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Hemodynamic observations in severe preeclampsia complicated by pulmonary edema
BASIC SCIENCE SECTION
Hemodynamic observations in severe preeclampsia complicated by pulmonary edema Thomas J. Benedetti, M.D., Richard Kates, M.D., and Virginia Williams, M.D. Seattle and Spokane, Washington Ten patients with severe preeclampsia complicated by pulmonary edema were studied with invasive hemodynamic monitoring. Eight of 10 patients developed pulmonary edema during the postpartum period. Five patients had alterations in the colloid osmotic pressure-pulmonary artery wedge pressure gradient related to elevations in the pulmonary artery wedge pressure and a reduction in the colloid osmotic pressure. Three patients had hemodynamic findings consistent with pulmonary capillary leak. Two patients had evidence of left ventricular failure. In three of the patients, the central venous pressure was significantly lower than the simultaneously determined pulmonary artery wedge pressure during the acute phase of the pulmonary edema. (AM J 0BSTET GYNECOL 1985;152:330-4.)
Key words: Severe preeclampsia, pulmonary edema, volume overload, colloid osmotic pressure, pulmonary artery wedge pressure
Pulmonary edema in the pregnant hypertensive pa tient has been postulated to occur by any one of three mechanisms: increased intravascular hydrostatic pres sure, increased capillary permeability, and low vascular oncotic pressure.' In nonpregnant patients, the latter mechanism may infrequently cause pulmonary edema but can potentiate its development when combined with either of the first two events. 2 We previously speculated that a reduction in intravascular colloid osmotic pres sure may play an important role in the development of pulmonary edema in the hypertensive pregnant pa tient.3 However, few patients with pulmonary edema have been subjected to invasive monitoring as well as measurement of colloid osmotic pressure. Since it is difficult to differentiate among the three mechanisms on clinical grounds, little information is available on the frequency with which these various factors lead to the development of pulmonary edema in hypertensive pregnant patients.
From the Departments of Obstetrics and Gynecology and Anesthesia, University of Washington, and the Inland Empire Perinatal Center. Received for publication May 7, 1984; revised October 24, 1984; accepted january 16, 1985. Reprint requests: Dr. Thomas ]. Benedetti, Department of Obstet rics and Gynecology, University of Washington, Seattle, WA 98195.
330
Material and methods This report details the occurrence of pulmonary edema in 10 patients with severe preeclampsia. This series of patients was collected over a 4-year period in two tertiary care referral centers, the University of Washington, Seattle, Washington, and the Inland Em pire Perinatal Center, Spokane, Washington. All pa tients in this series were studied with a flow-directed pulmonary artery catheter either during the develop ment of pulmonary edema or shortly after the devel opment of pulmonary edema but before pharmacologic therapy was directed at relieving the hypoxemia. Standard clinical procedures were used for care and interpretation of the catheter readings, and standard formulas were used for hemodynamic calculations. 3 The diagnosis of pulmonary edema was made on the basis of the clinical respiratory distress associated with hypoxemia (Po2 <70 mm Hg with FI 0 2 = 0.21), on blood gas determination, and confirmatory radio graphic evidence. Colloid osmotic pressure was either calculated from total protein determination or mea sured directly by means of a Wescor oncometer! The diagnosis of left ventricular failure was made when there was increased pulmonary artery wedge pressure associated with a low left ventricular stroke work index. •· 5 Altered capillary permeability was made when there was a normal pulmonary artery wedge pres sure and a normal or elevated left ventricular stroke
Pulmonary edema in severe preeclampsia 331
Volume 152 Number 3
work index (normal left ventricular stroke work in dex = 55 to 85 gm · min · M- 2 ) . Alternatively, this di agnosis was made when the ratio of protein in the pul monary edema fluid to protein in the patient's serum exceeded 0.4. 6 Altered hydrostatic-oncotic forces were diagnosed when the left ventricular stroke work index was normal and the pulmonary artery wedge pressure was elevated, so that the difference between the colloid osmotic pressure and the pulmonary artery pressure was .-;;:4 mm Hg (colloid ·osmotic pressure-pulmonary artery wedge pressure gradient .-;;:4 mm Hg) . Results
Complete hemodynamic data were available on all 10 patients with acute pulmonary edema. The age range of the patients was from 20 to 37 years (mean, 27 years) . Six patients were primiparous, three were secundiparous, and one was grand multiparous. The gestational age range was from 27 to 35 weeks (mean, 31.6 weeks) . Nine of the 10 patients were delivered by cesarean section. All patients, except Patient No. 2, were being treated with magnesium sulfate and hydralazine prior to or at the onset of pulmonary edema. Table I shows the individual hemodynamic data. The patients were categorized on the basis of the mechanism of development of pulmonary edema, Five patients (Nos. 1 through 5) demonstrated alterations in the hy drostatic oncotic forces , three patients (Nos. 6 through 8) showed evidence of permeability pulmonary edema, and two patients (Nos. 9 and 10) showed evidence of left ventricular failure . These data are graphically plot ted in Fig. 1. Table II illustrates the time of onset of pulmonary edema and the relationship to measured filling pres sures. For eight of the 10 patients, pulmonary edema developed after delivery. The range of onset was 5 to 24 hours (mean, 12.6 hours). Six of the eight patients developed respiratory insufficiency between 9 and 15 hours post partum. In all patients, central venous pres sure immediately post partum was between 0 and 6 mm Hg. However, there was a progressive rise iri the central venous pressure in moSt of the patients until the onset of pulmonary edema was recognized. In three of the patients (Nos. 1, 3, and 8), the measurements of central venous pressure did not reflect the simultaneously re corded wedge pressure. In those three patients, the wedge pressure was significantly higher than the cen tral venous pressure. Table III illustrates the volume status of each patient in the critical period before the onset of pulmonary edema. Large volumes of fluid were frequently justified by clinicai need (preoperative hypotension, preload for anesthesia). In some cases, the large volumes of fluid
140 120
~
:e I
100
...
