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.

42 What is the clinical significance of a dicrotic pulse?

It suggests low cardiac output and increased systemic vascular resistance, as in severe congestive cardiomyopathy or tamponade (especially during inspiration). Hence, it often coexists with pulsus alternans and gallop sounds. In these patients, the low cardiac output reduces the primary wave, thus increasing the likelihood of feeling the secondary one. In addition, a dicrotic pulse also has been reported in young healthy individuals as a result of fever.

43 What is a hypokinetic pulse?

From the Greek hypo (diminished) and kinesis (movement), this is a pulse of diminished amplitude. Causes include:

A small pulse is also called parvus (“small” in Latin), which usually presents as a slow upstroke (tardus, “delayed” in Latin). A reduced and delayed pulse (parvus and tardus) narrows significantly the differential diagnosis of a hypokinetic pulse, making AS more likely.

44 Is there any difference in sensitivity/specificify for tardus versus parvus?

A pulsus tardus is a better predictor of AS, with 30–90% sensitivity and even higher specificity. Instead, a pulse with small amplitude (parvus) but normal upstroke usually suggests decreased left ventricular contraction and/or filling. Hence, it argues for cardiomyopathy or mitral stenosis.

45 Can arterial characteristics modify a pulsus tardus?

Yes. The stiffer the vessel, the brisker the upstroke. That is why atherosclerosis may obliterate a pulsus tardus. And that is also why older AS patients may lack the typical arterial findings. This atherosclerosis-induced “acceleration” may even occur on central arteries.

46 Are there any other manifestations of arterial delay?

The apical–carotid and brachio–radial delay (respectively, a palpable delay between the apical and carotid impulse, and brachial and radial impulse). Both can occur in patients with valvular AS.

47 What is the carotid shudder?

It is a palpable thrill felt at the peak of the carotid pulse in patients with AS, AR, or both. It represents the transmission of the murmur to the artery and is a relatively specific but rather insensitive sign of aortic valvular disease (Fig. 10-5).

Figure 10-5 Carotid pulse tracing from a patient with significant valvular aortic stenosis. Note the delayed upstroke and shudder that represents the transmitted murmur.

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

48 What is an anacrotic pulse?

Another sign of AS. The pulse is not only small (parvus) and slow (tardus), but also has an anacrotic notch on its ascending limb. This is visible on arterial tracings but not palpable. Hence, it has little clinical relevance. The name derives from the Greek ana (upwards) and krotos (impulse), and refers to the upstroke (or ascending) limb of the arterial tracing. It is an abbreviation for “anadicrotic” (twice beating on the upstroke).

49 What is a hyperkinetic pulse?

A pulse with large amplitude and rapid upstroke (from the Greek hyper, large, and kinesis, motion). It is often referred to as pulsus celer (which is Latin for “fast”), to distinguish it from the slow and small pulse (tardus and parvus) of AS. The large volume of a hyperkinetic pulse reflects increased stroke volume, whereas the quick rise reflects increased velocity of contraction.

50 What are the causes of a hyperkinetic pulse?

Usually the high-output states (including AR), which are typically associated with a widening pulse pressure. Yet, a hyperkinetic pulse can also occur in mitral regurgitation or HOCM, but in this case the pulse pressure is normal. Finally, a hyperkinetic pulse may be felt in patients with decreased arterial compliance, like elderly individuals (especially if hypertensive).

51 What is Corrigan’s pulse?

It is one of the various names for the bounding and quickly collapsing pulse of aortic regurgitation. This is both visible and palpable. Another common term for it is “water hammer,” but also cannonball, collapsing, or pistol-shot pulse. Corrigan’s may be so brisk as to cause other typical findings, such as De Musset’s or Lincoln’s signs (see Chapter 1, questions 53 and 54).

52 Who was Corrigan?

Sir Dominic J. Corrigan (1802–1880) was an Irishman; in fact, the longest-serving president of the Irish College of Physicians, and a member of Parliament for the city of Dublin. He also was a personal physician to Queen Victoria. In 1832, he published a treatise titled “On Permanent Patency of the Mouth of the Aorta, or Inadequacy of the Aortic Valve,” in which he reported a series of observations on AR. He also reported the visible (not palpable) characteristics of his famous pulse. Still, a brisk arterial pulse had been described by De Vieussens 100 years before, but Corrigan was the first to make the correlation between this pulse and aortic regurgitation.

53 What is a water hammer?

A very popular Victorian toy. It consisted of a sealed test tube, partially filled with water or mercury, and all in a vacuum. Since solids and liquids fall at the same rate in a vacuum, the inversion of the tube caused the column of fluid to fall rather precipitously, hitting the glass with a brisk jolt. This made the Victorian children happy and the gadget almost as popular as today’s electronic gizmos. The comparison between the slapping impact of a water hammer and the brisk bounding pulse of AR was first made in 1844 by the English physician Thomas Watson. It remains part of medical lore today, long after the demise of its homonymous toy.

54 What is the best way to feel a Corrigan’s pulse?

By elevating the patient’s arm while at the same time feeling the radial artery at the wrist. Raising the arm higher than the heart reduces the intra-radial diastolic pressure, collapses the vessel, and thus facilitates the palpability of the subsequent systolic thrust.

