Arterial Pulse

Assessing the Pulses

The examiner uses tactile receptors in the tips of the fingers to sense movement of the arterial wall associated with the pressure pulse as it passes the site of palpation. Measurements in the proximal aorta show cyclic movement in both diameter and length proportional to the pulse pressure. In more peripheral arteries with connective tissue attachments, however, the detectable movement is small and variable, with radial expansion by only approximately 2% of the end-diastolic cross-sectional area.

The usual technique for palpating the arterial pulse is to press with the examining fingers until the maximum pulse is sensed. The pulse is felt as changing displacement superimposed on the baseline displacement produced by compressing the artery. The examiner should apply varying degrees of pressure while concentrating on the separate phases of the pulse wave. This method, referred to as trisection, is useful for assessing the upstroke, systolic peak, and diastolic slope of the arterial pulse.

Readily palpable pulses in healthy individuals include the brachial, radial, and ulnar arteries of the upper extremities and the femoral, popliteal, dorsalis pedis, and posterior tibial arteries of the lower extremities. The aorta also can be palpated in thin people.

The carotid pulse is usually best examined with the sternocleidomastoid muscles relaxed and the head rotated slightly toward the examiner. The carotid pulse can be timed from the first heart sound, which is heard slightly before the pulsation. The carotid pulse should be palpated in the lower half of the patient's neck to avoid carotid sinus compression.

Normally, the incident (or percussion wave) begins with systolic ejection (just after S₁) and is the predominant monophasic pulse appreciated at the bedside. The incisura or dicrotic notch signifies aortic valve closure (Fig. 2).

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Fig. 2 Normal pulse. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 2 Normal pulse. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

The carotid artery pulse wave occurs within 40 milliseconds of the ascending aortic pulse and reflects aortic valve and ascending aortic function. The aortic pulse is best appreciated in the epigastrium (abdominal aorta). The temporal arteries can be easily palpated and aid in the diagnosis of temporal arteritis or polymyalgia rheumatica. One of the two pedal pulses may not be palpable in a normal patient because of unusual anatomy (posterior tibial, < 5%; dorsal pedis, < 10%), but each pair should be symmetric. True congenital absence of a pulse is rare (< 2%), and in most cases, pulses can be obtained with a handheld Doppler device when not palpable.

The grading of the pulse are:

• Complete absence of pulsation

• Small or reduced pulsation

• Normal or average pulsation

• Large or bounding pulsation

Simultaneous Palpation of Pulse in the Upper and Lower Extremities

Brachial pulses should be palpated simultaneously as well.7

• If there is a delay between the upper and lower extremity pulses or absence of femoral pulsations, coarctation of the aorta should be considered.

• Absent or weak pulses in the arm may result from

  • Previous subclavian flap repair of a coarctation of the aorta

  • Systemic-to-pulmonary artery shunts (i.e., classic Blalock-Taussig shunt)

• Bounding pulses reflect aortic runoff as in aortic regurgitation (AR), patent ductus arteriosus (PDA), or hyperkinetic states such as fever, anemia, and thyrotoxicosis, or in pathologic states such as severe bradycardia, AR, arteriovenous fistula (AVF) or arteriovenous malformations (AVMs).

• Diminished pulses are ominous in children and may suggest cardiac failure or shock.

The contour of the pulses depends on

• The stroke volume

• Ejection velocity

• Vascular capacity and compliance

• Systemic resistance

The palpable pulse reflects the merging of both the ante-grade pulsatile flow of blood and reflection of the propagated pulse returning from the peripheral arteries. The arterial pulse upstroke increases with distance from the heart.

Normal Contour of Pulse (Normal Arterial Pulse)

The normal carotid pulse has a smooth, rapid upstroke or ascending limb to a smooth, dome-shaped summit. Then a downstroke occurs that is somewhat less rapid than the upstroke. The dicrotic notch and secondary diastolic wave are usually not felt but can be palpable in some normal individuals, particularly during fever, exercise, or excitement. The dicrotic notch usually occurs approximately 300 milliseconds after the onset of the pulse wave when corrected for heart rate.

