Hemodynamics in patients with severe toxemia during labor and delivery

Hemodynamics in patients with severe toxemia during labor and delivery TERET\CE D. RAFFERTY, M.D. RICHARD L. BERKOWITZ, M.D. Xne Hm•r11. Coiii/Pt/11'111 Three patients with severe pre-eclampsia-toxemia were studied with thermodilution tip pulmonary artery catheters. All patients were delivered by cesarean section with general anesthesia and endotracheal intubation. The left ventricular stroke work indices (LVSWI) of these patients were higher than those of normal nonpregnant subjects. There was no evidence of myocardial depression in terms of either cardiac index or the LVSWI-pulmonary capillary wedge pressure (Frank-Starling) relationship. Pulmonary arteriolar resistance (PAR) was found to be within or below the normal nonpregnant range, suggesting that in severe toxemia the pulmonary vasculature is not involved in a primary vasospastic process. At delivery a rise in cardiac index (CI) and mean pulmonary capillary wedge pressure (J5CWP) occurred. The PCWP was higher in the postpartum period than prior to delivery. This was felt to represent an increase in circulating blood volume. The therapeutic significance of these findings is discussed. (AM. J. Oesrer. GvNECOL. 138:263, 1980.)

is a vasospastic disorder which is characterized by an increase in systemic arrenolar resistance 1 along with a decrease in circulating blood volume." It has been reported that cardiac output is within normal limits for pregnancy in toxemic patients, 1 which suggests a compensatory increase in left ventricular work to offset the elevated peripheral resistance. The magnitude of this response, however, is unknown. In view of the svstemic nature of PET, it is not unreasonable to suppose that pulmonary hypertension might be an integral part of the syndrome. The extent to which the pulmonary vasculature is involved in the disease process is also unknown. The importance of intravasntlar volume replacement in the management of toxemic patients continues to be a source of controversy.'<- 4 These basic questions concerning the consequences of severe toxemia on the maternal circulaton svstern remain unanswered. Lntii fairiv recently, it has not been possible to obtain sophisticated central hemodynamic data at the bedside. (PET)

PRE-ECLA:\1PSIA-TOXEl\IIA

With the advent of thermodilution-tipped, How-directed pulmonary artery catheters. however. this is no longer the case. In this studv, Swan-Ganz (SG) catheters were utilized not only as a guide to thnapv but also as investigational tools in an attempt to darifv the central hemodynamics of severe PET in the period surrounding deliverv. Clinical material

Three patients. ranging in age t rom I i to ::!8 years, were studied on the high-risk obstetrics 'en·ice of the Yale-New Haven Hospital (Table I). All had severe toxemia as defined by an acute hvpertcnsive episode occurring in the last trimester, with admission blood pressures in excess of i 70/120 mm Hg and proteinuria (3+ to 4+). :\'one of these patients had an antecedent history oi hvpenension. One of the dm'c patients (B . .J .) had eclampsia, and none was in o;pontaneous labor at the time of admission. Thev \\Tre all treated with an intr;wenous loading dose of 1 gm of magne"

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SIUITI SUJI
From the Departments of .4nesthesiology and Obstetrics and Gvnerology, Yale Unir•ersitv Srhool of Medicine. Reaiverljf>r puhliration Fdmmry 26, 1979. Re<•iserl Februarv 22, 1980.

Aaepterl May 29, 1980. Reprint requnt1.· Richard L. Berkowitz, M.D., Depa rtmmt of' Ohstetrirs and Gynecology, Yale U niversit_~ School of Medicin.-, 331 Cedar St., New Haven, Conner/i(u/ (}(,51 0. 0002-9378/H0/190263+08$00.HO/O

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1980 The C:. V. Mosby Co.

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gm/hour. Two of the three patients U. 1.. and \of. C.) received oxytocin stimulation for l to fi hours. All three patients were delivered bv ces;treau section with general anesthesia following a rap1d inductionintubation sequence. Induction of anesthesia was accomplished with intravenous thiopental ( 1.:1 to 3 mg/kg) immediately followed by endotracheal intubation facilitated by intravenous succinylcholine (0.5 to I mg/kg). Ventilation was controlled with l)()q nitrous

263

264

Rafferty and Berkowitz Am.

