- Email: [email protected]
Does central venous pressure accurately reflect hemodynamic and fluid volume patterns in the critical surgical patient?
Does Central Venous Pressure Accurately Reflect Hemodynamic and Fluid Volume Patterns in the Critical Surgical Patient?
Dominic A. DeLaurentis, MD, Philadelphia, Pennsylvania Martin Hayes, MD, Philadelphia, Pennsylvania Teruo Matsumoto, MD, Philadelphia, Pennsylvania Charles C. Wolferth, Jr, MD, Philadelphia, Pennsylvania
Accurate assessment of the circulating blood volume and extracellular fluid volume is necessary for intelligent management of the critically ill surgical patient. Fluid overload can cause congestive heart failure or it may produce pulmonarysequestration of fluid with subsequent respiratory distress. Both situations should be avoided. However, adequate fluid therapy must be given even when the patient's myocardium is lJrimarily or secondarily damaged. Central venous pressure monitoring is commonly used as an aid in determining the adequacy of fluid replacement in critical patients. If in these patients the central venous pressure is low or in the low normal range, colloid solution or salt-containing fluid is administered in the belief that the volume load is insufficient. If the central venous pressure is high, additional colloid solution or fluid is withheld [•]. However, in critically ill patients it is incorrect to assume thatthe right atrial pressure, which is measured by a properly placed From the Department of Surgery, The Hahnemann Medical College and Hospital, and the Betty and Milton Kroungold Shock and Trauma Unit, Philadelphia, Pennsylvania. Reprint requests should be addressedto Dr DeLaurentts,The Hahnemann Medical College and Hospital, 230 North Broad Street, Phila. delphia, Pennsylvania 19102.
Volume 126; September 1973
central venous pressure catheter, is always an accurate reflection of the pressures found in the left heart. Disparate-hemodynamic forces between the right and left ventricles can occur and must be taken into consideration when parenteral fluids are given to sick patients [2]. Elevation of the central venous pressure can be caused by a variety of pathologic entities which exert their effects between the aor_tic valve and the tip of the measuring catheter, but these may not be related to body fluid volumes. Congestive heart failure, valvular heart disease, myocardial infarction, left atrial myxoma, pulmonary hypertension, cot pulmonale, and congenital heart disease are examples of such entities. Here again, the central venous pressure may be in the normal or in the low range and yet the patient may have pulmonary edema and left ventricular failure. The pressure which best defines left ventricular function and the ability of the heart to handle a fluid load is the left ventricular end diastolic pressure. This cannot be measured routinely in most critical patients. The next best measurements that directly reflect left ventricular pressure changes and reserve are the left atrial and pulmonary capillary wedge pressures. When'these pressures are elevated, the indication is that the left ventricle is failing, cannot empty
4t5
DeLaurentis et al
completely, has a poor output, and cannot accept any further fluid load. These pressures seem to be much more sensitive than the central venous pressure in determining fluid m a n a g e m e n t in critically ill surgical patients.
