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Hemodynamic responses of patients with heart disease to pregnancy and exercise
Hemodynamic
responses of patients with heart
disease to pregnancy and exercise KENT
UELAND,
MILES
J.
JAMES
METCALFE,
Seattle,
NOVY,
Washington,
M.D. M.D.” M.D. and Portland,
Oregon
Twenty-one patients with various valve lesions (New York Heart Association Functional Classes Z and ZZ) underwent serial hemodynamic studies during pregnancy and post Qartum. Cardiac output in the patients with heart disease was below normal at rest in the nonpregnant state. Pregnancy accentuated this hemodynamic difference, especially in patients with mitral stenosis and aortic stenosis and less in patients with aortic insuficiency or Qulmonic stenosis. The increase of cardiac outQut during light exercise was lower than normal in patients with all types of valve lesions, and the abnormality was accentuated during pregnancy. This was especially marked in the patients with mitral stenosis. It aQQears that valvular heart disease, even when symptomatically mild, results in reduced hemodynamic responses, at least to the demands of pregnancy and exercise. Factors other than changes in circulating blood volume must be involved because all the cardiac patients showed a normal rise during pregnancy. All of the pregnant cardiac patients showed evidence of some cardiac reserve, and none encountered dificulty attributable to their cardiac disease during pregnancy, labor, 07 delivery. However, several infants were born prematurely by weight or gestational age while others were small even though delivered at term. This suggests that patients with heart disease, even of Classes Z and ZZ severity, may have a suficiently limited blood flow and oxygen suQQly to the fetus to interfere with Qroger growth and development.
CLINICAL RESEARCH is enlarging our understanding of normal maternal cardiodynamics during pregnancy and clarifying some of the major influential factors. Both gestational age and body position significantly affect hemodynamics in normal pregnant women.’ Only a few reports have dealt with hemodynamic changes in pregnant patients with heart disease. Robbee and Bruce and Johnson2 reported on the physical working capacity and exercise tolerance of pregnant cardiac patients. The present investigation was undertaken to define further the hemodynamic characteristics of pregnant women with heart disease. The experimental design is the same as that previously reported for normal women,’ who serve as a group for comparison.
From the Department of Obstetrics and Gynecology, University of Washington School of Medicine, and The Heart Research Laboratory, Department of. E;t;y Untversrty of Oregon Medtcal This investigation was supported in part by United States Public Health Service Cardiovascular Program Project Grant No. HE 06336, Research Grant No. 06042, and Training Grant NO. HE 05499 from the National Heart Institute and the Oregon Heart Association, as well as Ford Foundation Grant No. 63-568-A (Training Program in Biology of Reproduction). Received
for publication
Accepted
for
publication
Dec.
27, 1971.
Jan. 27, 1972.
Reprint requests: Dr. K. Ueland, Dept. Ob./Gyn., University of Washington, Seattle, Washington 98195. *Present address: Department of Obstetrics and Gynecology, University of Oregon Medical School. 47
48
Ueland,
Novy, and Metcalfe
Am
May 1, 1972 J. Obstet. Gynecol.
Table I
Subject
Cardiac
B. P. K. B. L. B.
19 18 23
1.41 1.74 1.74
B. S.
25 25 17
1.82 1.56 1.42
24
1.51 1.74 1.56 1.68 1.49 1.60 1.81 1.57 1.46 1.62 1.72 1.60 1.46 1.62 1.43
ii.;:
J.
M. T. I. G. P. c. B. C. B. N. B. R. M. E. M. D. H. B. E. F. Y. R. M. B. S. H. D. C. P. R.
39 ;i;
19 28 19
21 17 28 21 22 19 ;i
*Body surface tPredominant @Xteria
Heart
I II II II II I I II II I I I II II I I I I
Association.
amtic
and
valve.
methods
Twenty-one patients with heart disease were studied during pregnancy and the puerperium. Table I lists the cardiac lesions di-
agnosed clinically or by cardiac catheterization in order of their hemodynamic predominance for each patient. The cardiac functional classification, based on New York Heart Association criteria, is also included. All patients were studied 6 to 8 weeks post partum and at one or two of the following periods during gestation: 20 to 24 weeks,
28 to 32 weeks, and 38 to 40 weeks. The studies were carried out in the morning, and the patients were fasting. A polyethylene
I I I
commissurotomy.
1IStarr-Edwards
Materials
Mitral stenosis Mitral stenosis,! mitral insufficiency Mitral stenosis,$ aortic stenosis, aortic insufficiency Mitral stenosis3 Mitral stenosis Mitral stenosis, aortic stenosis, aortic insufficiency Mitral stenosis Mitral stenosis Aortic insufficiency .4ortic insufficiency Aortic insufficiency, mitral insufficiency Aortic insufficiency Aortic stenosis Aortic stenosis Aortic stenosis SE. valvejl SE. valve/l Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis
area post partum. lesion listed first.
of New York
gPostmitral
Functional class$
lest’onst
catheter
was inserted
into
an ante-
cubital vein through a 16 or 18 gauge needle. A brachial artery was entered percutaneously with a Cournand needle, and a polyethylene catheter was threaded through the needle for 8 to 10 cm. Measurements were not made until pulse and respiratory rates stabilized following the catheterizations. Each patient was studied : ( 1) supine; (2) lying on the
side; (3) sitting before exercise; (4) while exercising, after at least 3 minutes of exercise, and (5) sitting, 10 minutes after stopping exercise. Blood pressure was measured with a Statham pressuretransducer. Heart rate was determined from the arterial pressure tracings which were continuously recorded. Cardiac output was measured by the dye-dilution technique, with the use of indocyanine green dye and a continuously recording densitometer. Exercise was performed on a bicycle ergometer at a load of 100 kilopon meters (k.p.m.). At the end of the procedure, plasma volume was determined by the dye dilution technique with Evans blue dye. Hematocrits were determined on arterial blood, and blood volumes were calculated from the plasma volume and hematocrit. Results
Table II shows the data for cardiac output
at different
gestational
ages and
body
Volume Number
113 1
Responses of heart patients
-
IO
Mean norm&
---1Std.deviotion 0 CIOSSI
SUPINE
l
subjects normt
to pregnancy
0
3 ---
Normal Subjects
subjects
CIOSSII
120
/-----&,
SUPINE
and exercise
Mean 1 Std. deviation o- Class I *-Class
49
I[
1
400 IO
1
SIDE 1201
SIDE
------*
lo
1SITTING SITTING I201
20-24 Weeks -
28-32 Gestation
38-M
Fig. 1. Cardiac output-mitral
6-8 Pos~turrl stenosis.
positions, grouped according to predominant value lesion and functional class. Mean values for normal pregnant women with their ranges and standard deviations? are included for comparison. Table III gives the values for heart rate. The data for resting cardiac output in patients with mitral stenosis of Functional Classes I and II are presented graphically in Fig. 1, against the means and standard deviations of values for normal women. The cardiac output of patients with mitral stenosis did not increase as much as that of normal women in response to the demands of pregnancy. Most values of cardiac output in these 8 patients (regardless of posture, stage of gestation, or functional class) were below the mean for normal pregnant women and showed little change from the postpartum values. Heart rate, on the other hand, was more variable and generally within the range for normal patients (Fig. 2). Stroke volume,
.