J.

Ouobn I. l\1~11 Obstet. C\lleL<>l

Table I. Demographic data Patient

Condition

Admission BP (mm Hg)

J.L.

Pre-eclampsia

180/120

Pre-eclampsia Eclantpsia

198/122 i86/i24

M.C. D

u.

T

J·

28 15

5'6" A 11111

...

j

j

156

94

1.8 11.~~ ""

Fetus

Term, Ap 4,6, BW 2,H30 gm, baby li\·ed ! day (metastatic neuroblastoma) 31 wk,Ap8,6,BW 1,140gm 33 wk. Ap 7,8, BW 1,800 gm

BP: Blood pressure; Ap: Apgar score; BW: birth weight.

oxide and 40% oxygen. After delivery of the baby supplementary anesthesia was provided by halothane (0.5%) or intravenous morphine 0.05 to 0.1 mg/kg). Further muscle relaxation was accomplished by additional succinylcholine. The antepartum rate of crystalloid Huid administration is shown in Tables II, III, and IV. Two patients also received 25 gm of salt-poor albumin (SPA) in the postpartum period. Magnesium sulfate infusion was maintained for at least 24 hours following delivery. All patients had received or were receiving hydralazine therapy during the period studied. Methods

Radiopaque flow-directed catheters (Swan-Ganz catheter, Model No. 934-13l-7F, Edwards Laboratories) were inserted with local anesthesia in the antepartum period via the right internal jugular vein, and waveform characteristics and intravascular pressures were used as guides to placement. Catheter position was confirmed by chest roentgenography. A Teflon catheter (No. 20 angiocath) was inserted percutaneously into the radial artery of each patient. Intravascular pressures were recorded with Bentley transducers (No. 800) calibrated with mercury. The zero reference point was the middle of the anteroposterior chest. All determinations were made at endexpiration. Cardiac output was measured in duplicate by the thermodilution method with a cardiac output analogue computer (Edwards Laboratories No. 95100). The antepartum measurements were determined between uterine contractions without the influence of oxytocin stimulation. During the antepartum period measurements were obtained with the patient lying on the left side to eliminate obstruction of venous return and aortic How by the gravid uterus. During the cesarean sections the right hip was elevated by a blanket roll for the same reason. Measurements were obtained 60 and 30 minutes prior to cesarean section. At deiivery two sets of determinations were performed. Hemodynamic variables were aiso determined houriy for g hours after delivery.

All values for cardiac output, stroke work, and the resistances were expressed as indices in order to allow for variations in body size. Cardiac index, left ventricular stroke work index (LVSWI), total peripheral resistance, pulmonary arteriolar resistance. and body surface area (BSA) were calculated according to the formulas in Table V. Results

Left ventricular function. The normal range of the LVSWI in pregnancy is not known. Each of our three patients had indices which were well above the normal resting nonpregnant range (56.4 ± 3.6 gm m/sq m)."· 6 When L VSWI. expressed as a function of mean pulmonary capillary wedge pressure (PCWP) (FrankStarling relationship), was examined in order to assess left ventricular function, all data points fell within or above the normal rangei (Fig. 1). Pulmonary vasculature-all periods. The normal arteriolar resistance in pregnancy is not known. The pulmonary arteriolar resistance of our patients wa~ consistently within or below the normal nonpregnant range (2.0 ± 0.9 mm Hg L~t sq m). 3 • " No simultaneously determined pulmonary arterial diastolic pressure (PADP)-PCWP gradient was in excess of 7 mm Hg in any patient. Antepartum period. The pulmonary arterial systolic, diastolic, and mean pressures and the PCWPs were higher post partum than antepartum. Mean and diastolic systemic arterial pressure and heart rate were lower postpartum (Tables II, III, and IV). Delivery period. The delivery period, as compared with the antepartum period, was marked by a rise in systemic arterial blood pressure, pulmonary arterial systolic and mean pressures, and PCWP. A rise in cardiac index and stroke work index also occurred (Tables II, III, and IV). Postpartum period. Diastolic systemic arterial blood pressure and ieft ventricuiar stroke work indices were lower postpartum than during delivery. Total peripherai resistance aiso feii post partum (Tabies II. iii. and IV).

