We may describe the actions of the heart chambers as independent actions, but they do not function independently. Instead, their actions are regulated so that the atrial walls contract while the ventricular walls are relaxed, and ventricular walls contract while the atrial walls are relaxed. Such a series of events constitutes a complete heartbeat, or a cardiac cycle.

During a cardiac cycle, the pressure within the chambers of the heart rises and falls continuously as blood is moved from chamber to chamber. When the atria are relaxed, blood flows into them from the vena cavae and pulmonary veins. As the atria fill, the pressure inside gradually increases. About 70 percent of the entering blood flows directly into the ventricles through the atrioventricular opening before the atrial walls contract.
During atrial contraction (atrial systole), the atrial pressure rises suddenly, forcing the remaining 30 percent of the atrial blood into the ventricles. This is followed by atrial relaxation (atrial diastole)
As the ventricles contract (ventricular systole), the tricuspid and bicuspid valves guarding the atrioventricular openings close passively (due to the pressure of blood forced upward, against the valves) and begin to bulge back into the atria, causing the atrial pressure to rise sharply. At the same time, the papillary muscles contract, and by pulling on the chordae tendineae, they prevent the cusps of these valves from inverting too far into the atria.

• Atrial pressure soon falls, however, as the blood flows out of the ventricles into the arteries. During the ventricular contraction, the tricuspid and bicuspid valves remain closed, and the atrial pressure gradually increases as the atria fill with the blood. When the ventricles relax (ventricular diastole), these valves open passively, the blood flows through them into the ventricles, and the atrial pressure drops to a low point.
• Pressure in the ventricles is low while they are filling, but when the atria contract, the ventricular pressure increases slightly. Then, as the ventricles contract, the ventricular pressure rises sharply, and as soon as the pressure exceeds that in the atria, the tricuspid and bicuspid valves close.
• The ventricular pressure continues to increase until it exceeds the pressure into the pulmonary trunk and aorta. Then, the pulmonary and aortic valves open, and blood is ejected from the ventricles into these arteries. When the ventricles are nearly empty, the ventricular pressure begins to drop, and it continues to drop as the ventricles relax. when the ventricular pressure is less than that in the arteries, the pulmonary and aortic valves are closed by arterial blood flowing back toward the ventricles.
• As soon as the ventricular pressure falls below that of the atria, the tricuspid and bicuspid valves open, and the ventricles begin to fill once more.

The sounds associated with a heartbeat can be heard with a stethoscope and are described as a lub-dub sound. The sound is due to vibrations through the heart tissue that is created as the blood flow suddenly speeds or slows with the contraction and relaxation of the heart chambers and with the opening and closing of the valves.

The first part of a heart sound (lub) occurs during the ventricular contraction, when the tricuspid and bicuspid are closing. The second part (dub) occurs during ventricular relaxation, when the pulmonary and aortic valves are closing.

The sounds that the heart makes can be diagnositc for certain heart disorders. One such example is cases of Endocarditis, or an inflammation of the endocardium. This can cause a change of shape for the valves (valvular stenosis), preventing proper closure, and allow some backflow of blood. This leads to an abnormal heart sound, called a murmur. The degree of murmur indicates the degree of valvular damage, which can be repaired with surgery.

Cardiac muscle fibers function much like those of skeletal muscles. In cardiac muscle, however, the fibers are interconnected in branching networks that spread in all directions through the heart. This allows an impulse travels to all parts of the heart when any portion of this net is stimulated. The whole structure contracts as a unit in a wave-like manner. Cardiac muscle cells are also connected by specialized regions of membrane called intercalated disks. These disks are highly folded potions of cell membrane which increases the surface area connecting two cells and reduces the electrical resistance between cells, thus allowing them to act more as one unit.

A mass of merging cells that act as a unit is called a functional syncytium. There are two such structures in the heart - one in the atrial walls and another in the ventricular walls. These masses of muscle fibers are separated from each other by portions of the heart's fibrous skeleton, except for a small area in the right atrial floor. in this region, the atrial syncytium and the ventricular syncytium are connected by fibers of the cardiac conduction system. These units allow for the coordination of contraction between the atria and ventricles.