Graphic recordings of the arterial pulses frequently show two positive deflections during systole, the first shoulder being referred to as the percussion wave and the second as the tidal wave. In the normal proximal aortic pulse, the percussion wave is caused by arrival of the impulse generated by LV ejection, the tidal wave can represent its echo from the upper part of the body, and the dicrotic or diastolic wave is a reflection from the lower part of the body.

Amplitude of Pulse

Because peripheral pulse contour is determined by LV ejection and vascular properties, emphasis is placed on the presence or absence of a pulse and on hypokinetic or hyperkinetic pulses.

Regular Pulse

Bisferiens Pulse

The bisferiens (from the Latin twice beating) pulse has a waveform characterized by two positive waves during systole. The pulse wave upstroke rises rapidly and forcefully, producing the first systolic peak (percussion wave). A brief decline in pressure is followed by a smaller and somewhat slower-rising positive pulse wave (tidal wave). Abnormalities of LV ejection and reflected waves from peripheral arteries contribute to the prominence of the second systolic wave in the bisferiens pulse. The bisferiens pulse is sometimes more easily palpable in a brachial or radial artery. The bisferiens pulse can be elicited by maneuvers that decrease the LV size or increase its contractility (Figs. 3, 4).

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Fig. 3 Bifid pulse with two systolic peaks. Example is severe aortic regurgitation. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 3 Bifid pulse with two systolic peaks. Example is severe aortic regurgitation. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 4 Bifid pulse with two systolic peaks. The second peak (tidal or reflected wave) is of lower amplitude than the initial percussion wave. Example is hypertrophic obstructive cardiomyopathy (HOCM). A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 4 Bifid pulse with two systolic peaks. The second peak (tidal or reflected wave) is of lower amplitude than the initial percussion wave. Example is hypertrophic obstructive cardiomyopathy (HOCM). A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

Bisferiens pulse occurs

• In patients with pure AR.

• When some AS accompanies the severe AR.

• Hypertrophic cardiomyopathy (HCM): Many of whom have a pressure gradient in the LV outflow tract. The midsystolic negative wave usually coincides with a marked decrease in the rate of LV ejection. The second systolic wave, or tidal wave, is most likely produced by reflected waves from the periphery. A physical finding nearly specific for HCM is a much smaller arterial pressure pulse in the cardiac cycle following a premature ventricular beat.

Dicrotic Arterial Pulse

The dicrotic (from the Greek dikrotos, “double beating”) pulse is a twice-peaked pulse with one peak in systole and the second in diastole, the latter caused by an accentuated and palpable dicrotic wave that follows the second heart sound. It is usually best felt in the carotids, although it also can be palpated over more peripheral arteries. Major abnormalities include a short systolic ejection phase, a low dicrotic notch, a large diastolic wave, a narrow pulse pressure, a diminished rate of rise in the pulse, and the lack of distinct percussion and tidal waves. Low cardiac output states can allow the systolic and diastolic pulses to become nearly equal and potentially palpable (Fig. 5).

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Fig. 5 Bifid pulse with systolic and diastolic peaks. Example is intra-aortic balloon counterpulsation. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 5 Bifid pulse with systolic and diastolic peaks. Example is intra-aortic balloon counterpulsation. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

Causes of dicrotic pulse are

• Low cardiac output states

• Patient with fever or after exercise in a normal individual and is consistent with increased vascular compliance

• Pulse is intra-aortic balloon counterpulsation

Pulsus Parvus Et Tardus

Severe AS may be suggested by an arterial pulse that is small and has a delayed systolic peak. Occasionally, there can be a detectable shoulder on the upstroke of the carotid pulse, referred to as anacrotic. Palpable coarse vibrations are often present as a systolic thrill over the slowly rising carotid pulse. The parvus et tardus pulse is much easier to detect in the carotid arteries than in more distal arteries (Fig. 6).