Hemodynamics 1n severe toxemra

\'l)lunw I :1:--:

265

\umber:\

Comment Left ventricular function. Because of the wide range of BSAs the cardiac outputs and other related variables of our patients were expressed as indices. Quantitative comparison of these data with those of healthy nonpregnant patients was possible because the inclusion of BS:\ measurements in the original reports permitted appropriate adjustments to be made.';."·" This type of rcanalvsis of the studies on pregnant women published b\ L'eland and Hansen'" and Assali and associates' could not he performed. \\'hen compared with normal resting. nonpregnant individuals.n. "· n the patients with PET demonstrated elevations of cardiac index of approxi matelv .'iW\. Cardi;~c work is increased during pregnancy in order to maintain the elevation in cardiac output which normall\ occurs. I 11 PET demands on the heart are even greater because systemic \·ascular resistance is increased. Determination of left ventricular stroke work requires a knowledge of the stroke volume index (cardiac index divided by heart rate) as well as the differences between mean arterial pressure and PC\'\'P. Values for these indices in normal pregnant patients have not been published; theref(Jre, comparisons were made with normal. nonpregnant control subjects. The values fill· I.VS\VJ in the PET patients were well above the normal nonpregnant resting range. 3 · 6 · " Although a cardiomvopathy has been reported in association with I'F'T. there was no evidence ofimpairecl contractility in terms oi' the L\'S\\11-PC:\VP relationship in our patiems. Pulmonary vasculature. Our data. when compared to those of healthv nonpregnant control subjects, revealed no increase in pulmonary arteriolar resistance."· '' Values during normal pregnancy were not available for comparison. Furthermore, the gradient between the pulmonary artery diastolic pressure and PCWP was within normal limits.'' These observations suggest that in PET the pulmonary vasculature. unlike its systemic counterpart. is not involved in a primary vasospastic process that is hemodynamically significant. Central intravascular pressures. Swan-Ganz catheterization permits the ongoing determination of pulrnonan arterv pressure and PC\VP. The latter is an intravasndar measun·ment which, in the absence of mitral \ alw· disease, reflects left ventricular enddiastolic volume. :\ change in \'entricular wall compliance rna\ alter the measured intravascular pressure. In our st udv this \
90 1-

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70

•

•

•

•

•

PC\\P ~lHI

~"

30

35

(mmH~l

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Lj\1

Fig. I. This graph distinguishes hetiHTil tin-·, k>.ds of \t'lltricular competence, Each of our three pali,.rl!' denton>~ rated excellent \entricular function b1 these nitn! '· <'\Til in tlw presence of marked!\ elevated PCWP \ alues . i \lodifwd from Ros.s, J.. Jr .. and Braunwald. E.: Tlw ''"'" n l'i• lentricuLtr funnion in man ln increasing resist all<,. ''' • • Tli' inda1 t'Jl'','

:llltl'par/um fH-riorl. The reported hlood 1olume deficits in PET cover a \1ide spectrum. C:hc,], ., '"stated th;tt in severe disease tht' plasma volume lll
266

Rafferty and Berkowitz

J.

Am.

October I. I'!HI I Obstet. Cvnt·«>l.

Table II. Measured and derived variables in Patient J. L. * Timr Variable

BP (S/D/M) HR PA (S/D/M)

1 Y2 hr AP

1 hr AP

Y2 hr AP

Intubation

Delivery

1 hr PP

140/96/110 104 18/5/9

150/100/117 102 21/8/12

160/100/120 120 25112/16

240/140/ln 140 42/18/26

180/100/127 110 36/13/24

180/70/107 124 30/13/19

..

~

0 0

A

J.Vl'l'.l

co Cl SVI LVSWI PAR TPR Fluids: D5 /W and D5 /RL (ml) SPA (gm) l:rine output (ml) EBL (ml) Hct.

