Approach to Cardiac Disease Diagnosis-2

Approach to Cardiac Disease Diagnosis


Michael H. Crawford, MD

Physical Findings



A. PHYSICAL EXAMINATION

The physical examination is less important than the history in patients with ischemic heart disease, but it is of critical value in patients with congenital and valvular heart disease. In the latter two categories, the physician can often make specific anatomic and etiologic diagnoses based on the physical examination. Certain abnormal murmurs and heart sounds are specific for structural abnormalities of the heart. The physical examination is also important for confirming the diagnosis and establishing the severity of heart failure, and it is the only way to diagnose systemic hypertension because this diagnosis is based on elevated blood pressure recordings.

1. Blood pressure—Proper measurement of the systemic arterial pressure by cuff sphygmomanometry is one of the keystones of the cardiovascular physical examination. We recommend that the brachial artery be palpated and the diaphragm of the stethoscope be placed over it, rather than merely sticking the stethoscope in the antecubital fossa. Current methodologic standards dictate that the onset and disappearance of the Korotkoff sounds define the systolic and diastolic pressures, respectively. Although this is the best approach in most cases, there are exceptions. For example, in patients in whom the diastolic pressure drops to near zero, the point of muffling of the sounds is usually recorded as the diastolic pressure. Because the diagnosis of systemic hypertension involves repeated measures under the same conditions, the operator should record the arm used and the position of the patient to allow reproducible measurements to be made on serial visits.
If the blood pressure is to be taken a second time, the patient should be in another position, such as standing, to determine any orthostatic changes in blood pressure. Orthostatic changes are a very important physical finding, especially in patients complaining of transient central nervous system symptoms, weakness, or unstable gait. The technique involves having the patient assume the upright position for at least 90 s before taking the pressure to be sure that the maximum orthostatic effect is measured. Although measuring the pressure in other extremities may be of value in certain vascular diseases, it provides little information in a routine examination beyond palpating pulses in all the extremities. Keep in mind, in general, that the pulse pressure (the difference between systolic and diastolic blood pressures) is a crude measure of left ventricular stroke volume. A widened pulse pressure suggests that the stroke volume is large; a narrowed pressure, that the stroke volume is small.


2. Peripheral pulses—When examining the peripheral pulses, the physician is really conducting three examinations. The first is an examination of the cardiac rate and rhythm, the second is an assessment of the characteristics of the pulse as a reflection of cardiac activity, and the third is an assessment of the adequacy of the arterial conduit being examined. The pulse rate and rhythm are usually determined in a convenient peripheral artery, such as the radial. If a pulse is irregular, it is better to auscultate the heart; some cardiac contractions during rhythm disturbances do not generate a stroke volume sufficient to cause a palpable peripheral pulse. In many ways, the heart rate reflects the health of the circulatory system. A rapid pulse suggests increased catecholamine levels, which may be due to cardiac disease, such as heart failure; a slow pulse represents an excess of vagal tone, which may be due to disease or athletic training.
To assess the characteristics of the cardiac contraction through the pulse, it is usually best to select an artery close to the heart, such as the carotid. Bounding high-amplitude carotid pulses suggest an increase in stroke volume and should be accompanied by a wide pulse pressure on the blood pressure measurement. A weak carotid pulse suggests a reduced stroke volume. Usually the strength of the pulse is graded on a scale of 1 to 4, where 2 is a normal pulse amplitude, 3 or 4 is a hyperdynamic pulse, and 1 is a weak pulse. A low-amplitude, slow-rising pulse, which may be associated with a palpable vibration (thrill), suggests aortic stenosis. A bifid pulse (beating twice in systole) can be a sign of hypertrophic obstructive cardiomyopathy, severe aortic regurgitation, or the combination of moderately severe aortic stenosis and regurgitation. A dicrotic pulse (an exaggerated, early, diastolic wave) is found in severe heart failure. Pulsus alternans (alternate strong and weak pulses) is also a sign of severe heart failure. When evaluating the adequacy of the arterial conduits, all palpable pulses can be assessed and graded on a scale of 0 to 4, where 4 is a fully normal conduit, and anything below that is reduced, including 0—which indicates an absent pulse. The major


pulses routinely palpated on physical examination are the radial, brachial, carotid, femoral, dorsalis pedis, and posterior tibial. In special situations, the abdominal aorta and the ulnar, subclavian, popliteal, axillary, temporal, and intercostal arteries are palpated. In assessing the abdominal aorta, it is important to make note of the width of the aorta because an increase suggests an abdominal aortic aneurysm. It is particularly important to palpate the abdominal aorta in older individuals because abdominal aortic aneurysms are more prevalent in those older than 70. An audible bruit is a clue to significantly obstructed large arteries. During a routine examination, bruits are sought with the bell of the stethoscope placed over the carotids, abdominal aorta, and femorals at the groin. Other arteries may be auscultated under special circumstances, such as suspected temporal arteritis or vertebrobasilar insufficiency.