55 What is a pulsus durus?

A pulse so hardened that it is difficult to compress (durus, hard in Latin). This is usually a finding of arteriosclerosis, which may be associated with Osler’s sign (see Chapter 2, questions 70–72).

56 Can the compressibility of the arterial pulse predict the systolic blood pressure?

Yes. To do so, palpate the radial artery with the fingers of your left hand, while at the same time compressing the brachial artery with the thumb of your right hand. Push on the brachial until you have obliterated the radial pulse. If this requires mild force, the blood pressure is probably around 120   mmHg or less. If it requires intermediate force, the blood pressure is 120–160   mmHg. Finally, if it requires high force, the blood pressure is probably above 160   mmHg.

57 How do you auscultate for carotid bruits?

By placing your bell on the neck in a quiet room and with a relaxed patient. Auscultate from just behind the upper end of the thyroid cartilage to immediately below the angle of the jaw.

58 What other findings can mimic a carotid bruit?

Most carotid bruits are heard in systole. Only a few are both systolic and diastolic. Why this is so is unclear. The major issue of a bruit, of course, is ruling out carotid artery stenosis.

59 What is the interobserver agreement on carotid bruits?

Quite good for detecting bruits, but only fair for evaluating their intensity, pitch, or duration.

60 Can carotid bruits occur in children?

Yes. In fact, they are present in 20% of children younger than 15 years of age.

61 And what about adults?

They occur in 1% of healthy adults. Still, prevalence and incidence increase with age. For example, prevalence of asymptomatic bruits rises from 2.3% between 45 and 54 years, to 8.2% above age 75. In fact, incidence of new bruits is 1% per year in adults ≥ 65—twice the rate of people aged 45–54. Finally, bruits are very common in high output states. In hemodialysis patients, they are often louder on the side of the A-V fistula, frequently associated with a subclavian bruit.

62 What is the significance of a carotid bruit in asymptomatic ambulatory patients?

It depends on the age. In a 50-year-old man, an asymptomatic carotid bruit is associated with increased incidence of both cerebrovascular and cardiovascular events, with average annual rates of stroke and transient ischemic attacks that are three times higher. This increased risk decreases sharply with age, becoming essentially nonexistent among people older than 75.

63 What is the significance of a carotid bruit in an asymptomatic preoperative patient?

It depends on the surgery. Asymptomatic preoperative bruits are rather common in the surgical population (10% of patients), a prevalence much higher than in the general population (4.4%). Yet, they do not necessarily predict increased risk of perioperative stroke, although they do predict transient postoperative dysfunction and behavioral abnormalities. Still, in patients undergoing by-pass heart surgery, the incidence of hemodynamically significant carotid artery stenosis is high (2.8–11.8%, with no correlation in the asymptomatic patient between presence of a bruit and severity of carotid disease). Risk of perioperative stroke is age related (1–3% in patients of all ages, but 3.8 times higher in those older than 70). Hence, detecting a bruit prior to coronary revascularization is ominous, and it mandates further diagnostic studies.

64 What is the correlation between symptomatic carotid bruit and high-grade stenosis?

It’s high. In fact, bruits presenting with transient ischemic attacks (TIAs) or minor strokes in the anterior circulation should be evaluated aggressively for the presence of high-grade (70–99%) carotid stenosis, since endarterectomy markedly decreases mortality and stroke rates. Still, while presence of a bruit significantly increases the likelihood of high-grade carotid stenosis, its absence doesn’t exclude disease. Moreover, a bruit heard over the bifurcation may reflect a narrowed external carotid artery and thus occur in angiographically normal or completely occluded internal carotids. Hence, surgical decisions should not be based on physical exam alone; imaging is mandatory.

65 What is the history behind the examination of neck veins?

The first report of venous pulsations goes back to the 17th century, when the Italian Giovanni Maria Lancisi (1654–1720) described a “systolic fluctuation of the external jugular vein” in a patient with tricuspid regurgitation (i.e., the large systolic jugular wave replacing the normal trough that is still referred to as the Lancisi’s sign—in these patients, also watch for earlobe pulsations, especially on the right side). In 1867, Pierre Carl Potain carefully described the jugular waveform in a paper titled “Movements and Sounds that Take Place in The Jugular Veins.” Forty years later, the Scottish Sir James MacKenzie published The Study of the Pulse, a seminal work, which summarized 20 years of clinical assessment of both venous and arterial pulsations, and established the jugular venous pulse as one of the essential elements of cardiovascular examination. It also contributed the standard waveform terminology (A, C, and V waves and X–Y descent) still used nowadays. Yet, it was only in the 1950s that the examination of the jugular venous pulse (and pressure) became a standard component of bedside assessment, thanks to the influence of the charismatic British physician Paul Wood.

66 What is the role of physical exam in assessing neck veins?

67 What is the central venous pressure (CVP)?

The pressure within the right atrium/superior vena cava system (i.e., the right ventricular filling pressure). As pulmonary capillary wedge pressure reflects left ventricular end-diastolic pressure (in the absence of mitral stenosis), so central venous pressure reflects right ventricular end-diastolic pressure (in the absence of tricuspid stenosis).

