9.12: Electrophysiology of Cardiac Contractile Cells

In cardiac contractile muscle fibers, the action potential pattern exhibits a more stable resting phase than conductive cells. The resting membrane potential for atrial myofibers is approximately -80 mV, while for ventricular muscle fibers, it is around -90 mV. The behavior of action potentials is quite distinct in cardiac contractile cells, featuring rapid depolarization followed by a plateau phase and eventual repolarization. This phenomenon contributes to the extended refractory periods essential for these cardiac muscle cells to pump blood before they can generate another action potential. These cardiac myocytes do not usually initiate their own electrical impulses; instead, they await a signal from a conductive cell (such as the SA node) to trigger an action potential.

Upon receiving an action potential from a pacemaker cell and the depolarization reaches the threshold of -75 mV, voltage-gated sodium channels open in a positive-feedback manner. This results in a rapid influx of sodium ions, raising the membrane potential to approximately +30 mV. At this point, the sodium channels close. This rapid depolarization phase typically lasts 3–5 ms (as indicated by the orange line; phase 0). Subsequently, the plateau phase follows. In the initial part of the plateau phase, only the slow potassium ion channels are open, leading to a gradual decline in the membrane potential (phase 1). Soon afterward, the L-type or slow calcium ion channels open, permitting the entry of calcium ions, which helps maintain a membrane potential of approximately 0 mV. During this phase, potassium ion channels are also open, allowing potassium ions to exit the cell while calcium ions enter. This period involves the inward movement of calcium ions and the outward movement of potassium ions, lasting approximately 175 ms (illustrated by the purple line; phase 2). Following this, the calcium ion channels close, while the potassium ion channels remain open, facilitating the exit of more potassium ions and initiating the repolarization phase (phase 3). The repolarization phase lasts about 75 ms. As the membrane potential drops to its resting levels, the potassium ion channels close again (phase 4), and the cycle repeats (Figure 15). The sequence takes place over 250 to 300 ms.

Figure 15 | Action Potential in the Cardiac Contractile Cells | ²⁷  (a) Note the long plateau phase due to the influx of calcium ions. The extended refractory period allows the cell to fully contract before another electrical event can occur. The numbers 0, 1, 2. 3, 4 indicate the phase of the action potential. (b) The action potential for heart muscle is compared to that of skeletal muscle

Once an action potential is triggered, a cardiac muscle cell enters a period when it can not initiate another action potential for a specific duration. This safeguarding period is known as the refractory period, lasting approximately 250 ms, and is crucial for protecting the heart. The cardiac refractory period is divided into two phases: absolute and relative refractory periods. A new action potential cannot be generated during the absolute refractory period, ensuring a controlled rhythm. Conversely, the relative refractory period allows for a new action potential if a strong stimulus is applied.

A comparison of the action potential in the contractile cells of cardiac muscle and skeletal muscle fiber is illustrated in Figure 15b. The duration of an action potential and the refractory period is significantly shorter in skeletal muscle compared to cardiac muscle contractile cells. Figure 15b also shows the resulting contraction pattern following each action potential. Due to the extended refractory period in cardiac muscle fibers, an entire contraction cycle must conclude before a new one can be initiated. This contraction pattern differs from skeletal muscle, where a further contraction might begin before the previous cycle ends, given the shorter refractory period. This occurrence is termed tetanus, common in skeletal muscle but not observed in cardiac muscle. Cardiac muscle cells undergo twitch-like contractions marked by prolonged refractory periods followed by brief relaxation periods. This relaxation period is crucial to allow the heart to fill with blood for the subsequent cycle. The lengthy refractory period prevents the risk of tetany, a condition where muscles involuntarily remain contracted. In the heart, tetany is incompatible with life as it impedes the heart's ability to pump blood effectively.

The sequence of gradual depolarization, followed by swift depolarization and repolarization, is observed in the SA node and selects other conducting cells within the heart. Serving as the primary pacemaker, the SA node surpasses the threshold for depolarization more rapidly than any other part of the conduction system. It launches impulses propagating to other conducting cells, orchestrating the heart's rhythm. Operating autonomously, the SA node triggers a heart impulse around 80 to 100 times per minute. While each component of the conduction system can generate its own impulse, the initiation rate gradually decreases from the SA node down to the Purkinje fibers.

Without the SA node's influence, the AV node would establish a heart rate ranging from 40 to 60 beats per minute. If the AV node lost its pacemaker role, the AV bundle would generate impulses approximately 30 to 40 times per minute. The bundle branches would exhibit an intrinsic rate of 20 to 30 impulses per minute, while the Purkinje fibers would fire at roughly 15 to 30 impulses per minute. Though some exceptionally trained aerobic athletes might showcase resting heart rates between 30 and 40 beats per minute (the lowest documented value being 28 beats per minute for cyclist Miguel Indurain), for most individuals, heart rates below 50 beats per minute would indicate bradycardia, a condition characterized by a slow heart rate. As rates dip significantly below this threshold, the heart's ability to supply essential tissues with sufficient blood becomes compromised, leading to organ failure, multisystem failure, and eventual death.²⁸

 

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