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American Heart Association~, Fighting Heart Disease and Stroke Inspection and Palpation of Venous and Arterial Pulses Examination of the Heart Part 2 Examination of the Heart Inspection and Palpation of Venous and Arterial Pulses Prepared on behalf of the Council on Clinical Cardiology of the American Heart Association Michael H. Crawford, MD Robert S. Flinn Professor of Medicine Chief, Division of Cardiology University of New Mexico School of Medicine Albuquerque, New Mexico Based on a text prepared by Noble O. Fowler, MD, in 1978 Part 2 Contents Examination of the Heart A Series of Booklets Part 1 The Clinical History Mark E. Silverman, MD Part 2 Inspection and Palpation of Venous and Arterial Pulses Michael H. Crawford, MD Part 3 Examination of the Precordium: Inspection and Palpation Robert C. Schlant, MD, and J. Willis Hurst, MD Part 4 Auscultation of the Heart James A. Shaver, MD, James J. Leonard, MD, and Donald F. Leon, MD Part 5 The Electrocardiogram Masood Akhtar, MD Available from your local American Heart Association ©1972, 1978, 1990 American Heart Association 1 Cervical Veins 1 Anatomy 3 Physiology 4 Examination 4 Patient Position 5 Lighting 6 Timing Separating Venous and Arterial Pulsations 6 8 Pathologic Findings 8 Increased Pressure 10 Prominent a Waves 10 Prominent v Waves 12 Cannon a Waves 13 Constrictive Pericarditis 14 Hepatojugular Reflux Test 15 Arterial Pulses Anatomy 15 Physiology 15 16 Examination 17 Pathologic Findings Differences in Peripheral Pulses 17 19 Hyperkinetic Pulse 20 Pulsus Bisferiens Hypokinetic Pulse 21 21 Pulsus Parvus et Tardus 22 Dicrotic Pulse 22 Pulsus Alternans 24 Pulsus Paradoxus Arrhythmias 26 27 Special Tests 27 Allen’s Test 27 Valsalva’s Maneuver Suggested Reading 29 Cervical Veins Anatomy As seen in Figure 1, the internal jugular veins arise from the transverse sinuses in the posterior compartment and descend from the jugular foramina at the base of the skull. They course down the sides of the neck, lateral to the internal carotid artery in the superior part of the neck, then anterior to the common carotid artery at the base of the neck, where they join the subclavian veins to form the innominate veins. The left internal jugular vein is usually smaller than the right and contains a pair of valves in the lower part near the junction with the left innominate vein. The right and left innominate veins form the superior vena cava, which is connected to the right atrium. The internal jugular veins lie behind the sternocleidomastoid muscles. A triangle is formed at the base of these muscles by each muscle splitting just before attachment to the clavicle. These triangles bounded by the two heads of the sternocleidomastoid muscles and the clavicles are called the internal jugular triangles. In acute care medicine, they are important as a site for internal jugular cannulation. The external jugular veins are formed below the ears by the confluence of superficial veins from the scalp and proceed superficially and laterally along the neck, joining the subclavian veins at the internal jugular triangles. The external jugular veins have two pairs of valves, one at the entrance to the subclavian veins and one in the midportion, approximately 4 cm above the clavicle. Physiology Caroti~ Internal Jugular Sternocleido mastoid Muscle External Jugular The height of the column of blood in the right internal jugular vein reflects right atrial pressure since there are no valves or other obstructions from this vein down to the right atrium. The left internal jugular and two external jugular veins are less reliable for estimating right atrial pressure because of the presence of valves and the fact that the left innominate vein must cross the mediastinum and may be relatively obstructed by the great vessels and other mediastinal structures. Inspiration augments flow through the right heart into the lungs, which normally results in a decrease in mean pressure in the right atrium and the right internal jugular vein. Pressure rises again during expiration. Recordings of right atrial pressure reveal several waveforms (Figure 2). First is the a wave, generated by atrial contraction during the latter part of diastole, followed by the x descent, which represents atrial relaxation. The x descent is interrupted by ascent of the v wave, generated by continued filling of the right atrium during ventricular systole while the tricuspid valve is closed. The v wave is terminated by onset of the tricuspid valve opening, which permits blood to flow passively from the right atrium to the right ventricle in early diastole. The v wave is followed by the y descent as right atrial pressure decreases during mid-diastole. Occasionally, a c wave is evident on the x descent, caused in the right atrium by upward displacement of the tricuspid valve early in systole. In recordings over the right internal jugular vein in the neck, the c wave may also be due to transmission of the upstroke of the underlying carotid arterial pulse. A Subclavian Vein ! Figure 1. Anatomy of cervical veins, From Ewy GA: Evaluation of the neck veins. Hosp Pract 1987;22:72-75,79-80. Reproduced with permission. Figure 2. Internal jugular venous waveforms in relation to first (S1) and second (S2) heart sounds. From Ewy GA: Evaluation of the neck veins. Hosp Pract 1987;22:72-75,79-80. Reproduced with permission. 