The four valves of the heart serve to keep blood flowing in a forward direction. The cusps of the mitral and tricuspid valves are attached to thin strands of fibrous tissue termed chordae tendineae (Fig. 32-2). Chordae are anchored in the papillary muscles of the ventricles. This support system prevents the eversion of the leaflets into the atria during ventricular contraction. The pulmonic and aortic valves (also known as semilunar valves) prevent blood from regurgitating into the ventricles at the end of each ventricular contraction.

FIG. 32-2 Anatomic structures of the heart and heart valves.

The myocardium has its own blood supply, the coronary circulation (Fig. 32-3). Blood flow into the two major coronary arteries occurs primarily during diastole (relaxation of the myocardium). The left coronary artery arises from the aorta and divides into two main branches: the left anterior descending artery and the left circumflex artery. These arteries supply the left atrium, the left ventricle, the interventricular septum, and a portion of the right ventricle. The right coronary artery also arises from the aorta, and its branches supply the right atrium, the right ventricle, and a portion of the posterior wall of the left ventricle. In 90% of people the atrioventricular (AV) node and the bundle of His receive blood supply from the right coronary artery. For this reason, blockage of this artery often causes serious defects in cardiac conduction.

The divisions of coronary veins parallel the coronary arteries. Most of the blood from the coronary system drains into the coronary sinus (a large channel), which empties into the right atrium near the entrance of the inferior vena cava.

Conduction System.

The conduction system is specialized nerve tissue responsible for creating and transporting the electrical impulse, or action potential. This impulse starts depolarization and subsequently cardiac contraction (Fig. 32-4, A). The electrical impulse is normally started by the sinoatrial (SA) node (the pacemaker of the heart). Each impulse coming from the SA node travels through interatrial pathways to depolarize the atria, resulting in a contraction.

The electrical impulse travels from the atria to the AV node through internodal pathways. The excitation then moves through the bundle of His and the left and right bundle branches. The left bundle branch has two fascicles (divisions): anterior and posterior. The action potential moves through the walls of both ventricles by means of Purkinje fibers. The ventricular conduction system delivers the impulse within 0.12 second. This triggers a synchronized right and left ventricular contraction.

The result of the cardiac cycle is the ejection of blood into the pulmonary and systemic circulations. It ends with repolarization when the contractile fiber cells and the conduction pathway cells regain their resting polarized condition. Cardiac muscle cells have a compensatory mechanism that makes them unresponsive or refractory to restimulation during the action potential. During ventricular contraction, there is an absolute refractory period during which cardiac muscle does not respond to any stimuli. After this period, cardiac muscle gradually recovers its excitability, and a relative refractory period occurs by early diastole.

Electrocardiogram.

The electrical activity of the heart can be detected on the body surface using electrodes and is recorded on an electrocardiogram (ECG). The letters P, QRS, T, and U are used to identify the separate waveforms (Fig. 32-4, B). The first wave, P, begins with the firing of the SA node and represents depolarization of the atria. The QRS complex represents depolarization from the AV node throughout the ventricles. There is a delay of impulse transmission through the AV node that accounts for the time between the beginning of the P wave and the beginning of the QRS wave. The T wave represents repolarization of the ventricles. The U wave, if seen, may represent repolarization of the Purkinje fibers, or it may be associated with hypokalemia.²

Intervals between these waves (PR, QRS, and QT intervals) reflect the time it takes for the impulse to travel from one area of the heart to another. These time intervals can be measured, and changes from these time references often indicate pathologic conditions. (See Chapter 36 for a complete discussion of ECG monitoring.)

Vascular System

Blood Vessels.

The three major types of blood vessels in the vascular system are the arteries, veins, and capillaries. Arteries, except for the pulmonary artery, carry oxygenated blood away from the heart. Veins, except for the pulmonary veins, carry deoxygenated blood toward the heart. Small branches of arteries and veins are arterioles and venules, respectively. Blood circulates from the left side of the heart into arteries, arterioles, capillaries, venules, and veins, and then back to the right side of the heart.

