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 ).

Heart within the pericardium.

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 ).

Cross section of the cardiac muscle.

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 ).

Views of the heart.

A, Anterior. B, Posterior.

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 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 ).

Anterior cross section showing the valves and chambers of the heart.

The atrioventricular 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 atrioventricular 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.”

Blood flow through the heart.

A, Systole. B, Diastole.

(From Canobbio, 1990.)

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 ).

Events of the cardiac cycle, showing venous pressure waves, electrocardiogram (ECG; the graphic representing the electrical activity during the cardiac cycle), and heart sounds in systole and diastole.

PCG, Phonocardiogram.

(Modified from Guzzetta and Dossey, 1992.)

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 atrioventricular node (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 ).

Cardiac conduction.

(From Canobbio, 1990.)

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 repolarization, 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.

Usual electrocardiogram waveform.

(From Berne and Levy, 1996.)

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, including 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 ( Figs. 15.10 and 15.11 ).

Anatomy of the fetal heart.

(From Thompson et al, 1997.)

Fetal circulation.

A, In utero. B, After delivery.

(From Ross and Wilson, 2011.)

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 total 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 out 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 the 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 these age-associated changes in heart architecture and contractile properties, the aged heart continues to function reasonably well at rest. Long-standing hypertensive disease, infarcts, and/or other insults and loss of physical conditioning may lead to severe compromise of the heart and to increasingly 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.

History of Present Illness

Chest Pain ( Boxes 15.1 and 15.2 )

• •
  

  Onset and duration: sudden, gradual, or vague onset, length of episode; cyclic nature; relation to physical exertion, rest, emotional experience, eating, coughing, cold temperatures, trauma; awakens from sleep

  
  
• •
  

  Character: aching, sharp, tingling, burning, pressure, stabbing, crushing, or clenched fist (Levine) sign

  
  
• •
  

  Location: radiating down arms, to neck, jaws, teeth, scapula; relief with rest or position change

  
  
• •
  

  Severity: interference with activity, need to stop all activity until it subsides, disrupts sleep, severity on a scale of 0 to 10

  
  
• •
  

  Associated symptoms: anxiety; dyspnea (shortness of breath); diaphoresis (sweating); dizziness; nausea or vomiting; faintness; cold, clammy skin; cyanosis; pallor; swelling or edema (noted anywhere, constant or at certain times during day)

  
  
• •
  

  Treatment: rest, position change, exercise, nitroglycerin

  
  
• •
  

  Medications: digoxin, diuretics, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium channel blockers, nonsteroidal antiinflammatory or antihypertensive medications

Risk Factors

Cardiac Disease

• •
  

  Gender (men more at risk than women; women’s risk is increased in the postmenopausal years and with oral contraceptive use)

  
  
• •
  

  Hyperlipidemia

  
  
• •
  

  Elevated homocysteine level

  
  
• •
  

  Smoking

  
  
• •
  

  Family history of cardiovascular disease, diabetes, hyperlipidemia, hypertension, or sudden death in young adults

  
  
• •
  

  Diabetes mellitus

  
  
• •
  

  Obesity: dietary habits, including an excessively fatty diet

  
  
• •
  

  Sedentary lifestyle without exercise

  
  
• •
  

  Fatigue: unusual or persistent, inability to keep up with contemporaries, inability to maintain usual activities, bedtime earlier

  
  
• •
  

  Associated symptoms: dyspnea on exertion, chest pain, palpitations, orthopnea (shortness of breath [dyspnea, ] when lying flat), paroxysmal nocturnal dyspnea (dyspnea that awakens someone from sleep), anorexia, nausea, vomiting

  
  
• •
  

  Medications: beta-blockers

  
  
• •
  

  Cough:

  
  
  
  
  • •
    

    Onset and duration

    
    
  • •
    

    Character: dry, wet, nighttime, aggravated by lying down

    
    
  • •
    

    Medications: ACE inhibitors

  
  
  
  
• •
  

  Difficulty breathing (dyspnea, orthopnea)

  
  
• •
  

  Worsening or remaining stable

  
  
• •
  

  At rest or aggravated by exertion (how much?) (see Box 15.3 ); on level ground, climbing stairs

  
  
• •
  

  Position: lying down or eased by resting on pillows (how many? or sleep in a recliner?)

