The pacemaker physiology refers to the mechanisms by which the heart's sinoatrial node (SAN) generates rhythmic electrical impulses, initiating each heartbeat.
Sinoatrial Node (SAN) and Automaticity
The SAN, a specialized group of cardiac cells, possesses the intrinsic property of automaticity. This means it can spontaneously depolarize and generate action potentials without external stimulation. This spontaneous depolarization is what dictates the heart rate.
The Pacemaker Potential (Phase 4 Depolarization)
Unlike other cardiac cells that maintain a stable resting membrane potential, SAN cells exhibit a slow, continuous depolarization during phase 4 (diastole) known as the pacemaker potential or diastolic depolarization. This gradual depolarization is crucial for initiating each heartbeat.
Ionic Mechanisms of the Pacemaker Potential
Several ion currents contribute to the pacemaker potential:
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Decreasing Potassium Efflux (IK): Potassium channels gradually close after repolarization of the previous action potential, reducing the outward flow of K+ ions and causing the membrane potential to drift upwards.
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"Funny" Current (If): This unique inward current is activated by hyperpolarization (negative membrane potentials). If is carried by sodium ions (Na+) and contributes to the initial depolarizing phase. It's termed "funny" because it's activated at hyperpolarized potentials, unlike most other ion channels.
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T-type Calcium Channels (ICaT): As the membrane potential depolarizes further, transient (T-type) calcium channels open, allowing a small influx of Ca2+, further contributing to depolarization.
Threshold and Action Potential
Once the pacemaker potential reaches a threshold voltage, voltage-gated L-type calcium channels (ICaL) open, causing a rapid influx of Ca2+ and resulting in the action potential. This influx is responsible for the upstroke (Phase 0) of the SAN action potential. Note: unlike ventricular myocytes where Na+ influx is critical for phase 0, Ca2+ drives the upstroke in the SAN.
Repolarization
Repolarization (Phase 3) occurs primarily due to the opening of voltage-gated potassium channels (K+ efflux), restoring the negative membrane potential. The cycle then restarts with the slow diastolic depolarization of phase 4.
Modulation of Pacemaker Activity
The autonomic nervous system and circulating hormones can modulate pacemaker activity and, therefore, heart rate:
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Sympathetic Nervous System (Norepinephrine): Increases the slope of the pacemaker potential, primarily by increasing If and ICaL, leading to a faster heart rate (positive chronotropic effect).
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Parasympathetic Nervous System (Acetylcholine): Decreases the slope of the pacemaker potential by decreasing If and increasing IK, leading to a slower heart rate (negative chronotropic effect).
Pacemaker Hierarchy
While the SAN is the primary pacemaker, other cardiac tissues (e.g., AV node, Purkinje fibers) also possess automaticity. However, their intrinsic firing rates are slower than the SAN. The SAN, with its faster firing rate, normally suppresses the activity of these latent pacemakers. If the SAN fails, one of these latent pacemakers can take over, albeit at a slower heart rate.
In summary, the pacemaker physiology is a complex interplay of ion channels and autonomic influences that allows the SAN to generate rhythmic electrical impulses, driving the rhythmic contraction of the heart.