Background The development of a pulmonary artery catheter with a balloon at its tip, which can be flowdirected, has allowed the obtaining of repeated m e a s u r e m e n t s of pulmonary capillary wedge pressures at the bedside [,3]. This permits accurate assessment of left atrial pressure which usually reflects left ventricular function. With this catheter, continuous evaluation of pulmonary hemodynamics i n t e r m s of pulmonary artery pressure becomes a clinical reality rather than a laboratory procedure. The relation of central venous pressure to pulmonary capillary wedge pressure in patients with myocardial infarction was~studied by Forrester et al [4]. They found t h a t the central venous pressure did not correlate well with left ventricular filling pressure, pulmonary capillary wedge pressure, or x-ray evidence of congestive heart failure. T h e y
TABLE I
Correlation between Central Venous Pressure and Pulmonary Artery Pressure in Thirty-Two Consecutive Patients Number of Patients
Low CVP and PAP Normal CVP and PAP High CVP and PAP Total
4 9 3 16
Low CVP and normal PAP Low CVP and high PAP Normal CVP and high PAP Total
4 4 8 16
Result: Correlation : 50%
T A B L E II
Response to Colloid Infusion Number of Patients Unchanged CVP]~
14
Increased PAP J Increased CVP~ Increased P A P I Total
416
8 22
also concluded that changes in central venous pressure were of lit Lle value during trials of fluid loading or diuresis. A recent s t u d y ill our S h o c k / T r a u m a Unit showed that central venous pressure and pulmonary artery pressure correlated in only 50 per cent of the surgical patients studied. (Table I.) In this study, patients without myocardial infarction and with normal central venous pressure were found to be in congestive heart failure as determined b y pulmonary artery and pulmonary capillary wedge pressures, x-ray films, and auscultatory data. Moreover, central venous pressure changes were not nearly as reliable or as sensitive during fluid challenge and diuresis as were pulmonary artery and pulmonary capillary wedge pressures. (Table II.) M c H u g h et al [5] showed a close correlation between the x-ray findings of pulmonary e d e m a and pulmonary capillary wedge pressures. T h e y found that the redistribution of blood flow in the puhnonary artery fr~Jm the base of the lung to the upper zones occurred when wedge pressures were elevated to 12 mm Hg. Hilar markings indical~ing central pulmonary venous congestion correlated with wedge pressures in the range of 15 mm Hg. Wedge pressures of 18 m m Hg or over revealed perihilar rosette formation on chest roentgenogram and were associated with frank congestive heart failure. We have observed similar changes in acutely ill, general surgical patients.
Measurement of Pulmonary Pressures In our S h o c k / T r a u m a Unit, the n u m b e r 7F Swan-Ganz catheter is routinely used. This size catheter is easier to insert than is the 5F "model since it has less tendency to kink and twist, and its balloon capacity of 1.5 cc withstands accidental overinflation better than does the 0.8 cc balloon on the 5F model. We usually introduce the catheter by cutdown into an antecubital vein or, less frequently, into the external jugular vein. After. the catheter is introduced into the vein, its p l a c e m e n t proceeds according to the technic described by Swan et al [3]. We can u s u a l l y p e r f o r m the entire procedure, including cutdown, in a b o u t twenty minutes. Although complications such as ventricular arrhythmia, catheter kinking, and pulmonary artery perforation have been reported, we have noted only five complications in more than 200 insertions. Four of these complications consisted of transient p a t t e r n s o f premature ventricular contraction as t h e catheter traversed the right
The American Journal of Surgery
Centra'. Venous Pressure Monitoring
ventricle. In one patient, i n t r a v e n t r i c u l a r knotting was noted on chest roentgenogram; however, the c a t h e t e r was withdrawn a n d replaced without difficulty. With the c a t h e t e r in place a n d connected to a strain gauge transducer, c o n t i n u o u s : p u l m o nary artery pressure is easily monitored. T h e balloon is i n t e r m i t t e n t l y inflated and a capillary wedge pressure is r e c o r d e d . Normal p u l m o n a r y capillary w e d g e p r e s s u r e is 5 t o 8 m m Hg. T h e cat h e t e r tip will usually lodge in the right mid-lung field, probably as a result of a n a t o m i c a n d flow factors since t h e r i g h t p u l m o n a r y artery has a less acute takeoff from the outflow t r a c t t h a n does the left p u l m o n a r y artery and it receives 60 per cent of the right ventricular stroke volume. F r e q u e n t irrigation of the c a t h e t e r to p r e v e n t clotting is performed with 3 to 5 cc of heparinized saline solution every hour. Several of our p a t i e n t s have had a c a t h e t e r in place for more t h a n t e n days a n d have had no clinical or x-ray evidence of traum a to the lung. Bursting of the latex balloon at the tip of the catheter frequently occurs after three or four d a y s with subsequent loss of the ability to record pulmonary capillary wedge pressure. In this event~ the pulmonary artery diastolic pressure can be used as a substitute.