•
~
.& 80 § ~ ;..,J
60 40
20
51015
20253035
PAW (mmHg) Fig. 1. Ventricular function curve 5 illustrating myocardial per formance for each of 10 patients listed in Table i. LVSWI, Left ventricular stroke work index. PAW, Pulmonary artery wedge pressure. • Patients l through 5. *Patients 6 though 8. o Patients 9 and 10.
were the result of intraoperative administration of blood and crystalloid to correct intraoperative loss, in traoperative falls in blood pressure, coagulopathy, or thrombocytopenia. Comment
In this group of patients, the most common reasons for the development of pulmonary edema was an al teration in the hydrostatic oncqtic forces that occurred within 15 hours postpartum. This alteration in forces occurred because of a combination of mild-to-moderate lowering of colloid osmotic pressure (mean = 15.3 mm Hg) and mild-to-moderate elevations in the left ven tricular filling pressures reflected by the pulmo~ary artery wedge pressure (mean, 18.6 mm Hg). None of these patients had evidence of left ventricular dys function, and the elevations in filling pressures were not of significant magnitude to account for pulmonary edema without simultaneous lowering of intravascular oncotic forces. All patients except Nos . 4 and 8 received colloidal fluid prior to the onset of the pulmonary edema. This
332
Benedetti, Kates, and Williams
June I, 1985
Am J Obstet Gynecol
Table I. Hemodynamic data
Patient No.
1
2
3
4
5 6 7 8 9 10
Blood pressure
Cardiac output (Limin)
Cardiac index (Liminlm 2)
Stroke volume (ml)
155/105 160/110 130/100 182/116 140/60 160/90 171/98 160/80 164/82 130/90
7.6 12.5 8.9 7.9 8.5 13.3 8.1 I 1.0 6.6 4.3
4.25 7.2 4.9 4.9 5.0 6.9
80 l01 89 78 85 133 81 103 75 54
4.4
6.9 3.4 2.7
Pulmonary artery systolic pressure (mm Hg)
Pulmonary artery diastolic pressure (mm Hg)
Pulmonary artery wedge pressure (mmHg)
35 34 30
25 16 18 15 20 8 10 20 20 20
22 20 17 14 20
22
40 23
22
35 40 34
Central venous pressure (mmHg)
7 15 10 14 16 8 6 10 18 12
4
6 20 20 18
.Patients 1 through 5: Altered hydrostatic forces. Patients 6 through 8: Permeability defect. Patients 9 and 10: Left ventricular failure.
Table 11. Filling pressures and time of onset of pulmonary edema
Onset of pulmonary edema (hr)
Postpartum central venous pressure (0-1 hr) (mm Hg)
Central venous pressure at onset of pulmonary edema (mm Hg)
Pulmonary artery wedge pressure at onset of pulmonary edema (mm Hg)
12 Hr postpartum Antepartum 12 Hr post parium 12 Hr post partum 9 Hr post partum 24 Hr post partum 12 Hr post partum 5 Hr post partum Antepartum 15 Hr postpartum
6 NA 6 5 0 0 3 5 NA 6
7 15 10 14 16 8
22
Patient No.*
1
2 3 4 5 6 7 8 9 10
6
10 18 12
20 17 14 20 4 6 20 20 18
NA = Not available. *Patients as in Table I. See footnote.
Table III. Fluid management Patient No.
