Original Article
A Noninvasive Method of Predicting Pulmonary-Capillary Wedge Pressure
N Engl J Med 1992; 327:1715-1720December 10, 1992
- Abstract
- Abstract
Background.
The noninvasive prediction of pulmonary-capillary wedge pressure (PCWP) is important for the recognition and treatment of a variety of cardiovascular disorders. The response of the arterial pressure to the Valsalva maneuver has been shown to correlate with the PCWP. We therefore devised a noninvasive method to measure this pressure response at the bedside and correlated these measurements with the PCWP measured directly with a pulmonary-artery catheter.
Methods.
Simultaneous, blinded, noninvasive measurements of the ratio of the final amplitude to the initial amplitude of the pulse wave form during the stress phase of the Valsalva maneuver (pulse-amplitude ratio) and direct measurements of the PCWP were obtained in 20 clinically stable patients and in 14 clinically unstable patients who were receiving vasoactive agents, 12 of whom also had endotracheal tubes in place.
Results.
Using linear regression analysis, we found that the pulse-amplitude ratio strongly correlated with the measured PCWP over a range of base-line values from 4 to 32 mm Hg for the 20 clinically stable patients (R2 = 0.80) and the 14 clinically unstable patients (R2 = 0.85). The method also correctly predicted changes in the PCWP after the administration of nitroglycerin or furosemide and after expansion of the intravascular volume (R2 = 0.79).
Conclusions.
These preliminary data indicate that a simple noninvasive method can accurately predict the PCWP and changes in the PCWP in response to medical therapy. (N Engl J Med 1992;327:1715–20.)
Article Activity
- Article
THE pulmonary-capillary wedge pressure (PCWP) is an important indicator of cardiac function and intravascular and pulmonary venous volume. Clinical and radiographic methods of detecting congestive heart failure are insensitive to increases in the PCWP,1 , 2 and hemodynamic monitoring of this pressure with use of a balloon-tipped, flow-directed catheter has therefore become commonplace in acutely ill patients.3 Because it is an invasive procedure and occasionally causes serious complications, pulmonary-artery catheterization is not an acceptable alternative either for screening or as a guide to routine therapy for congestive heart failure.4 5 6 A noninvasive method of estimating the PCWP could contribute to the early detection of congestive heart failure — an important goal now that early treatment of heart failure has been shown to reduce mortality and rates of hospitalization for congestive heart failure.7
Since 1944, reports have indicated that the contour of the strain phase of the arterial wave-form response to the Valsalva maneuver is related to the PCWP and to left ventricular end-diastolic pressure.8 9 10 11 12 We developed a noninvasive sensing and recording system that provides a reproducible estimate of the arterial response to the Valsalva maneuver and tested it by comparison with direct measurements of the PCWP. This prospective, blinded study provides preliminary data indicating that this method can predict the PCWP with a clinically meaningful degree of accuracy.
Methods
Phases of the Response of the Arterial Pressure to the Valsalva Maneuver
The Valsalva maneuver raises intrathoracic pressure, diminishes venous return to the heart and stroke volume, and increases venous pressure. Arterial-pressure tracings generally show four distinct phases in response to the Valsalva maneuver.12 In phase 1, the arterial pressure rises as a result of transmission to the periphery of the increased intrathoracic pressure; in phase 2, reductions in systolic, diastolic, and pulse pressures occur as a result of reduced venous return with continuing strain; phase 3 begins with the release of the strain, which results in a sudden drop in arterial pressure; and in phase 4 the arterial pressure overshoots to levels above control, with a widened pulse pressure.
A Noninvasive Method of Determining PCWP
Our noninvasive, peripheral-artery pulse-processing system consists of a pressurized pulse detector and conditioning assembly (pressurizer, amplifier, and filter) that transmits the reflected arterial-pulse contour from one of the patient's fingers to a personal computer. A mouthpiece is connected by tubing to a pressure transducer that is connected to the personal computer to provide a continuous indication of strain pressure on a video screen controlled by the computer system. The signal-conditioning system provides continuous operator-adjusted gain, with a capacity to increase the signal up to 500 times. This system has been previously described.13
The Valsalva maneuver was performed by asking the patient, after a normal inspiration, to exhale with enough force to elevate a marker on the video monitor first to 10 to 20 mm Hg, then to 20 to 30 mm Hg, and finally to 30 to 40 mm Hg, if he or she tolerated this pressure. In the course of these practice maneuvers, the patients learned to maintain the strain-phase pressure within approximately 5 mm Hg throughout the strain phase. The strain phase was maintained for 10 to 12 seconds. A tiny air leak was placed in the mouthpiece to ensure that airway pressure was produced from the thoracic cavity and not the pharynx. Among patients with endotracheal tubes in place, intrathoracic pressure was increased by the application of an anesthesia bag with an occluding exit valve to the patient's endotracheal-tube connector, guided by continuous pressure monitoring with a manometer.