Normal Central Venous Pressure and Elevated Pul. monary Artery Pressure and Pubnonary Wedge Pressure A sixty-nine year old man with cirrhosis of the liver was transferred to The Hahnemann Medical College and Hospital because of a perforated marginal ulcer. During surgery hypotension developed after massive blood loss. Blood and fluid replacement failed to reverse the hypotension, and vasopressors were given. On the patient's admission to the Shock/Trauma Unit the central venous pressure was-12 cm H20, the mean pulmonary artery pressure was 25 m m Hg, and the pulmonary wedge pressure was 16ram Hg. A blood pressure of 100 systolic could only be maintained with the administration of Aramine ®. Although the central venous pressure data suggested that further volume loading might be indicated, the pulmonary artery pressure and pulmonary wedge pressure data suggested a cardiogenic component; f~rther fluid administration was therefore withheld. The electrocardiogram revealed acute myocardial infarction of the posterior wall, and he was given digitalis and diuretics which resulted in a decrease in the pulmonary artery and pulmonary capillary wedge pressures. As diuresis proceeded, colloid solution and blood were slowly replaced. The rate of replacement was tittered by the pulmonary wedge pressure values. As blood and colloid solution were given, the blood pressure gradually increased until the administration of Aramine could finally be discontinued.
Clinical Application Abnormal p u h n o n a r y artery pressures m a y occur in the following situations: (1) states of increased p u l m o n a r y a r t e r y flow as i n left to right shunts; (2) states of increased p u l m o n a r y vascular resistance secondary to cardiac dysfunction, pulm o n a r y venous obstruction, or chronic lung disease; (3) hypoxia regardless of cause; (4) pulmonary emboli; (5) too m u c h or too rapid parenteral fluid administration. Elevations of p u l m o n a r y capillary wedge pressure m a y be n o t e d in t h e following circumstances: (1) p u l m o n a r y venous obstruction secondary to valvular heart disease or m y x o m a ; (2) congestive h e a r t failure; (3) too m u c h or too rapid parenteral fluid administration. T h e Swan-Ganz c a t h e t e r is useful in the differential diagnosis of cardiopulmon a r y problems. For example, an elevated pulmon a r y artery pressure with normal p u l m o n a r y wedge pressure Would indicate to us a p r i m a r y p u l m o n a r y problem, such as p u l m o n a r y emboli, whereas an elevated p u l m o n a r y a r t e r y pressure with e l b v a t e d p u l m o n a r y c a p i l l a r y wedge press u r e w o u l d point to a p r i m a r y c a r d i a c problem or fluid overload. T h e following cases a r e illustrative.
Yolumm124, September 11173
Eleva ted Central Venous Pressure, Pulmonary Artery Pressure, and Pulmonary Wedge Pressure A sixty-three year old woman was admitted to The Hahnemann Medical College and Hospital because of abdominal pain, fever, and dehydration. She had pyelonephritis with obstruction of the left kidney. An indwelling-ureteral catheter was placed and shortly thereafter she had shaking chills, fever, and hypotension. The central venous pressure was found to be low. The rapid administration of fluids was accompanied by a rapid rise in central venous pressure with continued hypotension. The diagnosis of septic shock was made and the patient was transferred to t h e Shock/Trauma Unit. A Swan-Ganz catheter was inserted and the pulmonary artery pressure was found to be 32 mm Hg and the pulmonary wedge pressure 24 mm Hg. The central venous pressm'e was 16 cm H20. The electrocardiogram revealed an acute anteroseptal infarction. Blood cultures were positive for Escherichia cMi. Thus, although volume was required, it was contraindicated in the presence of congestive heart failure. After treatment with a pharmacologic dose of steroids and intravenous digitalis, the patient was placed on vasopressor therapy. Lasix~-induced diuresis was started along with pressor-induced normotension until normal pulmonary wedge pressure values were obtained. At this time large doses of colloid Solution and normal saline were given
417
DeLaurentis et al
by titration against pulmonary wedge pressure. Keflin® and gentamicin sulfate were administered. The patient was gradually weaned from vasopressors without difficulty. After four days the patient was transferred from the unit and subsequently discharged from the hospital. Low Central Venous Pressure, Elevated Pulmonary Artery Pressure, and Normal Pulmonary Wedge Pressure A forty year old man was admitted to t h e Shock/ Trauma Unit because of flail chest, lung contusion, skull fracture, and shock. The central venous pressure was 4 c m H20, m e a n pulmonary artery pressure 27 m m Hg, and pulmonary wedge pressure 4 m m Hg. Cardiac output was 2.44 L per minute, Since the patient was thought to be hypovolemic, large volumes of colloid and crystalloidsolutions were given. Cardiac output increased to 5.14 L per minute; pulmonary wedge pressure and central venous pressure remained within normal limits. The pulmonary artery pressure remained elevated, and the urine output and blood pressure improved. Large doses of steroids combined with volume ventilation resulted in a gradual decrease in the abnormally elevated pulmonary artery pressure. In this patient we judged that the increased pulmonary artery pressure represented changes in pulmonary hemodynamics secondary to the lung injury whereas the low central venous and pulmonary capillary wedge pressures were indicativeof hypovolemia.