60-
40-
20-24 28-32 38-40 Gestation Post&A-n Weeks Fig. 2. Heart rate-mitral stenosis.
like cardiac output, showed a diminished response to pregnancy, with little change from the nonpregnant values. Fig. 3 shows the cardiac output values for patients with aortic regurgitation. In two of the four patients, the values were above the mean for normal patients in all positions throughout pregnancy. The one patient with a persistently low cardiac output, both during pregnancy and post partum, had both aortic insufficiency and mitral insufficiency (Functional Class II). The heart rate response in three of the four patients was either within the normal range or above, while the patient with the combined lesions showed a consistently low vaIue (Table III). The cardiac output values of three patients with aortic stenosis (Functional Class
tUeland
and
*Starr-Edwards
associates.7
aortic
deviation
hearts-f
Range Mean Standard
Normal
valve
5.3-7.1 6.4 +O 6
-
5.49
Aortic stenosis, Class II*
Pulmonic stenosis, Class I
4.96
Aortic stenosis, Class I
5.8-8.5 6.9 +1.0
-
-
4.6-7.3 5.9 +0.9
-
4.72
4.66
3.77 7.05
3.79 7.36
3.90 6.48
Aortic insufficiency, Class II
5.90 7.87
6.55 8.08
6.66 8.00
3.15
3.36
Aortic insufficiency, Class I
3.79 2.62
-
4.20
Mitral stenosis, Class II
-
3.95
-
I
4.71
4.97 4.9-9.6 7.0 -11.4
4.98 7.65
4.88 5.28
-
4.10
6.34 7.30
8.00
4.81 7.47
3.85
4.15
6.70 4.68 6.40 4.82
5.90 4.61 4.99
9.17
5.18 6.44
7.19 3.63 6.29 3.85
5.10 4.65 5.05 4.68
28-32 Weeks
age, and maternal
3.6-8.5 6.1 21.4
gestational
2.47
20.24 Weeks
per minute),
-
(liters
2.30
lesion
I
I
output
Mitral stenosis, Class I
Cardiac
Table II. Cardiac
4.5-9.8 6.4 21.5
4.71 4.84 5.09
4.87
-
4.91 5.63 4.70
7.80
5.62 6.84
6.18 4.04 5.17 3.00
5.30 4.36 4.95 4.74
Gestation
posture
I
3.8-4.9 4.5 +0.5
3.99 4.75 4.54 5.45
-
-
4.65 4.87
5
-
3.79 -
4.3-7.1 5.7 ‘1.0
6.10
4.57 5.90
-
5.78 5.85
-
38-40 Weeks
4.2-5.7 5.2 TO.6
4.30 4.92 5.10 4.85
-
4.60 5.60
-
-
3.8-5.8 5.1 +0.7
5.18 3.64 3.98 4.44
4.83 3.03
5.13 4.51 4.06
2.86 3.56
4.40 4.06
-
-
5.30 3.07 4.75 3.89
4.67 3.58 4.75 4.57
5.36 4.39 3.41 5.02
-
4.85 4.24 4.45
3.0.5 3.56
4.69 3.93
4.15 3.91 5.19 4.27 3.66 4.51 3.68
3.3-5.8 4.6 ‘0.8
4.39 2.56 3.18 4.19
4.06 2.88
4.53 4.06 3.32
2.74 2.86
3.80 3.70
3.45 3.48 4.41 2.6”
3.71 2.64 4.25 4.55
post fiartum
3.7-6.7 5.0 -_+0.9
6-8 Weeks
-
-
3.70
(
9 B zg br .- g. n* 2 .+
5 ;r Q F
lesion
72 -
90
Aortic stenosis, Class I
Aortic stenosis, Class II*
tUeland
and
*Starr-Edwards
associates.’
aortic
deviation
hearts?
Range Mean Standard
Normal
74 211
59-84
72 90
Aortic insufficiency, Class II
Pulmonic stenosis, Class I
ii
84
Supine
1
58-85 73 f10
-
61-108 83 ?I5
-
90 -
102 -
92 96
84 86
96
90
84
-
1 Sitting
gestational
82 -
Side
20-24 Weeks
(beats per minute),
Aortic insufficiency, Class I
Mitral stenosis, Class II
valve.
Pulse rate
Mitral stenosis, Class I
Cardiac
Table III.
82 +10
60-96
78
81 60-100 83 513
80 70
-
82 93
-
102
-
95 108
72 74
76 81 68 86
Side
80 78
84
-
72 78 105
102
102 105
96 66 100 72
80 81 57 81
Supine
28-32 Weeks
age, and maternal
64-l 23 92 217
88 86 75
80
-
88 100 105
93
96 105
108 82 116 84
80 78 69 84
Sitting
Posture
Gestation
posture
86 +7
75-96
80 68 80 81
-
83 ?12
68-96
84
72 88
80-105 89 29
80 84 86 93
-
-
-
92 -
Sitting
100 81
(
84 81
90
Side
88 78
-
-
-
90
Supine
38-40 Weeks 6-8
57-81 70 27
76 68 60 67
70 64
66 72 66
60 77
70 62
78 66 92 84
78 54 56 72
1 Supine
1 )
Weeks
57-81 70 Z8
60 70 73
68 71
68 64
84 76
-
75 60 60 71
Side
72-100 at r;
81 90 78 81
88 74
84 93 89
72 78
84 73
96
“9: 110
83 64 66 80
1 Sitting
post partum
F
s a -0 ;i, fD 2 : Y 2 n 2 2
u 9tD
8 2 6 R 5
52
Ueland,
Novy, and Metcalfe
> ---
N0rfl-KJl subjects
IO-
SUPINE
Am.
Mean 1 Std. deviation o-class I *-Class
II
. 8-
o_---
---I 0
---.
‘. 0
6-
*.
&--, 0
---__----
4
. .
2-
I
I
2
IO
lo
lo1
4-
--___-----
.
SITTING
I
1
I
,
SIDE
SITTING
.
4
#
21
,
20-24 \
Weeks Fig.
3. Cardiac
1
28-32 Gestation output-aortic
I
38-40
o
!
.
I
101 SIDE
1
Clc3SSII (S.E.VOlWl
-.
6
l
Std. deviatfon Class I .
--------.*A
a---_
4-
May 1, 1972 J, Obstet. Gynecol.
20124
6-8 Postghl
insufficiency.
I) and two patients with Starr-Edwards aortic valve prostheses(Functional ClassII) are shown in Fig. 4. In general, cardiac output was lower than the mean for normal patients at each stage of pregnancy and post par-turn. The two patients with Starr-Edwards aortic valve prostheses showed persistently low values for cardiac output in both the supine and sitting positions during pregnancy and post partum. Fig. 5 shows data from our four patients with pulmonic stenosis(Functional ClassI). The cardiac output tended to be lower than normal in all positions and was especially evident in the sitting position, but the effect was not as marked as in patients with mitral or aortic stenosis.The heart rate and
Weeks Fig.
28-32
38:40
Gestation
4. Cardiac
output-aortic
6l8 POS&-L”rn stenosis.
stroke volume of the patients with pulmonic stenosis were usually within one standard deviation of those of the normal patients but were generally below the mean for normal . pregnant women (Table III). The hemodynamic limitation of these patients became even more apparent with exercise. In normal patients (Table IV), there was a very constant increment in cardiac output throughout gestation in response to a standardized bout of mild exercise on a bicycle ergometer. The per cent increase during exercise was similar to that encountered 6 to 8 weeks post partum (70 to 80 per cent), but the absolute change was greater during pregnancy, the increment ranging, on the average, from 4.1 to 4.6 L.
