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The heart has four chambers (right and left atria and ventricles) separated by the AV valves (tricuspid and mitral) and semilunar valves (pulmonary and aortic), which enforce unidirectional blood flow through the pulmonary and systemic circuits. The intrinsic conduction system — sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, bundle branches, and Purkinje fibers — generates and propagates action potentials that coordinate atrial and ventricular contraction. Cardiac muscle cells are connected by gap junctions at intercalated discs, allowing the myocardium to act as a functional syncytium. The ECG waveform (P, QRS, T) maps to specific events in the conduction cycle.
Trace the path of a single action potential through the conduction system and match each step to its ECG waveform. Use a cross-sectional heart diagram to identify chambers, valves, and great vessels simultaneously.
Your prerequisite in cardiac electrophysiology established how individual cardiac muscle cells generate action potentials with a prolonged plateau phase that prevents tetanus and ensures a full mechanical contraction before the cell can be restimulated. Now the question is: how does a heart composed of billions of such cells beat in coordinated sequence rather than as a chaotic, independent riot of depolarizations? The answer is architectural — the heart is wired with a specialized conduction system that functions simultaneously as a pacemaker, a relay station with a deliberate delay, and a rapid distribution network.
The sinoatrial (SA) node, embedded in the right atrial wall near the superior vena cava, is the intrinsic pacemaker. It spontaneously depolarizes at 60–100 times per minute — faster than any other cardiac tissue — and therefore normally dictates heart rate. From the SA node, depolarization spreads through atrial muscle via gap junctions at intercalated discs, the structures that make the myocardium a functional syncytium: electrically coupled cardiomyocytes propagate the action potential cell-to-cell without synaptic delay, so the entire atrial mass contracts as a single coordinated unit. The resulting wave of atrial contraction sweeps inward and downward, pushing blood through the open AV valves — the tricuspid on the right and the mitral (bicuspid) on the left — into the ventricles. These valves open passively when atrial pressure exceeds ventricular pressure and close passively when the gradient reverses; no active mechanism is needed.
The depolarization wave cannot jump directly from atria to ventricles — a fibrous skeleton of connective tissue electrically insulates the two chambers except at one point: the atrioventricular (AV) node. This creates a deliberate delay of roughly 0.1 seconds, giving the atria time to fully contract and top off ventricular filling before ventricular contraction begins. The AV node passes the signal into the bundle of His, which splits into right and left bundle branches coursing down the interventricular septum. These terminate in the Purkinje fiber network, which fans rapidly across the endocardial surface of both ventricles. The Purkinje system distributes depolarization simultaneously to the entire ventricular wall, producing the coordinated, apex-to-base squeeze that ejects blood efficiently into the aorta and pulmonary trunk past the closed, then forcibly opened, semilunar valves (aortic and pulmonary).
The ECG maps each stage onto a waveform in real time. The P wave reflects atrial depolarization spreading from the SA node. The PR interval spans from atrial depolarization through the AV nodal delay — its duration reflects how long conduction through the AV node takes. The sharp, brief QRS complex reflects rapid ventricular depolarization via the Purkinje system; its brevity indicates how efficiently the conduction network distributes the signal. The T wave reflects ventricular repolarization. (Atrial repolarization occurs during this interval but is electrically masked by the QRS.) When any component of this system fails — SA node suppression causing an escape rhythm, AV nodal block lengthening the PR interval or causing dropped beats, bundle branch block broadening the QRS — the ECG waveform deforms in ways that map precisely back to the anatomy. Reading an ECG is, at bottom, reading the conduction system's anatomy through the electrical footprint it leaves on the body surface.