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Fig. 6 Anacrotic pulse with slow upstroke and peak near S₂. Example is aortic stenosis. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

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Fig. 6 Anacrotic pulse with slow upstroke and peak near S₂. Example is aortic stenosis. A₂, aortic component of S₂; P₂, pulmonic component of S₂; S₁, first heart sound; S₂, second heart sound; S₄, fourth heart sound.

Most middle-aged patients with uncomplicated severe AS have a parvus et tardus pulse, but this pulse can also occur in relatively mild stenosis. Conversely, an apparently normal arterial pulse is not unusual in elderly patients with severe AS who have decreased distensibility of the large arteries. Severe LV failure often results in a small, weak pulse that can be difficult to distinguish from that of AS. Carotid-apical delay is assessed during simultaneous auscultation of the heart sounds; the carotid upstroke should be coincident with S₁. This finding is less accurate in older hypertensive patients with reduced vascular compliance and stiffer carotid arteries.

Pulsus Alternans

Pulsus alternans is defined by the beat-to-beat variability of the pulse amplitude. It is present when only every other phase 1 Korotkoff sound is audible as the cuff pressure is slowly lowered, in a patient with a regular heart rhythm, independent of the respiratory cycle. These amplitude changes will be emphasized in a peripheral artery and may be easiest to detect in the femoral pulse, which normally has a slightly wider pulse pressure than the carotid artery. The patient's respiration should be held because the small changes in arterial pressure caused by normal respiration can obscure the recognition of pulsus alternans. Pulsus alternans can be confirmed by using a sphygmomanometer and is usually associated with an LV third heart sound.

In pulsus alternans, beats occur at regular intervals with a regular alternation of the systolic height of the pressure pulses. Rarely, pulsus alternans is so marked that the weaker pulses are not felt at all. When pulsus alternans is noticed first after a premature beat, the extent of the difference in systolic pressure in alternating beats can decline for several cycles until the pulse amplitude is again constant. The initiation of post-premature ventricular beat pulsus alternans is probably related to the increased duration of LV filling after the premature beat.

Sustained pulsus alternans is seen in severe depression of LV performance. Sustained pulsus alternans is likely caused by alteration of the contractile state of at least part of the myocardium, which can be caused by the failure of electromechanical coupling in some cells during the weaker contraction. A subsequent stronger contraction would then represent contraction of all cells, some of which were potentiated (Fig. 7).

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Fig. 7 Pulsus alternans.

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Fig. 7 Pulsus alternans.

Pulsus alternans is generally seen in

• Pulsus alternans is generally seen in severe heart failure.

• It is exaggerated in severe AR, hypertension, and hypovolemic states.

• It can also occur for several beats after supraventricular tachycardia in normal persons or when the respiratory rate is half the pulse rate.

It is attributed to cyclic changes in intracellular calcium levels and action potential duration. Association with electrocardiographic T-wave alternans appears to increase arrhythmic risk.

Irregular Pulse

An irregular pulse can be caused by

• AF

• Premature beats arising in the atria, atrioventricular junction, or ventricles

• Second-degree atrioventricular block

Premature complexes are among the most common causes of an irregular pulse.10 AF causes an irregularly, irregular pulse. Not only will the rate of the pulse be irregular, but the pulse amplitude will also vary. This results from variable stroke volumes during systole. Short R-R intervals during AF do not allow adequate time for LV diastolic filling, resulting in a low stroke volume and the absence of palpable peripheral pulse. This results in a “pulse deficit,” during which the peripheral pulse is not as rapid as the apical rate.10 Post extrasystolic potentiation contributes to the beat-to-beat variability of the pulse in AF. Simultaneous auscultation of the heart and palpation of the radial pulse can allow measurements of an apical to radial pulse deficit. Controlled AF should have no pulse deficit; that is, all central heartbeats are transmitted to the radial pulse and the peripheral circulation. Premature beats of any origin can cause irregularities of the pulse. If the premature beats alternate with normal sinus beats, bigeminy results. The results can be a pulse beat that has a strong, large-amplitude pulse (hyperkinetic) alternating with a weak, low-amplitude pulse (hypokinetic). Irregularities of the pulse rate or rhythm require an ECG for final diagnosis of the cardiac arrhythmia.11 12