18

10

14.4 6.5 62.9 90.7 0.76 16.8

14.2 6.4 63.2 93.8 0.92 18.1

12.0 5.4 45.4 68.0 1.1 22.0

850

800

300

30

20

30

~1

18.4 8.3 59.7 126.7 0.95 20.8

i6

16.4 7.4 67.7 14.1 0.53 23.3 500

80 800

120

35.1

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AP: Antepartum; PP: postpartum; S/D/M: systoiic/diastoiic/mean; HR: heart rate; PA: pulmonary artery; CO: cardiac output; Cl: cardiac index; SVI: stroke volume index; PAR: pulmonary arteriolar resistance (indexed as HR units); TPR: total peripheral resistance (indexed as HR units); D5 W: 5% dextrose in water; D5 RL: 5% dextrose in Ringer's lactate; EBL: estimated blood loss: ~ Hct.: hematocrit; IM: intramuscularly. *This patient presented at term with a BP of 180/120 mm Hg and a 17 pound weight gain in the week prior to admission. She was treated with a 4 gn1 loading dose of intravenous l\rigS04 and then started on a continuous infusion of 1 g1n/hr. She was also given a single bolus injection of 5 mg of hydralazine intravenously after which the BP ranged from 130 to 140/90 to 100 mm Hg. Labor was augmented with intravenous oxytocin, but 9 hours after admission and 6 hours after the initiation of the oxytocin infusion, she underwent a primary cesarean section for failure to progress. Because of significant oliguria vigorous hydration was undertaken during the AP period with the Swan-Ganz catheter in place. She received a total of 8,100 ml of D5 /W and D5 /RL along with 25 gm of SPA prior to delivery. Urine output during this period was 225 mi.

Table III. Measured and derived variables in Patient M. C.* Time Variable

BP (S/D/M) HR PA (S/D/M) PCWP

co

I Yz hr AP

1 hr AP

hhrAP

Intubation

Delivery

1 hr PP

190/110/137 110 27/14/18

180/108/132 98 22/11/15 6 10.4 5.7 58.9 !0! 1.5 22.8

190/90/123 100 16/5/9 8.6 4.7 47.7 83.8 1.6 27.2

200/100/133 111 20/6/11 2 12.4 6.8 62.0 ! !0.5 1.3 19.3

160/90/113 78 32/15/20 6 9.1 5.0 64.8 !03.! 2.7 24.3

180/80/113 87 16/6/9 2 7.4 4.1 47.2 84.! 1.7 32.3

600

575

300

300

625

40

20

20

100 600

100

Hydralazine, 5 mg IV

38.7 Hydralazine, 5 mg IV

:~

CI SVI LVS\VI PAR TPR Fluids: D5 /W and D5/RL (ml) SPA (gm) Urine output (ml) EBL (ml) Hct. Medications

l

Phenobarbital 60 mg IV and 60 mg IM

For abbreviations see footnote to Table II. IV: Intravenously. *1"'his patient presented to an out!yi~g hospital with an initial BP of220/ 140 mm Hg_ She was treated with a 4 grn loading dose of intravenous MgS04 and started on a continuous infusion of l gm/hr. She was also given 10 mg of hydralazine intravenously and then transferred to YNHH. Admission BP was 190/110 mm Hg and three intermittent intravenous bolus injections of 5 mg of hydralazine were given during the AP course to maintain BPs in the range of 180 to 190/~00 t? 110 m_m .Hg. I.ntravenou~ oxyto~in was administered but discontinued after 4 hours because of late fetal heart rate decelerations m assoCiation wtth hyperstlmulauon at 4 mU/min. The patient underwent primary cesarean section 6 hours following admission for failure to progress. She received a total of 2,025 ml of D5 /RL and D5 /W and had a urinary output of 330 mi in the hospital prior to delivery.

Hemodynamics in severe toxemia

Volume l:lK !"umher :l

267

Time 'I hr PP

160/90/1 l:l lOR 29/12/li'i

1-lO/R0/100 102 23/14/17 !6

3 hr PP

4 hr PP

5 hr PP

6 hr PP

172/90/117 110 25/12/16 !4

152/80/104 104 24/11/16 !4 14.2 6.4 62.0 R4.4 0.46 17.6

156/90/112 108 30/10/17 20 15.2 6.9 63.9 80.0 0.14 16.2

150/90/110 110 32/15/21 20 14./l

170/90/117 110 32118/23

61.1 74.8 0.14 16.:l

15.3 6.Y ti3.2 81.6 0.28 16.i'i

:150 25 60

275

175

100

100

150

120

!50

150

145

~JO

500 120

7 hrPP

8 hr PP

2 hr PP

!7

22

6~

.I

15.3 6.9 64.:\ R4.0 0.2H !1)2

:H.H

JOO

29.9 Phenobarbital,

MnrnhlnP H.O.>.Jot"so•••,.,_!