Calculation of the Pulse-Amplitude Ratio
The ratio of the final (minimal) to the initial (maximal) amplitude of the three steady-state beats of the strain phase as inscribed by the noninvasive peripheral-artery pulse-processing system was defined as the pulse-amplitude ratio, as shown in Figures 1Figure 1
Information Recorded by the Noninvasive Peripheral-Artery Pulse-Processing System in a Patient with Stable Coronary Artery Disease. and 2Figure 2
Tracings from a Patient at Base Line (Pulse-Amplitude Ratio [PAR], 0.57; PCWP, 14 mm Hg), after the Administration of Nitroglycerin (PAR, 0.39; PCWP, 8 mm Hg), and after Volume Expansion (PAR, 1.06; PCWP, 19 mm Hg)..Enrollment of Patients
Patients scheduled for elective cardiac catheterization and patients in both the medical and surgical intensive care units who had well-functioning balloon-tipped catheters in the pulmonary artery for the measurement of the PCWP were enrolled in the study. The research protocol was approved by the institutional review board of the BrocktonWest Roxbury Veterans Affairs Medical Center. The procedure was explained and informed consent was obtained from all the patients.
A total of 34 patients were enrolled for the study of the PCWP and pulse-amplitude ratio. The first 20 patients selected, the clinically stable group, were not intubated and were not receiving vasoactive drugs; 19 of these patients had documented coronary artery disease, 10 had hypertension, 3 had diabetes mellitus, 2 had atrial fibrillation, and 1 had chronic obstructive pulmonary disease. During the course of the study, 15 of these stable patients had changes induced in their hemodynamic status, either a reduction in central venous volume by the administration of sublingual nitroglycerin or oral furosemide, or expansion of central venous volume by the administration of angiographic contrast medium. The PCWP and pulse-amplitude ratio were measured serially to document these changes. Fourteen additional patients, the clinically unstable group, were receiving vasoactive drugs; 12 of these patients also had endotracheal tubes in place. Eight of these patients were receiving low-dose infusions of dopamine, six were receiving infusions of nitroglycerin, two were receiving infusions of sodium nitroprusside, one was receiving a continuous infusion of aminophylline, and one was receiving a continuous infusion of esmolol.
Protocol for Measuring the PCWP and Pulse-Amplitude Ratio at Base Line
The PCWP and pulse-amplitude ratio were directly measured simultaneously under base-line conditions after informed consent was obtained from the patients. The PCWP was measured directly in a steady state with the patient in the supine position with use of a 7-French single-lumen balloon-tipped catheter (Arrow International, Reading, Pa.) and reusable transducers (Medex, Hilliard, Ohio) leveled to the midaxillary line. The pulmonary-wedge position was confirmed in the catheterization laboratory by direct fluoroscopic observation of the catheter tip and by the appearance of a typical wedge-pressure tracing. Base-line right atrial mean pressures were also obtained in all 14 patients studied in the catheterization laboratory.
The same system was used in the medical and surgical intensive care units, except that the transducer systems for the measurement of the PCWP were disposable. In the intensive care units, the wave form was accepted as representative of the PCWP only when it exhibited distinct a and v waves and a distinct change from the pulmonary-artery wave form and pressure. The pulse-amplitude ratio was measured by positioning the detector around one finger of an unencumbered arm and pressurizing the detector system and the finger with a small cuff applied externally, as described above and reported earlier.13 A mouthpiece attached to the device through flexible tubing was then placed in the patient's mouth in preparation for the performance of the Valsalva maneuver. In the intubated patients, the anesthesia bag and pressure-monitor assembly were connected directly to the endotracheal tube. The strain phase of the Valsalva maneuver was maintained in the range of 30 to 40 mm Hg or passive pressure in the range of 25 to 35 mm Hg was applied through the endotracheal tube, guided by an on-line pressure manometer, insofar as practicable, for 10 to 12 seconds.
