184 J AM cou. CARDIOl 1983:1:184-98 The Physiologic Mechanisms of Cardiac and Vascular Physical Signs JOSEPH K. PERLOFF, MD, FACC Los Angeles. California Examination of the heart and circulation includes five relate cardiac and vascular physicalsigns to their mech• items: 1) the patient's physical appearance, 2) the ar• anisms, focusing on each of the five sources. It draws terial pulse, 3) the jugular venous pulse and peripheral liberally on early accounts, emphasizing that modern veins, 4) the movements of the heart-observation, pal• investigative techniques often serve chiefly to verify hy• pation and percussion of the precordium, and 5) aus• potheses posed in the past. cultation. This report deals with specific examples that I shall begin by acknowledging three debts. The first is to chain of events, has provided answers to many of the re• the late Paul Wood and his staff at the Institute of Car• maining questions (2,3). diology , London, where my under standing of the physio• Let us now tum to specific examples that relate cardiac logic meaning of cardiac and vascular physical signs began. and vascular physical signs to their mechanisms, focusin g The second debt is to the Fulbright Foundation and the on each of the five sources mentioned. In so doing, certain Institute for International Education for making my year in illustrative examples will be selected. No attempt will be England possible. The third debt is to the National Institutes made to be comprehensive. of Health for providing my first research grant , which sup• ported the continuation of these studies in the United States. That grant was approved exactl y 25 years ago , the year The Physical Appearance during which the first issue of the official journal of the Cyanosis and clubbing of the digits serve as useful points American College of Cardiology was published. of departure. Differential cyanosis and clubbing exist when Examination of the heart and circulation focuses on five these signs are present in the feet but not in the hands, and items: I) the patient's physical appearance, 2) the arterial reflect a right to left shunt through a patent ductus arteriosus pulse , 3) the jugular venous pulse and peripheral veins, 4) with intact ventricular septum (4). The physiologic mech• the movements of the heart-observation, palpation and anism requires that pulmonary vascular resistance exceed percu ssion of the precordium, and 5) auscultation (I). The systemic resistance so that unoxygenated blood from the pul• chain of events that has culminated in our present under• monary trunk flows through the ductus into the aorta just standing of the physiologic mechanisms of the physical signs distal to the left subclavian artery (Fig. I); the toes are began with bedside observations by a host of brilliant cli• cyanosed and clubbed selectively. In another form of dif• nicians; their descriptions of specific signs stand today as ferential cyanosis-designated by convention " reversed models of clarity. Then followed the graphic record that differential cyano sis" - the opposite is true. The toes are allowed more refined analysis of the arterial pulse, the jug• less cyanotic and clubbed than the fingers (4). This dis• ular venous pulse , precordial movement and heart sounds tinctive physical appearance also has a relatively precise and murmurs. The next major step , the cardiac catheter. pathoph ysiologic basis-the aorta is right ventricular in or• permitted hemodynamic, angiographic and intracardiac igin (cyanotic hands), while the pulmonary trunk is either phonocardiographic observations not previousl y possible . right ventricular or biventricular in origin, arising just above Echocard iograph y. the most recent advance in this exciting a ventricular septal defect so that oxygenated blood from the left ventricle enters the pulmonary trunk . In the presence of high pulmonary vascular resistance. this oxygenated blood From the Divisions of Cardiology, Departments of Medicine and Pe• flows through a patent ductu s arteriosus into the descending diatrics, UCLA Center for the Health Sciences. Los Angeles, California. Address for reprints: Joseph K. Perloff, MD. UCLA Center for the aorta and to the lower limbs (relatively acyanotic feet) (4). Health Sciences, Room 47-123. Los Angeles. California 90024. Thus. sophisticated diagnoses are based on nothing more © 1983 by the American College of Cardiol ogy 0735-1097/83/010184-15$03.00 MECHANISMS OF CARDIOVASCULAR PHYSICAL SIGNS J AM Call CARDIOl 185 1983;1:184-98 Righ'·'....." .hun' Desc Ao a b than comparison of the physical appearances of upper and Figure 1. (a) Schematic illustration of the mechanism of differential cy• lower limbs. anosis and clubbing. Unoxygenated blood from the pulmonary trunk (PT) flows through the patent ductus arteriosus (PDA) and enters the aorta (Ao) distal to the left subclavian artery (LSA). (b) A catheter takes this course in a 13 year old girl with reversed flow through a large ductus. Desc Ao The Arterial Pulse = descending aorta. Analysis of waveform. This