1 What are the main components of the cardiovascular physical examination?

These five components have been compared to the fingers of a hand, insofar as they are all needed to grab a diagnosis. Cardiac exam also could be compared to the evaluation of a pump, starting with the feeding and exit pipes and ultimately focusing on the pump itself: using your eyes (inspection of the PMI), your touch (palpation of the PMI), and your ears. Auscultation, the queen of cardiovascular examination, is in fact the longest (and largest) of these metaphoric fingers, and thus capable of reaching the farthest. Still, physical examination is only one of five more general components of the cardiovascular assessment. The other four are:

2 What aspects of general appearance should be observed in evaluating cardiac patients?

As suggested by Perloff, one should sequentially evaluate the following nine areas:

See Tables 10-1 and 10-2.

Table 10-1 Diagnostic Clues: Body and Facies, Gestures and Gait, Face and Ears

Body Appearance and Facies

The anasarca of congestive heart failure

The struggling, anguished, frightened, orthopneic, and diaphoretic look of pulmonary edema

The tall stature, long extremities (with arm span exceeding patient’s height), and sparse subcutaneous fat of Marfan’s syndrome (mitral valve prolapse, aortic dilation, and dissection)

The long extremities, kyphoscoliosis, and pectus carinatum of homocystinuria (arterial thrombosis)

The tall stature and long extremities of Klinefelter’s syndrome (atrial or ventricular septal defects, patent ductus arteriosus, and even tetralogy of Fallot)

The tall stature and thick extremities of acromegaly (hypertension, cardiomyopathy, and conduction defects)

The short stature, webbed neck, low hairline, small chin, wide-set nipples, and sexual infantilism of Turner’s syndrome (coarctation of the aorta and valvular pulmonic stenosis)

The dwarfism and polydactyly of Ellis-van Creveld syndrome (atrial septal defects and common atrium)

The morbid obesity and somnolence of obstructive sleep apnea (hypoventilation, pulmonary hypertension, and cor pulmonale)

The truncal obesity, thin extremities, moon face, and buffalo hump of hypertensive patients with Cushing’s syndrome

The mesomorphic, overweight, balding, hairy, and tense middle-aged patient with coronary artery disease

The hammer toes and pes cavus of Friedreich’s ataxia (hypertrophic cardiomyopathy, angina, and sick sinus syndrome)

The straight lower back of ankylosing spondylitis (aortic regurgitation and complete heart block)

Gestures, Gait, and Stance

The Levine’s sign (clenched fist over the chest of patients with an acute myocardial infarction)

The preferential squatting of tetralogy of Fallot

The ataxic gait of tertiary syphilis (associated with aortic aneurysm and regurgitation)

The waddling gait, lumbar lordosis, and calves pseudohypertrophy of Duchenne’s muscular dystrophy (associated with hypertrophic cardiomyopathy and a pseudo infarction pattern on ECG)

Face and Ears

Pulsatility of the earlobes (tricuspid regurgitation)

Head bobbing (De Musset’s and Lincoln’s signs)

The round and chubby face of congenital pulmonary stenosis

The hypertelorism, pigmented moles, webbed neck, and low-set ears of Turner’s syndrome

The round and chubby face of congenital valvular pulmonic stenosis

The elfin face (small chin, malformed teeth, wide-set eyes, patulous lips, baggy cheeks, blunt and upturned nose) of congenital stenosis of the pulmonary arteries and supravalvular aortic stenosis—often associated with hypercalcemia and mental retardation.

The unilateral lower facial weakness of infants with cardiofacial syndrome—this can be encountered in 5–10% of infants with congenital heart disease (usually ventricular septal defect); often noticeable only during crying.

The premature aging of Werner’s syndrome and progeria (associated with premature coronary artery and systemic atherosclerotic disease)

The drooping eyelids, expressionless face, receding hairline, and bilateral cataracts of Steinert’s disease (myotonic dystrophy, associated with conduction disorders, mitral valve prolapse)

The epicanthic fold, protruding tongue, small ears, short nose, and flat bridge of Down syndrome (endocardial cushion defects)

The dry and brittle hair, loss of lateral eyebrows, puffy eyelids, apathetic face, protruding tongue, thick and sallow skin of myxedema (associated with pericardial and coronary artery disease)

The macroglossia not only of Down syndrome and myxedema, but also of amyloidosis (linked to restrictive cardiomyopathy, congestive heart failure)