Volume Number
113 1
Responses
per minute during pregnancy as compared to 3.4 L. per minute post partum. In patients with mitral stenosis (Functional Classes I and II), however, the increase in cardiac output with exercise was markedly diminished, whether expressed as an absolute value or as a percentage of resting cardiac output, amounting to half or less of the increments achieved by normal pregnant women. Heart rate data are given in Table V. The small increase in cardiac output was achieved mostly by an increase in stroke volume. Post partum, on the other hand, the per cent rise in cardiac output evoked by standard exercise was similar in the women with mitral stenosis to that achieved by normal women, although the absolute rise in cardiac output was greater in the normal subjects. As already noted, the two patients with aortic insufficiency (Functional Class I) showed a normal rise of cardiac output (Table IV) during pregnancy, but when mild exercise was superimposed the cardiac output response was only half that seen in the normal pregnant patients. Also, the two patients with Class I aortic stenosis and the two with Starr-Edwards aortic valves (Class II) all had a diminished cardiac output response to exercise. In contrast with these results, two of three patients with pulmonic stenosis (Functional Class I) showed a normal rise in cardiac output in response to exercise. It is of interest and importance to note that all patients-both normal and those with heart disease Functional Classes I and II-showed complete hemodynamic recovery from exercise within 10 minutes at all stages of pregnancy and during the puerperium, as judged by a return of cardiac output to pre-exercise levels. Table VI shows the plasma volume, hematocrit, and blood volume changes in normal patients and in those with heart disease at 28 to 32 weeks’ gestation and 6 to 8 weeks post partum. With the exception of a rather low hematocrit in the normal patients at 28 to 32 weeks’ gestation, the values are very similar, especially when one expresses blood volume on the basis of maternal weight. During pregnancy, the normal pa-
of
heart
patients
IO-
to pregnancy
and
exercise
53
SIDE
.~
8-
-------,‘---,_
:
?3-
----a_
2 .a!
4-
<
22 ‘*
8
1
SITTING
6
-------
4
0 0
2-1
,
20-24,
I
I
28-32 38-40 Weeks Gestation Fig. 5. Cardiac output-pulmonic
6-8 Post;t”rn
stenosis.
tients had an average blood volume of 99.8 C.C. per kilogram versus 100.3 C.C. per kilogram for the patients with heart disease. Nonpregnant averages were 75.2 and 77.8 C.C. per kilogram, respectively. Comment
Fig. 6 summarizesour data on cardiac output and shows that the average in our patients with heart diseaseof Functional Classes I and II was decreased below normal, even at rest in the nonpregnant state. Pregnancy accentuated the hemodynamic deviation from normal, especially in patients with mitral stenosisor aortic stenosisand lessclearly in patients with aortic insufficiency or pulmonic stenosis.In several instances, the mean cardiac output for the patients with heart diseasewas below the normal average by more
=
sitting.
tUehnd
and
*Starr-Edwards
Sit.
=
associates.’
aortic
Ex.
Normal hear&f Range Mean Standard deviation
valve.
exercise.
4.6-7.3 5.9 21.2
8.8-12.1 10.4 +1.3
-
-
-
6.93 -
4.72 -
Aortic stenosis, Class II*
stenosis,
6.30
4.66 -
Aortic stenosis, Class I
I
5.73
3.77
Aortic insufficiency, Class II
Pulmonic Class
9.63 10.96
5.74 4.20
4.35
Ex.
5.90 7.87
1
Aortic insufficiency, Class I
2.62
3.?9
Mitral stenosis, Class II
Sit.
Weeks (
-
per minute),
20-24
(liters
3.95
output
Cardiac lesion Mitral stenosis, Class I
Table IV. Cardiac
4.8-7.6 6.0 21.0
-
3.40
4.10
6.70 6.74
230
3.93
3.97
Sit.
1
gestational
4.5-7.3 5.9 9.0
4.71 4.84 -
4.87
4.91 5.63
-
5.62 6.84
6.18 4.04 5.17 3.00
5.30 4.36
Sit.
1
a.90 7.61
6.90
5.77 7.52
a.20 9.79
7.12 4.60 7.95 5.23
7.30 6.99
Ex.
Weeks
7.2-11.5 10.0 21.5
28-32
age, and exercise
5.8-7.1 6.6 20.4
5.01 4.68 -
4.90
4.17 3.83
-
4.74 5.46
3.72 3.90
3.14 4.22
sit.
Posture
Gestation
1
I
5.5-5.7 5.6 ‘co.1
4.30 4.92 5.10
4.60
-
3.70
Sit.
7.80 7.30 6.82
-
7.00
5.41
Ex.
Weeks
9.2-11.1 10.2 tl.O
38-40 1
5.9-6.8 6.3 50.4
4.44 4.04 -
-
5.10
3.5-5.8 4.8 to.9
4.39 2.56 3.28
4.06 2.88
4.53 4.06
2.74
3.80 3.70
-
3.71 2.64
Sit.
3.45 3.48 4.41 2.62
1
6-8
-
3.89 -
Sit.
( 1
7.26 4.53 5.53
6.65 3.40
6.59 6.97
5.27
5.50 6.21
6.72 4.79 7.34 4.41
6.28 5.46
Ex.
post
5.6-10.9 a.2 21.9
Weeks 1
4.1-6.0 4.9 fO.a
4.03 3.03 3.25
3.6’ 2.36
4.14 3.76
9 ia _..
3.63 3.71
3.54 3.20 3.64 9-.3,-3
3.80 2.69
sit.
partum
is 2 Q =z m
Z 2 Y . Q z
E 2 .Q
c
lesion
and
associates.’
aortic
tUeland
deviation
*Starr-Edwards
heartst
Range Mean Standard
Normal
valve.
61-108 88 215
90 -
Aortic stenosis, Class II+
Pulmonic stenosis, Class I
114 -
102
Aortic stenosis, Class I
94-126 115 211
102
108
92
108 100
104 a5 114
Ex.
Aortic insufficiency, Class II
)
a4 86
;6
a4 90
-
Sit.
Aortic insufficiency, Class I
Mitral stenosis, Class II
Mitral stenosis, Class I
Cardiac
)
1
82-108 94 213
-
64-1 la 91 216
88 86
80
-
96 105
108 a2 116 a4
80 78
Sit.
88 100
1
)
98-132 116 212
120 120 -
92
96 120
114 126
120 a4 140 94
104 102
Ex.
28-32 Weeks
age, and exercise
96 -
102
96 90
90
;6 a0
Sit.
gestational
20-24 Weeks
Table V. Pulse rate (beats per minute),
1
78-108 95 212
104 92 -
100 99 a0
102 120
82 94
aa a4
Sit.
Posture
Gestation
1
88-105 97 f9
a0 a4 86
100 -
-
92 -
Sit.
)
120-136 128 26
loa loa 98
125
-
120
Ex.
38-40 Weeks )
96-120 108 217
86 95 80
)
115 108 a4
108 a4
102 120
92
96 100
124 92 144 100
106 94
Ex.
1
78
a2
Sit.
a co 2 Y2 0 2
96
72 76-96 86 +a
a -0
96
100 80
96
96
80
88 68
to4 a4 116 80
post partum
95-128 111 +13
Weeks
72-100 a5 f7
a1 90 78
aa 74
ii
104 -
72
-
aa 92 110 96
a3 64
Sit.
a4 73
)
6-8
-
90
Sit.
1
56
Ueland,
Novy,
and
May 1, 1972 Am. J. Obstet. Gynecol.
Metcalfe
Exercise
“I
T
(Top
of bar)
T
T
8-T : P .?? . 4 4-
est (base
2-
0
of bar) Normal
&IA1
n Ail Ii. D. q MS 0
20 - 24
Weeks II
28
-
Std.
- 32
38-40
6-8 Postpartum
Gestation deviation
Fig. 6. Cardiac output.
Table VI. Plasma volume,
hematocrit, 28-32
Plasma volume (L.) Heart
disease
Hematocrit (%I
and blood Weeks’
volume
gestation
6-8
volume I
CL.)
Weeks
post
CL.)
Hct. (%)
Blood volume (L.)
c.c./Kg.
