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Nuggets, Pearls, and Vignettes of Master Heart Failure Clinicians

2001; Wiley; Volume: 7; Issue: 6 Linguagem: Inglês

10.1111/j.1527-5299.2001.01167.x

1751-7133

Carl V. Leier, James B. Young, T. Barry Levine, Ileana L. Piña, Paul W. Armstrong, Michael B. Fowler, Lynne Warner‐Stevenson, Jay N. Cohn, J. B. O'Connell, Michael R. Bristow, John M. Nicklas, David E. Johnstone, Jonathan G. Howlett, Héctor O. Ventura, Thomas D. Giles, Barry Greenberg, Kanu Chatterjee, Robert C. Bourge, Clyde W. Yancy, Stephen S. Gottleib,

Cardiovascular Syncope and Autonomic Disorders

Vital signs should be carefully measured. This important component of the examination is oftentimes ignored, performed by ancillary medical personnel in a haphazard manner, or incompletely evaluated. Positional blood pressure and heart rate are important in patients receiving vasodilator drugs. Several characteristics of the blood pressure and pulse dynamics give important clues to the severity of heart failure. For example, the presence of atrial fibrillation or frequent premature ventricular contractions has significant prognostic and therapeutic implications. These dysrhythmias can be inferred from analysis of the cardiac rhythm during pulse palpation, palpation of the cardiac apex, and cardiac auscultation. The respiratory rate and pattern are important because tachypnea may reflect the severity of pulmonary congestion or compromise and certain periodic respiratory patterns can frequently be seen (even in the outpatient department) that correlate with the later stages of severe circulatory failure (that is, Cheyne-Stokes respirations). The respiratory rate should actually be counted, as estimates are inaccurate. Furthermore, the respiratory rate should be assessed with the patient sitting quietly as well as after moving up onto the examination table or around the room. An increase in respiratory rate with simple exertion indicates more severe cardiac failure and decompensation, and may portend a poor prognosis. Cough, wheezing, and prolonged expiratory phase are also important, quick, and simple findings of obvious importance. Assessment of the blood pressure response to Valsalva's maneuver, calculation of proportional pulse pressure (pulse pressure divided by systolic blood pressure [SBP]), determination of augmented jugular vein distention after abdominal compression (hepatojugular reflux), and precordial percussion and palpation to identify cardiomegaly are simple procedures that should be performed in every patient during every examination when heart failure or left ventricular (LV) dysfunction is suspected. Distention of jugular veins or further distention after gentle abdominal pressure suggests central venous congestion with volume overload. In patients with known substantive ventricular dysfunction, I prefer to assess neck veins with the patient sitting upright or standing. Jugular venous distention and positive hepatojugular reflux in a standing patient imply particularly egregious congestion. A proportional pulse pressure of less than 0.25 has a very high association with a cardiac index of less than 2.5 L/min/m2. Use of Valsalva's maneuver at the bedside with sphygmomanometric determination of arterial blood pressure response was first detailed in patients with heart failure in the mid-1950s. This simple technique has proven to be reasonably useful in differentiating cardiac from pulmonary causes of dyspnea, and in identifying patients with a significantly depressed LV ejection fraction (EF). The SBP is first obtained with the patient breathing normally in the supine position. Cuff pressure is then increased to about 15 mm Hg above the systolic pressure, and the patient is asked to perform the Valsalva maneuver at the end of a normal respiratory cycle. The Valsalva is held for 10 seconds, and the patient is subsequently instructed to relax, with resumption of the normal respiratory pattern. Korotkoff sounds will appear at the initiation of the Valsalva strain phase. In patients with normal ventricular function, the Korotkoff sound will disappear within a few seconds and will not be heard during continued straining, but will return 3–10 seconds after resumption of a normal breathing pattern (the so-called sinusoidal pattern). Patients with moderate depression of LV systolic function will initially appear to have the sinusoidal pattern, but Korotkoff sounds will not reappear during the relaxation phase (absent overshoot pattern). In patients with severely depressed LV systolic dysfunction and elevation of left heart pressures, Korotkoff sounds will be heard throughout the straining phase, with disappearance of the sounds after relaxation (“square wave” pattern). The square wave response pattern noted in patients who survive myocardial infarction, for example, is a sign of very poor prognosis. Cardiomegaly is suggested by a laterally displaced heart border, detected by percussion or palpation of the cardiac apical impulse. LV or RV lifts and a rocking and heaving left thorax are all associated with substantial ventricular dysfunction, pulmonary hypertension, and poor prognosis. Soft heart sounds, particularly if accompanied by a loud S3 gallop, are also associated with substantial ventricular dysfunction and congestion. If listened to carefully, most heart failure patients have heart murmurs. Generally, these are related to mitral or tricuspid regurgitation. The intensity of the murmur is not usually associated with the severity of valvular regurgitation, as substantial