68 Which veins should be evaluated for assessing venous pulse and CVP?

Central veins, as much in direct communication with the right atrium as possible. The ideal one is therefore the internal jugular. Of course, as part of a comprehensive examination, all visible veins should be evaluated. Since this chapter focuses on the cardiovascular exam, we will limit our discussion to jugular waveform and central venous pressure. Evaluation of peripheral veins is covered in Chapter 22, The Extremities and Peripheral Vascular Exam, questions 41–62.

69 What is the clinical value of jugular venous distention and pulse?

It is a “poor man’s” monitor of right heart hemodynamics. More specifically:

70 How difficult is it to evaluate the jugular veins?

Quite difficult, especially in patients with very low CVP or short and fat necks. It is especially difficult during mechanical ventilation or situations characterized by wide respiratory swings in CVP (such as status asthmaticus, or respiratory distress of any etiology). In fact, critically ill patients offer the greatest challenge to the assessment of jugular venous pulse and pressure. In one intensive care unit study, jugular venous pulsations were adequate for examination in only 20% of the patients, and central venous pressure could be measured by physical exam in only one half of the cases. In another study, central venous pressure could be accurately determined in two thirds of critically ill patients. Thus, the more severe and acute the patient’s condition, the more difficult and inaccurate is the bedside determination of jugular venous pulse and pressure.

71 Should one inspect the right or the left internal jugular vein?

Ideally the right, since it is in a more direct line with the right atrium and thus better suited to function as both a manometer for venous pressure and a conduit for atrial pulsations. Moreover, CVP may be spuriously higher on the left as compared to the right because of the left innominate vein’s compression between the aortic arch and the sternum.

72 Can the external jugulars be used for evaluating central venous pressure?

Theoretically not, practically yes. “Not” because:

Hence, if the only visible vein is the external jugular, do what Yogi Berra recommends you should do when coming to a fork on the road: take it.

73 But don’t external jugulars have valves?

They do, but so do the internal jugulars. Yet, this doesn’t interfere with estimation of CVP since the normal flow of blood is toward the heart, and not from it. It might interfere, though, with the evaluation of the venous pulse (see question 79).

74 Still, aren’t the internal jugulars too deep for an accurate inspection?

They are quite deep and thus not as visible as the external jugular (in fact, if you see a plump subcutaneous neck vein, as turgid as the one on the dorsum of your hand, it is probably the external jugular) yet the pulsations of the internal can be transmitted quite well through the overlying sternocleidomastoids, making its waveform recognizable as a skin flickering.

75 What is the anatomy of internal and external jugular veins?

The external jugulars lie above the sternocleidomastoid muscles, coursing obliquely from behind and laterally toward the angle of the jaw (Fig. 10-6). The internal jugulars lie instead below the sternocleidomastoids, crossing them in a vertical straight line. At the junction with the subclavian veins, the internal jugulars create a dilation known as the bulb, which is often visible between the two heads of the sternocleidomastoid muscles.

Figure 10-6 Important landmarks of the venous pulse. The external jugular veins are easily seen lateral to the sternocleidomastoid muscle, extending vertically toward the back of the ear.

(From Adair OV, Havranek EP [eds]: Cardiology Secrets. Philadelphia, Hanley & Belfus, 1995.)

76 How do you examine neck veins?

By carefully positioning the patient (so that the veins fill enough to become visible) and then by tangentially shining a light across the neck. The venous pulse will only be visible, not palpable.

77 How important is the patient’s position during examination of the neck veins?

Of enormous importance:

78 How do you tell apart the carotid pulse from the jugular venous pulse?

By the following differentiating features:

Table 10-3 Differentiation Between Jugular and Carotid Pulses

(Adapted from Cook DJ, Simel N: Does this patient have abnormal central venous pressure? JAMA 275:630–634, 1996; and Abrams J: Essentials of Cardiac Physical Diagnosis. Philadelphia, Lea & Febiger, 1987.)

79 How do you evaluate the jugular venous pulse?

With great difficulty and lots of practice.

If you still have difficulty in relating the various jugular ascents/descents to the cardiac cycle, either auscultate the heart or simultaneously palpate the right radial artery and left carotid.

Note that the external jugulars transmit the pulse poorly. So, while they are adequate for estimating central venous pressure, they are not well suited for jugular pulse evaluation.

80 What are the components of the jugular waveform?

It depends on whether you are looking at a patient or a tracing. Jugular vein undulations reflect phasic pressure changes in the right atrium. Yet, because the fluctuations in venous pressure are so mild (3–7   mmHg, or 4–11   cmH₂O), peaks and troughs of the venous pulse can be easily recorded, but remain difficult to appreciate at the bedside. As a result:

Figure 10-7 Simultaneous recording of an electrocardiogram (top tracing), jugular venous pressure waves (middle tracing), and carotid pressure waves (bottom tracing).

(From Adair OV, Havranek EP [eds]: Cardiology Secrets. Philadelphia, Hanley & Belfus, 1995.)

81 What is the physiology of the jugular venous pulse?

The jugular venous pulse reflects the relationship between volume of blood in the venous system, venous vascular tone, and right heart hemodynamics. Hence, during diastole it reflects right ventricular filling pressure, whereas during systole it reflects right atrial pressure.