Plasma volume
Blood
i
c.c./Kg.
parturn
patients
Range Mean Standard deviation
3.04-5.48 3.86 ‘0.65
29-43 35.9 23.50
4.32-8.48 6.05 k1.90
74.1-130.5 100.3 212.4
2.00-3.55 2.68 50.35
32-51 39.4 +4.2
3.21-6.10 4.40 to.71
65.5-94.1 77.8 28.9
6 Normal patients Range Mean Standard deviation
3.54-6.10 4.66 Al.10
27-35 31.1 T3.2
5.45-8.78 6.74 f1.31
70.5-129.7 99.8 224.0
2.40-3.06 2.72 f0.26
35-41 38.5 f4.7
3.93-5.68 4.70 to.23
64.8-87.2 75.2 kg.6
than one standard deviation. This finding was somewhat unexpected in these asymptomatic cardiac patients. In considering explanations other than their valvular heart disease, a smaller body surface area may have played a small part, although its calculation during pregnancy is of questionable validity. When postpartum weight and height were used, the average body surface area was 1.68 for our normal subjects, 1.60 for all our patients with heart disease, 1.56 for those with mitral stenosis, and 1.64 for those with aortic stenosis. Another factor which might have influenced the diminished cardiac output found in our cardiac patients is careful sodium restriction, avoidance of excessive weight gain, and use of diuretics to which they were
subjected during pregnancy. If these therapeutic measures played a part, factors other than changes in circulating blood volume must be involved, because all our cardiac patients showed a normal rise of blood volume during pregnancy (Table VI). This was also shown by Robbe.B In 1969, we reported on the hemodynamic responses to light exercise in a group of normal pregnant women.’ In six subjects, the cardiac output response to an exercise load of 100 k.p.m. per minute seemed fairly constant throughout pregnancy, with increments of 4.5 L. at 20 to 24 weeks, 4.1 L. at 28 to 32 weeks, and 4.6 L. at 38 to 40 weeks of gestation. Post partum, cardiac output rose only 3.4 L. in response to the same exer-
Volume 113 Number
Responses of heart patients
1
to pregnancy
and exercise
57
Table VII Increment Investigator Guzman 1970 Ueland 1969 Ihrman,*
*The
and
Exercise
Caplaq3
and associates,’
1960
authors’
comment:
Weeks’ gestation
load
Cardiac output
during Heart
for 4 min.
< 20 29-35 36-40
1.7 1.8 1.4
5.2 11.9 15.8
100 k.p.m.
for 3 min.
20-24 38-32 38-40
2.2 1.7 1.9
3.2 4.6 16.6
200 k.p.m.
for 6 min.
“Consistently
higher
than
non-pregnant
cise. Thus, the absolute rise in cardiac output in response to light exercise was higher during pregnancy than in the nonpregnant state. However, in our normal subjects,the average per cent rise in cardiac output was the same at all study periods, including the postpartum study, due to the fact that the resting cardiac output was significantly elevated during pregnancy. Referring again to Fig. 6, the cardiovascular response to light exercise differed from normal in patients with all types of heart disease,and the abnormality was accentuated during pregnancy. Especially in patients with mitral stenosis, the smaller rise in resting cardiac output during pregnancy, combined with a lessthan normal responseto exercise, resulted in values of cardiac output well below the mean value achieved by normal pregnant women. Post par-turn, the patients with heart disease showed a percentage rise in cardiac output during exercise that was similar to that of normal women, but the absolute values for cardiac output, at rest and during exercise, were significantly lower than those found in the normal subjects. The cardiac output and heart rate responsesof our patients with aortic stenosis were similar to those encountered in the patients with mitral stenosis, although the deviations from normal were not so pronounced. Patients with predominant aortic regurgitation and those with pure pulmonary stenosisalso showed diminished cardiac output responsesto pregnancy and to exercise.
control
Not Not Not
given given given
Stroke volume
rate
150 k.p.m.
20 28 36
exercise
9.1 12.1 14.1
Not Not Not
given* given* given* 17.5 14.5 6.2
Not Not Not
given given given
~alues.“~
Thus, it appears that valvular diseaseof all these varieties, even when symptomatically mild, results in reduced hemodynamic responsesto the demands of pregnancy and exercise. These findings are in general agreement with those reported by Robbe, who found a higher pulse rate responseto standard work loads on the bicycle ergometer during late pregnancy (36 weeks’ gestation) than post partum in patients with pure mitral valvular diseaseor mitral and aortic valvular disease combined. We studied only one patient with mitral stenosis (Functional Class I) late in pregnancy, and her heart rate increased 28 beats per minute, as compared to a rise of 23 beats per minute post partum. When all heart diseasepatients are considered, heart rate during exercise was higher at 28 to 32 weeks’ gestation (110 beats per minute) and 38 to 40 weeks’ gestation (112 beats per minute), compared to a postpartum average of 104 beats per minute. Bruce and Johnson2 showed that pregnant patients with even minimal cardiac impairment from mitral stenosis, aortic regurgitation, or congenital cardiac defects had a greater tachycardia than normal pregnant women in responseto exercise. However, their patients were studied in the recumbent position, and the altered hemodynamics produced by the gravid uterus may have influenced their results. As pregnancy advances, the hemodynamic mechanism by which an increasedblood flow is supplied to the peripheral tissuesin normal
58
Ueland,
Novy,
and
May 1, 1972 -41x1. J. Obstet. Gynecol.
Metcalfe
Table VIII Cardiac
lesion*
Functional
Mitral stenosis Mitral stenosis,$. mitral insufficiency Mitral stenosis,$ aortic stenosis, aortic insufficiency Mitral stenosis$ Mitral stenosis Mitral stenosis, aortic stenosis, aortic insufficiency Mitral stenosis Mitral stenosis Aortic insufficiency Aortic insufficiency Aortic insufficiency, mitral insufficiency Aortic insufficiency Aortic stenosis Aortic stenosis Aortic stenosis S.E. valves S.E. valves Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis “Predominant tCriteria $Postmitral &Starr
lesion of New
York
listed Heart
class?
Fetal weight (Gm.)
Weeks’ gestation at delivery
I I
2,540 2,848
42 41
I I
3,345 1,786 3,005
43 34 40
2,650 3,062 3,045 2,565 2,183 2,325 3,430 2,637 2,551 3,045 4,026 3,245 3,629 3,260 2,722 2.580
40 40 38 41 38 35 39 40 40 40 40 40 40 40 40 40
II II II II I I II II I I I II II I I I I
first. Association.
commissurotomy.
Edwards
aortic
valve.
women appears to change. Table VII compares the data from three studies of hemodynamic responses to exercise in normal pregnant patients. The table lists cardiac output, heart rate, and stroke volume as values in excess of those obtained in the same group of patients in the nonpregnant state. The
rise in cardiac output recorded by Guzman and Caplar? in responseto an exercise load of 150 k.p.m. for 4 minutes was quite similar to that found by the authors7 and did not increase with advancing pregnancy. The heart rate responsewas similar in all three studies and, in contrast with cardiac output, showed a progressive increase as pregnancy continued. Therefore, in normal women, with advancing gestation, the increase of cardiac output with exercise was achieved more and more by an increase in heart rate, and the stroke volume response to exercise became less as pregnancy advanced. It should be noted, however, that, according to our data, the stroke volume was higher at all stagesof gestation when compared to that of the nonpregnant individuals.
