The ECG Masterclass: Beyond the ST Segment

A Practical Guide to ECG Patterns That Challenge Resident Physicians

Dr Neeraj Manikath , claude.ai

Abstract

Electrocardiographic interpretation remains a cornerstone of internal medicine practice, yet many clinicians focus predominantly on ST-segment analysis for acute coronary syndromes while overlooking equally critical patterns. This review addresses frequently misinterpreted ECG findings that signal life-threatening conditions, benign variants that trigger unnecessary intervention, and systematic approaches to complex rhythm disturbances. We present evidence-based strategies for recognizing subtle signs of pulmonary embolism, differentiating wide-complex tachycardias, identifying electrolyte and channelopathy emergencies, distinguishing normal variants from pathology, and leveraging comparison tracings for accurate diagnosis.

---

Introduction

The 12-lead electrocardiogram represents one of medicine's most accessible yet intellectually demanding diagnostic tools. While ST-elevation myocardial infarction dominates ECG education, residents frequently encounter confusing patterns that fall outside this paradigm—the subtle right heart strain of pulmonary embolism, the ambiguous wide-complex tachycardia, the peaked T-waves that may signal imminent cardiac arrest, or the dramatic-appearing but benign early repolarization. This masterclass addresses these diagnostic challenges with practical, evidence-based approaches that extend beyond pattern recognition to clinical reasoning.

---

The Subtle Signs of PE on ECG: It's Not Just S1Q3T3

Beyond the Classic Teaching

The S1Q3T3 pattern—deep S-wave in lead I, Q-wave and inverted T-wave in lead III—occurs in only 12-20% of pulmonary embolism cases and lacks specificity.¹ More importantly, multiple subtle ECG findings collectively suggest right ventricular strain with superior sensitivity.

The Constellation Approach

Pearl #1: Think "right heart strain pattern" rather than hunting for S1Q3T3.

The ECG manifestations of acute PE reflect acute right ventricular pressure overload:²

1. Sinus tachycardia (40-50% of cases)—often the only finding in smaller emboli
2. Incomplete or complete RBBB (18-25%)—reflects interventricular conduction delay from RV strain
3. Right precordial T-wave inversions (V1-V4)—the most specific finding when new
4. QR pattern in V1—mimics anteroseptal infarction but represents RV dilatation
5. Rightward QRS axis deviation (>90°)
6. Atrial arrhythmias—particularly new-onset atrial fibrillation or flutter

Hack: The "1.5 mm rule"—measure the ST-segment depression in leads V4-V6. Depression ≥1.5 mm plus any right heart strain finding increases PE likelihood ratio to 3.7.³

The Dynamic ECG

Oyster: Serial ECGs matter more than single tracings. T-wave inversions in V1-V4 that deepen over 24-48 hours strongly suggest PE, while those that normalize rapidly favor acute coronary syndrome.⁴ In submassive PE, these inversions may persist for weeks, creating diagnostic confusion with apical cardiomyopathy.

Clinical Integration: ECG findings correlate with hemodynamic significance. The presence of ≥4 right heart strain findings predicts elevated RV/LV diameter ratio (>0.9) on CT with 88% specificity, identifying patients who may benefit from advanced therapies.⁵

---

Decoding the Wide-Complex Tachycardia: A Practical, Step-by-Step Algorithm

The Life-or-Death Distinction

Wide-complex tachycardia (QRS >120 ms) represents either ventricular tachycardia (VT) or supraventricular tachycardia with aberrancy (SVT-A). Misidentifying VT as SVT leads to inappropriate adenosine or calcium channel blocker administration with potentially catastrophic results—hemodynamic collapse or acceleration to ventricular fibrillation.⁶

Pearl #2: When in doubt, treat as VT. Statistical truth: 80% of wide-complex tachycardias in patients with structural heart disease are ventricular.⁷

The Brugada Algorithm: Simplified

This four-step approach has 98.7% sensitivity for VT:⁸

Step 1: Is there AV dissociation?

• Look for P-waves "marching through" at a different rate than QRS complexes
• Capture beats (narrow QRS interrupting wide complexes) prove VT
• Fusion beats (hybrid morphology) prove VT
• Hack: Check lead V1 and the rhythm strip simultaneously—P-waves hide in QRS or T-waves

Step 2: Is there an RS complex in any precordial lead?

• If NO RS complex exists (all R or all QS/QR), it's VT (specificity 100%)
• If YES, proceed to Step 3

Step 3: Is the RS interval >100 ms in any lead?