Fluid preceding pulmonary edema
5000 ml/24 hr 2
9000 ml/24 hr
3
1000 ml/5 hr
4
6500 ml/12 hr
5
7000 ml/12 hr
6
4500 ml/24 hr
7
7000 ml/3 hr
8
6000 ml/24 hr
9
5500 ml/24 hr
10
7000 ml/12 hr
Rationale for fluid
Fluid components
A nesthesialdelivery
Intraoperative replacement Hypotensive after epidural anesthesia Low hematocrit (28) Oliguria
Crystalloid + colloid + blood Crystalloid + colloid
Quadruplets
Preload for epidural anesthesia Excess intravenous intake Hypotension
Crystalloid + colloid
General anesthesia, cesarean section Epidural anesthe sia, cesarean section General anesthesia; cesarean section General anesthesia, cesarean section Epidural anesthe sia, cesarean section General anesthesia, General anesthesia, cesarean section General anesthesia, cesarean section Epidural anesthe· sia, cesarean section General anesthesia, cesarean section
Eclampsia, hepatic rupture Twins
Intraoperative replacement Excess intravenous and oral intake Intraoperative replacement
Blood Crystalloid
Crystalloid + colloid Crystalloid + colloid + blood Crystalloid Crystalloid + colloid Crystalloid + colloid + blood
cesarean section
Other factors
Diabetes, chronic hypertension Thrombocytopenia
Pulmonary edema in severe preeclampsia 333
Volume !52 Number 3
Colloid osmotic preSS!lre (mm Hg)
Systemic vascular resistance (dynessec · cm - 5)
Left ventricular stroke work index (gm · min · M- 2)
Colloid osmotic pressurepulmonary artery wedge pressure gradient (mm Hg)
10.4 18.8 15.6 14.8 17.9 17.2 16.5 11.9 17.9 16.5
1206 714 885 1357 978 631 1145 557 823 1693
74 100 62 82 68 102 69 90 46.4 39
-11.6 -1.2 -1.4 0.8 -2.0 13.0 10.5 -8.0 -2.0 -1.5
fluid (blood products and albumin) is known to have strong osmotic effects on the movement of fluid be tween the intravascular and extravascular space. When fluid is administered to the severely preeclamptic pa tient, movement of significant amounts of Ruid from the overexpanded extravascular space to the intravas cular space can result. We hypothesize that, when this effect is added to the usual mobilization of fluid from extravascular compartment to intravascular compart ment that occurs after delivery, a progressive rise in the pulmonary artery wedge pressure occurs. Our data are consistent with this hypothesis. It was previously shown that pregnancy results in the lowering of tht; colloid osmotic pressure, and that the preeclamptic patient has colloid osmotic pressure even lower than that of the normal pregnant patient. 3 The colloid osmotic pressure falls in the postpartum period both in normal and in preeclamptic pregnancies. The combination of a low intravascular oncotic pressure and progressjve rise in hydrostatic pressure can explain pulmonary edema in these patients. The most frequent time for this to occur was within 15 hours postpartum (Table II). In light of these observations, we think that it is wise to monitor central pressures closely in the postpartum period in severely preeclamptic patients who have received significant amount of colloidal fluid in the antepartum or intraoperative period. Many authors have questioned the administration of colloidal fluid to the severely hypertensive patient. We previously advised giving only maintenance fluid dur ing labor. 3 However, clinical circumstances may dictate the need for a colloidal fluid . These circumstances in clude acute volume loss, severe thrombocytopenia, or coagulopathy. We also have used volume loading with a combination of crystalloid fluid and colloidal fluid prior to the induction of epidural anesthesia, and have shown that when this is expertly done, with adequate monitoring of vascular pressure, it is safe for both the fetus and the mother. 7 The use of colloidal fluid without
a
adequate monitoring of pressure may increase the risk of pulmonary edema. The second most common mechanism for the de velopment of pulmonary edema was alteration in cap illary permeability. One of these three patients (No. 8) was the only fatality in the series. She developed acute respiratory insufficiency within 12 hours post partum and initially showed elevated filling pressures. How ever, after diuresis had lowered the pulmonary artery wedge pressure to 12 mm Hg, she began to exude large amounts of proteinaceous material from the endotr;l cheal tube. She eventually developed chronic adult re spiratory distress syndrome and died on the twenty second post partum diiy. Sectioning of the lungs at au topsy provided no evidence for amniotic fluid embo lism. The other two patients showed normal ventricular function and normal wedge pressures in the face of altered oxygenation, and both recovered. Altered cap illary permeability can develop in other organ systems, such as the kidney. In severe preeclampsia, perme ability defects in the lungs are uncommon, and the triggering mechanism is frequently associated with acute volume loss or amniotic fluid embolism, or sepsis .~ Two patients showed evidence of ventricular failure . Patient No. 9 had multiple medical problems, so that ventricular failure in this patient was not surprising. However, the other patient had no predisposing factors and her left ventricular dysfunction was rather tran sient, lasting only 8 hours. Potent diuresis led to a low ering of the pulmonary artery wedge pressure to 12 mm Hg, which resulted in the normalization of cardiac performance. Other investigators 7 have reported left ventricular failure as a result of high systemic resistance which responded to afterload reduction. Most patients in this series had received large amounts qf fluid prior to the development of pulmo nary edema. This was often not appreciated by the physician~ until pulmonary edema developed post par tum. One reason for the excess volume given during the intraoperative period in some patients was a pre cipitate fall in blood pressure just after the delivery of the fetus. Fig~ 2 illustrates sim~ltaneous recordings of the pulmonary artery pressure and the intra-arterial pressure in a patient who experienced a fall in blood pressure. In our experience, this event has usually not been associated with excessive volume loss. The pre cipitate fall in intravascular pressures occurs in both the systemic and pulmonary circulations. This phenom enon might be explained by the relief of a selective aortic obstruction by the gravid uterus. In that case, the pregnant uterus might have been acting in a fashion similar to an antigravity suit. The delivery of the fetus would relieve the obstruction and create a large, tran siently underfilled space. This would result in a pre cipitate fall in pressure until adequate volume homeo stasis was restored.