Arteries and Arterioles.

The arterial system differs from the venous system by the amount and type of tissue that make up arterial walls (Fig. 32-5). The large arteries have thick walls composed mainly of elastic tissue. This elastic property cushions the impact of the pressure created by ventricular contraction and provides recoil that propels blood forward into the circulation. Large arteries also contain some smooth muscle. Examples of large arteries are the aorta and the pulmonary artery.

FIG. 32-5 Comparative thickness of layers of the artery, vein, and capillary.

Arterioles have relatively little elastic tissue and more smooth muscle. Arterioles serve as the major control of arterial BP and distribution of blood flow. They respond readily to local conditions such as low oxygen (O₂) and increasing levels of carbon dioxide (CO₂) by dilating or constricting.

The innermost lining of the arteries is the endothelium. The endothelium serves to maintain hemostasis, promote blood flow, and, under normal conditions, inhibit blood coagulation. When the endothelial surface is disrupted (e.g., rupture of an atherosclerotic plaque), the coagulation cascade is initiated and results in the formation of a fibrin clot.

Capillaries.

The thin capillary wall is made up of endothelial cells, with no elastic or muscle tissue (see Fig. 32-5). The exchange of cellular nutrients and metabolic end products takes place through these thin-walled vessels. Capillaries connect the arterioles and venules.

Veins and Venules.

Veins are large-diameter, thin-walled vessels that return blood to the right atrium (see Fig. 32-5). The venous system is a low-pressure, high-volume system. The larger veins contain semilunar valves at intervals to maintain the blood flow toward the heart and to prevent backward flow. The amount of blood in the venous system is affected by a number of factors, including arterial flow, compression of veins by skeletal muscles, alterations in thoracic and abdominal pressures, and right atrial pressure.

The largest veins are the superior vena cava, which returns blood to the heart from the head, neck, and arms, and the inferior vena cava, which returns blood to the heart from the lower part of the body. These large-diameter vessels are affected by the pressure in the right side of the heart. Elevated right atrial pressure can cause distended neck veins or liver engorgement as a result of resistance to blood flow.

Venules are relatively small vessels made up of a small amount of muscle and connective tissue. Venules collect blood from the capillary beds and channel it to the larger veins.

Regulation of Cardiovascular System

Autonomic Nervous System.

The autonomic nervous system consists of the sympathetic nervous system and the parasympathetic nervous system (see Chapter 56).

Effect on Heart.

Stimulation of the sympathetic nervous system increases the HR, the speed of impulse conduction through the AV node, and the force of atrial and ventricular contractions. This effect is mediated by specific sites in the heart called beta (β)-adrenergic receptors, which are receptors for norepinephrine and epinephrine.

In contrast, stimulation of the parasympathetic system (mediated by the vagus nerve) slows the HR by decreasing the impulses from the SA node, and thus conduction through the AV node.

Effect on Blood Vessels.

The source of neural control of blood vessels is the sympathetic nervous system. The alpha₁ (α₁)-adrenergic receptors are located in vascular smooth muscles. Stimulation of α₁-adrenergic receptors results in vasoconstriction. Decreased stimulation to α₁-adrenergic receptors causes vasodilation. (Sympathetic nervous system receptors that influence BP are presented in Table 33-1.)

The parasympathetic nerves have selective distribution in the blood vessels. For example, blood vessels in skeletal muscle do not receive parasympathetic input.

Baroreceptors.

Baroreceptors in the aortic arch and carotid sinus (at the origin of the internal carotid artery) are sensitive to stretch or pressure within the arterial system. Stimulation of these receptors (e.g., volume overload) sends information to the vasomotor center in the brainstem. This results in temporary inhibition of the sympathetic nervous system and enhancement of the parasympathetic influence, causing a decreased HR and peripheral vasodilation. Decreased arterial pressure causes the opposite effect.

Chemoreceptors.