82 What is the physiology of the various ascents and descents of the jugular venous pulse?

It is the physiology of right-sided chambers. Thus, assessing the jugular venous pulse is important, not only to visualize peaks and troughs, but also to relate these undulations to various physiologic and clinical events, such as the ECG, the carotid pulse, and the heart sounds. More specifically:

Clinically, the only visible peaks are A and V; the only visible troughs are a combination of X₁ and X (which we will herein refer to as “X”) and Y; the A wave is usually more prominent than the V wave, whereas the X descent is usually more prominent than the Y descent. Overall, it is easier to time the pulse by using the X and Y descents than the A and V waves.

83 Who was Wenckebach?

Karel F. Wenckebach (1864–1940) was a Dutch physician. Building on an 1873 observation by the Italian physiologist Luigi Luciani, he reported in 1899 the phenomenon that still carries his name. He described it in a 40-year-old woman who had presented with an irregular pulse. Wenckebach based his conclusions on tracings of the patient’s arterial pulse, observations of her venous pulse, and intra-atrial and intraventricular recordings in a frog. His insight preceded the invention of electrocardiography by 2 years, the discovery of the atrioventricular node by 7 years, and the description of the sinoatrial node by 8 years. Still, despite his genius he remained a simple and unassuming man who was full of charm, had a self-deprecating humor, and a life-long love for the arts and the English countryside. He was famous for quipping that he was not a great man, just a “happy man.” His colleagues loved him and many affectionately referred to him as “Venky.” His many friends included Sir William Osler and James MacKenzie (with whom he maintained a long correspondence, praising him for his 1902 book The Study of the Pulse). A master of physical diagnosis and a pioneer in arrhythmias, Wenckebach linked his name not only to the homonymous phenomenon, but also to one of the first reports on the beneficial use of quinine in atrial fibrillation. He taught at Utrecht, Groningen, Strasbourg, and, finally, Vienna, where he died of urosepsis just after the onset of World War II.

84 What is the influence of respiration on the jugular venous pulse?

Inspiration increases venous return. This, in turn, distends the right-sided chambers and, because of the Starling effect, makes right atrial and right ventricular contraction stronger. As a result, the jugular venous pulse becomes more visible in inspiration, with brisker X and Y descents (i.e., the troughs of the venous pulse). Even the positive waves become more accentuated. Conversely, exhalation lessens the A wave, so much so to make “V” dominant.

85 What is the influence of respiration on the jugular venous pressure?

The opposite. Inspiration lowers the mean jugular venous pressure, exhalation increases it.

86 Which diseases can be diagnosed by jugular venous pulse?

Quite a few. Some are both common and important, affecting either waves or descents (see Fig. 10-8).

Figure 10-8 Jugular venous pulsation: Normal and disease patterns.

87 What are the most important abnormalities of jugular waves?

For both this and the next question, see Fig. 10-9.

Figure 10-9 Normal and abnormal venous pulses.

(From Adair OV, Havranek EP [eds]: Cardiology Secrets. Philadelphia, Hanley & Belfus, 1995.)

88 What are the most important abnormalities of jugular descents?

89 How do you estimate the CVP?

Figure 10-10 Measurement of jugular venous pressure.

This method relies on the fact that the zero point of the entire right-sided manometer (i.e., the point where central venous pressure is, by convention, zero) is the center of the right atrium. This is vertically situated at 5   cm below the sternal angle, a relationship that is present in subjects of normal size and shape, regardless of their body position. Thus, using the sternal angle as the external reference point, the vertical distance (in centimeters) to the top of the column of blood in the jugular vein will provide the JVP. Adding 5 to the JVP will yield the CVP.

90 How is “Louis” pronounced?

It depends. If you refer to the sternal angle, it should be “French-like,” since it was indeed the French surgeon Antoine Louis who first described it (Dr. Louis is much more famous for having co-authored with the internist Joseph-Ignace Guillotin the homonymous capital punishment device, which presumably chopped aristocrats’ heads just above the angle of Louis). If, on the other hand, you are referring to the maneuver that relies on the sternal angle for estimating central venous pressure, then you should pronounce it “English-like,” since it was the British physician Sir Thomas Lewis (student of MacKenzie) who first realized that the normal jugular vein distention is never more than 2–3   cm above the angle of Louis. A subsequent variant of this observation (i.e., that central venous pressure can be estimated at the bedside by adding 5 to the vertical height of the internal jugular vein above the angle of Louis) is what we call today the “method of Lewis.” Hence, it doesn’t really matter how you pronounce it, since either will be correct.

91 What is the normal central venous pressure?

As estimated by the method of Lewis, a normal central venous pressure should be <7   cm H₂O (some authors have suggested 8   cm H₂O). This means that the jugular venous pressure (i.e., distention) should not be >2–3   cm (two fingerbreadths) above the angle of Louis.

92 Is there any faster way to assess central venous pressure?

Yes. A nice, quick and dirty method consists in having the patient sit up. Visible neck veins in the upright position indicate a central venous pressure >7   cm H₂O, which is pathologic. This is because the clavicles lie at a vertical distance of about 2   cm above the sternal angle. Hence, if central venous pressure is normal, the veins should not be visible).

93 Are there alternative methods to assess the CVP?

Yes, but they have not been validated:

Both these methods may give falsely high readings because of local obstruction or peripheral venous constriction. Hence, they are not recommended for general use.

