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Electrocardiography

Chapter 247 | Part 6: Disorders of the Cardiovascular System · Part 6 – Cardiovascular Disorders · Chapter 247

Key Clinical Points

  1. The ECG records depolarization and repolarization electrical activity from the atrial and ventricular myocardium.
  2. Normal QRS axis ranges from -30° to +100°; values < -30° indicate left axis deviation; > +90° indicate right axis deviation.
  3. Left ventricular hypertrophy (LVH) criteria: Sv1 + (Rv5 or Rv6) > 35 mm; RaVL + Sv3 > 20 mm (women) or > 28 mm (men).
  4. Hyperkalemia progression: T-wave peaking → QRS widening → P-wave diminution → sine-wave pattern → asystole.
  5. Wellens' T wave sign: Deep, symmetric T-wave inversions in V1–V6 indicating high-grade LAD stenosis.
  6. Osborn waves (J point elevation) are a specific finding in systemic hypothermia.
  7. Cardiac tamponade triad: Sinus tachycardia, low QRS voltage, and electrical alternans.
  8. A normal ECG throughout an acute infarct is rare; persistent chest pain without changes requires investigation of non-coronary causes.
  9. Primary repolarization abnormalities (e.g., ischemia, electrolyte issues) are independent of QRS changes, unlike secondary ones seen in bundle branch blocks.
  10. ST-segment elevation indicates transmural injury and is a primary indicator for emergency reperfusion therapy.

DEFINITION & OVERVIEW

• Definition (Harrison's 22e): An electrocardiogram (ECG or EKG) is a graphical representation of electrical activity generated by the heart. • Mechanism: Signals are detected via metallic electrodes on extremities and chest wall, then amplified/recorded. • Utility: Noninvasive, inexpensive, and versatile tool for detecting arrhythmias, conduction disturbances, and myocardial ischemia/infarction. • Additional Findings: Can reveal metabolic disturbances, drug toxicities, and risk of sudden cardiac arrest.

ETIOLOGY & PATHOPHYSIOLOGY

• Source of Activity: Electrical currents from pacemaker cells, specialized conduction tissue, and heart muscle. • Conduction Pathway: SA node → Atria → AV junction → His bundle → Bundle branches (Right/Left) → Purkinje fibers → Ventricular myocardium. • Waveform Correlation: - Phase 0 (rapid upstroke) → QRS onset - Phase 2 (plateau) → ST segment - Phase 3 (active repolarization) → T wave • Factors Influencing Intervals: - Reduced Na+ influx (e.g., hyperkalemia, flecainide) → increased QRS duration. - Prolonged phase 2 or 3 (e.g., amiodarone, hypocalcemia) → increased QT interval. - Shortened repolarization (e.g., hypercalcemia, digoxin) → abbreviated QT.

CLINICAL FEATURES

Atrial and Ventricular Morphology

• Atrial Findings: - Right atrial overload → P-pulmonale (P wave ≥ 2.5 mm in lead II). - Left atrial abnormality → P-mitrale (biphasic/notched P wave in lead II; notched appearance in V1). • Ventricular Morphology: - R-wave progression: Increase in R-amplitude and decrease in S-amplitude from right to left. - Transition zone: Point where R ≈ S (typically V3 or V4). • QRS Axis: - Normal: -30° to +100° - Left axis deviation (< -30°) → LVH, left anterior fascicular block, or inferior MI. - Right axis deviation (> +90° to +100°) → RV overload, RBBB, dextrocardia, or left posterior fascicular block. • U-wave: - Normal: Small (≤ 1 mm) following T wave. - Abnormal increase → hypokalemia or drugs (dofetilide, amiodarone, sotalol, quinidine). - Large U waves → marker of risk for torsades de pointes.

Cardiac Enlargement and Hypertrophy

• Right Ventricular Hypertrophy (RVH): - Tall R wave in V1 (R ≥ S) or qR pattern in V1/V2. - Associated with ST depression and T-wave inversion in right to mid-precordial leads. - Note: Chronic cor pulmonale often shows diminished R waves (slow progression) due to emphysema/diaphragm displacement. • Left Ventricular Hypertrophy (LVH): - High risk for sudden cardiac death. - Repolarization abnormalities (ST depression, T-wave inversion) in leads with prominent R waves. - Table 1: Voltage Criteria for LVH - Sv1 + (Rv5 or Rv6) > 35 mm - RaVL + Sv3 > 20 mm (women); > 28 mm (men) - Note: Sensitivity decreases in older adults, obese patients, and those with RBBB.

