21. Cardiovascular System Disorders

Cardiovascular System: Disorders

Physical Assessment

A thorough physical assessment is the foundation for the nursing database and the formation of nursing diagnoses and collaborative problems. Any changes noted during the course of illness can be compared with this initial database. The nurse evaluates the client's vital signs on admission to the hospital or during the initial visit to the clinic or health care provider's office.

GENERAL APPEARANCE

Physical assessment begins with the client's general appear­ance. The nurse assesses the following areas: general build and appearance, skin color, distress level, level of conscious­ness, shortness of breath, position, and verbal responses.

Clients with chronic heart failure may appear malnour­ished, thin, and cachectic. Latent signs of severe heart failure are ascites, jaundice, and anasarca (generalized edema) as a result of prolonged congestion of the liver. Heart failure may cause fluid retention, and clients may have engorged neck veins and generalized dependent edema.

Coronary artery disease is suspected in clients with yellow, lipid-filled plaques on the upper eyelids (xanthelasma) or ear-lobe creases. Clients with poor cardiac output and decreased cerebral perfusion may experience mental confusion, memory loss, and slowed verbal responses.

INTEGUMENTARY SYSTEM

Assessment and evaluation of the integumentary system are determined primarily by the color and temperature of the skin. The best areas in which to assess circulation include the nail beds, mucous membranes, and conjunctival mucosa because small blood vessels are located near the surface of the skin.

Skin Color

If there is normal blood flow or adequate perfusion to a given area in light-colored skin, it appears pink, perhaps rosy in color, and it is warm to the touch. Decreased flow is depicted as cool, pale, and moist skin. Pallor is characteristic of anemia and can be seen in areas such as the nail beds, palms, and con-junctival mucous membranes.

A bluish or darkened discoloration of the skin and mucous membranes in Caucasians is referred to as cyanosis. This con­dition results from an increased amount of deoxygenated he­moglobin. Dark-skinned individuals may express cyanosis as a graying of the same tissues.

Central cyanosis involves decreased oxygenation of the ar­terial blood in the lungs and appears as a bluish tinge of the conjunctivae and the mucous membranes of the mouth and tongue. Central cyanosis may indicate impaired lung function or a right-to-left shunt found in congenital heart conditions. Because of impaired circulation, there is a marked desatura-tion of hemoglobin in the peripheral tissues, which produces a bluish or darkened discoloration of the nail beds, earlobes, lips, and toes.

Peripheral cyanosis occurs when blood flow to the periph­eral vessels is decreased by peripheral vasoconstriction. The clamping down of the peripheral blood vessels results from a low cardiac output or an increased extraction of oxygen from the peripheral tissues. Peripheral cyanosis localized in an ex­tremity is usually a result of arterial or venous obstruction.

 

Skin Temperature

Skin temperature can be assessed for symmetry by touching different areas of the client's body (e.g., arms, hands, legs, and feet) with the dorsal surface of the hand or fingers. De­creased blood flow results in decreased skin temperature. Skin temperature is lowered in several clinical conditions, in­cluding heart failure, peripheral vascular disease, and shock.

 

EXTREMITIES

The nurse assesses the client's hands, arms, feet, and legs for skin changes, vascular changes, clubbing, capillary filling, and edema. Skin mobility and turgor are affected by the fluid status of the client. Dehydration and aging reduce skin turgor, and edema decreases skin mobility. Vascular changes in an af­fected extremity may include paresthesia, muscle fatigue and discomfort, numbness, pain, coolness, and loss of hair distri­bution from a reduced blood supply.

Clubbing of the fingers and toes results from chronic oxy­gen deprivation in these tissue beds. Clubbing is characteris­tic in clients with advanced chronic pulmonary disease, con­genital heart defects, and cor pulmonale. Clubbing can be identified by assessing the angle of the nail bed. The angle of the normal nail bed is 160 degrees. With clubbing, this angle increases to greater than 180 degrees, and the base of the nail becomes spongy.

Capillary filling of the fingers and the toes is an indicator of peripheral circulation. Pressing or blanching the nail bed of a finger or a toe produces a whitening effect; when pressure is released, a brisk return of color should occur. If color returns within 3 seconds, peripheral circulation is considered intact. If the capillary refill time exceeds 3 seconds, the lack of cir­culation may be due to arterial insufficiency from atheroscle­rosis or spasm. Older adults typically have a prolonged capil­lary refill. Rubor (dusky redness) that replaces pallor in a dependent foot suggests arterial insufficiency.

Peripheral edema is a common finding in clients with car­diovascular problems. The location of edema helps the nurse to determine its potential cause. Bilateral edema of the legs may be seen in clients with heart failure or chronic venous in­sufficiency. Abdominal and leg edema can be seen in clients with heart disease and cirrhosis of the liver. Localized edema in one extremity may be the result of venous obstruction (thrombosis) or lymphatic blockage of the extremity (lymph-edema). Edema may also be noted in dependent areas, such as the sacrum, when a client is confined to bed.

The nurse documents the location of edema as precisely as possible (e.g., midtibial or sacral) and the number of centime­ters from an anatomic landmark. Although some health care severe (or 1 + , 2+, 3 + , or 4+), there is no universal scale. In addition, these values are not precise and are subjective. In­stead of using a grading scale, the nurse determines whether the edema is pitting (the skin can be indented) or nonpitting, the depth of the pit (in millimeters), and the amount of time the pit lasts (in seconds).

 

 BLOOD PRESSURE

Arterial blood pressure is measured indirectly by sphygmomanometry.

Normal blood pressure in adults older than 45 years of age ranges from 90 to 140 mm Hg for systolic pressure and from 60 to 90 mm Hg for diastolic pressure (AHA, 1998). A blood pressure that exceeds 135/85 mm Hg increases the workload of the left ventricle and oxygen consumption. Approximately 50 million Americans (one out of every 5 Americans) have hypertension, which is defined as a blood pressure greater than 140/90 mm Hg. Although the cause of hypertension is not known in 90% of people, it can be effectively controlled with lifestyle modification and/or medication. Hypertension is a cause of approximately 5 million deaths each year on its own and is a major contributor to the development of coro­nary artery disease and heart failure.

A blood pressure less than 90/60 mm Hg may be inade­quate for providing proper and sufficient nutrition to body cells. In certain circumstances, such as shock and hypoten­sion, the Korotkoff sounds are less audible or are absent. In these cases the nurse might palpate the blood pressure, use an ultrasonic device (Doppler device), or obtain a direct meas­urement by arterial catheter. When blood pressure is palpated, the diastolic pressure is usually not obtainable.

Postural Blood Pressure

Clients may report dizziness or lightheadedness when they move from a flat, supine position to a sitting or a standing po­sition at the edge of the bed. Normally these symptoms are transient and pass quickly; pronounced symptoms may be due to orthostatic (postural) hypotension. Postural hypotension occurs when blood pressure is not adequately maintained while moving from a lying to a sitting or standing position. It is defined as a decrease of more than 20 mm Hg of the sys­tolic pressure or more than 10 mm Hg of the diastolic pres­sure, as well as a 10% to 20% increase in heart rate. The causes of postural hypotension include medications, depletion of blood volume, prolonged bedrest, and age-related changes or disorders of the autonomic nervous system.

To detect orthostatic changes in blood pressure, the nurse first measures the blood pressure when the client is supine. After remaining supine for at least 3 minutes, the client changes position to sitting or standing. Normally systolic pressure drops slightly or remains unchanged as the client rises, whereas diastolic pressure rises slightly. After the posi­tion change, a time delay of 1 to 5 minutes should be permit­ted before auscultating blood pressure and palpating the radial pulse. The cuff should remain in the proper position on the client's arm. The nurse observes and records any signs or symptoms of distress. If the client is unable to tolerate the po­sition change, he or she is returned to the previous position of comfort.

Paradoxical Blood Pressure

Paradoxical blood pressure is defined as an exaggerated de­crease in systolic pressure by more than 10 mm Hg during the inspiratory phase of the respiratory cycle (normal is 3 to 10 mm Hg). Certain clinical conditions that potentially alter the filling pressures in the right and left ventricles may produce a paradoxical blood pressure. Such conditions include pericar-dial tamponade, constrictive pericarditis, and pulmonary hy­pertension. During inspiration, the filling pressures normally

decrease slightly. However, the decreased fluid volume in the ventricles resulting from these pathologic conditions pro­duces an exaggerated or marked reduction in cardiac output.