The paroxysmal facial and neck flushing of carcinoid syndrome (with pulmonic stenosis and tricuspid stenosis/regurgitation)

The saddle-shaped nose of polychondritis (associated with aortic aneurysm)

The tightening of skin and mouth, scattered telangiectasias, and hyperpigmentation/hypopigmentation of scleroderma (with pulmonary hypertension, pericarditis, and myocarditis)

The flushed cheeks and cyanotic lips of mitral stenosis (acrocyanosis)

The gargoylism of Hurler’s syndrome (associated with mitral and/or aortic disease)

The short palpebral fissures, small upper lip, and hypoplastic mandible of fetal alcohol syndrome (associated with atrial or ventricular septal defects)

The diagonal earlobe crease as a (questionable) marker of coronary artery disease (earlobe sign [also known as Frank’s sign])

Table 10-2 Diagnostic Clues: Eyes, Extremities, Skin, Thorax, and Abdomen

Eyes

Xanthelasmhas of dyslipidemia and coronary artery disease (CAD)

The enlarged lacrimal glands of sarcoidosis (restrictive cardiomyopathy, conduction defects, and, possibly, cor pulmonale)

The cataracts and deafness of “rubella syndrome” (patent ductus arteriosus [PDA] or stenosis of the pulmonary artery)

The stare and proptosis of increased central venous pressure The lid lag, stare, and exophthalmos of hyperthyroidism (tachyarrhythmias, angina, and high output failure)

The conjunctival petechiae of endocarditis

The conjunctivitis of Reiter’s disease (pericarditis, aortic regurgitation, and prolongation of the P-R interval)

The blue sclerae of osteogenesis imperfecta (aortic regurgitation)

The icteric sclerae of cirrhosis

The Brushfield’s spots (small white spots on the periphery of the iris, usually crescentic and with an outward concavity, frequently but not exclusively seen in Down syndrome—endocardial cushion defects)

The fissuring of the iris (coloboma) of total anomalous pulmonary venous return

The dislocated lens of Marfan’s syndrome

The retinal changes of hypertension and diabetes (CAD and congestive heart failure)

The Roth spots of bacterial endocarditis

Extremities

The cyanosis and clubbing of “central mixing” (right-to-left shunts, pulmonary arteriovenous fistulas, and drainage of the inferior vena cava into left atrium)

The differential cyanosis and clubbing of PDA with pulmonary hypertension (the reversed shunt limits cyanosis and clubbing to the feet, but spares hands)

The “reversed” differential cyanosis and clubbing of transposition (aorta originating from the right ventricle): hands are cyanotic and clubbed, but feet are normal

The sudden pallor, pain, and coldness of peripheral embolization

Osler’s nodes (swollen, tender, raised, pea-sized lesion of finger pads, palms, and soles) and Janeway lesions (small, nontender, erythematous or hemorrhagic lesions of the palms or soles) of bacterial endocarditis

The clubbing, splinter hemorrhages of endocarditis

The Raynaud’s of scleroderma

The simian line of Down’s syndrome (atrial septal defect [ASD])

The hyperextensible joints of osteogenesis imperfecta (aortic regurgitation)

The nicotine finger stains of chain smokers (CAD)

The leg edema of congestive heart failure

The tightly tapered and contracted fingers of scleroderma, with ischemic ulcers and hypoplastic nails (often associated with pulmonary hypertension and myocardial disease, pericarditis, and valvulopathy)

The arachnodactyly, hyperextensible joints (especially knees, wrists, and fingers), and flat feet of Marfan’s syndrome (associated with aortic disease and regurgitation)

The ulnar deviation of rheumatoid arthritis (pericardial, valvular, or myocardial disease)

The mainline track lines of addicts (tricuspid regurgitation, septic emboli, and endocarditis)

The liver palms (thenar and hypothenar erythema) of chronic hepatic congestion

Skin

The jaundice or hepatic congestion

The cyanosis of right-to-left shunt

The pallor of anemia and high output failure

The bronzing of hemochromatosis (restrictive cardiomyopathy)

The telangiectasias of Rendu-Osler-Weber (at times associated with pulmonary arteriovenous fistulae)

The neurofibromas, café-au-lait spots, and axillary freckles (Crowe’s sign) of von Recklinghausen’s (pheochromocytomas)

The symmetric vitiligo (especially of the distal extremities) of hyperthyroidism

The butterfly rash of SLE (endo-myo- pericarditis)

