Heart

Anatomy and Physiology

The heart is positioned behind the sternum and the contiguous parts of the third to the sixth costal cartilages. The area of the chest overlying the heart is the precordium. Because of the heart’s conelike shape, the broader upper portion is called the base, and the narrower lower tip of the heart is the apex ( Fig. 15.1 ).

The position of the heart can vary considerably depending on body build, configuration of the chest, and level of the diaphragm. In a tall, slender person, the heart tends to hang vertically and to be positioned centrally. With a shorter person, it tends to lie more to the left and more horizontally. Occasionally, the heart may be positioned to the right, either rotated or displaced, or as a mirror image (dextrocardia). Situs inversus is when the heart and stomach are placed to the right and the liver to the left.

Structure

The pericardium is a tough, double-walled, fibrous sac encasing and protecting the heart. Several milliliters of fluid are present between the inner and outer layers of the pericardium, providing for low-friction movement ( Fig. 15.2 ).

The epicardium, the thin outermost muscle layer, covers the surface of the heart and extends onto the great vessels. The myocardium, the thick muscular middle layer, is responsible for the pumping action of the heart. The endocardium, the innermost layer, lines the chambers of the heart and covers the heart valves and the small muscles associated with the opening and closing of these valves ( Fig. 15.3 ).

The heart is divided into four chambers. The two upper chambers are the right and left atria (or auricles, because of their earlike shape), and the bottom chambers are the right and left ventricles. The left atrium and left ventricle together are referred to as the left heart; the right atrium and right ventricle together are referred to as the right heart. The left heart and right heart are divided by a blood-tight partition called the interventricular septum (see Fig. 15.1 ). On the anterior external surface of the heart, the coronary sulcus separates the atria from the ventricles ( Fig. 15.4 ).

The atria are small, thin-walled structures acting primarily as reservoirs for blood returning to the heart from the veins throughout the body. The ventricles are large, thick-walled chambers that pump blood to the lungs and throughout the body. The right and left ventricles together form the primary muscle mass of the heart. In the adult heart, the left ventricle mass is greater than that of the right ventricle because the higher pressure in the systemic circulation requires a greater force of contraction (and more muscle mass) in order for blood to be successfully pumped throughout the body. The adult heart is about 12 cm long, 8 cm wide at the widest point, and 6 cm in its anteroposterior diameter.

Most of the anterior surface of the heart is formed by the right ventricle. The left ventricle is positioned behind the right but extends anteriorly, forming the left border of the heart (see Fig. 15.4 ). The left atrium is above the left ventricle, forming the more posterior aspect of the heart. The heart is, in effect, turned ventrally on its axis, putting its right side more forward. The left ventricle’s contraction and thrust result in the apical impulse usually felt in the fifth left intercostal space at the midclavicular line. The right atrium lies above and slightly to the right of the right ventricle, participating in the formation of the right border of the heart.

The four chambers of the heart are connected by two sets of valves, the atrioventricular (AV) and semilunar valves. In the fully formed heart that is free of defect, these are the only intracardiac pathways and permit the flow of blood in only one direction ( Fig. 15.5 ).

The AV valves, situated between the atria and the ventricles, include the tricuspid and mitral valves. The tricuspid valve, which has three cusps (or leaflets), separates the right atrium from the right ventricle. The mitral valve, which has two cusps, separates the left atrium from the left ventricle. When the atria contract (diastole), the AV valves open, allowing blood to flow into the ventricles. When the ventricles contract (systole), these valves snap shut, preventing blood from flowing back into the atria ( Fig. 15.6 ). See Clinical Pearl, “Order of Valves.”

The two semilunar valves each have three cusps. The pulmonic valve separates the right ventricle from the pulmonary artery. The aortic valve lies between the left ventricle and the aorta. Contraction of the ventricles (systole) opens the semilunar valves, causing blood to rush into the pulmonary artery and aorta. When the ventricles relax (diastole), the valves close, shutting off any backward flow into the ventricles (see Fig. 15.6 ).

Cardiac Cycle

The heart contracts and relaxes rhythmically, creating a two-phase cardiac cycle. During systole, the ventricles contract, ejecting blood from the left ventricle into the aorta and simultaneously from the right ventricle into the pulmonary artery. During diastole, the ventricles dilate, drawing blood into the ventricles as the atria contract, thereby moving blood from the atria to the ventricles (see Fig. 15.6 ). The volume of blood and the pressure under which it is returned to the heart vary with the degree of body activity, physical and metabolic (e.g., with exercise or fever).

As systole begins, ventricular contraction raises the pressure in the ventricles and forces the mitral and tricuspid valves closed, preventing backflow. This valve closure produces the first heart sound (S ₁ ), the characteristic “lub.” The intraventricular pressure rises until it exceeds that in the aorta and pulmonary artery. Then the aortic and pulmonic valves are forced open, and ejection of blood into the arteries begins. Valve opening is usually a silent event ( Fig. 15.7 ).