Congenital Heart Disease

The Closing Ductus Physiology Like in Hypoplastic Left-Sided Herat Syndrome

A sudden deterioration takes place with rapidly progressive congestive failure and shock as the ductus arteriosus constricts. There are decreased systemic blood flow (SBF) and increased pulmonary blood flow (PBF), which are largely independent of the pulmonary vascular resistance (PVR). The peripheral pulses are weak to absent.17

Coarctation of Aorta

The hallmark physical findings in coarctation consist of discrepant arterial pulses and systolic blood pressures in the upper and lower extremities. Arterial pulses below the coarctation are diminished in amplitude and delayed in timing compared with the proximal pulses. Systolic blood pressure is elevated proximal to the coarctation, and a systolic pressure gradient is present between the arm and leg.

Several clinical circumstances may make detection of pulse and pressure discrepancies difficult.

• The coarctation pressure gradient may be minimal, sometimes as a result of a mild coarctation, but also in an infant with heart failure and diminished cardiac output or with a large PDA. Descending aorta flow may be maintained by a right-to-left ductal shunt, and in the presence of a large ventricular septal defect, the perfusion may be well oxygenated and pulsatile.

• Detection of arterial pulse and pressure differences may be difficult because of variations in brachiocephalic artery anatomy.

  • An anomalous right subclavian artery arises distal to the coarctation in approximately 3 to 4% of cases. In these patients, the arterial pulse and blood pressure are identical in the right arm and leg, and discrepancies are detected only in the left arm.

  • In other patients, the left subclavian artery arises adjacent to the coarctation, and its orifice may be stenotic. In such patients, a bounding arterial pulse and elevated systolic pressure will be detected only in the right arm.

  • Rarely, patients may present with an anomalous right subclavian artery and a stenotic left subclavian artery. In these patients, arterial differences in the four extremities will not be detected, although carotid artery pulsations will be bounding.18

• Associated significant AR coexists.

Aortic Arch Interruption

Absent upper and lower limb pulses, with a palpable superficial temporal pulse, are a helpful clue to the diagnosis.19

Hypoplastic Left-Sided Heart Syndrome

The upper and lower extremity pulses are palpable and symmetric early but are reduced later as ductal closure ensues.20

Tetralogy of Fallot

Arterial pulses will be normal in uncomplicated tetralogy of Fallot (TOF).

The pulse pressure may be widened reflecting arterial diastolic runoff in the presence of21

• Aortopulmonary collaterals

• Palliative surgical shunt

• PDA

Tricuspid Atresia

Peripheral pulses are normal except when associated with coarctation of the aorta.

Uhl's Anomaly

In Uhl's anomaly, at physical examination, along with cyanosis, hepatomegaly, jugular venous distension with a dominant a wave, the quiet precordium, and peripheral pulses often are diminished in amplitude.22

Left Ventricular Inflow Obstruction

Decreased pulse volume due to congestive cardiac failure (CCF).

Pulmonary Atresia with Intact Ventricular Septal Defect

The peripheral pulses and blood pressure usually are normal in the neonatal period, even with a PDA, because the runoff into the lungs is not excessive during the first few weeks of life. In cyanotic patients, the pulses are normal. However, in patients beyond the first 4 to 6 weeks of age in whom PBF through a PDA, collaterals, or surgically created shunt is substantial, the pulses are bounding and only minimal cyanosis may be present.23

Truncus Arteriosus

The peripheral pulses are accentuated and may be bounding if truncal valve regurgitation is there, if not then normal pulse. The pulse pressure usually is increased owing to runoff into the pulmonary vascular bed during diastole.24