The eyelid purplish discoloration of dermatomyositis (cardiomyopathy, heart block, and pericarditis)

The skin nodules and macules of sarcoidosis (cardiomyopathy and blocks)

The xanthomas of dyslipidemia

The hyperextensible skin (and joints) of Ehlers-Danlos (mitral valve prolapse)

The coarse and sallow skin of hypothyroidism

The skin nodules (sebaceous adenomas), shagreen patches, and periungual fibromas of tuberous sclerosis (rhabdomyomas of the heart and arrhythmias)

Thorax and Abdomen

The thoracic bulges of ventricular septal defect/ASD

The pectus carinatum, pectus excavatum, and kyphoscoliosis of Marfan’s syndrome

The akyphotic and straight back of mitral valve prolapse

The systolic (and rarely diastolic) murmurs of pectus carinatum, excavatum, straight back

The barrel chest of emphysema (cor pulmonale)

The shield chest of Turner’s syndrome

The cor pulmonale of severe kyphoscoliosis

The ascites of right-sided or biventricular failure

The hepatic pulsation of tricuspid regurgitation

The positive abdominojugular reflux of congestive heart failure

3 Which arteries should be examined during the evaluation of the arterial pulse?

It depends on what you are trying to evaluate. If you are simply assessing the presence of peripheral pulses, all accessible arteries should be examined. The following points are especially important:

Since this section focuses on the bedside examination of the arterial wave as part of the cardiovascular exam, we will exclusively discuss evaluation of central arteries. Assessment of peripheral vessels is discussed in Chapter 22, Extremities and Peripheral Vascular Exam, questions 1–25.

4 Isn’t the radial artery the most commonly used vessel for the evaluation of the pulse?

No—and if so, it shouldn’t be, since the radial artery is only suited for evaluation of pulse rate and rhythm, especially in fully clothed patients—a feature that made it quite popular in the prudish Victorian times of Dr. MacKenzie. Conversely, the radial artery is not suited for evaluation of the wave contour, which requires a vessel large and central enough to retain most of the original characteristics of the aortic waveform. For that, the optimal choice is a carotid, brachial, or femoral artery, because amplitude and upstroke can only be appreciated in large central arteries (such as carotids and brachials), being otherwise missed in small peripheral arteries, like the radials. In fact, some findings (like the bifid pulse of hypertrophic obstructive cardiomyopathy [HOCM]) can only be appreciated on arterial tracing.

5 What alterations occur in peripheral arteries?

The major ones are an increase in amplitude and upstroke velocity. As the distance from the aortic valve increases, the primary percussion wave that is transmitted downward along the aorta begins to merge with the secondary waves that reverberate back from more peripheral arteries. This fusion leads to greater amplitude and upstroke velocity in peripheral as compared to central arteries (Fig. 10-1). This phenomenon is similar to that occurring at the shoreline, where waves tend to be taller. It is also the mechanism behind Hill’s sign, the higher indirect systolic pressure of lower extremities as compared to upper extremities (see Chapter 2, Vital Signs, questions 110–115).

Figure 10-1 Arterial pulse contour alteration in the peripheral circulation. As the distance increases from the peripheral artery to the central aorta, the amplitude and upstroke velocity of the pulse contour also increase and the dicrotic notch becomes lower. The higher systolic pressure in peripheral arteries is another reason why the arterial pulse is best evaluated at the carotid artery rather than distally.

(Adapted from Abrams J: Essentials of Cardiac Physical Diagnosis. Baltimore, Williams & Wilkins, 1987.)

6 Are there any findings that are better evaluated in peripheral rather than central arteries?

Pulsus paradoxus and pulsus alternans. Both are best felt over smaller arteries (such as the radial), since the greater amplitude produced by these vessels magnifies the subtle arterial findings of both paradoxus and alternans. Yet, the contour of the arterial pulse should not be examined in peripheral vessels, since the normal alterations in amplitude and upstroke of these arteries might make the pulse of aortic stenosis inappropriately (and misleadingly) brisk.

7 What alterations result from decreased arterial compliance?

The same encountered in peripheral arteries: stiffer vessels conduct the waveform with greater velocity, giving the pulse higher amplitude and brisker upstroke, even though stroke volume might be weak and diminished (as in aortic stenosis). Hence, the arterial pulse of hypertensive, atherosclerotic, and older patients is less reliable for detecting left ventricular outflow obstruction.