2 3 Examination Lighting Patient Position Examination of the character of the waves in the neck veins is often facilitated by proper lighting in the examining room (Figure 4). The best technique is to direct tangential light across the neck to highlight lowamplitude venous pulsations. In normal individuals, the most prominent characteristic of the internal jugular venous pulse may be the x descent, which is accentuated during inspiration and becomes more shallow during expiration. In older individuals and patients with heart disease, tl’ie a wave may be the most prominent pulsation. The v wave is usually the most difficult to observe unless pathologic conditions exist (see below). Since right atrial pressure is often very low, optimal positioning of the patient to visualize the column of venous blood above the level of the clavicle is critical. The examiner must position the patient’s upper thorax so that the column of blood in the internal jugular vein is visible in the neck. In general, in positioning the patient, the lower the pressure in the venous system, the more supine the patient’s position should be; the higher the pressure, the more upright the patient’s position should be. This is best accomplished by using an examining table that breaks in the middle, allowing the entire thorax to be raised and lowered. Raising and lowering the head alone is usually not sufficient. The overall height o~f the pulsating column is an indicator of mean right atrial pressure, which can be estimated based on a simple anatomic fact (Figure 3). In most individuals, the center of the right atrium is approximately 5 cm from the attachment of the second rib to the sternomanubrial junction (sternal angle of Louis). This relation is maintained in every position between supine and sitting upright. Thus, the vertical height of the column of blood in the neck can be estimated from the sternal angle, to which 5 cm is added to obtain an estimate of mean right atrial pressure in centimeters of blood. This amount can then be converted to millimeters of mercury by multiplying by 0.736. Normal values are less than 8 cm of blood or less than 6 mm Hg. Obviously, this estimation may be erroneous in patients with deformed chest walls or malpositioning of the heart. Figure 4. Proper positioning and lighting for examining cervical venous pulses. Note that light soume is tangential to neck veins being examined and that examining table breaks at patient’s hips so neck is not flexed. Photo courtesy of Noble O. Fowler, MD. Figure 3. Estimating right atrial pressure with column of blood in right internal jugular vein (see text for details). From O’Rourke RA: Physical examination of the arteries and veins (including blood pressure determination), in Hurst JW (ed): The Heart, ed 6. New York, McGraw-Hill Book Co, 1985, pp 138-151. Reproduced with permission. 4 5 Timing Timing the various waves may be difficult, especially in patients with rapid heart rates. The best way to determine correct timing of cervical venous pulsations is to palpate the carotid pulse on the opposite side of the neck. The a wave occurs just before the carotid pulse and the v wave just after it. Alternatively, the physician can auscultate the heart and note that the a wave occurs just before the first heart sound and the v wave just after the second heart sound. Finally, the apical precordial impulse can be observed and its timing substituted for that of the carotid artery. Separating Venous and Arterial Pulsations It is occasionally difficult to distinguish between venous pulsations and those of the underlying internal or common carotid artery. This can be accomplished in several ways. First, the carotid upstroke is usually one dominant wave, whereas the venous pulse should have two waves. Venous pulsations are also more lateral to carotid pulsations, especially in the superior part of the neck. Perhaps the best way to distinguish pulsations is to apply light pressure at the base of the neck, which results in cessation of venous pulsations but does not influence the higher pressure of the carotid artery pulsations (Figure 5). Figure 5. Light pressure at base of neck, shown here with a tongue blade, is useful for identifying external jugular veins and obliterating internal jugular vein pulsations to separate them from carotid pulsations. Photo courtesy of Noble O. Fowler, MD. 6 7 Pathologic Findings Increased Pressure Several cardiac diseases cause increased right atrial pressure. If neck pulsations are not seen in the patient in the supine position, the trunk must be progressively elevated to the full upright position until venous pulsations are observed. If the jugular venous pressure is very high (greater than 15 cm of blood), rhythmic movement of the earlobes may be noted because of transmission of pulsations to the confluence of venous drainage in this area. Prominent carotid pulsations usually do not cause movement of the earlobe because the carotid artery is more medial in the upper part of the neck. The importance of locating the jugular venous pulse cannot be overemphasized. In the patient with edema and ascites, the presence or absence of elevated jugular venous pressure is critical in differential diagnosis of cardiac versus hepatic disease. Occasionally with very high jugular Figure 6. Left panel shows distention of left external and left anterior jugular veins without venous distention of right veins. At right, normal right external jugular vein is shown by applying pressure near its termination, confirming that previous invisibility was related to normal venous pressure on right. Patient’s head and trunk are elevated 45° from horizontal position. Venous pressure was 14 