- Email: [email protected]
The Valsalva Maneuver: A Bedside “Biomarker” for Heart Failure
The American Journal of Medicine (2006) 119, 117-122
REVIEW
The Valsalva Maneuver: A Bedside “Biomarker” for Heart Failure G. Michael Felker, MD, MHS,a Phillip S. Cuculich, MD,b Mihai Gheorghiade, MDb a
Duke Clinical Research Institute, Durham, NC; and bNorthwestern University, Chicago, Ill. ABSTRACT Accurate assessment of volume status remains an important clinical goal in the management of patients with heart failure. Although physical examination can provide clues to volume status, its sensitivity and reproducibility are limited. Other noninvasive methods, such as measurement of natriuretic peptides or the use of impedance cardiography, are not well validated. The cardiovascular response to the Valsalva maneuver had been proposed as a simple, inexpensive bedside test for estimating filling pressures in patients with heart failure. Our objective was to summarize and critically evaluate the evidence for the use of the Valsalva maneuver in evaluating volume status in patients with heart failure. Studies have demonstrated a significant correlation between the cardiovascular response to the Valsalva maneuver and invasively measured ventricular filling pressures in patients with clinical heart failure. Although often overlooked in clinical training and practice, the cardiovascular response to the Valsalva maneuver is a potentially useful, noninvasive means of evaluating filling pressures in patients with heart failure. © 2006 Elsevier Inc. All rights reserved. KEYWORDS: Heart failure; Diagnosis; Physical examination; Valsalva maneuver
The epidemic of chronic heart failure has led to a rapid increase in hospitalizations for acute decompensated heart failure, with more than a million hospitalizations annually in the United States.1 Although a variety of clinical syndromes exist within the spectrum of decompensated heart failure, the majority of heart failure hospitalizations in clinical practice are related to volume overload and elevated ventricular filling pressures rather than low output states.2 Theoretically, many such heart failure hospitalizations could be prevented by early recognition and treatment of elevated filling pressures, but this strategy is difficult to apply because of the lack of tools to assess ventricular filling pressures in patients with chronic heart failure. Although ventricular filling pressures can be accurately assessed using pulmonary artery catheterization, this approach is highly invasive and associated with significant risks, making it an impractical means of assessing volume status Requests for reprints should be addressed to Michael Felker, MD, MHS, Duke Clinical Research Institute, PO Box 17969, Durham, NC 27715. E-mail address: [email protected]
0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2005.06.059
in the majority of patients with heart failure.3 Physical examination may provide important clues to filling pressures, but is also associated with substantial limitations and poor sensitivity.4 In addition, physical findings of volume overload, such as peripheral edema and elevated jugular venous pressure, are late signs that are often not present until ventricular filling pressures are extremely elevated, particularly in patients with long-standing chronic heart failure.5 Thus, there may be a disassociation between “hemodynamic congestion” (ie, elevation of left ventricular filling pressures) and “clinical congestion” (ie, physical signs of volume overload). It is therefore apparent that an accurate, reliable, inexpensive, and noninvasive means of quantifying “hemodynamic congestion” would be a major advance in heart failure management. This clinical need has led to a significant interest in the use of natriuretic peptides (brain natriuretic peptide and N-terminal prohormone brain natriuretic peptide) or impedance cardiography as tools for evaluating filling pressures and volume status in acute and chronic heart failure.6,7 Recently, novel implantable ambulatory devices have been developed to provide continuous estimation of ventricular filling pressures to optimize heart
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in blood pressure (phase 1) that remains elevated during the failure management.8 Another method of noninvasively esentire strain (phase 2) and returns to resting levels at release timating ventricular filling pressures, the cardiovascular re(phase 3). Stroke volume follows the same pattern.11,12 Careful sponse to the Valsalva maneuver, has been shown to be accurate, reliable, and noninvasive in a variety of clinical physiologic studies suggest the “square wave” response is the settings. Despite these promising data, the response to the result of maintenance of left ventricular filling during the strain Valsalva maneuver continues to phase, despite the decrease in right be little used in the clinical evalsided venous return.13 Maintenance of left ventricular volume is preuation of patients with heart failCLINICAL SIGNIFICANCE sumed to be related to increased ure. This review will summarize central blood volume that serves as available data on the response to ● Assessment of volume status is an ima reservoir to maintain left ventricthe Valsalva maneuver as a meaportant clinical goal in heart failure ular filling despite decreased venous sure of ventricular filling presmanagement, but this remains difficult return. With decreasing central sures and volume status and sugto assess accurately at the bedside using blood volume from diuresis, the regest potential roles for this test in currently available methods. sponse to the Valsalva maneuver the management of patients with normalizes.14 heart failure. ● The cardiovascular response to the Val-
CARDIOVASCULAR RESPONSE TO THE VALSALVA MANEUVER
salva maneuver has been shown to provide a reasonably accurate, non-invasive assessment of volume status and ventricular filling pressures in patients with heart failure.
