General Cardiovascular Exam



General Cardiovascular Exam


Timothy J. O’Connor

William H. Fennell

John W. McEvoy



INTRODUCTION

Physical examination of the cardiovascular system remains central to the contemporary practice of clinical medicine, despite technologic advances. The physical examination is an immediately available, rapid, repeatable, and noninvasive tool to not only identify the presence, nature, and severity of cardiovascular disease but also assess response of medical therapy and guide future therapy. The diagnostic value of the physical examination is user dependent. It relies on a thorough and accurate recording of the patient’s presenting complaint and prior medical history, demands a thorough understanding of the concepts on which the physical examination is based, and requires the adoption of a standardized and systematic approach to the examination.




FUNDAMENTALS AND CLINICAL APPLICATION OF THE PHYSICAL EXAMINATION

Before focusing on the examination of the heart itself, pertinent “extracardiac” aspects of the physical examination that are important in the comprehensive assessment of the cardiovascular patient are described. These include the general appearance of the patient; assessment of the skin, extremities, head, and neck; as well as examination of the chest wall and the abdomen.


The Extracardiac Examination


General Appearance

The starting point of the cardiovascular examination begins with an assessment of the general appearance of the patient. An overall appraisal of the patient’s status can aid quick identification of the acutely unwell patient and provide vital clues to underlying cardiac conditions. Is the patient in obvious pain? What is their posture, demeanor, level of consciousness, and breathing pattern? Is the patient cyanotic, pale, or diaphoretic (sweaty)? In addition, a number of syndromes with important cardiovascular associations may be evident from the patient’s appearance, such as Marfan syndrome, Turner syndrome, and Down syndrome (Table 2.1).

With respect to posture, patients with acute pericarditis often find relief of their chest pain with sitting forward and with short shallow breathing. In the acute heart failure patient, lying supine may cause significant distress and indicate pulmonary edema. Sitting forward with hands supported on knees and breathing through pursed lips (tripod position) may direct suspicion toward a pulmonary etiology of dyspnea rather than a cardiac one.

The patient’s breathing pattern should be routinely assessed. Inspection can identify abnormal patterns of breathing such as Kussmaul breathing or Cheyne-Stokes breathing. Kussmaul breathing is rapid, deep, and labored breathing associated with underlying metabolic acidosis. Cheyne-Stokes breathing is a pattern of crescendo-decrescendo breathing with periods of apnea, which is well recognized in congestive heart failure and is associated with increased mortality.1

Early identification of the acutely unwell patient is critically important. Besides general inspection, assessment of vital signs, such as respiratory rate, peripheral oxygen saturation, heart rate, blood pressure, and temperature, can help dictate the pace of assessment and any therapeutic actions that may be required. For example, a speedy bedside hemodynamic assessment of perfusion (warm vs cold) and congestion (wet vs dry) (Figure 2.1) helps guide initial management in acute heart failure. Determination of the patient’s level of consciousness contributes to assessment of cerebral and systemic perfusion.

Inspection of the patient’s nutritional status and degree of frailty can also help direct their cardiovascular care. The
presence of cachexia may indicate an underlying systemic disorder or malignancy but may also be present in advanced chronic heart failure. Frailty has been shown to be a strong risk factor for adverse outcomes in cardiovascular disease, and quantitative frailty assessments are increasingly used in advanced heart failure as well as in the assessment of heart valve disease and determining a patient’s suitability for intervention. Examples of such frailty assessments include both individual measures (handgrip strength, 5-meter gait speed) and multi-item frailty scales such as the Fried scale.2









Skin

A detailed examination of the skin may draw attention toward abnormalities that are manifestations of underlying cardiac disease or other disorders (inherited or systemic) with important cardiovascular sequelae.