All of our pregnant cardiac patients showed an increase in cardiac output during some cardiac reserve. exercise, indicating None of the mothers encountered any diiculty attributable to their cardiac disease during pregnancy, labor, or delivery. However, several infants were born prematurely by weight or gestational age, and several more were small, even though delivered at term (Table VIII). These findings suggest that the mother with valvular heart disease, even of Class I or II severity, may have a sufficiently limited blood flow and oxygen supply to her fetus that its proper growth and development are impaired. This suggestion can be found in the analyses by Niswander and associates5of the charts of 327 pregnant women with heart disease.The incidence of birth weight I 2,000 grams was 6.1 per cent, 2,001 to 2,500 grams, 11.9 per cent, and 2 2,501 grams, 82.0 per cent. This is comparable to our figures for 21 patients of 4.8, 14.3, and 80.9 per cent, respectively. These are all quite different from those of the contol group of Niswander and associ-
Volume Number
113 1
Responses of heart patients
ates5 If the birth weights of the 12 infants delivered at 40 weeks’ gestation are analyzed, the mean weight is 3,034 grams. This is much lower than the mean birth weight reported by Babson and colleagues1 for a white middle-class population in Oregon of 3,534 grams for boys and 3,389 grams for girls. Maternal deaths due to heart disease have been reduced strikingly in the past 50 years. In our care of pregnant cardiac patients, perhaps more thought and effort should be directed toward improvement of the uterine environment for fetal growth and development. This might be accomplished by such
to pregnancy
and exercise
59
measures as : ( I ) restricting maternal physical activity; (2) stressing proper maternal posture, with avoidance of abdominal compression and the supine position; (3) maximizing the oxygen-carrying capacity of the blood by prompt and continued iron supplementation; (4) avoiding sodium restriction and the use of oral diuretics which limit the normal rise of maternal blood volume and may thereby limit cardiac output and uterine blood flow; (5) using graded elastic stockings to prevent venous pooling in the lower extremities, thus augmenting venous return.
REFERENCES
1. 2. 3. 4.
Babson, S. C., Behrman, R. E., and Lessel, R.: Pediatrics 45: 937, 1970. Bruce, R. A., and Johnson, W. P.: Clin. Obstet. Gynecol. 4: 665, 1961. Guzman, C. A., and Caplan, R.: AM. J. OBSTET.GYNECOL. 108:600,1970. Ihrman, K.: Acta Sot. Med. Ups. 65: 335, 1960.
5.
6. 7.
Niswander, K. R., Berendes, H., Deutschberger, J., Lipko, N., and Westphal, M. C.: AM. J. OBSTET. GYNECOL. 98: 871, 1967. Robbe, H.: Acta Obstet. Gynecol. Stand. 38: 1, 1959. Ueland, K., Novy, M. J., Peterson, E. N., and Metcalfe, P.: AM. J. OBSTET. GYNECOL. 104: 856, 1969.
responses of patients with heart
disease to pregnancy and exercise KENT
UELAND,
MILES
J.
JAMES
METCALFE,
Seattle,
NOVY,
Washington,
M.D. M.D.” M.D. and Portland,
Oregon
Twenty-one patients with various valve lesions (New York Heart Association Functional Classes Z and ZZ) underwent serial hemodynamic studies during pregnancy and post Qartum. Cardiac output in the patients with heart disease was below normal at rest in the nonpregnant state. Pregnancy accentuated this hemodynamic difference, especially in patients with mitral stenosis and aortic stenosis and less in patients with aortic insuficiency or Qulmonic stenosis. The increase of cardiac outQut during light exercise was lower than normal in patients with all types of valve lesions, and the abnormality was accentuated during pregnancy. This was especially marked in the patients with mitral stenosis. It aQQears that valvular heart disease, even when symptomatically mild, results in reduced hemodynamic responses, at least to the demands of pregnancy and exercise. Factors other than changes in circulating blood volume must be involved because all the cardiac patients showed a normal rise during pregnancy. All of the pregnant cardiac patients showed evidence of some cardiac reserve, and none encountered dificulty attributable to their cardiac disease during pregnancy, labor, 07 delivery. However, several infants were born prematurely by weight or gestational age while others were small even though delivered at term. This suggests that patients with heart disease, even of Classes Z and ZZ severity, may have a suficiently limited blood flow and oxygen suQQly to the fetus to interfere with Qroger growth and development.
CLINICAL RESEARCH is enlarging our understanding of normal maternal cardiodynamics during pregnancy and clarifying some of the major influential factors. Both gestational age and body position significantly affect hemodynamics in normal pregnant women.’ Only a few reports have dealt with hemodynamic changes in pregnant patients with heart disease. Robbee and Bruce and Johnson2 reported on the physical working capacity and exercise tolerance of pregnant cardiac patients. The present investigation was undertaken to define further the hemodynamic characteristics of pregnant women with heart disease. The experimental design is the same as that previously reported for normal women,’ who serve as a group for comparison.
From the Department of Obstetrics and Gynecology, University of Washington School of Medicine, and The Heart Research Laboratory, Department of. E;t;y Untversrty of Oregon Medtcal This investigation was supported in part by United States Public Health Service Cardiovascular Program Project Grant No. HE 06336, Research Grant No. 06042, and Training Grant NO. HE 05499 from the National Heart Institute and the Oregon Heart Association, as well as Ford Foundation Grant No. 63-568-A (Training Program in Biology of Reproduction). Received
for publication
Accepted
for
publication
Dec.
27, 1971.
Jan. 27, 1972.
Reprint requests: Dr. K. Ueland, Dept. Ob./Gyn., University of Washington, Seattle, Washington 98195. *Present address: Department of Obstetrics and Gynecology, University of Oregon Medical School. 47
48
Ueland,
Novy, and Metcalfe
Am
May 1, 1972 J. Obstet. Gynecol.
Table I
Subject
Cardiac
B. P. K. B. L. B.
19 18 23
1.41 1.74 1.74
B. S.
25 25 17
1.82 1.56 1.42
24
1.51 1.74 1.56 1.68 1.49 1.60 1.81 1.57 1.46 1.62 1.72 1.60 1.46 1.62 1.43
ii.;:
J.
M. T. I. G. P. c. B. C. B. N. B. R. M. E. M. D. H. B. E. F. Y. R. M. B. S. H. D. C. P. R.
39 ;i;
19 28 19
21 17 28 21 22 19 ;i
*Body surface tPredominant @Xteria
Heart
I II II II II I I II II I I I II II I I I I
Association.
amtic
and
valve.
methods
Twenty-one patients with heart disease were studied during pregnancy and the puerperium. Table I lists the cardiac lesions di-
agnosed clinically or by cardiac catheterization in order of their hemodynamic predominance for each patient. The cardiac functional classification, based on New York Heart Association criteria, is also included. All patients were studied 6 to 8 weeks post partum and at one or two of the following periods during gestation: 20 to 24 weeks,
28 to 32 weeks, and 38 to 40 weeks. The studies were carried out in the morning, and the patients were fasting. A polyethylene
I I I
commissurotomy.
1IStarr-Edwards
Materials
Mitral stenosis Mitral stenosis,! mitral insufficiency Mitral stenosis,$ aortic stenosis, aortic insufficiency Mitral stenosis3 Mitral stenosis Mitral stenosis, aortic stenosis, aortic insufficiency Mitral stenosis Mitral stenosis Aortic insufficiency .4ortic insufficiency Aortic insufficiency, mitral insufficiency Aortic insufficiency Aortic stenosis Aortic stenosis Aortic stenosis SE. valvejl SE. valve/l Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis
area post partum. lesion listed first.