8 What about vasoconstricted arteries?

Highly constricted arteries may also have a diminished pulse, even when stroke volume is normal or increased.

9 What is the best technique for evaluating the arterial pulse in carotid arteries?

First, inspect the carotids in the upper triangular spaces, medial to the sternocleidomastoids. Look for the visible and abnormal pulsations of aortic regurgitation. Then listen over the vessel to rule out bruits. If negative, apply the thumb or index finger over the carotids, one vessel at a time. Vary pressure for optimal evaluation of pulse characteristics (especially amplitude and contour). Remember that light pressure is often more valuable. As always, practice and experience are crucial.

10 What is the best technique for evaluating the arterial pulse in brachial arteries?

First, use the fingers of your left hand to palpate the radial artery of the patient’s right arm. Then, use the thumb of your right hand to compress the patient’s brachial artery until the radial pulse is completely obliterated. At this point, release very gently the pressure over the brachial artery until you feel the radial pulse again. Your thumb has now become like a “poor man’s” transducer, allowing you to feel both amplitude and contour of the brachial pulse.

11 What should you evaluate when examining the arterial pulse?

You should evaluate the upstroke, the peak, and the downstroke of the waveform. More specifically, you should focus on the following eight characteristics:

12 What are the characteristics of a normal arterial pulse?

A normal arterial pulse comprises a primary (systolic) and a secondary (diastolic) wave. These are separated by a dicrotic notch (dikrotos, double-beating in Greek), which corresponds to the closure of the semilunar valves (S₂) (see Fig. 10-2).

Figure 10-2 Normal arterial pulse. Note the rapid upstroke, the rounded summit or peak, and the falloff in late systole.

(Adapted from Abrams J: Essentials of Cardiac Physical Diagnosis. Baltimore, Williams & Wilkins, 1987.)

13 Are both the primary and secondary waves palpable?

No. Neither the dicrotic notch nor the secondary wave is normally felt, only the primary wave. Yet, in certain pathologic conditions, a double-peaked pulse may indeed become palpable. Yet in these cases, the two spikes are usually systolic. More rarely, the second spike coincides with diastole.

14 How are primary and secondary waves generated?

15 What is the significance of a normal rate of rise of the arterial pulse?

It argues against the presence of significant aortic stenosis (AS), but only in the young (elderly patients may have spuriously brisk pulses—previously discussed). Hence, a normal rate of rise can be useful in evaluating a benign systolic ejection murmur.

16 What is the meaning of a slow rate of rise of the arterial pulse?

A pulse that is reduced (parvus) and delayed (tardus) argues for aortic valvular stenosis. This also may be occasionally accompanied by a palpable thrill.

17 Is there any correlation between the slow rise of the arterial pulse and the severity of AS?

Yes. If ventricular function is good, a slower upstroke correlates with a higher transvalvular gradient. In left ventricular failure, however, parvus and tardus may occur even with mild AS.

18 How can you differentiate supravalvular from valvular aortic stenosis?

Supravalvular AS is associated with right-to-left asymmetry of the arterial pulse: the right brachial is normal while the left resembles the pulse of valvular AS (see Fig. 10-3). This is akin to aortic coarctation and underscores the importance of examining both pulses.

Figure 10-3 The brachial pulse in supravalvular stenosis (A). In the right brachial artery, the rate of rise is brisker and the pulse pressure greater because of an increase in systolic pressure. The left brachial arterial pulse resembles the valvular or discrete subvalvular stenosis (C). Normal (B) is shown for comparison.

(Adapted from Perloff JK: Physical Examination of the Heart and Circulation. Philadelphia, WB Saunders, 1990.)

19 And what about subvalvular stenosis?

In subvalvular stenosis of the hypertrophic variety (HOCM), the arterial pulse is usually brisk and with a double systolic impulse.

20 What is the significance of a brisk arterial upstroke?

It depends on whether it is associated with normal or widened pulse pressure. If associated with normal pulse pressure, a brisk upstroke usually indicates two conditions:

If associated with widened pulse pressure, a brisk upstroke indicates aortic regurgitation (AR). In contrast to MR, VSD, or HOCM, the AR pulse has rapid upstroke and collapse.

21 In addition to AR, which other processes cause rapid upstroke and widened pulse pressure?

The most common are the hyperkinetic heart syndromes (high output states). These include anemia, fever, exercise, thyrotoxicosis, pregnancy, cirrhosis, beriberi, Paget’s disease, arteriovenous fistulas, patent ductus arteriosus, aortic regurgitation, and anxiety—all typically associated with rapid ventricular contraction and low peripheral vascular resistance.