334
Benedetti, Kates, and Williams
June I, 1985 Am J Obstet Gynecol
CIS
~
50
Fig. 2. Intra-arterial (BP) and pulmonary (PA) pressure during cesarean section (CIS) delivery. Paper speed is 3 em/min.
The usual treatment of this event is with intravenous ephedrine and volume replacement. If this volume re placement is administered by the anesthesiologist with out good communication with the obstetrician, serious volume overload in the postpartum period can result as the fluid is mobilized from the overloaded extravas cular space. Further investigation into this event is nec essary to determine etiologic mechanisms and whether pharmacologic intervention without volume replace ment will correct this hypotensive event. This study again demonstrated the poor correlation between the central venous pressure and the pulmo nary artery wedge pressure in some patients with severe preeclampsia. This observation has been made in pa tients witho11t pulmonary edema as well as in those with pulmonary edema. 9 · 10 In this series, five of 10 patients had a difference of ;;.5 mm Hg, and two patients had a difference of ;;.I 0 mm Hg. This difference appears to become clinically relevant when the central venous pressure exceeds 6 mm Hg. Neither this study nor any other in the literature shows any patients in whom the central venous pressure was 6 em or less accompanied by an el~vation in pulmonary artery wedge pressure that could potentiate the development of pulmonary edema. It is important to: recognize that patients in whom the central venous pressure is consistently grea~er than 6 mm Hg may have a much higher pul monary artery wedge pressure. If respiratory insuffi ciency develops, a pulmonary artery catheter should be
used to characterize the hemodynamic picture so that appropriate therapy can be selected and the response to therapy monitored. REFERENCES I. Benedetti TJ. In Cardiac problems in pregnancy, New York: Alan R. Liss, 1982:179-90.
2. Crandall ED, Staub NC, Goldberg HS, Effrog RM. Recent developments in pulmonary edema. Ann Int Med 1983; 99 :808-22. 3. Benedetti TJ, Carlson RW. Studies of colloid osmotic pres sure in pregnancy-induce d hypertension. AM J OBSTET GYNECOL 1979;135:308-11. 4. Cotton DB , Benedetti TJ . Use of the Swan-Ganz catheter. Obstet Gynecol 1980;56:641-5. 5. Berkowitz RI, Rafferty TD. Invasive hemodynamic mon itoring in critically ill pregnant patients: role of Swan Ganz catheterization. , AM j 0BSTET GYNECOL 1980; 137:127. 6. Fein A, Grossman RF, Jones· JG, Overland E, Pitts L, Murry J, Staub NC. The value of edema fluid protein measurement in patients with pulmonary edema. Am J Med 1979;67:32-8. 7. Benedetti TJ, Benedetti JK, Stenchever MS. Severe pre eclampsia maternal and fetal outcome. Clin Exp Hyper tens [B) 1982;263:401-16. 8. Anderson FH, LynchJP,Johnson TRB. Adult respiratory distress syndrome in obstetrics and gynecology. Obstet Gynecol 1980;55:291-5. 9. Strauss RG, Keefer JR, Burke T, Civett JM. Hemody namic monitoring of cardiogenic pulmonary edema com plicating toxemia of pregnancy. Obstet Gynecol 1980; 55: 170-4. 10. Benedetti TJ, Cotton DB, Read JA, Miller FC. Hemo dynamic observations in severe preeclampsia using a flow directed pulmonary artery catheter. AM J OBSTET GYNE COL 1980;136:465-70.