418
Summary Pulmonary artery pressures and pulmonary capillary wedge pressures more accurately reflect left ventricular function t h a n do central venous pressures. In more t h a n 200 patients, we found t h a t monitoring of hemodynamics via right heart catheterization with the Swan-Ganz catheter is superior to central venous pressure monitoring. All critical shrgical patients a d m i t t e d to our S h o c k / T r a u m a Unit are routinely monitored by means of this catheter.
References 1. Mogil RA, DeLaurentis DA, Rosemond GP: The infraclavicular venipuncture, Arch Surg 95: 320, 1967. 2, Civetta JM, Gabel JC, Laver MB: Disparate ventrtcular function in surgical patients. Surg Forum 22: 136, 1971. 3, Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D: Catheterization of the heart In man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283: 447. 19~'0. 4. Forrester JS, Diamond G, McHugh TJ, Swan HJC: Filling prossures in right and left sides of heart in acute myocardla! infarction. N EngIJ Med 285: 190, 1971. 5. McHugh TJ, Forrester JS, Adler L, Zion D, Swan HJC: Pulmonary vascular congestion in acute myocardial infarction: hemodynamic and radlologic correlations. Ann Intern Med 76: 29, 1972.
The American Joumd Of Surgery
Dominic A. DeLaurentis, MD, Philadelphia, Pennsylvania Martin Hayes, MD, Philadelphia, Pennsylvania Teruo Matsumoto, MD, Philadelphia, Pennsylvania Charles C. Wolferth, Jr, MD, Philadelphia, Pennsylvania
Accurate assessment of the circulating blood volume and extracellular fluid volume is necessary for intelligent management of the critically ill surgical patient. Fluid overload can cause congestive heart failure or it may produce pulmonarysequestration of fluid with subsequent respiratory distress. Both situations should be avoided. However, adequate fluid therapy must be given even when the patient's myocardium is lJrimarily or secondarily damaged. Central venous pressure monitoring is commonly used as an aid in determining the adequacy of fluid replacement in critical patients. If in these patients the central venous pressure is low or in the low normal range, colloid solution or salt-containing fluid is administered in the belief that the volume load is insufficient. If the central venous pressure is high, additional colloid solution or fluid is withheld [•]. However, in critically ill patients it is incorrect to assume thatthe right atrial pressure, which is measured by a properly placed From the Department of Surgery, The Hahnemann Medical College and Hospital, and the Betty and Milton Kroungold Shock and Trauma Unit, Philadelphia, Pennsylvania. Reprint requests should be addressedto Dr DeLaurentts,The Hahnemann Medical College and Hospital, 230 North Broad Street, Phila. delphia, Pennsylvania 19102.
