Figure 17-2 shows anterior and posterior views of the external heart surfaces. The right ventricle constitutes most of the anterior portion of the heart; the left ventricle is located more posteriorly. (Notice the small size of the atria compared with the ventricles.)

Figure 17-2 The heart and coronary arteries. A, Anterior view. B, Posterior view. (From Thibodeau GA, Patton KT: *Anatomy & physiology,* ed 3, St Louis, 1996, Mosby.)

Pericardium

The heart is covered with a loose-fitting membranous sac called the pericardium (Figure 17-3). The pericardium consists of a tough, fibrous outer portion continuous with the connective tissue covering the great vessels. Inferiorly, it attaches to the surface of the diaphragm. The fibrous pericardium limits overexpansion of the heart, holding it in place in the mediastinum. Inside the fibrous pericardium is a thin transparent membrane called the serous pericardium. The serous pericardium is a closed envelope containing a small amount of pericardial fluid. The part of the membrane that lines the inner surface of the fibrous pericardium is the parietal pericardium. The visceral pericardium, also known as the epicardium, is the part of the serous pericardium that is fused to the heart’s surface. The space between the parietal and visceral pericardium is the pericardial space. The fluid in this space lubricates the membranes, allowing smooth, frictionless movement. As the heart beats, it moves easily in its lubricated, fibrous jacket, protected from friction with other mediastinal structures. Figure 17-4 shows a close-up cross-section of the pericardial membranes.

Figure 17-4 Cross-section of the wall of the heart. (From Thibodeau GA, Patton KT: *Anatomy & physiology,* ed 3, St Louis, 1996, Mosby.)

Heart Wall

Three layers of tissue form the heart wall (see Figure 17-4): epicardium (visceral pericardium), myocardium, and endocardium. The myocardium is the heart muscle forming the bulk of the heart wall. This muscle wraps around the heart’s chambers in such a way that contraction ejects blood with great force. The endocardium lines the inner surfaces of the heart’s chambers; it resembles the smooth endothelial lining of the blood vessels (see Figure 17-4).

Heart Chambers and Valves

The heart is actually two separate muscular pumps—the right heart and the left heart—connected in sequence. The right heart pumps blood through the pulmonary circulation to the left heart, which pumps blood through the systemic circulation back to the right heart. Each heart consists of two chambers: an atrium located superiorly to a ventricle (Figure 17-5). The atria are weak pumps that prime the more powerful ventricles; they passively funnel blood into the ventricles except when they contract at the last instant to complete the filling process actively.

Figure 17-5 Valves and chambers of the heart. (From Patton KT, Thibodeau GA: *Anatomy & physiology,* ed 7, St. Louis, 2010, Mosby.)

The atria are thin-walled collecting chambers, whereas the ventricles are heavily muscled pumping chambers; the inner surfaces of the ventricles are muscle bundles undercut by open spaces called trabeculae carneae (see Figure 17-4). These irregular surfaces may prevent endocardial wrinkling and damage during ventricular contraction.¹ The muscle mass of the left ventricle is greater than the muscle mass of the right ventricle (see Figure 17-5) because the left ventricle pumps against a much greater resistance (systemic vascular resistance [SVR]) than the right ventricle (pulmonary vascular resistance [PVR]). The left ventricle is more spherical in cross-section than the right ventricle (Figure 17-6). The thinner walled right ventricle is crescent-shaped, appearing to wrap partly around and “hug” the left ventricle. This arrangement tends to flatten the right ventricle during left ventricular contraction, aiding ejection of blood by the right ventricle.

Figure 17-6 Cross-section of the ventricles.

The right atrium receives deoxygenated systemic venous blood from the superior and inferior vena cava and coronary venous blood from the coronary sinus. The left atrium receives oxygenated pulmonary venous blood from four pulmonary veins, two from each lung. Both atria channel their blood into the ventricles through one-way atrioventricular (AV) valves. These valves prevent backflow of blood into the atria during ventricular contraction. The right AV valve is the tricuspid valve (three cusps or leaflets); the left AV valve is the bicuspid (mitral) valve (two cusps). The two atria are separated by the interatrial septum, which prevents mixing of oxygenated and deoxygenated blood. A small depression in this septum marks the former location of the foramen ovale, an opening between the left and right atria during fetal life (see Chapter 16).

