The Normal Physiology of the Heart

Vikkineshwaran Siva Subramaniam The heart normally functions to support the process of maintaining homeostasis of the body by propelling blood which transports nutrients, waste products, chemicals etc. Cardiac muscle cell action potentials differ sharply from those of skeletal muscle cells in three important ways that promote synchronous rhythmic excitation of the heart: they can be self-generating, they can be conducted directly from cell to cell and they have longer durations which prevents tetanus occurring. The cardiovascular system is mediated intrinsically by the cardiac autoregulator mechanism while extrinsically by nervous and humoral effects. The cardiac cycle is the sequence of events that make up one heartbeat. It starts with blood entering and then getting pumped out of the heart. Two events occur during this cycle: the electrical events followed by the mechanical events. The cardiac cycle can also be divided into two phases: systolic and diastolic phase. The electrical events of the heart happen between specialised cells, called the pacemaker cells. A special property of these cells is that they have an inherent rhythmicity and can depolarize spontaneously. These cells are found in the sinoatrial node, the atrioventricular node, Bundle of His, and Purkinje cells. The SA node, having the fastest depolarization rate usually sets the heart rate. In its absence, the AV node, Bundle of His and Purkinje cells will still depolarize rhythmically but at a much slower rate. The pacemaker cells are responsible for the automaticity characteristic of the heart. The contractile myocardial tissues are not capable to this special pacemaker property and hence they can only respond to receiving impulse by contracting and passing along the impulse. The cardiac cycle begins with depolarization initiating from SA node and spreading throughout the atrium. This results in atrial systole. The impulse will then reach the AV node. There will be a small delay here, giving time for the ventricles to completely fill. Impulses will then travel from the AV node to the Bundle of His and then branch left and right travelling via the Purkinje cells throughout the ventricles and produce ventricular systole.

The electrocardiogram (ECG) is used to record the spread of electrical potentials and acts as a diagnostic tool in studying the heat. The mechanical events of the heart involve pressure changes in the heart chambers and blood vessels, and the opening and closing of the valves. The events occurring can be matched with the cardiac cycle pattern obtained in ECG. In an ECG, the P wave resembles atrial depolarization; QRS complex resembles the ventricular depolarization while the T wave resembles ventricular repolarization. Almost 70% of the blood flows without any contraction, from the atrium into the ventricle. Atrial contraction increases ventricular filling by 10% and this contraction is shown in P wave. R wave coincides with ventricular contraction, where the intraventricular pressure increases closing mitral and tricuspid valves. This produces first heart sound. When the ventricular pressure gets higher than the pressure in aorta and pulmonary vein, the semilunar valves open and ventricular ejection follows. Blood release will decrease pressure in ventricles and the semilunar valves close producing second heart sound. This happens at T wave. Aortic valve closes slightly earlier than pulmonic valve producing the third heart sound which can be heard in children and young adults. The normal adult blood volume is about 5l, of which 1.5l are in the heart and lungs, 0.9l in pulmonary arteries, capillaries and veins and 75ml in pulmonary capillaries. About 0.6l of blood is in the heart, of which left ventricular EDV is 140ml, stroke volume 90ml and ejection fraction about 70% for each ventricle. At rest, the normal pressure is usually higher in ventricles than atrium. The systolic pressure is always higher than diastolic. Left ventricle has the highest pressure while right atrium the lowest pressure. Cardiac output is the volume of blood pumped out by heart and is expressed in cardiac index. The mean cardiac index in about 3.5l/min/m 2. Estimated pulmonary or systemic vascular resistance is the difference between mean inflow and outflow pressures, divided by flow through the respective circulations. Flow equals cardiac output in normal individuals. Stroke work is the estimated product of stroke volume and mean ejection pressure. Hearts performance can be equated to cardiac output, which is stroke volume multiplied by the heart rate. Stroke volume is affected by preload, afterload and contractility. According to the Frank Starling mechanism, the heart
2

pumps blood that is returned to it. Increasing venous return and ventricular preload leads to an increase in stroke volume. Hearts contractile response depends on the intrinsic state of the muscle, autonomic stimulation and extrinsic inotropic influences. Afterload can be viewed as the load that the heart must eject blood against. It is closely related to aortic and pulmonary resistance. An increase in ventricular volume will cause the ventricle to increase in diameter, also cause a rise in the intraventricular pressure and surface area. This leads to an increase in wall tension. An increased wall tension will result in an increase in the myocardial oxygen demand, so contraction becomes less efficient. Coronary blood flow accounts for about 4% of cardiac output. The heart extracts most (70%) of the oxygen carried in the coronary circulation. The arteriovenous difference for oxygen across the heart is ~110 ml/litre, compared with ~40 ml/litre for the whole body under resting conditions. Elevated myocardial oxygen requirements are met largely by increases in coronary blood flow. Most of this supply is to the left ventricle, two-thirds occurring during diastole. Myocardial oxygen requirements and coronary blood flow are finely adjusted - major determinants are myocardial metabolism, aortic pressure, myocardial extravascular compression during systole, and the level of neurohumoral control. Coronary flow is closely related to coronary perfusion pressure and myocardial oxygen consumption. Sharp increases in flow occur when coronary venous oxygen content falls below 5 ml/100 ml. There are individual contributions from endothelial-derived nitric oxide, adenosine, vasodilator prostaglandins, and myocardial oxygen and carbon dioxide tensions. In addition, there is diurnal variation in systemic autonomic function; the normal early morning adrenergic surge results in increased vascular tone and blood pressure. Adverse cardiac events (e.g. acute myocardial infarction) occur more commonly at this time. Exercise leads to an increase in cardiac output. Sympathetic stimulation increases while parasympathetic decreases. Heart rate increases, venous return increases and vasodilation is seen in active areas. There is a marked reduction in total peripheral vascular resistance, which reduces afterload and encourages greater systolic emptying of the left ventricle. Despite the reduced peripheral
3

resistance, systolic blood pressure and pulse pressure both increase due to elevated cardiac output, but pulmonary pressure only slightly. The speed and force of cardiac contraction is increased, ejection fraction and stroke volume elevated, and enhanced adrenergic stimulation results in a left shift of the Frank Starling curve. There is a rapid rise in coronary blood flow to meet myocardial oxygen requirement. Hemodynamic and ventilator responses take about 2-3 minutes to equilibrate and adjust oxygen supply to the greater demand of a new steady workload. The heart rate at peak exercise is about 200beats/minute in healthy 20year olds while 170beats/minutes at 65years. Determinant of duration of exercise are limiting symptoms like shortness of breath, fatigue and muscle pain. When exercise stops, cardiopulmonary and metabolic changes return rapidly to resting levels, exponentially at first. Reduced circulatory function slows the recovery rate. Regular exercise to about 60% of maximal heart rate for 20-30 three times a week is the minimum requirement for improved effort tolerance through a training effect. The resting heart rate becomes slower, cardiac output is maintained by increased EDV and stroke volume, the heart rate response to a standard submaximal workload is reduced and skin circulations to working muscles and oxygen extraction from perfusing blood is improved. Rhythmic exercise causes a rise in blood pressure while isometric exercise is not recommended for cardiac patients because it causes an increase in afterload. Regular exercise may partly prevent endothelial dysfunction associated with ageing, improve nitric oxide availability and reduce blood pressure in normotensive and mildly hypertensive individuals via modulation of catecholamine release. Amongst other diverse exercise-induced hormonal changes, reduced glucosestimulated insulin release is of particular clinical relevance in individuals with type2 diabetes.