mitral insufficiency might have attenuated “noise” if the left atrial pressure is significantly elevated. Nonetheless, loud murmurs generally are of concern. Many findings that are routinely sought are well known and described, such as pulmonary rales, wheezes (cardiac asthma), ascites, hepatomegaly, and peripheral edema. Other findings, however, may be equally important and can provide further insight into both the chronicity and severity of the disease process (see Table I). Cachexia, for example, points to long-standing heart failure that is often end-stage. Sometimes the findings of cachexia can be subtle (e.g., just temporal muscle wasting). Petechiae or ecchymoses might suggest coagulopathy secondary to hepatic congestion. Examination of the integument can point toward the presence of systemic diseases, such as scleroderma, systemic sarcoidosis, myxedema, Graves' disease, or Rendu-Osler-Weber syndrome (small cutaneous and mucosal arteriovenous malformations/angiomata). Feeling the peripheral pulse for a long period of time will give the clinician great insight into the integrity and dynamics of the circulation in general. The importance of characterizing cardiac rhythm has already been mentioned. Certainly this time is well spent in the exam room because it creates a certain intimacy between the care giver and the patient that helps establish rapport and confidence. Pulse volume and regularity, and the presence of “dicrotism,” are important. I find these aspects best assessed by feeling the brachial and radial arteries of both arms, with varying degrees of pressure placed over the artery. Pulsus alternans and pulsus paradoxus implicate advanced stages of cardiac failure. Dicrotism, like many of the other subtle findings, is also associated with a poorer prognosis and is seen in the latter stages of heart failure, when patients are substantively volume-overloaded and hypotensive, but with diminished afterload. The dicrotic pulse is a “double-hump” pulse, with the second pulsation generally obliterated as pressure over the artery from one's fingers increases. It is not the same as the bisferious pulse noted in carotid arteries of patients with idiopathic hypertrophic subaortic stenosis. Other “physical findings” that can also give clinicians insight into the patient's clinical situation include observing a pack of cigarettes in a patient's pocket, particularly when the patient has just denied being a smoker! A casual glance into an open purse, briefcase, or package sometimes confirms the same, or often will allow inference of dietary indiscretion (e.g., when a partially consumed bag of Fritos is noted to be carefully tucked away). Interestingly, heart failure patients often will walk into an initial evaluation carrying handy containers of Gatorade™ or large cups of a carbonated soft drink or water, which they will consume during the interview. Observing the patient while walking with him/her to the examination room gives great insight into the stage of a patient's heart failure syndrome and degree of decompensation. Of course, a patient who shows up in a wheelchair and on oxygen can be telling, particularly if the wheelchair is not used to support non-CHF musculoskeletal difficulties. Finally, a coughing or wheezing patient presents a telling tale on physical examination. In summary, a patient's history and physical examination are always very important. Additional laboratory testing with further diagnostic evaluation is critical to developing the overall patient picture and therapeutic plan. To recapitulate, the diagnostic evaluation of a patient with heart failure should, in the end, be used to answer several key questions. It is critical to determine if heart failure is present, the cause(s) of the difficulty or precipitated deterioration, and the severity and degree of impairment. When these questions are answered, the patient's long-term prognosis can generally be determined and therapeutic strategies designed to address both the acute and chronic problems. —James B. Young I have found the onset of Cheyne-Stokes respirations to be an ominous sign. Although consultation with a pulmonologist may be of benefit, intensification of heart failure therapy, with or without inotropic support, is critical to the resolution of this symptom. —T. Barry Levine Loss of concentration for detailed tasks, such as performing mathematical operations or reading, may be an early sign of low cardiac output in patients with chronic heart failure who have been otherwise stable. —Ileana Piña Bilateral palpation of the radial pulses to screen for arm blood pressure and pulse differences permits selection of the best arm for repeated blood pressure measurements. This maneuver may also be informative in the detection of severe peripheral (e.g., subclavian, brachial) atherosclerosis in this era of vascular intervention. Oscillometric blood pressure measurement usually provides a more accurate measurement of SBP than that obtained via the first Korotkoff sound (Crit Care Med. 1984;12:965). The systolic pressure determined by the Korotkoff method is often erroneously lower than direct or oscillometric pressures and thus has been the basis for inappropriately withholding or reducing doses of important, needed medication (because of “hypotension”) in an otherwise asymptomatic patient. —Paul W. Armstrong Elevated systemic venous pressure and raised neck veins are often missed in heart failure because the examination is performed while the patient is lying flat. There is also a general failure to detect venous