Chemoreceptors are located in the aortic and carotid bodies and the medulla. They are capable of causing changes in respiratory rate and BP in response to increased arterial CO₂ pressure (hypercapnia) and, to a lesser degree, decreased plasma pH (acidosis) and arterial O₂ pressure (hypoxia). When the chemoreceptors in the medulla are triggered, they stimulate the vasomotor center to increase BP.⁴

Blood Pressure

The arterial blood pressure is a measure of the pressure exerted by blood against the walls of the arterial system. The systolic blood pressure (SBP) is the peak pressure exerted against the arteries when the heart contracts. The diastolic blood pressure (DBP) is the residual pressure in the arterial system during ventricular relaxation (or filling). BP is usually expressed as the ratio of systolic to diastolic pressure.

The two main factors influencing BP are cardiac output (CO) and systemic vascular resistance (SVR):

BP=CO×SVR

SVR is the force opposing the movement of blood. This force is created primarily in small arteries and arterioles. Normal blood pressure is SBP less than 120 mm Hg and DBP less than 80 mm Hg ⁵ (see Chapter 33).

Measurement of Arterial Blood Pressure.

BP can be measured by invasive and noninvasive techniques. The invasive technique consists of catheter insertion into an artery. The catheter is attached to a transducer, and the pressure is measured directly (see Chapter 66).

Noninvasive, indirect measurement of BP can be done with a sphygmomanometer and a stethoscope. The sphygmomanometer consists of an inflatable cuff and a pressure gauge. The BP is measured by auscultating for sounds of turbulent blood flow through a compressed artery (termed Korotkoff sounds). The brachial artery is the recommended site for taking a BP.

After placing the appropriate size cuff on the upper arm, inflate the cuff to a pressure 20 to 30 mm Hg above the SBP. This causes blood flow in the artery to cease. If the SBP is not known, estimate the pressure by palpating the brachial pulse and inflating the cuff until the pulse ceases. The pressure noted at this time is the estimated SBP. Inflate the BP cuff 20 to 30 mm Hg above this number.

As the pressure in the cuff is lowered, auscultate the artery for Korotkoff sounds. There are five phases of Korotkoff sounds. The first phase is a tapping sound caused by the spurt of blood into the constricted artery as the pressure in the cuff is gradually deflated. This sound is noted as the SBP. The fifth phase occurs when the sound disappears, which is noted as the DBP.⁶ BP is recorded as SBP/DBP (e.g., 120/80 mm Hg). Sometimes, an auscultatory gap occurs, which is a loss of sound between the SBP and the DBP. Proper BP technique (e.g., using the correct cuff size, positioning arm at heart level) is essential for accurate readings⁶ (see Table 33-11).

Another noninvasive way to measure BP indirectly is an automated device that uses oscillometric measurements to assess BP. Though this method does not involve auscultation, the same attention to proper technique is essential for accuracy. Finally, SBP (and pulse) can be assessed using a Doppler ultrasonic flowmeter. The hand-held transducer is positioned over the artery (identified by audible, pulsatile sounds). The cuff is applied above the artery, inflated until the sounds disappear, and then another 20 to 30 mm Hg beyond that point. The cuff is then slowly deflated until sounds return. This point is the SBP.⁶

Pulse Pressure and Mean Arterial Pressure.

Pulse pressure is the difference between the SBP and DBP. It is normally about one third of the SBP. If the BP is 120/80 mm Hg, the pulse pressure is 40 mm Hg. An increased pulse pressure due to an increased SBP may occur during exercise or in individuals with atherosclerosis of the larger arteries. A decreased pulse pressure may be found in heart failure or hypovolemia.

Another measurement related to BP is mean arterial pressure (MAP). The MAP refers to the average pressure within the arterial system that is felt by organs in the body. It is not the average of the diastolic and systolic pressures because the length of diastole exceeds that of systole at normal HRs. MAP is calculated as follows:

MAP=(SBP+2 DBP)÷3

A person with a BP of 120/60 mm Hg has an estimated MAP of 80 mm Hg. In patients with invasive BP monitoring, this value is automatically calculated and takes the patient’s HR into consideration (see Chapter 66).

