The heart’s rhythmic beating is driven by specialized electrical activity known as pacemaker potential. This spontaneous electrical impulse generation allows the heart to continuously pump blood throughout the body. Pacemaker potential is a fundamental process that ensures the heart’s consistent function.
The Heart’s Natural Pacemaker
The primary site for initiating the heart’s rhythmic contractions is the sinoatrial (SA) node, the natural pacemaker. Located in the upper back wall of the right atrium, the SA node is a cluster of specialized cardiac muscle cells. These cells possess the unique ability to spontaneously generate electrical impulses.
The SA node maintains its role as the heart’s primary pacemaker because its cells depolarize faster than other potential pacemaker cells. This inherent fastest rate of depolarization sets the overall heart rhythm, typically producing 60-100 electrical impulses per minute in a resting adult. The electrical signals from the SA node spread throughout the atria, causing them to contract, before moving to other parts of the heart’s conduction system.
While the SA node is the dominant pacemaker, other areas, such as the atrioventricular (AV) node and Purkinje fibers, also have the capacity for spontaneous depolarization. These are “latent” or “backup” pacemakers. They normally do not initiate heartbeats because the SA node’s faster rate suppresses their rhythm, a phenomenon known as overdrive suppression. However, if the SA node fails or its impulses are blocked, these latent pacemakers can take over, albeit at slower rates (e.g., the AV node at 40-60 beats per minute, Purkinje fibers at 20-40 beats per minute).
The Electrical Steps of Pacemaker Potential
The pacemaker potential in these specialized cells involves distinct electrical phases driven by the controlled movement of ions across the cell membrane. Unlike other heart cells, pacemaker cells do not have a stable resting potential; instead, their membrane potential slowly depolarizes after each action potential, leading to the next beat. This continuous cycle ensures the heart’s automaticity.
The process begins with Phase 4, the slow diastolic depolarization. During this phase, the membrane potential gradually becomes more positive, moving from -60 mV towards a threshold potential of -40 mV. This slow depolarization is largely due to the “funny current” (If), which is a slow inward current of both sodium and potassium ions through hyperpolarization-activated cyclic nucleotide-gated (HCN) channels. These channels open at very negative membrane potentials, allowing a net influx of positive charge into the cell.
As Phase 4 progresses, transient or T-type calcium channels also contribute to the depolarization as the membrane potential becomes less negative, at -50 mV. These channels allow a small influx of calcium ions, further pushing the membrane potential towards the threshold.
Once the membrane potential reaches the threshold of -40 mV, Phase 0, the rapid depolarization phase, is triggered. This swift increase in voltage is caused by the rapid influx of calcium ions through long-lasting, voltage-gated L-type calcium channels. These L-type channels open once the threshold is met, allowing significant calcium to enter the cell, which generates the upstroke of the action potential, reaching a peak of +10 mV.
Phase 3, the repolarization phase, begins after the action potential peaks. During this phase, the L-type calcium channels inactivate and close, stopping the inward calcium current. Simultaneously, voltage-gated potassium channels open, allowing potassium ions to flow out of the cell. This outward movement of positive potassium charges causes the membrane potential to rapidly become more negative, returning to the maximum diastolic potential of -60 mV. The repolarization sets the stage for the next spontaneous Phase 4 depolarization, restarting the cycle.
Modulation of Heart Rate
While pacemaker cells spontaneously generate electrical impulses, heart rate is continuously adjusted by external factors, primarily the autonomic nervous system. This system, composed of sympathetic and parasympathetic branches, modulates the rate of phase 4 depolarization in the SA node, altering heart rate to meet the body’s demands.
Sympathetic stimulation, associated with the “fight-or-flight” response, increases heart rate. Norepinephrine, released by sympathetic nerves, binds to beta-adrenoceptors on pacemaker cells. This binding increases the slope of phase 4 depolarization by enhancing the funny current and increasing the influx of slow inward calcium currents. This faster depolarization leads to an increased firing rate and a faster heart rate.
Conversely, parasympathetic stimulation, mediated by the vagus nerve, slows heart rate. Acetylcholine, released by the vagus nerve, binds to muscarinic receptors on SA node cells. This action decreases the slope of phase 4 depolarization by reducing the funny current and slow inward calcium currents, and by increasing potassium ion efflux. This slower depolarization prolongs the time to reach the threshold, resulting in a decreased firing rate and a slower heart rate. Parasympathetic activity can also hyperpolarize the pacemaker cell.
Other factors, such as circulating hormones like epinephrine (which acts similarly to norepinephrine) and thyroid hormones, also influence heart rate by affecting pacemaker activity. For instance, hyperthyroidism can lead to tachycardia, while hypothyroidism can cause bradycardia.