• Conduction Delays: - Complete block → QRS ≥ 120 ms. - Incomplete block → QRS 110–120 ms. • Right Bundle Branch Block (RBBB): - Terminus: Right and anterior → rSR' in V1. • Left Bundle Branch Block (LBBB): - Terminus: Left and posterior → QS in V1; R in V6. - Marker of high risk: Coronary heart disease, hypertensive heart disease, aortic valve disease, or cardiomyopathy. • Repolarization Dynamics: - Secondary changes: T wave opposite to last QRS deflection (seen in BBB). - Primary changes: Independent of QRS; caused by ischemia, electrolyte imbalance, or digoxin. • Fascicular Blocks: - Left anterior → axis more negative than -45°. - Left posterior → axis more rightward than +110° (rare as isolated finding). • Other Patterns: - Brugada: RBBB-like morphology with ST elevation in V1–V2. - Preexcitation: WPW patterns (prolonged QRS without conduction delay).

DIFFERENTIAL DIAGNOSIS

ST-Segment Elevations

• General Principles: - Normal ECG during acute infarct is rare. - Ischemia masked by LBBB, pacemaker patterns, or WPW. - Overdiagnosis risk: ST elevation/T-wave inversion can occur in pericarditis, LVH, or as normal variants. • Table 2: Differential Diagnosis of ST-Segment Elevations - Myocardial ischemia/infarction (Atherosclerotic or nonatherosclerotic like Takotsubo). - Acute pericarditis. - Normal variants (e.g., benign early repolarization). - LVH / LBBB (typically V1–V3). - Acute pulmonary embolism. - Brugada patterns. - Class 1C antiarrhythmic drugs. - DC cardioversion (transient). - Hypercalcemia/Hyperkalemia (usually V1–V3). - Hypothermia (J [Osborn] waves). - Myocarditis syndromes. - Tumor invading left ventricle. - Trauma to ventricles.

INVESTIGATIONS & DIAGNOSIS

  1. Initial Screening → 12-lead ECG to assess heart rate, rhythm, and QRS axis (Normal: -30° to +100°).
  2. Conduction Analysis → Measure QRS duration (≥ 120 ms for complete BBB) and identify specific patterns (e.g., rSR' in V1 for RBBB; QS in V1/R in V6 for LBBB).
  3. Repolarization Evaluation → Assess ST-segment, T-wave morphology, and QT interval to differentiate primary vs. secondary changes.
  4. Clinical Correlation → Identify specific syndromes based on morphology (e.g., Wellens' sign for LAD stenosis; 'peaked' T waves for hyperkalemia; Osborn waves for hypothermia).

MANAGEMENT & TREATMENT

  1. Acute Ischemia Management → Identify ST-segment elevation (transmural injury) → initiate emergency reperfusion therapy (minutes to hours).
  2. Metabolic/Electrolyte Emergency → Identify hyperkalemia (peaked T, QRS widening) or hypocalcemia (prolonged QT) → immediate electrolyte correction.
  3. Structural Identification → Recognize pericardial effusion with tamponade (triad: tachycardia, low voltage, electrical alternans) → prompt clinical intervention.

KEY PEARLS & HIGH-YIELD POINTS

• Wellens' Syndrome: Deep T-wave inversions in V1–V6 without ST elevation indicate high-grade LAD stenosis. • Hyperkalemia Sequence: Peaked T → QRS widening → P-wave loss → Sine wave. • Calcium Effects: Hypocalcemia prolongs QT; Hypercalcemia shortes QT. • Tamponade Triad: Sinus tachycardia + Low voltage + Electrical alternans. • Osborn Wave: Convex J-point elevation in hypothermia.

Reference Tables

TABLE 247-1 Differential Diagnosis of ST-Segment Elevations Myocardial ischemia/infarction

Harrison's 22e, p.1874

  • Myocardial ischemia/infarction
    Noninfarction transmural ischemia (e.g., Prinzmetal’s syndrome)
    Acute myocardial infarction
    Due to atherosclerotic coronary occlusion
    Due to nonatherosclerotic causes (e.g., takotsubo syndrome, co
    dissection)
    Post-myocardial infarction (left ventricular motion abnormality/ane
    Acute pericarditis
    Normal variants (including benign “early repolarization” patterns)
    Left ventricular hypertrophy/left bundle branch blocka
    Other (rarer)
    Acute pulmonary embolisma
    Brugada patterns (right bundle branch block–like morphology with
    elevations in right precordial leads)
    Class 1C antiarrhythmic drugsa
    DC cardioversion (transient)
    Hypercalcemiaa
    Hyperkalemiaa
    Hypothermia (J [Osborn] waves)
    Nonischemic myocardial injury
    Myocarditis syndromes (infectious and noninfectious)
    Tumor invading left ventricle
    Trauma to ventricles