mm Hg in left antecubital vein and 6 mm Hg in right antecubital vein. Left innominate vein was compressed by dissecting aneurysm, which was responsible for elevation in venous pressure limited to left upper extremity and left side of head and neck. Photo courtesy of Noble O. Fowler, MD. 8 Figure 7. Collateral venous pattern in patient with superior vena cava obstruction as demonstrated by venography. Photo courtesy of Noble O. Fowler, MD. 9 venous pressure, venous pulsations will not be noticed even in the full upright position. In this case, the external jugular veins are usually distended, suggesting very high venous pressure. The absence of venous pulsations even in the supine position suggests low central venous pressure. Unilateral cervical venous engorgement sometimes occurs because of localized obstructions in the venous drainage system. An example of this is seen in Figure 6, where compression in the mediastinum by an enlarged aorta led to cervical venous engorgement. Obstruction of the superior vena cava not only results in bilateral high venous pressure but usually causes formation of collateral venous channels through which venous blood flow from the upper body is diverted to the unobstructed lower body venous channels and the right atrium via the inferior vena cava. These channels often occur in subcutaneous areas over the upper thorax as shown in Figure 7. They also may result in venous stars, or small skin veins arranged in a radial pattern from a central source. Venous stars can be distinguished from cutaneous arterial angiomata (spiders) by compressing the central vessel and quickly releasing it. If blood flow returns from the periphery inward toward the central vessel, it is a venous star; the reverse is true of spider angiomata. V ¯ I I | X i I Y I -0.2 see. JUGULAR VENOUS PULSE TRICUSPID STENOSIS Figure 8. Jugular venous pulse recording in patient with tricuspid stenosis. Electrocardiogram Prominent a Waves Any condition that accentuates right atrial contraction or elevates right atrial pressure can result in a large a wave. Pulmonary hypertension is a common cause of large a waves because of high right-sided pressures and vigorous atrial contraction observed in this condition. For example, in mitral valve disease, pulmonary thromboembolism, and car pulmonale, the a wave may become the predominant wave of the venous pulse. In tricuspid valve stenosis, or atresia, the a wave may become very large because of the accentuated atrial contraction in the presence of obstruction to atrioventricular flow. In tricuspid stenosis, the y descent is gradual and prolonged, reflecting the diminished rate of atrioventricular flow through the narrowed tricuspid valve (Figure 8). Prominent v Waves cardiogram s., s, s, s_, r: ;" ~ ,,- ,." b - Jugular Venous Pu I se ISOLATED TRICUSPID INSUFFICIENCY Figure 9. Jugular venous pulse in severe tricuspid insufficiency. Pulse is almost entirely composed of large regurgitant or c-v wave, thus superficially resembling carotid arterial pulse. $1, first heart sound; S2, second heart sound. Large v waves may be seen in concert with large a waves when right atrial pressure is elevated by any cause. Large v waves exceeding the height of the a waves are usually caused by tricuspid regurgitation. In this condition, the tricuspid valve is incompetent and allows blood to regurgitate retrogradely into the right atrium during ventricular systole. The more severe the tricuspid regurgitation in general, the higher and the earlier the v wave. In wide-open tricuspid valve incompetence, the right atrial pressure wave may resemble the right ventricular pressure wave leading to one large dominant wave in the neck coinciding with the carotid pulse and the apical impulse (Figure 9). 10 11 Cannon a Waves The presence of various rhythm disorders may lead to the regular or irregular occurrence of abnormal cervical venous waveforms. An example is the cannon a wave, which occurs when there is a right atrial contraction during ventricular systole, while the tricuspid valve is closed. In this situation, blood does not enter the right ventricle during atrial contraction and regurgitates up the jugular veins, causing a large a wave. Irregular cannon a waves are seen during complete heart block when there is dissociation between atrial and ventricular contraction (Figure 10). Regular cannon a waves can be observed in junctional tachycardia when there is Jugular Venous Electrocardio gram P ORS T ORS T CANNON "~l" WAVES IN COMPLETE ATRIOVENTRICULAR BLOCK Figure 10. Irregular cannon a waves in patient with complete heart block. retrograde activation of the atria from the junctional focus, causing atrial contraction to occur simultaneously with ventricular systole in every cardiac cycle (Figure 11). Constrictive Pericarditis A thickened and rigid pericardium restricts cardiac filling so that right atrial and internal jugular venous pressures are elevated. Elevated atrial pressure results in more rapid filling, but the limitation of ventricular filling caused by the noncompliant pericardium abruptly terminates filling. Thus, the large pressure gradient to filling and abrupt termination of filling during both the early and later phases of diastole result in prominent x and y descents. The overall pattern is that of a jerky, saw-tooth waveform created by the heightened a and v waves and more accentuated x and y descents (Figure 12). In addition, venous pressure does not respond normally to respiration since right heart blood flow to the lungs can no longer be effectively augmented by inspiration due to the pericardial constriction. The jugular venous pulse pressure does not decrease during inspiration and may actually increase. Increased blood flow into the thorax caused by negative intrathoracic pressure produced by inspiration may not be accommodated by the constricted right ventricle; thus, right atrial pressure rises inappropriately during inspiration. This inspiratory increase in venous pressure is termed Kussmaul’s sign. It is not specific for constrictive pericarditis and can occur in other conditions such as severe right ventricular failure or right ventricular myocardial infarction. Jugular Venous Pulse Y IIIIII Y Y Y IIiII!!IIIII I<--- I sec.