QUANTIFYING THE CARDIOVASCULAR RESPONSE TO VALSALVA MANEUVER
The Valsalva maneuver was first described in 1704 as a sustained The hemodynamic changes asso● Further studies are needed to prospecforced expiratory effort or strain ciated with the Valsalva maneutively define the role of the Valsalva maagainst a closed glottis. The carver can be assessed with a varineuver in the clinical management of diovascular effects of the Valsalva ety of noninvasive methods, patients with heart failure. maneuver were described in 1851 including bedside sphygmomawhen Weber observed that “all the nometry, echocardiography, and sounds associated with the movephotoplethysmography of artement of the heart disappear” in response to the strain.9 In rial pressure waveforms. Bedside sphygmomanometry 1944, Hamilton and colleagues first reported an abnormal provides a qualitative assessment of the cardiovascular cardiovascular response to the Valsalva maneuver in paresponse to the Valsalva maneuver based on the “absent tients with congestive heart failure.10 overshoot” and “square wave” patterns of systolic blood The normal arterial blood pressure response to the maneupressure in heart failure. Systolic blood pressure is obver is an initial increase associated with the onset of straining tained while the patient is breathing quietly with normal (phase 1), followed by a sharp decrease to below baseline tidal volumes. Cuff pressure is then raised 15 mm Hg levels as the straining is maintained (phase 2). At the release of above resting systolic pressure, and the patient is asked to strain there is a short decrease of arterial pressure (phase 3), perform the Valsalva maneuver for 10 seconds and then which is followed by a distinct overshoot of the arterial presresume normal respirations. During the entire Valsalva sure (phase 4), creating a typical sinusoidal response (Figure 1, maneuver and for 30 seconds afterward, the cuff pressure 11 A). The changes in arterial pressure during the four phases of should be locked 15 mm Hg above the baseline systolic the Valsalva maneuver are the result of an acute increase in blood pressure while Korotkoff sounds are sought by intrathoracic pressure (phase 1), decreased stroke volume secauscultation over the brachial artery. Typically, only ondary to decreased venous return with compensatory increase phases 2 and 4 are registered, phase 1 and 3 being too in peripheral vascular resistance and reflex increase in heart short to be noticed. In healthy patients, Korotkoff sounds rate (phase 2), an acute decrease in the level of intrathoracic are heard only after release of straining, or phase 4. In pressure (phase 3), and a distinct increase in stroke volume patients with mild heart failure, Korotkoff sounds are over control level with concomitant decrease in peripheral absent during both phases 2 and 4 (absent overshoot). In vascular resistance and reflex bradycardia (phase 4). patients with severe heart failure, Korotkoff sounds are In patients with heart failure there are 2 distinct patterns of appreciated during phase 2 but not phase 4 (square wave) arterial pressure wave responses to the Valsalva maneuver: the (Table 1). This method has been demonstrated to be a “absent overshoot” response and the “square wave” response. reasonable screening test for left ventricular systolic dys“Absent overshoot” (Figure 1, B) is observed in patients with function in unselected outpatients in a cardiology less severe heart failure and manifests as normal phases 1 to 3 clinic.15 with an absence of arterial pressure overshoot after release of Echocardiographic evaluation of the cardiac response to the strain. The “square wave” response (Figure 1, C), seen in more severe heart failure, is characterized by an initial increase Valsalva maneuver has identified differences in atrial and
Felker, Cuculich, and Gheorghiade
Valsalva Maneuver in Heart Failure
119
CORRELATION OF VALSALVA MANEUVER WITH VENTRICULAR FILLING PRESSURES
Figure 1 Blood pressure response to Valsalva maneuver in various clinical situations. A, Sinusoidal arterial pressure response (normal). B, “Absent overshoot” arterial pressure response (mild heart failure). C, “Square wave” response (severe heart failure). Adapted from Zema MJ, Restivo B, Sos T, et al. Left ventricular dysfunction— bedside Valsalva manoeuvre. Br Heart J. 1980;44(5):560-569.
ventricular dimensions between patients with and without heart failure.16-18 Alternatively, cardiovascular response to the Valsalva maneuver can be quantified peripherally by measuring arterial pressure waveforms during the strain phase. The most frequently used measurement is the pulse amplitude ratio, a ratio of the minimal pulse pressure at the end of the strain phase to the maximum pulse pressure at initiation of the strain phase. Portable bedside devices that quantify these responses have been developed and validated.19,20 As described next, the pulse amplitude ratio has been shown to correlate very closely with ventricular filling pressures in a variety of clinical settings.
Table 1
The evaluation of patients with chronic heart failure for evidence of volume overload is crucial in preventing clinical decompensation. At present, noninvasive estimation of volume status is accomplished primarily by assessment of daily weights or by signs of elevated filling pressures on physical examination (increased jugular venous distention, hepatojugular reflux, peripheral edema). Unfortunately, these signs are insensitive, difficult to assess, and primarily reflect right-sided rather than left-sided filling pressures.5 Available data demonstrate that Valsalva maneuver is an accurate means for assessing cardiac filling pressures in a variety of heart failure populations. McIntyre and colleagues19 compared the pulse amplitude ratio during the Valsalva maneuver to directly measured pulmonary capillary wedge pressure in stable patients undergoing elective cardiac catheterization and critically ill patients undergoing placement of a pulmonary artery catheter in an intensive care unit. No patient had a primary diagnosis of heart failure. In both the stable and unstable patient groups, there was a strong correlation between the pulse amplitude ratio during Valsalva maneuver and invasively measured pulmonary capillary wedge pressure (r ⫽ 0.80 for the clinically stable group and 0.85 for the clinically unstable group). In addition, changes in pulmonary capillary wedge pressure induced by volume loading or diuresis correlated well with changes in noninvasive pulse amplitude ratio (r ⫽ 0.79). A subsequent study in patients with chronic heart failure compared predicted pulmonary capillary wedge pressure (based on Valsalva maneuver) to invasively measured pulmonary capillary wedge pressure in 30 patients with chronic heart failure, demonstrating a very high correlation between the 2 (r ⫽ 0.9, P ⬍ .001) (Figure 2). Noninvasive assessment predicted a pulmonary capillary wedge pressure of ⱖ 18 mm Hg with a sensitivity of 91% and specificity of 100%.21 A study by Sharma et al.20 compared the accuracy of noninvasive device measurement (VeriCor, CVP Diagnostics, Inc., Boston, Mass) to both invasively measured pulmonary capillary wedge pressure and left ventricular enddiastolic pressure in patients undergoing right- and leftsided heart catheterization. The noninvasive device measurement was found to have significant correlation with
Korotkoff sounds during beside performance of the Valsalva maneuver
Systolic BP response
Phase 2 (straining)
Phase 4 (relaxation)
Sinusoidal response (Normal) “Absent overshoot” response (Mild heart failure) “Square wave” response (Severe heart failure)
Korotkoff sounds NOT heard Korotkoff sounds NOT heard Korotkoff sounds heard
Korotkoff sounds heard
BP ⫽ blood pressure.