Hemodynamic observations in severe preeclampsia complicated by pulmonary edema Thomas J. Benedetti, M.D., Richard Kates, M.D., and Virginia Williams, M.D. Seattle and Spokane, Washington Ten patients with severe preeclampsia complicated by pulmonary edema were studied with invasive hemodynamic monitoring. Eight of 10 patients developed pulmonary edema during the postpartum period. Five patients had alterations in the colloid osmotic pressure-pulmonary artery wedge pressure gradient related to elevations in the pulmonary artery wedge pressure and a reduction in the colloid osmotic pressure. Three patients had hemodynamic findings consistent with pulmonary capillary leak. Two patients had evidence of left ventricular failure. In three of the patients, the central venous pressure was significantly lower than the simultaneously determined pulmonary artery wedge pressure during the acute phase of the pulmonary edema. (AM J 0BSTET GYNECOL 1985;152:330-4.)
Key words: Severe preeclampsia, pulmonary edema, volume overload, colloid osmotic pressure, pulmonary artery wedge pressure
Pulmonary edema in the pregnant hypertensive pa tient has been postulated to occur by any one of three mechanisms: increased intravascular hydrostatic pres sure, increased capillary permeability, and low vascular oncotic pressure.' In nonpregnant patients, the latter mechanism may infrequently cause pulmonary edema but can potentiate its development when combined with either of the first two events. 2 We previously speculated that a reduction in intravascular colloid osmotic pres sure may play an important role in the development of pulmonary edema in the hypertensive pregnant pa tient.3 However, few patients with pulmonary edema have been subjected to invasive monitoring as well as measurement of colloid osmotic pressure. Since it is difficult to differentiate among the three mechanisms on clinical grounds, little information is available on the frequency with which these various factors lead to the development of pulmonary edema in hypertensive pregnant patients.
From the Departments of Obstetrics and Gynecology and Anesthesia, University of Washington, and the Inland Empire Perinatal Center. Received for publication May 7, 1984; revised October 24, 1984; accepted january 16, 1985. Reprint requests: Dr. Thomas ]. Benedetti, Department of Obstet rics and Gynecology, University of Washington, Seattle, WA 98195.
330
Material and methods This report details the occurrence of pulmonary edema in 10 patients with severe preeclampsia. This series of patients was collected over a 4-year period in two tertiary care referral centers, the University of Washington, Seattle, Washington, and the Inland Em pire Perinatal Center, Spokane, Washington. All pa tients in this series were studied with a flow-directed pulmonary artery catheter either during the develop ment of pulmonary edema or shortly after the devel opment of pulmonary edema but before pharmacologic therapy was directed at relieving the hypoxemia. Standard clinical procedures were used for care and interpretation of the catheter readings, and standard formulas were used for hemodynamic calculations. 3 The diagnosis of pulmonary edema was made on the basis of the clinical respiratory distress associated with hypoxemia (Po2 <70 mm Hg with FI 0 2 = 0.21), on blood gas determination, and confirmatory radio graphic evidence. Colloid osmotic pressure was either calculated from total protein determination or mea sured directly by means of a Wescor oncometer! The diagnosis of left ventricular failure was made when there was increased pulmonary artery wedge pressure associated with a low left ventricular stroke work index. •· 5 Altered capillary permeability was made when there was a normal pulmonary artery wedge pres sure and a normal or elevated left ventricular stroke
Pulmonary edema in severe preeclampsia 331
Volume 152 Number 3
work index (normal left ventricular stroke work in dex = 55 to 85 gm · min · M- 2 ) . Alternatively, this di agnosis was made when the ratio of protein in the pul monary edema fluid to protein in the patient's serum exceeded 0.4. 6 Altered hydrostatic-oncotic forces were diagnosed when the left ventricular stroke work index was normal and the pulmonary artery wedge pressure was elevated, so that the difference between the colloid osmotic pressure and the pulmonary artery pressure was .-;;:4 mm Hg (colloid ·osmotic pressure-pulmonary artery wedge pressure gradient .-;;:4 mm Hg) . Results
Complete hemodynamic data were available on all 10 patients with acute pulmonary edema. The age range of the patients was from 20 to 37 years (mean, 27 years) . Six patients were primiparous, three were secundiparous, and one was grand multiparous. The gestational age range was from 27 to 35 weeks (mean, 31.6 weeks) . Nine of the 10 patients were delivered by cesarean section. All patients, except Patient No. 2, were being treated with magnesium sulfate and hydralazine prior to or at the onset of pulmonary edema. Table I shows the individual hemodynamic data. The patients were categorized on the basis of the mechanism of development of pulmonary edema, Five patients (Nos. 1 through 5) demonstrated alterations in the hy drostatic oncotic forces , three patients (Nos. 6 through 8) showed evidence of permeability pulmonary edema, and two patients (Nos. 9 and 10) showed evidence of left ventricular failure . These data are graphically plot ted in Fig. 1. Table II illustrates the time of onset of pulmonary edema and the relationship to measured filling pres sures. For eight of the 10 patients, pulmonary edema developed after delivery. The range of onset was 5 to 24 hours (mean, 12.6 hours). Six of the eight patients developed respiratory insufficiency between 9 and 15 hours post partum. In all patients, central venous pres sure immediately post partum was between 0 and 6 mm Hg. However, there was a progressive rise iri the central venous pressure in moSt of the patients until the onset of pulmonary edema was recognized. In three of the patients (Nos. 1, 3, and 8), the measurements of central venous pressure did not reflect the simultaneously re corded wedge pressure. In those three patients, the wedge pressure was significantly higher than the cen tral venous pressure. Table III illustrates the volume status of each patient in the critical period before the onset of pulmonary edema. Large volumes of fluid were frequently justified by clinicai need (preoperative hypotension, preload for anesthesia). In some cases, the large volumes of fluid
140 120
~
:e I
100
...