When the ventricles are almost empty, the pressure in the ventricles falls below that in the aorta and pulmonary artery, allowing the aortic and pulmonic valves to close. Closure of these valves causes the second heart sound (S ₂ ), the “dub.” The second heart sound has two components: A ₂ is produced by aortic valve closure, and P ₂ is produced by pulmonic valve closure. As ventricular pressure falls below atrial pressure, the mitral and tricuspid valves open to allow the blood collected in the atria to refill the relaxed ventricles. Diastole is a relatively passive interval until ventricular filling is almost complete. This filling sometimes produces a third heart sound (S ₃ ). Then the atria contract to ensure the ejection of any remaining blood. This can sometimes be heard as a fourth heart sound (S ₄ ). The cycle begins anew, with ventricular contraction and atrial refilling occurring at about the same time. The cardiac cycle continues without resting and constantly adjusts to the variable demands of work, rest, digestion, and illness.

The events of the cardiac cycle are not exactly identical on both sides of the heart. In fact, pressures in the right ventricle, right atrium, and pulmonary artery are lower than in the left side of the heart, and the same events occur slightly later on the right side than on the left. The effect is that heart sounds sometimes have two distinct components, the first produced by the left side and the second by the right side. For example, the aortic valve closes slightly before the pulmonic, so that S ₂ is often heard as two distinct components, referred to as a “split S ₂ ” (A ₂ , then P ₂ ).

Closure of the heart valves during the cardiac cycle produces heart sounds in rapid succession. Although the valves are anatomically close to each other, their sounds are best heard in an area away from the anatomic site because the sound is transmitted in the direction of blood flow (see Fig. 15.15 ).

Electrical Activity

An intrinsic electrical conduction system enables the heart to contract and coordinates the sequence of muscular contractions taking place during the cardiac cycle. An electrical impulse stimulates each myocardial contraction. The impulse originates in and is paced by the sinoatrial node (SA node), located in the wall of the right atrium. The impulse then travels through both atria to the AV node, located in the atrial septum. In the AV node, the impulse is delayed but then passes down the bundle of His to the Purkinje fibers (heart muscle cells specialized for electrical conduction), located in the ventricular myocardium. Ventricular contraction is initiated at the apex and proceeds toward the base of the heart ( Fig. 15.8 ).

An electrocardiogram (ECG) is a graphic recording of electrical activity during the cardiac cycle. The ECG records electrical current generated by the movement of ions in and out of the myocardial cell membranes. The ECG records two basic events: depolarization, which is the spread of a stimulus through the heart muscle, and re polarization, which is the return of the stimulated heart muscle to a resting state. The ECG records electrical activity as specific waves ( Fig. 15.9 ):

• P wave—the spread of a stimulus through the atria (atrial depolarization)

• PR interval—the time from initial stimulation of the atria to initial stimulation of the ventricles, usually 0.12 to 0.20 second

• QRS complex—the spread of a stimulus through the ventricles (ventricular depolarization), less than 0.12 second

• ST segment and T wave—the return of stimulated ventricular muscle to a resting state (ventricular repolarization)

• U wave—a small deflection rarely seen just after the T wave, thought to be related to repolarization of the Purkinje fibers. They are commonly seen with bradycardia. This is also seen sometimes with electrolyte abnormalities, hypothermia, and hypothyroidism.

• QT interval—the time elapsed from the onset of ventricular depolarization until the completion of ventricular repolarization. The interval varies with the cardiac rate.

Because the electrical stimulus starts the cycle, it precedes the mechanical response by a brief moment. The sequence of myocardial depolarization is the cause of events on the left side of the heart occurring slightly before those on the right. When the heart is beating at a rate of 68 to 72 beats/min, ventricular systole is shorter than diastole. As the rate increases to about 120 beats/min, because of stress or pathologic factors, the two phases of the cardiac cycle tend to approximate each other in length.

Infants and Children

Fetal circulation, which includes the umbilical vessels, compensates for the nonfunctional fetal lungs. Blood flows from the right atrium into the left atrium via the foramen ovale ( Fig. 15.10 ). The right ventricle pumps blood through the patent ductus arteriosus rather than into the lungs. The right and left ventricles are equal in weight and muscle mass because they both pump blood into the systemic circulation, unlike the adult heart ( Fig. 15.11 ; see also Fig. 15.10 ).

The changes at birth include closure of the ductus arteriosus, usually within 24 to 48 hours, and the functional closure of the interatrial foramen ovale as pressure rises in the left atrium. The mass of the left ventricle increases after birth in response to the left ventricle assuming responsibility for systemic circulation. By 1 year of age, the relative sizes of the left and right ventricles approximate the adult ratio of 2:1.

The heart lies more horizontally in the chest in infants and young children compared with adults. As a result, the apex of the heart rides higher, sometimes well into the fourth left intercostal space. In most cases, the adult heart position is reached by age 7 years.