Throughout the heart are clumps and strands of specialized cardiac muscle tissue whose fibers contain only a few myofibrils. These portions of tissue are not designed for contraction, but instead they initiate and distribute impulses (cardiac impulses) through the myocardium. They are the cardiac conduction system, which functions to coordinate the events occurring during the cardiac cycle.

A key portion of the conduction system is called the sinoatrial node (S-A node). It consists of a small mass of specialized muscle tissue just beneath the epicardium. It is located in the posterior wall of the right atrium, below the opening of the superior vena cava, and its fibers are continuous with those of the atrial syncytium.

The cells of the S-A node have the ability to excite themselves, without being stimulated by nerve fibers or any other source, The cells of the S-A node initiate impulses that spread into the myocardium and stimulate the cardiac muscle fibers to contract. This activity is rhythmic, with the S-A node initiating one impulse after another, seventy to eighty times a minute. Because it is responsible for the rhythmic contractions of the heart, it is often called a pacemaker.

As a cardiac impulse travels from the S-A node into the atrial synctium, the right and left atria contract almost simultaneously. The impulse does not pass directly into the ventricular syncytium, separated from the atrial synctium by the fibrous skeleton of the heart, the cardiac impulse passes along fibers of the conduction system that are continuous with atrial muscle fibers. These conducting fibers lead to a mass of specialized muscle tissue called the atrioventricular node (A-V node). This node, located in the floor of the right atrium near the septum between the atria (interatrial septum) and just beneath the endocardium, provides the only normal conduction pathway between the atrial and ventricular syncytia.

The fibers that conduct the cardiac impulse into the A-V node (internodal fibers) have very small diameters, and because small fibers conduct impulses slowly, they cause the impulse to be delayed. The impulse is delayed still more as it travels through the A-V node, and this delay allows time for the atria to empty and the ventricles to fill with blood. Once the cardiac impulse reaches the other side of the A-V node, it passes into a group of large fibers that make up the A-V bundle (Bundle of His), and the impulse moves rapidly through them. The A-V bundle enters the upper part of the interventricular septum, and divides into right and left branches that lie just beneath the endocardium. About halfway down the septum, the branches give rise to the enlarged Purkinje fibers. The Purkinje fibers spread from the interventricular septum, into the papillary muscles, which project inward from the ventricular walls, and then continue downward to the apex of the heart. There, they curve around the tips of the ventricles and pass upward over the lateral walls of these chambers. Along the way, the Purkinje fibers give off many small branches, which become continuous with cardiac muscle fibers.

The muscle fibers in the ventricular walls are arranged in irregular whorls, so that when they are stimulated by the impulses on the Purkinje fibers, the ventricular walls contract with a twisting motion. This action squeezes, or wrings, the blood out of the ventricular chambers and forces it into the aorta.

A recording of the electrical changes that occur in the myocardium during a cardiac cycle is called an electrocardiogram (ECG). These changes result from the depolarization and repolarization (movement of the electrical pulse over the muscle cells) associated with the action potentials occurring in contracting cardiac muscle fibers. Because the body fluids can conduct electrical currents, such changes can be detected on the surface of the body.

To record an ECG, electrodes are placed at certain locations on the skin. These electrodes are connected by wires to an instrument that responds to very weak electrical changes by causing a pen or stylus to mark on a moving strip of paper. When the instrument is operating, up-and-down movements of the pen correspond to electrical changes occurring as a result of myocardial activity.

Because the paper moves past the pen at a known rate, the distance between pen deflections can be used to measure the time elapsing between the various phases of the cardiac cycle.

The normal ECG pattern includes several deflections, or waves, during each cardiac cycle. Between cycles, the muscle fibers remained polarized, and no detectable electrical changes occur. Consequently, the pen does not move but creates a baseline as the paper passes through the instrument. When the S-A node triggers a cardiac impulse, however, the atrial fibers are stimulated to depolarize, and an electrical change occurs. As a result, the pen is deflected, and when this electrical change is completed, the pen returns to the base position. This first pen movement produces a P wave that is caused by depolarization of the atrial fibers just before they contract.