Hepatojugular reflux is determined by locating the internal jugular vein after positioning the client with the head of the bed elevated to 45 degrees. The nurse compresses the right upper abdomen for 30 to 40 seconds. Sudden distention of the neck veins after abdominal compression is usually indicative of right-sided heart failure.

Pulse Pressure

The difference between the systolic and diastolic values is re­ferred to as pulse pressure. A normal pulse pressure for an adult is 30 to 40 mm Hg. This value can be used as an indi­rect measure of cardiac output. A more precise measurement, proportional pulse pressure, is calculated as follows:

Proportional pulse pressure = (Systolic blood pressure - Diastolic blood pressure)/ Systolic blood pressure

A proportional pulse pressure less than 25% usually indi­cates a cardiac index of less than 2.2, as well as a critically low cardiac output (Stevenson & Braunwald, 1998). Nar­rowed pulse pressure is rarely normal and results from in­creased peripheral vascular resistance or decreased stroke vol­ume in clients with heart failure, hypovolemia, or shock. Narrowed pulse pressure can also be seen in clients who have mitral stenosis or regurgitation. An increased pulse pressure may be seen in clients with slow heart rates, aortic regurgita­tion, atherosclerosis, hypertension, and aging.

Ankle Brachial Index

The ankle brachial index (ABI) can be used to assess the vascular status of the lower extremities. The nurse applies a blood pressure cuff to the lower extremities just above the malleoli and measures the systolic pressure by Doppler ul­trasound at both the dorsalis pedis and posterior tibial pulses. The higher of these two pressures is then divided by the higher of the two brachial pulses to obtain the ankle brachial index:

Normal values for ABI are 1 or higher, because blood pres­sure in the legs is usually higher than blood pressure in the arms. ABI values less than 0.80 usually indicate moderate vascular disease, whereas values less than 0.50 indicate severe vascular compromise.

VENOUS AND ARTERIAL PULSATIONS

Venous Pulsations

The nurse observes the venous pulsations in the neck to assess the adequacy of blood volume and central venous pressure (CVP). The nurse can assess jugular venous pressure (JVP) to estimate the filling volume and pressure on the right side of the heart . The right internal jugular vein is usu­ally used to estimate JVP.

JVP is normally 3 to 10 cm H2O. Increases in JVP are usu­ally caused by right ventricular failure. Other causes include tricuspid regurgitation or stenosis, pulmonary hypertension, cardiac tamponade, constrictive pericarditis, hypervolemia, and superior vena cava obstruction.

Arterial Pulsations

Assessment of arterial pulsations gives the nurse information about
vascular integrity and circulation.

For clients with sus­pected or actual vascular disease, all major peripheral pulses, including the temporal, carotid, brachial, radial, ulnar, femoral, popliteal, posterior tibial, and dorsalis pedis pulses, need to be assessed for presence or absence, amplitude, con­tour, rhythm, rate, and equality. The nurse examines the pe­ripheral arteries in a head-to-toe approach with a side-to-side comparison.

A hypokinetic pulse is a weak pulsation indicative of a nar­row pulse pressure. It is seen in clients with hypovolemia, aortic stenosis, and decreased cardiac output.

A hyperkinetic pulse is a large, "bounding" pulse caused by an increased ejection of blood. It is seen in clients with a high cardiac output (with exercise or thyrotoxicosis) and in those with increased sympathetic system activity (with pain, fever, or anxiety).

In pulsus alternans, a weak pulse alternates with a strong pulse despite a regular heart rhythm. It is seen in clients with severely depressed cardiac function. Clients may be asked to hold their breath to exclude any false readings. The nurse may palpate the brachial or radial arteries to assess this condition, but it is more accurately assessed by auscultation of blood pressure.

Auscultation of the major arteries (e.g., carotid and aorta) is necessary to assess for bruits. Bruits are swishing sounds that may develop in narrowed arteries and are usually associated with atherosclerotic disease. The nurse can assess for the ab­sence or presence of bruits by placing the bell of the stetho­scope over the skin of the carotid artery while the client holds his or her breath. Normally there are no sounds if the artery has uninterrupted blood flow. A bruit may develop when the inter­nal diameter of the vessel is narrowed by 50% or more, but this does not indicate the severity of disease in the arteries. Sever­ity is determined by Doppler flow studies and arteriography.

 

PRECORDIUM

Assessment of the precordium (the area over the heart) in­volves inspection, palpation, percussion, and auscultation. In most settings the medical-surgical nurse seldom performs precordial palpation and percussion. However, the critical care nurse should perform a complete assessment (McGrath & Cox, 1998). The nurse places the client in a supine position, with the head of the bed slightly elevated for comfort. Some clients may require elevation of the head of the bed to 45 de­grees for ease and comfort in breathing.

Inspection

A cardiac examination is usually performed in a systematic order, beginning with inspection. The nurse inspects the chest from the side, at a right angle, and downward over areas of the precordium where vibrations are visible. Cardiac motion is of low amplitude, and sometimes the inward movements are more easily detected by the naked eye.

The nurse examines the entire precordium, focusing on the seven precordial areas and noting any promi­nent precordial pulsations.

Movement over the aortic, pulmonic, and tricuspid areas is abnormal. Pulsations in the mi­tral area (the apex of the heart) are considered normal and are referred to as the apical impulse, or the point of maximal im­pulse (PMI). The PMI should be located at the left fifth in­tercostal space (ICS) in the midclavicular line. If the apical impulse appears in more than one intercostal space and has shifted lateral to the midclavicular line, it may indicate left ventricular hypertrophy.

Palpation

The nurse palpates with the fingers and the most sensitive part of the palm of the hand to detect precordial motion and thrills, respectively. The nurse palpates by inching his or her hand in a Z pattern along the chest, starting with the aortic area and passing through all seven areas. Turning the client on his or her left side brings the heart closer to the surface of the chest. This may be helpful in achieving maximum tac­tile sensitivity.

An abnormal forceful thrust accompanied by a sustaining outward movement over the left anterior side of the chest usu­ally indicates left ventricular enlargement. An outward sys­tolic lift along the left sternal border that extends from the fourth to the fifth intercostal space represents right ventricu­lar enlargement.

Heaves and lifts are terms found with pulsations associated with valvular diseases or pulmonary hypertension. Thrills are vibrations associated with abnormal heart valve function (mi­tral regurgitation, tricuspid regurgitation, and pulmonic steno­sis). When palpating for heaves or thrills, the nurse should consider several factors, including location, amplitude, dura­tion, distribution, and timing in relation to the cardiac cycle.

Percussion

Cardiac size is determined most accurately by chest x-ray examination; percussion is now rarely used to determine the size of the heart. However, the size of the left ventricle can be estimated by locating the apical impulse by inspection and palpation.

Auscultation

Auscultation evaluates heart rate and rhythm, cardiac cycle (systole and diastole), and valvular function. The technique of auscultation requires a good-quality stethoscope and exten­sive clinical practice. The medical-surgical nurse needs to be familiar with normal heart sounds. The critical care nurse, telemetry nurse, and advance practice nurse should be able to identify common abnormal heart sounds.

 

The nurse evaluates heart sounds in a systematic order. Ex­amination usually begins at the aortic outflow tract area and progresses slowly to the apex of the heart. The diaphragm of the stethoscope is pressed tightly against the chest to listen for high-frequency sounds and is useful in listening to the first and second heart sounds and high-frequency murmurs. The nurse then repeats the progression from the base to the apex of the heart using the bell of the stethoscope, which is held lightly against the chest. The bell is able to screen out high-frequency sounds and is useful in listening for low-frequency gallops (diastolic filling sounds) and murmurs.

The nurse auscultates by inching a stethoscope in a Zpattern across the base of the heart, down the left sternal border, then over to the apex.  Auscultation checks for heart rate and rhythm, murmurs, extrasystolic sounds, and rubs in the presence of a current or suspected cardiac problem.

 NORMAL HEART SOUNDS

The first heart sound (S,) is created by the closure of the mi­tral and tricuspid valves (atrioventricular valves). When auscultated, the first heart sound is softer and longer; it is of a low pitch and is best heard at the lower left sternal border or the apex of the heart. It may be identified by palpating the carotid pulse while listening. S, marks the be­ginning of ventricular systole and occurs right after the QRS complex on the electrocardiogram (ECG).