!50 mg IM

10 mg IM

Time 3 hrPP

4 hr PP

5 hr PP

6 hr PP

7 hr PP

8 hr PP

9 hr PP

180/90/120 92

180/86/117 84

190/80/117 93

200/60/106 98

210/601110 88

21/9/13

23/12/16

.1UI 101<::<:

o..-1./"'lo/nn

30/18/22

29/19/22

8 9.4 5.2 56.7 86.4 0.95 22.9

12 10.5 5.8 69.4 99.! 0.68 20.0

190/94/126 80 25/17/20 15 11.4 6.3 79.1 !08.7 0.78 18.3

20 10.4 5.7 62.1 76.0 0.34 19.0

18 14.:3 7.9 81.0 9'7.0 0.50 I:U

20 12.7 7.0 80.0 98.! 0.28 15..')

220/85/130 97 33/20/24 20 12.4 6.H 71.0 !06.2 0.58 18.8

450

150

325

275

175

200

175

100

75

510 25 50

15

25

30

45

45

2hrPP

32.3 Morphine, 15 mg IM

268

Rafferty and Berkowitz

Octobn l. l 'JHII .\111. j. Obstt"t. ( ,, nc«>l

Table IV. Measured and derived variables in Patient B.

J. * Timr

Variablr

BP (S/D/M) HR PA (S/D/M) PCWP

I hr AP

Y2 hr AP

Intubation

Delivery

l hr PP

186/124/145 112

170/90/117 116

160/90/113 116 28/ !6/20 14 8.3 6.4 53.4 74.6 0.93 17.5

162/90/114 110 28/!4!19

116/80/42 105 !8/2/9

co

CI SVI LVSWI PAR TPR

14

7.8 6.0 54.9 74.7 0.66 18.8

·I

6.7 :i.l

49.4 59.9 057 17.7

Fluids:

D5 W and D5 RL (ml) SPA (gm) Urine output (ml) EBL(m!) Hct. Medications

700

500

150

350

20

60 600

60

35 Hydralazine, i5 rng iV

For abbreviations see footnotes to Tables II and II I. *This patient had three seizures at home and one on admission to the hospital. Fifty minutes after stabilization with an intravenous loading dose of 4 gm of MgS0 4 followed by a continuous infusion and 15 mg of hydralazine administered as an :ntrave?ous bo~us a primary c~sarean section. \V~s performed. 11.. Swan-Canz catheter was inserted in the operating roon1 Immediately pnor to the operatiOn. The data withm the box represent the high-output state referred to within the text. 1

Therefore, our hemodynamic findings indirectly support Chesley's assertion. Some investigators have stated that the decrease in blood volume observed in PET has no hemodynamic relevance.'1 We believe that this conclusion requires qualification. The assumption that the associated reduction in left ventricular filling pressure is invariably slight may not be valid. Vasodilating agents, an integral part of the management of acutely ill toxemic patients, can be expected to produce some venous dilatation. Epidural anesthesia may further compound this problem. Circulatory reHexes cannot be expected to compensate totally for abrupt changes of major magnitude in patients who are already hypovolemic. Based on these observations we believe that if low indices of ventricular filling pressure are present in severe toxemia they should be corrected along with the other therapeutic measures being taken. A further reduction of cardiac preload secondary to an absolute or relative intravascular volume loss may result in hemodynamic decompensation. Deliver; paiod. Dramatic increases were noted in systemic and pulmonary blood pressures as well as PCWP values and cardiac indices during delivery. This was undoubtedly clue in part to extrusion of blood from the uteropiacentai bed into the central circulation, resulting in increased cardiac preload. The rapid induction-