CONCEPT QUESTION 17-2

What are the consequences of a mitral valve that leaks or allows backflow of blood during ventricular systole?

Each ventricle has a large outflow tract located superiorly near the AV valves. The right ventricle pumps blood through the pulmonary semilunar valve into the pulmonary trunk, whereas the left ventricle pumps blood through the aortic semilunar valve into the aorta (see Figure 17-5). These valves prevent backflow of blood into the ventricles during ventricular relaxation. The interventricular septum separates right and left ventricles, preventing mixing of oxygenated and unoxygenated blood.

Each ventricle contains cone-shaped pillars called papillary muscles from which thin, strong connective tissue strings (chordae tendineae) attach to tricuspid and mitral valve cusps (see Figure 17-5). The chordae tendineae tether the AV valve leaflets, preventing them from bulging up into the atria and opening during ventricular contraction (called regurgitation). When the ventricles relax, these valves open again, allowing blood to fill the ventricles. Most of the ventricular filling is a passive process; the atria do not contract until very near the end of ventricular relaxation (diastolic) time.

Clinical Focus 17-1 Cardiac Tamponade

A previously healthy, 32-year-old man presents to the emergency department with a severe chest wall injury sustained in an automobile accident. He is conscious and anxious and complains of dyspnea and chest pain. Physical examination reveals the following: distended neck veins; tachycardia; systolic blood pressure 90 mm Hg; muffled, distant heart sounds; and loss of the carotid artery pulse during inspiration.

Discussion

This patient exhibits signs and symptoms of cardiac tamponade, in which fluid enters the pericardial space and builds up pressure, restricting the normal movements of the heart. The left ventricle fails to fill properly because its expansion is restricted. Penetrating or nonpenetrating chest wall trauma may cause acute cardiac tamponade. This patient’s distended neck or jugular veins indicate high venous pressure caused by inadequate left ventricular stroke volume—that is, inadequate pumping causes blood to dam up throughout the entire pulmonary vascular system, all the way to the vena cava. The body increases the heart rate in an attempt to sustain the cardiac output; nevertheless, in severe tamponade, systolic pressure decreases because of low stroke volume. The jacket of fluid in the pericardial sac muffles the normal heart sounds. The loss of pulse during inspiration is a sign of pulsus paradoxus, or paradoxical pulse. Pulsus paradoxus is defined as an inspiratory reduction in blood pressure exceeding 10 mm Hg. Inspiration increases venous blood flow into the right atrium and right ventricle; this distends these chambers, crowding and further impeding left ventricular filling. Consequently, the left ventricular stroke volume decreases markedly during inspiration, and the pulse weakens or disappears. The emergency treatment of acute cardiac tamponade in this clinical setting is pericardiocentesis. In this procedure, a long, large-bore needle is inserted through the chest wall into the pericardial space to drain the fluid and restore normal heart-filling pressures.

Cardiac Skeleton and Valvular Function

A tough set of connected rings (fibrous annuli) form a semirigid framework to which the heart valves and cardiac muscle are attached (Figure 17-7, A). This framework forms a fibrous skeleton, which is an electrical insulator and a physical barrier between atrial and ventricular muscle masses. The only electrical connection between atrial and ventricular muscle is a single bundle of specialized conductive tissue that penetrates the fibrous skeleton (discussed in a later section).

Figure 17-7 The cardiac skeleton and heart valves. A, Posterior view. Note the muscle fiber arrangement. B, View from above. The ventricles are relaxing—the atrioventricular (AV) valves are open. C, The ventricles are contracting—the semilunar (SL) valves are open, and the AV valves are closed. (From Patton KT, Thibodeau GA: *Anatomy & physiology,* ed 7, St. Louis, 2010, Mosby.)