  
  
• •
  

  Paroxysmal nocturnal dyspnea (recurring attacks of shortness of breath that wake the patient up at night gasping for air, coughing, wheezing and feeling like they aresuffocating)

  
  
• •
  

  Loss of consciousness (transient syncope)

  
  
• •
  

  Associated symptoms: palpitation, dysrhythmia

  
  
• •
  

  When occurs: unusual exertion, sudden turning of neck (carotid sinus effect), looking upward (vertebral artery occlusion), change in posture

Box 15.1

Chest Pain

The presence of chest pain suggests heart disease, and it has many causes. “Angina pectoris” is traditionally described as a pressure or choking sensation, substernal or into the neck. The discomfort, which can be intense, may radiate to the jaw and down the left (and sometimes the right) arm. It often begins during strenuous physical activity, eating, exposure to intense cold, windy weather, or exposure to emotional stress. Relief may occur in minutes if the activity can be stopped. Signs of angina pectoris may vary in location, intensity, and radiation, and often arise from sources other than the heart. In women it may vary from the classic signs in men. The “precordial catch,” for example, is a sudden, sharp, relatively brief pain that does not radiate, occurs most often at rest, is unrelated to exertion, and may not have a discoverable cause.

Some Possible Causes of Chest Pain

Cardiac

• 
  

  Angina

  
  
• 
  

  Acute myocardial infarction

  
  
• 
  

  Coronary insufficiency

  
  
• 
  

  Myocardial infarction

  
  
• 
  

  Nonobstructive, nonspastic angina

  
  
• 
  

  Mitral valve prolapse

Aortic

• 
  

  Dissection of the aorta

Pleuropericardial Pain

• 
  

  Pericarditis

  
  
• 
  

  Pleurisy

  
  
• 
  

  Pneumothorax

  
  
• 
  

  Mediastinal emphysema

Gastrointestinal Disease

• 
  

  Hiatus hernia

  
  
• 
  

  Reflux esophagitis

  
  
• 
  

  Esophageal rupture

  
  
• 
  

  Esophageal spasm

  
  
• 
  

  Cholecystitis

  
  
• 
  

  Peptic ulcer disease

  
  
• 
  

  Pancreatitis

Pulmonary Disease

• 
  

  Pulmonary hypertension

  
  
• 
  

  Pneumonia

  
  
• 
  

  Pulmonary embolus

  
  
• 
  

  Bronchial hyperreactivity

  
  
• 
  

  Tension pneumothorax

Musculoskeletal

• 
  

  Cervical radiculopathy

  
  
• 
  

  Shoulder disorder or dysfunction (e.g., arthritis, bursitis, rotator cuff injury, biceps tendonitis)

  
  
• 
  

  Costochondral disorder

  
  
• 
  

  Xiphodynia

Psychoneurotic

• 
  

  Recreational drug use (e.g., cocaine)

  
  
• 
  

  Herpes zoster: when lesions occur in thoracic region

Unlike in adults, chest pain in children and adolescents is seldom due to a cardiac problem. It is often difficult to find a cause, but trauma, exercise-induced asthma, and, even in a somewhat younger child, the use of cocaine should be among the considerations.

Box 15.2

Characteristics of Chest Pain

TYPE	CHARACTERISTICS
Cardiac	Substernal; provoked by effort, emotion, eating; relieved by rest and/or nitroglycerin; often accompanied by diaphoresis, occasionally by nausea
Pleural	Precipitated by breathing or coughing; usually described as sharp; present during respiration; absent when breath held
Esophageal	Burning, substernal, occasional radiation to the shoulder; nocturnal occurrence, usually when lying flat; relief with food, antacids, sometimes nitroglycerin
From a peptic ulcer	Almost always infradiaphragmatic and epigastric; nocturnal occurrence and daytime attacks relieved by food; unrelated to activity
Biliary	Usually under right scapula, prolonged in duration; often occurring after eating; will trigger angina more often than mimic it
Arthritis/bursitis	Usually lasts for hours; local tenderness and/or pain with movement
Cervical	Associated with injury; provoked by activity, persists after activity; painful on palpation and/or movement
Musculoskeletal (chest)	Intensified or provoked by movement, particularly twisting or costochondral bending; long-lasting; often associated with focal tenderness
Psychoneurotic	Associated with/after anxiety; poorly described; located in intramammary region

 

Box 15.3

Adapted from Department of Health and Human, 2008 .

