Electrophysiology of Heart

The heart is the pump that supplies blood and nutrients to the body organs for maintenance of proper functions. The mechanical events of the heart are triggered by changes in the electrical properties of the cardiac cells. An inherent and rhythmical electrical activity is the reason for the heart’s lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers.

Because they are self-excitable. Autorhythmic fibers repeatedly generate action potentials that trigger heart contractions. During embryonic development, only about 1% of the cardiac muscle fibers become autorhythmic fibers. They act as a pacemaker, setting the rhythm of electrical excitation that causes contraction of the heart.

Under normal circumstances, electric impulses are generated spontaneously from the sinoatrial (SA) node, transmitted by the atrial myocardium to the atrioventricular (AV) node, and then sent to the ventricular myocardium via the bundle of His, bundle branches, and Purkinje fibers.

The cell membrane usually maintains a stable negative potential at resting state (resting membrane potential). When the membrane potential is elevated above a threshold potential, an abrupt increase in the membrane potential will occur ("depolarization") and be followed by a plateau of positive potential, before the membrane potential gradually returns to the resting level ("repolarization"). This change in the membrane potential is termed action potential."

Action potential is a complex event that involves movement of various ions across the cell membrane, either actively or passively. The changes in membrane potential are modified by changes in the extracellular and intracellular concentration of ions such as Na+, Ca2+, and K+.

Depolarisation → Contraction

Repolarisation → Relaxation

Cardiac excitation normally begins in the Sinoatrial (SA) node.

SA node cells they repeatedly depolarize to threshold spontaneously. The spontaneous de-polarization is a pacemaker potential.

Each action potential from the SA node propagates throughout heart. following the action potential, the two atria contract at the same time By conducting along atrial muscle fibers, the action potential reaches the atrioventricular (AV) node from the AV node, the action potential enters the atrioven-tricular (AV) bundle(also known as the bundle of His After propagating through the AV bundle, the action potential enters both the right and left bundle branches.

The bundle branches extend toward the apex of the heart. The large-diameter Purkinje fibers rapidly conduct the action potential. Then the ventricles contract, pushing the blood upward to-ward the semilunar valves.

The electrophysiological conduction of heart has 5 phases.

Phase 0: Depolarization

In normal resting phase, the contractile fibers have a stable resting membrane potential that is close to 90 mV.

When a contractile fiber is brought to threshold by an action potential from neighboring fibers, its voltage-gated fast Na+ channels open. “fast” because they open very rapidly in response to a threshold-level depolarization.

Na+ concentration is higher in interstitial fluid (outside cell), whereas K+. are found more inside cardiac muscles.

Inflow of Na+ produces a rapid depolarization Fast Na+ channels start to open one by one and Na+ leaks into the cell, further raising the Transmembrane Potential (TMP) to 30 mV in very short duration (1-2 m sec.)

Phase 1: Partial Repolarization

Partial repolarization because of a rapid decrease in sodium ion passage as fast sodium channels close.

Immediately following rapid depolarization, the inactivation of the Na+ channel and subsequent activation of the outward K+ channel.

TMP is now slightly positive. Some K+ channels open briefly and an outward flow of K+ returns back the TMP to approximately 0 mV.

Phase 2: The plateau phase

L-type Ca2+ channels are still open and there is a small, constant inward current of Ca2+ and outward movement of K+ maintains a concentration gradient through delayed rectifier K+ channels.

These two countercurrents are electrically balanced, and the TMP is maintained at a plateau just below 0 mV throughout phase 2.

Phase 3: Repolarization

Ca2+ channels are gradually inactivated.

Persistent outflow of K+, now exceeding Ca2+ inflow, brings TMP back towards resting potential of −90 mV to prepare the cell for a new cycle of depolarization.

Normal transmembrane ionic concentration gradients are restored by returning Na+ and Ca2+ ions to the extracellular environment, and K+ ions to the cell interior. The pumps involved include the sarcolemmalNa+-Ca2+ exchanger, Ca2+-ATPase and Na+-K+-ATPase.

Resting membrane potential (−90 mV), resulting from the activity of the Na+/K+ ATPase pump which creates a negative intracellular potential because of the exchange of three sodium ions for only two potassium ions.

Phase 4: Resting Phase

The resting potential in a cardiomyocyte is −90 mV due to a constant outward leak of K+ through inward rectifier channels.

Na+ and Ca2+ channels are closed at resting TMP.