The spiral arrangement of ventricular muscle fibers (see Figure 17-7, A) propels blood upward into the aorta and pulmonary artery during contraction. This action “wrings” blood

Clinical Focus 17-2 Effects of a Ventricular Septal Defect

Ventricular septal defect (VSD) is the most common congenital malformation of the heart reported in children. In VSD, a defect in the septum dividing the right and left ventricles allows blood to flow directly from one chamber to the other. The functional disturbance caused by a VSD depends mainly on its size and the pulmonary vascular resistance. Normally, left ventricular pressure greatly exceeds right ventricular pressure, causing a left-to-right shunt through the VSD. That is, some oxygenated blood mixes with deoxygenated blood and is pumped back into the pulmonary circulation. A small, high-resistance VSD permits only a small left-to-right shunt. A large VSD is more likely to allow some mixing of right ventricular deoxygenated blood with oxygenated left ventricular blood (i.e., right-to-left shunt). This is especially true if pulmonary vascular resistance is elevated or if the pulmonic valve is narrowed; in these circumstances, right ventricular pressure rises, increasing right-to-left shunting. In very large defects, both ventricles act as a single pumping chamber with two outlets, equalizing the pulmonary and systemic pressures. In any case, only right-to-left shunting causes systemic arterial hypoxemia. Left-to-right shunting merely returns already oxygenated blood to the pulmonary circulation for reoxygenation. Left-to-right shunting increases right ventricular work. The treatment for a large, symptomatic VSD is surgical correction.

out of ventricles from apex to base. As the heart contracts, it rotates to the right, swinging the left ventricle to the front of the chest; this creates the PMI.

The fibrous rings supporting the tricuspid and mitral valves are more compliant than the rings supporting the semilunar valves. For this reason, mitral and tricuspid rings are compressed to smaller sizes during ventricular systole; consequently, their valve cusps are larger than the area to be covered; this ensures a complete seal during contraction.¹ If the size disproportion is too great, the valve cusps balloon upward into the atrium during ventricular contraction (prolapse). Heart valve function during ventricular diastole is illustrated in Figure 17-7, B; Figure 17-7, C, illustrates valvular function during ventricular systole. These illustrations correspond with ventricular filling (diastole) and ejection (systole) shown in Figure 17-8, A and B.

Figure 17-8 Action of valves and chambers when the ventricles are in diastole (A) and systole (B). (From Patton KT, Thibodeau GA: *Anatomy & physiology,* ed 7, St. Louis, 2010, Mosby.)

The crescent-shaped (semilunar) pulmonic and aortic valve cusps permit them to open fully during ventricular ejection and seal perfectly during ventricular diastole. The aortic diameter is slightly enlarged at the base just above the semilunar valves. This provides a space behind the valve cusps when they open during ventricular ejection, preventing them from occluding the coronary artery orifices.¹ Coronary arteries branch off from the aorta immediately above the semilunar valve. The enlarged aortic base also keeps the valve cusps away from the aortic wall. As the ventricles relax, the backflow of blood immediately catches the valve cusps and sharply closes them, preventing blood from flowing back into the ventricles.

Coronary Circulation

Coronary Arteries

The heart muscle itself receives its blood supply from the right and left coronary arteries, which arise from the aorta immediately above the aortic semilunar valve. These arteries and their branches lie on the heart’s surface (see Figure 17-2); smaller arteries penetrate into the cardiac muscle mass. Figure 17-9, A, illustrates the coronary arterial circulation. The heart relies almost exclusively on the two main coronary arteries for its oxygen supply. The endocardial surface obtains a very small amount of oxygen directly from the blood in the heart chambers.²

Figure 17-9 Coronary circulation. A, Arteries. B, Veins. (From Patton KT, Thibodeau GA: *Anatomy & physiology,* ed 7, St. Louis, 2010, Mosby.)

