The Cardiovascular Exam

(1)

Conventional Wisdom

…With careful practice the trained finger can become a most sensitive instrument in the examination of the pulse…from [its] examination we obtain information on three different points: first, concerning the rate and rhythm of the heart’s action; second, concerning certain events occurring in a cardiac revolution; third, concerning the character of the blood pressure in the artery…The trained finger can recognize a great variety in the apparent volume of the wave itself. Although the pulse wave occupies such a short space of time, yet the sensitive finger readily recognizes these different features. – J. MacKenzie, The Study of the Pulse , 1902

(2)

Generalities

Evaluation of the arterial pulse is a time-honored method of bedside examination. It can still provide valuable cardiovascular information. In selective processes (such as tamponade, aortic valve [AV] disease, and hypertrophic cardiomyopathy), it can even prove essential for securing a diagnosis. Yet, assessment of the characteristics of the arterial pulse requires skill and practice, and at times can be frustrating. It is worth the effort, though, and thus deserves attention even in our times of intraarterial monitoring.

• 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: (1) arteries on both sides should be compared to detect asymmetries suggestive of embolic, thrombotic, atherosclerotic, dissecting, or extrinsic occlusion; (2) arteries of upper and lower extremities should be simultaneously examined in hypertensive patients, to identify reduction in volume (or pulse delays) suggestive of aortic coarctation. And yet, if trying to evaluate the characteristics of the arterial waveform , you should examine only central arteries – carotid , brachial , or femoral . Since this section focuses on the bedside examination of the arterial wave as part of cardiovascular exam, we will exclusively discuss evaluation of central arteries. Assessment of peripheral vessels will be in the Extremities section.

• 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. This is because amplitude and upstroke can only be appreciated in large central arteries (such as carotids and brachial), being otherwise missed in small peripheral arteries, like the radials. In fact, some findings (like the bifid pulse of hypertrophic 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 (see Fig. 10.1 ). As the distance from the AV 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. 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 also Vital Signs ).

  

• 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 (AS) 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 AS). 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 (AR). Then listen over the vessel to rule out bruits. If negative, apply thumb or index 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. 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: (1) rate and rhythm; (2) volume and amplitude; (3) contour; (4) speed (or rate of rise) of the upstroke; (5) speed (or rate of collapse) of the downstroke; (6) stiffness (or distensibility) of the arterial wall; (7) presence of a palpable shudder or thrill ; (8) presence of audible bruits or transmitted murmurs .

• 12.

  What are the characteristics of a normal arterial pulse?

  A normal arterial pulse comprises a primary (systolic) and a secondary (diastolic) wave (see Fig. 10.2 ). These are separated by a dicrotic notch ( dikrotos , double-beating in Greek), which corresponds to the closure of the semilunar valves (S2).

  

• 13.

  Are both the primary and secondary wave palpable?

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

• 14.

  How are primary and secondary wave generated?

  • The primary wave derives from the ejection of blood into the aorta. Its early portion ( percussion wave) reflects discharge into the central aorta, while its mid-to-late portion ( tidal wave) reflects movement of blood from the central to the peripheral aorta. The two portions are separated by an anacrotic notch , only visible on tracing and usually not palpable.

  • The secondary wave is generated instead by the elastic back-reflection of the waveform, from the peripheral arteries of the lower half of the body.

• 15.

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

  It argues against the presence of significant AS, but only in the young (elderly patients may have spuriously brisk pulses – see earlier). 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 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 AS?

  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 ( Fig. 10.3 ). This is akin to aortic coarctation, and underscores the importance of examining both pulses.

  

• 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:

    • 1.

      the simultaneous emptying of the left ventricle (LV) into a high-pressure bed (the aorta) and a lower-pressure bed. The latter can be the right ventricle (RV; in patients with ventricular septal defect [VSD]) or the left atrium (LA; in patients with mitral regurgitation [MR]). Both will allow a rapid left ventricular emptying, which, in turn, generates a brisk arterial upstroke. The pulse pressure, however, remains normal.

    • 2.

      HOCM. Despite its association with left ventricular obstruction, this disease is characterized by a brisk and bifid pulse, due to the hypertrophic ventricle and its delayed obstruction.

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

• 21.

  Beside 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, Beri-Beri, Paget’s disease, arteriovenous fistulas, patent ductus arteriosus (PDA), AR, 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 Vital Signs section).

• 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, being 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. This is because smaller vessels tend to magnify 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 may also help eliciting 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 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 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.

• 29.

  What is a double-peaked pulse? ( Fig. 10.4 )

  

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

• 30.

  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.

• 31.

