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Reliability of Central Venous Pressure as an Indicator of Left Atrial Pressure* A Study in Patients with Mitral Valve Disease Hubert Bell, M.D.," David Stubbs, M.D., and David Pugh, M.D.OQ Central venous pressure (CVP) measurements have been used extensively in the management of critically ill patients. The value of CVP determinations was studied by determining the relationship of left atrial and right atrial pressares in 200 patients undergoing transsepta1 heart catheterization. All patients had mitral valve disease. The correlation coefficient of left atrial and right atrial pressure was 0.48. Low right atrial pressure (below 3 mm Hg) wss seen &I 18 of 91 patients with left atrial pressure 20 mm H g or greater. In 25 patients, acute pressure changes were induced by volume expansion, pachng, or drug infusion ( h o p terenol or phenylephrine). Increases in left atrial pressure hquently failed to be reflected in right atrial pressure changes. C e n W venous pressare may be misleading as a guide to left atrial pressure. entral venous pressure (OVP) measurements have been used extensively to provide guidelines in the treatment of critically ill patients. Since CVC and right atrial pressure are identical,' the clinical usefulness of CVP monitoring depends upon the relationship between left atrial and right atrial pressures. The superiority of CW over other methods of determining venous pressure has been established.2 Important clinical decisions have been based on CVP measurements and on the changes which occur during the course of observation and treatment.3-6 The following study was performed to determine the relationship of CVP to left atrial pressure. Patient material consisted of 200 consecutive ~ a t i e n t swith mitral valve disease undergoing cardiac catheterization. Patients with relatively pure mitral stenosis or mitral insdciency were included as well as patients with "mixed" mitral valve disease. Patients with associated aortic or tricuspid valve disease were excluded from the study. Transseptal technique was used to introduce a left atrial catheter ( Brockenbrough 8#F) in all patients. Pressure recordings were 'From the De artment of Medicine, Cardiovascular Section, University o h a n s a s Medical Center, Kansas City, Kansas. Supported in part by NIH Grant 5 TO1 HE05670-05. "Assistant Professor of Medicine. obtained with use of Statham pressure transducer (model P23D) and Electronics for Medicine recorder. Baseline right atrial pressure recordings were made through the transseptal catheter immediately before it was advanced into the left atrium. Pulmonary artery pressure measurements were obtained using a NIH 6 or 7F Dacron thin wall catheter and were recorded simultaneously with right and left atrial pressures. The Fick method was used to obtain cardiac output. In 25 patients, a significant rise in atrial pressure was induced by transvenous pacing, infusion of isoproterenol or phenylephrine, or volume expansion. The transsepta1 catheter was then rapidly withdrawn back into the right atrium while pressures were continuously recorded. Changes in pulmonary artery pressure were also continuously recorded. The rise in left atrial pressure was sustained for at least 15 minutes and in some patients for one hour. Volume expansion was accomplished by rapid infusion of 200 to 1000 ml of 5 percent dextrose and water into the venous circulation. Pacing was performed at a rate of 100-150/minute from the right atrium or right ventricle. Isoproterenol was infused at a rate of 5-10 pg/min. Phenylephrine was infused slowly over five to ten minutes to a total dose of 2-3 mg. The relationship between left atrial and right atrial pressures is summarized in Table 1 and Figure 1. The correlation coefficient of left atrial and right h t pressure atrial pressure was 0.48. ~ i ~ atrial Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21508/ on 04/29/2017 BELL, STUBBS AND PUGH FIGURE1 . Relationship between left atrial and right atrial pressures with standard error. equaled 0.228 of left atrial pressure. Four patients ( 4/31 ) with markedly elevated left atrial pressure (26 mm Hg or greater) had low right atrial pressures ( 3 mm Hg or less). Eighteen patients (18191) with left atrial pressure 20 m m Hg or greater had low right atrial pressure ( 3 mm Hg or less). Three patients (3139) with normal left atrial pressure ( 12 mm Hg or less) had elevated right atrial pressure ( 8 mm Hg or greater). In contrast, mean pulmonary artery pressure was elevated (25 mm Hg or greater) in 90 of 91 patients with left atrial pressure 20 mm Hg or greater. The correlation coefficient of left atrial and mean pulmonary artery pressure was 0.70 (Fig 2 ) . Mean pulmonary artery pressure equaled 1.23 of left atrial pressure. The effect of acute elevation of left atrial pressure on right atrial and pulmonary artery pressure is summarized in Table 2 and Figures 3 and 4. No consistent pattern of right atrial or pulmonary artery pressure change was observed in response to the left atrial pressure rise. Although in 16 patients a Table 1-7 3 or less MPA ...... .. I-Division of 200 patients according t o pressure relationships RA Pressurr (mm HR) 8 o r greater rise in left atrial pressure was reflected by a rise in right atrial pressure, in four of these a left atrial pressure rise of 10 mm Hg or greater was associated with a 1 mm Hg or less rise in right atrial pressure. In two patients, right atrial pressure increased despite no increase in left atrial pressure. In seven patients, a rise in left atrial pressure was not associated with a rise in right atrial pressure. L A Pressure (mm Hg) 11 or less 12-19 20-25 3 14 8 27 22 - 35 - 39 70 10 36 14 - 60 26 or Total greater Patients 17 10 4 31 38 87 75 200 FIGURE2. Relationship between left atrial and mean prllmonary artery pressures with standard error. CHEST, VOL. 59, NO. 2, FEBRUARY 1971 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21508/ on 04/29/2017 CENTRAL VENOUS PRESSURE AS INDICATOR OF LEFT ATRIAL PRESSURE 16 ' ARA mm Hg 8 0 x VOLUME EXPANSION WING NEOSYNEPHRINE - 0 . x FIGURE 3. Changes in left atrial and right atrial pressures with volume expansion, pacing, and drug infusion. A LA mn Hg -4 0 4 8 12 I // 1 I 1 16 " 28 32 36 D~scussro~ Important clinical decisions on critically ill patients have been based on right atrial (CVP) measurements. A low initial central venous pressure associated with low cardiac output has indicated that volume expansion therapy should be initiated.3 A rapid rise in central venous pressure, or a high initial CVP is usually an indication that volume expansion therapy should not continue.* Digitalis has been used when low cardiac output has been associated with a high CVP.5 Decisions regarding therapy for arrhythmias, eg digitalis, cardioversion, are based on the effect the arrhythmia has had on 28 o 24 x - I CVP. CVP monitoring - has also been used to determine the safety of vasoactive drugs, eg phenylephrine and isoproterenol.6 In our study, volume expansion, rapid pacing, phenylephrine and isoproterenol were selected to induce left atrial pressure changes because of their practical clinical implications. It would be ideal if left atrial pressure could be monitored in critically ill patients, but technical difficulties make this impractical for most patients. CVP is readily available and is assumed to reflect left atrial Pressure. Left atrial and right atrial pressures are similar under certain circumstances ie, VOLUME EXPANSION PACING NEOSYNEPHRINE ISOPROTERENOL X 20 A MPA 16- m m ~ q 12 - 0 FIGURE 4. Changes in left atrial and pulmonary artery pressures with volume expansion, pacing, and d ~ infusion. g -4 0 4 8 . . 12 16 CHEST, VOL. 59, NO. 2, FEBRUARY 1971 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21508/ on 04/29/2017 20 24 I I 28 32 I 36 BELL, STUBBS AND PUGH Table 2--Hemodynaniicr before and during volume exponrion Patient Lesion MS MS MI MS MS MS/MI MS MS MS/MI MS MS/MI MS MI MI MI MI MI MI MI MS MS/MI MS MS MS MS Time Pressure Cardiac (mm Hg) Output LA RA MPA (L/min) Baseline Volume Baseline Volume Baseline Volume Baseline Volume Baseline Volume Baseline Pacing Baseline Pacing Baseline Pacing Baseline Pacing Baseline Pacing Baseline Pacing Baseline Pacing Baseline Neosynephrine Baseline Neosynephrine Baseline Neosynephrine Baseline Neosynephrine Baseline Neosynephrine Baseline Neosynephrine Baseline Neosynephrine Baseline Isoproterenol Baseline Isoproterenol Baseline Isoproterenol Baseline Isoproterenol Baseline Isoproterenol Baseline Isoproterenol constrictive pericarditis and large atrial septa1 defects.' However, since elevated right atrial pressures usually occur only with right heart failure and elevated right ventricular end-diastolic pressures, elevated left atrial pressure may occur with normal CVP. Elevated CVP may occur with normal left atrial pressures in cor pulmonale. The information in our study emphasizes this lack of relationship since 20 percent of patients with left atrial pressure greater than 20 mm Hg have low right atrial pressure below 3 mm Hg. Similarly, 8 percent of patients with right atrial pressure greater than 8 mm Hg have normal left atrial pressures (below 12 mm Hg). Consequently, CVP frequently cannot be used as a measure of left atrial pressure. Volume expansion therapy has gained widespread popularity. By augmenting atrial pressure, the rapid infusion of intravenous fluids may augment stroke volume in accordance with the Frank-Starling principle. A plateau is eventually reached so that additional increments of fluid may result in increased filling pressure with very little augmentation of stroke volume.8 If volume expansion is continued past this point, pulmonary edema will eventually result. Recently, volume expansion therapy has been advocated even in the patient in cardiogenic shock following myocardial infarction.9 Cohn and Luria3 have stated that right and left atrial pressures rise symmetrically during volume expansion in normal subjects and that consistent rises in CVP are seen before left atrial pressure is increased to a dangerous level. A CVP rise of 3 cm water or more with each 100 ml of volume infused has been used as a guideline indicating abnormal rises in left atrial pressure.3 In our study, right atrial pressure did increase in four of five patients during volume infusion. However, in patient 5 this rise was associated with