-->l CONSTRICTIVE PERICARDITIS WITH ATRIAL FIBRILLATION Figure 12. Rapid y descent of jugular venous pulse in patient with constrictive pericarditis who is in atrial fibrillation. Figure 11. Regular cannon a waves during junctional tachycardia disappear after restoration of sinus rhythm by carotid sinus massage. 12 13 Hepatojugular Reflux Test Patients suspected of having cardiac decompensation, pulmonary hypertension, or right heart failure may have a normal resting jugular venous pressure. The hepatojugular reflux test is useful for ascertaining right ventricular reserve in these conditions. This test consists of placing the palm of the hand flat on the upper abdomen and pushing firmly for 10-15 seconds while observing the jugular venous pulse. This maneuver increases intra-abdominal pressure and the pressure gradient for venous flow from the abdomen to the thorax, resulting in augmented venous return. With normal cardiac function, this increased venous return will be readily accommodated by the heart without a change in right atrial pressure; hence, there is no discernible change in jugular venous pulsation. However, in patients with right ventricular dysfunction, pulmonary hypertension, or constrictive pericarditis, increased venous blood flow cannot be adequately accommodated, and pressure rises progressively in "the right atrium and internal jugular vein (Figure 13). The term hepatojugular reflux is in fact a misnomer since the jugular venous blood does not come exclusively from the liver. Indeed, there is no actual reflux of blood into the jugular venous system but rather a general increase in pressure due to lack of accommodation of increased flow from the abdomen to the thorax. Normal individuals may exhibit a brief rise in jugular pressure immediately after abdominal pressure has begun, but pressure will return to baseline during the remainder of the maneuver. ¯ .,IJJj jj j JJJ J j j.jj J JJ J J J J j JJ~lJ~lJ.j Figure 13. Elevation in right atrial (RA) pressure observed during abdominal pressure in patient with mild congestive heart failure. 14 Arterial Pulses Anatomy Perhaps because arterial pulsations can be readily appreciated, arterial palpation is one of the earliest practices in physical diagnosis. Evidence suggests that it was the major method of determining the presence or absence of life in ancient societies and is still used today in deciding whether to initiate cardiopulmonary resuscitation. Thus, a high level of expertise in arterial pulse palpation is important for every practicing physician. Arterial pulses are palpable because of their higher pressures and increased thickness of the arterial wall as compared with veins. The routine physical examination includes palpation of the carotid, subclavian, brachial, radial, abdominal aortic, femoral, popliteal, posterior tibial, and dorsalis pedis arterial pulses. It is beyond the scope of this publication to present the anatomy and physical examination approaches to all arteries, but certain major concepts and key diagnostic features are reviewed in detail. Physiology. Transmission of left ventricular blood pressure to the peripheral arterial system after the aortic valve has opened during cardiac systole is the origin of the arterial pulse. Its character is influenced by resistance to blood flow in the arterial system, distensibility of the arteries, and inertia of the blood mass. After the aortic valve opens, the velocity of blood flow in the aorta initially rises rapidly, leading to the anacrotic (Greek derivation meaning "upbeat") shoulder of the ascending aortic pressure tracing. Peak pressure occurs somewhat later, then falls in the latter part of systole until the aortic valve closes. Aortic valve closure abruptly ceases blood flow to the aorta, resulting in the incisura on the aortic pressure recording, followed by a small positive wave caused by elastic recoil of the aorta. Pressure then falls throughout diastole as blood runs off into the periphery. This character of the ascending aortic pulse wave recording changes as the arterial waveform is sampled more peripherally in the arterial system. The major changes are a progressive dampening of pressure waveform components and a delay in the time at which the peak pulse pressure arrives in relation to onset of systole, as indicated by the QRS complex on the electrocardiogram (ECG). For example, the carotid pulse occurs 30 msec after the QRS complex, the brachial pulse 60 msec 15 after the QRS complex, the radial pulse 80 msec after the QRS complex, and the femoral pulse 75 msec after the QRS complex. Finally, as the pulse wave moves peripherally, the various waves are distorted by influences of reflected waves from more peripheral arteries (Figure 14). For example, in the carotid pressure wave, the incisura is replaced by the smoother and later dicrotic notch followed