  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 can also be detected by a blood pressure cuff, as a closely split Korotkoff sound.

• 32.

  What is the diagnostic significance of a pulsus bisferiens?

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

  • Double Korotkoff sound . This is heard during measurement of systolic blood pressure, with the cuff being slowly deflated. It coincides with the systolic arterial peak.

  • Traube’s femoral sound(s) . Reported by Traube in 1867, this is a loud, explosive, and shot-like systolic sound heard over a large central artery (femoral, usually, but also brachial or carotid), in synchrony with the arterial pulse. It is detected whenever light pressure is applied with the stethoscope’s diaphragm over the artery, coupled with mild arterial compression distal to the stethoscope’s head. Although more often single (and thus called pistol shot sound ), it can also be double (hence referred to as Traube’s femoral double sounds ) and sometimes even triple. It reflects the sudden systolic distension of the arterial wall – like a sail filling with wind. A single shot occurs in approximately half of all AR patients, but may also take place in other high-output states. Double sounds occur in one-fourth of AR patients. Lack of arterial compression distal to the stethoscope’s head sharply decreases the test’s sensitivity, confining it to cases with severe left ventricular dilatation.

• 33.

  What is Duroziez’ 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’ sign has 58%–100% sensitivity and specificity for AR. False negatives may occur in mild disease, concomitant AS, inadequate ventricular filling (due to associated mitral [MS]), inadequate ventricular emptying (due to concomitant MR), or obstruction to waveform transmission (because of aortic coarctation). False positives may occur in all high-output conditions. Yet, 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, while 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 PDA, the only other high-output state characterized by both forward and reverse flow.

• 34.

  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.

• 35.

  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 signs of Traube nor Duroziez predict AR severity.

• 36.

  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 the aortic walls inward, 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.

• 37.

  What is the prognostic value of a pulsus bisferiens?

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

• 38.

  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 ).

• 39.

  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).

• 40.

  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 AV, 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.

• 41.

  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 has also been reported in young healthy individuals as a result of fever.

• 42.

  What is a hypokinetic pulse?

  From the Greek hypo (diminished) and kinesis (movement), this is a pulse of diminished amplitude . Causes include: (1) obstruction to left ventricular outflow (AS); (2) diminished left ventricular contraction (cardiomyopathy); and (3) diminished left ventricular filling (MS). 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.

• 43.

  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.

• 44.

  Are there any other manifestations of arterial delay?

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

• 45.

  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 insensitive sign of aortic valvular disease ( Fig. 10.5 ).

  

• 46.

  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 at the bedside. Hence, it has little clinical relevance. The name derives from the Greek ana (upward) 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) .

• 47.

  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, while the quick rise reflects increased velocity of contraction.

• 48.

  What are the causes of a hyperkinetic pulse?

  Usually the high-output states (including AR), which are typically associated with a widening pulse pressure . A hyperkinetic pulse can also occur in MR 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 they are hypertensive.

• 49.

  What is Corrigan’s pulse?

  It is one of the various names for the bounding and quickly collapsing pulse of AR. 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 to cause other typical findings, such as De Musset’s or Lincoln’s signs (see also Chapter 1 ).

• 50.

  Who was Corrigan?

  Sir Dominic J. Corrigan (1802–1880) was an Irishman. In fact, he was the longest-serving president of the Irish College of Physicians, and a member of Parliament for the city of Dublin. He was also 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 , where 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 AR.

• 51.

  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 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.

• 52.

  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 intraradial diastolic pressure, collapses the vessel, and thus facilitates the palpability of the subsequent systolic thrust.

• 53.

  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 ).

• 54.

  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 to 160 mmHg. Finally, if it requires high force, the blood pressure is probably above 160 mmHg.

• 55.

  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.

• 56.

  What other findings can mimic a carotid bruit?

  • Systolic heart murmurs. These are only transmitted to the neck. Hence, in contrast to a bruit, they are louder over the precordium than the neck.

  • Venous hums. These are innocent murmurs caused by flow in the internal jugular vein. In contrast to a carotid bruit, they are loudest in diastole (although, actually, continuous ) and can only be heard in a sitting position (see also later, under Jugular Veins Exam ).

  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 the exclusion of carotid artery stenosis .

• 57.

  Can carotid bruits occur in children?

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

• 58.

  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. 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.

• 59.

  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.

• 60.

  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 bypass 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.

• 61.

  What is the correlation between carotid bruit and symptomatic 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.