pulsation at the angle of the jaw. Gallop rhythm is often missed, as it is simply not “listened for.” —Michael B. Fowler If you are not willing to take the time to acquire and retain facility at reading jugular venous pulsations, you need to find a different population of patients (other than heart failure) to serve. —Lynne Warner-Stevenson The jugular venous pressure (JVP) is the single most important marker of the status of intravascular volume. Most patients with heart failure can be maintained in a satisfactory hemodynamic state with a JVP within normal limits and without a rise in pressure in response to right upper quadrant abdominal compression. In a few instances, however, when LV function is severely impaired or when there is an element of restriction (pericardial or myocardial), clinical stability requires maintenance of an elevated JVP. When a patient is stable, the level of the JVP (along with body weight) can serve as a baseline for all subsequent observations. Stable patients can usually be monitored at 3-month intervals. More labile patients may require more frequent clinic visits and drug adjustment. At each clinic visit, the JVP, as assessed by deep pulsation in the neck, is recorded before and after right upper quadrant abdominal compression. Two other maneuvers are often helpful: passive leg raising (which can be combined with right upper quadrant compression) and exercise by jogging in place and then returning to the supine position for assessment of a change in JVP. Patients who begin to complain of dyspnea on exertion almost always manifest a rise in JVP in response to these maneuvers. Such response should mandate an increase in the diuretic dosage. In contrast, the absence of any of these signs of intravascular volume expansion, along with fatigue, weakness, and modest azotemia, would be an indication to reduce the diuretic dose. —Jay N. Cohn In the physical diagnosis course, second-year medical students are typically introduced to the mysteries encoded in evaluation of JVP and pulsations. However, a true appreciation of the information that the neck veins can provide is underdeveloped at best in most clinicians. In fact, with the advent of echocardiography, by and large the expertise in cardiovascular physical examination has dramatically deteriorated and it is not uncommon for even cardiology fellows to record relatively sophomoric physical examinations on the medical record, and even to perform echocardiography (gasp!) prior to thoroughly examining the patient. However, in a heart failure practice, the neck veins provide an easily accessible tool in assessing JVP as an index of intravascular volume, right-sided filling characteristics, and even arrhythmias. Much has been written about assessing the jugular veins; however, this discussion will selectively deal with utilization in patients with CHF and consequently concentrate on estimation of JVP. Physical diagnosis textbooks quote various methodologies for estimating JVP at the bedside. Textbooks will suggest placing the patient in a position of anywhere from 25°–45° from the supine and estimating the zero at the mid-right atrial position, either directly or using anatomic landmarks, such as the manubrial sternal angle (angle of Louis) 5 cm above the mid-right atrium. If the height of the column is then estimated, a column detected >5 cm above the sternal angle indicates elevation of JVP (>10 cm H2O). However, this technique is extraordinarily cumbersome and, in fact, fraught with inaccuracies. Estimation of height and the bedside angle are all difficult to reproduce. A much easier technique employs the observation that at 90° (sitting up-right) the clavicle is approximately 10 cm above the right atrium in most normal adults. Since 10 cm of water is the upper limit of normal central venous (right atrial) pressure, the absence of visible jugular venous pulsations in a free-flowing system essentially eliminates elevated JVP. JVP can then be approximated by estimating the height to the top of the column (area of pulsations) from the clavicle (my fingers are 1.5 cm wide). Therefore, a recording of JVP of 10 cm of water). It is easy for trainees to understand this concept and add diuretics or venodilators if venous pressure is too high, or to reduce or maintain them. In our ambulatory practice, repetitive measurement of JVP is a key physical diagnostic observation that is recorded at every visit, and optimum venous pressure can easily be established over recurrent observations. The JVP is also helpful in identifying volume depletion. However, in order to approximate the venous pressure below 10 cm of water, a gradual reduction of the supine position angle should be accomplished. If there is no filling of the jugular veins in the flat supine position, the patient may be significantly volume-depleted. Although medical students are taught to measure hepatojugular reflux (abdominal jugular reflux), this technique in heart failure patients is useful only if JVP is not elevated. Elevation of the JVP implies that right-sided filling is already impaired, and the obvious expectation is positive hepatojugular reflux. The positive reflux sign can be informative in the circumstance of normal right-sided filling pressures when diastolic reserve is impaired, suggesting ventricular dysfunction. In general, this technique has little utility in the sequential assessment of heart failure. Observation of the jugular vein can include characterization of the waveforms that are seen in pericardial constriction, restrictive heart disease, pulmonary