of New York
gPostmitral
Functional class$
lest’onst
catheter
was inserted
into
an ante-
cubital vein through a 16 or 18 gauge needle. A brachial artery was entered percutaneously with a Cournand needle, and a polyethylene catheter was threaded through the needle for 8 to 10 cm. Measurements were not made until pulse and respiratory rates stabilized following the catheterizations. Each patient was studied : ( 1) supine; (2) lying on the
side; (3) sitting before exercise; (4) while exercising, after at least 3 minutes of exercise, and (5) sitting, 10 minutes after stopping exercise. Blood pressure was measured with a Statham pressuretransducer. Heart rate was determined from the arterial pressure tracings which were continuously recorded. Cardiac output was measured by the dye-dilution technique, with the use of indocyanine green dye and a continuously recording densitometer. Exercise was performed on a bicycle ergometer at a load of 100 kilopon meters (k.p.m.). At the end of the procedure, plasma volume was determined by the dye dilution technique with Evans blue dye. Hematocrits were determined on arterial blood, and blood volumes were calculated from the plasma volume and hematocrit. Results
Table II shows the data for cardiac output
at different
gestational
ages and
body
Volume Number
113 1
Responses of heart patients
-
IO
Mean norm&
---1Std.deviotion 0 CIOSSI
SUPINE
l
subjects normt
to pregnancy
0
3 ---
Normal Subjects
subjects
CIOSSII
120
/-----&,
SUPINE
and exercise
Mean 1 Std. deviation o- Class I *-Class
49
I[
1
400 IO
1
SIDE 1201
SIDE
------*
lo
1SITTING SITTING I201
20-24 Weeks -
28-32 Gestation
38-M
Fig. 1. Cardiac output-mitral
6-8 Pos~turrl stenosis.
positions, grouped according to predominant value lesion and functional class. Mean values for normal pregnant women with their ranges and standard deviations? are included for comparison. Table III gives the values for heart rate. The data for resting cardiac output in patients with mitral stenosis of Functional Classes I and II are presented graphically in Fig. 1, against the means and standard deviations of values for normal women. The cardiac output of patients with mitral stenosis did not increase as much as that of normal women in response to the demands of pregnancy. Most values of cardiac output in these 8 patients (regardless of posture, stage of gestation, or functional class) were below the mean for normal pregnant women and showed little change from the postpartum values. Heart rate, on the other hand, was more variable and generally within the range for normal patients (Fig. 2). Stroke volume,
.
60-
40-
20-24 28-32 38-40 Gestation Post&A-n Weeks Fig. 2. Heart rate-mitral stenosis.
like cardiac output, showed a diminished response to pregnancy, with little change from the nonpregnant values. Fig. 3 shows the cardiac output values for patients with aortic regurgitation. In two of the four patients, the values were above the mean for normal patients in all positions throughout pregnancy. The one patient with a persistently low cardiac output, both during pregnancy and post partum, had both aortic insufficiency and mitral insufficiency (Functional Class II). The heart rate response in three of the four patients was either within the normal range or above, while the patient with the combined lesions showed a consistently low vaIue (Table III). The cardiac output values of three patients with aortic stenosis (Functional Class
tUeland
and
*Starr-Edwards
associates.7
aortic
deviation
hearts-f
Range Mean Standard
Normal
valve
5.3-7.1 6.4 +O 6
-
5.49
Aortic stenosis, Class II*
Pulmonic stenosis, Class I
4.96
Aortic stenosis, Class I
5.8-8.5 6.9 +1.0
-
-
4.6-7.3 5.9 +0.9
-
4.72
4.66
3.77 7.05
3.79 7.36
3.90 6.48
Aortic insufficiency, Class II
5.90 7.87
6.55 8.08
6.66 8.00
3.15
3.36
Aortic insufficiency, Class I
3.79 2.62
-
4.20
Mitral stenosis, Class II
-
3.95
-
I
4.71
4.97 4.9-9.6 7.0 -11.4
4.98 7.65
4.88 5.28
-
4.10
6.34 7.30
8.00
4.81 7.47
3.85
4.15
6.70 4.68 6.40 4.82
5.90 4.61 4.99
9.17
5.18 6.44
7.19 3.63 6.29 3.85
5.10 4.65 5.05 4.68
28-32 Weeks
age, and maternal
3.6-8.5 6.1 21.4
gestational
2.47
20.24 Weeks
per minute),
-
(liters
2.30
lesion
I
I
output
Mitral stenosis, Class I
Cardiac
Table II. Cardiac
4.5-9.8 6.4 21.5
4.71 4.84 5.09
4.87
-
4.91 5.63 4.70
7.80
5.62 6.84
6.18 4.04 5.17 3.00
5.30 4.36 4.95 4.74
Gestation
posture
I
3.8-4.9 4.5 +0.5
3.99 4.75 4.54 5.45
-
-
4.65 4.87
5
-
3.79 -
4.3-7.1 5.7 ‘1.0
6.10
4.57 5.90
-
5.78 5.85
-
38-40 Weeks
4.2-5.7 5.2 TO.6
4.30 4.92 5.10 4.85
-
4.60 5.60
-
-
3.8-5.8 5.1 +0.7
5.18 3.64 3.98 4.44
4.83 3.03
5.13 4.51 4.06
2.86 3.56
4.40 4.06
-
-
5.30 3.07 4.75 3.89
4.67 3.58 4.75 4.57
5.36 4.39 3.41 5.02
-
4.85 4.24 4.45
3.0.5 3.56
4.69 3.93
4.15 3.91 5.19 4.27 3.66 4.51 3.68
3.3-5.8 4.6 ‘0.8
4.39 2.56 3.18 4.19
4.06 2.88
4.53 4.06 3.32
2.74 2.86
3.80 3.70
3.45 3.48 4.41 2.6”
3.71 2.64 4.25 4.55
post fiartum
3.7-6.7 5.0 -_+0.9
6-8 Weeks
-
-
3.70
(
9 B zg br .- g. n* 2 .+
5 ;r Q F
lesion
72 -
90
Aortic stenosis, Class I
Aortic stenosis, Class II*
tUeland
and
*Starr-Edwards
associates.’
aortic
deviation
hearts?
Range Mean Standard
Normal
74 211
59-84
72 90
Aortic insufficiency, Class II
Pulmonic stenosis, Class I
ii
84
Supine
1
58-85 73 f10
-
61-108 83 ?I5
-
90 -
102 -
92 96
84 86
96
90
84
-
1 Sitting
gestational
82 -
Side
20-24 Weeks
(beats per minute),
Aortic insufficiency, Class I
Mitral stenosis, Class II
valve.
Pulse rate
Mitral stenosis, Class I
Cardiac
Table III.
82 +10
60-96
78
81 60-100 83 513
80 70
-
82 93
-
102
-
95 108
72 74
76 81 68 86
Side
80 78
84
-
72 78 105
102
102 105
96 66 100 72
80 81 57 81
Supine
28-32 Weeks
age, and maternal
64-l 23 92 217
88 86 75
80
-
88 100 105
93
96 105
108 82 116 84
80 78 69 84
Sitting
Posture
Gestation
posture
86 +7
75-96
80 68 80 81
-
83 ?12
68-96
84
72 88
80-105 89 29
80 84 86 93
-
-
-
92 -
Sitting
100 81
(
84 81
90
Side
88 78
-
-
-
90
Supine
38-40 Weeks 6-8
57-81 70 27
76 68 60 67
70 64
66 72 66
60 77
70 62
78 66 92 84
78 54 56 72
1 Supine
1 )
Weeks
57-81 70 Z8
60 70 73
68 71
68 64
84 76
-
75 60 60 71
Side
72-100 at r;
81 90 78 81
88 74
84 93 89
72 78
84 73
96
“9: 110
83 64 66 80
1 Sitting
post partum
F
s a -0 ;i, fD 2 : Y 2 n 2 2
u 9tD
8 2 6 R 5
52
Ueland,
Novy, and Metcalfe
> ---
N0rfl-KJl subjects
IO-
SUPINE
Am.
Mean 1 Std. deviation o-class I *-Class
II
. 8-
o_---
---I 0
---.
‘. 0
6-
*.
&--, 0
---__----
4
. .
2-
I
I
2
IO
lo
lo1
4-
--___-----
.
SITTING
I
1
I
,
SIDE
SITTING
.
4
#
21
,
20-24 \
Weeks Fig.