Bluish discoloration of the skin and/or mucous membranes can indicate cyanosis. Approximately 2 g/dL or more of deoxyhemoglobin in subpapillary capillaries is required for cyanosis to manifest. Central cyanosis causes bluish discoloration of both the skin and mucous membranes (including the tongue) and is typically seen in disorders with right-to-left shunting of blood such as in congenital heart disease with pulmonary hypertension. Peripheral cyanosis, seen in disorders such as severe heart failure, spares the mucous membranes and is indicative of diminished blood flow and increased oxygen extraction in the peripheral circulation. Blue-gray cutaneous discoloration of sun-exposed skin infrequently occurs in patients on long-term amiodarone therapy.







Tanned or bronzed hyperpigmentation of the skin on the face, dorsal hands, and extensor forearms may indicate hemochromatosis, a disorder of iron storage that can result in diabetes and dilated cardiomyopathy. A plum or red discoloration of the cheeks with a butterfly pattern (i.e., malar flush) is a known manifestation of mitral stenosis. Systemic disorders such as systemic lupus erythematosus (SLE) can also present with malar erythema and provide clues to a systemic cause of cardiac disease (eg, Libman-Sacks endocarditis in SLE).

Disorders of lipid metabolism resulting from genetic disease or secondary etiologies can present with yellow cutaneous lesions (termed xanthomas) at various body sites. Xanthomas can be seen on the eyelids (where they are termed xanthelasmas), neck, palms, chest, or along extensor tendons of the extremities. Tendonous xanthomata typically indicate type IIa hyperlipoproteinemia (otherwise known as familial hypercholesterolemia or FH). Xanthelasmas involve soft yellow plaques on the upper and lower eyelids. Discrete yellow macules/papules along the creases of the palms (palmar xanthomata) are associated with type III familial hyperlipoproteinemia (defined by the Fredrickson-Levy classification). Tuberous and tuberoeruptive xanthomata are painless yellow nodules that are not attached to tendons and can be located on the buttocks, hands, and knees and are associated with types IIa and III familial hyperlipoproteinemias. Eruptive xanthomata are crops of small erythematous yellow papules that suddenly appear on extensor surfaces and are linked with types I and V hyperlipoproteinemias. Cholesterol embolization syndrome resulting from disruption of atheromatous plaques of the aorta and other arteries can manifest with ulceration, purpura, painful nodules, or livedo reticularis (particularly in the lower extremities).

Nontender red or hemorrhagic macules of the palms and soles (Janeway lesions) and painful, raised, erythematous nodules involving the pulp of the fingers and toes (Osler nodes) are well-known manifestations of infective endocarditis. Telangiectasia are seen in patients with systemic disorders such as scleroderma (associated with pulmonary hypertension, right heart failure, and nonischemic cardiomyopathy) or SLE (associated with pericarditis and Libman-Sacks endocarditis, among other cardiac sequelae), whereas hereditary telangiectasia of the lips, tongue, and mucous membranes is a finding of Osler-Weber-Rendu syndrome (associated with pulmonary arteriovenous malformations causing right-to-left intracardiac shunting).

Extensive freckle-like brown spots (lentigines) on the face, neck, and trunk can be cutaneous manifestations of rare inherited cardiovascular syndromes such as Carney syndrome (associated with cardiac myxomas) and LEOPARD syndrome (Lentigines, Electrocardiographic conduction abnormalities, Ocular hypertelorism, Pulmonary stenosis, Abnormal genitalia, Retardation of growth, and Deafness). Pseudoxanthoma elasticum (associated with premature coronary artery disease) is a genetic disorder of connective tissue resulting in leathery, inelastic “plucked chicken” skin appearance of the flexural areas of the neck, axilla, and inguinal regions.


Head and Neck

A stepwise review of the face should begin with an examination of the eyes. For example, yellow discoloration of the sclera (scleral icterus) may be seen in severe heart failure with hepatic congestion, whereas patients with osteogenesis imperfecta have blue sclera and may potentially manifest mitral regurgitation or aortic regurgitation. As highlighted earlier, disorders of lipid metabolism can result in yellow deposits around the eyelids (xanthelasmas) or a gray circle around the outer rim of the pupil (arcus senilis). Bilateral periorbital ecchymosis is a characteristic sign of amyloidosis, a condition with major cardiac manifestations (most notably heart failure with preserved ejection fraction).