hypertension, and tricuspid regurgitation. The jugular venous waveforms may be very helpful in the diagnosis of arrhythmia (e.g., f waves in atrial flutter or cannon A waves in atrioventricular (AV) dissociation, high-grade heart block, and occasionally in ventricular tachycardia). However, diagnosing AV block from the neck vein, as noted by Mobitz and Wenckebach in an era when specific rhythm disturbances were described by determining the timing of A and V waves, before electrocardiography (EKG) was invented, is now rarely necessary. Mastering the ability to gain information from JVP is not passé. Important information can still be obtained from careful evaluation of the neck veins. This technique is easy to learn and is a great aid in management of fluid status in patients with heart failure. —John B. O'Connell Palpation of the internal jugular vein can be very helpful. It is oftentimes the only way to determine the level and extent of jugular venous distention in patients with “short, fat necks.” It has also served me well in expediting placement of central venous catheters, sheath placement for endomyocardial biopsies, and related procedures. —Carl V. Leier Don't bother evaluating neck veins in other than the 90°(sitting upright) position, since any true elevation will be visible above the clavicle in that position. This eliminates the need to extrapolate pressures from angles, and it saves time. —Michael R. Bristow Assess jugular venous distention with the patient in an upright position. The level of jugular venous distention in patients who are semi-supine is difficult to reproduce. Furthermore, I believe it is inaccurate to extrapolate venous pressure by triangulation from the observed vertical level of venous distention. Any clinically significant venous distention will be visible when the patient is upright. The level of venous distention is also easy to reproduce in the upright position and does not require triangulation. The jugular vein is a collapsible vessel. It is not a rigid vessel, and the intravascular pressure does not produce a simple meniscus in the blood filling the vein. Rather, the jugular distends to lesser degrees at higher vertical levels. In the upright position, the column of blood in the jugular vein resembles an inverted cone more than a cylinder. When venous pressure is extraordinarily high, the vein is fully distended and the tip of the column of blood extends above the jaw, even in the upright position. However, at more moderate levels of pressure, the cone of blood distends the vein in the neck to different degrees at various levels of the neck (less on top and more toward the lower region). Since it is difficult to assign a specific level of jugular distention in a vein distended by a cone, it is more appropriate to assign categories of venous distention. I categorize jugular distention in the upright position as absent, mild (the cone distends only the lower portion of the neck), moderate (the cone distends the entire neck, but the tip of the cone can still be visualized in the neck), or severe (the tip of the cone extends well above the jaw and the vein in the neck is fully distended). Reassess jugular distention during the Valsalva maneuver. Jugular venous distention can be difficult to assess because the internal jugular vein is often buried 2–4 cm beneath the skin or its pulsation may not be discernible from nearby carotid pulsation. During Valsalva, the jugular vein of a patient with normal venous pressures will slowly and progressively distend. In patients with elevated venous pressures, Valsalva will not produce a rising venous wave in the neck. Thus, Valsalva can assist the clinician in improving the specificity of the assessment of jugular venous distention. —John M. Nicklas In patients with advanced CHF, the examination should begin in the sitting position with the legs comfortably over the side of the examining table. An elevated JVP is rarely missed in this position. The lungs can also be examined at the same time, avoiding unnecessary movement of the patient with advanced symptoms. Palpation of the digital pulses in a patient with CHF may be helpful in the assessment of the pulse pressure and, if present, generally is a favorable sign. A digital throb in a patient with congestive heart failure suggests that the patient is compliant with the vasodilator regimen. A precordial murmur that radiates through to the back is usually mitral regurgitation and is less likely aortic stenosis or tricuspid regurgitation. In an adult patient presenting with an elevated JVP and no obvious signs of left heart failure, still suspect an LV origin. The most common etiology is restrictive physiology (hypertension, hypertrophic cardiomyopathy), which is more common than constrictive pericarditis. —David E. JohnstoneJonathan Howlett We have found the 2×2 matrix of wet/dry + warm/cold to be a very useful way of describing heart failure and triggering an initial plan of therapy (see Table II). This is now described (Circulation. 