by the dicrotic wave. Figure 14. Intra-arterial recordings from various locations (see text for details). From O’Rourke RA: Physical examination of the arteries and veins (including blood pressure determination), in Hurst JW (ed): The Heart, ed 6. New York, McGraw-Hill Book Co, 1985, pp 138-151. Reproduced with permission. The second major use of arterial pulse palpation is to assess the magnitude of the left ventricular ejection impulse. The carotid pulse is usually used for this assessment since it is most readily palpated and is in proximity to the heart. Accentuated pulses represent an increase in pulse pressure (the difference between peak systolic and end-diastolic arterial pressure). Proximal aortic pulse pressure is proportional to left ventricular stroke volume. However, arterial distensibility influences this relation. If distensibility decreases because of age or disease, arterial pulse pressure will be higher with a constant stroke volume. The pads of the fingertips should be used to determine the character of the carotid pulse. Some examiners suggest using the thumb, which has a larger area for palpating. The timing of the pulse in relation to venous waves and cardiac events such as heart sounds and the apical impulse should be measured first, then the character of the pulse in terms of its fullness, rate of rise, and abnormal pulsations. The normal carotid pulse rises rapidly and tapers more slowly, is easily palpable, and occurs just after the first heart sound between the a and v waves of the jugular venous waveform and synchronous with the apical impulse in the precordial area. Pathologic Findings Examination There are two issues concerning examination of arterial pulses. First is use of the palpable pulse to determine patency of the artery. For this purpose, the pulses are usually graded on one of several numerical scales. In one scale, 0 designates an absent pulse and 2+ a normal pulse; 1 + therefore is a reduced pulse. Another system popular with vascular surgeons uses a scale of 0-4+ for more gradations of reduced pulses. These systems do not consider accentuated pulses since increased pulses are more often a reflection of the magnitude of the systolic ejection than of peripheral vascular patency. Many clinicians blend the two systems and refer to a 2+ pulse as representing a normally patent artery with normal cardiac function and 4+ as a normally patent artery with an increased left ventricular systolic ejection impulse. In this system, a 1 ÷ pulse represents either reduced arterial patency or reduced cardiac function. Therefore, it is recommended that physicians specify the aspect of interpretation when grading a pulse. 16 Differences in Peripheral Pulses The peripheral pulses should be evaluated bilaterally for patency. Impairment of one or both carotid pulses can be caused by atherosclerotic narrowing and occlusion by thrombus or aortic arch disease resulting from arteritis (e.g., Takayasu’s syndrome and syphilis). Unequal radial pulses can result from aortic arch disease, dissecting aortic aneurysm, a cervical rib, the scalenus anticus syndrome, arterial embolism, and thrombosis, which may be due to previous cardiac catheterization or trauma. The right subclavian artery occasionally arises from the aorta more distally than the left (anomalous subclavian artery) and courses behind the esophagus, resulting in reduced pulses in the right arm. Accentuated pulses in the right arm can be caused by supravalvular aortic stenosis. Femoral pulses may be impaired with atherosclerosis of the external or common lilac arteries. On palpation, the normal femoral pulses should slightly precede the radial pulses. The femoral pulses may be absent or impaired bilaterally in Leriche’s syndrome (i.e., thrombotic occlusion of the aortic bifurcation). They may be impaired either unilaterally or bilaterally in dissecting aneurysm. Absent femoral pulses may result from thrombotic 17 occlusion of the aortic bifurcation or bilateral common lilac artery sclerosis with thrombosis or saddle embolism to the aortic bifurcation. In a child or young adult, if neither femoral pulse can be palpated or if both femoral pulses are equally weakened and delayed, coarctation of the aorta is a likely possibility. This is especially true if hypertension exists in the upper extremities (Figure 15). Rarely, hypertension in the upper extremities and a weak or absent femoral pulse result from coarctation of the abdominal aorta, which often involves the renal arteries. With coarctation of the thoracic aorta, the carotid pulses are often exaggerated. Weak or absent femoral pulses are rarely found to be related to pseudoxanthoma elasticum. The external lilac arteries may be hypoplastic, simulating coarctation of the aorta. Bilateral absence of either the dorsalis pedis or the posterior tibial pulses occasionally occur in normal individuals. Bilateral absence of both or unilateral absence of either usually indicates arterial obstructive disease, more often resulting from arteriosclerosis than from embolism, arteritis, or trauma. When the dorsalis pedis or the posterior tibial pulses are abnormal, the more proximal pulsations of the popliteal and femoral arteries and the abdominal aorta should be evaluated to determine the site and cause of obstruction. Hyperkinetic Pulse A rapidly rising carotid pulse of increased amplitude suggests a widened pulse pressure and increased left ventricular stroke volume. Widened pulse pressure can be caused by high cardiac output states such as anxiety, thyrotoxicosis, anemia, or