[1]. From the lungs, blood enters the heart upon relaxation and before being ejected out to the tissues during the contraction phase. The process of contraction and relaxation are influenced by ions such as calcium, sodium, and potassium.

Jeremy Pinnell, Turner, Simon, and Simon Howell, asserts that in this state, its inner surface is charged with negative ions while the outer one has positive ones[2]. The negatively charged ions are the negatively charged nucleic acids and proteins. The positive ones include the sodium and potassium ions, which are on the outer and inner surface of the sarcolemma respectively. The unstimulated state of the sarcolemma is called the resting potential of the sarcolemma.

On the other hand, the resting potential can be disturbed resulting in depolarization. During the depolarization process, the cardiac cells enter the active phase called the action potential. In the cardiac fibers, there is a sequence of events that result in depolarization and finally cardiac fiber contraction. Depolarization occurs rapidly from -290 mV to +10 mV when the fast opening channels of sodium ions of the sarcolemma open. That allows the influx of the Na+ into the heart muscle cells. After that, the channels close rapidly. From that point forward, a plateau phase occurs in which the calcium ions enter the cytoplasm of the cardiac fibers from the sarcoplasmic reticulum located in the cell. On the same line, some calcium ions enter the cell through the slow opening calcium ion channels of the sarcolemma. Once the calcium ions are inside the cell cytoplasm, they bind to troponin that triggers the binding of the cross-bridge resulting in the sliding of actin past the myosin filaments. It is the sliding of these filaments that produces the cellular contraction. During the time, calcium is entering the cells, the channels of K+ that happen to leak some potassium out of the cell become impermeable to the ions. Due to that, in addition to prolonged release of Ca+, the depolarization phase extends. On a plotted graph of the action potential against time, this depolarization phase looks like a plateau. After the long phase of depolarization, repolarization phase sets in, which leads to the relaxation process of the cardiac fibers.

Repolarization occurs when the potassium ion channels open. Potassium the moves out of the cell by a process called diffusion[3]. Concurrently, calcium ion channels close, restricting the movement of these ions. With all these events in place, the original polarization state of the cardiac fiber sarcolemma is restored. The only difference from the previous state is that there is a reversal of the Na+ and K+ on each side of the sarcolemma.

After that, the refractory period sets in. The concentration of sodium and potassium ions is restored to their initial sides of the plasma membrane of the fibers. That is aided by the sodium-potassium ion pumps, which pump the respective ions to their appropriate sides of the sarcolemma. Once this happens, the cardiac fibers can’t contract anymore potassium and sodium ions are restored to their previous membrane resting potential states. The resting membrane potential of the cardiac fibers is about -90mV[4]. The refractory period of these fibers is a bit longer than that of the skeletal fibers. With this in place, the cardiac muscle fibers cannot go into titanic contraction. Such a refractory period gives the heart chambers time to refill with adequate blood before the next phase of contraction, which leads to ejection of blood from the heart chambers into the arteries.

In summary, the relaxation phase is coupled with refilling of the heart with blood. During the contraction phase, the heart ejects the same blood to the appropriate body tissues. The contraction phase is marked with depolarization of the sarcolemma. On the other hand, the repolarization phase is the one that is coupled with the relaxation of the myocardial fibers. If the appropriate ions and channels aren’t functioning well, then the cardiac fibers may not contract and relax well, which can compromise the heart function.

Bibliography

Brazier, Mary. A History of Neurophysiology in the 19th Century. New York: Raven Press, 1988.

Grodins, Fred. “Integrative cardiovascular physiology: a mathematical synthesis of cardiac and blood vessel hemodynamics.” Quarterly Review of Biology (1959): 93-116.

Katz, Arnold and Beverly Lorell. “Regulation of cardiac contraction and relaxation.” Circulation 102, no. Suppl 4 (2000): Iv-69.

Pinnell, Jeremy, Simon Turner, and Simon Howell. “Cardiac muscle physiology.” Continuing Education in Anaesthesia, Critical Care & Pain 7, no. 3 (2007): 85-88.

[1] Fred Grodins. ‘‘Integrative cardiovascular physiology: a mathematical synthesis of cardiac and blood vessel hemodynamics.’’ (Quarterly Review of Biology 1959): 93-116.

[2]. Jeremy Pinnell, Turner Simon and Simon Howell. ‘‘Cardiac muscle physiology.’’ In Continuing Education in Anaesthesia (Critical Care & Pain 7, no. 3, 2007): 85-88.

[3] Mary Brazier. A History of Neurophysiology in the 19th Century (New York: Raven Press, 1988), 462-507.

[4] Katz, Arnold Katz and Lorell Beverly. “Regulation of cardiac contraction and relaxation.” (Circulation 102, no. Suppl 4, 2000): Iv-69.