Generalities

Observation of the jugular venous pulse and measurement of the CVP are more recent acquisitions than the evaluation of the arterial pulse. Yet, they can still provide a wealth of valuable clinical information; especially when trying to assess intravascular volume, evaluate right ventricular function, test the integrity of pulmonic and tricuspid valves, and investigate the status of the pericardium. Skills are difficult. At times even intimidating. Yet, they are worth the effort, even in our times of invasive hemodynamic monitoring.

• 62.

  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 (TR; 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, 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 examination, thanks to the influence of the charismatic British physician Paul Wood.

• 63.

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

  Twofold: (1) To estimate the CVP and (2) To evaluate the venous pulse .

• 64.

  What is the central venous pressure (CVP)?

  The pressure within the right atrium (RA)/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 MS ), so CVP reflects right ventricular end-diastolic pressure (in the absence of tricuspid stenosis [TS]).

• 65.

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

  Central veins, as much in direct communication with the RA as possible. The ideal one is therefore the internal jugular .

• 66.

  What is the clinical value of jugular venous distension and pulse?

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

  • Evaluation of jugular venous distension provides a noninvasive estimate of CVP and intravascular volume.

  • Evaluation of jugular waveform provides instead additional information on right ventricular function, the status of tricuspid and pulmonic valves, and the presence (or absence) of pericardial constriction.

• 67.

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

  Ideally the right, since it is in a more direct line with the RA, 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. This is because of the left innominate vein’s compression between aortic arch and sternum.

• 68.

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

  Both the internal and external jugular veins can actually be used for estimating CVP, since they yield comparable estimates. 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.

• 69.

  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 evaluation of the venous pulse (see later).

• 70.

  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). And yet, the pulsations of the internal can be transmitted quite well through the overlying sternocleidomastoids, making its waveform recognizable as a skin flickering.

• 71.

  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 lay instead below the sternocleidomastoids, crossing them in a vertical straight line. At the junction with the subclavian veins, the internal jugulars create a dilatation known as the bulb , which is often visible between the two heads of the sternocleidomastoid muscles.

  

• 72.

  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. Venous pulse will only be visible and, unless the right ventricular pressure is extremely high, is not palpable.

• 73.

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

  Of enormous importance:

  • The head should be supported, so that the neck muscles are fully relaxed and not impinging upon the jugular veins.

  • The trunk should be inclined and raised. The angle of inclination must allow the top of the column of blood in the internal jugular to reach above the clavicle but still to remain below the jaw. This inclination will vary depending on CVP:

    • In patients with normal CVP , the required angle is usually 30–45 degrees above the horizontal.

    • In patients with elevated CVP , the required angle is >45 degrees. In fact, patients with severe venous congestion may have to sit upright and take a deep inspiration in order to lower the meniscus down into full view. In some of these patients the level of venous pulsation may still remain behind the angle of the jaw, where it will appear to flicker the earlobes.

    • In patients with very high CVP , the internal jugular will be so “full” that pulsations may not be visible even when the patient is fully upright. The risk in this case is to overlook the high venous pressure and call it normal.

    • In patients with low CVP , the required angle is usually between 0 and 30 degrees.

    • In patients with very low CVP , the neck veins will be so empty that pulsations may not be visible at all, even when the patient is fully horizontal.

  Hence, to get a good look at venous pulsations you may need to vary patient’s position based on volume status .

• 74.

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

  By the following differentiating features:

  • The waveform is different: the venous pulsation is diffuse, at least bifid , and with a slow upward deflection. Conversely, the carotid pulse is well localized, single , and with a fast outward deflection. Also, the most striking event in the venous pulse are the descents, while in the arterial pulse is the ascent.

  • The response to position is different: the carotid pulse never varies with position. The venous pulsations classically do so. In fact, as the patient sits up or stands, they move down toward the clavicle and may even disappear below it. Conversely, as the patient reclines, venous pulsations gradually climb toward the angle of the jaw. They may even disappear behind the auricle.

  • The response to respiration is different: in the absence of intrathoracic disease (and Kussmaul’s sign – see later), the top of the venous waveform descends toward the heart during inspiration (because of lower intrathoracic pressure and greater venous return). The carotid pulse, instead, remains unchanged. The only exception is pulsus paradoxus, and even in this case, the variation is rarely visible, at most palpable. Note that inspiration makes jugular “pulsations” more visible (by enhancing venous return), even though it also lowers the mean jugular “pressure.”

  • The response to palpation is different: the jugular venous pulse is usually too light to be palpable. Even gentle pressure will collapse the vein, engorge its more distal segment, and obliterate the pulse. Conversely, the carotid is not only palpable but quite forceful too.

  • The response to abdominal pressure is different: sustained pressure on the abdomen (the abdominojugular reflux test , see later) will not change the carotid pulse, but will increase (at least momentarily) even the normal venous pulse.