is one of the most im• portant aspects of the examination of the arterial pulse. In (I) drew a careful distinction between pulsus bigeminus and severe valvular aortic stenosis (Fig. 2), the arterial pulse is pulsus altemans, the latter a term that Traube introduced. diminished (small) with a slow ascending limb (parvus), He wrote, "The following case...demonstrates a variation but in addition, the peak is illdefined and late (tardus) (5). of the pulsus bigerninus: I designated it the name of 'pulsus Mackenzie (6) understood the physiologic mechanism, writ• altemans'. .It involves a succession of high and low ing, "When there is marked narrowing of the aortic orifice, pulses, in such a manner that a low pulse regularly the full effect of the ventricular systole upon the arterial follows a high pulse...." Traube's report included a pho• column is not at once developed, as the aortic stenosis offers tograph of typical beat to beat alternans recorded with Mar• an increased resistance. Hence, the impact of the pulse wave ey's sphygmograph applied to the radial artery. The mech• on the finger is not sudden, but feels to push against the anism of pulsus bigeminus is clear enough (simple fixed finger in a somewhat leisurely fashion. The tracing in such coupling as in digitalis toxicity). Pulsus alternans is one a case represents a slanting of the stroke with an interruption reflection of depressed left ventricular function, but the pre• near the top-an anacrotic-pulse tracing." cise mechanism of the beat to beat alternation in rate of rise Characteristics of arterial pulse. A strong arterial pulse and peak pressure remains elusive. occurs either with or without increased pulse pressure, the Differential pulsations. With regard to differential pul• latter epitomized by the visible Corrigan's pulse of chronic sations, coarctation of the aorta epitomizes the relation be• free aortic regurgitation (7). An increasedarterialpulse (strong, tween simple physical signs and their anatomic and phys• hyperkinetic) with normal pulse pressure is a feature of iologic mechanisms (4). Important variations in the anatomic chronic severe mitral regurgitation, for example (small water• location of the coarctation can be inferred from bedside hammer pulse) because the left ventricle ejects at a high analysis of the arterial pulse. Equal and brisk brachial and velocity while the diastolic pressure in the aortic root re• carotid pulses with absent or diminished femoral pulses mains normal (8). Similarly, high velocity left ventricular place the coarctation distal to the left subclavian artery. ejection accounts for the brisk arterial pulse with normal When right and left brachial arterial pulses are compared, pulse pressure in hypertrophic obstructive cardiomyopathy. an absent or relatively small left brachial pulse means that Pulsus bigeminus and alternans. Ludwig Traube (1872) the coarctation compromises the orifice of the left subclavian 186 J AM cou, CARDIOl PERlOFF 1983:1:184--98 P QRS Figure 2. (a) Apexeardiogram showing mid-dia• stolic and presystolic distension (arrows) of the left ventricle in a patient with valvular aortic ste• nosis and heart failure. (b) Left ventricular (LV) pressure pulse with identical configuration (ar• rows ). The brachial artery pulse (BA) shows the typical slow rate of rise and sustained peak of severe aortic stenosis. a artery . Absence or diminution of the right brachial pulse stantly finds clinical evidence of the ready occurrence of implies anomalous origin ofthe right subclavian artery distal tricuspid incompetence in the study of the venous pulse." to the coarctation. In supravalvular aortic stenosis , differ• A tall V wave with a rapid Y descent implies that the ential pulsations take the form of an increase in pulse pres• tricuspid orifice is unobstructed . Conversely, a tall V wave sure and rate of rise of right brachial and carotid pulses. with an inappropriately slow, gentle Y descent is a feature The zone of supravalvular stenosis directs a high velocity of obstruction at the tricuspid orifice, typically rheumatic jet into the innominate artery, disproportionately increasing tricuspid stenosis with atrial fibrillation (10). Despite a tall the systolic pressure in the right carotid and subclavian V crest , the Y descent is slow because the stenotic tricuspid arteries (4,5). In addition, the Coanda effect (affinity of a orifice puts an effective break on the rate of right ventricular jet stream to adhere to a wall) carries the high velocity jet filling in the presence of a high right atrial pressure . into the orifice of the innominate artery (4). Constrictive pericarditis. The jugular venous pulse in constrictive pericarditis is distinctive, and its mechanism is clear (13). The A and V waves are high and equal yet The Jugular Venous Pulse inconspicious because the marked elevation of mean right Giant A waves. In 1867, Potain not only accurately atrial pressure puts the crests above the angle of the jaw described the normal waveform of the internal jugular vein, (Fig.