22 What is pulsus paradoxus?

It is an exaggerated fall in systolic blood pressure during quiet inspiration. In contrast to evaluation of arterial contour and amplitude, pulsus paradoxus is best detected in a peripheral vessel, such as the radial. Although palpable at times, optimal detection of the pulsus paradoxus usually requires a sphygmomanometer (see Chapter 2, Vital Signs, questions 85–103).

23 What is pulsus alternans?

It is the alternation of strong and weak arterial pulses, despite regular rate and rhythm. First described by Traube in 1872, pulsus alternans is often associated with alternation of strong and feeble heart sounds (auscultatory alternans). Both indicate severe left ventricular dysfunction (from ischemia, hypertension, or valvular cardiomyopathy), with worse ejection fraction and higher pulmonary capillary pressure. Hence, they are often associated with an S₃ gallop.

24 What is electrical alternans?

It’s a beat-to-beat alternation of tall and small QRS complexes, still within the realm of a regular heart rate. It may also present as beat-to-beat variation in the direction, amplitude, and duration of any other component of the ECG waveform, although the QRS is usually the predominant one. Undetectable on physical exam, it may coexist with mechanical alternans (which manifests itself through pulsus alternans). The clinical significance of electrical alternans is its association with large pericardial effusions, seen in 5–10% of patients with tamponade.

25 What is the best way to feel a pulsus alternans?

Not on the carotids. Like pulsus paradoxus, pulsus alternans is best assessed in peripheral arteries because smaller vessels tend to magnify those variations in volume and amplitude that are crucial for the detection of both findings. To feel a pulsus alternans, either palpate the radial artery at the wrist or use the blood pressure cuff at the arm (beat-to-beat fluctuations in arterial pulse are paralleled by beat-to-beat fluctuations in systolic blood pressure). Slowly deflate the cuff until you hear the first Korotkoff sounds. Notice that only the stronger ejections do indeed produce a sound. After further deflating the cuff, notice that the weaker ejections become detectable, too, causing in fact a doubling of Korotkoff sounds. The difference in systolic blood pressure between stronger and weaker ejections is usually 15–20   mmHg, not too dissimilar from that of pulsus paradoxus. Finally, ask the patient to take a deep breath, or suddenly assume an upright position. This also may help elicit pulsus alternans.

26 What is the mechanism of pulsus alternans?

There are two schools of thought: one based on contractility and the other on hemodynamics. The contractility school attributes the pulse-to-pulse variation to a beat-to-beat change in left ventricular diameter, which, in turn, leads to a cycling of weaker and stronger ejections through swings in the Starling curve position. The hemodynamic school attributes, instead, the variation in left ventricular ejection to a relative change in systolic and diastolic duration. Whenever ejection lengthens (because of increased left ventricular filling), diastole is proportionally shortened. This, in turn, leads to a shorter (and weaker) ejection during the following cycle, with a subsequent proportional increase in diastolic filling. This will then trigger a new cycle of stronger ejection and shorter diastole, with reinitiation of the seesaw.

27 Can pulsus alternans ever be normal?

It may be encountered in very rapid heart rates (for example, paroxysmal tachycardia), where it does not carry the same ominous implications.

28 What is total alternans?

It’s a pulsus alternans in which the weak pulse is too small to be detected so that the rate at the wrist is always half that at the apex.

29 What is a bigeminal pulse?

It is also a pulse in which beats occur in pairs (and with different strength), except that this time the rhythm is irregular, and the cause is a bigeminy.

30 What is a double-peaked pulse?

It is a pulse characterized by two palpable spikes per cycle (Fig. 10-4). The first peak always occurs in systole, whereas the second may instead occur during either systole (as part of the primary wave: pulsus bisferiens and bifid pulse) or diastole (as part of the secondary wave: dicrotic pulse).

Figure 10-4 Double-peaked arterial pulses. A, Bisferiens pulse, commonly found in severe aortic regurgitation or mild aortic stenosis with moderate aortic regurgitation. B, “Spike and dome” arterial pulse of hypertrophic cardiomyopathy or idiopathic hypertrophic subaortic stenosis. This unusual contour is recordable but not readily palpable. C, Dicrotic pulse. In this waveform, the second palpable component is a diastolic reflection wave.