94 How precise is the clinical assessment of CVP?

When well performed (and in stable patients), it can be quite accurate, with bedside estimates of CVP within 4   cm H₂O of intravenous catheter measurement in almost 90% of the cases. Still, interobserver (and intraobserver) variability may be as high as 7   cm. This becomes especially problematic in the unstable patient, where expertise plays an important role. For instance:

95 So what conclusions can be drawn about the clinical use of CVP assessment?

When compared to the gold standard of a central venous catheter, clinical measurement of CVP is overall poor, especially in the acutely ill patient. In the aforementioned study of 50 critically ill patients, for example, the pooled accuracy of the test was 56%. All groups involved (students, residents, and attending physicians) tended to underestimate central venous pressure (see question 96), and level of expertise was not a guarantee of accuracy. In fact, the correlation coefficient between clinical assessment and central venous catheter recording was highest for medical students (0.74), a little lower for residents (0.71), and lowest for staff physicians (0.65). These correlations slightly improved after exclusion of patients on mechanical ventilation, suggesting that CVP assessment is more accurate in patients who breathe spontaneously. Hence, bedside assessment of CVP is only accurate at the extremes of presentation:

96 Why does bedside assessment tend to underestimate central venous pressure?

Because the semi-erect (or erect) position required for the neck veins’ visualization lengthens the distance between the angle of Louis and the zero reference point by as many as 3   cm. To reduce this underestimation, many physicians measure CVP in exhalation.

97 What is the significance of a low jugular venous pressure?

It reflects a low CVP, usually due to intravascular depletion from GI (vomiting, diarrhea), urinary (diuretics, uncontrolled diabetes mellitus, or diabetes insipidus), or third space losses.

98 What is the significance of an elevated jugular venous pressure?

It usually reflects a high CVP. This can be due to either hypervolemia or impedements to right-sided filling. Among the latter are (in a rostrocaudal fashion):

Finally, CVP does not predict left-sided ejection fraction.

99 What is the significance of neck vein distention in assessing chronic heart failure?

In a prospective study of 52 patients undergoing in-hospital evaluation for heart transplantation, Butman et al. found that jugular venous distention, a positive abdominojugular test, pulmonary crackles, and a left-sided S₃ all independently predicted higher right-sided pressures and worse cardiac performance. Jugular venous distention (whether at rest or inducible) had the best sensitivity (81%), specificity (80%), and predictive accuracy (81%) for elevation of pulmonary capillary wedge pressure. In fact, the probability of an elevated “wedge” was 0.86 when either variable was present. Hence, the bedside cardiovascular examination of patients with chronic heart failure is quite useful for identifying increased right- and left-sided pressures. In this study, baseline or induced jugular venous distention was both sensitive and specific.

100 What is the prognostic significance of abnormal jugular venous pressure in heart failure?

Together with S₃, it represents an ominous prognostic variable, independently associated with adverse outcomes, including progression of heart failure. This was shown by Drazner et al. in a large study of 2569 patients with either symptomatic heart failure or a history of it. In multivariate analyses adjusted for other markers of heart failure severity, elevated jugular venous pressure was associated with a significant increase in the risk of death or hospitalization for heart failure. The presence of S₃ was similarly (and independently) associated with increased risk.

101 How are the neck veins in tamponade?

Distended. This is a must, together with dyspnea/tachypnea, tachycardia, and clear lungs. Given this constellation of four symptoms/findings, the differential diagnosis is narrowed to five major entities: right ventricular infarction, massive pulmonary embolism, constrictive pericarditis, tension pneumothorax, and tamponade. The first four present with a positive Kussmaul’s sign in approximately one half of the cases, but never have a pulsus paradoxus >21   mmHg. Conversely, tamponade comes with no Kussmaul’s, but does present with a pulsus of 20–50   mmHg (see Chapter 2, questions 92–95).

102 What is the significance of leg swelling without increased central venous pressure?

It reflects either bilateral venous insufficiency or noncardiac edema (usually hepatic or renal). This is because any cardiac (or pulmonary) disease resulting in right ventricular failure would manifest itself through an increase in central venous pressure.

103 What is the significance of leg edema plus ascites in the absence of increased CVP?

It also argues in favor of a hepatic or renal cause (cirrhotics do not have high CVP). Conversely, a high CVP in patients with ascites and edema argues in favor of an underlying cardiac etiology.

104 What is the prognostic value of an increased CVP in preoperative patients?

If untreated, it predicts postoperative pulmonary edema and/or infarction.

105 What are the jugular findings of right ventricular infarction?

106 What is the hepatojugular reflux?

An old term for the abdominojugular reflux, a maneuver first described by the British William Pasteur in 1885 as a sign of TR, and then rekindled in 1898 by the French Edouard Rondot. Rondot also is the author of the unfortunate term “hepatojugular reflux” and the first to suggest that a positive response is not pathognomonic of TR, but can also occur in other disorders.

107 What is it used for?

To unmask subclinical right ventricular failure (and silent tricuspid regurgitation) but also to confirm symptomatic left ventricular failure (see question 113). Hence, the “Pasteur-Rondot maneuver” is a very helpful tool, albeit one that is often misused and misinterpreted.