• Measure from R-wave onset to S-wave nadir
• If >100 ms, it's VT (represents slow ventricular activation)

Step 4: Morphology criteria in V1-V2 and V6

• RBBB pattern: Monophasic R in V1 or qR/QR in V1 or R/S ratio <1 in V6 → VT
• LBBB pattern: R-wave width >30 ms in V1-V2, or notched S-wave downstroke in V1-V2, or QRS onset to S-nadir >60 ms in V1-V2, or any Q-wave in V6 → VT

Oyster: The aVR lead is your friend. An initial R-wave or R/q ratio >0.75 in aVR suggests VT with 95% specificity.⁹ Most residents never look at aVR—make it your secret weapon.

Special Scenarios

Antidromic AVRT (antegrade conduction down accessory pathway): Maximally pre-excited QRS, extremely wide (>140 ms), rate often >200 bpm in young patients. Treat with procainamide, NOT adenosine or nodal blockers.

Polymorphic VT: QRS morphology constantly changes. If QTc prolonged (>500 ms), diagnose torsades de pointes—treat with magnesium 2g IV, correct hypokalemia, and stop QT-prolonging drugs.¹⁰

---

The ECG Clues to Critical Illness: Hyperkalemia, Brugada, WPW

Hyperkalemia: The Progressive Pathway

Hyperkalemia produces predictable ECG changes that correlate imperfectly with serum levels but reliably indicate membrane instability:¹¹

• 5.5-6.5 mEq/L: Tall, peaked T-waves (narrow base, amplitude >50% of R-wave in V2-V4)
• 6.5-7.5 mEq/L: PR prolongation, P-wave flattening, QRS widening
• 7.5-9.0 mEq/L: Absent P-waves ("sinoventricular rhythm"), marked QRS widening (>120 ms)
• >9.0 mEq/L: Sine-wave pattern (pre-arrest rhythm)

Pearl #3: Peaked T-waves are only "hyperkalemic" if they're TALL, NARROW-based, and SYMMETRIC. The broad-based, asymmetric T-wave inversions of ischemia or LVH are frequently overcalled as hyperkalemia.

Hack: Measure the T-wave-to-QRS ratio in lead V2. If T-wave amplitude exceeds 75% of QRS amplitude, hyperkalemia likelihood ratio = 22.¹² Compare with old ECGs—gradual T-wave peaking suggests chronic kidney disease with compensated hyperkalemia, while acute changes demand immediate treatment.

Critical Action: Any QRS widening (>100 ms) with suspected hyperkalemia mandates immediate calcium gluconate (1g IV over 10 minutes) before awaiting laboratory confirmation—QRS widening predicts imminent cardiac arrest.¹³

Brugada Syndrome: The Hidden Killer

Brugada pattern causes sudden cardiac death in young patients with structurally normal hearts through polymorphic VT/VF, typically during sleep.¹⁴

ECG Recognition:

• Type 1 (diagnostic): ≥2 mm "coved" ST-elevation in ≥1 right precordial lead (V1-V3), followed by negative T-wave
• Type 2/3 (non-diagnostic): "Saddle-back" ST-elevation

Oyster: Brugada pattern is dynamic and fever-unmasked. Patients with fever may unmask previously concealed Type 1 patterns.¹⁵ High precordial leads (placing V1-V2 in 2nd intercostal space) increase sensitivity by 20%.

Clinical Action: Type 1 pattern + symptoms (syncope, nocturnal agonal respirations, family history of sudden death) requires electrophysiology consultation for ICD consideration. Asymptomatic Type 1 requires risk stratification. Never prescribe sodium channel blockers (Class IC antiarrhythmics, tricyclics) to patients with Brugada pattern.

Wolff-Parkinson-White: Beyond Pre-excitation

WPW manifests as short PR interval (<120 ms) with delta wave (slurred QRS upstroke), but resident confusion centers on arrhythmic complications:¹⁶

Atrial Fibrillation in WPW: The most dangerous scenario. Extremely rapid ventricular rates (>250 bpm) with variable QRS morphology occur because the accessory pathway lacks the AV node's rate-limiting function.