Very few connections exist between the major coronary arteries; blood flow can take few detours if its main route becomes obstructed. This lack of collateral circulation explains why sudden coronary artery occlusion, such as occurs with a blood clot, is life threatening. The heart muscle supplied by the occluded artery becomes hypoxic (ischemic), which can lead to myocardial tissue death, or myocardial infarction (MI). If the narrowing of coronary arteries progresses gradually over a long time, some collateral circulation develops to supply ischemic areas; this lessens the chances that a blocked coronary artery will cause an MI.²

Ischemia produced by coronary artery occlusion stimulates myocardial nociceptive (pain-eliciting) fibers, producing the characteristic pain known as angina pectoris.³ This pain is often felt beneath the sternum, in the left arm, and in the neck. Frequent attacks of angina are associated with a greatly increased risk of coronary artery occlusion. About 35% of all deaths in the United States are caused by coronary artery disease.²

The left anterior descending and circumflex branches of the left coronary artery supply the anterior and lateral portions of the left ventricle (see Figure 17-9, A). The right coronary artery supplies the right ventricle and the posterior part of the left ventricle. The left and right atria receive blood from small branches of left and right coronary arteries. The right coronary artery is the dominant supplier of blood to the heart in about 50% of people; in about 30% of people, blood flow is equal through right and left coronary arteries; and the left artery predominates in about 20% of people.²

Clinical Focus 17-3 Pulmonary Effects of Mitral Valve Regurgitation and Stenosis

A patient with diagnosed severe mitral valve stenosis is in the cardiac intensive care unit. This patient requires oxygen and shows signs and symptoms of pulmonary edema on physical examination and chest x-ray film. What is the connection between this patient’s cardiac and pulmonary problems?

Discussion

Mitral valve stenosis is a condition characterized by a narrowed, stiff mitral valve. The narrowed valve creates high resistance to blood flow, increasing pulmonary venous and capillary pressures. A stenosed valve is likely to seal improperly during left ventricular systole, allowing some backflow of blood (regurgitation), further increasing pulmonary vascular pressures. Hydrostatic pulmonary edema is a common consequence of mitral valve stenosis, which accounts for the hypoxemia and dyspnea that often accompany mitral stenosis. Severe cases require surgical correction.

Coronary Veins

The coronary venous drainage (see Figure 17-9, B) follows a path generally parallel to the path of the coronary arteries. The cardiac veins converge to empty into a large venous cavity within the right atrium, the coronary sinus. In addition, the thebesian veins (not shown) empty directly into all heart chambers; this venous drainage into the left heart contributes to the normal anatomical shunt that prevents arterial blood from being fully saturated with oxygen. About 75% of coronary venous flow is through the coronary sinus.²

Oxygen Requirements and Coronary Blood Flow

Even at rest, the myocardium extracts about 70% of the oxygen from its arterial blood flow compared with a 25% extraction rate for the whole body.² During exercise, this extraction rate is higher still. Because heart muscle cannot extract much additional oxygen from the blood, the only way it can receive more oxygen is through increased coronary blood flow. Myocardial oxygenation is highly dependent on blood flow.

Myocardial oxygen need is the major factor governing coronary blood flow. Increased metabolic activity and myocardial hypoxia cause the release of a potent coronary vasodilator called adenosine.³

Diastolic Time and Coronary Blood Flow

At rest, coronary blood flow is about 225 mL per minute, or between 4% and 5% of the cardiac output; during heavy exercise, coronary blood flow can triple or quadruple to meet the extra oxygen demands of the myocardium.² Most coronary perfusion occurs during ventricular relaxation (diastole), opposite to flow through other vascular beds of the body. The powerful contractile force of the ventricles during systole compresses the coronary vessels, momentarily stopping or reversing the direction of their blood flow.³ Thus, sufficient diastolic time (normally about two times as long as systolic time) is important for adequate coronary blood flow. Extreme tachycardia, especially in persons with narrowed coronary arteries, may shorten diastolic time so much that coronary blood flow becomes inadequate. In healthy people, the effect of this shortened diastolic time is overridden by the coronary vasodilation that occurs with increased myocardial oxygen demand.