Serial Observations after the Induction of Hemodynamic Alterations
Sublingual nitroglycerin (0.4 mg) was given to selected patients, and the PCWP and pulse-amplitude ratio were measured again five minutes later. Simultaneous testing was also performed after the administration of angiographic contrast medium, which produced intravascular volume loading (approximately 125 ml of diatrizoate meglumine), when indicated as part of the planned diagnostic procedure.
Of the 14 patients evaluated in the cardiac-catheterization laboratory, 6 were excluded from testing with nitroglycerin because they were thought to be clinically unsuitable, leaving 8 patients for our analysis of paired observations before and after nitroglycerin challenge. Measurements were made after volume loading in 10 of the 14 patients studied in the catheterization laboratory. For the six patients who had base-line studies in bed in the medical intensive care unit, neither nitroglycerin nor contrast medium was administered, but when diuretic therapy (40 mg of furosemide orally) was administered as a part of the patient's therapy (as was the case for three patients), simultaneous determination of PCWP and pulse-amplitude ratio was carried out between 2.5 and 4 hours later.
Collection and Interpretation of Data
The direct measurements of the PCWP and the noninvasive measurements of the pulse-amplitude ratio were interpreted in a blinded manner by two separate investigators. The direct measurements of the PCWP and data on the pulse-amplitude ratio were submitted to a third investigator for analysis.
The PCWP tracings were read by a supervised cardiology fellow who was blinded to the pulse-amplitude ratios, and the tracings from the peripheral-artery pulse-processing system were read to derive values for the pulse-amplitude ratio by a physician who was experienced in reading these tracings and who was blinded to the results of the catheterization and to the sequence of the study.
Regression Analysis
Standard least-squares linear regression analysis was used to investigate the capacity of the pulse-amplitude ratio to predict the PCWP corresponding to the base-line values.14 Separate regression analyses were conducted for the 20 clinically stable patients and the 14 clinically unstable patients. For the 15 patients in whom alterations in hemodynamic status were induced during the study, regression of the first change in the PCWP on the change in the pulse-amplitude ratio was performed similarly.
Results
PCWP and Pulse-Amplitude Ratio at Base Line
Simultaneous blinded observations of the pulse-amplitude ratio and PCWP measured directly at the time of cardiac catheterization or in the intensive care unit were obtained in 34 patients. Linear regression analysis was used to compare direct measurements of the PCWP with the pulse-amplitude ratio at base line for the 20 clinically stable patients and the 14 clinically unstable patients who were receiving vasoactive drugs or had endotracheal tubes in place (Fig. 3Figure 3
Comparison of Direct Base-Line Measurements of the PCWP with the Pulse-Amplitude Ratio in 20 Patients Who Were Clinically Stable and 14 Patients Who Were Clinically Unstable.). These base-line measurements indicated that the pulse-amplitude ratio predicted the measured PCWP over a range of values from 4 mm Hg to 32 mm Hg with good accuracy (R2 = 0.80, root-mean-square error = ±3.72 mm Hg for the 20 clinically stable patients; R2 = 0.85, root-mean-square error = ±2.35 mm Hg for the 14 clinically unstable patients).The Pulse-Amplitude Ratio and the Right Atrial Mean Pressure as Predictors of PCWP
Both the right atrial mean pressure and the PCWP were measured in the patients studied in the catheterization laboratory; in these patients, the pulse-amplitude ratio correlated with the PCWP (R2 = 0.86) better than with the right atrial mean pressure (R2 = 0.70).
Changes in the PCWP and Pulse-Amplitude Ratio after Alterations in Hemodynamic Status
We measured the PCWP and pulse-amplitude ratio for the first alteration induced in the patients' hemodynamic status after the base-line measurements for the 15 patients in the clinically stable group who had such alterations. For 11 of these patients, the first alteration in hemodynamic status was a reduction in central venous volume induced by nitroglycerin or furosemide; for the other 4, the first alteration was an increase in central venous volume produced by the injection of angiographic contrast medium (resulting in volume loading).
