Cardiac Output

Contractility of myocardial cells depends on the intracellular [Ca2+], which is regulated by Ca2+ entry across the cell membrane during the plateau of the action potential and by Ca2+ uptake into and release from the sarcoplasmic reticulum (SR). Ca2+ binds to troponin C and removes the inhibition of actin–myosin interaction, allowing contraction (shortening) to occur.

Factors That Cause a Hypoeffective Heart
► (1) Increased arterial pressure against which the heart must pump, such as in hypertension.
► (2) Inhibition of nervous excitation of the heart.
► (3) Pathological factors that cause abnormal heart rhythm or rate of heartbeat.
► (4) Coronary artery blockage, causing a "heart attack”.
► (5) Valvular heart disease.
► (6) Congenital heart disease.
► (7) Myocarditis, an inflammation of the heart muscle.

Explanation:
About 10% of the total blood volume can be removed with almost no effect on arterial pressure or cardiac output, but greater blood loss usually diminishes the cardiac output first and falls to zero when about 40% to 45% of the total blood volume has been removed.

Although heart function is obviously crucial in

determining cardiac output, the various factors of the  peripheral circulation that affect flow of blood into the heart  from the veins, called venous return, are normally the  primary controllers of cardiac output.

(Ref. Guyton & Hall-14th, P-245

কোন ব্যাখ্যা যোগ হয় নি।

Reference-Ganong physiology/26th/P-580/T-32-3

Explanation:

Explanation:

Explanation:

[Ganong 24th p-524]

A negative inotropic effect is one that decreases myocardial contractility. Contractility is the ability to develop tension at a fixed muscle length. Factors that decrease contractility are those that decrease the intracellular [Ca2+]. Increasing heart rate increases intracellular [Ca2+] because more Ca2+ ions enter the cell during the plateau of each action potential. Sympathetic stimulation and norepinephrine increase intracellular [Ca2+] by increasing entry during the plateau and increasing the storage of Ca2+ by the sarcoplasmic reticulum (SR) [for later release]. Cardiac glycosides increase intracellular [Ca2+] by inhibiting the Na+–K+ pump, thereby inhibiting Na+–Ca2+ exchange (a mechanism that pumps Ca2+ out of the cell). Acetylcholine (ACh) has a negative inotropic effect on the atria.