The first heart sound can be accentuated or intensified in conditions such as exercise, hyperthyroidism, and mitral stenosis. A decrease in sound intensity occurs in clients with mitral regurgitation and heart failure.

The second heart sound (S2) is caused mainly by the clos­ing of the aortic and pulmonic valves (semilunar valves). S2 is characteristically shorter. It is higher pitched and is heard best at the base of the heart at the end of ventricular systole.

The splitting of heart sounds is often difficult to differenti­ate from diastolic filling sounds (gallops). A splitting of S1 (closure of the mitral valve followed by closure of the tricuspid valve) occurs physiologically because left ventricular con­traction occurs slightly before right ventricular contraction. However, closure of the mitral valve is louder than closure of the tricuspid valve, so splitting is often not heard. Normal splitting of S2 occurs because of the longer systolic phase of the right ventricle. Splitting of S, and S2 can be accentuated by inspiration (increased venous return), and it narrows dur­ing expiration.

Psychosocial Assessment

To many people, their heart is a symbol of their ability to ex­ist, survive, and love. A client with a heart-related illness, whether acute or chronic, usually perceives it as a major life crisis. The client and families and significant others confront not only the possibility of death but also fears about pain, dis­ability, lack of self-esteem, physical dependence, and changes in family dynamics. The nurse may assess the meaning of the illness to the client and family members by asking, "What do you understand about what happened to you (or the client)?" and "What does that mean to you?" When the client or fam­ily members perceive the stressor as overwhelming, formerly adequate support systems may no longer be effective. In these circumstances, the client and family members attempt to cope to regain a sense or feeling of control.

Coping behaviors vary among clients. Those who feel helpless to meet the demands of the situation may exhibit be­haviors such as disorganization, fear, and anxiety. The nurse may ask the client or family members, "Have you ever en­countered such a situation before?", "How did you manage that situation?", and "To whom can you turn for help?" The answers to these questions often reassure the client that he or she has encountered difficult situations in the past and has the ability and resources to cope with them.

A common and normal response is denial, which is a de­fense mechanism that enables the client to cope with threat­ening circumstances. The client may deny that he or she has the current cardiovascular condition, may state that it was present but is now absent, or may be excessively cheerful. Denying the seriousness of the illness while following the treatment regimen is a protective response. Denial becomes maladaptive when the client is noncompliant with significant portions of medical and nursing care.

Family members and significant others may be more anx­ious than the client. Often they recall all events of the illness, are unprotected by denial, and are afraid of recurrence. Dis­agreements often occur between the client and family mem­bers over compliance with appropriate follow-up care.

 

CURRENT HEALTH PROBLEMS   

Inquiring about major concerns helps the nurse to establish priorities in nursing care and management. The client is asked to describe his or her health concerns. The nurse expands on the description of these concerns by obtaining information about their onset, duration, chronology, frequency, location, quality, intensity, associated symptoms, and precipitating, ag­gravating, and relieving factors. Major symptoms identified by clients with cardiovascular disease include chest pain or discomfort, dyspnea, fatigue, palpitations, weight gain, syn­cope, and extremity pain.

 Chest Pain

Chest pain or discomfort, a cardinal symptom of heart dis­ease, can result from ischemic heart disease, pericarditis, and aortic dissection. Chest pain can also be due to noncardiac conditions such as pleurisy, pulmonary embolus, hiatal her­nia, and anxiety. Nurses must thoroughly evaluate the nature and characteristics of the chest pain. Because chest pain re­sulting from myocardial ischemia is life threatening and can lead to serious complications, its cause should be considered ischemic (reduced or obstructed blood flow to the myo­cardium) until proven otherwise.

When assessing for chest pain, the nurse uses alternative terms such as "discomfort," "heaviness," and "indigestion." Clients often do not experience pain in the chest but instead feel discomfort or indigestion. The client may also describe the sensation as aching, choking, strangling, tingling, squeez­ing, constricting, or vise-like.

The nurse asks the client to identify when the pain was first noticed (onset). Did the pain begin suddenly or develop grad­ually (manner of onset)? How long did it last (duration)? If the client has repeated chest pain episodes, the nurse assesses how often the pain occurs (frequency). The nurse asks whether this pain is different from any other episodes of pain. The nurse asks the client to describe what activities he or she was doing when it first occurred, such as sleeping, arguing, or running (precipitating factors). The client can be asked to point to the area where the chest pain occurred (location) and to describe how the pain spread (radiation).

In addition, the client describes how the pain feels and whether it is sharp or dull (quality). To understand the sever­ity of the pain, the nurse asks the client to grade it from 0 to 10, with 0 indicating an absence of pain and 10 indicating se­vere pain (intensity). The client may also report other signs and symptoms that occur at the same time (associated symp­toms), such as dyspnea, diaphoresis, nausea, and vomiting. Other factors that need to be addressed are those that may have made the chest pain worse (aggravating factors) or less intense (relieving factors). Chest pain may arise from a vari­ety of sources. By obtaining the appropriate in­formation, the nurse may assist in identifying the source of the chest discomfort.

Dyspnea

Dyspnea can occur as a result of both cardiac and pulmonary disease. Dyspnea is objectively described as difficult or la­bored breathing and is subjectively experienced as uncom­fortable breathing or shortness of breath. When obtaining the client's history, the nurse ascertains what factors precipitate and relieve dyspnea, what level of activity produces dyspnea, and the client's body position when dyspnea occurred.

There are several types of dyspnea. Dyspnea that is associ­ated with activity, such as climbing stairs, is referred to as dyspnea on exertion (DOE). This is usually an early symptom of heart failure.

The client with advanced heart disease may experience or-thopnea, or dyspnea that appears when the client lies flat. The client may use several pillows at night to elevate the head and chest or may sleep in a recliner to prevent nighttime breath-lessness. The severity of orthopnea is measured by the num­ber of pillows or the amount of head elevation needed to pro­vide restful sleep. Orthopnea is usually relieved within a matter of minutes by sitting up or standing.

Paroxysmal nocturnal dyspnea develops after the client has been lying down for several hours. In this position, blood from the lower extremities is redistributed to the venous sys­tem, which increases venous return to the heart. A diseased heart is unable to compensate for the increased volume and is ineffective in pumping the additional fluid into the circulatory system. Pulmonary congestion results. The client awakens abruptly, often with a feeling of suffocation and panic. The client usually sits upright with the legs dangled over the bed­side to relieve the dyspnea. This sensation may last for 20 minutes before disappearing.

Fatigue

Fatigue may be described as a feeling of tiredness or weariness resulting from activity. The client may complain that a certain activity takes longer to complete or that he or she tires easily after activity. Although fatigue in itself is not diagnostic of heart disease, many people with heart failure are limited by leg fatigue during exercise. Fatigue that occurs after mild activity and exertion usually indicates inadequate cardiac output (low stroke volume) and anaerobic metabolism in skeletal muscle. The nurse questions the client to determine the time of day he or she experiences fatigue as well as the activities that he or she can perform. Fatigue resulting from decreased cardiac output is often worse in the evening. The nurse asks whether the client can perform the same activities as a year ago or the same activities as others of the same age. Often the client lim­its activities in response to fatigue and unless questioned is unaware how much less active he or she has become.

Palpitations

A feeling of fluttering in the chest or an unpleasant awareness of the heartbeat is referred to as palpitations. Palpitations may result from a change in heart rate or rhythm or from an increase in the force of heart contractions. Rhythm distur­bances that may cause palpitations include paroxysmal supraventricular tachycardia, premature contractions, and si­nus tachycardia. Those that occur during or after strenuous physical activity, such as running and swimming, may indi­cate overexertion or possibly heart disease. Noncardiac fac­tors that may precipitate palpitations include anxiety, stress, fatigue, insomnia, hyperthyroidism, and the ingestion of caf­feine, nicotine, or alcohol.

Weight Gain

A sudden weight increase of 2.2 pounds (1 kg) can result from an accumulation of excessive fluid (1 L) in the interstitial spaces. This condition is commonly known as edema. It is possible for weight gains of up to 10 to 15 pounds (4.5 to 6.8 kg, or 4 to 7 L of fluid) to occur before edema is apparent. The nurse should inquire whether the client has noticed a tightness of shoes, indentations from socks, or tightness of rings.

