19-Inspection and Palpation of the Precordium PDF

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19 – Inspection and Palpation of the precordium The precordium is the front of the chest wall over the heart. Inspection 

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The general appearance should be evaluated. The patient may appear tired because of a chronic low cardiac output. The respiratory rate may be rapid in cases of pulmonary venous congestion. Look for any scars or masses, which may be indicative of previous operations. Signs of cyanosis. Central cyanosis, often associated with clubbing of the fingers and toes, indicates right-to-left cardiac or extracardiac shunting or inadequate oxygenation of blood by the lungs. Cyanosis (peripheral) in the distal extremities, cool skin, and increased sweating result from vasoconstriction in patients with severe heart failure. Pulsations (apex beat), also examine the valve areas for pulsations. Coldness of extremities, which could be a sign of reduced cardiac output. Vasoconstriction of the cutaneous bed, allows the body to circulate blood to the vital organs, to compensate for the failing heart ability to pump enough blood.

When inspecting the precordium it is important to look for scars suggesting cardiac surgery. A midline sternotomy suggests a coronary artery bypass graft (CABG) or valve replacement. A left submammary thoracotomy scar suggests mitral valvotomy. It is also important to note if the patient has an implantable pacemaker or cardiovertor/defibrillator. There will be a scar just below the left (occasionally right) clavicle and a bulge in the skin may be visible. Signs of chest deformity should be noted as this can affect examination of the heart. For example, pectus carinatum (‘pigeon chest’) or pectus excavatum (funnel chest) can displace the heart, affecting palpation and auscultation of the precordium. The patient may have a barrel-shaped chest with an increased anteroposterior diameter, a straight-back syndrome kyphoscoliosis, or ankylosing spondylitis. Each may produce or be associated with cardiac abnormalities. Asymmetry of the thorax due to convex bulging of the precordium suggests the presence of heart disease since childhood. Exaggerated movements of the cardiac apex often can be detected from this observation point. In patients with an abnormally prominent apical impulse and in some thin, normal individuals, the apical impulse or apex beat can be seen. The presystolic apical motion associated with the atrial contribution to ventricular filling (S4) sometimes may be visualized, as may the diastolic waveform due to rapid ventricular filling (S3). When precordial pulsations are exaggerated, they become visible as well as palpable. In general, however, outward movements are best discerned by palpation, whereas inward movements usually are seen more easily than felt. Cyanosis Cyanosis refers to a bluish color of the skin and mucous membranes resulting from an increased quantity of reduced hemoglobin, or of hemoglobin derivatives, in the small blood vessels of those areas. It is usually most marked in the lips, nail beds, ears, and malar eminences. In general, cyanosis becomes apparent when the concentration of reduced hemoglobin in capillary blood exceeds 40 g/L (4 g/dL). Cyanosis may be subdivided into central and peripheral types. In the central type, the SaO2 (oxygen saturation) is reduced or an abnormal hemoglobin derivative is present, and the mucous membranes

and skin are both affected. Peripheral cyanosis is due to a slowing of blood flow and abnormally great extraction of O2 from normally saturated arterial blood. It results from vasoconstriction and diminished peripheral blood flow, such as occurs in cold exposure, shock, congestive failure, and peripheral vascular disease. Often in these conditions, the mucous membranes of the oral cavity or those beneath the tongue may be spared. Clinical differentiation between central and peripheral cyanosis may not always be simple, and in conditions such as cardiogenic shock with pulmonary edema there may be a mixture of both types. Clubbing The selective bullous enlargement of the distal segments of the fingers and toes due to proliferation of connective tissue, particularly on the dorsal surface, is termed clubbing; there is also increased sponginess of the soft tissue at the base of the nail. Clubbing may be hereditary, idiopathic, or acquired and associated with a variety of disorders, including cyanotic congenital heart disease, infective endocarditis, and a variety of pulmonary conditions (among them primary and metastatic lung cancer, bronchiectasis, lung abscess, cystic fibrosis, and mesothelioma), as well as with some gastrointestinal diseases (including inflammatory bowel disease and hepatic cirrhosis). The presence or absence of clubbing of the digits should be ascertained. The combination of cyanosis and clubbing is frequent in patients with congenital heart disease and right-to-left shunting and is seen occasionally in patients with pulmonary diseases such as lung abscess or pulmonary arteriovenous fistulae. In contrast, peripheral cyanosis or acutely developing central cyanosis is not associated with clubbed digits. Edema Edema is defined as a clinically apparent increase in the interstitial fluid volume, which may expand by several litres before the abnormality is evident. There are 4 main causes of edema: 1. 2. 3. 4.