• 75.

  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 RA. Yet, because the fluctuations in venous pressure are so mild (3–7 mmHg, or 4–11 cmH ₂ O), peaks and troughs of the venous pulse can be easily recorded but remain difficult to appreciate at the bedside. As a result:

  • On venous tracings the jugular pulse consists of three positive waves (A, C, and V) and three negative descents (X, X1, and Y). The A wave is followed by the X descent, the C wave by the X1 descent, and the V wave by the Y descent.

  • At the bedside the jugular venous pulse consists instead of only two positive waves (A and V – with A taller than V) and two negative descents (X1 and Y – with X1 steeper than Y). Neither the C wave nor the X descent are visible (C is usually lost in the A wave, and X is merged with X1). Note that descents are easier to spot than ascents.

• 76.

  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.

• 77.

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

  It is the physiology of right-sided chambers. Thus, in assessing the jugular venous pulse, it is important not only to visualize peaks and troughs but also to relate these undulations to various physiologic and clinical events, such as the EKG, the carotid pulse, and the heart sounds ( Fig. 10.7 ). More specifically:

  • The A wave (the first and dominant positive wave) is produced by right A trial contraction. It follows the P wave on EKG, coincides with the fourth heart sound (if present), and slightly precedes both first heart sound and carotid upstroke.

  • The C wave , the second positive wave (only visible on recordings), is produced by the bulging of the tricuspid cusps into the RA, and thus coincides with ventricular isovolumetric contraction. Note that a very small component of “C” is produced by the transmitted carotid pulsation – in fact, Mackenzie considered it an entirely C arotid artifact; hence the label “C.” Also, note that the interval between A and C corresponds to the P-R interval on EKG (this was one of the methods used by Wenckebach to describe the second-degree heart block that still carries his name). Because the C wave is not visible at the bedside, it is omitted from the remainder of our discussion.

  • The early X descent (located between A and C) is produced by right atrial relaxation. The most dominant later trough (X1 , i.e ., the “x-prime”) is produced instead by the pulling of the valvular cusps into the RV. This downward and forward movement of valve and atrium floor (descent of the base) coincides with right ventricular isotonic contraction and acts as a plunger, creating a sucking effect that draws blood from the great veins into the RA. The X1 descent occurs during systole , coincides with ventricular ejection and the carotid pulse, takes place between S1 and S2, and ends just before S2. Note that this discussion disregards the early X descent and uses instead this term to refer to the combined X and X1 troughs – only X1 is visible at the bedside.

  • The V wave (the third positive wave) occurs toward the end of V entricular systole and during the early phase of ventricular diastole. It coincides with the apex of the carotid pulse and peaks immediately after S2. Because the ventricle relaxes while the tricuspid valve is still closed, blood flowing into the RA starts building up, generating a positive wave.

  • The Y descent (the final negative trough) occurs during early ventricular diastole. It is due to the opening of the tricuspid valve and the emptying of the RA. It corresponds to S3.

  • 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 .

  

• 78.

  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 intraatrial 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. Yet, despite his genius, he remained a simple and unassuming man, full of charm, self-deprecating humor, and a 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.

• 79.

  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 contractions 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 to a point that V becomes dominant.

• 80.

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

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

• 81.

  Which diseases can be diagnosed by jugular venous pulse? ( Fig. 10.8 )

  

  Quite a few. Some are both common and important, affecting either waves or descents .

• 82.

  What are the most important abnormalities of jugular waves?

  For both this and the next question see Fig. 10.9 .

  • Giant A wave. In addition to TS, this can also occur in increased right ventricular end-diastolic pressure (from pulmonic stenosis [PS], primary pulmonary hypertension, pulmonary emboli, or chronic pulmonary disease). In these patients the large A wave reflects a strong atrial contraction against an increased ventricular resistance, presenting with a concomitantly blunted and small Y descent . The acoustic counterpart of a giant A wave is a right-sided S4, while its electric equivalent is a P pulmonale. Giant A waves may also be seen in marked left ventricular hypertrophy (LVH; like AS, severe hypertension, or hypertrophic obstructive cardiomyopathy). In these patients, the ventricular septum bulges toward the right, making right ventricular filling more difficult (the Bernheim effect, from Hippolyte Bernheim, the French physician and hypnotist who described it in 1910).

  • “Cannon” A waves are the hallmark of atrioventricular dissociation (i.e., the atrium contracts against a closed tricuspid valve). They are different from the other prominent outward waves (like the presystolic giant A wave), insofar as they begin just after S1, since they represent atrial contraction against a closed tricuspid valve. Giant A waves, on the other hand, begin just before S1 – like the large V waves of TR (see later). Intermittent cannon A waves reflect atrioventricular dissociation in a setting of ventricular tachycardia, while regular cannon A waves reflect atrioventricular dissociation in a setting of supraventricular tachycardia with retrograde atrial activation.