The changes in the PCWP from base line were then regressed on the changes in the pulse-amplitude ratio from base line (Fig. 4Figure 4
Change in the Mean PCWP and the Pulse-Amplitude Ratio in 15 Clinically Stable Patients in Whom Alterations in Hemodynamic Status Were Induced.). The changes induced in the PCWP were accurately reflected by the changes in the pulse-amplitude ratio (R2 = 0.79, root-mean-square error = ±2.69 mm Hg).Clinical Analysis
We considered how the pulse-amplitude ratio might be used in a clinical setting to characterize patients as having low, normal, or high values for the PCWP. It is crucial to distinguish patients with low PCWP values from those with high values, since the appropriate treatments for these groups are opposite. For these clinical analyses, we used the base-line values and multiple serial measurements of induced changes in the 15 clinically stable patients. In 35 base-line observations, the pulse-amplitude ratio correctly categorized 11 of the 12 patients with a markedly elevated PCWP (≥20 mm Hg), 14 of 17 with a normal PCWP (≤12 mm Hg), and 5 of 6 with mild-to-moderate increases in the PCWP (13 to 19 mm Hg). In the three patients incorrectly categorized as normal according to the pulse-amplitude ratio, the measured PCWP values were only 1 and 2 mm Hg above the range predicted by the pulse-amplitude ratio in two and 4 mm Hg above that range in the third; in one patient in whom the PCWP was predicted to be ≥20 mm Hg, the measured value was 19 mm Hg, and in one patient in whom the pulse-amplitude ratio predicted a PCWP of 13 to 19 mm Hg, the measured value was 10 mm Hg. Thus, the pulse-amplitude ratio predicted a PCWP in the correct clinical category for 30 of 35 base-line observations and was within 4 mm Hg of the measured PCWP for the other 5.
After the administration of nitroglycerin or furosemide, the pulse-amplitude ratio predicted a PCWP in the correct range for 9 of 11 patients. In one patient for whom the range was incorrectly predicted, the pulse-amplitude ratio underestimated the PCWP by 4 mm Hg (predicted PCWP, ≤12 mm Hg; measured PCWP, 16 mm Hg), whereas in the other, the ratio underestimated the range of the PCWP by 2 mm Hg (predicted PCWP, ≤12 mm Hg; measured PCWP, 14 mm Hg). The pulse-amplitude ratio changed in a different direction from the PCWP in only one patient, in whom the pulse-amplitude ratio increased from 1.00 to 1.21 while the PCWP fell from 32 mm Hg to 28 mm Hg. However, in this patient the pulse-amplitude ratio still predicted the correct range for both the PCWP value before the administration of nitroglycerin and the value after nitroglycerin (≥20 mm Hg). In the cases of two other patients, the pulse-amplitude ratio rose, but the PCWP range after the administration of nitroglycerin or furosemide was still accurately identified (13 to 19 mm Hg in one patient and ≤12 mm Hg in the other). The largest decline in the PCWP in the group after the administration of nitroglycerin or furosemide was in those who received furosemide in the medical intensive care unit and were studied 2.5 to 4 hours later. The PCWP declined by 12 mm Hg (from 20 to 8 mm Hg), 10 mm Hg (from 24 to 14 mm Hg), and 6 mm Hg (from 20 to 14 mm Hg) in the three patients in this group.
The PCWP rose in all 10 patients after volume loading, and the pulse-amplitude ratio predicted an increase in the PCWP in 9. In the one patient in whom the pulse-amplitude ratio declined, the ratio predicted a PCWP in the 13 to 19 mm Hg range both before and after volume loading, whereas the measured PCWP values were 12 and 13 mm Hg, respectively. In two other patients in this group, the pulse-amplitude ratio predicted that the PCWP would be ≥20 mm Hg when the measured PCWP values were 19 and 14 mm Hg. None of the patients had symptoms during testing, and no adverse effects were observed.