When the cardiac impulse reaches the ventricular fibers, they are stimulated to depolarize rapidly. Because the ventricular walls are much more extensive than those of the atria, the amount of electrical change is greater, and the pen is deflected to a greater degree than before. As before, when the electrical change is completed, the pen returns tot he baseline, leaving a mark called the QRS complex, which usually consists of a Q wave, an R wave, and S wave. This complex appear just prior to the contraction of the ventricular walls.

Near the end of the ECG pattern, the pen is deflected once again, producing a T wave. This wave is caused by the electrical changes occurring as the ventricular fiber become repolarized relatively slowly. The record of the atrial repolarization is missing from the pattern because the atrial fibers repolarize at the same time that the ventricular fibers depolarize. The recording of the atrial repolarization is thus obscured by the QRS complex.

The primary function for the heart is to pump the blood to the body cells, and when the needs of these cells change, the quantity of the blood pumped must change also. For example, during strenuous exercise, the amount of blood required by the skeletal muscles increases greatly, and the rate of the heartbeat increases in response to this need. Since the S-A node normally controls the heart rate, changes in this rate often involve factors that affect the pacemaker. These include the motor impulses carried on the parasympathetic and sympathetic nerve fibers.

The parasympathetic fibers that supply the heart arise from neurons in the medulla oblongata. Most of these fibers branch to the S-A and A-V nodes. When the nerve impulses reach their endings, these fibers secrete acetylcholine, which causes a decrease in S-A and A-V nodal activity. As a result, the rate of heartbeat decreases.

The parasympathetic fibers seem to carry impulses continually to the S-A and A-V nodes, and these impulses impose a braking action on the heart. Consequently, parasympathetic activity can cause the heart rate to change in either direction. An increase in the impulses causes a slowing of the heart, and a decrease in the impulses releases the parasympathetic brake and allows the heartbeat to increase. Sympathetic fibers also reach the heart and join the S-A and A-V nodes as well as other areas of the atrial and ventricular myocardium. The endings of these fibers secrete norepinephrine, and this substance causes an increase in the rate and force of myocardial contractions.

A normal balance between the inhibitory effects of the parasympathetic fibers and excitatory effects of the sympathetic fibers is controlled by the cardiac center of the medulla oblongata. This center receives sensory impulses from various parts of the circulatory system and relays motor impulses to the heart in response.

For example, receptors that are sensitive to being stretched are located in certain regions of the aorta (aortic sinus and aortic arch) and in the carotid arteries (carotid sinuses). These receptors, called pressoreceptors (baroreceptors), can detect changes in the blood pressure. For example, if the pressure rises, the pressoreceptors are stretched, and they signal the cardiac center in the medulla. In response, the medulla sends parasympathetic motor impulses to the heart, causing the heart rate and force of contraction to decrease. This response also causes the blood pressure to drop toward the normal level. If pressure is low, these receptors signal a need to increase rate (and thus increase pressure). Obvioulsy there is a fine balance to be achieved.

The cardiac control center can also be influenced by impulses from the cerebrum or hypothalamus. Such impulses may cause the heart rate to decrease, as occurs when a person faints following an emotional upset; or they may cause the heart rate to increase during a period of anxiety.

Two other factors that influence the heart rate are temperature change and the presence of various ions. Heart action is increased by a rising body temperature and is decreased by abnormally low body temperature. Consequently, a patient's body temperature is sometimes deliberately lowered (hypothermia) to slow the heart during surgery.

Of the ions that influence heart action, the most important are potassium (K+) and calcium (Ca++) ions. An excess of potassium ions (hyperkalemia) for example, results in a decrease in the rate and force of contractions. If the potassium concentration drops below normal (hypokalemia ), the heart may develop a serious abnormal rhythm (arrhythmia).

Excessive calcium ions (hypercalcemia) cause increased heart actions, and there is danger hat the heart will undergo a prolonged contraction. Conversely, low calcium concentration (hypocalcemia) depresses heart action.

Hormones may also effect the rate at which the heart will beat. The adrenal gland produces the hormone epinephrine (aka adrenaline), which stimulates the heart to beat faster. This hormone effects many structures, preparing them for stressful situations the body may encounter.