CONTENTS

• Tall R-wave in V1
• Right axis deviation (RAD)
  • Prominent S-I
    • LPFB (left posterior fascicular block)
  • RAD without S-I 
• Cor pulmonale (PE & RVH)
  • Diagnostic approach to PE & RVH
• Biventricular hypertrophy
• Lung hyperinflation pattern
  • Pneumothorax
  • Lead I sign
• Dextrocardia ➡️
• S1S2S3 pattern

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tall R-V1

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• Usually defined as either of the following (in the absence of RBBB): (19281932)
  • R>S in V1.
  • R-V1 > 6-7 mm.
• The approach to the etiology of tall R-V1 is as follows:

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[1] consider & exclude rare causes

(a) hypertrophic cardiomyopathy 📖

• High voltages, which meet LVH criteria.
• Sharp & deep septal Q-waves in lateral leads (I, aVL) and left precordial leads (V4-V6).
  • ⚠️ These may also be seen with posterior Q-wave MI.
• Duchenne muscular dystrophy may produce a similar pattern.

(b) Wolff-Parkinson-White syndrome.

(c) incorrectly high placement of V1 & V2 📖

(d) dextrocardia (V1 is functionally V2) 📖

(e) fascicular VT (may resemble RBBB+LAFB) 📖

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[2] remaining possibilities: posterior MI vs. RVH (vs. normal)

posterior MI (active or remote; Q-wave equivalent) 📖

• 🔑 Usually, there will be some inferior or lateral Q-waves (look carefully; they may be small).
  • ⚠️ Careful: QS waves in I and aVL don't distinguish between posterior MI vs. RVH. In this situation, examine V6 to determine whether there is qR (suggesting prior infarction) or Rs (suggesting terminal right axis deviation consistent with RVH).
• 🔑 Abnormal T-waves in right precordium:
  • Reperfused posterior OMI may cause prominent T-waves.
  • Hyperacute posterior OMI may cause TWI.
• 🔑 If posterior OMI is acute, STD in the right precordial leads may be seen.
• Morphology using a Mirror Test looks like a posterior MI.

RVH (right ventricular hypertrophy) ⚡️

• 🔑 Terminal RAD (prominent S-I +/- S-V6).
• 🔑 TWI in right precordial and/or inferior leads (especially III).
• 🔑 RAA (prominent, peaked P-waves in inferior leads).
• 🔑 qR in V1 (rarely seen but fairly specific for RVH).

(normal variant)

• ~1-3% of normal individuals may have a tall R-wave.
• This is a diagnosis of exclusion (e.g., following an unremarkable echocardiogram). (15495441)

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right axis deviation (RAD)

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#1 compare Lead I and Lead V6

• These should look similar (they're both left-pointing leads).
• If morphology is very different, consider lead malposition (e.g., technical dextrocardia 📖).

#2 subcategorize RAD:

• (a) Prominent S-wave in lead I: 📖
• (b) RAD without prominent S-I: 📖

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Prominent S-wave in Lead I (S-I)

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definition of prominent S-I?

• Size of S-I:
  • S-I >1-1.5 mm is often considered prominent in the literature.
  • S-I > R-I is definitely abnormal (since this indicates a right-axis deviation).
• Any coexisting S-wave in V6 supports the presence of an abnormality (normally, V6 lacks an S-wave).
  • ⚠️ A large S-wave in Lead I without any S-wave in V6 may raise the possibility of lead misplacement (since these leads generally have similar morphology).
• In the context of RBBB:
  • RBBB alone usually produces a relatively shallow, blunted R-wave in I.
  • RBBB with a prominent S-wave in Lead I suggests an additional pathology (e.g. RBBB + LPFB, RBBB + RV strain).

differential diagnosis of prominent S-I

1. Hyperkalemia. ⚡️
2. Na blocker toxicity. ⚡️
3. Brugada. ⚡️
4. Lung hyperinflation pattern. ⚡️
5. PE or RVH. ⚡️
6. BiV hypertrophy. 📖
7. Young people. ⚡️
8. LPFB (left posterior fascicular block). ⚡️

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[1/8] hyperkalemia 📖

• 🔑  Peaked T-waves.
• 🔑  P-waves widen, PR increases, and eventually, P-waves disappear.
• 🔑  Bradycardia, blocks, and/or pauses.
• 🔑  QRS widening (may mimic RBBB or VT; can be >200 ms).
• 🔑  Infarct mimic (STE in V1-V2; often triangular STE diving into TWI).