Korotkoff sounds NOT heard Korotkoff sounds NOT heard
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Figure 2 Relationship between pulse amplitude ratio during Valsalva maneuver (noninvasive PAWP) and invasively measured PAWP. Noninvasive PAWP was calculated from PAR by linear regression. PAWP, pulmonary artery wedge pressure; PAR, pulse amplitude ratio. Adapted from Givertz MM, Slawsky MT, Moraes DL, et al. Noninvasive determination of pulmonary artery wedge pressure in patients with chronic heart failure. Am J Cardiol. 2001;87(10):1213-1215.
left ventricular end-diastolic pressure (r ⫽ 0.86). Notably, this correlation was greater than that between the directly measured pulmonary capillary wedge pressure and the left ventricular end-diastolic pressure (r ⫽ 0.80). Direct comparison of device measurements and pulmonary capillary wedge pressure showed that 84% of the device measurements were within 4 mm Hg of the left ventricular enddiastolic pressure, compared with 41% of the pulmonary capillary wedge pressure measurements. The device used in this study was approved for use by the Food and Drug Administration to estimate left ventricular end-diastolic pressure in patients with signs and symptoms of heart failure. In addition to direct measurements of pulmonary capillary wedge pressure and left ventricular end-diastolic pressure, response to the Valsalva maneuver has been shown to correlate with other surrogate measures of left ventricular filling pressures, such as natriuretic peptide levels. A study of 45 patients with moderate heart failure demonstrated correlation between response to the Valsalva maneuver (as quantified by the pulse amplitude ratio) and levels of atrial natriuretic peptide (r ⫽ 0.75, P ⬍ .0001) and brain natriuretic peptide (r ⫽ 0.6, P ⬍ .0001) (Figure 3).22 No studies have directly compared the accuracy of Valsalva maneuver and brain natriuretic peptide measurements in predicting ventricular filling pressures, but the data of Givertz et al.21 compare favorably to available data on brain natriuretic peptide and invasively measured filling pressures.23 Heart failure in the setting of preserved systolic function (“diastolic dysfunction”) is an important clinical entity,
comprising greater than 50% of the population of patients with heart failure in the community.24 Clinically, this syndrome is characterized by frequent hospitalization and high resource use, typically because of elevated filling pressures and volume overload.25 Available data suggest that the relation between response to the Valsalva maneuver and ventricular filling pressures is not affected by ejection fraction (EF). Data suggest that pulse amplitude ratio correlates best with invasively measured pulmonary capillary wedge pressure (r ⫽ 0.77, P ⬍ .005) but not with cardiac index (r ⫽ 0.14, P ⫽ not significant) or EF (r ⫽ 0.09, P ⫽ not significant).26 These data have been corroborated by other small studies.27 Given that the cardinal symptoms of heart failure are related to elevated filling pressures and not to EF per se, heart failure is increasingly being seen as spectrum of disease states requiring similar treatment regardless of EF.28 Available data suggest that the use of the Valsalva maneuver as a tool for the assessment of volume status seems applicable to patients with heart failure regardless of EF.
PROGNOSTIC VALUE OF VALSALVA MANEUVER IN HEART FAILURE Accurate assessment of prognosis is critical in heart failure because of the need to triage patients among expensive, invasive therapies such as implantable defibrillators, cardiac resynchronization therapy, ventricular assist devices, and cardiac transplantation.29-32 A variety of parameters have been associated with prognosis in chronic heart failure.33-36 Recently, a growing body of research has focused on the role of natriuretic peptides (brain natriuretic peptide or Nterminal prohormone brain natriuretic peptide) in risk stratification of patients with heart failure.37,38 In contrast, few studies have investigated relationships between Valsalva maneuver and clinical end points. One small study has suggested that abnormal response to Valsalva maneuver is predictive of future heart failure episodes in patients on
Figure 3 Correlation of response to Valsalva maneuver (pulse amplitude ratio) and brain natriuretic peptide measurements in patients with heart failure. Adapted from Rocca HP, Weilenmann D, Rickli H, et al. Is blood pressure response to the Valsalva maneuver related to neurohormones, exercise capacity, and clinical findings in heart failure? Chest. 1999;116(4):861-867.
