D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Examination of the pulse

--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.--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.

*Inequality in the amplitude of the peripheral pulses may result from:

-Obstructive arterial diseases, most commonly atherosclerosis-Aortic dissection-Aortic aneurysm-Takayasu disease-Coarctation of the aorta-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 (also termed mechanical alternans)

--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.--The most important cause of pulsus alternans is left ventricular failure.--Pulsus alternans should not be diagnosed when the cardiac rhythm is irregular.--Pulsus alternans is more common with faster heart rate. --Pacing induced tachycardia can precipitate sustained pulsus alternans in patients with idiopathic dilated cardiomyopathy and is associated with worse prognosis.

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.--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. It is however rare in the absence of left ventricular systolic dysfunction.--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.

--The precise mechanism for pulsus alternans remains unclear.--Alternating preload (Frank-Starling mechanism) and incomplete relaxation have been proposed. --Changes in afterload, which is lower before the strong beat because of the lower output during the weak beat, may also contribute.--Also has been suggested that a change in ventricular contractility is the primary mechanism (Changes in sarcoplasmic calcium pumps with alternate strong and weak beats).

PULSUS PARADOXUS

-- Systolic arterial pressure normally falls during inspiration, although the magnitude of decrease usually does not exceed 8 to 12 mmHg.--A more marked inspiratory decrease in arterial pressure exceeding 20 mmHg is termed pulsus paradoxus {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 as interventricular septum shifts toward the left ventricular cavity during inspiration (reverse Bernheim phenomenon) + inspiratory decrease in pulmonary venous return to the left side of the heart}.-- 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.

--Pulsus paradoxus is an important physical finding in cardiac tamponade. Pulsus paradoxus may not occur despite cardiac tamponade in patients with hemodynamically significant aortic regurgitation and atrial septal defect.--pulsus paradoxus can occur in chronic obstructive pulmonary disease, morbid obesity, hypovolemic shock, and infrequently in constrictive pericarditis and restrictive cardiomyopathy.--In hypertrophic obstructive cardiomyopathy, arterial pressure occasionally rises during inspiration (reversed pulsus paradoxus); the precise mechanism for this phenomenon is unclear.

PULSUS BISFERIENS

--The normal carotid arterial pulse tracing and the central aortic pulse waveform consist of an early component, the percussion wave, which results from rapid left ventricular ejection, and a second smaller peak, the tidal wave, presumed to represent a reflected wave from the periphery (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).--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.

--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.-- Occasionally felt in patients with a large patent ductus arteriosus or arteriovenous fistula. --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.--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.

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).--In severe heart failure, hypovolemic shock, cardiac tamponade, conditions associated with a decreased stroke volume and elevated systemic vascular resistance.--During the immediate postoperative period following aortic valve replacement , mechanism 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.

Water hammer or Corrigan (or hyperkinetic) pulse

-- 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.--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. --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

**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.**Characteristics:--Anacrotic character (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): delayed peak and slower upstroke of the carotid pulse. 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.--Small amplitude (pulsus parvus): The amplitude of the pulse decreases with a diminished stroke volume.--Shudder (thrill) on the ascending limb: is frequently palpable on the ascending limb of the pulse.

**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.

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