systemic arteriovenous fistula. In adults, the most common cause is aortic regurgitation, where blood is regurgitated retrogradely from the aorta into the left ventricle during diastole. The regurgitated volume is ejected with the forward stroke volume during systole, increasing total left ventricular stroke output (Figure 16). This increased stroke volume together with the fall in diastolic pressure due to regurgitation may result in a marked increase in pulse pressure. It should be mentioned that increased pulse pressure can also occur in the elderly with a normal stroke volume, due to decreased distensibility of the arterial tree that magnifies the arterial pulse waves. In children, patent ductus arteriosus is a common cause. mm Hg 160 ECG ~ 8O ~00 4O Brochiol Artery ~, 150’ E I00 E 50 0 ECG FEMORAL ARTERY AORTIC 160-I Femoral Artery PRESSURE PULSE INSUFFICIENCY Figure 16. Hyperkinetic pulse recorded from femoral artery of patient with aortic regurgitation. K-I se c.-~ COARCTATION OF THE AORTA Figure 15, Brachial and femoral artery recordings from patient with coarctation of aorta. 18 19 Exaggeration of the right carotid pulse may be found with supravalvular aortic stenosis. In hypertensive patients who are middle-aged or older, the right common carotid artery just above the clavicle may show an exaggerated pulse and a seemingly increased diameter. This finding is often considered evidence of a carotid aneurysm. However, arteriograms usually show that such findings result from kinking or buckling of an elongated artery, not from a true aneurysm. Palpation of a carotid artery may disclose a vibration (thrill) with an associated audible bruit. Such a thrill may be caused by localized disease of the carotid artery. A systolic murmur is found with mild obstruction produced by thrombosis. A thrill in the carotid artery also may be referred from elsewhere, most commonly from valvular aortic stenosis. Thrills may be felt in high output states such as thyrotoxicosis, severe anemia, or beriberi heart disease and are usually of brief duration. Hypokinetic Pulse The cause of a reduction in left ventricular stroke volume will lead to a reduced pulse pressure or a hypokinetic pulse. A generalized decrease in systemic arterial pressure can also lead to a diminution in pulse pressure and a hypokinetic pulse. Thus, the major issue in evaluation of a hypokinetic pulse is to differentiate between cardiac and peripheral causes since both are associated with low systemic arterial pressure. For example, marked hypovolemia will result in reduced blood pressure that cannot be elevated by increased arterial tone or augmented cardiac activity. Pulsus Parvus et Tardus A carotid pulse that is slow-rising, late-peaking, and of low amplitude is characteristic of severe valvular aortic stenosis (Figure 18). In this condition, there also may be a palpable vibration (thrill) on the ascending limb of the pulse. It is often difficult to palpate the carotid pulses of such patients because of lowered pulse pressure and lack of a rapid rise on the upstroke of the pulse. This pulse must be distinguished from the hypokinetic pulse discussed above. Pulsus Bisferiens The pulsus bisferiens, or twice-beating pulse, has a double impulse during systole and is best appreciated in the carotid pulse (Figure 17). It has three major causes: The combination of aortic stenosis and insufficiency, severe aortic regurgitation without stenosis, and hypertrophic obstructive cardiomyopathy. The pathophysiology of the bisferious pulse in each of these conditions is somewhat different, and the three disease states are readily separated by other features of the physical examination. Electrocardioqram Inspiration Phono- cardiogram $1 ESM PzAz SI ESM PzA2 S~ ESM St Carotid Pulse 0.2s=. SEVERE AORTIC VALVULAR STENOSIS PULSUS Figure 18. Phonocardiogram and carotid pulse tracing from patient with severe aortic valve stenosis. S1, first heart sound; S2, second heart sound; ESM, ejection systolic murmur; A2, aortic valve component; P2, putmonic valve component. BISFERIENS IN AORTIC INSUFFICIENCY Figure 17. Brachial artery recordings from patient with severe aortic regurgitation. 20 21 Dicrotic Pulse The dicrotic pulse also beats twice, but the second pulse wave is in diastole and is an accentuation of the normal dicrotic wave of the carotid pulse. A dicrotic pulse has two major causes. One is severe left ventricular failure with a low stroke volume and high peripheral vascular resistance (Figure 19). Paradoxically, the dicrotic pulse can also be produced by high output states with extremely low systemic vascular resistance as occurs with a high fever and dehydration (i.e., typhoid fever). Thus, the pathophysiologic origins of an accentuated dicrotic wave are complex. Z5 25 0.50 0.49 0.50 PRIMARY MYOCARDIOPATHY 0.48 0.50 45° Heod-up tilt 0.48 Figure 20. Patient in Figure 19 also develops pulsus alternans after elevation to 45° head-up tilt. 0.54 0.55 PRIMARY MYOCARDIOPATHY 0.55 0.55 suspicion of pulsus alternans may be confirmed by use of a sphygmomanometer. In milder cases, if cuff pressure is lowered slowly, all sounds can be heard over the brachial artery distal to the cuff at the systolic pressure level, but these sounds alternate in intensity. In more advanced cases, when cuff pressure is raised above the systolic pressure level and then lowered very slowly, only the alternate strong beats are audible over the brachial artery at first. Then, as cuff pressure is lowered further, perhaps by 10 mm Hg, frequency of the Korotkoff sounds may suddenly double as the weaker beats also become audible. 