•
~
.& 80 § ~ ;..,J
60 40
20
51015
20253035
PAW (mmHg) Fig. 1. Ventricular function curve 5 illustrating myocardial per formance for each of 10 patients listed in Table i. LVSWI, Left ventricular stroke work index. PAW, Pulmonary artery wedge pressure. • Patients l through 5. *Patients 6 though 8. o Patients 9 and 10.
were the result of intraoperative administration of blood and crystalloid to correct intraoperative loss, in traoperative falls in blood pressure, coagulopathy, or thrombocytopenia. Comment
In this group of patients, the most common reasons for the development of pulmonary edema was an al teration in the hydrostatic oncqtic forces that occurred within 15 hours postpartum. This alteration in forces occurred because of a combination of mild-to-moderate lowering of colloid osmotic pressure (mean = 15.3 mm Hg) and mild-to-moderate elevations in the left ven tricular filling pressures reflected by the pulmo~ary artery wedge pressure (mean, 18.6 mm Hg). None of these patients had evidence of left ventricular dys function, and the elevations in filling pressures were not of significant magnitude to account for pulmonary edema without simultaneous lowering of intravascular oncotic forces. All patients except Nos . 4 and 8 received colloidal fluid prior to the onset of the pulmonary edema. This
332
Benedetti, Kates, and Williams
June I, 1985
Am J Obstet Gynecol
Table I. Hemodynamic data
Patient No.
1
2
3
4
5 6 7 8 9 10
Blood pressure
Cardiac output (Limin)
Cardiac index (Liminlm 2)
Stroke volume (ml)
155/105 160/110 130/100 182/116 140/60 160/90 171/98 160/80 164/82 130/90
7.6 12.5 8.9 7.9 8.5 13.3 8.1 I 1.0 6.6 4.3
4.25 7.2 4.9 4.9 5.0 6.9
80 l01 89 78 85 133 81 103 75 54
4.4
6.9 3.4 2.7
Pulmonary artery systolic pressure (mm Hg)
Pulmonary artery diastolic pressure (mm Hg)
Pulmonary artery wedge pressure (mmHg)
35 34 30
25 16 18 15 20 8 10 20 20 20
22 20 17 14 20
22
40 23
22
35 40 34
Central venous pressure (mmHg)
7 15 10 14 16 8 6 10 18 12
4
6 20 20 18
.Patients 1 through 5: Altered hydrostatic forces. Patients 6 through 8: Permeability defect. Patients 9 and 10: Left ventricular failure.
Table 11. Filling pressures and time of onset of pulmonary edema
Onset of pulmonary edema (hr)
Postpartum central venous pressure (0-1 hr) (mm Hg)
Central venous pressure at onset of pulmonary edema (mm Hg)
Pulmonary artery wedge pressure at onset of pulmonary edema (mm Hg)
12 Hr postpartum Antepartum 12 Hr post parium 12 Hr post partum 9 Hr post partum 24 Hr post partum 12 Hr post partum 5 Hr post partum Antepartum 15 Hr postpartum
6 NA 6 5 0 0 3 5 NA 6
7 15 10 14 16 8
22
Patient No.*
1
2 3 4 5 6 7 8 9 10
6
10 18 12
20 17 14 20 4 6 20 20 18
NA = Not available. *Patients as in Table I. See footnote.
Table III. Fluid management Patient No.