3. Cardiac
1
28-32 Gestation output-aortic
I
38-40
o
!
.
I
101 SIDE
1
Clc3SSII (S.E.VOlWl
-.
6
l
Std. deviatfon Class I .
--------.*A
a---_
4-
May 1, 1972 J, Obstet. Gynecol.
20124
6-8 Postghl
insufficiency.
I) and two patients with Starr-Edwards aortic valve prostheses(Functional ClassII) are shown in Fig. 4. In general, cardiac output was lower than the mean for normal patients at each stage of pregnancy and post par-turn. The two patients with Starr-Edwards aortic valve prostheses showed persistently low values for cardiac output in both the supine and sitting positions during pregnancy and post partum. Fig. 5 shows data from our four patients with pulmonic stenosis(Functional ClassI). The cardiac output tended to be lower than normal in all positions and was especially evident in the sitting position, but the effect was not as marked as in patients with mitral or aortic stenosis.The heart rate and
Weeks Fig.
28-32
38:40
Gestation
4. Cardiac
output-aortic
6l8 POS&-L”rn stenosis.
stroke volume of the patients with pulmonic stenosis were usually within one standard deviation of those of the normal patients but were generally below the mean for normal . pregnant women (Table III). The hemodynamic limitation of these patients became even more apparent with exercise. In normal patients (Table IV), there was a very constant increment in cardiac output throughout gestation in response to a standardized bout of mild exercise on a bicycle ergometer. The per cent increase during exercise was similar to that encountered 6 to 8 weeks post partum (70 to 80 per cent), but the absolute change was greater during pregnancy, the increment ranging, on the average, from 4.1 to 4.6 L.
Volume Number
113 1
Responses
per minute during pregnancy as compared to 3.4 L. per minute post partum. In patients with mitral stenosis (Functional Classes I and II), however, the increase in cardiac output with exercise was markedly diminished, whether expressed as an absolute value or as a percentage of resting cardiac output, amounting to half or less of the increments achieved by normal pregnant women. Heart rate data are given in Table V. The small increase in cardiac output was achieved mostly by an increase in stroke volume. Post partum, on the other hand, the per cent rise in cardiac output evoked by standard exercise was similar in the women with mitral stenosis to that achieved by normal women, although the absolute rise in cardiac output was greater in the normal subjects. As already noted, the two patients with aortic insufficiency (Functional Class I) showed a normal rise of cardiac output (Table IV) during pregnancy, but when mild exercise was superimposed the cardiac output response was only half that seen in the normal pregnant patients. Also, the two patients with Class I aortic stenosis and the two with Starr-Edwards aortic valves (Class II) all had a diminished cardiac output response to exercise. In contrast with these results, two of three patients with pulmonic stenosis (Functional Class I) showed a normal rise in cardiac output in response to exercise. It is of interest and importance to note that all patients-both normal and those with heart disease Functional Classes I and II-showed complete hemodynamic recovery from exercise within 10 minutes at all stages of pregnancy and during the puerperium, as judged by a return of cardiac output to pre-exercise levels. Table VI shows the plasma volume, hematocrit, and blood volume changes in normal patients and in those with heart disease at 28 to 32 weeks’ gestation and 6 to 8 weeks post partum. With the exception of a rather low hematocrit in the normal patients at 28 to 32 weeks’ gestation, the values are very similar, especially when one expresses blood volume on the basis of maternal weight. During pregnancy, the normal pa-
of
heart
patients
IO-
to pregnancy
and
exercise
53
SIDE
.~
8-
-------,‘---,_
:
?3-
----a_
2 .a!
4-
<
22 ‘*
8
1
SITTING
6
-------
4
0 0
2-1
,
20-24,
I
I
28-32 38-40 Weeks Gestation Fig. 5. Cardiac output-pulmonic
6-8 Post;t”rn
stenosis.
tients had an average blood volume of 99.8 C.C. per kilogram versus 100.3 C.C. per kilogram for the patients with heart disease. Nonpregnant averages were 75.2 and 77.8 C.C. per kilogram, respectively. Comment
Fig. 6 summarizesour data on cardiac output and shows that the average in our patients with heart diseaseof Functional Classes I and II was decreased below normal, even at rest in the nonpregnant state. Pregnancy accentuated the hemodynamic deviation from normal, especially in patients with mitral stenosisor aortic stenosisand lessclearly in patients with aortic insufficiency or pulmonic stenosis.In several instances, the mean cardiac output for the patients with heart diseasewas below the normal average by more
=
sitting.
tUehnd
and
*Starr-Edwards
Sit.
=
associates.’
aortic
Ex.
Normal hear&f Range Mean Standard deviation
valve.
exercise.
4.6-7.3 5.9 21.2
8.8-12.1 10.4 +1.3
-
-
-
6.93 -
4.72 -
Aortic stenosis, Class II*
stenosis,
6.30
4.66 -
Aortic stenosis, Class I
I
5.73
3.77
Aortic insufficiency, Class II
Pulmonic Class
9.63 10.96
5.74 4.20
4.35
Ex.
5.90 7.87
1
Aortic insufficiency, Class I
2.62
3.?9
Mitral stenosis, Class II
Sit.
Weeks (
-
per minute),
20-24
(liters
3.95
output
Cardiac lesion Mitral stenosis, Class I
Table IV. Cardiac
4.8-7.6 6.0 21.0
-
3.40
4.10
6.70 6.74
230
3.93
3.97
Sit.
1
gestational
4.5-7.3 5.9 9.0
4.71 4.84 -
4.87
4.91 5.63
-
5.62 6.84
6.18 4.04 5.17 3.00
5.30 4.36
Sit.
1
a.90 7.61
6.90
5.77 7.52
a.20 9.79
7.12 4.60 7.95 5.23
7.30 6.99
Ex.
Weeks
7.2-11.5 10.0 21.5
28-32
age, and exercise
5.8-7.1 6.6 20.4
5.01 4.68 -
4.90
4.17 3.83
-
4.74 5.46
3.72 3.90
3.14 4.22
sit.
Posture
Gestation
1
I
5.5-5.7 5.6 ‘co.1
4.30 4.92 5.10
4.60
-
3.70
Sit.
7.80 7.30 6.82
-
7.00
5.41
Ex.
Weeks
9.2-11.1 10.2 tl.O
38-40 1
5.9-6.8 6.3 50.4
4.44 4.04 -
-
5.10
3.5-5.8 4.8 to.9
4.39 2.56 3.28
4.06 2.88
4.53 4.06
2.74
3.80 3.70
-
3.71 2.64
Sit.
3.45 3.48 4.41 2.62
1
6-8
-
3.89 -
Sit.
( 1
7.26 4.53 5.53
6.65 3.40
6.59 6.97
5.27
5.50 6.21
6.72 4.79 7.34 4.41
6.28 5.46
Ex.
post
5.6-10.9 a.2 21.9
Weeks 1
4.1-6.0 4.9 fO.a
4.03 3.03 3.25
3.6’ 2.36
4.14 3.76
9 ia _..
3.63 3.71
3.54 3.20 3.64 9-.3,-3
3.80 2.69
sit.
partum
is 2 Q =z m
Z 2 Y . Q z
E 2 .Q
c
lesion
and
associates.’
aortic
tUeland
deviation
*Starr-Edwards
heartst
Range Mean Standard
Normal
valve.
61-108 88 215
90 -
Aortic stenosis, Class II+
Pulmonic stenosis, Class I
114 -
102
Aortic stenosis, Class I
94-126 115 211
102
108
92
108 100
104 a5 114
Ex.
Aortic insufficiency, Class II
)
a4 86
;6
a4 90
-
Sit.
