Bundle Branch Block: Causes, ECG Signs & Treatment | Pathology Review

A standard 12-lead ECG consists of three standard limb leads (I, II, III), three augmented limb leads (aVR, aVL, aVF), and six chest leads (V1-V6). In normal ECGs, P-waves, QRS complexes, and T-waves are typically positive in leads I, II, and III, while aVR shows inverted waves. Chest leads demonstrate progressive R-wave increase from V1 to V4/V5, with V6 showing smaller R-waves. The ST segment is usually isoelectric, with slight upsloping in V1-V2 being normal. Heart rate is measured between R-waves at 60-100 bpm in adults, calculated as 60 divided by R-R interval in seconds.

A standard 12-lead ECG provides 12 different views of cardiac electrical activity. The limb leads (I, II, III, aVR, aVL, aVF) are generated by electrodes on the four extremities, while precordial leads (V1-V6) are placed on the chest wall. The cardiac cycle consists of three main waveforms: the P wave representing atrial depolarization, the QRS complex representing ventricular depolarization, and the T wave representing ventricular repolarization. Each waveform has distinct morphology that varies by lead.

A normal ECG consists of P wave (atrial depolarization/contraction), PR interval (atrial depolarization to ventricular depolarization), QRS complex (ventricular depolarization/contraction), and T wave (ventricular repolarization/relaxation). The PR segment represents the delay at the AV node. The P wave forms when the atria contract, the QRS complex forms when ventricles contract, and the T wave forms when ventricles relax. These waveforms represent the complete electrical cycle of the heart.

ECG (Electrocardiogram) records electrical changes in the heart during the cardiac cycle. The cardiac cycle includes events from one heartbeat to the next. ECG captures weak electrical signals (millivolts) occurring rapidly (milliseconds), requiring special galvanometers. Electrodes are placed on the skin surface because electrical signals travel through blood and tissues. Standard lead colors are: Red (right arm), Yellow (left arm), Green (left leg), Black (right leg/ground). The bipolar lead system (Einthoven's triangle) uses three leads: Lead I (RA negative to LA positive), Lead II (RA negative to LL positive), Lead III (LA negative to LL positive), with the mathematical relationship Lead I + Lead III = Lead II. The unipolar lead system uses a single positive electrode with combined negative reference: aVR (RA positive), aVL (LA positive), aVF (LL positive). The standard 12-lead ECG system includes 3 bipolar leads, 3 augmented unipolar leads, and 6 chest leads (V1-V6) placed at specific locations on the chest wall. ECG waveforms are named: P wave (atrial depolarization), QRS complex (ventricular depolarization), T wave (ventricular repolarization), U wave (Purkinje fiber repolarization). The P wave precedes atrial contraction. Normal P wave duration is 0.08-0.11 seconds (2-3 small squares) and amplitude is 0.25 mV (2-3 small squares). The QRS complex represents ventricular depolarization, smaller than P wave because ventricles are smaller. Normal QRS duration is 0.06-0.10 seconds (1.5-2.5 small squares) and amplitude is 0.5-2.5 mV (5-25 small squares). The T wave follows ventricular depolarization. The U wave, which may appear after T wave, represents Purkinje fiber repolarization and is prominent in hypokalemia.

A normal ECG displays five main waves: P wave, QRS complex, and T wave. The P wave represents atrial depolarization (atrial contraction) and occurs when impulses from the SA node spread through both atria. The QRS complex represents ventricular depolarization (ventricular contraction) as impulses spread through the Bundle of His and Purkinje fibers. The T wave represents ventricular repolarization (ventricular relaxation) as the ventricular muscle cells recover. The U wave, when visible, represents Purkinje fiber repolarization but is not always present. These waves provide information about the heart's electrical and mechanical function.

The heart exists in three dimensions, requiring precordial leads to capture the third dimension (Z-axis). The RV sits anteriorly bulging toward the chest wall, while the LV curves away toward the apex. The normal 3D depolarization vector points down, left, and away from the chest wall toward the apex. Precordial leads are positioned to detect this three-dimensional vector: V1-V2 look anteriorly toward the chest wall, while V4-V6 look toward the apex. R-wave progression (increasing positive deflections from V1 to V6) reflects leads becoming increasingly aligned with the normal 3D depolarization vector.

This section covers the technical setup for 12-lead ECG recording. The 12 leads consist of 6 limb leads (3 bipolar: D1, D2, aVR; 3 unipolar: aVL, aVF, aVR) and 6 precordial leads (V1-V6). Bipolar leads have positive and negative electrodes: D1 (left arm positive, right arm negative), D2 (left leg positive, right arm negative), aVR (right arm positive, left arm and leg negative). Precordial leads are placed at specific intercostal spaces: V1 (4th ICS, right parasternal), V2 (4th ICS, left parasternal), V3 (between V2 and V4), V4 (5th ICS, midclavicular), V5 (same height, anterior axillary), V6 (same height, midaxillary). Vector cardiology explains that ventricular depolarization produces three vectors: septal (left to right), free wall (right to left), and basal (left to right, bottom to top). The free wall vector dominates due to left ventricular mass.

