Examination of the arterial pulse

May 13, 1999

Assessment of the arterial pulse characteristics is an integral part of the cardiovascular examination. Carotid, radial, brachial, femoral, posterior tibial, and dorsalis pedis pulses should be routinely examined bilaterally to ascertain any differences in the pulse amplitude, contour, or upstroke. Popliteal pulses should also be examined when lower extremity arterial disease is suspected.

The carotid pulse contour is very similar to that of the central aortic pulse; a delay in the onset of the ascending limb of the carotid pulse, compared with the central aortic pulse, is only about 20 msec. Thus, examination of the carotid pulse provides the most accurate representation of changes in the central aortic pulse. The brachial arterial pulse is examined to assess the volume and consistency of the peripheral vessels.

UNEQUAL OR DELAYED PULSES — Inequality in the amplitude of the peripheral pulses may result from:

  •  Obstructive arterial diseases, most commonly atherosclerosis
  •  Aortic dissection
  •  Aortic aneurysm
  •  Takayasu's disease
  •  Supravalvular aortic stenosis in which the right carotid, brachial, and radial pulses are larger in amplitude and volume than those on the left side because of the preferential streaming of the jet toward the innominate artery

Simultaneous palpation of the radial and femoral pulses is important to determine if there is a delay in pulse transmission. In normal adults, the upstrokes of the radial and femoral pulses normally appear simultaneously. A delay in the onset of the femoral pulse, generally associated with a diminished amplitude, suggests coarctation of the aorta.

PULSUS ALTERNANS — Pulsus alternans is a variation in pulse amplitude occurring with alternate beats due to changing systolic pressure. It is best appreciated by applying light pressure on the peripheral arterial pulse, and can be confirmed by measuring the blood pressure. When the cuff pressure is slowly released, phase I Korotkoff sounds are initially heard only during the alternate strong beats; with further release of cuff pressure, the softer sounds of the weak beat also appear. The degree of pulsus alternans can be quantitated by measuring the difference in systolic pressure between the strong and the weak beat.

Etiology — The most important cause of pulsus alternans is left ventricular failure. In clinical practice, true pulsus alternans is rarely seen in the absence of significant left ventricular myocardial failure, and should prompt further investigation to determine the severity and cause of left ventricular myocardial dysfunction.

Pulsus alternans also may be evident in the following situations:

  •  Left ventricular pulsus alternans without systemic arterial pulsus alternans has been observed in patients with hypertrophic cardiomyopathy and a significant rest or provocable outflow gradient [1]. The mechanism remains unclear; abolition of left ventricular alternans occurs after successful myomectomy. (See "Clinical manifestations of hypertrophic cardiomyopathy" and see "Evaluation of obstructive hypertrophic cardiomyopathy").

  •  Pulsus alternans is rarely encountered in patients with cardiac tamponade.

  •  It can occur in the presence of marked tachypnea when the respiratory rate is one-half the heart rate due to an inspiratory decrease in the pulse amplitude. The pulse abnormality disappears when respiration is held transiently.

  •  It may be seen in patients with severe aortic regurgitation.

  •  Pulsus alternans is frequently precipitated by ectopic beats; apparent pulsus alternans may be observed in patients with a bigeminal rhythm. In the latter situation, the premature beats are usually out of phase with the normal beats and postectopic pauses are appreciated. Simultaneous auscultation of the sequence of the heart sounds and palpation of the arterial pulse can differentiate between true pulsus alternans and apparent pulsus alternans due to bigeminy.

Pulsus alternans should not be diagnosed when the cardiac rhythm is irregular.

Mechanism — The precise mechanism for pulsus alternans remains unclear; alternating preload (Frank-Starling mechanism) and incomplete relaxation have been proposed [2]. Changes in afterload, which is lower after preceding the strong beat, may also contribute.

It also has been suggested that a change in ventricular contractility is the primary mechanism, causing changes in end-diastolic volume and pressure. In experimental animals, acute myocardial ischemia is associated with regional pulsus alternans, leading to the hypothesis that alternating potentiation and attenuation or deletion of contraction accounts for the pulse abnormality [3]. Thus pulsus alternans may result primarily from an alternating contractile state of the ventricle. The magnitude of the alteration of pressure and stroke volume during pulsus alternans, indices of pump function, reflects the interaction of an alternating contractile state with changes in preload and afterload.