  • The V wave is classically increased in TR, where it becomes the dominant wave, associated with a brisk Y collapse (a more gentle Y descent usually indicates concomitant regurgitation and stenosis). Abdominal compression may help to unmask more subtle and subclinical cases. Prominent V waves can become so large that they were dubbed by Paul Wood “the venous Corrigan.” In fact, they may even cause bobbing of the earlobes (the Lancisi’s sign). Since the CV merger responsible for the giant V wave entirely eliminates the X descent , a giant V wave is easy to spot; it starts just after S1 and leaves the patient with only one ascent (the V wave) and one descent (the Y descent). The giant V wave is not too sensitive for TR, being present in only 40% of the cases.

  • Equally prominent A and V waves can occur in atrial septal defect. The V wave in the higher-pressure LA is transmitted through the perforated septum into the RA , and from there to the jugular veins. This, however, is more commonly suggestive of simple right ventricular failure.

  

• 83.

  What are the most important abnormalities of jugular descents?

  • A prominent X descent is seen in patients with vigorous ventricular contraction (and thus requiring strong atrial contractions), like tamponade or right ventricular overload .

  • A diminished X descent (to the point of becoming even less prominent than the Y descent) is seen in atrial fibrillation or cardiomyopathy (wherein right ventricular contraction is not forceful enough to “pull down” the atrial floor).

  • A prominent Y descent is seen in patients with increased venous pressure, regardless of etiology. A very brisk Y descent is often referred to as Friedreich’s sign, from the German clinician and neurologist Nikolaus Friedreich, who described it in 1861. In combination with the prominent X descent it creates two steep troughs (the “W” sign). This occurs in one-third of constrictive pericarditis cases, where it is often associated with an early diastolic extra-sound (pericardial knock). Friedreich’s sign is not too sensitive for constrictive pericarditis, but quite specific, with the only differential diagnosis being restrictive cardiomyopathy.

  • A diminished – to-absent Y descent is seen in patients with increased CVP, like tamponade or TS. Note that the Y descent is usually minimal in normal subjects too; hence, an abnormally diminished Y descent has clinical significance only if the patient has high CVP.

• 84.

  How do you estimate the CVP?

  • By first positioning the patient , so that you can get a good view of the internal jugular vein and its oscillations. Although it is wise to start at 45 degrees, it doesn’t really matter which angle you use to raise the patient’s head, as long as it can adequately reveal the pulsations.

  • By identifying the highest point of jugular pulsation that is transmitted to the skin (i.e., the meniscus). This usually occurs during exhalation and coincides with the peak of “A” or “V” waves. It serves as a bedside pulsation manometer.

  • By finding the sternal angle of Louis (junction of the manubrium with the body of the sternum).

  • By measuring in centimeters the vertical height from sternal angle to the top of the jugular pulsation and then adding a correction factor, usually 5–10 cm, which is the distance from the center of the RA (the zero point) to the sternal angle.

  • In the past, 5 cm was thought to be the constant distance from the sternal angle to the center of the RA regardless of patient position, but recent evidence from cadavers and computerized tomography (CT) scans show that the 5 cm rule is only correct when the patient is supine. At angles between 30 and 90 degrees, 8–10 cm should be added (and even more if the patient has a larger than average chest wall, as in obesity).

• 85.

  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 Louís who first described it (Dr. Louis is much more famous for having coauthored with the internist Joseph-Ignace Guillotin the homonymous capital punishment device, which presumably chopped aristocrats’ heads just above their angle of Louis). If, on the other hand, you are referring to the maneuver that relies on the sternal angle for estimating CVP, 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 distension is never more than 2–3 cm above the angle of Louis. A subsequent variant of this observation (i.e., that CVP can be estimated at the bedside by adding 5 cm to the vertical height of the internal jugular vein above 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.

• 86.

  What is the normal central venous pressure?

  As estimated by the method of Lewis, a normal CVP should be less than 7 cmH ₂ O (some authors have suggested 8 cmH ₂ O).

• 87.

  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 CVP >10 cmH ₂ O, and thus pathologic (this is because the clavicles lie at a vertical distance of about 2 cm above the sternal angle. Hence, if CVP is normal, veins should not be visible).

• 88.

  Are there alternative methods to assess the central venous pressure?

  Yes, by using hand veins.

