CONTENTS

• LAD (left axis deviation)
• LAHB (left anterior hemiblock)
• iLBBB (incomplete left bundle branch block)
• LVH (left ventricular hypertrophy)
  • Diagnostic criteria
  • Differential diagnosis of LVH
  • Interpreting an ECG in the context of LVH
    • LVH versus MI
    • LVH plus ER (early repolarization)
• HCM (hypertrophic cardiomyopathy)
  • Apical HCM
• Extreme axis deviation (-90 to +180)

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LAD

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Left axis deviation is defined as an axis between -30 and -90 degrees.  

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[1/3] consider prior IMI 

• [1] Inferior complexes have a QS or Qr morphology. However, 1/3 of patients with prior IMI can regrow R-waves, so an absence of Q-waves doesn't exclude prior IMI.
• [2] QRS complex fragmentation suggests prior infarction.
• [3] Evidence of prior Q-wave MI elsewhere on the ECG (e.g., lateral Q-waves, tall R-V1).
• [4] LAD is often less pronounced in IMI than with LAHB (usually -45 to -90 degrees). (19228822)

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[2/3] consider LAHB, criteria as follows: ⚡️

• [1] QRS <120 ms (often ~100-120 ms).
• [2] Frontal axis between -45° to -90°:
  • Positive in Lead I.
  • Negative in aVF.
  • Substantially net negative in Lead II.
  • S-wave in aVF > R-wave in Lead I.
• [3] qR in aVL.
• [4] R-peak time in aVL of ≧45 ms. (19228822)

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[3/3] consider LVH ⚡️

Romhilt-Estes score (≧5)

• Voltage criteria (3 points): any of the following:
  • R or S in limb leads ≧20 mm.
  • S in V1 or V2 ≧30 mm.
  • R in V5 or V6 ≧30 mm.
• ST-T abnormalities: 3 points (1 with digoxin).
• Left atrial enlargement in V1 (terminal P-wave is >40ms and >1 mm): 3 points.
• Left axis deviation: 2 points.
• QRS >90 ms: 1 point.
• Delayed intrinsicoid deflection in V5 or V6 (>50 ms between the onset of QRS to R-wave peak): 1 point.

Voltage criteria

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LAHB

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diagnostic criteria for LAHB 

• [1] QRS <120 ms (often ~100-120 ms).
• [2] Frontal axis between -45° to -90°:
  • Positive in Lead I.
  • Negative in aVF.
  • Substantially net negative in Lead II.
  • S-wave in aVF > R-wave in Lead I.
• [3] qR in aVL.
• [4] R-peak time in aVL of ≧45 ms. (19228822)

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interpreting the rest of the ECG in the context of LAHB 

LVH is difficult to diagnose

• LAHB itself can cause:
  • Tall R-wave in aVL and I.
  • Left axis deviation.
  • Slight prolongation of the QRS complex.
• Features that support LVH:
  • LAA.
  • LVH strain morphology.
  • Maximal precordial QRS complex (R wave + S wave) + (S-III) >30 (M) or >28(F) mm suggests LVH. (23347023)

LAHB can confuse the diagnosis of prior Q-wave MI:

• High-lateral MI: LAHB may cause small Q-waves & TWI in I, aVL.
• Anterior MI: LAHB often causes poor R-wave progression with QS complexes in the right precordial leads.
• Inferior MI: LAHB can mask an old inferior MI by generating an R-wave in the inferior leads. (O'Keefe 2021)

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clinical associations with LAHB

• Acute MI.
• Hypertension, aortic valvular disease.
• Cardiomyopathy.
• Degenerative disease of the cardiac conduction system.
• It may rarely be a benign, isolated finding.