Syncope

Syncope refers to a transient loss of consciousness. The most common cause is decreased perfusion to the brain. Any con­dition that suddenly reduces cardiac output, resulting in de­creased cerebral blood flow, can potentiate a syncopal episode. Conditions such as cardiac rhythm disturbances (ventricular dysrhythmia or Stokes-Adams attack) and valvu­lar disorders (aortic stenosis) may potentiate this symptom.

Near-syncope refers to dizziness with an inability to re­main in an upright position. The nurse explores the circum­stances that lead to dizziness or syncope.

Extremity Pain

Extremity pain may be caused by two conditions: ischemia from atherosclerosis and venous insufficiency of the periph­eral blood vessels. Clients who report a moderate to severe cramping sensation in their legs or buttocks associated with an activity such as walking have intermittent claudication re­lated to reduced arterial tissue perfusion. Claudication pain is usually relieved by resting or lowering the affected extremity to decrease tissue demands or to enhance arterial blood flow. Leg pain that results from prolonged standing or sitting is re­lated to venous insufficiency from either incompetent valves or venous obstruction. This pain may be relieved by elevating the extremity.

FUNCTIONAL HISTORY

After the history of the client's cardiovascular status is ob­tained, he or she may be classified according to the New York Heart Association's Functional Classification (Table 33-2). The four classifications (I, II, III, and IV) depend on the de­gree to which ordinary physical activities (routine activities of daily living [ADLs]) are affected by heart disease.

ABNORMAL HEART SOUNDS

PARADOXICAL SPLITTING. Abnormal splitting of S2 is referred to as paradoxical splitting and is characteristic of a wider split heard on expiration. Paradoxical splitting of S2 is heard in clients with severe myocardial depression that causes early closure of the pulmonic valve or a delay in aortic valve closure. Such conditions include myocardial infarction, left bundle branch block, aortic stenosis, aortic regurgitation, and right ventricular pacing.

GALLOPS AND MURMURS. Gallops and murmurs are common abnormal heart sounds that may occur with heart disease.

GALLOPS. Diastolic filling sounds (S3) and (S4) are pro­duced when blood enters a noncompliant chamber during rapid ventricular filling. The third heart sound (S3) is pro­duced during the rapid passive filling phase of ventricular di­astole when blood flows from the atrium to a noncompliant ventricle. The sound arises from vibrations of the valves and supporting structures. The fourth heart sound (S4) occurs as blood enters the ventricles during the active filling phase at the end of ventricular diastole.

S3 is termed ventricular gallop, and S4 is referred to as atrial gallop. These sounds can be caused by decreased com­pliance of either or both ventricles. The nurse can best hear left ventricular diastolic filling sounds with the client on his or her left side. The bell of the stethoscope is placed at the apex and at the left lower sternal border during expiration.

An S3 heart sound is probably a normal finding in children or young adults up to 30 years of age. An S3 gallop in clients older than 40 years of age is considered abnormal and repre­sents a decrease in left ventricular compliance. S3 can be de­tected as an early sign of heart failure or as a ventricular sep-tal defect.

An atrial gallop (S4) may be heard in clients with hyper­tension, anemia, ventricular hypertrophy, myocardial infarc­tion, aortic or pulmonic stenosis, and pulmonary emboli. It may also be heard with advancing age because of a stiffened ventricle.

The auscultation of both S3 and S4, called a summation or a quadruple gallop, is an indication of severe heart failure. If the quadruple rhythm is present and the client has tachycardia (a shortened diastole), the two sounds may actually fuse to produce a rhythm that sounds like a horse galloping.

MURMURS. Murmurs reflect turbulent blood flow through normal or abnormal valves. They are classified ac­cording to their timing in the cardiac cycle: systolic murmurs (e.g., aortic stenosis and mitral regurgitation) occur between S, and S2, whereas diastolic murmurs (e.g., mitral stenosis and aortic regurgitation) occur between S2 and S,. Murmurs can occur during presystole, midsystole, or late systole or diastole or can last throughout both phases of the cardiac cycle. They are also graded according to their intensity, depending on their level of loudness.

The nurse describes the location of a murmur by where it is best heard on auscultation. Some murmurs transmit or radiate from their loudest point to other areas, including the neck, the back, and the axilla. The configuration is de­scribed as crescendo (increases in intensity) or decrescendo (decreases in intensity). The quality of murmurs can be fur­ther characterized as harsh, blowing, whistling, rumbling, or squeaking. They are also described by pitch, usually high or low.

PERICARDIAL FRICTION RUB. A pericardial fric­tion rub originates from the pericardial sac and occurs with the movements of the heart during the cardiac cycle. Rubs are usually transient and are a sign of inflammation, infection, or infiltration. Pericardial friction rubs may be heard in clients with pericarditis resulting from myocardial infarction and car­diac tamponade.

The three phases of cardiac movement—atrial systole, ventricular diastole, and ventricular systole—can produce three components of a rub. Usually only one or two compo­nents can be heard. A short, high-pitched scratchy sound is produced with each movement; the loudest component is heard in systole. The nurse may be most able to auscultate the rubs when the client sits, leans forward, and exhales. A peri­cardial friction rub is better heard with the diaphragm of the stethoscope.

An Overview of the Cardiovascular System

The evaluation of the cardiovascular system includes a thorough medical history, a detailed examination of the heart and the peripheral arterial and venous circulations, and appropriate laboratory studies. In addition to the electrocardiogram and chest x-ray, the availability of sophisticated noninvasive techniques (e.g., echocardiography and nuclear cardiology) and the continued improvement of cardiac catheterization and angiography have significantly enhanced the clinical work-up of the patient with a cardiovascular problem. A careful assessment will enable the clinician to identify the etiologic, anatomic, and physiologic components of a specific cardiovascular disorder, as well as to determine overall cardiac function.

History

The medical history in a patient with a cardiac problem is usually centered on symptoms due to myocardial ischemia, dysrhythmias, and reduction in ventricular function. The majority of these individuals will consult a physician because of chest pain, dyspnea, palpitations, ankle edema, or syncope. Any or all of these symptoms may also have extra-cardiac causes. Because symptoms of heart disease may be absent at rest and appear only during stress, the medical history has unique diagnostic importance. The patient's daily activities should be assessed for their role in precipitating the symptoms and in identifying these symptoms as cardiac in origin. A purely symptom-based classification of heart disease has major limitations, however, since functional abnormalities are often more extensive than those represented by symptoms alone. In addition, the anatomic and physiologic disturbances may develop to advanced stages before symptoms appear. Examples of the manner in which the principal symptoms of heart disease may serve as a guide to diagnosis will be highlighted.

Chest pain or discomfort has numerous cardiac causes (e.g., myocardial ischemia, pericarditis, pulmonary embolism, aortic dissection) as well as noncardiac etiologies (e.g., anxiety, cholecystitis, pneumonia). The pain of myocardial ischemia, characterized by a squeezing, strangling, or burning sensation, must be differentiated from pleuritic pain, which is sharp, stabbing, intensified by inspiration, and relieved by sitting up. Among the causes of myocardial ischemia are angina pectoris and myocardial infarction. Pleuritic pain usually accompanies pericarditis and pulmonary embolism.

Dyspnea (shortness of breath)  of cardiac origin must be distinguished from dyspnea due to pulmonary disease. Cardiac dyspnea, including paroxysmal nocturnal dyspnea (breathlessness at night) and orthopnea (dyspnea precipitated by assuming the recumbent position), is characteristically related to effort until the advanced stages of heart disease when it may become present at rest. Rapid progression of an episode of respiratory distress may result in a very severe form of dyspnea, acute pulmonary edema, i.e., "asthmatic" wheezes and a pink, frothy sputum.

Palpitations describe an awareness of the heartbeat. Although the underlying disturbance usually requires electrocardiographic confirmation, occasionally the cadence of the palpitations may be ascertained at the bedside. Palpitations may often be of no consequence.

Syncope of cardiac origin may be due either to an inability of the heart to maintain adequate cardiac output for a given level of activity or to a dysrhythmia that results in sudden loss of cardiac output. Left ventricular outflow tract obstruction (e.g., aortic stenosis or hypertrophic cardiomyopathy) commonly causes effort syncope, whereas syncopal episodes due to dysrhythmias can occur either at rest or during activity.