Exercise Intensity

• 
  

  Light: walking 10 to 15 steps, preparing a simple meal for one, retrieving a newspaper from just outside the door, pulling down a bedspread, brushing teeth

  
  
• 
  

  Moderate: making the bed, dusting and sweeping, walking a level short block, office filing

  
  
• 
  

  Moderately heavy: climbing one or two flights of stairs, lifting full cartons, long walks, sexual intercourse

  
  
• 
  

  Heavy: jogging, vigorous athletics of any kind, cleaning the entire house in less than a day, raking a large number of leaves, mowing a large lawn with a hand mower, shoveling deep snow

Auscultation positions.

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 ( Box 15.3 )

  
  
• •
  

  Use of recreational drugs: amyl nitrate, cocaine, injection drug use

Equipment

• •
  

  Stethoscope

  
  
• •
  

  Marking pencil

  
  
• •
  

  Centimeter ruler

The examination of the heart includes the following: inspection, palpation, and percussion of the chest and then auscultation of the heart. Performing a successful examination requires a competence of each procedure and an ability to integrate and interpret the findings in relation to the cardiac events they reflect.

Findings from examinations of other body systems have a significant impact on judgments made about the cardiovascular system. For example, crackles auscultated in the lungs, palpation of an enlarged liver, and observation of peripheral edema are signs of heart failure. Examples of other influencing factors may include the following:

• •
  

  Effect of a barrel chest or pectus deformity

  
  
• •
  

  Xanthelasma (yellowish deposit of fat underneath the skin)

  
  
• •
  

  Funduscopic changes of hypertension

  
  
• •
  

  Ascites, pitting edema, or elevated jugular venous pulse

  
  
• •
  

  Abdominal aortic bruit

In assessing cardiac function, it is a common error to auscultate the heart first. It is important to follow the proper sequence, beginning with inspection and proceeding to palpation, percussion, and performing auscultation last. Use a tangential light source to inspect the chest, allowing shadows to accent the surface flicker of any underlying cardiac movement. The room should be quiet because subtle, low-pitched sounds are hard to hear. Stand to the patient’s right, at least at the start. A thorough examination of the heart requires the patient to assume a variety of positions: sitting erect and leaning forward, lying supine, and left lateral recumbent position. These changes in position mandate a comfortable examining table on which movement is easy. Large breasts can make examination difficult. Either you or the patient can move the left breast up and to the left.

Inspection

In most adults the apical impulse is visible at about the midclavicular line in the fifth left intercostal space, but it is easily obscured by obesity, large breasts, or muscularity. In some patients it may be visible in the fourth left intercostal space. It should be seen in only one intercostal space if the heart is healthy. In some adults the apical impulse may become visible only when the patient sits up and the heart is brought closer to the anterior wall.

Examination findings are affected by the shape and thickness of the chest wall and the amount of tissue, air, and fluid through which the impulses are transmitted. For example, a readily visible and palpable impulse when the patient is supine suggests an intensity that may be the result of a problem. The absence of an apical impulse in addition to faint heart sounds, particularly when the patient is in the left lateral recumbent position, suggests some intervening extracardiac problem, such as pleural or pericardial fluid.

Inspection of other organs may reflect important information about the cardiac status. For example, inspecting the skin for cyanosis or venous distention and inspecting the nail bed for cyanosis and capillary refill time provide valuable clues to the cardiac evaluation.

Palpation

Make sure that your hands are warm, and with the patient supine, palpate the precordium. Use the proximal halves of the four fingers held gently together or use the whole hand. Touch lightly and let the cardiac movements rise to your hand because sensation decreases as you increase pressure.

As always, be methodical. One suggested sequence is to begin at the apex, move to the inferior left sternal border, then move up the sternum to the base and down the right sternal border and into the epigastrium or axillae if the circumstance dictates ( Fig. 15.12 ).

Sequence for palpation of the precordium.

A, Apex. B, Left sternal border. C, Base.

Feel for the apical impulse and identify its location by the intercostal space and the distance from the midsternal line. The point at which the apical impulse is most readily seen or felt should be described as the point of maximal impulse (PMI). The PMI is typically noted at the left fifth intercostal space, midclavicular line in adults and fourth intercostal space medial to the nipple in children. Determine the diameter of the area in which it is felt. Usually it is palpable within a small diameter—no more than 1 cm. The impulse is usually gentle and brief, not lasting as long as systole. In some adults, the apical impulse is not felt because of the thickness of the chest wall ( Fig. 15.13 ).

Palpation of the apical pulse.