A thorough examination of the dentition is important in ruling out active infection, which has implications for the likelihood of infectious endocarditis. The oral cavity may also expose a high-arched palate (Marfan syndrome), palatal petechiae (infective endocarditis), or macroglossia (amyloidosis, most typically of the light chain [AL] subtype). A bifid uvula is a recognized sign of Loeys-Dietz syndrome (which is a similar condition to Marfan syndrome in that it is also associated with aortopathy and aneurysmal changes of the aorta). As noted earlier malar rash involving the facial cheeks and nasal bridge with sparing of the nasolabial folds is indicative of SLE, whereas
the mitral facies of rheumatic mitral valve stenosis produces flushed plethoric cheeks with pink-purplish patches.

Dysmorphic facial features are a common sign of many inherited syndromes with associated congenital heart defects. Micrognathia, ocular hypertelorism, a short philtrum, and low-set ears can point toward underlying disorders, such as Noonan, Edwards, Turner, or Down syndrome. A webbed neck is a classical sign of Turner syndrome (Table 2.1). Individuals with myotonic dystrophy may have a long, thin face with drooping eyelids and a swanlike neck.

Although the examination of jugular venous pressure (JVP) is anatomically part of the head and neck examination, it is discussed in detail later in the “Cardiac examination” section.


Extremities

Inspection of the hands can provide valuable clues to underlying cardiovascular disorders, and the initial examination should focus on abnormalities of the digits and nail beds. Longitudinal red-brown hemorrhages under the nail suggest splinter hemorrhages, which have a wide etiology including infective endocarditis and systemic disorders, such as cutaneous vasculitis. Visible pulsation of the nail bed capillaries can suggest Quincke sign, a sign of severe aortic regurgitation. Abnormalities in the shape of the nail, such as koilonychia (spooning of the nail), are associated with a variety of conditions, such as iron deficiency anemia, hemochromatosis, and coronary disease. Skeletal abnormalities of the hands, such as arachnodactyly, are seen in Marfan syndrome. The absence of a thumb or a finger-sized thumb are manifestations seen in Holt-Oram syndrome. Clubbing is an increase in the soft tissue of the distal phalanx, which has a large differential but includes underlying cardiovascular etiologies like infective endocarditis, left atrial myxoma, or congenital heart disease with right-to-left shunting.

In the lower extremities, bilateral pitting edema is seen in many volume overload states, including heart failure, particularly if accompanied by a raised JVP. A clear identification of the extent of edema is important to guide and evaluate medical therapy, remembering that bedbound patients tend to manifest dependent edema in their sacrum and buttocks rather than their legs. Bilateral lower limb edema without a raised JVP makes the diagnosis of heart failure less likely and is seen in disorders such as chronic venous insufficiency; it is supported by signs such as varicose veins, venous ulceration, hyperpigmentation, stasis dermatitis, and lipodermatosclerosis. Unilateral swelling can suggest a localized venous thrombosis, lymphatic obstruction, or previous vein graft harvesting in the company of a medial longitudinal scar. Cold extremities with muscle wasting and loss of body hair may suggest underlying arterial disease. Cold extremities more generally may also reflect poor cardiac output if accompanied by other signs of poor organ perfusion. It is important to examine distal pulsations including the dorsal pedis, posterior tibial, and popliteal pulses. Differential clubbing and cyanosis of the toes (ie, without similar abnormalities noted in the fingers) can be a sign of patent ductus arteriosus with Eisenmenger syndrome.


Chest and Abdomen

Deformities of the chest wall can be acquired or congenital, and their presence can be associated with underlying cardiovascular pathology. Emphysema can cause a barrel-shaped chest and is associated with cor pulmonale and right heart failure. A pigeon chest (pectus carinatum) manifests with an outward bowing of the sternum, whereas a funnel chest (pectus excavatum) creates a localized depression of the sternum, and both are associated with connective tissue disorders. Severe kyphosis is a recognized sign of ankylosing spondylitis and may raise suspicion of coexisting aortic regurgitation.