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incomplete left bundle branch block (iLBBB)

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rough diagnostic criteria:

• [1] QRS ~110-120 ms.
• [2] Negative QRS complex in leads V1 and V2.
• [3] V5, V6, I, aVL: R-wave peak time >60 ms, often with notched/slurred R waves.
  • Notched/slurred R-wave may be seen only in aVL (especially if cardiomegaly contributes to delayed R-wave progression).
  • QRS notching/slurring in the lateral leads predicts progression to complete LBBB, potentially constituting the “truest” form of iLBBB. (31823461)
• [4] No septal Q-waves in I, V5, or V6.

differential diagnosis includes

• [1] LVH ⚡️ (although iLBBB may often coexist with LVH). (19281930)
• [2] LAHB. ⚡️
• [3] Prior anteroseptal MI is causing poor R-wave progression.
  • iLBBB can cause poor R-wave progression, so in the context of iLBBB, it's difficult to diagnose prior anteroseptal MI.
• [4] Complete LBBB: ⚡️
  • This hinges on the precise QRS duration, which is challenging to decipher.
  • Reciprocal morphologic changes might support a diagnosis of LBBB.

clinical significance of iLBBB

• iLBBB is often associated with cardiac pathology (e.g., ischemic heart disease, cardiomyopathy, valvular dysfunction, or congenital heart disease). (O'Keefe 2021)
• iLBBB can cause a rate-related complete LBBB.

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left ventricular hypertrophy (LVH)

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diagnostic features of LVH

Romhilt-Estes scoring system (4 = highly probable; ≧5 = definite)

• Voltage criteria (3 points): any of the following
  • R or S in limb leads ≧20 mm.
  • S in V1 or V2 ≧30 mm.
  • R in V5 or V6 ≧30 mm.
  • (⚠️ Voltage decreases with age and obesity.)
• ST-T shows LV strain pattern: 3 points (1 with digoxin).
• Left atrial enlargement in V1 (terminal P-wave is >40ms and >1 mm): 3 points.
• Left axis deviation: 2 points.
• QRS >90 ms: 1 point.
• Delayed intrinsicoid deflection in V5 or V6 (>50 ms): 1 point.

voltage criteria for LVH

• R-aVL >11 mm
  • Sensitivity ~10%; specificity ~93% (except with LAHB). 
• Cornell: R-aVL + SV3 >20♀/28♂
  • Sensitivity ~40%; specificity ~85%. 
• Peguero-Lo Presti: (Deepest precordial S) + (SV4) >23♀/28♂
  • Sensitivity ~60%; specificity ~90%. (28359515)
• Revised Sokolow-Lyon: SV1/2 + RV5/6 >35 (or >40 if under 30YO).
  • Sensitivity ~10%; specificity ~98%. 
  • Superior performance as compared to original Sokolow-Lyon criteria (SV1 + RV5/6). 

other features supporting LVH

• Poor R-wave progression from V1-V3.

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differential diagnosis of LVH includes:

[1/5] LAHB (left anterior hemiblock) 📖

• LAHB may cause R-aVL >11 mm and left axis deviation.
• Diagnostic criteria for LAHB:
  • [1] QRS <120 ms (often ~100-120 ms).
  • [2] Frontal axis between -45° to -90°:
    • Positive in Lead I.
    • Negative in aVF.
    • Substantially net negative in Lead II.
    • S-wave in aVF > R-wave in Lead I.
  • [3] qR in aVL.
  • [4] R-peak time in aVL of ≧45 ms.
• Features that suggest LVH within the context of LAHB:
  • LAA.
  • LVH strain morphology.
  • Maximal precordial QRS complex (R wave + S wave) + (S-III) >30 (M) or >28(F) mm. (23347023)

[2/5] HCM (hypertrophic cardiomyopathy) 📖

• Tall R-wave in V1.
• Deep septal Q-waves.

[3/5] Apical HCM 📖

• TWI is unusually deep (in comparison to R-wave voltages).

[4/5] Biventricular hypertrophy 📖

• Signs of RVH may include the following:
• [1] Right atrial abnormality or biatrial abnormality.
• [2] Tall R-wave in V1. However, there may be an S-wave in V1 that is much smaller than the S-wave in V2 (as if RVH is trying to generate a tall R-wave in V1, but only succeeds in erasing part of the S-wave).
• [3] RV strain pattern in the right precordial leads.
• [4] Vertical axis (~90°) or frank RAD (with S>R in Lead I).