Fluid preceding pulmonary edema
5000 ml/24 hr 2
9000 ml/24 hr
3
1000 ml/5 hr
4
6500 ml/12 hr
5
7000 ml/12 hr
6
4500 ml/24 hr
7
7000 ml/3 hr
8
6000 ml/24 hr
9
5500 ml/24 hr
10
7000 ml/12 hr
Rationale for fluid
Fluid components
A nesthesialdelivery
Intraoperative replacement Hypotensive after epidural anesthesia Low hematocrit (28) Oliguria
Crystalloid + colloid + blood Crystalloid + colloid
Quadruplets
Preload for epidural anesthesia Excess intravenous intake Hypotension
Crystalloid + colloid
General anesthesia, cesarean section Epidural anesthe sia, cesarean section General anesthesia; cesarean section General anesthesia, cesarean section Epidural anesthe sia, cesarean section General anesthesia, General anesthesia, cesarean section General anesthesia, cesarean section Epidural anesthe· sia, cesarean section General anesthesia, cesarean section
Eclampsia, hepatic rupture Twins
Intraoperative replacement Excess intravenous and oral intake Intraoperative replacement
Blood Crystalloid
Crystalloid + colloid Crystalloid + colloid + blood Crystalloid Crystalloid + colloid Crystalloid + colloid + blood
cesarean section
Other factors
Diabetes, chronic hypertension Thrombocytopenia
Pulmonary edema in severe preeclampsia 333
Volume !52 Number 3
Colloid osmotic preSS!lre (mm Hg)
Systemic vascular resistance (dynessec · cm - 5)
Left ventricular stroke work index (gm · min · M- 2)
Colloid osmotic pressurepulmonary artery wedge pressure gradient (mm Hg)
10.4 18.8 15.6 14.8 17.9 17.2 16.5 11.9 17.9 16.5
1206 714 885 1357 978 631 1145 557 823 1693
74 100 62 82 68 102 69 90 46.4 39
-11.6 -1.2 -1.4 0.8 -2.0 13.0 10.5 -8.0 -2.0 -1.5
fluid (blood products and albumin) is known to have strong osmotic effects on the movement of fluid be tween the intravascular and extravascular space. When fluid is administered to the severely preeclamptic pa tient, movement of significant amounts of Ruid from the overexpanded extravascular space to the intravas cular space can result. We hypothesize that, when this effect is added to the usual mobilization of fluid from extravascular compartment to intravascular compart ment that occurs after delivery, a progressive rise in the pulmonary artery wedge pressure occurs. Our data are consistent with this hypothesis. It was previously shown that pregnancy results in the lowering of tht; colloid osmotic pressure, and that the preeclamptic patient has colloid osmotic pressure even lower than that of the normal pregnant patient. 3 The colloid osmotic pressure falls in the postpartum period both in normal and in preeclamptic pregnancies. The combination of a low intravascular oncotic pressure and progressjve rise in hydrostatic pressure can explain pulmonary edema in these patients. The most frequent time for this to occur was within 15 hours postpartum (Table II). In light of these observations, we think that it is wise to monitor central pressures closely in the postpartum period in severely preeclamptic patients who have received significant amount of colloidal fluid in the antepartum or intraoperative period. Many authors have questioned the administration of colloidal fluid to the severely hypertensive patient. We previously advised giving only maintenance fluid dur ing labor. 3 However, clinical circumstances may dictate the need for a colloidal fluid . These circumstances in clude acute volume loss, severe thrombocytopenia, or coagulopathy. We also have used volume loading with a combination of crystalloid fluid and colloidal fluid prior to the induction of epidural anesthesia, and have shown that when this is expertly done, with adequate monitoring of vascular pressure, it is safe for both the fetus and the mother. 7 The use of colloidal fluid without
a
adequate monitoring of pressure may increase the risk of pulmonary edema. The second most common mechanism for the de velopment of pulmonary edema was alteration in cap illary permeability. One of these three patients (No. 8) was the only fatality in the series. She developed acute respiratory insufficiency within 12 hours post partum and initially showed elevated filling pressures. How ever, after diuresis had lowered the pulmonary artery wedge pressure to 12 mm Hg, she began to exude large amounts of proteinaceous material from the endotr;l cheal tube. She eventually developed chronic adult re spiratory distress syndrome and died on the twenty second post partum diiy. Sectioning of the lungs at au topsy provided no evidence for amniotic fluid embo lism. The other two patients showed normal ventricular function and normal wedge pressures in the face of altered oxygenation, and both recovered. Altered cap illary permeability can develop in other organ systems, such as the kidney. In severe preeclampsia, perme ability defects in the lungs are uncommon, and the triggering mechanism is frequently associated with acute volume loss or amniotic fluid embolism, or sepsis .~ Two patients showed evidence of ventricular failure . Patient No. 9 had multiple medical problems, so that ventricular failure in this patient was not surprising. However, the other patient had no predisposing factors and her left ventricular dysfunction was rather tran sient, lasting only 8 hours. Potent diuresis led to a low ering of the pulmonary artery wedge pressure to 12 mm Hg, which resulted in the normalization of cardiac performance. Other investigators 7 have reported left ventricular failure as a result of high systemic resistance which responded to afterload reduction. Most patients in this series had received large amounts qf fluid prior to the development of pulmo nary edema. This was often not appreciated by the physician~ until pulmonary edema developed post par tum. One reason for the excess volume given during the intraoperative period in some patients was a pre cipitate fall in blood pressure just after the delivery of the fetus. Fig~ 2 illustrates sim~ltaneous recordings of the pulmonary artery pressure and the intra-arterial pressure in a patient who experienced a fall in blood pressure. In our experience, this event has usually not been associated with excessive volume loss. The pre cipitate fall in intravascular pressures occurs in both the systemic and pulmonary circulations. This phenom enon might be explained by the relief of a selective aortic obstruction by the gravid uterus. In that case, the pregnant uterus might have been acting in a fashion similar to an antigravity suit. The delivery of the fetus would relieve the obstruction and create a large, tran siently underfilled space. This would result in a pre cipitate fall in pressure until adequate volume homeo stasis was restored.
