What Is Cardiac Action Potential?

The cardiomyocytes are striated muscles, which are not subject to conscious control and belong to involuntary muscles. Cardiomyocytes can be roughly divided into two categories: cardiac conduction system and working muscle cells. Cardiac conduction cells include the sinoatrial node, the atrioventricular node, and Pudd's fibers. Mainly conduct myocardial electrical impulses. Working muscle cells include atrial and ventricular muscles. Individual working muscle cells receive electrical impulses from the cardiac conduction system to produce a coupling of excitation and contraction. The entire atrial muscle or ventricle muscle as a whole to complete the pumping function.

Myocardial electrophysiology

characteristic:

The characteristic that myocardial cells can generate action potentials is called excitability. Cells in the cardiac conduction system can spontaneously generate action potentials, a feature called autonomy. The regular contraction of cardiomyocytes is called rhythmicity.

Sinoatrial node

Under normal circumstances, the sinoatrial node can generate action potentials spontaneously. The sinoatrial node generates electrical impulses at a rhythm of 60-100 times per minute. The electrical impulses are quickly spread to the left and right atria, and then the impulses are transmitted to In the ventricular Pu's fiber, the atrioventricular node is the only pathway between the atria. Impulse has a delay in atrioventricular node conduction, which takes about 0.15 seconds (this block effect is conducive to ventricular blood filling).

The impulse then quickly spreads to the entire ventricle along the Purdue fiber system, activating the entire ventricle in 0.1 seconds, thereby causing the ventricular muscles to contract synchronously and expel blood. The generation and conduction of impulses are accompanied by fine ion transport across the myocardial cell membrane, and if abnormal, it may produce arrhythmia.

When the myocardium is in a resting state, the intra-membrane potential is negative to the outer membrane, about -90 mV, and it is in a polarized state due to the high concentration of K + outflow in the myocardial cells. When myocardial cells are excited, they depolarize and then repolarize to form an action potential (AP). During membrane potential changes, ion channels undergo transitions that are closed, open, and inactivated. AP is divided into 5 phases, phase 0 is rapid depolarization, which is caused by Na + rapid inflow. Phase 1 is the early stage of rapid repolarization, which was caused by a transient outflow of K +. The 2-phase plateau is a slow repolarization, which is caused by Ca2 + and a small amount of Na + inflow and K + outflow. Phase 3 is the end of rapid repolarization, which is caused by K + outflow. The AP duration of 0 to 3 phases is called action potential duration (APD). Phase 4 is the resting phase. The membrane potential of non-autonomic cells is maintained at a resting level. Phase 4 auto-depolarization is caused by a Na + inward current. In autonomic cells, it is the spontaneous diastolic phase.

The resting membrane potential of the working muscles of the heart and the cells of the conduction system has a large negative value, a fast depolarization rate, and a rapid response to electrical activity. The depolarization is mainly caused by Na + influx. Membrane potentials of sinoatrial node and atrioventricular node cells are small, phase 0 depolarization amplitude and speed are low, conduction is slow, and there is a slow response to electrical activity. Depolarization is caused by Ca2 + influx. In addition, under certain pathological conditions (such as myocardial ischemia, hypoxia, drug poisoning, etc.), the membrane potential decreases (negative value decreases), which can cause fast-responding cells to exhibit slow-responding electrical activity.

Membrane reactivity refers to the relationship between the membrane potential level and its maximum upstroke slope of phase 0 (Vmax), which is related to the Na + current. Membrane reactivity represents the activity of sodium channels and is an important factor in determining the conduction speed. Generally, the faster the rise rate of phase 0, the larger the amplitude of the action potential, and the faster the conduction speed. Drugs can affect the rate of conduction by increasing or decreasing membrane reactivity.

When the membrane potential returns to about -60 mV during repolarization, the cell generates a spreadable action potential to the stimulus. The period from the beginning of depolarization to this is the effective refractory period (ERP), which generally corresponds to the length of the APD, but the degree can vary. Antiarrhythmic drugs can interrupt arrhythmia by prolonging ERP, which causes abnormal impulses to fall more into ERP.