Volume 126; September 1973
central venous pressure catheter, is always an accurate reflection of the pressures found in the left heart. Disparate-hemodynamic forces between the right and left ventricles can occur and must be taken into consideration when parenteral fluids are given to sick patients [2]. Elevation of the central venous pressure can be caused by a variety of pathologic entities which exert their effects between the aor_tic valve and the tip of the measuring catheter, but these may not be related to body fluid volumes. Congestive heart failure, valvular heart disease, myocardial infarction, left atrial myxoma, pulmonary hypertension, cot pulmonale, and congenital heart disease are examples of such entities. Here again, the central venous pressure may be in the normal or in the low range and yet the patient may have pulmonary edema and left ventricular failure. The pressure which best defines left ventricular function and the ability of the heart to handle a fluid load is the left ventricular end diastolic pressure. This cannot be measured routinely in most critical patients. The next best measurements that directly reflect left ventricular pressure changes and reserve are the left atrial and pulmonary capillary wedge pressures. When'these pressures are elevated, the indication is that the left ventricle is failing, cannot empty
4t5
DeLaurentis et al
completely, has a poor output, and cannot accept any further fluid load. These pressures seem to be much more sensitive than the central venous pressure in determining fluid m a n a g e m e n t in critically ill surgical patients.
Background The development of a pulmonary artery catheter with a balloon at its tip, which can be flowdirected, has allowed the obtaining of repeated m e a s u r e m e n t s of pulmonary capillary wedge pressures at the bedside [,3]. This permits accurate assessment of left atrial pressure which usually reflects left ventricular function. With this catheter, continuous evaluation of pulmonary hemodynamics i n t e r m s of pulmonary artery pressure becomes a clinical reality rather than a laboratory procedure. The relation of central venous pressure to pulmonary capillary wedge pressure in patients with myocardial infarction was~studied by Forrester et al [4]. They found t h a t the central venous pressure did not correlate well with left ventricular filling pressure, pulmonary capillary wedge pressure, or x-ray evidence of congestive heart failure. T h e y
TABLE I
Correlation between Central Venous Pressure and Pulmonary Artery Pressure in Thirty-Two Consecutive Patients Number of Patients
Low CVP and PAP Normal CVP and PAP High CVP and PAP Total
4 9 3 16
Low CVP and normal PAP Low CVP and high PAP Normal CVP and high PAP Total
4 4 8 16
Result: Correlation : 50%
T A B L E II
Response to Colloid Infusion Number of Patients Unchanged CVP]~
14
Increased PAP J Increased CVP~ Increased P A P I Total
416
8 22
also concluded that changes in central venous pressure were of lit Lle value during trials of fluid loading or diuresis. A recent s t u d y ill our S h o c k / T r a u m a Unit showed that central venous pressure and pulmonary artery pressure correlated in only 50 per cent of the surgical patients studied. (Table I.) In this study, patients without myocardial infarction and with normal central venous pressure were found to be in congestive heart failure as determined b y pulmonary artery and pulmonary capillary wedge pressures, x-ray films, and auscultatory data. Moreover, central venous pressure changes were not nearly as reliable or as sensitive during fluid challenge and diuresis as were pulmonary artery and pulmonary capillary wedge pressures. (Table II.) M c H u g h et al [5] showed a close correlation between the x-ray findings of pulmonary e d e m a and pulmonary capillary wedge pressures. T h e y found that the redistribution of blood flow in the puhnonary artery fr~Jm the base of the lung to the upper zones occurred when wedge pressures were elevated to 12 mm Hg. Hilar markings indical~ing central pulmonary venous congestion correlated with wedge pressures in the range of 15 mm Hg. Wedge pressures of 18 m m Hg or over revealed perihilar rosette formation on chest roentgenogram and were associated with frank congestive heart failure. We have observed similar changes in acutely ill, general surgical patients.