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[2/8] sodium channel blockers 📖

• 🔑  May cause tall R-wave in aVR.
• 🔑  QT prolongation.
• 🔑  QRS prolongation often occurs (may cause an incomplete or complete RBBB pattern).

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[3/8] Brugada syndrome 📖

• Coved STE in V1, or in V2, or in multiple leads within V1-V3
  • Followed by TWI.
  • STE at least 2 mm.

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[4/8] lung hyperinflation pattern 📖

• 🔑 Prominent P-waves in inferior leads.
• 🔑 Lead-I sign (low voltage in lead I).
• 🔑 Low voltage (sometimes with shrinkage of QRS voltage in V4->V5->V6).
• 🔑 Slow R-wave progression in V1-V3.
• 🔑 S-waves in V6 and Lead I.
• ⚠️ No unexplained features suggest PE/RVH (e.g., right precordial TWI, RBBB, tall R-V1). 📖

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[5/8] PE or RVH 

• Discussed below: ⚡️

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[6/8] Biventricular hypertrophy

• LVH may disguise many typical findings from RVH.
• If there are findings to support both LVH and RVH, consider BiV hypertrophy. 📖

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[7/8] young patients

• Right axis deviation may be a benign finding in very young adults.
• This may also be more common among athletes.

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[8/8] dx of exclusion = LPFB (left posterior fascicular block)

diagnostic criteria for isolated LPFB 

• [1] RAD (usually between +90 and +140 degrees) with a narrow QRS complex.
• [2] RAD involving the terminal portion of the QRS complex:
  • rS in leads I and aVL
  • qR in lead III (Q-wave should be <40 ms).
• [3] Exclusion of another etiology of RAD, especially RVH and vertical heart (as listed above).
  • There shouldn't be RAA (right atrial abnormality).
  • ⚠️ Isolated LPFB is uncommon, so be cautious about making this diagnosis.

other morphologic effects of LPFB

• Inferior TWI can occur.
• Poor R-wave progression.
• rS waves in I and aVL may mask a prior lateral Q-wave MI.
• QRS complex may be slightly wide.

clinical significance of LPFB

• LPFB rarely occurs alone or in normal hearts. LPFB is usually associated with RBBB (as a form of bifascicular block).
• Causes of LPFB include:
  • Coronary artery disease is the most frequent cause, especially large septal MI.
  • Hypertension.
  • Aortic valve disease.
  • Cardiac skeleton calcification. (de Luna 2022)

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right axis deviation without S-I

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Right axis deviation without S-I is due to a shift in the initial axis of the QRS complex.  Two causes include: 

lateral Q-wave infarct

• Suggested by Q-wave in Lead I (versus RVH, which has negative forces at the end of the QRS complex).
  • If there is a QS complex in lead I, then look at lead V1 to make this distinction (qR in V1 strongly suggests RVH rather than Q-wave infarct).
• TWI in I, aVL, V5, and V6 often seen

dextrocardia 📖

• Everything is negative in left limb leads (I and aVL).

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diagnostic approach to PE & RVH

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Please note that “PE” is used here to refer to an ECG pattern of acute RV strain. Identical changes can also be caused by any cause of acutely increased pulmonary vascular resistance (e.g., severe asthma or ARDS).  However, non-PE etiologies are usually more obvious from the remainder of the clinical examination.  

rapid evaluation for PE/RVH

[#1] consider features seen in PE and/or RVH:

• 🔑 Terminal RAD (prominent S-I +/- S-V6).
• 🔑 TWI in right precordial and/or inferior leads (especially III).
• 🔑 RV strain pattern with STD in V1-V4 (and, to a lesser degree, the inferior leads).
• 🔑 RBBB (complete or incomplete).
• 🔑 RAA (prominent, peaked P-waves in inferior leads).

[#2] consider features that are suggestive of RVH:

• 🔑 V1 with one of the following:
  • Tall R-wave (R>S, or R>6-7 mm) is the most specific feature but is insensitive. (Tall R-V1 has a relatively narrow differential diagnosis: 📖)
  • RSR' with R' >10 mm.
  • qR pattern.
• 🔑 V6 with a very prominent S-wave (S>R, or S>7 mm).
• 🔑 (R-V1 plus S-V5/6) >10.5 mm.
• 🔑 Stable imaging compared to prior (ECG, echo, and/or CT).

full discussion of potential findings in PE/RVH: five key points

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[#1/5] vertical axis

Lead I: 