If the apical impulse is more vigorous than expected, characterize it as a “heave” or “lift.” An apical impulse that is more forceful and widely distributed, fills systole, or is displaced laterally and downward may indicate increased cardiac output or left ventricular hypertrophy. A lift along the left sternal border may be caused by right ventricular hypertrophy. A loss of thrust may be related to overlying fluid or air or to displacement beneath the sternum. Displacement of the apical impulse to the right without a loss or gain in thrust suggests dextrocardia, diaphragmatic hernia, distended stomach, or a pulmonary abnormality.

Feel for a thrill—a fine, palpable, rushing vibration, a palpable murmur, often, but not always, over the base of the heart in the area of the right or left second intercostal space. It generally indicates turbulence or a disruption of the expected blood flow related to some defect in the closure of the aortic or pulmonic valve (generally aortic or pulmonic stenosis), pulmonary hypertension, or atrial septal defect ( Box 15.4 ). Locate each sensation in terms of its intercostal space and relationship to the midsternal, midclavicular, or axillary lines. Chapter 14 describes the method for counting ribs and intercostal spaces.

While palpating the precordium, use your other hand to palpate the carotid artery so that you can describe the finding in relation to the cardiac cycle. The carotid pulse and S ₁ are practically synchronous. The carotid pulse is located just medial to and below the angle of the jaw ( Fig. 15.14 ).

Palpation of the carotid artery to time events felt over the precordium.

Percussion

Percussion is of limited value in defining the borders of the heart or determining its size because the shape of the chest is relatively rigid and can make the more malleable heart conform. Left ventricular size is better judged by the location of the apical impulse. The right ventricle tends to enlarge in the anteroposterior diameter rather than laterally, thus diminishing the value of percussion of the right heart border. Obesity, unusual muscular development, and some pathologic conditions (e.g., presence of air or fluids) can also easily distort the findings. A chest radiograph is far more useful in defining the heart borders.

If radiographic facilities are unavailable, percussion can be used to estimate the size of the heart. Begin tapping at the anterior axillary line, moving medially along the intercostal spaces toward the sternal border. The change from a resonant to a dull note marks the cardiac border. Note these points with a marking pen and the outline of the heart is visually defined. On the left, the loss of resonance will generally be close to the PMI at the apex of the heart. Measure this point from the midsternal line at each intercostal space and record that distance. When percussing the right cardiac border, a change in resonance is usually noted when the right sternal border is encountered. The right heart border is only found if it extends beyond the sternal border.

Auscultation

Because all heart sounds are of relatively low frequency, in a range somewhat difficult for the human ear to detect, you must ensure a quiet environment. Because shivering and movement increase adventitious sound and because comfort is important, make certain the patient is warm and relaxed before beginning. Always place a comfortably warm stethoscope on the unclothed chest. You must also learn to appreciate the differences in findings when the chest is thin and nonmuscular (i.e., sounds are louder, closer) or muscular or obese (i.e., sounds are dimmer, more distant).

Because sound is transmitted in the direction of blood flow, specific heart sounds are best heard in areas where the blood flows after it passes through a valve (see Clinical Pearl, “Heart Sounds” ). Approach each of the precordial areas systematically in a sequence that is comfortable for you, working your way from base to apex or apex to base ( Box 15.5 ). Because the site of the apex of the heart may be changed by elevation of the diaphragm from pregnancy, ascites, or other intraabdominal condition, many healthcare providers prefer to begin their examination at the base of the heart.

Box 15.5

Procedure for Auscultating the Heart

Adopt a routine for the various positions the patient is asked to assume for auscultating the heart; however, be prepared to alter the sequence if the patient’s condition requires it. Instruct the patient when to breathe comfortably and when to hold the breath in expiration and inspiration. Listen carefully for each heart sound, isolating each component of the cardiac cycle, especially while the respirations are momentarily suspended. The following sequence is suggested:

Patient sitting up and leaning slightly forward and, preferably, in expiration: listen in all five areas ( Fig. 15.16, A ). This is the best position to hear relatively high-pitched murmurs with the stethoscope diaphragm.

Patient supine: listen in all five areas (see Fig. 15.16, B ).

Patient left lateral recumbent: listen in all five areas. This is the best position to hear the low-pitched filling sounds in diastole with the stethoscope bell (see Fig. 15.16, C ).

Other positions depend on your findings. Patient right lateral recumbent is the best position for evaluating a right rotated heart of dextrocardia. Listen in all five areas.

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