Pregnant Patients

The pregnant patient’s blood volume increases 40% to 50% over prepregnancy level. The rise is mainly due to an increase in plasma volume, which begins in the first trimester and reaches a maximum after the 30th week. On average, plasma volume increases 50% with a single pregnancy and as much as 70% with a twin pregnancy. The heart works harder to accommodate the increased heart rate and stroke volume required for the expanded blood volume. The left ventricle increases in both wall thickness and mass. The blood volume returns to prepregnancy levels within 3 to 4 weeks after delivery ( Table 15.1 ).

TABLE 15.1

Hemodynamic Changes During Pregnancy

Stage
Hemodynamic Variable	First Trimester	Second Trimester	Third Trimester	Labor And Delivery	Postpartum Period
Heart rate	Increased	Peaks at 28th week	Slightly decreased	Increased; bradycardia at delivery	Prepregnancy level within 2–6 weeks
Blood pressure	Prepregnancy level	Slightly decreased	Prepregnancy level	Prepregnancy level	Prepregnancy level
Blood volume	Increased	Peaks at 20th week	Gradually decreased	Rises sharply	Prepregnancy level within 2–6 weeks
Stroke volume	Increased	Peaks at 28th week	Gradually decreased	Decreased	Prepregnancy level within 2–6 weeks
Cardiac output	Increased	Peaks at 20th week	Slightly decreased	Increased	Prepregnancy level within 2–6 weeks
Systemic vascular resistance	Decreased	Decreased	Decreased	Sharply decreased at delivery	Prepregnancy level within 2–6 weeks

The cardiac output increases approximately 30% to 40% over that of the nonpregnant state and reaches its highest level by about 25 to 32 weeks of gestation. This level is maintained until term. Cardiac output returns to prepregnancy levels about 2 weeks after delivery. As the uterus enlarges and the diaphragm moves upward in pregnancy, the position of the heart is shifted toward a horizontal position, with slight axis rotation.

Older Adults

Heart size may decrease with age unless hypertension or heart disease causes enlargement. The left ventricular wall thickens, and the valves tend to fibrose and calcify. Stroke volume decreases, and cardiac output during exercise declines by 30% to 40%. The endocardium thickens. The myocardium becomes less elastic and more rigid so that recovery of myocardial contractility is delayed. The response to stress and increased oxygen demand is less efficient. Tachycardia is poorly tolerated, and after any type of stress, the return to an expected heart rate takes longer. Despite age-associated changes in heart architecture and contractile properties, the heart continues to function reasonably well at rest. Long-standing hypertensive disease, infarcts, and/or other insults, as well as loss of physical conditioning, may lead to severe compromise of the heart and to significant decline in cardiac output.

Cardiac function is further compromised by fibrosis and sclerosis in the region of the SA node and in the heart valves (particularly the mitral valve and aortic cusps) and by increased vagal tone. ECG changes occur secondary to cellular alteration, to fibrosis within the conduction system, and to neurogenic changes.

Review of Related History

For each of the symptoms or conditions discussed in this section, particular topics to include in the history of the present illness are listed. Responses to questions about these topics provide clues for individualizing the physical examination and the development of a diagnostic evaluation for the patient. Questions regarding medication use (prescription and over-the-counter preparations), as well as complementary and alternative therapies, are relevant for each area.

History of Present Illness

Past Medical History

• Cardiac surgery or hospitalization for cardiac evaluation or disorder

• Congenital heart disease

• Rhythm disorder

• Acute rheumatic fever, characterized by unexplained fever, swollen joints, Sydenham chorea (St. Vitus dance), abdominal pain, skin rash (erythema marginatum) or nodules

• Kawasaki disease (see Chapter 16 )

• Chronic illness: hypertension, bleeding disorder, hyperlipidemia, diabetes, thyroid dysfunction, coronary artery disease, obesity

Family History

• Long QT syndrome

• Marfan syndrome (a genetic disorder of the connective tissue associated with mitral valve prolapse/regurgitation, aortic regurgitation, and aortic dissection)

• Diabetes

• Heart disease

• Dyslipidemia

• Hypertension

• Obesity

• Congenital heart disease: Once it occurs in a family, the likelihood of its recurring increases.

• Family members with risk factor: morbidity, mortality related to cardiovascular system; ages at time of illness or death; sudden death, particularly in young and middle-aged relatives

Personal and Social History

• Employment: physical demands, environmental hazards such as heat, chemicals, dust, sources of emotional stress

• Tobacco use: type (cigarettes, cigars, pipe, chewing tobacco, snuff), duration of use, amount, age started and stopped; pack-years (number of years smoking times number of packs per day)

• Nutritional status

• Usual diet: proportion of fat, use of salt, food preferences, history of dieting, caffeine intake

• Weight: loss or gain, amount and rate

• Alcohol consumption: amount, frequency, duration of current intake

• Known hypercholesterolemia and/or elevated triglycerides (see Risk Factors, “Cardiac Disease”)

• Relaxation/hobbies

• Exercise: type, amount, frequency, intensity (see Box 15.3 )

• Use of illicit drugs: amyl nitrate, cocaine, injection drug use