108 What is the physiology of the abdominojugular reflux?

It is a cardiac stress test for patients whose jugular venous pressure is either normal or only borderline elevated (hence, no need to use it in patients who already have jugular venous distention). Steady pressure onto the abdomen increases venous return by shifting blood from the splanchnic bed into the thorax and right atrium, like a sort of “poor man’s” fluid challenge. If the right ventricle cannot handle this extra load, there will be sustained increase in JVP.

109 Does abdominal pressure cause any change in cardiac output?

No. Moreover, the changes in central venous pressure that result from this maneuver cannot be attributed to variations in esophageal pressure or to a compression of the heart by elevation of the diaphragm. Instead, various observations are consistent with the overall hypothesis, that the increased right-sided filling pressure induced by abdominal compression does indeed reflect both the volume of blood in the abdominal veins and the ability of the ventricles to respond to an increased venous return. Hence, its value for unmasking congestive heart failure.

110 Is compression of the liver necessary to elicit a response?

No. In fact, it can actually be detrimental in patients with passive hepatic congestion, since compression of the right upper quadrant (and a distended glissonian capsule) might indeed elicit pain and a Valsalva’s response. As a result, pressure over the periumbilical area (or any other area of the abdomen) has become the method of choice. Hence, the more current term of abdominojugular (reflux) test.

111 How do you perform an abdominojugular test?

By observing the jugular venous pressure before, during, and after abdominal compression:

112 When is the abdominojugular test considered positive?

When there is an increase in jugular venous pressure of more than 3   cm in height (which, according to Ducas, is the upper limit of normal) that remains sustained though all 15 seconds of compression. Conversely, the test is considered negative when any of the following occurs:

A positive “reflux” is sometimes easier to observe as an abrupt fall in JVP when the pressure is being released. For the test to be positive, this drop should be at least 4   cm (Ewy et al).

113 What is the significance of a positive abdominojugular reflux?

In patients presenting with dyspnea and/or angina, it argues in favor of bi-ventricular failure and suggests a pulmonary capillary wedge pressure >15   mmHg. This was confirmed at cardiac catheterization by Ewy et al. Patients with positive response also had lower left ventricular ejection fraction and stroke volume and higher mean pulmonary arterial and right atrial pressure, confirming biventricular failure. Conversely, a negative test in a patient with dyspnea would strongly argue against the presence of increased left atrial pressure.

In the absence of left ventricular failure, a positive test points instead to the right chambers, suggesting an inability of the atrium and ventricle to handle an increased venous return. This is particularly useful in subclinical cases, where a positive test has high sensitivity and specificity for predicting right atrial pressure >9   mmHg and right ventricular end-diastolic pressure >12   mmHg. Differential diagnosis includes impaired right ventricular preload (increased intravascular volume), decreased right ventricular compliance (right ventricular hypertrophy), decreased right ventricular systolic function (right ventricular infarction), or elevated right ventricular afterload (pulmonary hypertension).

Tricuspid regurgitation, tricuspid stenosis, restrictive cardiomyopathy, and constrictive pericarditis are also a common cause of a positive test. The only condition not presenting with a positive abdominojugular reflux is cardiac tamponade. Hence, the test is not specific to any one disorder, but is instead a reflection of either a right ventricle that cannot accommodate an increased return or a left ventricle that is dysfunctional.

114 Shouldn’t the abdominal pressure be applied for at least 1 minute?

No. This was recommended in the past, but it is not the case anymore. In fact, Ewy used 10 seconds, and so did Ducas, who also showed that CVP stabilized by that point and did not change over the subsequent 60 seconds. Sochowski, on the other hand, showed that 62 of 65 patients stabilized their pressure by 15 seconds. Hence, the choice of 15 seconds.

115 What is Kussmaul’s sign?

It is the paradoxical increase in JVP that occurs during inspiration. Jugular venous pressure normally decreases during inspiration because the inspiratory fall in intrathoracic pressure creates a “sucking effect” on venous return. Thus, Kussmaul’s sign is a true physiologic paradox. This can be explained by the inability of the right heart to handle an increased venous return.

116 Which disease processes are associated with a positive Kussmaul’s?

Those that interfere with venous return and right ventricular filling. The original description was in a patient with constrictive pericarditis (Kussmaul’s is still seen in one third of severe and advanced cases, where it is often associated with a positive abdominojugular reflux). Nowadays, however, the most common cause is severe heart failure, independent of etiology. Working backwards from the heart to the superior vena cava, other causes of this sign include:

Remember that Kussmaul’s is also present in 33–100% of patients with right ventricular infarction. Thus, in a setting of acute myocardial infarction, Kussmaul’s should not be interpreted as a sign of tamponade, but as a clue to concomitant right ventricular injury.

117 What can be said about the association of pulsus paradoxus and Kussmaul’s sign?

Both were first described by Kussmaul, yet Kussmaul’s never occurs in “pure” tamponade (if it does, concomitant epimyocardial fibrosis is present); however, it does occur in one third of patients with “pure” constrictive pericarditis. Pulsus paradoxus, on the other hand, does not occur in “pure,” totally dry constrictive pericarditis (if it does, a concomitant amount of pericardial effusion is present). Still, it does occur in almost all patients with tamponade.

