INTRODUCTION Cardiac Location and Structures The heart is the driving force of the circulatory system, contracting about 70 times/minute to pump an adequate volume of blood with sufficient pressure to perfuse all body organs and tissues. The muscular organ, about the size of a clenched fist, weights from 300 to 400 g. It is located within the mediastinum of the thoratic cavity, above the diaphragm and between the lungs. This location subjects the hearts activity to influence from all pressure variances during respiration, Fassler, (1991). Intrathoracic pressure varies with the respiratory cycle. On inspiration, the heart moves slightly vertically, and the increased negative pressure generated in the thoracic cavity increases venous blood return to the heart and pulmonary blood flow.

On respiration, the heart moves slightly horizontally as the diaphragm rises, and a decreased negative pressure is generated. The pericardial sac is a fibrous membrane that doubles over onto itself to form two surfaces. A small amount of pericardial fluid in the sac allows the two surfaces to slide over each other without friction as the heart beats. The pericardium performs several functions. First, it provides shock-absorbing protection.

Second, it acts as a protective barrier against bacterial invasion from the lungs. Third, because of its fibrous nature, it protects the heart from sudden overdistention and increase in size, Fassler, (1991). The heart has three tissue layers: the epicardium (outer layer), the myocardium (middle layer), and the endocardium (inner layer). The epicardium is the thin inner layer of the pericardium. The myocardium, thickest of the three layers, is composed of muscle fibers that contract, creating the pumping effect of cardiac activity.

The endocardium, a smooth, membranous layer that lines all cardiac chambers and valve leaflets, is continuous with the intima, or lining, of the aorta and arteries, Fassler, (1991). The hearts four chambers the right and left atria and left atria and the right and left ventricles are separated by the interatrial and interventricular septa. The atria are thin-walled, low-pressure chambers that serve primarily as reservoirs for blood flow into the ventricles. The ventricles are formed by muscle fibers that contract to eject blood to the pulmonary vasculature (right) and systemic circulation (left). Because the left ventricle must achieve the high pressure needed for systemic circulation, it is much thicker than the right ventricle, (Fig. #1), Fassler, (1991).

The right atrium receives venous blood from the body via the venae cavae. The superior vena cava returns blood from the structures above the diaphragm, and the inferior vena cava drains venous blood from below the diaphragm. The coronary sinus returns venous blood to the right atrium. At the base of the right atrium is the tricuspid valve, which controls blood flow into the right ventricle and prevents back flow to the atrium during ventricular systole. The tight ventricle pumps blood through the pulmonary valve and the branches of the pulmonary artery to the lobes of the lungs, the pulmonary capillaries, and the alveolar capillaries that surround the alveoli, (Fig. #2), Fassler, (1991).

At the alveolar capillaries, gas exchange occurs, that is, blood gives off carbon dioxide and receives oxygen. Then, oxygenated blood returns through the pulmonary veins to the left atrium. The mitral valve at the base of the left atrium controls blood flow to the left ventricle and prevents backflow to the left atrium. Both the mitral and the tricuspid valves are attached to the strong chorae tendineae, fibrous filaments that arise from the papillary muscles of the ventricle Fig. (#1) Location of cardiac structures, Fassler, (1991).

Fig. (#2) Blood flow through the heart, Fassler, (1991). and work to prevent eversion of the valves when the ventricle contracts, The left ventricle pumps blood through the aortic valve into the aorta, (Fig. #3), Fassler, (1991). The basic contractile unit in the myocardium, the sarcomere, is composed of actin and myosin filaments, which are contractile proteins.

The degree to which actin and myosin overlap depends on the length of the sarcomere, which is determined by muscle stretch. Less overlap occurs during diastole, as the ventricle fills and the muscle stretches; more overlap occurs during diastole, when the muscle contracts. Contraction occurs when the action potential stimulates movement of calcium with energy release, causes the filaments to slide past each other and shorten sarcomere, Fassler, (1991). Cardiac Cycle The heart ejects blood during ventricular systole, which comprises approximately one-third of the cardiac cycle. The cardiac muscles relax during diastole, which comprises the remaining two-thirds of the cardiac cycle. The first phase of systole, called isovolumetric contraction, begins with closure of the tricuspid and mitral valves. Pressure in the walls of the ventricles builds in preparation for mechanical contraction.

