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Dr. Zema is Clinical Associate Professor of Medicine, State University of New York, and Chief, Division of Cardiology, Brookhaven Memorial Hospital Medical Center.
Correspondence to: Michael J. Zema, MD, FCCP, Chief, Division of Cardiology, Brookhaven Memorial Hospital Medical Center, 101 Hospital Rd, Patchogue, NY 11772
For decades, clinicians have diagnosed and treated the symptoms of left heart failure in their patients based on a carefully taken history, bedside physical examination, and chest radiograph. Symptoms such as orthopnea, paroxysmal nocturnal dyspnea, and dyspnea on exertion lack specificity, however, and may be seen in patients with chronic sinusitis as well as obstructive airways disease.1 2 The well-known physical findings of ventricular gallop sound, pulmonary rales, hepatojugular reflux, jugular venous distention, and peripheral edema, on the other hand, while reasonably specific in certain clinical settings, are unacceptably insensitive, making their absence in an individual patient of little value in excluding significant left ventricular dysfunction.3 4 5 Although it is far superior to the standard physical diagnostic signs, an upright chest radiograph that assesses the distribution of pulmonary blood flow and the presence or absence of radiographic cardiomegaly still has rather limited sensitivity, particularly for the detection of mild or moderate left ventricular dysfunction.2 3 4
Over the past decade, it has become increasingly clear, moreover, that the hemodynamic model of heart failure is an incomplete and imperfect one. Alterations of the renin-angiotensin,6 natriuretic peptide,7 and sympathetic nervous systems6 8 have been demonstrated in animal models and in man to correlate quite closely with measurable hemodynamic abnormalities, and often to precede their development.
While the diagnosis of congestive heart failure, therefore, may have as yet no "gold standard," we and others have found an unsurpassed correlation between the pattern of arterial pressure response detected by use of the bedside Valsalva maneuver and documented abnormal left ventricular hemodynamics, either systolic4 9 or diastolic4 10 dysfunction. Its use has proven, moreover, to be an extremely helpful clinical tool for the identification of patients with left ventricular disease who present with either acute11 or chronic2 dyspnea of unknown etiology. The maneuver can usually be performed quite satisfactorily by most subjects, even after only a very brief explanation.
The Valsalva maneuver has generally been divided by most cardiac
physiologists into four more or less well-defined phases: phase 1, the
onset of straining with its associated arterial pressure rise; phase 2,
straining; phase 3, the release of strain; and phase 4, arterial
pressure overshoot. Studies in man using the pressure-gradient
technique have shown that in normal subjects, the arterial pressure
response during the Valsalva maneuver is the result of an acute
increase in intrathoracic pressure (phase 1); decreased stroke volume
secondary to decreased venous return with compensatory rise in heart
rate and peripheral vascular resistance and subsequent narrowing of
pulse pressure (phase 2); an acute decrease in the level of
intrathoracic pressure (phase 3); and an acute increase in stroke
volume over control level while peripheral vascular resistance remains
transiently elevated (phase 4). During phase 2, with decreased venous
return, decreased stroke volume, and fall in systolic arterial
pressure, arterial baroreceptor hypotension causes decreased carotid
sinus nerve stimulation with enhanced 
and ß sympathetic efferent
traffic via the cardiac sympathetic nerves resulting in tachycardia
(ß), enhanced contractility (ß), and increased peripheral vascular
resistance (), the latter being responsible for the narrowing of
pulse pressure and decrease in pulse amplitude ratio. In patients with
heart failure, perhaps due to a resetting of the arterial baroreceptors
or enhanced resting -adrenergic tone, this decrease in pulse
amplitude ratio during phase 2 is blunted, as noted by Brunner-La Rocca
and coworkers in this issue of CHEST (see page 861) and by
others10
Likewise, the height of the arterial
pressure overshoot (phase 4) is diminished, a finding that can be
reproduced experimentally in normal subjects by the infusion of the
-agonist norepinephrine.12
In patients with
severe hemodynamic4
9
or neurohumoral manifestations of
heart failure (see Brunner-La Rocca and coworkers), physiologic events
during the Valsalva maneuver are even more abnormal. Stroke
volume initially increases (phase 1) but often continues to
remain elevated during the remainder of the strain phase (phase 2),
accounting for the rise in systolic BP above control levels (as seen in
the "BP VM > rest" subgroup by Brunner-La Rocca and
coworkers).
Brunner-La Rocca and coworkers have demonstrated in symptomatic patients with proven left ventricular dysfunction that pulse amplitude ratio measured during phase 2 of the Valsalva maneuver varies directly with plasma concentration of natriuretic peptide and inversely with indexes of functional capacity such as maximum oxygen uptake and exercise duration, thereby completing the integration of left ventricular hemodynamics, neuroendocrine balance, and patient functional capacity with the arterial pressure response elicited during the Valsalva maneuver.
Production of the phase 4 arterial pressure overshoot is dependent on the integrity of baroreceptor function,4 13 and as such can be interfered with by antiadrenergic drugs such as ß-blockers,4 limiting its clinical utility under those circumstances. Likewise, since the change in pulse pressure and hence pulse amplitude ratio during phase 2 appear to be dependent on an intact neural reflex arc involving sympathetic efferent output, it may be anticipated that sympatholytic agents will also interfere with their measurement. Brunner-La Rocca and coworkers do not reveal what percentage of their patients were taking ß-blocking agents. Of interest, however, is that 19 of their subjects (42%) were receiving amiodarone, which does possess noncardioselective ß-adrenergic blocking properties. It might prove interesting to reanalyze their data, excluding those subjects, to determine whether their reported correlations would be even more robust.
Considering the cost and time involved with currently available methods to objectively demonstrate the presence or absence of "congestive heart failure" (eg, exercise testing, natriuretic peptide and norepinephrine blood levels, radionuclide ventriculography, and echocardiography etc), one must ask whether or not it is time to incorporate the simple 30-s bedside Valsalva maneuver into the routine office examination. The arterial pressure response (which correlates with functional capacity, level of neurohormones, and cardiac hemodynamics) that occurs during the Valsalva maneuver (which is totally noninvasive, does not expose the patient to ionizing radiation, and can be completed in < 30 s) would appear to be a far more useful screening tool than either the chest radiograph or resting ECG, both of which are almost universally employed in patients in whom there is any question of clinical congestive heart failure. Although multiple patient populations must eventually be examined, preliminary information suggesting prognostic value, at least in postmyocardial infarction subjects, has already been published.14
Ultimately, performance of the Valsalva maneuver can be standardized, results can be directly recorded,15 and data can be digitized and transferred to a personal computer where, with appropriate software and minimal user interface, information can be derived from the pulse amplitude ratio and arterial pressure overshoot, permitting the creation of a statement of probability or likelihood of a congestive heart failure state. The physiology has been elucidated, the technology is available and reasonably inexpensive, the preliminary data are encouraging, and expectation, therefore, is justifiably high.
References
This article has been cited by other articles:
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  A. Schlegel Dyspnea and Heart Failure in the Emergency Department JAMA, March 8, 2006; 295(10): 1122 - 1122. [Full Text] [PDF]
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 D. Weilenmann, H. Rickli, F. Follath, W. Kiowski, and H. P. Brunner-La Rocca Noninvasive Evaluation of Pulmonary Capillary Wedge Pressure by BP Response to the Valsalva Maneuver* Chest, July 1, 2002; 122(1): 140 - 145. [Abstract] [Full Text] [PDF]
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