PULSUS PARADOXUS — Some respiratory variation of pulse amplitude should be observed during examination of the arterial pulse. Systolic arterial pressure normally falls during inspiration, although the magnitude of decrease usually does not exceed 8 to 12 mmHg. These changes in pulse amplitude are not usually appreciated by palpation but can be established with the sphygmomanometer.

A more marked inspiratory decrease in arterial pressure exceeding 20 mmHg is termed pulsus paradoxus. In contrast to the normal situation, this is easily detectable by palpation, although it should be evaluated with a sphygmomanometer. When the cuff pressure is slowly released, the systolic pressure at expiration is first noted. With further slow deflation of the cuff, the systolic pressure during inspiration can also be detected. The difference between the pressures during expiration and inspiration is the magnitude of pulsus paradoxus. The inspiratory decrease in systolic pressure is accentuated during very deep inspiration or Valsalva; thus, assessment of pulsus paradoxus should be made only during normal respiration.

Etiology — Pulsus paradoxus is an important physical finding in cardiac tamponade. (See "Pulsus paradoxus in pericardial disease"). In patients with suspected cardiac tamponade, echocardiography should be performed to detect pericardial effusion and ventricular diastolic collapse; the latter is more specific and sensitive than pulsus paradoxus for the diagnosis of tamponade [4]. Pulsus paradoxus may not occur despite cardiac tamponade in patients with hemodynamically significant aortic regurgitation and atrial septal defect. (See "Pericardial compressive syndromes").

In addition to tamponade, pulsus paradoxus can occur in chronic obstructive pulmonary disease, hypovolemic shock, and infrequently in constrictive pericarditis and restrictive cardiomyopathy. It is rarely observed in pulmonary embolism, pregnancy, marked obesity, and partial obstruction of the superior vena cava.

In hypertrophic obstructive cardiomyopathy, arterial pressure occasionally rises during inspiration (reversed pulsus paradoxus); the precise mechanism for this phenomenon is unclear [5].
In addition to changes in the amplitude, configurational changes of the carotid pulse may occur.

Mechanism — The mechanism for the marked inspiratory decrease in arterial pressure with pulsus paradoxus appears to be related to the inspiratory decline of left ventricular stroke volume due to an increase in right ventricular end-diastolic volume and decreased left ventricular end-diastolic volume. In cardiac tamponade, the interventricular septum shifts toward the left ventricular cavity during inspiration (reverse Bernheim's effect), a result of the normal increase in venous return to the right side, thereby decreasing left ventricular preload [6]. An inspiratory decrease in pulmonary venous return to the left side of the heart also has been thought to contribute to decreased left ventricular preload.

PULSUS BISFERIENS — The normal carotid arterial pulse tracing and the central aortic pulse waveform consist of an early, the percussion wave, that results from rapid left ventricular ejection, and a second smaller peak, the tidal wave, presumed to represent a reflected wave from the periphery. The tidal wave may increase in amplitude in hypertensive patients or in those with elevated systemic vascular resistance. Radial and femoral pulse tracings demonstrate a single sharp peak in normal circumstances.

Pulsus bisferiens is characterized by two systolic peaks of the aortic pulse during left ventricular ejection separated by a midsystolic dip. Both percussion and tidal waves are accentuated. It is difficult to establish with certainty that the two peaks are occurring in systole with simple palpation (pulsus bisferiens) versus one peak in systole and the other in diastole (dicrotic pulse).

Etiology — Pulsus bisferiens is frequently observed in patients with hemodynamically significant (but not mild) aortic regurgitation. In patients with mixed aortic stenosis and aortic regurgitation, bisferiens pulse occurs when regurgitation is the predominant lesion. The absence of pulsus bisferiens does not exclude significant aortic regurgitation.

In most patients with hypertrophic cardiomyopathy the carotid pulse upstroke is sharp and the amplitude is normal; pulsus bisferiens is rarely palpable but often recorded. The rapid upstroke and prominent percussion wave result from rapid left ventricular ejection into the aorta during early systole. This is followed by a rapid decline as left ventricular outflow tract obstruction ensues, a result of midsystolic obstruction and partial closure of the aortic valve. The second peak is related to the tidal wave. Occasionally, a bisferiens pulse is not present in the basal state but can be precipitated by Valsalva maneuver or by inhalation of amyl nitrite.

Pulsus bisferiens is occasionally felt in patients with a large patent ductus arteriosus or arteriovenous fistula. A bisferiens quality of the arterial pulse also is rarely noted in patients with significant mitral valve prolapse and, very rarely in normal individuals, particularly when there is a hyperdynamic circulatory state.