When ventricular pressure becomes higher than pressure in the aorta and pulmonary artery, the pulmonary and aortic valves open, allowing for paid ejection of blood. Blood is ejected rapidly at first and then more slowly as pressure decreases. Pressure in the ventricles continues to fall until the aortic and pulmonary valves close. Closure of the valves begins the first phase of diastole, called isovolumetric relaxation. During this time, ventricular pressure continues to decrease.

When pressure in the ventricles becomes less than atrial pressure, the tricuspid and mitral valves open, permitting rapid ventricular fillings. The ventricle continues to fill until atrial contraction occurs. Atrial Fig. (#3) Coronary Artery Circulation, Fassler, (1991) contraction contributes the final volume for ventricular filling, Fassler, (1991). Pulmonary Circulation The right side of the cardiac pump, consisting of the right atrium and right ventricle, delivers venous blood to the lungs for oxygenation. The thin-walled pulmonary vessels have little medial muscle and offer six times less resistance than systemic blood vessels.

Since the pulmonary vessels offer little resistance, the right ventricle is considered a low-pressure pump, Fassler, (1991). Systemic Circulation The left side of the cardiac pump, consisting of the left atrium and left ventricle, generates the high pressures necessary to overcome peripheral vascular resistance and to deliver oxygenated arterial blood to all body tissues. Because the left ventricle has a larger muscle mass than the right ventricle, must generate more pressure, and contract with greater strength, it has a greater need for oxygen. Thus, the left ventricle is particularly susceptible to the effects of deficient oxygen supply, Fassler, (1991). Coronary Circulation Coronary artery circulation delivers oxygenated blood to the heart, primarily during diastole.

The small coronary arteries branch off the aorta and encircle the heart at the epicardial layer. The arteries continue to branch and enter the myocardium and endocardium, becoming arterioles and then capillaries. The right coronary artery branches to the right from the aorta and supplies blood to the right atrium, the right ventricle, the sinoatrial (SA) and atrioventricular (AV) nodes of the conduction system, and, in most people, the inferior-posterior wall of the left ventricle. The left coronary artery bifurcates into the left anterior descending and circumflex coronary supplies the left atrium and the left ventricle. In some people, the circumflex artery also provides oxygenated blood to the posterior surfaces of the left atrium and left ventricle, Fassler, (1991). Hemodynamics Cardiac output refers to the volume of blood ejected by the left ventricle into the aorta in 1 minute-normally, about 4 to 6 liters/minute at rest.

Cardiac output is a product of the heart rate multiplied by the stroke volume, the amount of blood ejected from the left ventricle with each beat. The heart rate may vary form second to second or minute to minute. The stroke volume may vary from beat to beat, Fassler, (1991). Heart Rate A change in heart rate can dramatically affect cardiac output. For instance, when the heart rate increases, cardiac output may double or triple. In a person with heart disease, such an increase can be dangerous because it decrease diastolic filling time, increases oxygen demand, and decreases coronary artery perfusion time.

Conversely, if the heart rate falls below 50 beats/minute, cardiac output usually decreases, Fassler, (1991). Stroke Volume Variables influencing the stroke volume include preload, afterload and contractility. Preload is the volume of blood that fills the ventricle at the end of diastole. An increase in diastolic volume increases muscle stretch and subsequent stroke volume. Either excessive or inadequate preload can increase the hearts work load and decrease the stroke volume. Afterload, the resistance to flow from the ventricle, increase secondary to vasoconstriction in the peripheral blood vessels or to increased resistance, such as aortic stenosis.

Increases in afterload result in greater oxygen demand because the heart must use more contractile energy to eject blood. Contractility refers to the ability of cardiac muscle fibers to shorten. Calcium within the cell allows protein fibers to be attracted to each other causing muscle shortening. The contractile (or inotropic) state of the myocardium can be influenced by many factors. For instance, epinephrine, dopamine, and sympathetic nervous system stimulation exert a positive inotropic effect (increase contractility), whereas hypoxemia, acidosis, and such drugs as propranolol (Inderal) exert a negative inotropic effect (decrease contractility), Fassler, (1991). Arterial Blood Pressure The pressure exerted on the arterial wall as blood flows through the arteries is called arterial blood pressure, a product of the cardiac output and the total peripheral resistance, which is determined by blood viscosity and by the length and internal diameter of the vessels. Arteries have a medial or muscle layer in their wall that permits constriction or dilation of the vessel.