Edema a detectable excess of fluid in the interstitial spaces, is most commonly located in the ankles and feet and is referred to as peripheral or ankle edema. When due to cardiac disease, it is usually a late sign of congestive heart failure, specifically, right heart failure.

Additional symptoms that may herald a cardiovascular problem include claudication (extertional cramping of the muscles) most often of the lower extremities, fatigue, and hemoptysis (Table 7.1).

Table 7.1. Symptoms of Cardiovascular Diseases.

Table 7.1

Symptoms of Cardiovascular Diseases.

Physical Examination

Instruments needed for the cardiovascular examination are listed in Table 7.2. The examination involves inspection, palpation, and auscultation of the heart, arteries, and veins. The cardiac examination consists of evaluation of (1) the carotid arterial pulse and auscultation for carotid bruits; (2) the jugular venous pulse and auscultation for cervical venous hums; (3) the precordial impulses and palpation for heart sounds and murmurs; and (4) auscultation of the heart. The evaluation of the peripheral arteries, the aortic pulsation, elicitation of pulsus alternans, and a search for thrombophlebitis completes the cardiovascular examination (Table 7.3).

Table 7.2. Instruments Needed for Cardiovascular Examination.

Table 7.2

Instruments Needed for Cardiovascular Examination.

Table 7.3. Most Frequently Used Examination Sequence of the Cardiovascular System.

Table 7.3

Most Frequently Used Examination Sequence of the Cardiovascular System.

Special attention should be given to the patient's general appearance, since it can reflect the state of the circulation as well as noncardiac diseases that may involve the heart. The patient's color (pale, flushed, or cyanotic), facial features, body build, and obvious pulsations should be noted. The blood pressure and heart rate and rhythm are obtained with the vital signs, but must be integrated with the findings of the cardiovascular examination to arrive at the proper diagnosis.

Examination of the Heart

Carotid Arteries

Begin the cardiovascular examination by assessing the carotid arterial pulses . They are ordinarily examined while the patient is breathing normally and reclining with the trunk of the body elevated about 15 to 30 degrees (Figure 7.1). In order to examine the carotid arteries, the sternocleidomastoid (SCM) muscle should be relaxed and the head rotated slightly toward the examiner. The examiner places the forefinger or thumb, depending on individual preference, slightly over the artery in the groove just lateral to the trachea. Care should be taken always to palpate in the lower half of the neck in order to avoid the area of the carotid bulb, lest a hypersensitive carotid sinus reflex be evoked with resultant bradycardia and hypotension. It is important that the carotid pulses be palpated using light pressure, one side at a time, since bilateral carotid compression may produce cerebral ischemia and syncope; extreme caution should be exercised in patients who have a history of syncope or transient neurologic symptoms.

Figure 7.1. Examination of the carotid arterial pulse.

Figure 7.1

Examination of the carotid arterial pulse. Place the patient in the supine position with the trunk elevated approximately 30 degrees, the head turned slightly toward the side being examined and the chin elevated. Palpate the carotid artery by gently pressing

Listen to the heart with the stethoscope in order to identify the first (S1) and second (S2) heart sounds while simultaneously palpating the carotid artery. The heart sounds are used as reference points for the cardiac examination in order to determine which events occur in systole (between S1 and S2) and which in diastole (between S2 and S1). While listening to the heart sounds, the examiner carefully and slowly applies more and more pressure to the carotid artery until the maximum pulse is felt; palpation should be continued for 5 to 8 seconds. The examiner should then slowly release the pressure on the artery while attempting to form a mental image of the pulse wave. It may be possible to detect an anacrotic notch (halt on the upstroke) or a bisferiens pulse (bifid or double peak) more easily with light pressure than with heavy pressure. In patients with evidence of carotid arterial disease, palpation of the vessels obviously should be gentle.

Divide the carotid pulse wave into three parts: (1) ascending limb or upstroke; (2) peak; and (3) descending limb. Initially concentrate on the amplitude (size) of the carotid pulse and note whether it is normal, decreased, or increased. If necessary, use your own carotid pulse as a control. Next, direct attention to analysis of the pulse contour and note if there is a single or double peak, a shudder or thrill, and the location of the peak within systole (i.e., early, mid, or late). Then concentrate on the upstroke and note whether it is normal, rapid, or slow. Finally, concentrate on the down-stroke of the pulse, which is difficult to palpate reliably. If there is a rapid fall-off, for instance, the majority of the clownstroke will be completed during systole.

The normal carotid arterial pulse wave is illustrated in Figure 7.2 together with the heart sounds. The upstroke of the carotid tracing is moderately rapid and smooth, and begins just after the initial component of the first heart sound. The summit of the carotid pulse is smooth and dome shaped, and occurs approximately in the middle of systole. The descending limb from the systolic peak is usually less steep than the ascending limb. In most normal individuals, the carotid incisura or dicrotic notch is not palpable; however, one can usually sense a change to a less steep down-slope.

Figure 7.2. These graphics represent the normal cardiac pulsations and heart sounds.

Figure 7.2

These graphics represent the normal cardiac pulsations and heart sounds. The jugular venous pulsation normally has 3 positive waves—the a, c, and v waves and 2 negative troughs—x and y troughs. The "a" wave is approximately synchronous 

There are a variety of abnormal arterial pulses including the hypokinetic pulse commonly seen with left ventricular failure; the hyper kinetic pulse commonly seen with mitral or aortic regurgitation; and the bisferiens pulse seen with aortic regurgitation or hypertrophic cardiomyopathy. During routine palpation of the carotid pulse, pay particular attention to the amplitude of the pulse following any premature beat, A diminished pulse amplitude following a premature beat is suggestive of hypertrophic cardiomyopathy.

Auscultation should be performed along the course of the carotid artery in order to detect any bruits. The location of maximum intensity of the bruit should be noted, as well as the pitch and duration of the sound. It is necessary for the patient to stop breathing during auscultation to eliminate the harsh sounds of tracheal breathing that could mask a low-pitched carotid bruit.

Figure 7.3. Auscultation of the carotid artery.

Figure 7.3

Auscultation of the carotid artery. Lightly apply the bell of the stethoscope over the course of the carotid artery, from the base of the neck to angle of the jaw, during full expiration.

Jugular Veins

The jugular venous pulse is usually examined next. It includes observation of venous wave form, assessment of the response of the venous pressure to abdominal compression, estimation of the central venous pressure (CVP), and auscultation for cervical venous hums. Venous pulsations are examined by inspection of either the external or internal jugular veins, although the latter are generally more reliable because they more directly reflect right atrial hemodynamics.

The position of the patient is extremely important for the examination of the jugular veins (Figure 7.4). Relax the neck muscles by placing a small pillow behind the neck. The head should not be rotated more than a few degrees, since rotation may tense the SCM muscle and obscure the transmission of venous pulsations. The trunk of the body should be elevated until maximal venous pulsations are noted. The degree of trunk elevation varies from subject to subject and must be established for each person. In most normal individuals, the maximum pulsation of the internal jugular vein is usually observed when the trunk is inclined to about 15 to 30 degrees. In patients with elevated venous pressure, it may be necessary to elevate the trunk more than 45 degrees to visualize the maximum venous pulsation. At times there is venous distention without visible waves and the pulsations are only seen with the patient upright at 90 degrees.

Figure 7.4. Anatomy of the blood vessels in the neck.

Figure 7.4

Anatomy of the blood vessels in the neck. Evaluation of the jugular venous pulse and the carotid artery are best accomplished with the patient supine, the neck muscles relaxed by placing a small pillow under the head and the trunk elevated until the maximal

Look for pulsations of the internal jugular vein by standing just behind the patient and looking down alongside the SCM muscle or by bending over in front of the patient and looking directly along the SCM muscles. Direct your study of the wave form to whichever internal jugular pulse is easier to see. For most patients, the right internal jugular vein is superior for accurate evaluation of the venous wave form. The internal jugular venous pulsations may be highlighted by shining a beam of light from a penlight tangentially across the skin overlying the left internal jugular vein. This technique may amplify the wave form by casting a shadow of its pulsations on the pillow or bed sheet behind the neck.