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CIS
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Fig. 2. Intra-arterial (BP) and pulmonary (PA) pressure during cesarean section (CIS) delivery. Paper speed is 3 em/min.
The usual treatment of this event is with intravenous ephedrine and volume replacement. If this volume re placement is administered by the anesthesiologist with out good communication with the obstetrician, serious volume overload in the postpartum period can result as the fluid is mobilized from the overloaded extravas cular space. Further investigation into this event is nec essary to determine etiologic mechanisms and whether pharmacologic intervention without volume replace ment will correct this hypotensive event. This study again demonstrated the poor correlation between the central venous pressure and the pulmo nary artery wedge pressure in some patients with severe preeclampsia. This observation has been made in pa tients witho11t pulmonary edema as well as in those with pulmonary edema. 9 · 10 In this series, five of 10 patients had a difference of ;;.5 mm Hg, and two patients had a difference of ;;.I 0 mm Hg. This difference appears to become clinically relevant when the central venous pressure exceeds 6 mm Hg. Neither this study nor any other in the literature shows any patients in whom the central venous pressure was 6 em or less accompanied by an el~vation in pulmonary artery wedge pressure that could potentiate the development of pulmonary edema. It is important to: recognize that patients in whom the central venous pressure is consistently grea~er than 6 mm Hg may have a much higher pul monary artery wedge pressure. If respiratory insuffi ciency develops, a pulmonary artery catheter should be
used to characterize the hemodynamic picture so that appropriate therapy can be selected and the response to therapy monitored. REFERENCES I. Benedetti TJ. In Cardiac problems in pregnancy, New York: Alan R. Liss, 1982:179-90.
2. Crandall ED, Staub NC, Goldberg HS, Effrog RM. Recent developments in pulmonary edema. Ann Int Med 1983; 99 :808-22. 3. Benedetti TJ, Carlson RW. Studies of colloid osmotic pres sure in pregnancy-induce d hypertension. AM J OBSTET GYNECOL 1979;135:308-11. 4. Cotton DB , Benedetti TJ . Use of the Swan-Ganz catheter. Obstet Gynecol 1980;56:641-5. 5. Berkowitz RI, Rafferty TD. Invasive hemodynamic mon itoring in critically ill pregnant patients: role of Swan Ganz catheterization. , AM j 0BSTET GYNECOL 1980; 137:127. 6. Fein A, Grossman RF, Jones· JG, Overland E, Pitts L, Murry J, Staub NC. The value of edema fluid protein measurement in patients with pulmonary edema. Am J Med 1979;67:32-8. 7. Benedetti TJ, Benedetti JK, Stenchever MS. Severe pre eclampsia maternal and fetal outcome. Clin Exp Hyper tens [B) 1982;263:401-16. 8. Anderson FH, LynchJP,Johnson TRB. Adult respiratory distress syndrome in obstetrics and gynecology. Obstet Gynecol 1980;55:291-5. 9. Strauss RG, Keefer JR, Burke T, Civett JM. Hemody namic monitoring of cardiogenic pulmonary edema com plicating toxemia of pregnancy. Obstet Gynecol 1980; 55: 170-4. 10. Benedetti TJ, Cotton DB, Read JA, Miller FC. Hemo dynamic observations in severe preeclampsia using a flow directed pulmonary artery catheter. AM J OBSTET GYNE COL 1980;136:465-70.