Electrocardiography¶
Chapter 247 | Part 6: Disorders of the Cardiovascular System
KEY CLINICAL POINTS¶
- ECG records electrical activity of the heart, with P wave (atrial depolarization), QRS complex (ventricular depolarization), and T wave (ventricular repolarization).
- 12 leads (6 limb + 6 chest) provide spatial orientation of cardiac electrical activity; QRS axis determines ventricular depolarization direction.
- Abnormalities include bundle branch blocks, myocardial ischemia/infarction, electrolyte disturbances (e.g., hyperkalemia/hypokalemia), and drug effects (e.g., class 1A/III antiarrhythmics).
- QT interval varies inversely with heart rate; corrected QT (QTc) formulas (e.g., Framingham) are used to assess for prolonged repolarization.
- ECG is critical for diagnosing arrhythmias, ischemia, infarction, and monitoring drug/toxin effects.
1. DEFINITION & OVERVIEW¶
An electrocardiogram (ECG) is a graphical representation of the heart's electrical activity, recorded via electrodes on the extremities and chest. It captures depolarization (P wave, QRS complex) and repolarization (T wave) processes. The ECG is a noninvasive, rapid tool for diagnosing arrhythmias, conduction disturbances, myocardial ischemia/infarction, and metabolic disturbances.
Table 247-1: Differential Diagnosis of ST-Segment Elevations¶
| Differential Diagnosis | Key Features |
|---|---|
| Myocardial ischemia/infarction | ST elevation, Q waves, reciprocal changes |
| Acute pericarditis | Diffuse ST elevation, PR depression, T-wave inversion |
| Brugada syndrome | Right precordial ST elevation, coved T waves |
| Hyperkalemia | Peaked T waves, widened QRS, sine-wave pattern |
| Early repolarization | Benign ST elevation, no reciprocal changes |
| Left ventricular hypertrophy | Left axis deviation, tall R waves in V5–V6 |
| Pulmonary embolism | Sudden onset, right axis deviation, SnQnTn pattern |
1.1 Basic ECG Waveforms and Intervals¶
The ECG waveform includes the P wave (atrial depolarization), QRS complex (ventricular depolarization), and ST-T-U complex (ventricular repolarization). Key intervals include PR (atrioventricular delay), QRS (ventricular depolarization duration), and QT (ventricular repolarization duration). The RR interval reflects heart rate.
1.2 ECG Leads and Orientation¶
The 12-lead ECG includes limb leads (I, II, III, aVR, aVL, aVF) and chest leads (V1–V6). Limb leads assess frontal plane activity, while chest leads evaluate horizontal plane. The hexaxial diagram defines lead orientations, with the mean QRS axis measured relative to lead I.
2. ETIOLOGY & PATHOPHYSIOLOGY¶
The heart's electrical activity originates in the sinoatrial node, propagates through the atrioventricular node and bundle of His, and spreads via Purkinje fibers. Depolarization and repolarization generate vectors that form the ECG. Abnormalities arise from conduction delays (e.g., bundle branch blocks), myocardial ischemia, electrolyte imbalances, or drug effects.
2.1 Conduction System Abnormalities¶
Right bundle branch block (RBBB) shows rSR ′ in V1 and qRS in V6; left bundle branch block (LBBB) demonstrates wide, predominantly negative QRS in V1 and positive in V6. These alter the QRS vector and repolarization patterns.
2.2 Repolarization Abnormalities¶
ST-T changes reflect repolarization disturbances. Hyperkalemia causes peaked T waves, widened QRS, and sine-wave patterns. Hypokalemia leads to prominent U waves and prolonged QT. Drugs like amiodarone and digoxin affect repolarization duration.
3. CLINICAL FEATURES¶
ECG findings correlate with clinical conditions: ST elevation indicates acute myocardial infarction, T-wave inversions suggest ischemia or infarction, and Q waves may denote prior infarction. P-wave abnormalities (e.g., peaked P waves in hyperkalemia) reflect atrial depolarization changes.
3.1 Myocardial Ischemia/Infarction¶
Acute ischemia causes ST elevation (transmural) or depression (subendocardial). Infarction may show Q waves, T-wave inversions, and reciprocal changes. Wellens' sign (T-wave inversions in V1–V4) indicates critical left anterior descending artery stenosis.