• [#1] Prominent S-I ⚡️
  • A prominent S-wave in Lead I is often seen in PE or RVH.
  • This reflects the right-axis deviation of the terminal portion of the QRS complex.
  • This finding is supported if an S-wave in V6 is also seen.
• [#2] Lead I may become net negative (i.e., S>R), so the average axis points to the right.
• [#3] An entirely negative QRS complex in Lead I may occasionally be seen if the QRS axis points entirely to the right. Such profound right-axis deviation could suggest a combination of multiple processes shifting the axis to the right (e.g., lung hyperinflation plus right ventricular strain).

axis shift from baseline

• >+30 degree axis shift compared to prior ECG suggests acuity. (de Luna 2022)

SI-QIII-TIII (McGinn-White pattern)

• This was initially defined as requiring S-I and Q-III both >1.5 mm. This constellation of features combines terminal right-axis deviation (SI-QIII) with TWI in III.
• The SI-QIII-TIII pattern has a likelihood ratio of ~3.7 for PE. (19766353)
• Causes of this pattern include PE, RVH, and inferior MI. 📖

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[#2/5] horizontal axis & V1 

V1

• Tall R in V1 suggests RVH:
  • Often defined as R>S or R>6-7 mm.
  • Tall R-V1 is relatively specific for RVH, but it is insensitive.
  • Acute PE doesn't cause a tall R-wave in V1 (in the absence of RBBB or incomplete RBBB).
  • The differential diagnosis of tall R-V1 is relatively narrow (discussed above: ⚡️).
• RSR' in V1 (iRBBB) 📖
  • This may occur in either PE or RVH.
  • If R' is >10 mm, this may be more suggestive of RVH. (O'Keefe 2021)
  • rsR' is also associated with atrial septal defect (which causes more dilation than hypertrophy).
• qR, QR, or Qr in V1:
  • These patterns suggest RV dilation, which causes the septum to assume a D-shaped configuration that tilts away from V1.  🌊
  • A tall R-wave in V1 (qR or QR) suggests RVH, whereas a smaller R-wave (Qr) suggests PE.
  • Within the context of PE, Qr in V1 is a very poor prognostic sign (carrying a 4.7 odds ratio for mortality, as discussed below).
  • Other causes of qR in V1 include:
    • RBBB plus anteroseptal Q-wave MI.
    • Rarely may occur with LPFB (left posterior fascicular block).
    • Cardiac amyloidosis (possibly due to blunting of electrical signals from the left ventricle, causing the right ventricle to be electrically dominant). (38048086)

S-wave in V6

• Normally, there should be no S-wave in V6. RV dilation may shift the intraventricular septum so that leads V5-V6 are positioned over the septum (rather than the left ventricle). This clockwise shift causes delayed R-wave progression. 🌊
• A small/moderate S-wave in V6 may be seen in either PE or RVH.
• A large S-wave in V6 (e.g., >7 mm or S>R) suggests RVH.

(R-V1 + S-V5/6) >10.5 mm in RVH

• This might be the best single index for evaluating RVH (with a sensitivity of 70% and specificity of 85% in one series). (30475826)
• This is fundamentally an integration of a prominent R-wave in V1 and a prominent S-wave in V5/6 (features which are both discussed above).
• This may be falsely negative in patients with small QRS complexes.

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[#3/5] RAA

RAA in PE

• RAA may develop acutely due to pressure overload, with subsequent improvement following thrombolysis.
• Prominent Peaked P-waves in the inferior leads may be notable (even if they don't satisfy all criteria for RAA).

peaked P-wave in lead II in RVH

• Frontal plane:
  • Peaked P-wave in II may be more commonly seen. (18711612)
  • The P-wave axis may be right-deviated so that the P-wave is flattened in lead I. This may suggest the presence of emphysema. 
• P-wave in V1 may be biphasic, with a tall initial component >1.5 mm. (de Luna 2022)

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[#4/5] TWI and ST shifts in the right precordium +/- inferior leads

RVH: RV strain pattern can occur

• This refers to STD +/- TWI in V1-V4 (and, to a lesser degree, the inferior leads).
• Features that may suggest strain:
  • [1] If present, the combination of TWI in the right precordium and inferior leads suggests RV strain.
  • [2] STD has a gradual down-sloping, “strainy” morphology.
• Differential diagnosis: ST shifts can mimic a posterior or lateral OMI (see figure below).
• 💡 RV strain may be absent in a chronic, compensated RVH. (O'Keefe 2021)

