Equine Physiology Workbook

The Frank-Starling Law of Heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations. For example, if the left side of the heart pumps a little more blood than the right, the volume of blood returning to the heart (venous return) increases. This increases EDV and causes the right ventricle to contract more forcefully on the next beat, bringing the two sides back into balance.

2) Contractility: the forcefulness of contraction of individual ventricular muscle fibres.

Contractility is really the strength of contraction at any given preload. Certain substances can increase or decrease contractility. Positive Inotropic Agent : increases contractility. These often promote Ca++ inflow during cardiac action potentials which strengthens the force of contraction. Stimulation of the sympathetic nervous system, hormones such as epinephrine and norepinephrine, and increased Ca++ levels in the interstitial fluid. Negative Inotropic Agent : decrease contractility. Examples include inhibition of the sympathetic nervous system, anoxia, acidosis, some anesthetics, and increased K+ levels in the interstitial fluid. Drugs such as Ca++ channel blockers also have a negative inotropic effect and ultimately decrease the strength of the heartbeat. 3) Afterload: the pressure that must be exceeded before ejection of blood from the ventricles can occur. Ejection of blood from the heart begins when pressure in the right ventricle exceeds the pressure in the pulmonary trunk (~ 20mmHg) and when pressure in the left ventricle exceeds the pressure in the aorta (~ 80mmHg). The higher pressure(s) cause the blood to push the valves open. Therefore: Afterload can more accurately be defined as the pressure that must be overcome before a semilunar valve can open . Increased afterload reduces stroke volume as more blood remains in the ventricles at the end of systole.

Regulation of Heart Rate

The SA node sets the pace and if left alone, would set a constant HR of ~ 100 beats/min.

Since tissues require different volumes of blood under different conditions, we cannot have a constant HR. Stroke volume may decrease in cases of blood loss. Therefore, homeostatic mechanisms affect heart rate and contractility and ultimately cardiac output. The most important regulators of this are the ANS and hormones released by the adrenal medullae.

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