  • One is the Von Recklinghausen’s maneuver . This consists in asking the patient to lie supine, with the palm of one hand laid down over the thigh and the other laid down over the bed (thereby 5–10 cm below the first hand). Patients have high CVP if the veins of both hands are engorged; normal CVP if only the lower hand veins are engorged.

  • An alternative but similar maneuver consists in inspecting the veins of the back of the hand in a reclining patient as the arm is slowly, and passively, raised. The level at which the veins collapse can then be related to the angle of Louis and the CVP measured.

• 89.

  What is the significance of a low jugular venous pressure?

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

• 90.

  What is the significance of an elevated jugular venous pressure?

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

  • Superior vena cava obstruction (in this case, there will be no jugular venous pulse and the abdominojugular reflux test will be negative)

  • Obstruction to right ventricular inflow (such as TS and right atrial myxoma, but also constrictive pericarditis or tamponade, where neck veins distension is a sine qua non )

  • TR

  • Decreased right ventricular compliance with increased end-diastolic (and right atrial) pressure. Possible causes include right ventricular failure or infarction, PS, and pulmonary hypertension

  • Left ventricular failure . This is a common cause of pulmonary hypertension. In fact, in patients presenting with either angina or dyspnea, a high CVP argues in favor of left ventricular failure. Conversely, normal neck veins are unhelpful in separating normal from increased left-atrial pressure. Finally, CVP does not predict left-sided ejection fraction.

• 91.

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

  In a prospective study of 52 patients undergoing in-hospital evaluation for heart transplantation, found that jugular venous distension, a positive abdominojugular test, pulmonary crackles, and a left-sided S3 all independently predicted higher right-sided pressures and worse cardiac performance. Jugular venous distension (whether at rest or inducible), had the best operating characteristics. 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 distension were both sensitive and specific.

• 92.

  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 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.

• 93.

  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 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.

• 94.

  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 leading to right ventricular failure would manifest itself through an increase in CVP.

• 95.

  What is the significance of leg edema plus ascites in the absence of increased central venous pressure?

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

• 96.

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

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

• 97.

  What are the jugular findings of right ventricular infarction?

  • The right ventricular filling pressure is increased (as a result of an ischemic and less compliant chamber). Since the ventricle also becomes unable to handle incoming venous flow, the mean jugular (and central) venous pressures will be similarly increased.

  • The jugular venous pulse exhibits a prominent “A” wave. It also shows “X” and “Y” descents so steep they can mimic constrictive pericarditis. Jugular venous pressure and waveform are both significantly affected by the concomitant magnitude of damage to the interventricular septum (IVS) and left ventricular free wall.

  • Positive Kussmaul's sign is as specific as a jugular venous pressure (JVP) increase, but less sensitive.

  • The abdominojugular reflux test can be positive.

  • Finally, an associated TR will give additional findings, such as giant V waves, pulsatile liver, and right earlobe bobbing.

• 98.

  What is 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 is also 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.

• 99.

  What is it used for?

  To unmask subclinical right ventricular failure (and silent TR), but also to confirm symptomatic left ventricular failure (see later). Hence, the “Pasteur-Rondot maneuver” is a very helpful tool, albeit one that is often used (and interpreted) incorrectly.

• 100.

  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 RA, like a sort of poor man’s fluid challenge . If the RV cannot handle this extra load, there will be sustained increase in JVP.

• 101.

  Does abdominal pressure cause any change in cardiac output?

  No. Moreover, the changes in CVP 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 detecting congestive heart failure.

• 102.

  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 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 .

• 103.

  How do you perform an abdominojugular test?

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

  • Position the supine patient so that the jugular venous pulsations are properly monitored (an angle of 45 degrees will usually suffice). Then instruct him/her to relax and breathe normally through the open mouth. This will avoid the false-positive increase in jugular venous pressure caused by a Valsalva's maneuver inadvertently triggered by abdominal discomfort.

  • Apply your hand over the patient’s mid-abdomen (periumbilical area), with fingers widely spread and palm gently rested. Once the patient is well relaxed, apply gradual and progressive pressure for at least 10 seconds: firm, inward, cephalad, and soon reaching a steady level of 20–35 mmHg. This can be confirmed by placing an unrolled bladder of a standard adult blood pressure cuff between the examiner's hand and the patient's abdomen. The cuff should be partially inflated with six full-bulb compressions.

  • Note that the precision of the test may vary based on the force of abdominal compression. Different investigators have in fact suggested different forces: Ducas (1983) recommended 35 mmHg (equivalent to a weight of approximately 8 kg), while used 20 mmHg.

  • Throughout the maneuver (i.e., before, during or after compression), observe the column of blood in the internal and external jugular veins.

