Transcript Pulse - シーサー株式会社

Pulse
The pulse has been studied for centuries.
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Information gained:
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Frequency, regularity
Patency of peripheral arteries
Characteristics of the arterial pressure pulse wave
The arterial pulse contour changes to the periphery:
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Resistance: viscosity, vessel geometry opposes flow; HR
independent
Inertia: mass opposes rate of change of flow, HR dependent
Compliance: distensibility opposes changes of blood volume,
HR-dependent
Location of Pulses
Carotid – similar to central aortic pulse (delay of
20msec)
 Radial – used to assess the volume and consistency
of the peripheral vessels.
 Brachial
 Femoral
 Posterior tibial
 Dorsalis pedis
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Look for any differences in the pulse amplitude,
contour, or upstroke.
Factors Influencing the Pulse
Stroke volume
 Rate of ejection
 Distensibility of peripheral arteries
 Peripheral resistance
 Pulse rate
 Pulse pressure
 Size of the vessel
 Distance from the heart
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Normal Pulse (1/2)
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The normal central aortic pulse wave is characterized by a
fairly rapid rise to a somewhat rounded peak.
The anacrotic shoulder, present on the ascending limb,
occurs at the time of peak rate of aortic flow just before
maximum pressure is reached.
The less steep descending limb is interrupted by a sharp
downward deflection, coincident with AV closure, called
incisura.
The pulse pressure is about 30-40 mmHg.
Normal Pulse (2/2)
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As the pulse wave is
transmitted peripherally,
the initial upstrokes
becomes steeper, the
anacrotic shoulder becomes
less apparent, and the
incisura is replaced by the
smoother dicrotic notch.
Abnormal Pulses
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Inequality in the amplitude of the peripheral
pulses:
Obstructive arterial diseases , most commonly
artherosclerosis
 Aortic dissection
 Aortic aneurysm
 Takayasu arteritis (pulseless disease)
 Supravalvular aortic stenosis (fixed form of LVOT
caused by narrowing of ascending aorta)
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Pulsus Parvus
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The pressure is diminished, and the pulse feels weak
and small, reflecting decreased stroke volume (e.g.
heart failure), restrictive pericardial disease,
hypovolemia, mitral stenosis, and increased
peripheral resistance (e.g. exposure to cold, severe
CHF).
Pulsus Parvus et Tardus (weak and delayed):
→Aortic Stenosis
Aortic Stenosis (1/2)
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LVOT obstruction
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Reduces SV, prolongs LV total ejection time, and
retards the rate of initial stroke output into the
aorta and distal arterial system.
Anacrotic character (anacrotic pulse)
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Interruption of the upstroke of the carotid pulse.
AS is likely to be hemodynamically significant
when the anacrotic notch is felt immediately after
the onset of the upstroke.
Aortic Stenosis (2/2)
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Delayed upstroke of the ascending limb
(pulsus tardus)
Prolonged LV ejection time.
 Appreciated by simultaneous palpation of carotid
pulse and auscultation fo the interval between S1
and S2.
 Normally the carotid pulse occurs closer to S1; in
severe AS closer to S2.
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Thrill (carotid shudder)
Bisferiens Pulse
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Increased arterial pulse with a double systolic
peak.
Second peak, the tidal wave, presumed to represent
a reflected wave from the periphery.
 Causes: hemodynamically significant AR
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HCM: rarely palpable; rapid LV ejection during early
systole, rapid decline due to LVOT obstruction, and
tidal wave from periphery.
Bigeminal Pulse
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Normal beat alternating with a premature contraction.
SV of the premature beat diminished, and pulse varies
in amplitude accordingly.
May masquerade as pulsus alternans
Causes: decreased BP (e.g. severe HF, hypovolemic
shock, cardiac tamponade) and peripheral resistance
(e.g. fever), s/p aortic valve replacement.
Present in normal individuals after exercise.
Pulsus Alternans (1/2)
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Variation in pulse amplitude occurring with alternate beats due
to changing systolic pressure.
When the cuff pressure is slowly released while taking BP,
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.
Degree of pulsus alternans can be quantitated by measuring the
pressure difference between the strong and the weak beat.
Pulsus Alternans (2/2)
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Causes:
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Left ventricular failure – usually accompanied by a leftsided S3.
May be seen in patients with severe AR
Frequently precipitated by ectopic beats (bigeminal pulse)
Mechanisms:
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Alternating preload and afterload, incomplete relaxation,
Change in ventricular contractility, causing changes in enddiastolic volume and pressure.
Pulsus Paradoxus (1/2)
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Pressure drop > 20 mmHg during inspiration.
Normally, systolic arterial pressure falls 8-12 mmHg during
inspiration.
Evaluated with sphygmomanometer:
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when the cuff 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.
Pulsus Paradoxus (2/2)
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Causes:
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Cardiac Tamponade
COPD, hypervolemic shock
infrequently in constrictive pericarditis and rescrictive
cardiomyopathy.
Mechanism:
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Decreased LV-SV due to an increased RV-EDV and
decreased LV-EDV during inspiration.
In cardiac tamponade, the interventricular septum shifts
toward the LV cavity during inspiration (reverse
Bernheim’s effect) b/c of increased venous return to RV,
decreasing the LV preload.
Decrease in pulmonary venous return to the LV during
inspiration also contributes to decreased LV preload.
Bounding Pulses (1/2)
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A.K.A. water-hammer pulse or the Corrigan pulse.
Most commonly in chronic, hemodynamically significant AR.
Seen in many conditions associated with increased stroke
volume: PDA, large arteriovenous fistula, hyperkinetic states,
thyrotoxicosis anemia, and extreme bradycardia.
Not seen in acute AR, since SV may not have increased
appreciably.
Bounding Pulses (2/2)
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Physical signs of aortic insufficiency are related to the high pulse
pressure and the rapid decrease in blood pressure during diastole
due to the AI:
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Lighthouse sign (blanching & flushing of forehead)
de Musset's sign (head nodding in time with the heart beat)
Ladolfi's sign (alternating constriction & dilatation of pupil)
Becker's sign (pulsations of retinal vessels)
Müller's sign (pulsations of uvula)
Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
(Watson's) Water-hammer pulse
Quincke's sign (pulsation of the capillary bed in the nail)
Mayen's sign (diastolic drop of BP>15 mm Hg with arm raised)
Rosenbach's sign (pulsatile liver)
Gerhardt's sign (enlarged spleen)
Duroziez's sign (systolic and diastolic murmurs heard over the femoral artery when it is gradually compressed)
Hill's sign (A ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures, seen in chronic severe AI)
Traube's sign (a double sound heard over the femoral artery when it is compressed distally)
Lincoln sign (pulsatile popliteal)
Sherman sign (dorsalis pedis pulse is quickly located & unexpectedly prominent in age>75 yr)