The normal jugular venous pulse consists of intermittent increases in the volume of blood in the veins caused by slowing or halting of blood flow in the right atrium. Because they are low-pressure impulses, venous pulsations are not palpable and therefore are interpreted by inspection rather than by palpation, in contrast to the carotid arterial pulse. Generally, internal and external jugular venous pulsations may be eliminated by applying gentle pressure below the point of observation. This procedure also may produce increased distention of the vein by blocking the flow of blood to the heart. The visible venous pulsations in the neck are slower and more undulating than the brisk, forceful arterial pulse waves. Respiration may produce marked changes in venous pulsations, whereas arterial pulses normally change relatively little. Under normal circumstances, inspiration decreases intrathoracic pressure and increases return of blood to the heart from the peripheral veins. The result is to reduce the mean level of venous pulsation and distention; the opposite occurs during expiration.

Abdominal pressure may also be used to distinguish venous from arterial neck pulsations. This test is best performed with the patient lying comfortably in bed at the optimal angle for observing the internal jugular venous pulsations. The patient is instructed to continue normal breathing in order to avoid performance of a Valsalva maneuver. Moderately firm pressure is then slowly applied for about 30 seconds with the palm of the hand pressing on the abdomen, usually on the right side (over the liver). Normally this maneuver produces no visible change in the arterial pulse, but a slight increase in the prominence of the jugular venous pulsations. In the presence of heart failure the jugular venous pulsations may be markedly increased. The response of jugular venous pulse to abdominal compression is known as the hepato-jugular reflux test. It is useful not only for distinguishing venous from arterial pulsations but also in unmasking occult abnormalities of circulatory function.

The normally visible jugular venous pulsations consist of two outward pulsations or positive waves ("a" and "v") and two descents or collapses or negative waves ("x" and "y") as shown in Figure 7.2. The "c" wave, a positive wave that follows the "a" wave, may be recorded, but is seldom seen at the bedside. The carotid pulse may be used to time venous pulsations, but the heart sounds generally are preferable at the bedside. The "a" wave, the larger of the two visible positive waves, begins before S1 and precedes the upstroke of the carotid pulse. The negative "x" and "y" waves occupy systole and diastole, respectively. The "v" wave occurs in late systole virtually synchronous with S2. Frequently, it is easier to visualize jugular descents because they are the largest and fastest movements.

The internal jugular veins are also used to estimate central venous pressure. The technique is similar to that for evaluation of the internal jugular venous wave form (Figure 7.5). The patient is examined at the optimum degree of trunk elevation for inspection of the venous pulse. While the patient is breathing gently or preferably at the end of a normal expiration, the highest point of visible pulsation of the internal jugular vein is determined (Figure 7.5). The CVP can then be estimated by measuring the vertical distance between the midright atrium and the top of the column of venous blood in relation to a fixed reference point, the sternal angle (of Louis). The vertical distance between the top of the column of venous blood and the level of the sternal angle is normally 2 cm. For convenience at the bedside, the sternal angle is chosen as a reference point because it has a relatively constant relationship, in all positions, to the midpoint of the right atrium (i.e., 5 cm above the mid-right atrium).

Figure 7.5. Estimation of the central venous pressure (CVP).

Figure 7.5

Estimation of the central venous pressure (CVP). Place the patient in the supine position with the head slightly elevated on a pillow to relax the sternocleidomastoid muscle. Elevate the trunk by adjusting the head of the bed so as to maximize the internal 

The normal CVP is less than or equal to 7 cm H2O (i.e., 5 + 2 cm). The most common cause of an elevated CVP is failure of the right ventricle secondary to failure of the left ventricle. Earlobe and rarely eyeball pulsations are evidence of markedly elevated venous pressure.

Central venous pressure may also be estimated by examining the veins of the dorsum of the hand. To perform this determination, the patient should be in either a sitting or lying position at a 30-degree elevation or greater, and the hand should be kept below the level of the heart long enough for the veins of the dorsum of the hand to become distended. The arm is then slowly and passively raised while the physician observes the veins. Care should be taken that the arm is not flexed excessively at either the shoulder or the elbow and that the upper arm is not constricted by-clothing. Normally, the veins will be seen to collapse when the level of the dorsum of the hand reaches the sternal angle or the level of the suprasternal notch. The vertical distance above the sternal angle at which the veins collapse should be recorded as well as the position of the patient during the test.

Auscultation at the base of the neck, just above the clavicle and lateral to the clavicular attachment of the SCM muscle, with the patient sitting, enables one to determine if a cervical venous hum is present. The cervical venous hum is a continuous whining or roaring noise throughout systole and diastole produced by the flow of blood through the internal jugular veins. It occurs more frequently on the right than on the left, but may be present bilaterally. It is loudest with the patient sitting, during inspiration, and in diastole. It may be increased by turning the head away from the side being auscultated. It is obliterated by applying light pressure directly above the point of auscultation, the Valsalva maneuver, compression of the internal jugular vein, or lying down. An arterial bruit, in contrast, is loudest in systole, unaffected by light pressure, the Valsalva maneuver, and the patient's changing position. The venous hum is a frequent finding in normal individuals, but may also be a clue to high-output states (e.g., thyrotoxicosis).

Precordial Movements and Thrills

The precordial examination, performed next, consists of inspection and palpation of the anterior chest wall. Precordial movements should be evaluated at the apex (left ventricle), lower left parasternal edge (right ventricle), upper left (pulmonary artery) and upper right (aorta) parasternal edges, and epigastric and sternoclavicular areas (Figure 7.6). It is best to examine the precordium with the patient supine because if the patient is turned on the left side, the apical region of the heart is displaced against the lateral chest wall, distorting the chest movements. Inspect the chest wall by positioning yourself on the patient's right side and looking tangentially across the fourth, fifth, and sixth intercostal spaces. Ask the patient to take a deep breath and then to exhale slowly as you look for a discrete area of apical movement. The following are the factors to be considered about any precordial movement that can be seen or felt: (1) location; (2) amplitude; (3) duration; (4) time of the impulse in the cardiac cycle; and (5) contour.

Figure 7.6. Anteroposterior view of the chest indicating the major precordial areas to be examined.

Figure 7.6

Anteroposterior view of the chest indicating the major precordial areas to be examined. Try to detect by both inspection and palpation any abnormal pulsations that the underlying cardiac chambers and great vessels may produce. Auscultation is routinely

Locate the apex impulse by placing the palm and fingers of your right hand over the left precordium in the fourth, fifth, and sixth intercostal spaces near the midclavicular line (Figure 7.7). If unable to palpate an impulse, move your hand laterally to the anterior axillary line. If still unable to locate the impulse, ask the patient to roll onto the left side and attempt to palpate the apex as just described (Figure 7.8). Always state in which patient position the apex impulse was identified because the left lateral decubitus position distorts a normal apex and makes it appear or feel unduly sustained. If still unable to locate the apex impulse, inspect the right precordium in a manner similar to that used for the left precordium. On rare occasions the impulse may be visible in the right chest, providing the initial clue to the presence of dextrocardia.

Figure 7.7. Examination of the apex impulse in the supine position.

Figure 7.7

Examination of the apex impulse in the supine position. Place the patient in the supine position elevating the trunk approximately 30–45 degrees. Position yourself on the patient's right side and place the flat part of your right hand over the 

Figure 7.8. Examination of the apex impulse with the patient in the left lateral decubitus position.

Figure 7.8

Examination of the apex impulse with the patient in the left lateral decubitus position. If the apex impulse cannot be located with the patient supine, ask the patient to roll to his left side and attempt to palpate the apex with the fingers of your right

Record the location of the apex impulse by noting its distance from either the midsternal or midclavicular line and the intercostal space in which it is felt. Also record the approximate diameter (cm) of the apex. The amplitude and duration of the apical pulsation may be more important than its location and size; therefore, state whether the impulse is of normal, increased, or diminished force and whether it occupies half or more than half of systole. If necessary, palpate your own apex impulse for comparison. In addition, if a single pulsation is palpated, determine whether its force is uniform throughout systole or whether there is a late systolic accentuation or bulge.