Felker, Cuculich, and Gheorghiade
Valsalva Maneuver in Heart Failure
hemodialysis.39 When tested several weeks after an acute myocardial infarction, an abnormal response to Valsalva maneuver predicted future sudden cardiac death.40 The most common reason for hospitalization in patients with congestive heart failure is volume overload, typically treated with intravenous diuretics.2 Objective measures of the adequacy of diuresis during acute hospitalizations are lacking, and decisions to discharge patients with heart failure are usually based on clinical judgment. Lack of objective criteria to define “successful treatment” has contributed to high rates of rehospitalization.1 Stevenson et al.41 have demonstrated that the ability to achieve decreased filling pressures with aggressive medical therapy is a powerful predictor of future clinical stability. Low levels of brain natriuretic peptide at discharge have been shown to predict freedom from hospitalization, presumably because of adequacy of diuresis and restoration of physiologic homeostasis.42 Decreasing intravascular volume has clearly been shown to normalize the response to the Valsalva maneuver in human studies.14,19 These data suggest the possibility of a role for response to Valsalva maneuver as a simple bedside assessment of the adequacy of diuresis and readiness for discharge, a concept that could be tested prospectively.
CONCLUSIONS Accumulated data suggest that the Valsalva maneuver is a useful tool in the assessment of patients with heart failure. Bedside sphygmomanometry can provide a qualitative assessment of volume status, and commercially available arterial waveform devices provide a rapid and reliable measurement of cardiovascular dynamics that predict left ventricular filling pressures in a variety of clinical settings. Potential uses for the Valsalva maneuver in patients with heart failure include bedside assessment of filling pressures, judging adequacy of diuresis during hospitalization, and stratifying risk for future events. Despite the potential advantages of accurately estimating filling pressures at the bedside, measurement of cardiovascular response to the Valsalva maneuver is seldom taught in medical schools and remains little used in clinical practice. Given the increasing costs of heart failure care, further research into the potential uses of this inexpensive bedside tool seems justified as a means to control cost and improve outcomes in patients with heart failure.
References 1. Felker GM, Adams KF, Konstam MA, et al. The problem of decompensated heart failure: nomenclature, classification, and risk stratification. Am Heart J. 2003;145(2):S18-S25. 2. Fonarow GC, Adams KF Jr, Abraham WT, et al. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA. 2005;293(5):572-580. 3. Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA. 1996;276(11):889-897. 4. Sanders GP, Mendes LA, Colucci WS, Givertz MM. Noninvasive methods for detecting elevated left-sided cardiac filling pressure. J Card Fail. 2000;6:157-164.
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5. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989; 261(6):884-888. 6. Rodeheffer RJ. Measuring plasma B-type natriuretic peptide in heart failure: good to go in 2004? J Am Coll Cardiol. 2004;44:740-749. 7. Yancy CW, Abraham WT. Non-invasive hemodynamic monitoring in heart failure: utilization of impedance cardiography. Congest Heart Fail. 2003;9:241-250. 8. Magalski A, Adamson P, Gadler F, et al. Continuous ambulatory right heart pressure measurements with an implantable hemodynamic monitor: a multicenter, 12-month follow-up study of patients with chronic heart failure. J Card Fail. 2002;8(2):63-70. 9. Derbes VJ, Kerr A. Valsalva’s maneuver and Weber’s experiment. N Engl J Med. 1955;253:822-823. 10. Hamilton WF, Woodbury RA, Haper HT. Arterial cerebrospinal and venous pressures in man during cough and strain. Am J Physiol. 1944;14:42-50. 11. Zema MJ, Restivo B, Sos T, et al. Left ventricular dysfunction— bedside Valsalva manoeuvre. Br Heart J. 1980;44(5):560-569. 12. Greenfield JC, Cox RL, Hernandez RR, et al. Pressure-flow studies in man during Valsalva maneuver with observations on mechanical proprieties of the ascending aorta. Circulation. 1967;35:653-661. 13. Little WC, Barr WK, Crawford MH. Altered effect of the Valsalva maneuver on left ventricular volume in patients with cardiomyopathy. Circulation. 1985;71(2):227-233. 14. Weilenmann D, Rickli H, Follath F, et al. Noninvasive evaluation of pulmonary capillary wedge pressure by BP response to the Valsalva maneuver. Chest. 2002;122(1):140-145. 15. Zema MJ, Caccavano M, Kligfield P. Detection of left ventricular dysfunction in ambulatory subjects with the bedside Valsalva maneuver. Am J Med. 1983;75(2):241-248. 16. Parisi AF, Harrington JJ, Askenazi J, et al. Echocardiographic evaluation of the Valsalva maneuver in healthy subjects and patients with and without heart failure. Circulation. 1976;54(6):921-927. 17. Robertson D, Stevens RM, Friesinger GC, Oates JA. The effect of the Valsalva maneuver on echocardiographic dimensions in man. Circulation. 1977;55(4):596 –562. 18. Little WC, Barr WK, Crawford MH. Altered effect of the Valsalva maneuver on left ventricular volume in patients with cardiomyopathy. Circulation. 1985;71(2):227-233. 19. McIntyre KM, Vita JA, Lambrew CT, et al. A noninvasive method of predicting pulmonary capillary wedge pressure. N Engl J Med. 1992; 327:1715-1720. 20. Sharma GVRK, Woods PA, Lambrew CT, et al. Evaluation of a noninvasive system for determining left ventricular filling pressure. Arch Intern Med. 2002;162(18):2084-2088. 21. Givertz MM, Slawsky MT, Moraes DL, et al. Noninvasive determination of pulmonary artery wedge pressure in patients with chronic heart failure. Am J Cardiol. 2001;87(10):1213-1215. 22. Rocca HP, Weilenmann D, Rickli H, et al. Is blood pressure response to the Valsalva maneuver related to neurohormones, exercise capacity, and clinical findings in heart failure? Chest. 1999;116(4):861-867. 23. Kazanegra R, Cheng V, Garcia A, et al. A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study. J Card Fail. 2001;7(1):21-29. 24. Hogg K, Swedberg K, McMurray J. Heart failure with preserved left ventricular systolic function: epidemiology, clinical characteristics, and prognosis. J Am Coll Cardiol. 2004;43(3):317-327. 25. Philbin EF, Rocco TA, Lindenmuth NW, et al. Systolic versus diastolic heart failure in community practice: clinical features, outcomes, and the use of angiotensin-converting enzyme inhibitors. Am J Med. 2000;109(8):605-613. 26. Bernaldi L, Saviolo R, Spodick DH. Do hemodynamic responses to the Valsalva maneuver reflect myocardial dysfunction? Chest. 1989;95: 986-991.