[5/5] Dilated cardiomyopathy 📖

• Suggested by the combination of:
• [1] LVH meeting voltage criteria, which is driven by large precordial voltages.
• [2] Low voltage in limb leads (<8 mm).
• [3] Delayed R-wave progression (R<S in V4).

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expected ECG changes in the context of LVH

intervals

• It may be slightly widened.
• May see notching of QRS in mid-precordial leads.

vertical axis

• LAD often occurs (but not necessarily).
• Any right axis deviation suggests biventricular hypertrophy. 📖

horizontal axis

• V1-V3: poor R-wave progression with a QS pattern may occur (can mimic prior anterior MI).

chambers

• LAA is expected.
• RAA suggests biventricular hypertrophy. 📖

early LVH: absence of classic strain pattern

• Initially, the classic LV strain is absent.
• Lateral leads may show ST segment flattening (+/- depression) with a symmetric upright T-wave.

later LVH: strain pattern

• STD with TWI in leads with tall R-waves (V4-V6, I, aVL):
  • STD should be down-sloping and asymmetric.
  • TWI should be asymmetric with a rapid return to baseline. Overshoot of terminal positivity can occur, which may produce an inverted U-wave in the left chest leads (overshoot suggests LVH rather than ischemia). (11992349)
  • The pattern is usually maximal in V5-V6 (e.g., TWI in V6 > TWI in V4).
• STE in V1-V3 and aVR:
  • Usually, STE is ~2-4 mm and proportional to the preceding S-wave.
  • Mirror test: Flip V1-V3 vertically. If this resembles an LVH strain pattern (with downsloping ST depression), that supports the diagnosis of LVH-induced secondary changes.
  • Lack of STE in leads with deep S-waves may indicate relative ST segment depression!  
• PseudoWellens-A pattern may occur:
  • This seems to be a transitional phenomenon that occurs as the R-waves transition from negative to positive. The morphology of leads with pseudo-Wellens will often look like a hybrid of the right precordium (which only has STE) and the left precordium (which only has TWI).
  • There should be high voltages plus strain morphology seen in the precordial leads. 
  • True Wellen's pattern usually causes TWI in V2-V4, whereas pseudoWellens tends to cause TWI from V3-V6.

other potential abnormalities

• Prominent T-waves.
• Prominent or inverted U-waves.

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sorting out MI versus LVH: five signs of potential badness

Caution: ⚠️ It is often impossible to sort this out from a single ECG.  Comparison to baseline and serial evolution over time can also help. Below are some general concepts that may serve as red flags for the presence of ischemia:

[1] scary morphology 🚩

• Unequivocally hyperacute T-waves support acute ischemia.
• (LVH can mimic hyperacute T-waves, but T-waves are more concave and sometimes saddleback shaped.)

[2] deviation from the expected pattern 🚩, e.g.:

• TWI is concordant with the QRS complex (it should be discordant).
• ST depression followed by upright T-waves.
• Biphasic T-waves (e.g., reciprocal down-up T-waves).

[3] disproportionality 🚩

• QRS complex should be much larger than the T-wave.
• ST elevation should be mild in comparison to the size of the preceding QRS complex.

[4] regionality 🚩

• Be careful if morphology in one region looks unusual but morphology elsewhere looks typical for LVH.

[5] voltage loss 🚩

• The larger the QRS complex is, the more likely it is to be benign (ischemia causes a loss of R-wave amplitude).
• If some leads show unexpectedly low QRS voltages – beware!

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LVH combined with benign early repolarization

• This involves a combination of:
  • (1) LVH: Voltage and morphology criteria met (e.g., TWI in lateral precordial leads).
  • (2) Benign early repolarization: Causes J-waves and more STE than would otherwise occur in isolated LVH.
• This combination is a very challenging MI mimic.
• J-waves and a saddle-back morphology may support a benign etiology rather than ischemia. However, note that J-waves can be caused by acute myocardial infarction.

