levels to high-normal range, while looking for underlying causes

Take home points

2 main types of polymorphic ventricular tachycardia

Generic polymorphic VT (normal QTc)
- Usually associated with ACS
- Treat for cardiac ischemia, refer to EP for Brugada syndrome
Torsades de pointes (type of PVT with long QTc)
- If persistent and unstable, defibrillate and give IV magnesium
- If intermittent, use IV magnesium and electrical or chemical overdrive pacing as needed
- After conversion, continue magnesium infusion, and look for and treat the underlying cause of the long QT interval
Be careful about trusting the computer interpretation! Interval calculations can be unreliable when there is significant artifact

Further Reading:

Viskin S, Chorin E, Viskin D, et al. Polymorphic Ventricular Tachycardia: Terminology, Mechanism, Diagnosis, and Emergency Therapy. Circulation. 2021 Sep 7;144(10):823-839. PMID: 34491774

Key Teaching Points

Differential diagnosis for T wave inversions in V1-V2

Anteroseptal ischemia
Persistent juvenile T-wave pattern
Pulmonary embolism
RVH with strain
(I)RBBB (usually with ST depression, rsR’, and lateral s waves)
WPW
Brugada syndrome
Arrhythmogenic right ventricular dysplasia/cardiomyopathy
Lead misplacement (V1/V2) placed too high on the chest

Normal ECG Lead Placement

Take home points

When the V1-V2 electrodes are placed too high on the chest…

Incomplete right bundle branch block-type pattern
- Often with an Rsr’ pattern as opposed to typical (I)RBBB patterns that have rsR’ (have a larger second upward deflection, consider lead misplacement when the first upward deflection is higher than the second)
ST segment elevation
T wave inversions
- Normal in V1, but not usually normal in V2
Inverted P waves
- Normal in V1, but not usually normal in V2

Reference:
Walsh B. Misplacing V1 and V2 can have clinical consequences. Am J Emerg Med. 2018 May;36(5):865-870. PMID: 29472037

Amal Mattu’s ECG Case of the Week – July 11, 2022

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