In a normal individual the apex impulse is a tapping, early systolic outward thrust that occurs in the fifth intercostal space in the midclavicular line. It is localized to a small area not more than 1 to 2 cm (dime-sized) in diameter. The outward thrust is brief, lasting about one-half of systole, and is of minimal amplitude. Normally, diastolic pulsations are not palpable. Left ventricular hypertrophy, for instance, results in exaggeration of the normal left ventricular thrust both in amplitude and duration. It is nondisplaced, sustained (occupying more than one-half of systole), and 2 to3 cm (quarter-sized). Left ventricular dilation, in contrast, results in downward and lateral displacement of the apex below the fifth interspace.

The lower left parasternal region of the chest is best evaluated by looking at the chest from the side and by placing the heel of the hand over or just to the left of the sternum (Figure 7.9). If a left parasternal impulse or lift is appreciated, determine if the impulse is sustained throughout systole, vigorous or slight, and begins with or after the onset of the apex impulse. Determine its onset by placing your right hand over the apex impulse and your left palm over the left parasternal impulse. The right ventricle is really an anterior structure, and when enlarged, it may lift the anterior portion of the chest including the sternum. In normal individuals the parasternal region usually retracts (moves inward) during ejection and is not palpable.

Figure 7.9. Palpation of the left parasternal impulse.

Figure 7.9

Palpation of the left parasternal impulse. Place the patient in the supine position with the trunk elevated 30–45 degrees. Place the heel of your right hand, with the hand slightly cocked up, together with downward pressure (arrow) of your left 

Right ventricular hypertrophy and/or dilation results in a sustained systolic lift of the lower parasternal region of the chest. This lift is present in patients with high right ventricular pressure (pulmonary arterial hypertension or pulmonic stenosis) or volume overload (tricuspid regurgitation or atrial septal defect), but is infrequently seen in chronic lung disease if right-sided heart failure is not present. The pulsations of the main pulmonary artery are also often visible and palpable, especially in patients with parasternal pulsations.

Patients with acute myocardial infarction or with angina pectoris may have an outward paradoxical precordial movement that often can be seen or palpated at the apex, the anterior precordium, or in an "ectopic" area. The impulse is usually sustained throughout systole, frequently with a second systolic bulge, and is often difficult to distinguish from that of left ventricular hypertrophy by palpation alone if the bulge occurs in the region of the apex. In order to time systolic and diastolic cardiac movements accurately, it is essential to inspect and palpate the precordium while actually listening to the heart sounds.

The early diastolic and late diastolic (presystolic) precordial movements are the visible and palpable counterparts of the third (S3) and fourth (S4) heart sounds, respectively. They may be felt at the cardiac apex with the patient in the left lateral decubitus position. Careful inspection of the precordium with the naked eye or observing the motions of a wooden stick taped over the cardiac apex best demonstrates any precordial impulses that correlate with audible S3 and S4 sounds. The right-sided S4, seen and felt at the lower left sternal edge, occurs slightly earlier in diastole than the left-sided S4. It often correlates with a very prominent jugular "a" wave and a sustained outward movement (lift) in the lower left parasternal area.

Heart murmurs that can be palpated are referred to as thrills . The diastolic rumble of mitral stenosis and the systolic murmur of mitral regurgitation may be palpated at the cardiac apex. The harsh systolic murmur of aortic stenosis may cut across the palm of the hand toward the right side of the neck, while the thrill of pulmonic stenosis cuts across the palm of the hand to the left side of the neck. The thrill due to ventricular septal defect is usually located in the third and fourth intercostal spaces near the left sternal border. Heart sounds may also be palpable. For instance, the loud S1 of mitral stenosis may be palpated at the apex.

Heart Sounds and Murmurs

Auscultation  of the heart is performed after examining the jugular venous pulse, carotid pulse, and precordial movements because acoustic events can best be interpreted after the other components of the cardiac examination have been evaluated. Auscultation of the heart should, therefore, not be performed as an isolated event because heart sounds, murmurs and pulse tracings must all be integrated in order to understand normal and altered cardiac physiology and anatomy. Attempt to study two and occasionally three aspects of the cardiac examination simultaneously. Then pictorially display the heart sounds and correlate them, by use of a diagram, with any murmurs heard, the jugular venous wave form, the carotid pulse, and the apex impulse to best understand the patient's cardiac problem (Figure 7.2).

Proper use of a quality stethoscope is essential for an accurate auscultatory examination. The important parts of the stethoscope are the ear pieces, the tubing, and the chest pieces. The ear pieces must fit the ear canal snugly without going to an uncomfortable depth. The tubing should be as short as possible, but long enough to be comfortable and convenient for the user; 10 to 12 inches is an ideal length. The chest pieces, the bell, and the diaphragm should be combined into one housing. A diaphragm pressed firmly on the chest filters out low-frequency vibrations and amplifies high-frequency vibrations. It is routinely used to hear the first and second heart sounds, systolic murmurs, and the diastolic murmur of aortic regurgitation. The bell should be applied to the chest with very light pressure, barely creating an air seal, so low-frequency sounds and murmurs are appreciated. It is used to hear the third and fourth heart sounds and the diastolic murmur (rumble) of mitral stenosis. A trumpet-shaped bell is much better than a shallow one.

Auscultation usually begins at the aortic area (upper right sternal edge). The stethoscope is then moved sequentially to the pulmonary (upper left sternal edge), tricuspid (lower left sternal edge), and mitral (apex) areas. It is helpful to palpate the carotid pulse or apex impulse simultaneously to time the acoustic events as systolic or diastolic. A finger on the carotid artery will sense the systolic thrust that is virtually coincident with S1. Use of a more distant artery for this purpose leads to error because of the time it takes the pulse wave to reach the periphery.

The heart sounds are usually the first auscultatory events identified. They are brief, discrete, auditory vibrations of varying intensity (loudness) and frequency (pitch). The first heart sound  identifies the onset of systole. It is normally split into mitral (M1) and tricuspid (T1) components that are temporally related to closure of the respective atrioventricular (A-V) valves. The second heart sound  identifies the end of systole and the onset of diastole. It is normally split into aortic (A2) and pulmonic (P2) components that are temporally related to closure of the respective semilunar valves. The second sound is louder than S1 in the aortic listening area; S1 is louder at the apex.

In the aortic area, listen for the first and second heart sounds, the aortic ejection sound, and the murmurs of aortic stenosis and aortic regurgitation with the stethoscope diaphragm. Then move the diaphragm to the second and third left intercostal spaces in order to appreciate the aortic and pulmonic components of S2, the pulmonary ejection sound, and the murmurs of pulmonic stenosis and pulmonary and aortic regurgitation. Continue to the fourth and fifth intercostal spaces along the left sternal border and listen for the murmurs of tricuspid regurgitation and tricuspid stenosis and the murmur produced by ventricular septal defect. Right ventricular S3 and S4 sounds (gallops) can best be heard in this area with the stethoscope bell. The diaphragm should be moved to the third and fourth intercostal spaces to the right of the sternum to judge whether a murmur of aortic regurgitation is louder along the left or right sternal border.

The diaphragm should then be positioned at the cardiac apex where S1 and S2 should again be studied. An aortic ejection sound, a mid to late systolic click, the opening snap of mitral stenosis, the systolic murmur of mitral regurgitation, and occasionally the high-pitched murmur of aortic regurgitation are also heard in this area with the diaphragm.

The bell of the stethoscope should then be positioned over the apical impulse with the patient turned to the left lateral position to listen for low-frequency diastolic sounds and murmurs.

Have the patient exercise (5 to 10 sit-ups), or cough if myocardial infarction is suspected, to "bring out" the murmur of mitral stenosis and the S3 and S4 gallop sounds. The third and fourth heart sounds  are low pitched and may be audible as well as palpable. They are best heard at the cardiac apex when generated from the left ventricle and at the lower left sternal edge when generated from the right ventricle.

The technique known as inching may help determine whether extra cardiac sounds are systolic or diastolic. The examiner moves the stethoscope inch by inch from the aortic area to the apex while focusing attention on S2. Determine whether the extra sound precedes (systolic) or follows (diastolic) S2. The acoustic events can best be appreciated by a careful review of the hemodynamic curves of the cardiac cycle.