Transposition of the Great Arteries

A large, persistent PDA can modify the clinical findings in the neonate with transposition of the great arteries/intact ventricular septum (TGA/IVS) because a large intercirculatory shunt may be present. Characteristically, these infants present quite early with prominent tachypnea and relatively slight cyanosis. Importantly, the classic signs indicative of a large PDA, such as continuous murmur, bounding pulses, and a prominent mid-diastolic rumble, are present in fewer than half of this group.25

Congenital Anomalies of the Aortic Root

Aortic-LV defect (tunnel) and aneurysm of sinus of Valsalva: Many of patients with aortic-LV defect present in infancy with CHF. They have signs resembling marked aortic incompetence—a wide pulse pressure with a low diastolic blood pressure, a hyperactive dilated LV and enlarged left atrium, and a loud to-and-fro murmur at the base.26

Aortic Arch Anomalies

Physical findings of pulse discrepancy, depending on branching pattern, are helpful only after restoration of satisfactory cardiac output. Absence of all limb pulses suggests interruption type B with anomalous subclavian artery, that is, both carotid arteries proximal and both subclavian arteries distal to the interruption. Strong carotid pulses help differentiate interrupted arch from critical AS in which all pulses are diminished.27

Left aortic arch with isolated subclavian artery: In many cases there may be no symptoms or simply absence of the right arm pulse.

Isolated brachiocephalic arteries: Cases of isolated brachiocephalic arteries may have diminished pulses or lower blood pressure in the affected artery. If the ductus remains patent, pulmonary artery steal can occur with flow down the vertebral artery through the ductus into the low-resistance pulmonary artery. The diagnosis should be suspected in any patient with right aortic arch and diminished pulse amplitude or blood pressure in the left arm.28

Cervical arches: In the presence of a pulsatile neck mass, a presumptive diagnosis can be made by notation of loss of femoral pulses during brief compression of the mass.29

Mitral stenosis

The arterial pulse is usually normal, but in patients with a reduced stroke volume, the pulse may be low in volume.

Mitral Regurgitation

Brisk arterial pulses are frequently present. Palpation of the arterial pulse is helpful in differentiating AS from MR, both of which may produce a prominent systolic murmur at the base of the heart and apex. The carotid arterial upstroke is sharp in severe MR and delayed in AS; the volume of the pulse may be normal or reduced in the presence of heart failure.30

Acute Severe Aortic Regurgitation

Patients with acute severe AR are tachycardic and tachypneic. Unlike the clinical examination found with significant chronic AR, the pulse pressure is often narrow and the pulses are not increased or bounding.31

Chronic Severe Aortic Regurgitation

On examination, significant chronic AR results in a wide pulse pressure (elevated systolic and low diastolic pressures) and bounding pulses. The water-hammer pulse in severe AR is named after a Victorian toy. In patients with chronic, severe AR, the head may bob with each heartbeat (de Musset's sign), and there are water hammer pulses, with abrupt distention and quick collapse (Corrigan's pulse). The arterial pulse is often prominent and can be best appreciated by palpation of the radial artery with the patient's arm elevated. A bisferiens pulse may be present and is more readily recognized in the brachial and femoral arteries than in the carotid arteries. A variety of auscultatory findings provide confirmation of a wide pulse pressure. Traube's sign (a.k.a. pistol shot sounds) refers to booming systolic and diastolic sounds heard over the femoral artery, Müller's sign consists of systolic pulsations of the uvula, and Duroziez's sign consists of a systolic murmur heard over the femoral artery when it is compressed proximally and a diastolic murmur when it is compressed distally. Capillary pulsations (Quincke's sign) can be detected by transmitting a light through the patient's fingertips or exerting gentle pressure on the tip of a fingernail.30

Aortic Stenosis

With severe stenosis, the arterial pulse may be decreased, with a slow rate of rise. If there is associated AR, however, the pulses may be increased.