3.2 Bundle Branch Blocks¶
RBBB: rSR ′ in V1, qRS in V6; LBBB: wide QRS with negative V1 and positive V6. These patterns may mimic ischemia but are distinct from infarction patterns.
4. DIFFERENTIAL DIAGNOSIS¶
ST-segment elevations may arise from myocardial infarction, pericarditis, Brugada syndrome, hyperkalemia, or early repolarization. T-wave inversions can indicate ischemia, infarction, or nonischemic conditions like hypertrophy or electrolyte disturbances.
4.1 ST-Segment Elevation¶
Differential diagnosis includes acute MI, pericarditis, Brugada syndrome, hyperkalemia, and early repolarization. Reciprocal changes (e.g., ST depression in II, III, aVF with anterior elevation) suggest infarction.
4.2 T-Wave Abnormalities¶
Inversions may reflect ischemia, infarction, or nonischemic causes like hypertrophy, electrolyte imbalances, or drug effects. Prominent U waves suggest hypokalemia or digitalis toxicity.
5. INVESTIGATIONS & DIAGNOSIS¶
ECG interpretation involves assessing waveforms, intervals, and lead orientations. The Framingham formula (QTc = QT + 0.154*(1000 - RR)) and square root method (QTc = QT/ √ RR) correct for heart rate. Abnormalities like prolonged QTc (>460 ms in women, >450 ms in men) suggest risk for torsades de pointes.
5.1 Lead Configuration¶
Limb leads (I, II, III, aVR, aVL, aVF) and chest leads (V1–V6) provide spatial data. The hexaxial diagram determines QRS axis, with normal range –30° to +100°.
5.2 QT Interval Correction¶
QTc formulas (e.g., Framingham, Bazett) adjust for heart rate. Prolonged QTc (>460 ms) increases risk of torsades de pointes, while shortened QTc may indicate hypercalcemia or digitalis effect.
6. MANAGEMENT & TREATMENT¶
Management depends on the underlying cause: reperfusion therapy for MI, electrolyte correction for hyperkalemia/hypokalemia, and drug adjustments for antiarrhythmics. Monitoring includes serial ECGs and serial cardiac enzymes for infarction.
6.1 Acute Myocardial Infarction¶
ST-segment elevation MI (STEMI) requires reperfusion therapy (thrombolysis, PCI). Non-ST elevation MI (NSTEMI) involves antiplatelet agents, anticoagulants, and risk stratification.
6.2 Electrolyte and Drug Effects¶
Hyperkalemia: calcium gluconate, insulin, and dialysis. Hypokalemia: potassium supplementation. Antiarrhythmic drugs (e.g., amiodarone) may prolong QT and require monitoring.
7. PROGNOSIS & COMPLICATIONS¶
ECG abnormalities predict outcomes: prolonged QT increases torsades risk, bundle branch blocks may indicate underlying disease, and ST changes correlate with infarct size. Complications include arrhythmias, heart failure, and sudden cardiac death.
7.1 Arrhythmia Risk¶
Prolonged QTc (>460 ms) and Brugada patterns increase risk of ventricular tachycardia. Left ventricular hypertrophy correlates with higher cardiovascular mortality.
7.2 Infarction Outcomes¶
Q-wave infarction has worse prognosis than non-Q-wave. ST elevation resolution and T-wave inversion patterns guide infarct evolution and reperfusion success.
8. SPECIAL CONSIDERATIONS¶
ECG interpretation varies by population: athletes may show benign early repolarization, while elderly may have low voltage. Pregnancy requires monitoring for fetal effects, and pacemaker rhythms must be distinguished from native rhythms.
8.1 Pediatric Considerations¶
Children may show right axis deviation as a normal variant. Neonatal ECGs may have prolonged QT due to immature repolarization.
8.2 Pregnancy¶
ECG changes in pregnancy include increased heart rate and possible left axis deviation. Fetal heart rate monitoring is critical for maternal and fetal well-being.
9. KEY POINTS & CLINICAL PEARLS¶
ECG is essential for diagnosing cardiac conditions. Key pearls: 1) Use Framingham formula for QTc correction. 2) Recognize bundle branch block patterns. 3) Differentiate ST elevation in MI vs. pericarditis. 4) Monitor for electrolyte and drug effects on repolarization. 5) Assess QRS axis for ventricular hypertrophy or conduction delays.