Thus, peripheral vascular resistance and blood pressure are affected by vasoconstriction and vasodilation, Fassler, (1991). Cardiac Innervation Innervation of the heart involves the autonomic nervous system and the baroreceptor and Bainbridge reflexes. Autonomic Nervous System The autonomic nervous system influences cardiac activity through sympathetic and parasympathetic verve fibers. Sympathetic fibers are found in the atrial and ventricular walls, the SA and AV nodes. The sympathetic effect on the heart is mediated through beta receptor sites and release of norepinephrine. Stimulation of beta receptors increase heart rate, conduction velocity, and contractility. The major effects are usually on the SA node, increasing heart rate, and the myocardial muscle.

The sympathetic nervous system also has receptor, sites, primarily alpha and beta receptors in peripheral blood vessels. When the sympathetic nervous system is stimulated, the alpha effects predominate in the blood vessels and cause vasoconstriction. The parasympathetic effects on the heart are mediated through release of acetylcholine at nerve endings in the SA node, atrial muscle, and AV node. Parasympathetic or vagal stimulation decrease heart rate and conduction velocity, Fassler, (1991). Baroreceptor and Bainbridge Reflexes The baroreceptor reflex mediates heart rate as well as peripheral vascular resistance.

The baroreceptors-specialized pressure-sensitive tissue located in the aortic arch and carotid sinuses-increase their rate of discharge when they are stretched by increase blood pressure. Impulses are transmitted to the cardiovascular center in the medulla. The cardiovascular center decreases sympathetic stimulation and increases parasympathetic stimulation, thereby decreasing heart rate initiating blood vessel dilation. Conversely, baroreceptors also respond to decreasing blood pressure by increasing heart rate and vasoconstriction, Fassler, (1991). The Bainbridge reflex is thought to be mediated by stretch receptors in the atria.

These receptors may respond to increased volume and cause an increase in heart rate. Contractility is unaffected by the Bainbridge reflex, Fassler, (1991). CORRELATION OF PHYSIOLOGIC EVENTS TO ELECTRICAL EVENTS RECORDED ON THE ECG Through out the cardiac cycle the heart produces a series of action potentials. This sequence of action potential produces a series of deflections that represents different events within the cardiac cycle. The classic series of deflections constituting one cardiac cycle is: P wave, QRS complex, and T wave.

The significance of these deflections (and the intervals between) is explained as follows, (Graph #1), (Fig. #4), Murphy, (1991). P Wave The first wave of the cycle, the P wave, represents the spread of electrical depolarization throughout the atria, Murphy, (1991). PR Interval The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. It represents the time it takes for the electrical impulse to travel from the atria to the ventricles.

Thus the PR interval has two components: (1) the P wave (time needed to depolarize the atria) and (2) the PR segment (end of P wave to beginning of the QRS complex, representing the time the impulse spends in the AV node), Murphy, (1991). QRS Complex Fig. (#4) Normal cardiac intervals, Murphy, (1991). The QRS complex represents the spread of electrical depolarization throughout ventricular muscle. The QRS complex is composed of several wave outlined in detail below, Murphy, (1991). Q Wave The Q wave is the first negative deflection preceding an R wave (regardless of the size of the deflection).

A Q wave is always downward in direction. This wave usually represents depolarization of the muscular interventricular septum in the frontal leads (I, II, III, aVR, aVL, aVF). Abnormally deep Q waves in these leads are often seen with myocardial infarction, Murphy, (1991). R Wave The R wave is the first positive deflection of the complex. In the frontal leads this wave represents depolarization of the main bulk of ventricular muscle.

An R wave is always directed upward regardless of a preceding Q wave, Murphy, (1991). S Wave The S wave is the negative deflection following an R wave. An S wave usually represents the late depolarization of the last bit of left ventricular muscle. In the anterior precordial leads (V, to V3) the S wave is large because of the normal slightly posteriorly directed mean QRS vector, Murphy, (1991). T Wave T wave represents ventricular repolarization. ST Segment The ST segment is mea …