The carotid upstroke directly reflects the arterial pressure waveform. The expected finding with severe AS reveals a slow-rising, late-peaking, low-amplitude carotid pulse and the parvus and tardus carotid impulse. When present, this finding is specific for severe AS. However, many adults with AS have concurrent conditions, such as AR or systemic hypertension, that affect the arterial pressure curve and the carotid impulse. Thus, an apparently normal carotid impulse is not reliable for excluding the diagnosis of severe AS. With severe AS, radiation of the murmur to the carotids may result in a palpable thrill or carotid shudder.32

When the LV fails and stroke volume falls, the systolic murmur of AS becomes softer; rarely, it disappears altogether. The slow rise in the arterial pulse is more difficult to recognize. Stated simply, with LV failure, the clinical picture changes from typical AS to that of severe LV failure with a low cardiac output. Thus, occult AS may be a cause of intractable heart failure, and severe AS should be ruled out by echocardiography in patients with heart failure of unknown cause because operative treatment may be lifesaving and result in substantial clinical improvement.32

In more severe cases of neonatal AS, the left heart may not have the capacity to handle the entire cardiac output and closure of the ductus arteriosus may result in circulatory collapse. Such infants are pale and poorly perfused, with poor pulses, hepatomegaly, tachycardia, gallop rhythm, hyperdynamic right ventricular impulse, tachypnea with retractions, and usually but not always a systolic heart murmur.33

In supravalvular AS, the pulse in the right arm is frequently greater than that in the left arm because of Coanda's effect. This pulse disparity may relate to the tendency of a jet stream to adhere to a vessel wall (Coanda's effect) and selective streaming of blood into the innominate artery. Differences in upper extremity blood pressures and carotid artery pulses may also result from stenosis of the aortic arch branches.34

Cardiac Tamponade

The characteristic features of cardiac tamponade include low cardiac output, elevated central venous pressures, a paradoxical pulse, muffled or diminished heart sounds, and tachycardia.38

The second characteristic hemodynamic finding is the paradoxical pulse. In severe tamponade, the arterial pulse is impalpable during inspiration.

The mechanism of the paradoxical pulse is multifactorial, but respiratory changes in systemic venous return are certainly important. In tamponade, in contrast to constriction, the normal inspiratory increase in systemic venous return is retained. Therefore, the normal decline in systemic venous pressure on inspiration is present (and Kussmaul's sign is absent). The increase in right-sided heart filling occurs, once again, under conditions in which total heart volume is fixed and left-sided heart volume is markedly reduced to start. The interventricular septum shifts to the left in exaggerated fashion on inspiration, encroaching on the LV such that its stroke volume and pressure generation are further reduced. Although the inspiratory increase in right-sided heart volume (preload) causes an increase in right ventricular stroke volume, this requires several cardiac cycles to increase LV filling and stroke volume and to counteract the septal shift. Other factors that may contribute to the paradoxical pulse include increased afterload caused by transmission of negative intrathoracic pressure to the aorta and traction on the pericardium caused by descent of the diaphragm, which increases pericardial pressure. Associated with these mechanisms are the striking findings that left- and right-sided heart pressure and stroke volume variations are exaggerated and 180 degrees out of phase.

Cardiac tamponade without paradoxical pulse occurs

• When there are preexisting elevations in diastolic pressures or volume. Examples are patients with LV dysfunction, AR, and atrial septal defect.

• In patients with retrograde bleeding into the pericardial sac due to aortic dissection; tamponade can occur without a paradoxical pulse because of aortic valve disruption and regurgitation.39

Constrictive Pericarditis

Paradoxical pulse occurs in perhaps one-third of patients with constriction, especially when there is an effusive-constrictive picture.