Vectorcardiography is a method that accompanies electrocardiography by recording cardiac electrical activity in three planes (frontal, horizontal, sagittal) using seven electrodes. It generates three loops: P (atrial depolarization), QRS (ventricular depolarization), and T (ventricular repolarization). Each tear represents 2 milliseconds of conduction time. Different delay patterns indicate specific conditions: initial delay suggests preexcitation (Wolff-Parkinson-White), mid-final delay indicates left bundle branch block, terminal delay shows right bundle branch block. Ventricular depolarization involves four vectors: septal, lower septum, free walls, and basal vectors. Body habitus affects rotation: obese patients show clockwise rotation with axis near +90 degrees, while long thin patients show counterclockwise rotation with axis near +15 degrees. The T loop has elliptical morphology with rotation varying by plane. Vectorcardiography has three key points: point E (sinoatrial node activation), point zero (end of P wave/start of QRS), and point J (end of ventricular depolarization/start of repolarization). It offers advantages: more didactic, vectorial loop records, tridimensional information, and higher sensitivity/specificity for chamber overload, fascicular blocks, and infarction. However, electrocardiography is more practical, reproducible, and cheaper, serving as the reference for conduction disorders, preexcitation, most arrhythmias, and acute infarction.

This segment covers the precordial leads and cardiac vector in ECG interpretation. The precordial leads (V1-V6) are unipolar leads placed on the chest at specific locations: V1 at the fourth intercostal space right sternal border, V2 at the fourth intercostal space left sternal border, V3 between V2 and V4, V4 at the fifth intercostal space midclavicular line, V5 at the fifth intercostal space anterior axillary line, and V6 at the fifth intercostal space midaxillary line. V1 and V2 normally show a small R wave and deep S wave. V3 and V4 show increasing R wave amplitude. V5 and V6 show large R waves. The transition from S-dominant to R-dominant leads normally occurs between V3 and V4. The cardiac vector represents the direction and magnitude of the heart's electrical activity, shown as an arrow. The normal electrical axis is between -30 degrees and +110 degrees. Left axis deviation (-30 to -90 degrees) indicates conditions like left ventricular hypertrophy. Right axis deviation (+90 to +180 degrees) indicates conditions like right ventricular hypertrophy.

An electrocardiogram represents cardiac electrical activity on millimeter paper, captured by electrodes placed on the precordial region and limbs. The 12 derivations function like photographic perspectives: frontal derivations (D1, D2, D3, aVR, aVL, aVF) and precordial derivations (V1-V6) each capture the heart from different angles. Electrical activity is represented as vectors with positive heads and negative tails. When electrodes capture the vector head, the wave is positive; when capturing the tail, the wave is negative. The P wave represents auricular depolarization; Q wave represents interventricular septum depolarization; R wave represents left ventricular depolarization; S wave represents right ventricular depolarization; T wave represents ventricular repolarization. Wave polarity depends on vector capture, not on whether the event is depolarization or repolarization.

Ischemia acutely increases tissue impedance by disrupting sodium-potassium ATPase function, causing extracellular potassium accumulation and altered resting membrane potential. Chronic ischemia reduces connexin 43 expression. Pathological hypertrophy (aortic stenosis, hypertrophic cardiomyopathy) relocates gap junctions from longitudinal to transverse cell aspects, disrupting coordinated activation and potentially creating arrhythmogenic substrates. Volume overload stretches myocytes, activating stretch-activated channels that alter resting membrane potential and capacitance, reducing conduction velocity.

This comprehensive section covers ECG interpretation for cardiac pathology. Hypertrophy diagnosis includes: right atrial (P wave amplitude >2.5mm), left atrial (P wave length >2mm), right ventricular (R in aVR >11mm, axis >+110°), and left ventricular (S criteria ≥35mm, Cornell voltage ≥28mm men/≥20mm women). Ischemic changes show peaked T waves progressing to inversion; infarction shows ST elevation and pathological Q waves (>0.04s, >25% QRS). Bundle branch blocks: right shows RSR' in V1/V2 >0.12s with right axis deviation; left shows RSR' in V5/V6 with left axis deviation. Electrolyte effects: hypocalcemia (narrow QRS, prolonged QT), hypercalcemia (short QT, tall T), hyperkalemia (peaked T, PR prolongation, QRS widening), hypokalemia (flattened T, O waves). Sinus node dysfunction includes bradycardia (<60 bpm, pathological if <40 bpm with symptoms), pause/arrest, and inability to reach 80% of expected maximum heart rate. AV conduction disorders range from first-degree block (PR >0.20s) to third-degree complete block with escape rhythm.

Myocardial infarction occurs when coronary artery blockage (usually by atherosclerotic plaque with thrombosis) causes myocardial death. Ischemia precedes infarction. Left ventricular hypertrophy involves myocardial thickening, commonly from hypertension or valvular disease, increasing cardiac workload. Right ventricular hypertrophy results from pulmonary hypertension. Right ventricular dilatation involves cavity enlargement, reducing pumping efficiency. These conditions can lead to heart failure if severe.

AV blocks represent progressive conduction system dysfunction: first-degree shows prolonged PR interval with 100% conduction (benign). Second-degree Mobitz Type I shows progressive PR lengthening before dropout; Mobitz Type II shows constant PR with intermittent dropout (more ominous). Third-degree (complete) block shows total dissociation between atria and ventricles, requiring urgent pacing. Myocardial infarction progresses through phases: hyperacute (tall T waves), acute (ST elevation), subacute (pathological Q waves), and chronic (persistent T inversion). Non-ST elevation MI shows no significant ST changes but elevated biomarkers. Ventricular hypertrophy shows characteristic patterns: left hypertrophy shows left axis deviation and increased voltage; right hypertrophy shows right axis deviation. Wolff-Parkinson-White syndrome creates accessory pathways causing delta waves and reentrant tachycardias.

The cardiac conduction system is susceptible to damage from conditions such as myocardial infarction (heart attack), ischemia (inadequate blood supply), and other coronary artery diseases. When blood supply to parts of the conduction system is disturbed, bizarre heart rhythms or abnormal sequences of contraction can occur, potentially severely affecting cardiac pumping effectiveness and even causing death.