0.55 Supine Figure 19. Brachial artery recording from patient with congestive heart failure due to primary cardiomyopathy. Puisus Aiternans Pulsus alternans is an alternation in the pulse amplitude on every other beat that is best appreciated in the radial artery. The examiner must be certain that the rhythm is regular since irregular rhythm can cause variations in pulse amplitude (see below). This is usually a sign of severe left ventricular dysfunction and heart failure (Figure 20). It is often associated with a tachycardia and may be present continuously or occur transiently after a premature ventricular contraction. In the latter situation, the difference in pulse amplitude diminishes over several beats and finally disappears. This is a subtle sign that can be discerned only by careful attention to the pulse amplitude. In addition, it is best to have the patient hold his or her breath to remove the effects of respiration on pulse amplitude. The 22 23 Pulsus Paradoxus Pulsus paradoxus is a classic physical finding of cardiac tamponade due to increased fluid in the pericardial space. In pericardial tamponade, unlike constrictive pericarditis, augmented right heart flow to the lungs can be accomplished during inspiration but only at the expense of left ventricular filling. Thus, the slight decrease in systemic arterial pressure during normal quiet respiration is markedly accentuated and becomes palpable (Figure 21). Once an inspiratory decrease in pulse amplitude is appreciated by palpation, the maximum difference in systolic blood pressure between inspiration and expiration is usually 20 mm Hg or more. Normally, this difference is less than 10 mm Hg and is due to a slight decrease in left ventricular stroke volume during inspiration and transmission of reduced intrathoracic pressure to the aorta. Occasionally in severe tamponade, peripheral arterial pressure approaches zero during inspiration, an observation that is the origin of the term pulsus paradoxus. Kussmaul, who described it, noted that the peripheral pulse disappeared during inspiration, yet the apical impulse of the heart was still visible, thus the term paradoxic pulse. However, in extreme degrees of pericardial tamponade, this sign may disappear if pericardial pressure approaches the point of mimicking constrictive pericarditis and right heart flow can no longer be augmented. In this situation, Kussmaul’s sign, an inspiratory increase in jugular venous pressure, should be noted. Pulsus paradoxus is not specific for pericardial tamponade and can occur in severe obstructive lung disease (Figure 22) and in patients with constrictive pericarditis, especially if the constriction is partial and not uniformly distributed throughout the pericardium. Reversed pulsus paradoxus has also been described in patients on positive pressure ventilators. During examination for a paradoxical pulse, the patient should breathe as normally as possible and should not be asked to breathe deeply. If the pulse wanes with inspiration in all accessible arteries and cardiac rhythm is regular, a paradoxical pulse is present. In instances when the examiner is uncertain, it may be desirable to use a blood pressure cuff to measure and confirm existence of a paradoxical pulse. The blood pressure cuff is inflated until no sounds are heard with the stethoscope over the brachial artery, and then gradually deflated until sounds are heard in expiration only. The cuff pressure is then lowered further until sounds are heard throughout the respiratory cycle. The difference between these two pressure levels is a measure of the magnitude of the paradoxical pulse. Any reading exceeding 10 mm Hg is probably significant. mm Hg 120 Inspiration Respiration ~ 80 40 0 ECG ~ Pneumogram Brochiol 150 Artery Ioo-L ~ ~ A.= ~.= Pressure 50-J mm Hg O~ CARDIAC TAMPONADE Figure 21. Exaggerated inspiratory decrease in brachial artery pressure in patient with cardiac tamponade (pulsus paradoxus). I sec PARADOXICAL PULSE IN EMPHYSEMA Figure 22. Pulsus paradoxus in patient with obstructive lung disease. 24 25 Special Tests Arrhythmias Cardiac arrhythmias often alter peripheral pulse characteristics. Irregular rhythms such as atrial fibrillation cause a variation in stroke volume from beat to beat and result in varying amplitude of the arterial pulse. Any interruption in cardiac activity due to arrhythmias can also be appreciated in the periphery by the absence of pulsations. For example, an interruption of the pulse frequency of exactly double one cardiac cycle suggests the presence of a premature ventricular contraction that usurped the next sinus beat and resulted in a compensatory pause before the following sinus beat. Under certain circumstances in which atrial activation is not transmitted to the ventricles, the peripheral pulses wax and wane in relation to the varying time interval between atrial and ventricular systole. This variation of pulse magnitude occurs most commonly in patients with ventricular tachycardia and patients with atrioventricular block or dissociation. An example is shown in Figure 23. It may be observed that the maximum pulse occurs when atrial systole precedes ventricular systole by a short interval. When there is a long interval or no preceding atrial beat, the pulse is at a minimum. This finding may be a valuable clue to diagnosis of ventricular tachycardia in patients who have a paroxysmal tachycardia of unknown variety. A blood pressure cuff may help demonstrate or confirm