Cardiac Conduction System

A specialized system of modified cardiac muscle tissue (distinct from nerve tissue) conducts regular electrical impulses that stimulate rhythmic, synchronized heart muscle contractions. This conduction system also transmits the impulses rapidly and uniformly throughout the heart, much more rapidly than over regular myocardial fibers. Rapid and uniform conduction of electrical impulses is important to ensure effective, properly timed pumping action of the heart. With normal impulse conduction, the atria contract to complete the ventricular filling process about one sixth of a second before the ventricles contract.² Figure 17-10 illustrates the electrical conduction system of the heart.

Figure 17-10 Conduction system of the heart. *Arrows* show direction of electrical current flow. (From Patton KT, Thibodeau GA: *Anatomy & physiology,* ed 7, St. Louis, 2010, Mosby.)

The sinoatrial (SA) node, embedded in the right atrial muscle near the superior vena cava, is responsible for initiating the electrical impulses that produce sequential atrial and ventricular contraction. The impulses of the SA node travel over specialized internodal pathways to the atrioventricular (AV) node at a velocity of about 1 m per second (regular atrial muscle conducts impulses at about 0.3 m per second). The AV node and the AV bundle slow the impulse velocity considerably before transmitting it into the ventricles. It takes the SA node impulse about 0.03 second to reach the AV node, which along with the AV bundle delays the impulse another 0.13 second before conducting it on to the ventricles; thus, about 0.16 second elapses from the time the SA node generates its impulse until the ventricles receive the signal.² This transmission delay prevents impulses from arriving at the ventricles too rapidly in succession; in this way, the ventricles have enough time to fill between contractions.

CONCEPT QUESTION 17-3

What is the effect of a very high heart rate on ventricular stroke volume?

The only electrical connection between atrial and ventricular muscle is the AV bundle (also known as the bundle of His). This bundle conducts impulses to the right and left bundle branches in the forward direction only (toward the ventricles). This one-way transmission prevents impulses from traveling backward from ventricles to atria. The bundle branches travel downward through the ventricular septum and subdivide many times to form the Purkinje fibers. Purkinje fibers spread out diffusely from the apex throughout the ventricles, transmitting

Clinical Focus 17-4 Surgical Treatment Options for Blocked Coronary Arteries

When blockage of the major coronary arteries is severe and life threatening, coronary artery bypass graft (CABG) surgery and coronary angioplasty are common treatment options. In CABG surgery, a vein taken from another part of the patient’s body (often the saphenous vein of the leg) is grafted such that it provides a channel around the vessel obstruction, allowing the hypoxic myocardium to be resupplied with blood. In an aortocoronary bypass graft, the grafted vein connects the aorta to the coronary artery distal to the obstruction site. Veins can be grafted from other nearby arteries as well. If more than one coronary artery is blocked, multiple bypass grafts are done.

In coronary angioplasty, a small stainless steel mesh sleeve called a stent is positioned over a small, balloon-tipped catheter about 1 mm in diameter; the catheter is usually introduced into a femoral artery and advanced through the abdominal and thoracic aorta and into the coronary artery until the deflated balloon and stent lie in the partially occluded part of the vessel. The balloon is abruptly inflated with high pressure, permanently dilating the stent, which keeps the artery propped open; the balloon is then deflated, and the catheter is withdrawn. After this procedure, blood flow through the vessel is often restored to normal, reoxygenating the myocardium. Before the advent of stents, vessels often became occluded again after balloon angioplasty, and CABG surgery was required; vessels with stents are less susceptible to reocclusion.

impulses at a velocity up to 4 m per second, which is about six times faster than the impulses can travel over regular ventricular muscle. It takes these impulses about 0.03 second to travel from the AV bundle to the Purkinje fibers, where they normally stimulate rapid, simultaneous ventricular contractions.²