Discussion
Hemodynamic studies have long suggested that the contour of the response of the arterial pressure to the Valsalva maneuver may be predictive of the PCWP.8 9 10 11 Hamilton et al. reported an association between a response characterized by an abrupt change followed by a plateau (a "square-wave" response) (Fig. 2) during phase 2 of the Valsalva maneuver (the strain phase) and the presence of congestive heart failure; we found such a response to be highly predictive of a PCWP of 20 mm Hg or higher.8 Other investigators showed that the response in normal subjects was characterized by a rapid decline in systolic pressure and pulse pressure during this phase as a result of an interruption in venous return, producing a decrease in arterial and pulse pressure, which had a sinusoidal appearance.8 , 9 , 15 Gorlin and coworkers10 made detailed correlations between hemodynamic measurements and wave-form responses to the Valsalva maneuver in a variety of cardiopulmonary conditions and showed that although both the right atrial mean pressure and the PCWP may be elevated when the response to the Valsalva maneuver is abnormal, elevation of the right atrial mean pressure with a normal PCWP does not appear to correlate with an abnormal response to the Valsalva maneuver.10 In their studies, the square-wave response was consistently associated with elevations of the PCWP in the range of 20 to 37 mm Hg, whereas the right atrial mean pressure was normal or only slightly elevated. It now appears that the square-wave response in most common clinical conditions in humans is related primarily to an elevation of the PCWP.10 , 11 , 13 , 15 , 16 One indispensable condition for a square-wave response appears to be the maintenance of left ventricular filling throughout the course of the strain phase of the Valsalva maneuver.15 16 17 18 It now appears, therefore, that the increase in intrathoracic pressure generated during the strain phase of the Valsalva maneuver impedes the return of venous blood to the heart.18 19 20 It has been demonstrated, in part in our laboratories, that left atrial and left ventricular dimensions and left ventricular stroke volume and arterial pressure decline in subjects with normal cardiovascular function as left ventricular filling falls precipitously in response to the Valsalva maneuver.21 22 23 24 Conversely, as pulmonary congestion progresses, causing the PCWP to rise, the response to the Valsalva maneuver may be expected to become progressively "squarer" in configuration.
A number of approaches have heretofore been taken to predict the PCWP noninvasively, including the use of Doppler echocardiographic techniques, but none have proved sufficiently reliable to be clinically useful.25 , 26 Since the contour of the response to the Valsalva maneuver seemed promising as a predictor of the PCWP, we made a series of pilot observations to determine the values for the pulse-amplitude ratio that corresponded to clinical breakpoints of 12 mm Hg and 20 mm Hg for the PCWP. We then obtained values for the PCWP by direct measurement with simultaneous testing for pulse-amplitude ratio in groups of patients with clinically stable and clinically unstable disease. Linear regression analysis indicated that the pulse-amplitude ratio correlated with the measured PCWP with a clinically useful degree of accuracy. Both the prediction of the clinical category of the PCWP by means of the pulse-amplitude ratio and the changes in the PCWP produced by volume loading or by the administration of nitroglycerin or furosemide were also sufficiently accurate to be useful clinically. Of the 10 incorrect categorizations, 5 were within 2 mm Hg of the measured PCWP, 3 were within 4 mm Hg, and 2 were within 6 mm Hg of the measured value. We believe that these errors would not have led to serious misinterpretation of the patients' clinical status. Passively induced increases in intrathoracic pressure in patients with endotracheal tubes in place who were receiving a variety of vasoactive agents showed a similar relation between the strain-phase contour as calibrated by the pulse-amplitude ratio and the PCWP.
The primary diagnosis of 30 of the 34 patients evaluated in this study was coronary heart disease. Although extensive, though unblinded, experience with more than 2100 patients over the past six years has indicated that the pulse-amplitude ratio is highly predictive of the directly measured PCWP in patients with other forms of acquired heart disease (hypertensive, valvular, myopathic, and pericardial processes), additional systematic studies will be necessary to evaluate this technique in a broader range of patients. The safety of this method should also be emphasized. In our experience with the more than 2100 patients with severe heart disease, there have been no instances in which myocardial ischemia or any form of hemodynamic, dysrhythmic, or conduction-system instability or neurologic symptoms has followed carefully monitored single or repeated Valsalva maneuvers.
These preliminary observations suggest that the pulse-amplitude ratio can predict the PCWP over a wide range of clinically relevant values, that it can identify increases and decreases in the PCWP in response to therapy or the exacerbation of heart failure, and that it can be useful in intubated patients and patients receiving vasoactive agents. Although this study indicates that the pulse-amplitude ratio is highly predictive of the PCWP in patients with coronary artery disease, additional studies will be required to validate and further refine these findings, both in patients with coronary artery disease and in those with other forms of heart disease.
