Chapter 29: Origin of the Heartbeat & Cardiac Electrical Activity

The regulation of the heart’s sequential contraction—where atrial systole precedes ventricular systole—is managed by a distinct electrical system known as the cardiac conduction system. This system's impulse generation typically begins at the sinoatrial (SA) node, which functions as the inherent pacemaker due to its inherently rapid spontaneous discharge rate, determining the overall heart rhythm. The depolarization spreads from the SA node through atrial pathways to the atrioventricular (AV) node, experiencing a crucial approximately 0.1 second delay (AV nodal delay) there due to slow conduction. The signal then travels quickly via the bundle of His, its branches, and the widespread Purkinje system to activate the ventricular muscle for contraction. Specialized pacemaker cells, notably in the SA and AV nodes, possess a unique electrical property called the prepotential (or pacemaker potential), characterized by a slow decay of membrane potential following each impulse. This depolarization is initiated by the "funny current" (Ih), carried by h or f channels, which eventually activates voltage-gated calcium channels, producing the rapid upstroke of the action potential. The electrocardiogram (ECG or EKG) is an extracellular recording of the summed electrical activity throughout the cardiac cycle, consisting of recognizable deflections: the P wave signals atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave marks ventricular repolarization. Neural input, particularly from the vagus nerve (parasympathetic), decreases the heart rate by hyperpolarizing nodal tissue and flattening the slope of the prepotential, while sympathetic stimulation increases the rate. Disruptions in this electrical rhythm produce cardiac arrhythmias, which can arise from abnormal, irritable ectopic foci or, more commonly, from a phenomenon known as reentry (or circus movement), where excitation propagates continuously within a closed circuit. Arrhythmias include types of heart block (e.g., first, second, or third-degree block, the latter resulting in independent, slow idioventricular rhythm), as well as rapid rhythms like atrial flutter, atrial fibrillation, and dangerous ventricular tachycardia or ventricular fibrillation. Conditions such as myocardial infarction interrupt blood flow, causing early changes like characteristic ST segment elevation on the ECG due to altered electrical potentials in the injured muscle. Furthermore, the heart is extremely sensitive to changes in blood electrolytes, particularly potassium. Elevated plasma potassium levels (hyperkalemia) manifest on the ECG as tall peaked T waves, eventually leading to QRS widening and atrial paralysis, potentially causing the heart to stop in diastole. Treatment options for these rhythm abnormalities range from antiarrhythmic drugs targeting ion channels (sodium, potassium, calcium) to implanting electronic pacemakers for slow rhythms or using catheter ablation to physically interrupt reentrant pathways.