Hemopericardium

These patients may also have the combination of acute volume overload due to disruption of the aortic valve and tamponade without a paradoxical pulse.40

Vascular Anomalies

Systemic AVMs or AVFs usually are associated with wide pulse pressure and bounding pulses. In the new-born period, congenital AVMs and AVFs may clinically resemble congenital heart defects (CHDs), leading to a delay in diagnosis. Diminished femoral pulses may mimic aortic coarctation.41 In contrast, in pulmonary AVM the arterial pulse is normal.42

Aortic Dissection

Absent pulses depend on the site and extending of dissection. The physical findings most typically associated with aortic dissection—pulse deficits, AR, and neurologic manifestations— are more characteristic of ascending than descending dissection. Pulse deficit was reported in 19% of type A and only 9% of type B dissections. Aortic dissection may extend into the iliac arteries and cause diminished femoral pulses (12%) and acute lower extremity ischemia. The pulse deficits may be intermittent because the intimal flap movement sporadically obstructs the arterial orifice or because of distal reentry of blood into the true lumen, which decompresses the false channel.43

Atheroembolism

Blue toe syndrome with presence of pedal pulses is typically present because the emboli tend to lodge in the more distal digital arteries and arterioles.44

Takayasu

During the active inflammatory pre-pulseless phase, the peripheral pulses and blood pressures may be normal, making diagnosis difficult. As the disease progresses into the chronic pulseless phase, there are additional symptoms and signs of absent or decreased brachial and radial pulses or carotid pulses with bruits over the cervical, supraclavicular, and abdominal regions.45

Pulse in Heart Failure

Physical findings of heart failure are45

• Tachycardia

• Extra beats or irregular rhythm

• Narrow pulse pressure or thready pulse

• Pulsus alternans

Pulse in Hypertension and Arteriosclerosis

In hypertension and arteriosclerosis, the pressure pulse amplitude is increased, the tidal wave is prominent, and the diastolic wave is absent. All features of the pulse can be explained by increased wave velocity. Reflected waves return to the proximal aorta during late systole, augmenting the tidal wave and increasing systolic pressure.

Chronic Kidney Disease (CKD) on Hemodialysis

Patients on chronic hemodialysis often have hyperdynamic pulses produced by the combination of a surgical AVF, anemia, and hypertension.

Pulse after Cardiac Catheterization

After removal of arterial sheath, just enough pressure is needed to prevent bleeding from the vessel, not necessarily completely occluding all flow through the vessel. While holding pressure, the pedal pulses should be palpated often to ensure adequate perfusion.

After a diagnostic catheterization, pulse loss is rare. Even in small infants, the use of a 3F pigtail catheter tapered to a 0.021-in wire should allow a safe retrograde arterial catheterization (although the catheter flow rate is low).

When loss of a pulse occurs, heparin is continuously infused until the pulse returns or for 12 to 24 hours. There is likely a component of arterial spasm, and heparin may prevent thrombus formation at the site of spasm. If the pulse does not return, treatment with streptokinase or tissue plasminogen activator (tPA) may be instituted unless contraindications are present.46

During Cardiopulmonary Resuscitation (CPR)

Palpation of either the femoral or carotid pulse is a method to know the adequacy of CPR compression.

Pulseless Electrical Activity

Pulseless electrical activity, formerly called electromechanical dissociation, is separated into primary and secondary forms. The common denominator in both is continued electrical rhythmicity of the heart in the absence of effective mechanical function. The secondary form includes the causes that result from an abrupt cessation of cardiac venous return, such as massive pulmonary embolism, acute malfunction of prosthetic valves, exsanguination, and cardiac tamponade from hemopericardium. Electrical mechanisms of cardiac arrest are divided into tachyarrhythmic and bradyarrhythmia-asystolic events.49

Patients who have a bradyarrhythmia or asystole, or pulseless electrical activity, at initial contact have the worst prognosis; only 9% of such patients in the Miami study were admitted to the hospital alive, and none was discharged.

Intermittent Loss of Pulses

• In cardiac tamponade: During inspiration pulse disappears.

• Cardiac herniation: One clue to the presence of cardiac herniation is sudden loss of pulse when the patient is repositioned, such as when moved to a stretcher.50

Pulse Rate as Component of Score for Prognostication

In pulmonary embolism: The Pulmonary Embolism Severity Index: PR > 110/min, then score is 20.51

Hypothyroidism

Mild degrees of bradycardia, diastolic hypertension, narrow pulse pressure and relatively quiet precordium, and decreased intensity of the apical impulse are all characteristic.