Intrinsic Regulation of heart in animals
Frank’s Starling Mechanism/Heterometric Regulation
Regulation of the cardiac function is independent of the nervous or humoral control. This was proved by the Starling’s experiment using Starling’s heart lung preparation i.e., isolating the heart from the body so as to remove humoral and neural influences. The heart is perfused through the aorta with an oxygenated solution containing nutrients essential to maintain normal cardiac function. In this preparation, contractility of the heart is studied by allowing the isolated heart to do work under various degrees of pressure and load made in the pulmonary artery or aorta. Starling’s law of heart was derived from these studies and was initially known as Heterometric autoregulation and it states that the force or contraction is a function of the initial length of the muscle fibres i.e upto a physiological limit, greater the initial length, greater is the force of contraction.
An increase in the venous return to the heart increases the input of blood into the ventricles which stretches the ventricular wall and induces a stronger contraction during systole. According to this law the heart makes adjustments to load upon the ventricles during each beat without any neural or humoral influences.
Preload is the amount of stretch on the heart prior to contracttion. The load is directly proportional to the volume of blood in the ventricles or end diastolic volume. Greater ventricular filling during diastole, stretches the muscle fibres, causes increased fibre length and a greater amount of Ca++ release during systole resulting in increased force of contraction and stroke volume.
After Load is the pressure that must be exceeded by the ventricles before blood can be ejected through the semilunar valves is called as after load. The resistance is determined by the diameter of the arterioles and pre-capillary sphincters which is controlled by the sympathetic system which in turn, controls the tone of the arteriole muscles as well as the diameter of the blood vessels. Any factor that increases after load, will increase end systolic volume and decrease stroke volume.
Homeometric autoregulation
This type of regulation occurs when aortic blood pressure increases due to increase in cardiac output or increase in peripheral resistance to blood flow. When venous return is normal but the arterial pressure is increased by peripheral resistance, causes a reduction in the ventricular discharge for few beats and accumulation of ventricular blood volume. This causes subendocardial ischemia resulting in reduced contractile strength. Subsequently, the subendocardial ischemia is relieved by vascular autoregulation, the contractile strength increases without changing the muscle fibre length to pump normal blood volume against increased arterial resistance known as homeometric autoregulation and the ventricular volume returns to normal. The significance of homeometric regulation is to allow the ventricles to eject the same stroke volume against varying degrees of arterial resistance without an increase in end diastolic pressure or increase in myocardial fibre length during diastole.
Cardiac output will change to match changing metabolic demands of the body. The outputs of both ventricles must be identical, and also equal to the venous return of blood from the body. During exercise of the muscles, the increased blood flow through the blood vessels is due to increased metabolism. This causes increased venous return and preload to right ventricular and pulmonary circulation. Consequently, more blood is delivered to the left ventricle and cardiac output increases. There will also be increased contractility and heart rate from the sympathetic activity associated with exercise to meet tissue requirements.