Blood enters the heart via the vena cava into the right atrium. From the right atrium the blood flows through the tricuspid valve into the right ventricle that serves to pump blood to the lungs for the exchange of gases. The blood is ejected through valves in the pulmonary artery. Upon return from the pulmonary vascular system the blood enters the left atrium via the pulmonary veins. Blood flows through the mitral valve to the thicker walled left ventricle that serves to forcefully pump blood through the aortic valve into the aorta and to the systemic vascular system.
The heart beats in an orderly sequence due to the characteristics of the heart muscle and a specialized electrical conduction system. Cardiac muscle is automatic, meaning that the tissue will spontaneously contract at a periodic rate that is without nervous or hormonal influences. It is also syncitial which means that if one cell has an action potential the electrical change will be transmitted to the others around it via gap junctions and the cells will contract as a unit.
Some cardiac muscle cells are specialized pacemaker cells. They spontaneously generate action potentials at a faster rate than other heart tissue. The primary pacemaker of the heart, the sinoatrial (SA) node, is located at the junction of the vena cava and right atrium. When these cells spontaneously discharge the impulse is carried via three tracts of internodal fibers to the secondary pacemaker called the atrioventricular (AV) node.
The electrical transmission is delayed a bit (about 0.1 second) at the AV node before rapidly traveling via the bundle of His and the Purkinje system to the ventricular muscle. The atria are electrically isolated from the ventricles by connective tissue except for the conductive bundle of His. The Purkinje system is a very rapid (4 m/s) conduction system that quickly distributes the electrical impulse to the ventricular muscle via branching fibers that radiate from the apex of the ventricles.
Heart rate must be regulated so that in times of metabolic need the tissues can be supplied with a greater flow of blood. Both the sympathetic and parasympathetic nervous systems alter the activity of the pacemakers to regulate the heart rate. In the adult the right vagus (parasympathetic) innervates mainly the SA node and the left vagus goes to the AV node. The sympathetic nervous system also innervates both nodes. Stimulation of the right vagus slows the rate of discharge of the pacemaker cells and therefore slows the heart rate. Stimulation of the left vagus causes the conduction speed through the AV node to decrease. The resting heart is normally under the influence of some parasympathetic stimulation.
Sympathetic stimulation at the SA node causes and increase in heart rate while stimulation on the left side causes faster conduction through the AV node. Besides the positive chronotropic effect (faster heart rate) sympathetic stimulation makes the heart muscle contract more forcefully (inotropic effect). This is in addition to the inherent inotropic effect of stretch on cardiac muscle known as the Frank-Starling effect. When more blood is returned to the heart the muscle is stretched causing the muscle to contract more forcefully. This adaptation allows the heart to pump the blood that is returned to it efficiently within a physiologic range of venous return.
The human heart rate without nervous system regulation would be 100 beats/min. With the normal vagal tone, the resting heart rate is about 70. If vagal influences are blocked, the heart rate increases to 150-180 due to sympathetic tone. Therefore, the conflicting influences of the sympathetic and parasympathetic systems are constantly in balance to regulate heart rate.
Coronary arteries that arise from the sinuses behind the aortic valve serve the heart muscle. The openings to these vessels are open throughout the cardiac cycle. The blood returns to the heart via the coronary veins which drain into the right atrium. Because contraction of the ventricle closes the coronary arteries feeding the subendocardial region of the left ventricle, this region is especially prone to damage due to ischemia. Blood flow in the coronary system is regulated by local chemical factors and adrenergic inputs.
At the start of ventricular systole the AV valves close and the ventricular pressure increases. When the ventricular pressure exceeds that of the aorta (80 mm Hg) and pulmonary arteries (10 mm Hg) the aortic and pulmonary valves open and blood is ejected. Left and right ventricular pressure rises to a maximum of about 120 mm Hg and 25 mm Hg, respectively. The AV valves are pulled down into the ventricle by the contraction of the ventricular muscle. About 70-90 ml of blood is ejected with each stroke, but about 50 ml remains in each ventricle. Cardiac output, an important index of cardiac function, is the product of stroke volume and heart rate.
Ventricular diastole begins with as the pressure drops and the aortic and pulmonary valves close. When the ventricular pressure falls below the atrial pressure the AV valves open and blood begins to quickly fill the ventricles.