this mechanism. This finding is absent in ventricular tachycardia when there is retrograde conduction from ventricles to atria. PPPPP PP PPP a. 60- COMPLETE ATRIOVENTRICULAR BLOCK VENTRICLES PACED AT 70/MINUTE Figure 23. Variation in pulse magnitude due to variable atrial contribution to ventricular filling in patient with complete atrioventricular block and escape ventricular rhythm of 70 beats/min. 26 Allen’s Test Small arteries in the hand cannot ordinarily be palpated, yet arterial defects due to trauma or arterial disease may lead to dysfunction of the hand. Adequacy of arterial circulation in the hand can be determined by Allen’s test, in which firm compression of the arteries against the distal ulnar and radial bones with the examiner’s fingers and thumbs occludes both the radial and ulnar pulse at the wrist. The patient then flexes the hand several times until all the blood has drained from the hand, as evidenced by pallor. The examiner then releases either the ulnar or radial artery and observes the flow of blood through the hand. Release of either artery should result in rapid full perfusion of the hand since both arteries are connected by collateral channels through the palmar arcade. With this technique, specific arterial insufficiencies in various regions of the wrist and hand can be determined. It is especially useful to ascertain the adequacy of ulnar artery perfusion of the hand before cannulating the radial artery in a critically ill patient. Valsa~va’s Maneuver When subtle degrees of cardiac dysfunction are suspected in a patient without overt congestive heart failure, the Valsalva maneuver can be used to detect this decrease in cardiac reserve. In Valsalva’s maneuver, the patient bears down against the closed glottis, which increases intrathoracic pressure and effectively ends venous flow into the thorax, markedly reducing cardiac filling, resulting in a progressive fall in blood pressure. The fall in blood pressure causes a reflex tachycardia, both of which can be experienced by palpating a peripheral arterial pulse during the maneuver. After 15 seconds of bearing down, the patient releases the maneuver and breathes normally. There is an immediate increase in venous return to the heart and, subsequently, left ventricular stroke volume, which results in an increase in blood pressure that is higher than before the maneuver because the reflex vasoconstriction that occurred during the strain phase results in increased vascular resistance. The increase in pulse amplitude is readily appreciated in a peripheral artery, as is the ensuing reflex bradycardia. This is the normal response to the Valsalva maneuver (Figure 24A). In the presence of reduced left ventricular performance, there may already be heightened sympathetic arterial tone. Thus, the fall in blood pressure during the maneuver does not result in the usual tachycardia, and there is no overshoot in blood pressure or reflex bradycardia (Figure 24B). If the patient has unrecognized overt heart failure, the so-called square wave pattern is seen. In this situation, increasing intrathoracic 27 pressure increases pulmonary venous flow from the lungs into the left ventricle since there is a great deal of excess blood in the lungs. This results in an elevation of blood pressure during the Valsalva maneuver and no appreciable reflex changes in heart rate. Once the strain phase is released and pulmonary venous return falls, blood pressure returns to baseline (Figure 24C). This abnormality in the Valsalva response is readily determined by palpating an arterial pulse. The square wave response to blood pressure in the Valsalva maneuver can also be observed in patients with large atrial septal defects. ~ IO0 o ~00 5O ~00 C Suggested Reading Dell’Italia L J, Starling MR, O’Rourke RA: Physical examination for exclusion of hemodynamically important right ventricular infarction. Ann Intern Med 1983;99:608-611 Ducas J, Magder S, McGregor M: Validity of the hepatojugular reflux as a clinical test for congestive heart failure. Am J Cardiol 1983;52:1299-1303 Ewy GA: Venous and arterial pulsations, in Horwitz LD, Groves BM (eds): Signs and Symptoms in Cardiology. Philadelphia, JB Lippincott Co, 1984, pp 135-155 Ewy GA: Evaluation of the neck veins. Hosp Pract 1987;22:72-75,79-80 Ewy GA: The abdominojugular test: Technique and hemodynamic correlates [published erratum appears in Ann Intern Med 1988;109:947]. Ann Intern Med 1988;109:456-460 O’Rourke RA: Physical examination of the arteries and veins (including blood pressure determination), in Hurst JW (ed): The Heart, ed’6. New York, McGraw-Hill Book Co, 1985, pp 138-151 O’Rourke RA, Crawford MH: Physical findings in heart failure and their physiologic basis, in Mason DT (ed): Congestive Heart Failure. New York, Yorke Medical Books, 1976, pp 183-190 START STOP Figure 24. Direct systemic arterial pressure recordings during Valsalva maneuver in three patients (see text for details). From O’Rourke RA, Crawford MH: Physical findings in heart failure and their physiologic basis, in Mason DT (ed): Congestive Heart Failure. New York, Yorke Medical Books, 1976, pp 183-190. Reproduced with permission. 28 29 Your contributions to the American Heart Association will support research that helps make publications like this possible. For more information, contact your local American Heart Association or call 1-800-AHA-USA 1 (1-800-242-8721). American Heart ~ Associations, Fighting Heart Disease and Stroke National Center 7272 Greenville Avenue Dallas, TX 75231-4596 70-1030 6-94 90 03 30 B