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Hypertrophic Cardiomyopathy (HCM)

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🔑 summary of key diagnostic findings

• [1] Voltage criteria for LVH (~60%).
  • HCM is suggested if LVH is epidemiologically unexpected (e.g., a young patient without HTN).
• [2] Exaggerated septal forces, such as:
  • [a] Tall R-wave in V1 and/or early R-wave transition. 📖
  • [b] Sharp & deep septal Q-waves in lateral leads (I, aVL) and left precordial leads (V4-V6).

arrhythmia

• AF may occur in ~10% of patients (loss of atrial kick may cause clinical deterioration). (de Luna 2022)
• Sudden death may result from VF/VT during exercise (a common cause of sudden death among athletes).
• Sinus node disease and AV block may occasionally occur. (O'Keefe 2021)

intervals

• QT prolongation in 15%. (O'Keefe 2021)

axis

• LAD in 20%.
• Tall R-wave in V1 📖, which may occur with TWI simulating RVH. (O'Keefe 2021)

chambers

• LAA in ~30% (due to reduced left ventricle compliance).
• LVH:
  • ~60% of patients meet voltage criteria for LVH. (O'Keefe 2021)
  • ST-T changes due to LVH are often seen.

septal Q-waves (70%), which are:

• Unusually deep (deeper than normal septal Q-waves).
• Narrow (helps distinguish them from Q-wave MI, which usually causes Q-waves >40 ms).
• Diffuse (may involve lateral and inferior leads, as well as tall R-wave in V1).
• Pseudoinfarction patterns may occur due to a combination of Q-waves plus ST-T changes due to LVH.

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differential diagnosis of HCM includes:

HCM vs. LVH

• A tall R-wave in V1 suggests HCM.
• Avoid over-calling HCM (when in doubt, LVH is statistically more likely).
• Obtain an echocardiogram when there is a clinical suspicion for HCM.

HCM vs. biventricular hypertrophy

• Discussed further here 📖

Duchenne muscular dystrophy

• This may cause tall R-wave in V1 with deep lateral Q-waves, closely mimicking HCM.
• Differentiation from HCM:
  • [1] Voltages may be lower than usually seen with HCM.
  • [2] Clinical history: ECG changes usually occur in severe, longstanding Duchenne muscular dystrophy that should be clinically evident. (15495441)
• ECG changes in Duchenne muscular dystrophy relate to fibrosis of the posterior basal and lateral myocardium (causing an imbalance in septal depolarization similar to HCM).  These findings don't correlate with echocardiographic abnormality or dilated cardiomyopathy. 🌊

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Apical HCM

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has some similarities with HCM

• Most features of HCM may occur (including voltage criteria for LVH and LAA).
• Abnormal septal Q-waves aren't seen (since hypertrophy doesn't involve the septum).

exaggerated LV strain pattern (giant TWI)

• If seen, this specifically suggests apical HCM.
• (1) Giant TWI:
  • It often involves V3-V5.
  • Inverted T-waves are larger than would generally be expected for LVH.
  • Disproportionate TWI may be seen in leads I and aVL, as compared to the preceding R-wave (more than would be expected for LVH).
• (2) ST depression.
• (Differential diagnosis of giant TWI: 📖).

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extreme axis deviation

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Extreme axis deviation is between -90 and +180 degrees (aka, north-west axis). Causes include:

• Misplaced limb leads (e.g., RA and LL reversal). 📖
• Ventricular rhythms:
  • Ventricular tachycardia.
  • AIVR (Accelerated idioventricular rhythm).
  • Ventricular escape rhythm.
• Wolf-Parkinson-White syndrome.
• Ventricular pacing.
• Hyperkalemia.
• Dextrocardia.
• Lung hyperinflation 📖 (vertically oriented heart) plus right ventricular hypertrophy.
• Myocardial infarction (especially inferior or posterior myocardial infarctions).
• Certain congenital heart diseases.

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questions & discussion

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