1. D . B A S E M E L S A I D E N A N Y
L E C T U R E R O F C A R D I O L O G Y
A I N S H A M S U N I V E R S I T Y
Examination of the pulse

2. --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.

3. *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.

5. 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.

6. 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.

7. --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).

8. 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.

9. --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.

10. 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.

11. --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.

12. 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.

13. 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.

14. 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.

15. Thank you