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27. Schmidt DE, Shah PK. Accurate detection of elevated left ventricular filling pressure by a simplified bedside application of the Valsalva maneuver. Am J Cardiol. 1993;71(5):462-465. 28. Konstam MA. “Systolic and diastolic dysfunction” in heart failure? Time for a new paradigm. J Card Fail 2003;9(1):1-3. 29. Bristow MR, Saxon LA, Boehmer J, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced chronic heart failure. N Engl J Med. 2004;350(21):2140-2150. 30. Rose EA, Gelijns AC, Moskowitz AJ, et al. Long term use of leftventricular assist device for end-stage heart failure. N Engl J Med. 2001;345:1435-1443. 31. Abraham WT, Fisher WG, Smith AL, et al. Cardiac resynchronization in chronic heart failure. N Engl J Med. 2002;346(24):1845-1853. 32. Hunt SA. Current status of cardiac transplantation. JAMA. 1998; 280(19):1692-1698. 33. Felker GM, Thompson RE, Hare JM, et al. Underlying causes and long-term survival in patients with initially unexplained cardiomyopathy. N Engl J Med. 2000;342(15):1077-1084. 34. Cohn JN, Levine TB, Olivari MT, et al. Plasma norepinephrine as a guide to prognosis in patients with chronic congestive heart failure. N Engl J Med. 1984;311:819-823. 35. Ezekowitz JA, McAlister FA, Armstrong PW. Anemia is common in heart failure and is associated with poor outcomes: insights from a cohort of 12 065 patients with new-onset heart failure. Circulation. 2003;107(2):223-225.
36. Aaronson KD, Schwartz JS, Chen TM, et al. Development and prospective validation of a clinical index to predict survival in ambulatory patients referred for cardiac transplant evaluation. Circulation. 1997; 95(12):2660-2667. 37. Berger R, Huelsman M, Strecker K, et al. B-type natriuretic peptide predicts sudden death in patients with chronic heart failure. Circulation. 2002;105(20):2392-2397. 38. Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001;37(2): 386-391. 39. an Kraaij D, Schuurmans M, Jansen R, et al. Use of the Valsalva manoeuvre to identify haemodialysis patients at risk of congestive heart failure. Nephrol Dial Transplant. 1998;13(6):1518-1523. 40. Zema MJ. Prognosis after myocardial-infarction—prediction in ambulatory patients by use of the bedside Valsalva maneuver. Angiology. 1985;36(2):96-104. 41. Stevenson LW, Tillisch JH, Hamilton M, et al. Importance of hemodynamic response to therapy in predicting survival with ejection fraction less than or equal to 20% secondary to ischemic or nonischemic dilated cardiomyopathy. Am J Cardiol. 1990;66(19):1348-1354. 42. Logeart D, Thabut G, Jourdain P, et al. Predischarge B-type natriuretic peptide assay for identifying patients at high risk of re-admission after decompensated heart failure. J Am Coll Cardiol. 2004;43(4):635-641.