Presented in part at the American College of Cardiology Scientific Sessions, Atlanta, March 4, 1991, and at the meeting of the American Federation for Clinical Research, Seattle, May 4, 1991.
The peripheral-artery pulse-processing system is protected by patent rights issued (or pending) to Dr. McIntyre. No financial support was provided for this study.
We are indebted to George Thibault, M.D., William L. Daley, M.D., M.P.H., Christopher R. Gill, M.D., G.V.R.K. Sharma, M.D., Jamil Kirdar, M.D., Shukri Khuri, M.D., Daniel Pietro, M.D., Ronald Dunlap, M.D., Bernard Kelley, Patricia Woods, R.N., M.S.N., Diane Lapsley, M.S., R.N., and Thomas P. Rocco, M.D., for their important contributions to this study, and to Ms. Stephanie Tribuna and Ms. Donna Kantarges for assistance in the preparation of the manuscript.
Source Information
From the Department of Medicine, Cardiology Section, and the Research and Development Service and the Department of Surgery, BrocktonWest Roxbury Veterans Affairs Medical Center and Harvard Medical School, Boston (K.M.M., J.A.V., J.F., J.L.); the Departments of Medicine and Surgery, Brigham and Women's Hospital, Boston (K.M.M., J.A.V., J.L.); the Departments of Cardiology and Research, Maine Medical Center, Portland, and the University of Vermont Medical School, Burlington (C.T.L.); and the Department of Epidemiology, Harvard School of Public Health, Boston (J.F.). Address reprint requests to Dr. McIntyre at the Veterans Affairs Medical Center, 1400 VFW Pky., West Roxbury, MA 02132.
- References
References
1
Stevenson
CrossRef | Web of Science | Medline2
Chakko
Web of Science | Medline3
Swan
Full Text | Web of Science | Medline4
Foote
Full Text | Web of Science | Medline5
Matthay
Web of Science | Medline6
Gill
CrossRef7
The SOLVD Investigators
Full Text | Web of Science | Medline8
Hamilton 9
Lee G de
CrossRef | Web of Science | Medline10
Gorlin
CrossRef | Web of Science | Medline11
Zema
CrossRef | Web of Science | Medline12
Braunwald E. Clinical manifestations of heart failure. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. 2nd ed. Vol. 1. Philadelphia: W.B. Saunders, 1984:500–1.
13
McIntyre 14
SAS/STAT user's guide, release 6.03 ed. Cary, N.C.: SAS Institute, 1988:193.
15
Sharpey-Schafer
CrossRef | Web of Science | Medline16
Judson
Web of Science | Medline17
Wilkinson
Web of Science | Medline18
Chevalier
Web of Science | Medline19
Stucki
Web of Science | Medline20
Sharpey-Schafer EP. Effect of respiratory acts on the circulation. In: Handbook of physiology: a critical, comprehensive presentation of physiological knowledge and concepts. Section 2, Circulation. Vol. 3. Washington, D.C.: American Physiological Society, 1965:1875–86.
21
Robertson
Web of Science | Medline22
Brooker
CrossRef | Web of Science | Medline23
Parisi
Web of Science | Medline24
Korner
Web of Science | Medline25
Askenazi
Full Text | Web of Science | Medline26
Rahko
- Citing Articles (19)
Citing Articles
1
Michael M. Givertz. (2011) Hemodynamic Monitoring to Guide Treatment of Acute Heart Failure. Journal of Cardiac Failure 17:9, 726-728
CrossRef2
G.V.R.K. Sharma, Patricia A. Woods, Nancy Lindsey, Carol O’Connell, Louise Connolly, Jacob Joseph, Kevin M. McIntyre. (2011) Noninvasive Monitoring of Left Ventricular End-Diastolic Pressure Reduces Rehospitalization Rates in Patients Hospitalized for Heart Failure: A Randomized Controlled Trial. Journal of Cardiac Failure 17:9, 718-725
CrossRef3
Dóra Paprika, Linda Judák, Anita Korsós, László Rudas, Éva Zöllei. (2011) The effects of acute blood loss on blood pressure recovery from the Valsalva maneuver. Autonomic Neuroscience 160:1-2, 103-106
CrossRef4
Marie Jennyfer Ng Kam Chuen, Gregory YH Lip, Robert J MacFadyen. (2007) Repeated assessment of physical biomeasures or blood biomarkers for the definition of volume status and cardiac loading in LVSD. Biomarkers in Medicine 1:3, 355-374