Measurement of Pulmonary Pressures In our S h o c k / T r a u m a Unit, the n u m b e r 7F Swan-Ganz catheter is routinely used. This size catheter is easier to insert than is the 5F "model since it has less tendency to kink and twist, and its balloon capacity of 1.5 cc withstands accidental overinflation better than does the 0.8 cc balloon on the 5F model. We usually introduce the catheter by cutdown into an antecubital vein or, less frequently, into the external jugular vein. After. the catheter is introduced into the vein, its p l a c e m e n t proceeds according to the technic described by Swan et al [3]. We can u s u a l l y p e r f o r m the entire procedure, including cutdown, in a b o u t twenty minutes. Although complications such as ventricular arrhythmia, catheter kinking, and pulmonary artery perforation have been reported, we have noted only five complications in more than 200 insertions. Four of these complications consisted of transient p a t t e r n s o f premature ventricular contraction as t h e catheter traversed the right
The American Journal of Surgery
Centra'. Venous Pressure Monitoring
ventricle. In one patient, i n t r a v e n t r i c u l a r knotting was noted on chest roentgenogram; however, the c a t h e t e r was withdrawn a n d replaced without difficulty. With the c a t h e t e r in place a n d connected to a strain gauge transducer, c o n t i n u o u s : p u l m o nary artery pressure is easily monitored. T h e balloon is i n t e r m i t t e n t l y inflated and a capillary wedge pressure is r e c o r d e d . Normal p u l m o n a r y capillary w e d g e p r e s s u r e is 5 t o 8 m m Hg. T h e cat h e t e r tip will usually lodge in the right mid-lung field, probably as a result of a n a t o m i c a n d flow factors since t h e r i g h t p u l m o n a r y artery has a less acute takeoff from the outflow t r a c t t h a n does the left p u l m o n a r y artery and it receives 60 per cent of the right ventricular stroke volume. F r e q u e n t irrigation of the c a t h e t e r to p r e v e n t clotting is performed with 3 to 5 cc of heparinized saline solution every hour. Several of our p a t i e n t s have had a c a t h e t e r in place for more t h a n t e n days a n d have had no clinical or x-ray evidence of traum a to the lung. Bursting of the latex balloon at the tip of the catheter frequently occurs after three or four d a y s with subsequent loss of the ability to record pulmonary capillary wedge pressure. In this event~ the pulmonary artery diastolic pressure can be used as a substitute.
Normal Central Venous Pressure and Elevated Pul. monary Artery Pressure and Pubnonary Wedge Pressure A sixty-nine year old man with cirrhosis of the liver was transferred to The Hahnemann Medical College and Hospital because of a perforated marginal ulcer. During surgery hypotension developed after massive blood loss. Blood and fluid replacement failed to reverse the hypotension, and vasopressors were given. On the patient's admission to the Shock/Trauma Unit the central venous pressure was-12 cm H20, the mean pulmonary artery pressure was 25 m m Hg, and the pulmonary wedge pressure was 16ram Hg. A blood pressure of 100 systolic could only be maintained with the administration of Aramine ®. Although the central venous pressure data suggested that further volume loading might be indicated, the pulmonary artery pressure and pulmonary wedge pressure data suggested a cardiogenic component; f~rther fluid administration was therefore withheld. The electrocardiogram revealed acute myocardial infarction of the posterior wall, and he was given digitalis and diuretics which resulted in a decrease in the pulmonary artery and pulmonary capillary wedge pressures. As diuresis proceeded, colloid solution and blood were slowly replaced. The rate of replacement was tittered by the pulmonary wedge pressure values. As blood and colloid solution were given, the blood pressure gradually increased until the administration of Aramine could finally be discontinued.
Clinical Application Abnormal p u h n o n a r y artery pressures m a y occur in the following situations: (1) states of increased p u l m o n a r y a r t e r y flow as i n left to right shunts; (2) states of increased p u l m o n a r y vascular resistance secondary to cardiac dysfunction, pulm o n a r y venous obstruction, or chronic lung disease; (3) hypoxia regardless of cause; (4) pulmonary emboli; (5) too m u c h or too rapid parenteral fluid administration. Elevations of p u l m o n a r y capillary wedge pressure m a y be n o t e d in t h e following circumstances: (1) p u l m o n a r y venous obstruction secondary to valvular heart disease or m y x o m a ; (2) congestive h e a r t failure; (3) too m u c h or too rapid parenteral fluid administration. T h e Swan-Ganz c a t h e t e r is useful in the differential diagnosis of cardiopulmon a r y problems. For example, an elevated pulmon a r y artery pressure with normal p u l m o n a r y wedge pressure Would indicate to us a p r i m a r y p u l m o n a r y problem, such as p u l m o n a r y emboli, whereas an elevated p u l m o n a r y a r t e r y pressure with e l b v a t e d p u l m o n a r y c a p i l l a r y wedge press u r e w o u l d point to a p r i m a r y c a r d i a c problem or fluid overload. T h e following cases a r e illustrative.