REVIEW
The Valsalva Maneuver: A Bedside “Biomarker” for Heart Failure G. Michael Felker, MD, MHS,a Phillip S. Cuculich, MD,b Mihai Gheorghiade, MDb a
Duke Clinical Research Institute, Durham, NC; and bNorthwestern University, Chicago, Ill. ABSTRACT Accurate assessment of volume status remains an important clinical goal in the management of patients with heart failure. Although physical examination can provide clues to volume status, its sensitivity and reproducibility are limited. Other noninvasive methods, such as measurement of natriuretic peptides or the use of impedance cardiography, are not well validated. The cardiovascular response to the Valsalva maneuver had been proposed as a simple, inexpensive bedside test for estimating filling pressures in patients with heart failure. Our objective was to summarize and critically evaluate the evidence for the use of the Valsalva maneuver in evaluating volume status in patients with heart failure. Studies have demonstrated a significant correlation between the cardiovascular response to the Valsalva maneuver and invasively measured ventricular filling pressures in patients with clinical heart failure. Although often overlooked in clinical training and practice, the cardiovascular response to the Valsalva maneuver is a potentially useful, noninvasive means of evaluating filling pressures in patients with heart failure. © 2006 Elsevier Inc. All rights reserved. KEYWORDS: Heart failure; Diagnosis; Physical examination; Valsalva maneuver
The epidemic of chronic heart failure has led to a rapid increase in hospitalizations for acute decompensated heart failure, with more than a million hospitalizations annually in the United States.1 Although a variety of clinical syndromes exist within the spectrum of decompensated heart failure, the majority of heart failure hospitalizations in clinical practice are related to volume overload and elevated ventricular filling pressures rather than low output states.2 Theoretically, many such heart failure hospitalizations could be prevented by early recognition and treatment of elevated filling pressures, but this strategy is difficult to apply because of the lack of tools to assess ventricular filling pressures in patients with chronic heart failure. Although ventricular filling pressures can be accurately assessed using pulmonary artery catheterization, this approach is highly invasive and associated with significant risks, making it an impractical means of assessing volume status Requests for reprints should be addressed to Michael Felker, MD, MHS, Duke Clinical Research Institute, PO Box 17969, Durham, NC 27715. E-mail address: [email protected]
0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2005.06.059
in the majority of patients with heart failure.3 Physical examination may provide important clues to filling pressures, but is also associated with substantial limitations and poor sensitivity.4 In addition, physical findings of volume overload, such as peripheral edema and elevated jugular venous pressure, are late signs that are often not present until ventricular filling pressures are extremely elevated, particularly in patients with long-standing chronic heart failure.5 Thus, there may be a disassociation between “hemodynamic congestion” (ie, elevation of left ventricular filling pressures) and “clinical congestion” (ie, physical signs of volume overload). It is therefore apparent that an accurate, reliable, inexpensive, and noninvasive means of quantifying “hemodynamic congestion” would be a major advance in heart failure management. This clinical need has led to a significant interest in the use of natriuretic peptides (brain natriuretic peptide and N-terminal prohormone brain natriuretic peptide) or impedance cardiography as tools for evaluating filling pressures and volume status in acute and chronic heart failure.6,7 Recently, novel implantable ambulatory devices have been developed to provide continuous estimation of ventricular filling pressures to optimize heart
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in blood pressure (phase 1) that remains elevated during the failure management.8 Another method of noninvasively esentire strain (phase 2) and returns to resting levels at release timating ventricular filling pressures, the cardiovascular re(phase 3). Stroke volume follows the same pattern.11,12 Careful sponse to the Valsalva maneuver, has been shown to be accurate, reliable, and noninvasive in a variety of clinical physiologic studies suggest the “square wave” response is the settings. Despite these promising data, the response to the result of maintenance of left ventricular filling during the strain Valsalva maneuver continues to phase, despite the decrease in right be little used in the clinical evalsided venous return.13 Maintenance of left ventricular volume is preuation of patients with heart failCLINICAL SIGNIFICANCE sumed to be related to increased ure. This review will summarize central blood volume that serves as available data on the response to ● Assessment of volume status is an ima reservoir to maintain left ventricthe Valsalva maneuver as a meaportant clinical goal in heart failure ular filling despite decreased venous sure of ventricular filling presmanagement, but this remains difficult return. With decreasing central sures and volume status and sugto assess accurately at the bedside using blood volume from diuresis, the regest potential roles for this test in currently available methods. sponse to the Valsalva maneuver the management of patients with normalizes.14 heart failure. ● The cardiovascular response to the Val-
CARDIOVASCULAR RESPONSE TO THE VALSALVA MANEUVER
salva maneuver has been shown to provide a reasonably accurate, non-invasive assessment of volume status and ventricular filling pressures in patients with heart failure.
QUANTIFYING THE CARDIOVASCULAR RESPONSE TO VALSALVA MANEUVER