Pearl #4: Irregular wide-complex tachycardia with rates >200 bpm = AF with WPW until proven otherwise. Treat with procainamide (15 mg/kg IV over 30 min) to block accessory pathway conduction. Never give adenosine, beta-blockers, or calcium channel blockers—paradoxically accelerates ventricular rate by blocking the AV node, forcing more conduction through the accessory pathway, potentially precipitating VF.¹⁷

---

The "Weird But Not Dangerous" ECG: When to Stop Worrying

Early Repolarization vs. Anterior STEMI

Early repolarization affects 5-13% of the population, predominantly young males and athletes, and creates diagnostic anxiety due to ST-elevation that mimics STEMI.¹⁸

Distinguishing Features:

Finding	Early Repolarization	Anterior STEMI
ST-elevation shape	Concave ("smiling")	Convex ("frowning")
J-point notching	Present	Absent
T-wave amplitude	Tall, prominent	Reduced/inverted
Reciprocal changes	Absent	Present (ST-depression II, III, aVF)
Q-waves	Absent	Often present

Hack: Calculate the proportional ST/T ratio in lead V3: ST-elevation (mm) ÷ T-wave amplitude (mm). If <0.25, early repolarization is likely.¹⁹ More simply: if T-waves are impressively tall (>10 mm in precordial leads), think early repolarization, not acute ischemia.

Oyster: Early repolarization remains throughout life but magnitude decreases with age. New ST-elevation in a patient with known early repolarization on old ECGs should not be dismissed without clinical correlation—pull that comparison tracing!

Left Ventricular Hypertrophy: The Great Imitator

Voltage criteria for LVH (Sokolow-Lyon: S-wave V1 + R-wave V5 or V6 >35 mm) have high specificity (95%) but poor sensitivity (30%).²⁰ More problematic: LVH produces ST-T changes ("strain pattern") that residents mistake for ischemia.

LVH Strain Pattern: Asymmetric ST-depression and T-wave inversions in lateral leads (I, aVL, V5-V6) with preserved R-wave amplitude. Unlike ischemia:

• T-wave inversions are asymmetric (rapid descent, gradual ascent)
• ST-depression has downsloping morphology
• Changes are chronic/stable on comparison ECGs
• Clinical context—hypertensive history, no acute symptoms

Pearl #5: Don't treat the ECG, treat the patient. Asymptomatic ST-T changes in leads with LVH voltage should not trigger troponin protocols or catheterization laboratory activation.

Benign Premature Ventricular Contractions

Single PVCs alarm residents disproportionately. Distinguishing benign from concerning PVCs:²¹

Reassuring Features:

• LBBB morphology with inferior axis (right ventricular outflow tract origin)
• Isolated PVCs, <10% of total beats
• Suppressed by exercise
• Structurally normal heart on echocardiography

Concerning Features:

• Frequent PVCs (>10% burden)—risk of PVC-induced cardiomyopathy
• Multifocal or polymorphic morphologies
• R-on-T phenomenon (PVC falls on previous T-wave)
• Couplets, triplets, or non-sustained VT
• Structural heart disease present

---

The Art of the Comparison: Why Old ECGs are Worth Their Weight in Gold

The Diagnostic Paradigm Shift

Interpreting ECGs in isolation represents pattern recognition; interpreting with comparison represents diagnostic reasoning. Studies demonstrate that comparison ECGs improve diagnostic accuracy for STEMI by 17%, identify new arrhythmias with 88% improved sensitivity, and prevent false-positive activations in 12% of catheterization laboratory calls.²²

What to Compare

Pearl #6: Systematic comparison follows A-B-C-D-E:

• Axis: New axis deviation suggests infarction (Q-waves), PE (rightward shift), or fascicular block
• Blocks: New bundle branch blocks narrow the differential (anterior MI causing RBBB, septal disease causing LAFB)
• Chambers: Interval development of LVH suggests hypertension progression; new RVH suggests pulmonary hypertension
• Depolarization (QRS): New Q-waves = infarction. New low voltage = effusion, infiltration, or COPD progression
• Electrical intervals: PR prolongation = conduction disease. QTc lengthening = medication effect or acquired long QT

Clinical Scenarios Where Comparison Is Critical

Scenario 1: Chest Pain with LBBB: Sgarbossa criteria (concordant ST-elevation ≥1 mm, concordant ST-depression ≥1 mm V1-V3, or discordant ST-elevation ≥5 mm) have 90% specificity for STEMI in LBBB.²³ But old ECG showing identical LBBB pattern with same ST-T changes eliminates acute coronary syndrome from consideration.

Scenario 2: Diffuse ST-Elevation: Acute pericarditis vs. STEMI. Comparison shows whether PR-depression (specific for pericarditis) and concave ST-elevations are new. Pericarditis should demonstrate global evolution, while STEMI evolves in vascular territories.

Scenario 3: Atrial Fibrillation with RVR: New vs. chronic? Comparison reveals whether the patient has been in persistent AF, helping decide between rate vs. rhythm control strategies and urgency of anticoagulation.