PE: TWI +/- STE occurs in up to 50% of patients

• Distribution:
  • Most notably in the right precordial leads.
  • Inferior leads: (TWI in III) > (TWI in aVF).
  • The combination of TWI in right precordial and inferior leads is highly suggestive of PE (especially TWI in III and V1 and additional precordial leads).
• Morphology of acute RV strain pattern in right precordial leads:
  • There is often a small degree of convex STE.
  • TWI is typically deepest in V1-V2 (but not always).
  • TWI may be relatively broad with a splayed, roller-coaster pattern.
• Differential diagnosis:
  • [1] Right precordial TWI can mimic Wellens pattern: 📖
  • [2] STE in III with STD in aVL can mimic an inferior OMI (PE vs. IMI discussed further here: 📖).
  • [3] STE in III combined with diffuse subendocardial ischemia can mimic the Aslanger pattern.
• Chronicity: TWI in V1-V4 is the most persistent of all ECG abnormalities, lasting an average of 40 days.

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[#5/5] diffuse subendocardial ischemia pattern 📖

• This involves diffuse STD (often greatest in V4-V6) plus STE in aVR and V1.
• This pattern usually suggests a massive PE with secondary hypoperfusion of the left ventricle as a manifestation of global shock.

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differential diagnostic considerations

differential diagnosis: Secundum ASD

• ECG features: (33707907)
  • [1] RVH (often including an incomplete RBBB pattern).
  • [2] Crochetage sign: notching near the apex of the R-wave in inferior leads (figure below).
    • If present in all inferior leads, the specificity for ASD is high.
    • It correlates with the degree of shunting and the size of the ASD. Following ASD closure, this sign disappears in about a third of patients. (33707907)
• ASD is one of the most common congenital heart disorders diagnosed in adulthood. (33707907)

differential diagnosis: ARVC (arrhythmogenic RV cardiomyopathy) 📖

• ARVC may mimic RVH, with the following findings:
  • Relatively tall R-wave in V1 (R>S).
  • Right axis deviation, with S>R in Lead I.
  • S-wave present in V6.
  • TWI in right precordial leads +/- inferior leads.
• ARVC is incredibly rare, so statistically speaking, these features will usually reflect RVH.
• Clues to the diagnosis of ARVC may include:
  • Although R>S in V1, the absolute size of the R-wave in V1 is small (less than would be expected in RVH).
  • An epsilon wave may be helpful (if seen).

related algorithms & differentials

• ECG findings:
  • Prominent S-I 📖
  • Tall R-V1 📖
  • STD 📖
  • RSR' in V1 📖
  • Diffuse STD & STE in aVR 📖
  • Right precordial STE 📖
• Diagnostic algorithms:
  • Inferior MI vs. PE 📖
  • Lateral OMI 📖
  • Posterior OMI 📖

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ECG for risk stratification in PE

predictors of mortality

• OR 4.7: Qr in V1.
• OR 4.3: STE in V1.
• OR 3.9: Complete RBBB.
• OR 3.4: SI-Q3-T3.
• OR 3.2: Right axis deviation.
• OR 3.1: STE in III.
• OR 2.5: STD in V4-V6 (subendocardial ischemia).
• OR 2.0: Atrial fibrillation.
• OR 1.6: TWI in precordial/inferior leads. (28628222)
• (For comparison, a positive troponin has an OR of  ~4.3). (31476570)

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biventricular hypertrophy

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💡 Consider BiV hypertrophy when there are signs of both right and left-sided chamber enlargement (e.g., RAA plus LVH).

RVH is suggested by:

• [1] Right atrial abnormality or biatrial abnormality.
• [2] A tall R-wave in V1 helps suggest RVH.
  • 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 right precordial leads.
• [4] Vertical or right-ward axis (prominent terminal S-wave in lead I).
  • Normally, LVH would cause left axis deviation.
  • A vertical axis (~90 degrees) or frank RAD may suggest BiV hypertrophy.

LVH is suggested by:

• [1] Left atrial abnormality or biatrial abnormality.
• [2] Standard voltage criteria may be met:
  • R-aVL >11 mm
  • Cornell: R-aVL + SV3 >20♀/28♂
  • Sokolow-Lyon: SV1/2 + RV5/6 >35 (or >40 if under 30YO).
  • Peguero-Lo Presti: (Deepest precordial S) + (SV4) >23♀/28♂
• [3] Katz-Wachtel phenomenon suggests biventricular hypertrophy:
  • Huge (>~50 mm) biphasic (R~S) QRS amplitude in V2-V4.
• [4] LV strain pattern.

differential diagnosis of biventricular hypertrophy

• Hypertrophic cardiomyopathy: 📖
  • HCM may cause tall R-waves in V1 that mimic RVH.
  • HCM can cause biatrial abnormality.