Careful examination of the entire chest wall should be carried out to identify any scars. A central sternotomy scar for coronary artery bypass or open cardiac valve surgery may be obvious; however, be sure to inspect for a “J” sternotomy (mini-sternotomy) or right mini-thoracotomy, seen in minimally invasive valve surgery. The scar of an indwelling cardiac implantable electronic device (CIED) can be located on either side of the upper chest wall but typically on the left. The presence of a CIED can be associated with rare complications, such as unilateral arm swelling or cutaneous venous congestion of the anterior chest wall, because of superior vena cava or subclavian vein obstruction.

Hepatomegaly can be present in right heart failure, and prominent or palpable systolic hepatic pulsations can indicate severe tricuspid regurgitation (TR). Ascites has a broad spectrum of etiologies but can be the result of chronic right heart failure (most notable in cases of constrictive pericarditis or restrictive cardiomyopathy). Splenomegaly is a well-recognized sign of subacute infective endocarditis. Careful and gentle palpation and auscultation of the abdomen should be done to rule out an abdominal aortic aneurysm or aortic or renal bruits.


Cardiac Examination


Jugular Venous Pressure

Assessment of the JVP remains a fundamental element of the cardiovascular examination and provides clinically useful information that allows estimation of the patient’s volume status, ventricular filling pressures, and response to medical therapy. This is because a distended internal jugular vein can discriminate between a high and low central venous pressure (CVP). Consequently, an increased JVP can be used to infer the presence of an increased pulmonary capillary wedge pressure (PCWP) among patients with advanced left heart failure.3

Evaluation of the JVP is difficult to master. The initial starting point begins with correct positioning of the patient. Full exposure of the neck and chest is essential to allow the physician to observe the venous pulse. The patient should be lying down at 45° to the horizontal with the head turned slightly to the left and chin extended. It is important not to overrotate the neck because doing so will cause contraction of the sternocleidomastoid muscle with resulting compression of the external and internal jugular veins and obstruction of view. Next, identify the internal jugular vein that lies lateral to the carotid artery and descends deep to the sternocleidomastoid
muscle (the external jugular vein descends anteriorly to the sternocleidomastoid muscle, traveling in a posterior and inferior direction). Differentiating the JVP pulsation from that of the carotid pulse requires observation of the pulse appearance, response to inspiration, and palpation (Table 2.2).








The next step is to determine the mean height of the JVP, which is an indicator of right atrial pressure (or right heart filling pressure). The units of measurement for JVP are in centimeters of water. The JVP is measured as the vertical distance in centimeters from the top of the venous pulsation down to the anterior angle formed by the junction of the manubrium and the body of the sternum (the so-called angle of Louis) (Figure 2.2A,B). A height of more than 3 cm (ie, anything visible above the clavicle) at 45° is considered an abnormal JVP and infers elevated right heart filling pressures. If an approximate estimation of CVP is also desired, the measured height of the JVP is then added to the distance from the sternal angle to the mid-right atrium. In the supine position at 45° to the horizontal, this distance is estimated at 5 cm. Thus, an appropriately measured JVP of 3 cm above the sternal angle can be estimated to reflect a CVP of 8 cm of water (note that cm of water can be converted to approximate millimeters of mercury for comparison with catheterization values [1.36 cm of water = 1 mm Hg]). A caveat is that this 5-cm value is an approximation of the distance between the sternal angle and the right atrium and can vary with such patient factors as increased age, smoking status, height, obesity, and increased anteroposterior chest wall diameter. Thus, it is our view that the primary utility in measuring the height of the JVP is in identifying a raised right heart filling pressure, rather than quantifying a specific value for CVP.

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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on General Cardiovascular Exam
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