intubation sequence associated with the light general anesthesia used in these patients may have cornpounded the situation. 1'1 Each hemodynamic profile required approximately 3 minutes to perform. Accordingly, within the time limits imposed by intubation and delivery, it was not possible to distinguish conc!ttsively between intubation, cesarean section delivery, and delivery of the placenta. Postpartum period. Ross and Braunwalcl 7 have shown that left ventricular function is normal when LVSWI increases in proportion to elevations of left ventricular encl-cliastolic pressure. 7 It is, therefore, important to know the LVSWI when interpreting the hemodynamic significance of an increase in PCWP. When this relationship was examined in our patients, no impairment of left ventricular contractility was detected (Fig. I). This was true despite the potentially depressant effect of concurrently aclministerecl magnesium sulfate. All three of the patients in this study received intravenous hydralazine. The cardiovascular effects of this agent include decreased vascular resistance and increased heart rate, stroke volume. and cardiac index. 11 While hydralazine may have contributed to the excellent ventricular function observed, it is uniikeiy to have played a major role because of the inconstancy of its adnuntstration and the :-,rnall dose~ entployed. During the postpartum pet·iod one patient (B. J .) re-

Hemodynamics in

Volume l:lH Number ~~

seven~

toxemia

269

--------------------------------------------------- ---------Timr -------.-----.----------.------------,-----------.-----------.---------,--·-----2 hr PP

JhrPP

1:>0180197 108 1H/4/7 6 fi.ti -~.1

47.:\ .57.9 0.19 17.:l

200

12.5

ilO

50

4 hr PP

5 hr PP

6 hr PP

I6:ll90/114 118 30/9/16 1.5 8.8 6.8 57.8 77.8 0.14 15.6

1801108/132 123

183II091n4 122 ~)4/ 16/22 21 8.9 6.8 56.5 86.9 0.14 18.4

70

20

7 hr PP

j

8 hr f'P

4 hr PP

.-------------160/90111:l 113

--,

154190/111 112

1 35/ 18/~4

!16/YOI991 105 !S/2/7

2:\ il.8 6.8 60.5 7:1.8 0.14 15.5

li.'-J 62.2 77. ~1 0.21-i Fr. I

4 6.7 S.1 50.9 ti\1.9 0.:",7 11-\.il

100

100

125

125

1125

85

60

tiS

20 9.1!

:ll Hydralazine, 20 mg iV

ceived diuretic therapy because of elevated indices of left heart filling pressure despite fluid restriction. Therapv was directed toward a high-output state characterized by hypertension, elevated cardiac and left ventricular stroke work indices, and PCWPs in excess of 20 mm Hg (Table li). The high-output state demonstrated by this patient might be responsible for manv cases of postpartum hypertension which are rel When this entity exists in the postpartum period the administration of a diuretic should facilitate concurrent vasodilator therapv. The high-output state we have observed may be analogous to that described by Davidson and Parry' 6 in a group of normal ~igerian women where fiuicl retention caused by a high salt intake was associated with postpartum pulmonary edema.

Conclusion The patients studied in this series were receiVIng drug and fluid therapy while the data were being collected. Our results, theref{>re, do not necessarily provide insight into the natural history of severe PET at the time of delivery and must be interpreted with this in mind. Three severelv toxemic patients have been demon-

Furosemide, 20 mg iV

Table V. Formulas for derived data R"L\

&..~"~'"a

l~n •••t ml \'~'1

=l-It {rrn0,72:) ')(' ur.r:>l€rht a.,._. \..._.aaa , . ._ ·~•a•

(kg) 0 ·" 2" . I sq m) = CO (~'I (I "I mm BSA

X

7J.R4

X

lO

1

CI SVI (ml/heatlsq m) = - ' -

HR

PAR(mmHgmin~ 1 sqm)

=

iMPAP- J>cWh

, · (indexed as HR units) ( ,j . (BP(M) - PCWPl TRP(mmHgmmL-'sqm= , -(indexedasHRumts) U LVSWI (gm mlsq m) = SVI x (BP(M) ~ -PCWP) x 0.0136 For abbreviations see footnote to Tahle I L M PAP: Mean pulmonary artery pressure.

strated to have higher LVSWls than health\, nonpregnant patients. In addition, the pulmonar) 'asculature did not seem to be involved in a primary 1 asospastic process. Finally, at least in terms of central imravascular pressures, the antepartum period was associated with a decrease in circulating blood volume At delivery, an increase in PCvVP and cardiac inde:-.. occurred primarily because of an increase in venous return. 'The postpartum period differed from the antepartum period in that it was associated with an incretsed PCWP. which seems to reHect an increase in circulating blood volume rather than a pathologic diminution of cardia( reserve. These tindings suggest that, coincident with the administration of vasodiiators, intravenous fluid rherap) should be aggressive during the antepartum period.