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lung hyperinflation pattern

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key features of lung hyperinflation pattern

• 🔑 Prominent P-waves in inferior leads (often with relatively small QRS complexes).
• 🔑 Lead-I sign (low voltage in lead I). ⚡️
• 🔑 Low voltage in the lateral precordial leads (sometimes with shrinkage of QRS voltage in V4->V5->V6).
• 🔑 Slow R-wave progression in V1-V3.
• Diagnosis of exclusion:
  • ⚠️ No unexplained features suggest PE/RVH (e.g., right precordial TWI, RBBB, tall R-V1). 📖
  • ⚠️ Findings aren't better explained by DCM 📖 (which may cause low limb lead voltages and poor R-wave progression).

related differential diagnoses

• Prominent S-I. ⚡️
• P-pulmonale. 📖
• Poor R-wave progression. 📖
• Low voltage in left precordial leads (V4-V6). 📖
• Low voltage in Lead I. ⚡️

basics concept of lung hyperinflation pattern

• This set of ECG findings seems to relate to patients with hyperinflated lungs, leading to vertical heart positioning with dextrorotation in the horizontal axis. (This pattern doesn't necessarily indicate the presence of RA dilation, RV hypertrophy, or pulmonary hypertension.)
• Causes include:
  • [1] Emphysema or asthma.
  • [2] Tall, thin people with a vertical heart configuration.
  • [3] Left-sided pneumothorax.
  • [4] Right-sided pneumothorax (may cause P-pulmonale and Lead-I signs, without affecting precordial leads as much as left-sided pneumothorax). (33757495)
• ⚠️ The NEW appearance of a lung hyperinflation pattern suggests either dynamic hyperinflation (due to acute exacerbation of COPD or asthma) or the development of pneumothorax.
  • 💡 Inferior P-wave amplitude may increase during COPD exacerbations, with subsequent reduction as patients improve! (12907543) 

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full description of ECG findings in the lung hyperinflation pattern 

P-wave axis >70 degrees

• Prominent P-waves in inferior leads (“P-mitrale” 📖).
  • ⚠️ Prominent P-waves may lead to atrial repolarization abnormalities that mimic ST deviation.
• Negative P-wave in aVL.

frontal QRS axis shifts towards vertical (+90)

• Low QRS voltage in Lead I (“Lead I sign”) – differential of this finding is below 👇
• Q-waves may occur in I and aVL (due to rightward axis shift).

poor R-wave progression

• This reflects the clockwise rotation of the heart.
• QS complexes may occur in V1-V3 (mimicking Q-waves; may be more prominent with tachycardia).
• Persistent S-waves may be seen in V6 and lead I.

low lateral precordial voltages

• The heart loses contact with the left precordium.
• Low voltages often occur in V4-V6. 🌊
• Other causes of low voltage in V4-V6 are discussed here: 📖

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left-sided pneumothorax

• More common:
  • Right-axis deviation (may reduce the voltage in Lead I).
  • Reduced precordial QRS amplitude, especially in lateral leads (may mimic prior anterior MI).
• Less common:
  • Symmetric T-wave inversion can occur.
  • PR depression can occur.
  • Rarely, STE in the inferior leads with reciprocal STD in I, aVL, and aVR that may mimic an inferior MI. (de Luna 2022)

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Lead I sign (low voltage in Lead I), aka Schamroth's sign

definition of Lead I sign

• [1] Lead I is nearly isoelectric (P, QRS, and T are all <2 mm in size).
• [2] This isn't simply due to the low voltage of the entire ECG. 📖

causes of Lead I sign

• Pulmonary hyperinflation (discussed above).
• Reverse Takotsubo Cardiomyopathy. 📖
• Lead misplacement (bilateral arm-leg reversal). 📖
  • 🔑 Precordial leads should be normal.
  • 🔑 Lead I is completely flat.

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S1S2S3 pattern

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definition

• Some authors define this as any S-waves in leads I, II, and III. However, this definition is frequently encountered, nonspecific, and clinically less helpful. (35839706)
• A true S1S2S3 pattern is probably best defined as S≧R in leads I, II, and III (this definition will be used for the rest of this section). (34505077)  This is exceedingly uncommon among normal people. (Chou 2008)

causes of true S1S2S3 pattern include:

• RVH (right ventricular hypertrophy).
• Emphysema.
• Incomplete RBBB (in some healthy people, S1S2S3 might occur with an RSR' in V1 – reflective of conduction delay rather than right ventricular hypertrophy). (Chou 2008)

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questions & discussion

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