2000;102:2443). We have found the Valsalva maneuver square wave response helpful in identifying marked volume overload, particularly when there are other potential causes of dyspnea. I am not sure whether it preferentially detects right-sided over left-sided volume overload, or if it is equally influenced by both. While devices have been developed to do this more precisely, it can be determined with a blood pressure cuff and a stethoscope. The enhanced x and y descents of the jugular venous pulse that occur during inspiration often accentuate the appearance and allow the height of the pulsation to be better detected. Kussmaul's sign of an actual increase in JVP during inspiration is common in patients with severe RV volume overload. A number of methods can be employed to determine adequacy of systemic perfusion: Proportional pulse pressure ([SBP − DBP]/SBP) less than 25% suggests a cardiac output index (CO/BSA) of <2.2 L/min/m2. (JAMA. 1989;261:884). (SBP/DBP=systolic/diastolic blood pressure;BSA=body surface area) Temperature of extremities—feeling forearms and calves may be more useful than hands and feet, which can be cool from anxiety without necessarily reflecting poor overall perfusion. Patients who are completely alert and oriented one minute and falling asleep the next may be showing signs of low output. This often occurs before frank confusion. In patients undergoing right-heart catheterization during transplant evaluation (based on 1000 patients studied), we found that a mean right atrial pressure of greater or less than 10 and pulmonary capillary wedge pressure (PCWP) of greater or less than 22 were concordant in 79% of patients. Thus, in the absence of other known confounding diseases, such as severe chronic obstructive pulmonary disease (COPD), if you can read the neck veins accurately, you can guess whether the PCWP is greater or less than 22 in about 80% of patients with chronic heart failure. (J Heart Lung Transplant. 1999;18:1). When PCWP is elevated in patients without known severe pulmonary disease, pulmonary artery systolic pressure is closely related to PCWP and is usually about 2 × PCWP. (J Heart Lung Transplant. 1999;18:1) —Lynne Warner Stevenson The best bedside measure of cardiac output is examination of the peripheral pulse volume, and in the absence of peripheral vascular disease, foot pulse volumes and skin temperature. Thus, my first maneuver at the bedside of a patient with potentially compromised cardiac function is to examine the feet! Always examine the precordium in the left lateral position, which is the best place to hear a soft S3 gallop. —Michael R. Bristow This is a quote from one of my respected and excellent attending physicians regarding palpation of the apical impulse relative to cardiac dilatation: “A dilatation extending outward to one fingerbreadth beyond the nipple line is usually recovered from; two fingerbreadths means an exceedingly dangerous condition; while three fingerbreadths is usually fatal.” I do believe that it is helpful from a clinical point of view. —Hector O. Ventura Heart failure with warm hands and pink nailbeds suggests high-output states (e.g., thyrotoxicosis, beri-beri). Reversible causes of heart failure may be suspected by simply touching the patient. Heart failure with warm hands and cyanotic nailbeds suggests cor pulmonale. Right heart failure usually predominates in the setting of elevated JVP, hepatomegaly, and dependent edema. Dyspnea and signs of right heart failure that occur after edema of the legs raise suspicion of pulmonary emboli. The importance of determining the chronology of symptoms and signs cannot be overemphasized. —Thomas D. Giles Physical examination is an excellent means of determining whether heart failure is the cause of the patient's symptoms. An aspect of the examination that is paid scant (if any) attention is the visual and tactile bedside assessment of the heart through the chest wall. Inspection, percussion, and palpation of the precordium are excellent means of assessing cardiac size, and they can provide important clues about the levels of intracardiac pressures and about ventricular function. Moreover, this part of the examination can be performed rapidly in a variety of clinical settings, is reliable even when the clinician is “acoustically challenged,” and costs nothing other than time and the interest of the examiner. Inspection of the precordium is initially best performed from the foot of the bed or examining table, with the observer positioned at the level of the supine patient and looking in a cranial direction. Ordinarily, the chest is symmetric and without a bulge on either side or over the sternum. Handedness and strenuous physical activity over a sustained period of time may increase the size of the chest muscles on the right or left side in some individuals. However, bulging of the ribs and sternum over the left precordium may be seen in patients with congenital abnormalities resulting in pulmonary hypertension. This is due to enlargement and leftward extension of the (anterior) right ventricle. These abnormalities of the chest wall are rare with pulmonary hypertension acquired during adulthood, since the opportunity to remodel developing bone has already passed. The precordium of the patient with a normal heart and normal body habitus is usually “quiet,” without obvious pulsation. Pulsatile movement of the left 2nd intercostal space close to the sternum suggests the presence of pulmonary hypertension, and this can be confirmed by palpation of the impulse in the same area. This finding is often accompanied by the tactile sensation of a sharp click due to brisk pulmonary valve closure. Patients with heart failure often have evidence of a parasternal heave, detectable with visual inspection. This outward movement of the sternum during systole is commonly referred to as an “RV heave.” It is important to recognize that this precordial movement can also occur in patients with mitral regurgitation who have either trivial or no increases in RV pressure. The parasternal lift in this case is due to rapid increase in press