Several additional areas should be ausculted (Figure 7.10), including (1) the inferior edge of the sternum and epigastrium, especially in patients with chronic obstructive lung disease, in whom heart sounds and murmurs are difficult to hear in the more conventional listening areas; (2) the first and second intercostal spaces below the left midclavicular area for the continuous (systolic and diastolic) murmur of patent ductus arteriosus; (3) the interscapular area of the back for the systolic murmur of coarctation of the aorta; (4) over the lung areas; (5) over the head, eyes, liver, sacrum, abdomen, as well as over tumors or bony overgrowths; and (6) over all scars to identify the continuous murmur of a peripheral A-V Fistula.

Figure 7.10. Anteroposterior view of the chest showing some additional areas shaded for auscultation.

Figure 7.10

Anteroposterior view of the chest showing some additional areas shaded for auscultation. The first and second left intercostal spaces at the mid clavicular line (MCL). The fifth intercostal space to the right of the sternum. The epigastric area just below 

Murmurs  are prolonged series of auditory vibrations that should be characterized according to (1) timing in the cardiac cycle (systolic, diastolic, continuous); (2) intensity (loudness); (3) frequency (pitch); (4) configuration (shape); (5) duration (long or short); (6) radiation (to other auscultatory areas); and (7) variation, if any, with respiration or other maneuvers (position change, Valsalva, etc.).

The classic way to time murmurs and heart sounds is with a finger on the carotid arterial pulse. The heart sound virtually coinciding with the carotid upstroke (pulse) is Sl and the heart sound just after the carotid pulse is S2. The intensity of a murmur is graded I to VI with I faint, III loud, IV palpable, and VI loud enough to be heard with the stethoscope just off the chest. The frequency of a murmur varies from low (rumbling) to mid (harsh) to high (blowing). The configuration is described as crescendo (increases progressively in intensity), decrescendo (decreases progressively in intensity), crescendo-decrescendo (diamond-shaped), or plateau (even). Of all the parameters by which a murmur is analyzed, its time of occurrence in the cardiac cycle and the precordial area of maximal intensity are easiest to learn and thus are most reliable.

The influence of respiration on the second sound is extremely important. The examiner will wish to note respiratory variation both during quiet breathing and at times during exaggerated breathing. The interval between the two audible components of S2 normally increases on inspiration and virtually disappears on expiration. The Valsalva maneuver may be used to exaggerate the effects of respiration. Variation in the cardiac cycle, as with atrial fibrillation or heart block, may also exert profound influences on S2 and on S1. When S2 is split, determine the relative loudness of each component (A2 and P2).

Examination of the Peripheral Arteries

The evaluation of the peripheral arterial pulses is an integral part of the cardiovascular examination. Palpation of the peripheral arteries may yield the following information: (1) frequency and regularity of the pulsations; (2) condition and patency of the peripheral arteries; and (3) characteristics of the arterial pulse wave. All of the following pulses should be examined thoroughly by palpation: temporals, brachials, radials, aortic, femorals, popliteals, posterior tibials, and the dorsalis pedii (Figure 7.11). When applicable, pulses should be examined bilaterally and graded as to quality of the impulse on a scale of 0 to 3 with 2 being normal, 0 absent, 1 decreased, and 3 increased. In addition, hair distribution should be checked on the toes and feet.

Figure 7.11. Location of the arteries that are routinely examined.

Figure 7.11

Location of the arteries that are routinely examined. The temporalis artery is located in front of the ear where it is very superficial and readily palpated. Pulses in the upper extremities can be identified at the brachial artery, just medial to the 

To examine the brachial artery, palpate along the course of the artery just medial to the biceps tendon and lateral to the medial epicondyle of the humerus. To examine the radial artery, palpate along the radial–volar aspect of the subject's forearm at the wrist.

The abdominal aorta is an upper abdominal, retroperitoneal structure that is best palpated by applying firm pressure with the flattened fingers of both hands to indent the epigastrium toward the vertebral column. The normal aortic pulse should be less than 6 cm in diameter. Auscultation should be performed over the aorta and along both iliac arteries into the lower abdominal quadrants to detect bruits.

The femoral artery is best palpated with the fingertips of the examining hand pressed firmly into the groin. Auscultation should be performed in this area as well.

The popliteal artery passes vertically through the deep portion of the popliteal space. It may be difficult or impossible to palpate in obese or very muscular individuals. The pulse is detected by pressing deeply into the popliteal space with the supporting fingertips.

The posterior tibial artery lies just posterior to the medial malleolus and is felt most readily by curling the fingers of the examining hand around the ankle.

The dorsalis pedis artery usually lies near the center of the long axis of the foot. Place the fingertips transversely across the dorsum of the forefoot near the ankle. This pulse often requires some searching and is congenitally absent in approximately 10% of normal individuals.

Information should be obtained by simultaneously palpating the radial and femoral arteries and noting the relative time of onset of the pulse at the two locations. Normally, the pulse wave arrives in these locations virtually simultaneously. In a patient with coarctation of the aorta, both onset and peak of the weak femoral pulses are delayed. Compared to the carotid pulse, the pulse wave in these more peripheral vessels arrives later and is characterized by a steeper initial wave that reaches a higher systolic peak, whereas the diastolic and the mean arterial pressures are lower.

Palpating peripheral arteries is the most important single maneuver in establishing whether or not chronic occlusive arterial disease is present. One may obtain an impression of thickness and hardness of the walls of the brachial, radial, and dorsalis pedis arteries by "rolling" the compressed vessel against the underlying tissue. Auscultation of the peripheral arteries is also very important. A systolic bruit over the abdominal aorta, iliac, or femoral arteries when the patient has been supine for more than 10 minutes usually signifies intimal disease, but not necessarily significant occlusion.

Pulsus alternans refers to a characteristic pulse pattern in which the beats occur at regular intervals, but with an alternation of the height of the pulse. This valuable sign should be searched for by palpating the femoral artery; less often, the radial artery may disclose that alternate pulses vary in amplitude. Have the patient hold his or her breath while you feel the pulse to make certain that the alternation of pulse volume is independent of respiration. The pulse rhythm should be regular, since alternation of the strength of cardiac beats commonly results from bigeminal rhythm. Rarely, pulsus alternans may feel irregular because of a slight delay in sensing the weaker beat.

When pulsus alternans is prominent, it may be confirmed and quantified by use of a sphygmomanometer. As the pressure is lowered in the sphygmomanometer, the examiner should routinely observe whether every Korotkoff sound is heard with equal intensity. As the cuff pressure is lowered further, the frequency of the sounds may suddenly double as the weaker beats also become audible. In most instances, the weak pulses are only slightly weaker than the strong beats. On rare occasions, a weak beat may be so small that no palpable pulse is detected at the periphery, so-called total alternans. Pulsus alternans is produced by an alternation in left ventricular contractile force associated with an alternation of left ventricular fiber length; it is a very valuable sign of left ventricular dysfunction. In most instances, it is found in association with a third heart sound.

Examination for Thrombophlebitis

The presence or absence of thrombophlebitis is an integral part of the cardiovascular database. Thrombophlebitis refers to venous inflammation with secondary thrombosis of the involved vein. It is most commonly noted in the deep veins of the leg and superficial veins of the arm. Superficial thrombophlebitis can be seen and felt, making the diagnosis easy in most cases. Most deep vein thromboses are clinically silent and cannot be detected by routine examination. When thrombophlebitis is confined to small venous channels beneath the subcutaneous tissue or in the pelvis, the lesions are neither visible nor palpable. Mild pain in the calf may be the only symptom, and tenderness may be the only sign.

The examiner should also compare the skin temperature in the two calves, since active phlebitis may create local warmth. Calf circumference should also be determined in all suspected cases. Pain is a prominent feature of muscular, synovial, or vascular leg diseases, and various tests have been used to identify the specific etiology. Homans's test (dorsiflexion sign) is used to detect irritability of the posterior leg muscles through which inflamed or thrombosed veins course. The Lowenberg cuff test is another helpful clinical maneuver for detection of calf vein thrombosis.

A summary of only the most common conditions associated with an abnormality on the cardiovascular examination is shown inTable 7.4.

Table 7.4. Common Conditions Associated with an Abnormality on the Cardiovascular Examination.

Table 7.4

Common Conditions Associated with an Abnormality on the Cardiovascular Examination.

Conclusion

An orderly process of history taking and physical examination together with selective application of modern laboratory technology should enable the clinician to arrive at an accurate diagnosis, estimate the degree of severity, formulate a logical plan of treatment,and better understand the pathophysiologic abnormalities in the patient with a cardiovascular problem.