An MAP greater than 60 mm Hg is needed to adequately perfuse and sustain the vital organs of an average person under most conditions. When the MAP falls below this number for a period of time, vital organs are underperfused and will become ischemic.

Gerontologic Considerations

Effects of Aging on the Cardiovascular System

One of the greatest risk factors for cardiovascular disease (CVD) is age. CVD remains the leading cause of death in adults older than age 85. It is the most common cause of hospitalization and the second leading cause of death in adults younger than age 85. The most common cardiovascular problem is coronary artery disease (CAD) secondary to atherosclerosis. It is difficult to separate normal aging changes from the pathophysiologic changes of atherosclerosis. Many of the physiologic changes in the cardiovascular system of older adults are a result of the combined effects of the aging process, disease, environmental factors, and lifetime health behaviors rather than just age alone.⁷

Age-related changes in the cardiovascular system and differences in assessment findings are presented in Table 32-1. With increased age, the amount of collagen in the heart increases and elastin decreases. These changes affect the myocardium’s ability to stretch and contract. One of the major changes in the cardiovascular system is the response to physical or emotional stress. In times of increased stress, CO and SV decrease due to reduced contractility and HR response. The resting supine HR is not markedly affected by aging. When the patient changes positions (e.g., sits upright), the sympathetic nerve pathway may be affected by fibrous tissue and fatty deposits, resulting in a blunted HR response.⁷

TABLE 32-1

GERONTOLOGIC ASSESSMENT DIFFERENCES
Cardiovascular System

Changes	Differences in Assessment Findings
Chest Wall
Kyphosis	Altered chest landmarks for palpation, percussion, and auscultation. Distant heart sounds.
Heart
Myocardial hypertrophy, ↑ collagen and scarring, ↓ elastin	↓ Cardiac reserve, heart failure.
Downward displacement	Difficulty in isolating apical pulse
↓ CO, HR, SV in response to exercise or stress	↓ Response to exercise and stress. Slowed recovery from activity.
Cellular aging and fibrosis of conduction system	↓ Amplitude of QRS complex and slight. lengthening of PR, QRS, and QT intervals. Irregular cardiac rhythms, ↓ maximal HR, ↓ HR variability.
Valvular rigidity from calcification, sclerosis, or fibrosis, impeding complete closure of valves	Systolic murmur (aortic or mitral) possible without an indication of cardiovascular disease.
Blood Vessels
Arterial stiffening caused by loss of elastin in arterial walls, thickening of intima of arteries, and progressive fibrosis of media	↑ In systolic BP and possible ↑ or ↓ in diastolic BP. Possible widened pulse pressure. Pedal pulses diminished. ↑ In intermittent claudication.
Venous tortuosity increased	Inflamed, painful, or cordlike varicosities. Dependent edema.

Cardiac valves become thicker and stiffer from lipid accumulation, degeneration of collagen, and fibrosis. The aortic and mitral valves are most frequently affected. These changes result in either regurgitation of blood when the valve should be closed or narrowing of the orifice of the valve (stenosis) when the valve should be open. The turbulent blood flow across the affected valve results in a murmur.

The number of pacemaker cells in the SA node decreases with age. By age 75, a person may have only 10% of the normal number of pacemaker cells. Although this is compatible with adequate SA node function, it may account for the frequency of some sinus dysrhythmias in older adults. Similar decreases also occur in the number of conduction cells in the internodal tracts, bundle of His, and bundle branches. These changes contribute to the development of atrial dysrhythmias and heart blocks. About 50% of older adults have an abnormal resting ECG that shows increases in the PR, QRS, and/or QT intervals.⁸

The autonomic nervous system control of the cardiovascular system changes with aging. The number and function of β-adrenergic receptors in the heart decrease with age. So the older adult not only has a decreased response to physical and emotional stress, but also is less sensitive to β-adrenergic agonist drugs. The lower maximum HR during exercise results in only a twofold increase in CO compared with the three or four times increase seen in younger adults.