a fall in left atrial pressure. In patient 3, right atrial pressure fell while left atrial pressure rose to 36 mm Hg. In patient 2, a 1 mm rise in right atrial pressure was associated with a 6 mm rise in left atrial pressure. Baseline mean pulmonary artery pressure showed good correlation with left atrial pressure. Mean pulmonary artery pressure was used in this study because of the technical difficulties of obtaining reliable pulmonary artery end-diastolic pressure. While marked elevations in mean pulmonary artery pressure occasionally occurred with only modestly elevated left atrial pressures, the absence of pulmonary hypertension reliably indicated that left atrial pressure was not markedly elevated. This lends support to the concept that mean pulmonary artery pressure rather than CVP should be used to make decisions regarding therapy. While the changes in mean pulmonary artery pressure with rises in left atrial pressure were not consistent, a normal mean pulmonary pressure excluded a marked elevation of left atrial pressure. Patients with mitral stenosis and insufficiency were used in this study because they provided a readily accessible group with chronic elevations of CHEST, VOL. 59, NO. 2, FEBRUARY 1971 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21508/ on 04/29/2017 CENTRAL VENOUS PRESSURE AS INDICATOR OF LEFT ATRIAL PRESSURE left atrial pressure. Mitral stenosis is uncommon among critically ill patients. The mechanism of left atrial pressure elevation is not the same in rnitral stenosis as in other forms of heart disease. In patients with mitral stenosis left atrial pressure cannot be used as an indicator of left ventricular end-diastolic pressure. However, both may have low cardiac outputs and chronically elevated left atrial pressure. Elevation of right heart pressure is presumably due to elevated left atrial pressures.10 Furthermore, mitral insuiliciency occurs with surprising frequency in critically ill patients. This may be due t o papillary muscle dysfunction or rupture or merely due to a markedly dilated left ventricle.11 Poor correlation exists between baseline left atrial and right atrial pressures. Significant differences between these pressures may occur with a frequency of 20 percent. Rapid changes in left atrial pressure induced by volume expansion, tachycardia, or vasoactive drugs may not be reflected in right atrial or pulmonary artery pressure changes. Baseline mean pulmonary artery pressure may be helpful in predicting left atrial pressure. If the mean pulmonary artery pressure is not elevated, it is likely left atrial pressure is normal or only slightly elevated. 173 REFERENCES 1 Zimmerman HA: Intravascular Catheterization, Springfield, Charles C Thomas, 1966 2 Weil MH, Shubin H, Rosoff L: Fluid repletion in circulatory shock. JAMA 192:668,1965 3 Cohn JN, Luria MH: Studies in clinical shock and hypotension. JAMA 193:891, 1964 4 Tristani FE, Cohn JN: Masked heart failure in shock. Circulation, Supplement 3,33 and 34, 1966 5 Siege1 JH, Creenspan M, Del Guercio LRM: Abnormal vascular tone, defective oxygen transport and myocardial failure in human septic shock. Ann Surgery 165:504, 1967 6 Hardaway RM, James PM, Anderson RW, et al: Intensive study and treatment of shock in man. JAMA 199:115, 1967 7 Albers WH, Hugenholb PC, Nadas AS: Constrictive pericarditis and atrial septal defect, secundum type. Amer J Cardiol23:850, 1969 8 Burton AC: Physiology and Biophysics of the Circulation, Chicago, Year Book, 1965 9 Nixon PC, Ikram H, Morton S: Cardiogenic shock treated with infusion of dextrose solution. Amer Heart J 73:843, 1967 10 Linhart JW, Hildner FJ, Barold SJ, et al: Myocardial function in patients with coronary artery disease. Amer J Cardiol23:379, 1969 11 Friedberg CF: Diseases of the Heart, Philadelphia, W. B. Saunders Co., 1966 Reprint requests: Dr. Bell, University of Kansas Medical Center, Kansas City, Kansas 66103 RESIDENT FELLOWSHIP PROGRAM American College of Chest Physicians In an effort to advance knowledge of chest diseases and their treatment, the American College of Chest Physicians has established a Resident Fellowship program through which medical graduates from other countries may receive assistance in postgraduate medical training in chest diseases in the United States. Under this program, the College aids qualified physicians in obtaining suitable postgraduate residencies in cardiopulmonary diseases at accredited hospitals or institutions in the United States. At this time, the College is offering the following fellowship for 1972: Eudowood Fellowship for Tuberculosis with a grant of $2,500.00 per year for postgraduate training in the United States in tuberculosis. All applicants must be ECFMG certified and the Resident Fellowship program of the College requires that the candidate be assured of a responsible position in the field of chest diseases when he returns to his country. Physicians who are interested should write to Dr. Arthur M. Olsen, Chairman of the Council on International Mairs, in care of the ACCP, 112 East,Chestnut Street, Chicago 6061 1. CHEST, VOL. 59, NO. 2, FEBRUARY 1971 Downloaded From: http://publications.chestnet.org/pdfaccess.ashx?url=/data/journals/chest/21508/ on 04/29/2017