A small pulsus paradoxus (>10 but <21   mmHg) occurs in two thirds of patients with right ventricular infarction, whereas Kussmaul’s occurs in 33–100% of right ventricular infarctions.

To avoid confusion, you should use a high cutoff for pulsus paradoxus (>21   mmHg). This will limit the positivity of the test to only tamponade, a condition where Kussmaul doesn’t occur.

118 What is the association between Kussmaul’s sign and the abdominojugular reflux?

They share the same pathophysiology. Both, for example, occur in situations of diffuse peripheral venous constriction with secondary increase in central venous pressure, such as severe heart failure and constrictive pericarditis. And both result from the inability of the heart to handle an increase in venous return, either because of pump failure or various mechanical impediments (constrictive pericarditis, tricuspid stenosis, and cor pulmonale—acute or chronic).

119 How can you improve the clinical examination of the jugular veins?

Blind examination of patients with indwelling central venous catheters may provide a valuable feedback. Pocket cards displaying the normal jugular pulse also may be helpful. Finally, evaluation of patients with tachycardia, irregular cardiac rhythms, rapid and deep respirations, or need for mechanical ventilation may provide very useful challenges and thus hone the skill.

120 What is the “venous hum”?

It is a functional murmur (see Chapter 12, questions 44 and 45) produced by turbulent flow in the internal jugular vein. It is continuous (albeit louder in diastole) and at times strong enough to be associated with a palpable thrill. It is best heard on the right side of the neck, just above the clavicle, but sometimes it can become audible over the sternal/parasternal areas, both right and left. This may lead to misdiagnoses of carotid disease, patent ductus arteriosus, or AR/AS.

121 What is the best way to elicit a venous hum?

Have the patient sit up, with head turned away from the side of auscultation (i.e., rotated 30–60 degrees leftward if listening over the right supraclavicular area). The hum vanishes upon reclining and similarly fades (or altogether disappears) with other maneuvers that reduce venous return, such as pressing over the jugular vein distal to the hum (i.e., just above the stethoscope) or performing Valsalva.

122 What is the mechanism of the venous hum?

It is a mild compression of the internal jugular vein by the transverse process of the atlas, in subjects with strong cardiac output and increased venous flow. Hence, it is common in young adults or patients with a high output state.

123 How prevalent is this finding?

It can be heard in 31–66% of normal children and 25% of young adults. It also is encountered in 2.3–27% of adult outpatients. It is especially common in situations of arteriovenous fistula, being present in 56–88% of patients undergoing dialysis and 34% of those in between sessions.

124 Can any other cardiac event be heard at the neck?

Beside transmitted systolic ejection murmurs, right-sided S₃, and S₄ gallops also may be heard over the neck. These usually occur in patients with right-ventricular failure and elevated right-sided pressure. Similarly, the murmur of TR may at times be heard over the neck.

125 What is the history behind precordial palpation?

It goes back 3500 years, to the Ebers Papyrus of 1550 B.C., which was the principal medical document of ancient Egypt. The papyrus covered 15 diseases of the abdomen, 29 of the eyes, and 18 of the skin. It also listed no fewer than 21 cough treatments. In a section titled “Beginning of the Secret of the Physicians: Knowledge of Heart’s Movement and Knowledge of the Heart,” palpation of the cardiac impulse was clearly described. Following that initial information, chest palpation remained part of the medical armamentarium up to medieval times. Only with William Harvey, though, did the motions of the heart become again a specific topic of scientific discussion. In his 1628 book De Motu Cordis, Harvey wrote: “[T]he heart is erected and rises upward to a point so that at this time it strikes against the breast and the pulse is felt externally.” Subsequently, important contributions to the art of precordial palpation came from Laënnec, his teacher Jean-Nicolas Corvisart, and Sir James MacKenzie.

126 Which precordial impulse can be appreciated on physical exam?

The only one that can be normally seen (and palpated) in healthy subjects is the apical impulse, also known as the PMI (point of maximal impulse)—a rather confusing term for what is nothing more than a brisk movement of left ventricle and septum against the chest wall. This is typically felt over the left fifth interspace midclavicular line, and can be absent in >50% of the cases. In disease states, additional precordial or chest wall impulses may occur, reflecting mechanical events of ventricles, atria, and large vessels. Hence, the need for a systematic search.

127 What precordial areas should be examined?

The same four used for cardiac auscultation. In addition to the apex per se (which reflects primarily the left ventricular impulse), you should palpate the two basilar areas (right and left parasternal interspaces, reflecting, respectively, the aortic and pulmonary outflow tracts) and the left lower sternal area (reflecting the right ventricular and atrial projection).

128 Can the right ventricle be appreciated in a normal person?

No. Right ventricular contraction produces neither visible nor palpable chest wall movements. Only occasionally (and usually in children or young people with narrow anteroposterior diameter) it may become possible to feel a gentle right ventricular activity. The same applies for the two basilar areas, which in the absence of pathology offer no palpable impulse.

129 How do you assess the precordial impulse(s)?

130 How do you time precordial events?

By simultaneously palpating the carotid, or by concomitantly auscultating for S₁ and S₂.