  • To avoid the risk of false positive neck vein distension from breath-holding or “bearing down,” consider a trial run. This can also be used to demonstrate in advance the force that will be applied onto the abdomen.

  • You might also look for a softening of the first heart sound during the application of abdominal pressure. This represents the auscultatory equivalent of a positive response.

• 104.

  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 [1983], is the upper limit of normal) that remains sustained through all 10 seconds of compression. Conversely, the test is considered negative when any of the following occurs:

  • No change in JVP.

  • Sustained change, but not large enough (i.e., ≤3 cm).

  • Enough change, but not sustained . In this case there may be an initial bulging of the external jugular vein at the beginning of abdominal compression (and also of the peaks and troughs of the internal jugular), and the JVP may even increase by more than 3 cm, but this is transient and returns to normal (or near normal) during the remainder of the compression.

  • 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.).

• 105.

  What is the significance of a positive abdominojugular reflux?

  • In patients presenting with dyspnea, the presence of abdominojugular reflux argues in favor of bi ventricular failure and suggests a pulmonary capillary wedge pressure >15 mmHg . This was confirmed at cardiac cath by Ewy et al. Patients with positive responses 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 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).

  • TR, TS, restrictive cardiomyopathy, and constrictive pericarditis are also common causes 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 instead a reflection of either a RV that cannot accommodate an increased return, or a LVLV that is dysfunctional.

  Pearl

  Although recently shown to correlate with pulmonary capillary wedge pressure (and thus reflecting left ventricular function) the abdominojugular maneuver is traditionally used to either augment or unmask a murmur of tricuspid regurgitation. For this, it has a specificity of 100% and a sensitivity of 66%, whereas the Rivera-Carvallo maneuver (inspiratory increase in intensity of the tricuspid regurgitation murmur) has a specificity of 100% and a sensitivity of 80%. When combined, the two have a sensitivity of 93% and a specificity of 100%.

• 106.

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

  No. This was recommended in the past, but it is not the case anymore. In fact, used 10 seconds, and so did Ducas (1983), 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.

• 107.

  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.

• 108.

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

  Those that interfere with venous return and right ventricular filling. The original description was in a patient with constrictive pericarditis (Kussmaul’s sign 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 backward from the heart to the superior vena cava, other causes of this sign include (1) cor pulmonale (acute or chronic); (2) constrictive pericarditis ; (3) restrictive cardiomyopathy (such as sarcoidosis, hemochromatosis, and amyloidosis); and (4) TS . Remember that Kussmaul’s sign is also present in 33%–100% of patients with right ventricular infarction . Thus, in a setting of acute myocardial infarction (MI), Kussmaul’s sign should not be interpreted as a sign of tamponade, but as a clue to concomitant right ventricular injury.

• 109.

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

  Both were first described by Kussmaul. And yet,

  • Kussmaul’s sign never occurs in “pure” tamponade (if it does, concomitant epimyocardial fibrosis is present); but 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, while Kussmaul’s sign 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’s sign doesn’t occur.

• 110.

  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 CVP, 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, TS, and cor pulmonale – acute or chronic).

• 111.

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

  Blind examination of patients with indwelling central venous catheters may provide valuable feedback. Pocket cards displaying the normal jugular pulse may also 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.

• 112.

  What is the “venous hum”?

  It is a functional murmur (see also Question 324) 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 can become audible over the sternal/parasternal areas, both right and left. This may lead to misdiagnoses of carotid disease, PDA, or AR/AS.

• 113.

  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 fades (or altogether disappears) with 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.

• 114.

  What is the mechanism of the venous hum?

  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 high-output state.

• 115.

  How prevalent is this finding?

  It can be heard in 31%–66% of normal children, and 25% of young adults. It is also 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.

• 116.

  Can any other cardiac event be heard at the neck?

  Besides transmitted systolic ejection murmurs, right-sided S3 and S4 gallops may also 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.

Generalities

Inspection and palpation of precordial impulse and movements completes the preauscultatory evaluation of the cardiovascular system. In fact, percussion of the cardiac area (although still quite accurate when competently performed) has become more a memory of the past than a standard of today’s practice. Conversely, evaluation of the precordial impulse remains a very important part of the exam. It can provide valuable information on intracardiac size and function and may even be the first clue of ventricular enlargement, well before any EKG or x-ray change.

• 117.

  What is the history behind precordial palpation?

  It goes back 3500 years, to the Ebers Papyrus of 1550 BC, 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 R.T.H. Laennec, his teacher Jean-Nicolas Corvisart, and Sir James MacKenzie.

• 118.