Increased filtration through capillaries due to increased pressure Decreased capillary colloidal osmotic pressure, so fluid is not drawn back into vessels Increased permeability Obstruction to lymph flow

The retention of salt and water by the kidneys alters the above-mentioned parameters, leading to edema. The effect of gravity ensures that edema is most prominent around the ankles, or over the sacrum in bedridden patients. In advanced heart failure edema may involve legs, genitalia and trunk. Transudation into the peritoneal cavity (ascites), pleural cavity and pericardial spaces may also occur. Subcutaneous edema that pits on digital pressure is a cardinal sign of congestive heart failure. Congestive Heart Failure. In this disorder the impaired systolic emptying of the ventricle(s) and/or the impairment of ventricular relaxation promotes an accumulation of blood in the venous circulation at the expense of the effective arterial volume. In mild heart failure, a small addition of total blood volume may repair the deficit of arterial volume and establish a new steady state. Through the operation of Starling’s law of the heart, an increase in ventricular diastolic volume promotes a more forceful contraction and may thereby restore the

cardiac output. However, if the cardiac disorder is more severe, fluid retention continues, and the addition in blood volume accumulates in the venous circulation. With reduction in cardiac output, a decrease in baroreflex-mediated inhibition of the vasomotor center activates renal vasoconstrictor nerves and the RAAS system, causing Na+ and H2O retention. Incomplete ventricular emptying (systolic heart failure) and/or inadequate ventricular relaxation (diastolic heart failure) both lead to an elevation of ventricular diastolic pressure. If the impairment of cardiac function primarily involves the right ventricle, pressures in the systemic veins and capillaries rise, augmenting the transudation of fluid into the interstitial space and enhancing the likelihood of peripheral edema. The elevated systemic venous pressure is transmitted to the thoracic duct with consequent reduction of lymph drainage, further increasing the accumulation of edema. If the impairment of cardiac function (incomplete ventricular emptying and/or inadequate relaxation) involves the left ventricle primarily, then pulmonary venous and capillary pressures rise. Pulmonary artery pressure rises and this, in turn, interferes with the emptying of the right ventricle, leading to an elevation of right ventricular diastolic and of central and systemic venous pressures, thereby enhancing the likelihood of the formation of peripheral edema. The elevation of pulmonary capillary pressure may cause pulmonary edema, which impairs gas exchange. The resultant hypoxemia may impair cardiac function further, sometimes causing a vicious circle. Palpation The location, amplitude, duration, and direction of the cardiac impulse usually can be best appreciated with the fingertips. The normal left ventricular apex impulse is located at or medial to the left midclavicular line in the fourth or fifth intercostal space. When palpating the apex beat, you should note the following:  Location: Normal is in the left 5th intercostal space at the midclavicular line  Amplitude: Normal is described as "a tap"  Duration: Normal is 2/3 the length of systole. Determine this by simultaneously palpating the radial pulse  Size: Normal is approximately 2.5cm, or the size of a quarter If you are unable to palpate the apex beat with the patient supine, try palpating the apex beat with the patient in the left lateral decubitus position Heaves - Palpate using the palm or heel of your hand along the left sternal border for signs of heaves. The presence of heaves is not normal. If the hand is lifted with each ventricular contraction then this is referred to as a left parasternal heave, usually due to right ventricular hypertrophy or volume overload. Left ventricular hypertrophy results in exaggeration of the amplitude, duration, and often size of the normal left ventricular thrust. The impulse may be displaced laterally and downward into the sixth or seventh intercostal space, particularly in patients with a left ventricular volume load such as occurs in cases of aortic regurgitation or dilated cardiomyopathy. Right ventricular hypertrophy often results in a sustained systolic lift at the lower left parasternal area, which starts in early systole and is synchronous with the left ventricular apical impulse. The apex beat will be shifted more to the left.

Abnormal precordial pulsations occur during systole in patients with left ventricular dys-synergy due to ischemic heart disease or due to diffuse myocardial disease from some other cause. They are most commonly felt in the left mid-precordium one or two interspaces above the left ventricular apex. A left parasternal lift is frequently present in patients with severe mitral regurgitation and is due to anterior displacement of the right ventricle by an enlarged, expanding left atrium. Pulmonary artery pulsation is often visible and palpable in the second left intercostal space. This pulsation usually denotes pulmonary hypertension or increased pulmonary blood flow. When the palm of the hand is placed over the precordium, the thrill of aortic stenosis crosses the palm toward the right side of the neck, while the thrill of pulmonic stenosis radiates more often to the left side of the neck. The thrill due to a ventricular septal defect is usually located in the third or fourth intercostal spaces near the left sternal border. Thrills – a palpable murmur. Palpate in each of the valve areas for thrills. The presence of a thrill is not normal. Thrills are palpable, low frequency vibrations associated with heart murmurs. The location of a thrill often helps identify its origin. Thrills are palpated most easily with the fingertips or with firm pressure, using either the palm of the hand or the proximal metacarpals. Sometimes thrills are felt better during a held end-expiration with moderate pressure applied from the right hand on top of the left hand, which is placed on the chest. Occasionally, palpable murmurs are more readily detected with the right palm placed over the anterior chest and the left hand supporting the posterior thorax with equal force. Anti-clockwise rotation of the left ventricle along its longitudinal axis occurs as the cardiac apex moves anteriorly and makes contact with the chest wall in early systole. The maximal outward movement occurs coincidental with or just after aortic valve opening. After rapid early ejection, the left ventricle moves away from the chest wall, and the apex retracts during latter systole and returns to baseline well before the second heart sound. The outward apex movement in early systole normally is palpable, but the later systolic inward movement is only visible. Palpable movements of the apex in diastole result from LV filling. The early diastolic outward movement due to rapid ventricular filling (F wave), which corresponds to the normal S3 sound, is occasionally palpable in normal children and young adults. Later diastolic filling due to left atrial contraction (a wave) is not normally palpable. Precordial motion is modified by age, chest wall thickness, lung disease, and pleural or pericardial effusion....