270

Rafferty and Berkowitz .\m

Diuretic therapy during this period should be specifically reserved for those instances where central fluid overload has been demonstrated. Following deliverv,

0< wbe1 I. l'liil! Oh-rct. ( ;mecol.

however, the rate of Huicl administration should lw ITduced and diuretics may be a w,eful thnapeuti' ad-junct in patients with a high-output state.

REFERENCES I. Assali, I\. S .. Holm, L. W .. and Parker. H. R.: Systemic and regional alterations in toxemia, Circulation (Suppl. 2) 29,30: II, 1964. 2. Chesley, L. C.: Plasma and red cell volumes during pregnancy. AM. J. 0BSTET. GvNECOL. 112:440, 1972. cl. Assali, N. S., and Vaughn, D. L.: Blood volume in preeclampsia: Fantasy and reality, AM. J. 0BSTET. Gvr-oECOL. 129:355, 1977. 4. (~oodlin, R. C .. Cotton, D. B., and Haesslein, H. C.: Severe edema-proteinuria-hypertension gestosis. AM . .J. 0BSTET. GY:'\ECOL. 132:595, 1978. 5. Holmgren, A., Johnsson, B., and Sjostrand, T.: Circulatory data in normal subjects at rest and during exercise in recumbent position, with special reference ti> the stroke volume at different work intensities, Acta Phystol. Scan d. 49:343, 1960. . 6. Parmlev, W .. Tomoda, H., Diamond, G .. Forrester, S .. and C~exells, C.: Dissociation between indices of pump performance and contractility in patients with coronary artery disease and acute n1yocardial infarction, Chest 67:141, 1975. 7. Ross, .J., Jr., and Braunwald, E.: The study of left ventricular function in man by increasing resistance to ventricular ejection with angiotensin, Circulation 29:7:~9. 1964. 8. Barrett-Boyes, B. G., and Wood, E. H.: Cardiac output and related measurements and pressure values in the

.J.

right heart and associated vessels, together with an anal~­ sis of the hemnrlvn;~mic resnonsP to the inh01btion of hitrh ;>xygen mi~tu~e~ heal~h·y ;t;bj~~t;. C:lin -~~~~~51:72, 1958. Snell, R., and Luchsinger. P. C.: Determination of external work and power of the left ventricle in intact man, Am. Heart J. 69:529, 1965. Ueland, K., and Hansen, J. :VI.: Maternal cardiovascular dynamics: Labor and delivery under local and caudal anesthesia. AM. J. OssTET. GYNECOI.. 103:8, 1969. Swan. H. J. C.: The role of hemodynamic monitoring in the management of the critically ill, Crit. Care Med. 3:H:), 1975. Chesley, L. C.: Hypertensive Disorders in Pregnancy. New York, 1978, Appleton-Century-Crofts, p. 20:\. Prys-Roberts, L. T., Meloche, G. R., and Foex, P.: Studies of anesthesia in relation to hypertension. II. Haemodvnamic consequences of induction and endotracheal intubation, Br.J. Anaesth. 43:531, 1971. Goodman, L. S., and Gilman, A.: The Pharmacological Basis of Therapeutics, ed. 5, 1'-~cw York. 1975. ~'lannillan Publishing Co., Inc., pp. 705-706. Sarnoff. S. J.. and Berglund, E.: Starling's Law of the heart studied by means of simuitaneous right and left ventricular function curves in the dog, Circulation 9:706, 1954. Davidson, N. McD., and Parry. E. H. 0.: Postpartum fluid retention, Q. J. Med. 47:431, 1978.

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9.

10.

II.

12. J:l.

14.

15.

16.

:r: L:r;.·