  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 – a rather confusing term for what is nothing more than a brisk movement of LV and septum against the chest wall. This is typically felt over the left fifth interspace, mid-clavicular 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.

• 119.

  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 aortic and pulmonary outflow tracts) and the left lower sternal area (reflecting right ventricular and atrial projection).

• 120.

  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.

• 121.

  How do you assess the precordial impulse(s)?

  • First inspect , since this may prove even more valuable than palpation. Shine a tangential light across the chest, which can help you visualize retractions and outward motions.

  • Then palpate the precordium, thoroughly assessing all major areas. With the patient in a supine position, localize impulses and evaluate their force . Then assess the impulse size by asking the patient to lie in left lateral decubitus. This might also help you elicit an otherwise undetectable apical impulse, as well as other impulses, such as a palpable S3 or S4. Use your palm to detect heaves or lifts (i.e., sustained precordial movements), the proximal metacarpals to identify thrills , and the finger pads to localize the various abnormalities.

• 122.

  How do you time precordial events?

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

• 123.

  Which characteristics of the apical impulse should be analyzed?

  • Location. Normally over the fifth left interspace mid-clavicular line, which usually (but not always) corresponds to the area just below the nipple. Volume loads to the LV (such as AR or MR) tend to displace the apical impulse downward and laterally. Conversely, pressure loads (such as AS 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 has 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 mid-systole. 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 systolic ejection murmur, consider instead severe pressure load from AS.

    • In patients with a diastolic murmur of AR (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 AR and VSD), 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 mid-clavicular line.

• 124.

  What are the most common abnormal apical movements?

  • A double systolic apical impulse can be seen in patients with HOCM. This may even present as a triple apical impulse (triple ripple) , with one impulse being presystolic (and corresponding to a strong atrial contraction) and the other two being instead systolic (corresponding to the initial ventricular contraction, and a delayed one necessary to overcome the outflow obstruction by the septum). A thrill is often present. Note that a double systolic impulse may also be encountered in patients with left ventricular dyskinesia due to either ischemia or aneurysm of the wall (see later). In fact, one-third of patients with ventricular aneurysm present with abnormal precordial findings.

  • A presystolic apical impulse represents the palpable equivalent of a fourth heart sound. It is an important finding because it provides a clue to reduced left ventricular compliance, as in the case of either ischemia or pressure load (such as AS or hypertension). In AS, a palpable S4 usually correlates with a significant gradient between the LV and aorta. It is often associated with a palpable thrill over the second right interspace.

  • An early-diastolic apical impulse represents the palpable equivalent of S3. It is more difficult to palpate than the presystolic impulse, and usually indicates a dilated LVLV. This can be the result of either volume load (i.e., MR) and/or left ventricular failure. In the latter, there may be an associated sustained apical impulse.

• 125.

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

  • A sustained movement that begins immediately after S1 usually reflects a pressure (or volume) load to the RV.

  • A sustained movement that begins late in systole reflects instead severe MR with dilatation of the LA.

  • A hyperdynamic movement can be a sign of atrial septal defect but is much more common in situations of high output, thin chests, or sternal malformations.

• 126.

  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.

• 127.

  What are the causes of a retracting impulse?

  Constrictive pericarditis (where up to 90% of patients may present with the finding) and severe TR . 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 RV) and a bulge over the epigastric and tricuspid area (now occupied by the enlarged RA).

• 128.

  What are the precordial findings of tricuspid regurgitation?

  In addition to those listed above, adult patients with TR may 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 is also appreciated.

• 129.

  What precordial evidence suggests mitral stenosis?

  Palpability of both first and second sound. 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 (OS) can become palpable too, and an apical diastolic thrill may at times be felt in left lateral decubitus. Since the apical impulse of MS 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 MR.

• 130.

  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 case 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 a left ventricular aneurysm or dyskinesia.

• 131.

  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.

• 132.

  What is a thrill?

  A palpable vibration associated with an audible murmur (see also Question 306). A thrill automatically qualifies the murmur as being ≥4/6 in intensity, and thus pathologic.

• 133.

  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.

(1)

Diastolic Extra Sounds

• 195.

  How many diastolic extra sounds can be encountered?

  Five. Of these, two are common (S4 and S3); one less common (the OS of MS or TS); and two very uncommon (the opening “plop” of atrioventricular myxoma and the pericardial knock). Only the S4 occurs late in diastole (or presystole ); all others are early diastolic. Two are low-pitched and soft (S3 and S4); two high-pitched and loud (OS and pericardial knock); and one medium-pitched and of varying intensity (tumor “plop”).

(2)

Systolic Extra Sounds