(Adapted from Perloff JK: Physical Examination of the Heart and Circulation. Philadelphia, WB Saunders, 1990.)

31 Define pulsus bisferiens.

From the Latin bis (twice) and ferio (to strike [i.e., a “double-strike”]), pulsus bisferiens is an arterial pulse with two palpable systolic peaks of equal strength. First described by Galen, it has a large amplitude and quick upstroke/downstroke.

32 What is the best way to detect a pulsus bisferiens?

Through light but firm compression of a large central artery, best if done by using the thumb and slightly elevating the patient’s arm. Too strong of a compression may actually miss it. A pulsus bisferiens also can be detected by blood pressure cuff, as a closely split Korotkoff sound.

33 What is the diagnostic significance of a pulsus bisferiens?

It usually reflects moderate to severe aortic regurgitation (with or without aortic stenosis), but can also occur in other high output states. In aortic regurgitation, however, the double pulse is not only palpable, but sometimes is even audible. For example, it can be detected as:

34 What is Duroziez’s double murmur?

It is a to-and-fro double murmur over a large central artery—usually the femoral, but also the brachial. It is elicited by applying gradual but firm compression with the stethoscope’s diaphragm. This produces not only a systolic murmur (which is normal), but also a diastolic one (which is instead pathologic, and typical of AR). Duroziez’s has 58–100% sensitivity and specificity for AR. False negatives may occur in mild disease, concomitant AS, inadequate ventricular filling (due to associated mitral stenosis), inadequate ventricular emptying (due to concomitant mitral regurgitation), or obstruction to waveform transmission (because of aortic coarctation). False positives may occur in all high-output conditions. In these disorders, the murmur is not to and fro, but continuous, like that of an arteriovenous fistula. Moreover, the double murmur of high-output states is usually caused by forward flow, whereas in AR only one murmur is due to forward flow; the other is caused instead by reverse flow. The two can be easily separated by applying pressure first on the more cephalad edge of the diaphragm (which enhances the murmur of forward flow), and then on its more caudad end (which enhances the reverse flow murmur). This allows identification not only of AR but also of patent ductus arteriosus, the only other high-output state characterized by both forward and reverse flow.

35 Who was Duroziez?

A colleague and friend of Charcot. Paul L. Duroziez (1826–1897) had a general medical practice in Paris, but no official academic appointment. After serving as a surgeon during the Franco–Prussian war of 1870, he became president of the French Society of Medicine and Chevalier of the Legion of Honor. He described his homonymous finding at age 35, in 1861.

36 What is the usefulness of all these auscultatory findings?

More historical than clinical, although the intensity of femoral pistol shot sounds does indeed correlate with height of pulse pressure. Yet, neither Traube nor Duroziez predicts AR severity.

37 What is the mechanism of pulsus bisferiens?

Not clear. One theory explains the trough between the two peaks as a result of the Venturi effect caused by rapid blood flow. This would pull inward the aortic walls and trigger a transient arrest in flow—which, in turn, would stop the Bernoulli effect, restart the flow, and thus lead to the secondary peak.

38 What is the prognostic value of a pulsus bisferiens?

It indicates a very large stroke volume. Hence, it may disappear with left ventricular dysfunction.

39 What is a bifid pulse?

It is the classic pulse of HOCM. In contrast to bisferiens, the bifid pulse (from the Latin bifidus, cleft) is not detectable at the bedside, unless there is severe outflow obstruction. In fact, most HOCM patients have a normal carotid pulse, with its bifid nature only appearing on tracings (where it presents as a spike and dome pattern).

40 What is the mechanism of the bifid pulse?

It is a very rapid, early systolic emptying of the ventricle (causing the first brisk peak), followed by an obstruction, and then by another emptying (causing the second peak).

41 What is a dicrotic pulse?

It is also a double-peaked pulse (from the Greek di, two, and krotos, beat), except that in this case the additional impulse originates in diastole, as an accentuation of the secondary (or dicrotic) wave. Although the secondary wave is normally seen only on arterial recordings, the dicrotic pulse can actually be felt—usually over the carotids. It is probably due to a rebound of blood against the closed aortic valve, causing a secondary elastic wave. Since this “rebound” requires very elastic arteries, it can only be felt in young patients—and never above the age of 45. The dicrotic pulse is the least common of all the double-peaked pulses, easily separated from bifid and bisferiens because of its diastolic timing and longer interval between peaks.