CrossRef5
2007. Congestive Heart Failure. , 518-528.
CrossRef6
Renee L. Bess, Shahabuddin Khan, Howard S. Rosman, Gerald I. Cohen, Zuhair Allebban, Julius M. Gardin. (2006) Technical Aspects of Diastology: Why Mitral Inflow and Tissue Doppler Imaging Are the Preferred Parameters?. Echocardiography 23:4, 332-339
CrossRef7
C. Gillard, C. Henuzet, J. Lallemande, A. Moscariello, M. Guillaume, A. Van Meerhaeghe. (2006) Operating characteristics of the finapress system to predict elevated left ventricular filling pressure. Clinical Cardiology 29:3, 107-111
CrossRef8
Morito Akiyama, Yukari Morofuji, Toshihiro Kamohara, Keiko Nishikubo, Masayoshi Tsubai, Osamu Fukuda, Naohiro Ueno. (2006) Flexible piezoelectric pressure sensors using oriented aluminum nitride thin films prepared on polyethylene terephthalate films. Journal of Applied Physics 100:11, 114318
CrossRef9
Jaap J. Remmen, Wim R. M. Aengevaeren, Freek W. A. Verheugt, Rene W. M. M. Jansen. (2005) Normal values of pulmonary capillary wedge pressure and the blood pressure response to the Valsalva manoeuvre in healthy elderly subjects. Clinical Physiology and Functional Imaging 25:6, 318-326
CrossRef10
J. J. Remmen, W. R. M. Aengevaeren, F. W. A. Verheugt, A. Bos, R. W. M. M. Jansen. (2005) Lower body positive pressure by anti-G garment inflation: a suitable method to increase pulmonary capillary wedge pressure in healthy elderly subjects. Clinical Physiology and Functional Imaging 25:1, 27-33
CrossRef11
Luís Beck da Silva, Lisa Mielniczuk, Marc Laberge, Anjali Anselm, Margaret Fraser, Kathryn Williams, Haissam Haddad. (2004) Persistent Orthopnea and the Prognosis of Patients in the Heart Failure Clinic. Congestive Heart Failure 10:4, 177-180
CrossRef12
Anju Nohria, Sui W Tsang, James C Fang, Eldrin F Lewis, John A Jarcho, Gilbert H Mudge, Lynne W Stevenson. (2003) Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. Journal of the American College of Cardiology 41:10, 1797-1804
CrossRef13
R. P. Patterson, J. Zhang. (2003) Impedance cardiographic measurement of the physiological response to the Valsalva manoeuvre. Medical & Biological Engineering & Computing 41:1, 40-43
CrossRef14
Roger M. Mills, Robert E. Hobbs. (2001) Drug Treatment of Patients with Decompensated Heart Failure. American Journal of Cardiovascular Drugs 1:2, 119-125
CrossRef15
Hans Peter Brunner-LaRocca, Hans Rickli, Christine Helena Attenhofer Jost, Rolf Jenni. (2000) Left Ventricular End-Diastolic Pressure Can Be Estimated by Either Changes in Transmitral Inflow Pattern During Valsalva Maneuver or Analysis of Pulmonary Venous Flow. Journal of the American Society of Echocardiography 13:6, 599-607
CrossRef16
Gregory P. Sanders, Lisa A. Mendes, Wilson S. Colucci, Michael M. Givertz. (2000) Noninvasive methods for detecting elevated left-sided cardiac filling pressure. Journal of Cardiac Failure 6:2, 157-164
CrossRef17
David M. Rothenberg, Kenneth J. Tuman. (2000) Pulmonary Artery Catheter: What Does the Literature Actually Tell Us?. International Anesthesiology Clinics 38:4, 171-187
CrossRef18
HANS-PETER BRUNNER-La ROCCA, CHRISTINE HELENA ATTENHOFER, ROLF JENNI. (1998) Can the Extent of Change of the Left Ventricular Doppler Inflow Pattern During the Valsalva Maneuver Predict an Elevated Left Ventricular End-Diastolic Pressure?. Echocardiography 15:3, 211-218
CrossRef19
(1993) Noninvasive Prediction of Pulmonary-Capillary Wedge Pressure. New England Journal of Medicine 328:19, 1423-1424
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