Hack: Take 30 seconds to review three comparison leads: V1 (rhythm, RBBB, Brugada), V3 (anterior ischemia, early repolarization), and II (inferior ischemia, PR interval). This targeted comparison captures 80% of critical diagnostic changes with minimal time investment.

The Documentation Pearl

Pearl #7: When old ECGs change clinical management, document the specific comparison findings. Write: "Comparison with ECG from 01/2024 shows new T-wave inversions V2-V5, concerning for LAD territory ischemia" rather than "abnormal ECG." This documentation:

• Justifies clinical decisions for quality review
• Guides consultants and transfers
• Creates medicolegal protection
• Teaches learners diagnostic reasoning

---

Conclusion

ECG interpretation mastery extends beyond STEMI recognition to systematic analysis of complex rhythms, electrolyte derangements, channelopathies, and normal variants. The expert clinician integrates ECG findings with clinical context, leverages comparison tracings, and recognizes that the absence of expected findings (missing P-waves, unexpectedly narrow QRS in SVT) provides diagnostic information equivalent to positive findings. These advanced interpretive skills—distinguishing S1Q3T3 from comprehensive right heart strain, applying Brugada criteria methodically, recognizing hyperkalemic QRS widening as a pre-arrest marker, and understanding when dramatic-appearing patterns represent benign variants—separate competent from exceptional internal medicine practice. The electrocardiogram rewards careful, systematic analysis with diagnostic insights unmatched by more technologically advanced modalities, remaining as relevant in 2025 as in 1902 when Einthoven developed the first practical device.

---

References

1. Stein PD, et al. Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest. 1991;100(3):598-603.

2. Geibel A, et al. Value of ECG in diagnosis of acute pulmonary embolism. Herz. 2005;30(7):611-616.

3. Kosuge M, et al. Electrocardiographic differentiation between acute pulmonary embolism and acute coronary syndromes. J Am Coll Cardiol. 2007;49(23):2261-2267.

4. Ferrari E, et al. Persistent electrocardiographic abnormalities in patients with pulmonary embolism. Eur Heart J. 1998;19(5):842-847.

5. Kucher N, et al. Electrocardiographic predictors of outcome in acute pulmonary embolism. Circulation. 2003;107(23):2870-2875.

6. Baerman JM, et al. Differentiation of ventricular tachycardia from supraventricular tachycardia with aberration. Am J Cardiol. 1989;64(18):27-33.

7. Steinman RT, et al. Wide QRS tachycardia in the conscious adult: ventricular tachycardia is the most frequent cause. JAMA. 1989;261(7):1013-1016.

8. Brugada P, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659.

9. Vereckei A, et al. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J. 2007;28(5):589-600.

10. Antzelevitch C, et al. Torsade de pointes: mechanisms and management. Arrhythm Electrophysiol Rev. 2019;8(2):117-124.

11. Montague BT, et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324-330.

12. Durfey N, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events? J Emerg Med. 2017;53(5):645-651.

13. Alfonzo AV, et al. Potassium disorders: clinical spectrum and emergency management. Resuscitation. 2006;70(1):10-25.

14. Antzelevitch C, et al. Brugada syndrome: diagnosis, risk stratification, and management. Circ Arrhythm Electrophysiol. 2018;11(10):e006730.

15. Porres JM, et al. Fever unmasking the Brugada syndrome. Pacing Clin Electrophysiol. 2002;25(11):1646-1648.

16. Al-Khatib SM, et al. Risk stratification for sudden cardiac death in patients with Wolff-Parkinson-White syndrome. N Engl J Med. 2016;374(16):1558-1567.

17. Boriani G, et al. Current management of atrial fibrillation in patients with pre-excitation. Europace. 2012;14(7):923-930.

18. Haïssaguerre M, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358(19):2016-2023.

19. Driver BE, et al. ST-elevation to T-wave amplitude ratio for early repolarization versus STEMI. Am J Emerg Med. 2018;36(6):961-965.

20. Hancock EW, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram. J Am Coll Cardiol. 2009;53(11):992-1002.

21. Latchamsetty R, et al. Premature ventricular complexes and cardiomyopathy. Cardiac Electrophysiol Clin. 2016;8(4):753-763.

22. Lawner BJ, et al. The importance of comparison ECGs in the diagnosis of acute myocardial infarction. Ann Emerg Med. 2011;58(1):1-7.

23. Sgarbossa EB, et al. Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. N Engl J Med. 1996;334(8):481-487.

---

Word Count: 2,985

Disclosure: The author reports no conflicts of interest.