3. Jugular venous pulse—Assessment of the jugular venous pulse can provide information about the central venous pressure and right-heart function. Examination of the right internal jugular vein is ideal for assessing central venous pressure because it is attached directly to the superior vena cava without intervening valves. The patient is positioned into the semiupright posture that permits visualization of the top of the right internal jugular venous blood column. The height of this column of blood, vertically from the sternal angle, is added to 5 cm of blood (the presumed distance to the center of the right atrium from the sternal angle) to obtain an estimate of central venous pressure in centimeters of blood. This can be converted to millimeters of mercury (mm Hg) with the formula:

mm Hg = cm blood × 0.736.

Examining the characteristics of the right internal jugular pulse is valuable for assessing right-heart function and rhythm disturbances. The normal jugular venous pulse has two distinct waves: a and v; the former coincides with atrial contraction and the latter with late ventricular systole. An absent a wave and an irregular pulse suggest atrial fibrillation. A large and early v wave suggests tricuspid regurgitation. The dips after the a and v waves are the x and y descents; the former coincide with atrial relaxation and the latter with early ventricular filling. In tricuspid stenosis the y descent is prolonged. Other applications of the jugular pulse examination are discussed in the chapters dealing with specific disorders.

4. Lungs—Evaluation of the lungs is an important part of the physical examination: Diseases of the lung can affect the heart, just as diseases of the heart can affect the lungs. The major finding of importance is rales at the pulmonary bases, indicating alveolar fluid collection. Although this is a significant finding in patients with congestive heart failure, it is not always possible to distinguish rales caused by heart failure from those caused by pulmonary disease. The presence of pleural fluid, although useful in the diagnosis of heart failure, can be due to other causes. Heart failure most commonly causes a right pleural effusion; it can cause effusions on both sides but is least likely to cause isolated left pleural effusion. The specific constellation of dullness at the left base with bronchial breath sounds suggests an increase in heart size from pericardial effusion (Ewart's sign) or another cause of cardiac enlargement; it is thought to be due to compression by the heart of a left lower lobe bronchus.

When right-heart failure develops or venous return is restricted from entering the heart, venous pressure in the abdomen increases, leading to hepatosplenomegaly and eventually ascites. None of these physical findings is specific for heart disease; they do, however, help establish the diagnosis. Heart failure also leads to generalized fluid retention, usually manifested as lower extremity edema or, in severe heart failure, anasarca.

Akhtar M: AHA Examination of the heart (Part 5)—The electrocardiogram. American Heart Association, 1990.
Cain M et al: ACC Expert consensus document: Signal-averaged electrocardiography. J Am Coll Cardiol 1996;27:238–249.
Cheitlin M, Albert JS, Armstrong WF et al: ACC/AHA guidelines for the clinical application of echocardiography: Executive summary—A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on Clinical Application of Echocardiography). J Am Coll Cardiol 1997;29:862–879.
Crawford MH, Berstein SJ, Deedwania PC et al: ACC/AHA guidelines for ambulatory electrocardiography: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee to Revise the Guidelines for Ambulatory Electrocardiography). J Am Coll Cardiol 1999;34:912–948.
Gibbons RJ, Balady GJ, Beasley JW et al: ACC/AHA guidelines for exercise testing: Executive summary: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on Exercise Testing). Circulation 1997;96:345–354.
Grundy SM, Pasternak R, Greenland P et al: ACC/AHA scientific statement: Assessment for cardiovascular risk by use of multiple-risk-factor assessment equations; A statement for healthcare professionals from the American Heart Association and the American College of Cardiology. J Am Coll Cardiol 1999;34:1348–1359.
O'Rourke R, Brundage BH, Froelicher VF et al: ACC/AHA expert consensus document: American College of Cardiology/American Heart Association expert consensus document on electron-beam computed tomography for the diagnosis and prognosis of coronary artery disease. J Am Coll Cardiol 2000;36:326–340.
Ritchie JL, Bateman TM, Bonow RO et al: ACC/AHA task force report: Guidelines for clinical use of cardiac radionuclide imaging; report of the American college of Cardiology/American Heart Association task force on assessment of diagnostic and therapeutic cardiovascular procedures (Committee on Radionuclide Imaging), developed in collaboration with the American Society of Nuclear Cardiology. J Am Coll Cardiol 1995;25:521–547.
Scanlon PJ, Faxon DP, Audet AM et al: ACC/AHA practice guidelines: ACC/AHA guidelines for coronary angiography: A report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on Coronary Angiography); Developed in collaboration with the Society of Cardiac Angiography and Interventions. J Am Coll Cardiol 1999;33:1756–1824.
Schlant RC, Adolph RJ, DiMarco JP et al: ACC/AHA guidelines for electrocardiography: A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Electrocardiography). J Am Coll Cardiol 1992;19:473–481.
Zipes DP, DiMarco JP, Gillette PC et al: ACC/AHA Task Force Report: Guidelines for clinical intracardiac electrophysiological and catheter ablation procedures; a report on the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Clinical Intracardiac Electrophysiologic and Catheter Ablation Procedures), developed in collaboration with the North American Society of Pacing and Electrophysiology. J Am Coll Cardiol 1995;26:555–573.