131 Which characteristics of the apical impulse should be analyzed?

Location: Normally over the fifth left interspace midclavicular line, which usually (but not always) corresponds to the area just below the nipple. Volume loads to the left ventricle (such as aortic or mitral regurgitation) tend to displace the apical impulse downward and laterally. Conversely, pressure loads (such as aortic stenosis or hypertension) tend to displace the impulse more upward and medially—at least initially. Still, a failing and decompensated ventricle, independent of its etiology, will typically present with a downward and lateral shift in PMI. Although not too sensitive, this finding is very specific for cardiomegaly, low ejection fraction, and high pulmonary capillary wedge pressure. Correlation of the PMI with anatomic landmarks (such as the left anterior axillary line) can be used to better characterize the displaced impulse.

Size: As measured in left lateral decubitus, the normal apical impulse is the size of a dime. Anything larger (nickel, quarter, or an old Eisenhower silver dollar) should be considered pathologic. A diameter >4   cm is quite specific for cardiomegaly.

Duration and timing: This is probably one of the most important characteristics. A normal apical duration is brief and never passes midsystole. Thus, a sustained impulse (i.e., one that continues into S₂ and beyond—often referred to as a “heave”) should be considered pathologic until proven otherwise, and is usually indicative of pressure load, volume load, or cardiomyopathy. For separating these conditions, use the overall clinical picture:

In patients with no murmurs, consider cardiomyopathy and a low ejection fraction.

In patients with a systolic ejection murmur, consider instead severe pressure load from AS.

In patients with a diastolic murmur of aortic regurgitation (which causes a volume load), consider the disease to be mild if the apical impulse is nonsustained.

Amplitude: This is not the length of the impulse, but its force. A hyperdynamic impulse (often referred to as a “thrust”) that is forceful enough to lift the examiner’s finger can be encountered in situations of volume overload and increased output (such as aortic regurgitation and ventricular septal defect), but may also be felt in normal subjects with very thin chests. Similarly, a hypodynamic impulse can be due to simple obesity, but also to congestive cardiomyopathy. In addition to being hypodynamic, the precordial impulse of these patients is large, somewhat sustained, and displaced downward/laterally.

Contour: A normal apical impulse is single. Double or triple impulses are clearly pathologic.

Hence, a normal apical impulse consists of a single, dime-sized, brief (barely beyond S1), early systolic, and nonsustained impulse, localized over the fifth interspace midclavicular line.

132 What are the most common abnormal apical movements?

133 What is the significance of a precordial movement in the left lower sternal area?

134 What is a retracting impulse?

One that moves inward in systole and outward in diastole. This is the opposite of the normal apical impulse, which has instead an early systolic outward movement followed by a mid to late systolic retraction. Timing of the events by either auscultation or carotid palpation is therefore key to separating the two.

135 What are the causes of a retracting impulse?

Constrictive pericarditis (where up to 90% of patients may present with the finding) and severe tricuspid regurgitation. In the latter condition, patients usually exhibit a peculiar rocking motion of the chest in systole, with a retraction at the apex (now occupied by the enlarged right ventricle) and a bulge over the epigastric and tricuspid areas (now occupied by the enlarged right atrium).

136 What are the precordial findings of tricuspid regurgitation?

In addition to those previously listed, adult patients with TR almost always have precordial evidence of pulmonary hypertension and right ventricular hypertrophy, such as a palpable P₂ over the pulmonic area and a right ventricular parasternal impulse. At times, the right ventricular impulse may even be palpable over the epigastric or subxiphoid area. A pulsatile liver in synchrony with each systole also is appreciated.

137 What precordial evidence suggests mitral stenosis?

Palpability of both first and second heart sounds. S₁ becomes palpable because of the sharp loudness characteristic of this disease, and S₂ (primarily its P₂ component) because of the concomitant pulmonary hypertension. Thus, the absence of a palpable P₂ argues strongly against the presence of pulmonary hypertension. Note that the opening snap can become palpable, too, and an apical diastolic thrill may at times be felt in left lateral decubitus. Since the apical impulse of mitral stenosis is usually hypodynamic (as a result of impaired left ventricular filling), the presence of a hyperkinetic impulse argues strongly against the purity of the disease and suggests instead the possibility of concomitant aortic or mitral regurgitation.

138 What precordial evidence suggests angina? Previous infarction?

In angina, the apical impulse is usually normal, but there may be a transiently palpable S₄ (presystolic impulse) or a dyskinetic apical area. Conversely, in cases of a preexisting infarction, the apical impulse may at times be just superior and medial to the normal apical location. Such an ectopic impulse usually suggests left ventricular aneurysm or dyskinesia.

139 What are the precordial findings of a dilated aorta or pulmonary artery?

A dilated pulmonary artery (as in patients with pulmonary hypertension) may often be felt at the upper left parasternal area. Conversely, a dilated aorta (as, for example, in patients with aortic aneurysm) may often be felt at the right parasternal area.

140 What is a thrill?

A palpable vibration associated with an audible murmur (see Chapter 12, question 7). A thrill automatically qualifies the murmur as being >4/6 in intensity and thus pathologic.

141 What is the value of precordial percussion?

When properly carried out, precordial percussion retains some clinical value. It can even outline the cardiac area with errors of only 1   cm. But given the difficulty in mastering this skill (and today’s ubiquity of sophisticated imaging), cardiac percussion has become one of those areas of physical examination that have clearly yielded to technology-based diagnosis.