Cardiac Electrical Activity

Cardiac Electrical Activity is the generation and propagation of self-originating electrical impulses within specialized and working myocardial tissue that initiate, coordinate, and sequence the mechanical contraction of the atria and ventricles, forming the electrical basis upon which the entire mechanical pumping cycle of the heart depends.

Intrinsic Rhythmicity of the Heart

Automaticity

Certain cardiac cells possess the intrinsic property of automaticity, the ability to spontaneously depolarize and generate action potentials without requiring external neural stimulation, a property arising from their unstable resting membrane potential that drifts progressively toward the threshold for firing.

The Pacemaker Hierarchy

Multiple regions of the heart possess automaticity, but the sinoatrial node normally depolarizes fastest and therefore sets the rhythm for the entire heart, suppressing the slower intrinsic rates of subsidiary pacemakers in the atrioventricular node and ventricular conduction tissue through a mechanism known as overdrive suppression.

The Cardiac Conduction Pathway

Sequential Route of Impulse Propagation

The electrical impulse originates in the sinoatrial node, spreads across the atrial myocardium to produce coordinated atrial contraction, converges upon the atrioventricular node, passes into the bundle of His, divides into the left and right bundle branches, and terminates in the Purkinje fiber network, which rapidly distributes the impulse throughout the ventricular myocardium.

The Atrioventricular Delay

Conduction through the atrioventricular node is deliberately slow compared to the surrounding tissue, introducing a delay that allows atrial contraction to complete ventricular filling before ventricular depolarization and contraction begin, optimizing the mechanical efficiency of each cardiac cycle.

Ionic Basis of Cardiac Electrical Activity

Pacemaker Potentials

In nodal tissue, the slow spontaneous depolarization between action potentials, termed the pacemaker potential, results from a combination of a decaying inward current, calcium channel activity, and declining potassium conductance, gradually driving the membrane potential toward threshold.

Working Myocardial Action Potentials

In contrast to nodal tissue, working atrial and ventricular myocardial cells exhibit a stable resting potential and a rapid depolarization upon stimulation, followed by a prolonged plateau phase sustained by inward calcium current balanced against outward potassium current, before repolarization restores the resting state.

Propagation and Synchrony

Cell-to-Cell Conduction

Electrical impulses propagate from cell to cell through gap junctions at the intercalated discs, allowing depolarization to spread continuously through the myocardial syncytium without requiring a separate conducting structure for every individual cell.

Rapid Ventricular Activation

The specialized Purkinje fiber network conducts impulses at a considerably higher velocity than ordinary myocardium, ensuring that the ventricular walls are activated nearly simultaneously, producing coordinated, efficient contraction rather than a slow, disorganized wave of activation.

Modulation by the Autonomic Nervous System

Sympathetic Influence

Sympathetic stimulation increases the rate of pacemaker depolarization and accelerates conduction through the atrioventricular node, increasing both heart rate and the speed of impulse transmission through the conduction system.

Parasympathetic Influence

Parasympathetic stimulation, delivered primarily through the vagus nerve, slows the rate of pacemaker depolarization and prolongs atrioventricular nodal conduction, decreasing heart rate and, at high levels, slowing transmission from atria to ventricles.

Relationship to Mechanical Function

Cardiac electrical activity precedes and determines the timing, sequence, and coordination of mechanical contraction, so that the orderly spread of depolarization from the sinoatrial node through the atria, across the atrioventricular delay, and rapidly throughout the ventricles establishes the precise temporal sequence necessary for effective, synchronized ejection of blood during each cardiac cycle.