The Valsalva maneuver was first described in 1704 as a sustained The hemodynamic changes asso● Further studies are needed to prospecforced expiratory effort or strain ciated with the Valsalva maneutively define the role of the Valsalva maagainst a closed glottis. The carver can be assessed with a varineuver in the clinical management of diovascular effects of the Valsalva ety of noninvasive methods, patients with heart failure. maneuver were described in 1851 including bedside sphygmomawhen Weber observed that “all the nometry, echocardiography, and sounds associated with the movephotoplethysmography of artement of the heart disappear” in response to the strain.9 In rial pressure waveforms. Bedside sphygmomanometry 1944, Hamilton and colleagues first reported an abnormal provides a qualitative assessment of the cardiovascular cardiovascular response to the Valsalva maneuver in paresponse to the Valsalva maneuver based on the “absent tients with congestive heart failure.10 overshoot” and “square wave” patterns of systolic blood The normal arterial blood pressure response to the maneupressure in heart failure. Systolic blood pressure is obver is an initial increase associated with the onset of straining tained while the patient is breathing quietly with normal (phase 1), followed by a sharp decrease to below baseline tidal volumes. Cuff pressure is then raised 15 mm Hg levels as the straining is maintained (phase 2). At the release of above resting systolic pressure, and the patient is asked to strain there is a short decrease of arterial pressure (phase 3), perform the Valsalva maneuver for 10 seconds and then which is followed by a distinct overshoot of the arterial presresume normal respirations. During the entire Valsalva sure (phase 4), creating a typical sinusoidal response (Figure 1, maneuver and for 30 seconds afterward, the cuff pressure 11 A). The changes in arterial pressure during the four phases of should be locked 15 mm Hg above the baseline systolic the Valsalva maneuver are the result of an acute increase in blood pressure while Korotkoff sounds are sought by intrathoracic pressure (phase 1), decreased stroke volume secauscultation over the brachial artery. Typically, only ondary to decreased venous return with compensatory increase phases 2 and 4 are registered, phase 1 and 3 being too in peripheral vascular resistance and reflex increase in heart short to be noticed. In healthy patients, Korotkoff sounds rate (phase 2), an acute decrease in the level of intrathoracic are heard only after release of straining, or phase 4. In pressure (phase 3), and a distinct increase in stroke volume patients with mild heart failure, Korotkoff sounds are over control level with concomitant decrease in peripheral absent during both phases 2 and 4 (absent overshoot). In vascular resistance and reflex bradycardia (phase 4). patients with severe heart failure, Korotkoff sounds are In patients with heart failure there are 2 distinct patterns of appreciated during phase 2 but not phase 4 (square wave) arterial pressure wave responses to the Valsalva maneuver: the (Table 1). This method has been demonstrated to be a “absent overshoot” response and the “square wave” response. reasonable screening test for left ventricular systolic dys“Absent overshoot” (Figure 1, B) is observed in patients with function in unselected outpatients in a cardiology less severe heart failure and manifests as normal phases 1 to 3 clinic.15 with an absence of arterial pressure overshoot after release of Echocardiographic evaluation of the cardiac response to the strain. The “square wave” response (Figure 1, C), seen in more severe heart failure, is characterized by an initial increase Valsalva maneuver has identified differences in atrial and
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CORRELATION OF VALSALVA MANEUVER WITH VENTRICULAR FILLING PRESSURES
Figure 1 Blood pressure response to Valsalva maneuver in various clinical situations. A, Sinusoidal arterial pressure response (normal). B, “Absent overshoot” arterial pressure response (mild heart failure). C, “Square wave” response (severe heart failure). Adapted from Zema MJ, Restivo B, Sos T, et al. Left ventricular dysfunction— bedside Valsalva manoeuvre. Br Heart J. 1980;44(5):560-569.
ventricular dimensions between patients with and without heart failure.16-18 Alternatively, cardiovascular response to the Valsalva maneuver can be quantified peripherally by measuring arterial pressure waveforms during the strain phase. The most frequently used measurement is the pulse amplitude ratio, a ratio of the minimal pulse pressure at the end of the strain phase to the maximum pulse pressure at initiation of the strain phase. Portable bedside devices that quantify these responses have been developed and validated.19,20 As described next, the pulse amplitude ratio has been shown to correlate very closely with ventricular filling pressures in a variety of clinical settings.
Table 1
The evaluation of patients with chronic heart failure for evidence of volume overload is crucial in preventing clinical decompensation. At present, noninvasive estimation of volume status is accomplished primarily by assessment of daily weights or by signs of elevated filling pressures on physical examination (increased jugular venous distention, hepatojugular reflux, peripheral edema). Unfortunately, these signs are insensitive, difficult to assess, and primarily reflect right-sided rather than left-sided filling pressures.5 Available data demonstrate that Valsalva maneuver is an accurate means for assessing cardiac filling pressures in a variety of heart failure populations. McIntyre and colleagues19 compared the pulse amplitude ratio during the Valsalva maneuver to directly measured pulmonary capillary wedge pressure in stable patients undergoing elective cardiac catheterization and critically ill patients undergoing placement of a pulmonary artery catheter in an intensive care unit. No patient had a primary diagnosis of heart failure. In both the stable and unstable patient groups, there was a strong correlation between the pulse amplitude ratio during Valsalva maneuver and invasively measured pulmonary capillary wedge pressure (r ⫽ 0.80 for the clinically stable group and 0.85 for the clinically unstable group). In addition, changes in pulmonary capillary wedge pressure induced by volume loading or diuresis correlated well with changes in noninvasive pulse amplitude ratio (r ⫽ 0.79). A subsequent study in patients with chronic heart failure compared predicted pulmonary capillary wedge pressure (based on Valsalva maneuver) to invasively measured pulmonary capillary wedge pressure in 30 patients with chronic heart failure, demonstrating a very high correlation between the 2 (r ⫽ 0.9, P ⬍ .001) (Figure 2). Noninvasive assessment predicted a pulmonary capillary wedge pressure of ⱖ 18 mm Hg with a sensitivity of 91% and specificity of 100%.21 A study by Sharma et al.20 compared the accuracy of noninvasive device measurement (VeriCor, CVP Diagnostics, Inc., Boston, Mass) to both invasively measured pulmonary capillary wedge pressure and left ventricular enddiastolic pressure in patients undergoing right- and leftsided heart catheterization. The noninvasive device measurement was found to have significant correlation with
Korotkoff sounds during beside performance of the Valsalva maneuver
Systolic BP response
Phase 2 (straining)
Phase 4 (relaxation)
Sinusoidal response (Normal) “Absent overshoot” response (Mild heart failure) “Square wave” response (Severe heart failure)
Korotkoff sounds NOT heard Korotkoff sounds NOT heard Korotkoff sounds heard
Korotkoff sounds heard
BP ⫽ blood pressure.