Mechanism — The mechanism of pulsus bisferiens is not clear. It appears to be related to a large, rapidly ejected left ventricular stroke volume associated with increased left ventricular and aortic dp/dt.

DICROTIC PULSE — A dicrotic pulse results from the accentuated diastolic dicrotic wave that follows the dicrotic notch. It tends to occur when the dicrotic notch is low, as in patients with decreased systemic arterial pressure and vascular resistance (eg, fever). A dicrotic pulse also may be present in patients with severe heart failure, hypovolemic shock, cardiac tamponade, conditions associated with a decreased stroke volume and elevated systemic vascular resistance, and during the immediate postoperative period following aortic valve replacement [7]. The precise mechanism for a dicrotic pulse in the last group is not clear; it is more frequently observed in patients with pump failure postoperatively. Dicrotic pulse is occasionally noted in normal individuals, particularly after exercise.

A dicrotic pulse is frequently confused with pulsus bisferiens at the bedside; it is almost impossible to distinguish between these two types of pulse configurations without a pulse recording. Thus, the potential exists for mistaken diagnosis of aortic regurgitation due to malfunction of a prosthetic valve.

CORRIGAN PULSE — The Corrigan or water-hammer pulse is characterized by an abrupt, very rapid upstroke of the peripheral pulse (percussion wave), followed by rapid collapse. It is best appreciated by raising the arm abruptly and feeling for the characteristics in the radial pulse.

The Corrigan pulse probably results from very rapid ejection of a large left ventricular stroke volume into a low resistance arterial system. Thus, it occurs most commonly in chronic, hemodynamically significant aortic regurgitation. A bounding arterial pulse is not diagnostic of aortic regurgitation; it can occur in many conditions associated with increased stroke volume such as patent ductus arteriosus, large arteriovenous fistulas, hyperkinetic states, thyrotoxicosis anemia, and extreme bradycardia. The typical pulse characteristics of chronic aortic regurgitation may not occur in acute aortic regurgitation, even when it is severe, since left ventricular stroke volume may not increase appreciably, the systemic vascular resistance may not be low, and the left ventricle is not dilated.

PULSES IN AORTIC STENOSIS — Characteristic changes in the morphology of the arterial pulse may occur in the presence of fixed left ventricular outflow tract obstruction, particularly valvular aortic stenosis. Careful examination of the arterial pulse provides useful information for the diagnosis and assessment of the severity of aortic stenosis.

Increased resistance to left ventricular ejection due to fixed obstruction reduces the stroke volume, prolongs left ventricular total ejection time, and retards the rate of initial stroke output into the aorta and distal arterial system. This results in a number of changes that can be appreciated with palpation of the carotid pulse:

  •  Anacrotic character (anacrotic pulse) — An anacrotic pulse gives the impression of interruption of the upstroke of the carotid pulse. Aortic stenosis is likely to be hemodynamically significant when the anacrotic notch is felt immediately after the onset of the upstroke. When an anacrotic notch occurs very early on the ascending limb of the arterial pulse, it can be appreciated in the radial pulse and suggests moderate to severe aortic stenosis.

  •  Delayed upstroke of the ascending limb (pulsus tardus) — A delayed peak and slower upstroke of the carotid pulse suggest a prolonged left ventricular ejection time. The delay can be appreciated by simultaneous palpation of the carotid pulse and auscultation of the interval between S1 and S2 (duration of systole). Normally the peak of the carotid pulse occurs closer to S1; in the presence of severe aortic stenosis, it is usually closer to S2. In the presence of fixed outflow obstruction, the central aortic pulse demonstrates a progressively slower rise of the ascending limb, a lower anacrotic shoulder, and a peak closer to the incisura as the severity of obstruction increases.

  •  Delayed peak

  •  Small amplitude (pulsus parvus) — The amplitude of the pulse decreases with a diminished stroke volume.

  •  Shudder (thrill) on the ascending limb — A thrill (carotid shudder) also is frequently palpable on the ascending limb of the pulse.

The diagnosis and severity of aortic stenosis should not be determined by changes in the carotid pulse configuration alone. The auscultatory findings of aortic stenosis and evidence for left ventricular hypertrophy should be sought.

The carotid arteries may become rigid and less compliant in elderly patients due to arteriosclerosis. The usual changes in the carotid pulse due to aortic stenosis are modified in this situation, particularly the amplitude, which may not decrease even in the presence of severe aortic stenosis.