Yolumm124, September 11173
Eleva ted Central Venous Pressure, Pulmonary Artery Pressure, and Pulmonary Wedge Pressure A sixty-three year old woman was admitted to The Hahnemann Medical College and Hospital because of abdominal pain, fever, and dehydration. She had pyelonephritis with obstruction of the left kidney. An indwelling-ureteral catheter was placed and shortly thereafter she had shaking chills, fever, and hypotension. The central venous pressure was found to be low. The rapid administration of fluids was accompanied by a rapid rise in central venous pressure with continued hypotension. The diagnosis of septic shock was made and the patient was transferred to t h e Shock/Trauma Unit. A Swan-Ganz catheter was inserted and the pulmonary artery pressure was found to be 32 mm Hg and the pulmonary wedge pressure 24 mm Hg. The central venous pressm'e was 16 cm H20. The electrocardiogram revealed an acute anteroseptal infarction. Blood cultures were positive for Escherichia cMi. Thus, although volume was required, it was contraindicated in the presence of congestive heart failure. After treatment with a pharmacologic dose of steroids and intravenous digitalis, the patient was placed on vasopressor therapy. Lasix~-induced diuresis was started along with pressor-induced normotension until normal pulmonary wedge pressure values were obtained. At this time large doses of colloid Solution and normal saline were given
417
DeLaurentis et al
by titration against pulmonary wedge pressure. Keflin® and gentamicin sulfate were administered. The patient was gradually weaned from vasopressors without difficulty. After four days the patient was transferred from the unit and subsequently discharged from the hospital. Low Central Venous Pressure, Elevated Pulmonary Artery Pressure, and Normal Pulmonary Wedge Pressure A forty year old man was admitted to t h e Shock/ Trauma Unit because of flail chest, lung contusion, skull fracture, and shock. The central venous pressure was 4 c m H20, m e a n pulmonary artery pressure 27 m m Hg, and pulmonary wedge pressure 4 m m Hg. Cardiac output was 2.44 L per minute, Since the patient was thought to be hypovolemic, large volumes of colloid and crystalloidsolutions were given. Cardiac output increased to 5.14 L per minute; pulmonary wedge pressure and central venous pressure remained within normal limits. The pulmonary artery pressure remained elevated, and the urine output and blood pressure improved. Large doses of steroids combined with volume ventilation resulted in a gradual decrease in the abnormally elevated pulmonary artery pressure. In this patient we judged that the increased pulmonary artery pressure represented changes in pulmonary hemodynamics secondary to the lung injury whereas the low central venous and pulmonary capillary wedge pressures were indicativeof hypovolemia.
418
Summary Pulmonary artery pressures and pulmonary capillary wedge pressures more accurately reflect left ventricular function t h a n do central venous pressures. In more t h a n 200 patients, we found t h a t monitoring of hemodynamics via right heart catheterization with the Swan-Ganz catheter is superior to central venous pressure monitoring. All critical shrgical patients a d m i t t e d to our S h o c k / T r a u m a Unit are routinely monitored by means of this catheter.
References 1. Mogil RA, DeLaurentis DA, Rosemond GP: The infraclavicular venipuncture, Arch Surg 95: 320, 1967. 2, Civetta JM, Gabel JC, Laver MB: Disparate ventrtcular function in surgical patients. Surg Forum 22: 136, 1971. 3, Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D: Catheterization of the heart In man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283: 447. 19~'0. 4. Forrester JS, Diamond G, McHugh TJ, Swan HJC: Filling prossures in right and left sides of heart in acute myocardla! infarction. N EngIJ Med 285: 190, 1971. 5. McHugh TJ, Forrester JS, Adler L, Zion D, Swan HJC: Pulmonary vascular congestion in acute myocardial infarction: hemodynamic and radlologic correlations. Ann Intern Med 76: 29, 1972.
The American Joumd Of Surgery