Korotkoff sounds NOT heard Korotkoff sounds NOT heard
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Figure 2 Relationship between pulse amplitude ratio during Valsalva maneuver (noninvasive PAWP) and invasively measured PAWP. Noninvasive PAWP was calculated from PAR by linear regression. PAWP, pulmonary artery wedge pressure; PAR, pulse amplitude ratio. Adapted from Givertz MM, Slawsky MT, Moraes DL, et al. Noninvasive determination of pulmonary artery wedge pressure in patients with chronic heart failure. Am J Cardiol. 2001;87(10):1213-1215.
left ventricular end-diastolic pressure (r ⫽ 0.86). Notably, this correlation was greater than that between the directly measured pulmonary capillary wedge pressure and the left ventricular end-diastolic pressure (r ⫽ 0.80). Direct comparison of device measurements and pulmonary capillary wedge pressure showed that 84% of the device measurements were within 4 mm Hg of the left ventricular enddiastolic pressure, compared with 41% of the pulmonary capillary wedge pressure measurements. The device used in this study was approved for use by the Food and Drug Administration to estimate left ventricular end-diastolic pressure in patients with signs and symptoms of heart failure. In addition to direct measurements of pulmonary capillary wedge pressure and left ventricular end-diastolic pressure, response to the Valsalva maneuver has been shown to correlate with other surrogate measures of left ventricular filling pressures, such as natriuretic peptide levels. A study of 45 patients with moderate heart failure demonstrated correlation between response to the Valsalva maneuver (as quantified by the pulse amplitude ratio) and levels of atrial natriuretic peptide (r ⫽ 0.75, P ⬍ .0001) and brain natriuretic peptide (r ⫽ 0.6, P ⬍ .0001) (Figure 3).22 No studies have directly compared the accuracy of Valsalva maneuver and brain natriuretic peptide measurements in predicting ventricular filling pressures, but the data of Givertz et al.21 compare favorably to available data on brain natriuretic peptide and invasively measured filling pressures.23 Heart failure in the setting of preserved systolic function (“diastolic dysfunction”) is an important clinical entity,
comprising greater than 50% of the population of patients with heart failure in the community.24 Clinically, this syndrome is characterized by frequent hospitalization and high resource use, typically because of elevated filling pressures and volume overload.25 Available data suggest that the relation between response to the Valsalva maneuver and ventricular filling pressures is not affected by ejection fraction (EF). Data suggest that pulse amplitude ratio correlates best with invasively measured pulmonary capillary wedge pressure (r ⫽ 0.77, P ⬍ .005) but not with cardiac index (r ⫽ 0.14, P ⫽ not significant) or EF (r ⫽ 0.09, P ⫽ not significant).26 These data have been corroborated by other small studies.27 Given that the cardinal symptoms of heart failure are related to elevated filling pressures and not to EF per se, heart failure is increasingly being seen as spectrum of disease states requiring similar treatment regardless of EF.28 Available data suggest that the use of the Valsalva maneuver as a tool for the assessment of volume status seems applicable to patients with heart failure regardless of EF.
PROGNOSTIC VALUE OF VALSALVA MANEUVER IN HEART FAILURE Accurate assessment of prognosis is critical in heart failure because of the need to triage patients among expensive, invasive therapies such as implantable defibrillators, cardiac resynchronization therapy, ventricular assist devices, and cardiac transplantation.29-32 A variety of parameters have been associated with prognosis in chronic heart failure.33-36 Recently, a growing body of research has focused on the role of natriuretic peptides (brain natriuretic peptide or Nterminal prohormone brain natriuretic peptide) in risk stratification of patients with heart failure.37,38 In contrast, few studies have investigated relationships between Valsalva maneuver and clinical end points. One small study has suggested that abnormal response to Valsalva maneuver is predictive of future heart failure episodes in patients on
Figure 3 Correlation of response to Valsalva maneuver (pulse amplitude ratio) and brain natriuretic peptide measurements in patients with heart failure. Adapted from Rocca HP, Weilenmann D, Rickli H, et al. Is blood pressure response to the Valsalva maneuver related to neurohormones, exercise capacity, and clinical findings in heart failure? Chest. 1999;116(4):861-867.
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hemodialysis.39 When tested several weeks after an acute myocardial infarction, an abnormal response to Valsalva maneuver predicted future sudden cardiac death.40 The most common reason for hospitalization in patients with congestive heart failure is volume overload, typically treated with intravenous diuretics.2 Objective measures of the adequacy of diuresis during acute hospitalizations are lacking, and decisions to discharge patients with heart failure are usually based on clinical judgment. Lack of objective criteria to define “successful treatment” has contributed to high rates of rehospitalization.1 Stevenson et al.41 have demonstrated that the ability to achieve decreased filling pressures with aggressive medical therapy is a powerful predictor of future clinical stability. Low levels of brain natriuretic peptide at discharge have been shown to predict freedom from hospitalization, presumably because of adequacy of diuresis and restoration of physiologic homeostasis.42 Decreasing intravascular volume has clearly been shown to normalize the response to the Valsalva maneuver in human studies.14,19 These data suggest the possibility of a role for response to Valsalva maneuver as a simple bedside assessment of the adequacy of diuresis and readiness for discharge, a concept that could be tested prospectively.
CONCLUSIONS Accumulated data suggest that the Valsalva maneuver is a useful tool in the assessment of patients with heart failure. Bedside sphygmomanometry can provide a qualitative assessment of volume status, and commercially available arterial waveform devices provide a rapid and reliable measurement of cardiovascular dynamics that predict left ventricular filling pressures in a variety of clinical settings. Potential uses for the Valsalva maneuver in patients with heart failure include bedside assessment of filling pressures, judging adequacy of diuresis during hospitalization, and stratifying risk for future events. Despite the potential advantages of accurately estimating filling pressures at the bedside, measurement of cardiovascular response to the Valsalva maneuver is seldom taught in medical schools and remains little used in clinical practice. Given the increasing costs of heart failure care, further research into the potential uses of this inexpensive bedside tool seems justified as a means to control cost and improve outcomes in patients with heart failure.
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