Arterial and venous blood vessels thicken and become less elastic with age.⁹ Arteries increase their sensitivity to vasopressin (antidiuretic hormone). With aging both of these changes contribute to a progressive increase in SBP and a decrease or no change in DBP. Thus an increase in the pulse pressure is found. Hypertension is not a normal consequence of aging, and should be treated. Valves in the large veins in the lower extremities have a reduced ability to return the blood to the heart, often resulting in dependent edema.

Orthostatic hypotension, which is estimated to be present in more than 30% of patients over age 70 with systolic hypertension, may be related to medications and/or decreased baroreceptor function.⁸ Postprandial hypotension (decrease in BP of at least 20 mm Hg that occurs within 75 minutes after eating) may also occur in about a third of otherwise healthy older adults. Both orthostatic and postprandial hypotension may be related to falls in older adults. Despite the changes associated with aging, the heart is able to function adequately under most circumstances.

Case Study

Patient Introduction

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L.P., a 63-year-old Asian American man, is brought to the emergency department by ambulance at 6 am after calling 911 with complaints of chest pain, shortness of breath (SOB), palpitations, and dizziness. The paramedics have started an IV and oxygen at 2 L/min via nasal cannula. They also administered four chewable baby ASA and a nitroglycerin tablet, and they obtained a 12-lead ECG. L.P. is pain free on arrival but still complains of palpitations and dizziness.

Critical Thinking

As you read through this assessment chapter, think about L.P.’s symptoms with the following questions in mind:

1. What are the possible causes of L.P.’s chest pain, SOB, palpitations, and dizziness?

2. What would be your major focus when assessing L.P.?

3. What questions would you ask L.P.?

4. What should be included in the physical assessment? What would you be looking for?

5. What diagnostic studies would you expect to be ordered?

Assessment of Cardiovascular System

Subjective Data

A careful health history and physical examination will help you distinguish symptoms that reflect a cardiovascular problem from problems of other body systems. Explore and document all cues that alert you to the possibility of underlying cardiovascular problems.

Many illnesses affect the cardiovascular system directly or indirectly. Ask the patient about a history of chest pain, shortness of breath, fatigue, alcohol and tobacco use, anemia, rheumatic fever, streptococcal throat infections, congenital heart disease, stroke, palpitations, dizziness with position changes, syncope, hypertension, thrombophlebitis, intermittent claudication, varicosities, and edema.

Medications.

Assess the patient’s current and past use of medications. This includes over-the-counter (OTC) drugs, herbal supplements, and prescription drugs. For example, aspirin prolongs the blood clotting time, and is found in many drugs used to treat cold symptoms. List all of the patient’s drugs. Include dosage, time of last dose, and the patient’s understanding of the drug’s purpose and side effects. Many noncardiac drugs can adversely affect the cardiovascular system and should be assessed (Table 32-2).

TABLE 32-2

CARDIOVASCULAR EFFECTS OF NONCARDIAC DRUGS *

Drug Classification	Examples	Cardiovascular Effects
Anticancer agents	daunorubicin (Cerubidine) doxorubicin (Adriamycin)	Dysrhythmias, cardiomyopathy
Antipsychotics	chlorpromazine (Thorazine) haloperidol (Haldol)	Dysrhythmias, orthostatic hypotension
Corticosteroids	cortisone (Cortone) prednisone (Orasone)	Hypotension, edema, potassium depletion
Hormone therapy, oral contraceptives	estrogen + progestin (Ortho-Novum, Prempro, Tri-Norinyl)	Myocardial infarction, thromboembolism, stroke, hypertension
Nonsteroidal antiinflammatory drugs (NSAIDs) †	ibuprofen (Motrin) celecoxib (Celebrex)	Hypertension, myocardial infarction, stroke
Psychostimulants	cocaine amphetamines	Tachycardia, angina, myocardial infarction, hypertension, dysrhythmias
Tricyclic antidepressants	amitriptyline (Elavil) doxepin (Sinequan)	Dysrhythmias, orthostatic hypotension