Aortic insufficiency, Class I
Mitral stenosis, Class II
Mitral stenosis, Class I
Cardiac
)
1
82-108 94 213
-
64-1 la 91 216
88 86
80
-
96 105
108 a2 116 a4
80 78
Sit.
88 100
1
)
98-132 116 212
120 120 -
92
96 120
114 126
120 a4 140 94
104 102
Ex.
28-32 Weeks
age, and exercise
96 -
102
96 90
90
;6 a0
Sit.
gestational
20-24 Weeks
Table V. Pulse rate (beats per minute),
1
78-108 95 212
104 92 -
100 99 a0
102 120
82 94
aa a4
Sit.
Posture
Gestation
1
88-105 97 f9
a0 a4 86
100 -
-
92 -
Sit.
)
120-136 128 26
loa loa 98
125
-
120
Ex.
38-40 Weeks )
96-120 108 217
86 95 80
)
115 108 a4
108 a4
102 120
92
96 100
124 92 144 100
106 94
Ex.
1
78
a2
Sit.
a co 2 Y2 0 2
96
72 76-96 86 +a
a -0
96
100 80
96
96
80
88 68
to4 a4 116 80
post partum
95-128 111 +13
Weeks
72-100 a5 f7
a1 90 78
aa 74
ii
104 -
72
-
aa 92 110 96
a3 64
Sit.
a4 73
)
6-8
-
90
Sit.
1
56
Ueland,
Novy,
and
May 1, 1972 Am. J. Obstet. Gynecol.
Metcalfe
Exercise
“I
T
(Top
of bar)
T
T
8-T : P .?? . 4 4-
est (base
2-
0
of bar) Normal
&IA1
n Ail Ii. D. q MS 0
20 - 24
Weeks II
28
-
Std.
- 32
38-40
6-8 Postpartum
Gestation deviation
Fig. 6. Cardiac output.
Table VI. Plasma volume,
hematocrit, 28-32
Plasma volume (L.) Heart
disease
Hematocrit (%I
and blood Weeks’
volume
gestation
6-8
volume I
CL.)
Weeks
post
CL.)
Hct. (%)
Blood volume (L.)
c.c./Kg.
Plasma volume
Blood
i
c.c./Kg.
parturn
patients
Range Mean Standard deviation
3.04-5.48 3.86 ‘0.65
29-43 35.9 23.50
4.32-8.48 6.05 k1.90
74.1-130.5 100.3 212.4
2.00-3.55 2.68 50.35
32-51 39.4 +4.2
3.21-6.10 4.40 to.71
65.5-94.1 77.8 28.9
6 Normal patients Range Mean Standard deviation
3.54-6.10 4.66 Al.10
27-35 31.1 T3.2
5.45-8.78 6.74 f1.31
70.5-129.7 99.8 224.0
2.40-3.06 2.72 f0.26
35-41 38.5 f4.7
3.93-5.68 4.70 to.23
64.8-87.2 75.2 kg.6
than one standard deviation. This finding was somewhat unexpected in these asymptomatic cardiac patients. In considering explanations other than their valvular heart disease, a smaller body surface area may have played a small part, although its calculation during pregnancy is of questionable validity. When postpartum weight and height were used, the average body surface area was 1.68 for our normal subjects, 1.60 for all our patients with heart disease, 1.56 for those with mitral stenosis, and 1.64 for those with aortic stenosis. Another factor which might have influenced the diminished cardiac output found in our cardiac patients is careful sodium restriction, avoidance of excessive weight gain, and use of diuretics to which they were
subjected during pregnancy. If these therapeutic measures played a part, factors other than changes in circulating blood volume must be involved, because all our cardiac patients showed a normal rise of blood volume during pregnancy (Table VI). This was also shown by Robbe.B In 1969, we reported on the hemodynamic responses to light exercise in a group of normal pregnant women.’ In six subjects, the cardiac output response to an exercise load of 100 k.p.m. per minute seemed fairly constant throughout pregnancy, with increments of 4.5 L. at 20 to 24 weeks, 4.1 L. at 28 to 32 weeks, and 4.6 L. at 38 to 40 weeks of gestation. Post partum, cardiac output rose only 3.4 L. in response to the same exer-
Volume 113 Number
Responses of heart patients
1
to pregnancy
and exercise
57
Table VII Increment Investigator Guzman 1970 Ueland 1969 Ihrman,*
*The
and
Exercise
Caplaq3
and associates,’
1960
authors’
comment:
Weeks’ gestation
load
Cardiac output
during Heart
for 4 min.
< 20 29-35 36-40
1.7 1.8 1.4
5.2 11.9 15.8
100 k.p.m.
for 3 min.
20-24 38-32 38-40
2.2 1.7 1.9
3.2 4.6 16.6
200 k.p.m.
for 6 min.
“Consistently
higher
than
non-pregnant
cise. Thus, the absolute rise in cardiac output in response to light exercise was higher during pregnancy than in the nonpregnant state. However, in our normal subjects,the average per cent rise in cardiac output was the same at all study periods, including the postpartum study, due to the fact that the resting cardiac output was significantly elevated during pregnancy. Referring again to Fig. 6, the cardiovascular response to light exercise differed from normal in patients with all types of heart disease,and the abnormality was accentuated during pregnancy. Especially in patients with mitral stenosis, the smaller rise in resting cardiac output during pregnancy, combined with a lessthan normal responseto exercise, resulted in values of cardiac output well below the mean value achieved by normal pregnant women. Post par-turn, the patients with heart disease showed a percentage rise in cardiac output during exercise that was similar to that of normal women, but the absolute values for cardiac output, at rest and during exercise, were significantly lower than those found in the normal subjects. The cardiac output and heart rate responsesof our patients with aortic stenosis were similar to those encountered in the patients with mitral stenosis, although the deviations from normal were not so pronounced. Patients with predominant aortic regurgitation and those with pure pulmonary stenosisalso showed diminished cardiac output responsesto pregnancy and to exercise.
control
Not Not Not
given given given
Stroke volume
rate
150 k.p.m.
20 28 36
exercise
9.1 12.1 14.1
Not Not Not
given* given* given* 17.5 14.5 6.2
Not Not Not
given given given
~alues.“~
Thus, it appears that valvular diseaseof all these varieties, even when symptomatically mild, results in reduced hemodynamic responsesto the demands of pregnancy and exercise. These findings are in general agreement with those reported by Robbe, who found a higher pulse rate responseto standard work loads on the bicycle ergometer during late pregnancy (36 weeks’ gestation) than post partum in patients with pure mitral valvular diseaseor mitral and aortic valvular disease combined. We studied only one patient with mitral stenosis (Functional Class I) late in pregnancy, and her heart rate increased 28 beats per minute, as compared to a rise of 23 beats per minute post partum. When all heart diseasepatients are considered, heart rate during exercise was higher at 28 to 32 weeks’ gestation (110 beats per minute) and 38 to 40 weeks’ gestation (112 beats per minute), compared to a postpartum average of 104 beats per minute. Bruce and Johnson2 showed that pregnant patients with even minimal cardiac impairment from mitral stenosis, aortic regurgitation, or congenital cardiac defects had a greater tachycardia than normal pregnant women in responseto exercise. However, their patients were studied in the recumbent position, and the altered hemodynamics produced by the gravid uterus may have influenced their results. As pregnancy advances, the hemodynamic mechanism by which an increasedblood flow is supplied to the peripheral tissuesin normal
58
Ueland,
Novy,
and
May 1, 1972 -41x1. J. Obstet. Gynecol.
Metcalfe
Table VIII Cardiac
lesion*
Functional
Mitral stenosis Mitral stenosis,$. mitral insufficiency Mitral stenosis,$ aortic stenosis, aortic insufficiency Mitral stenosis$ Mitral stenosis Mitral stenosis, aortic stenosis, aortic insufficiency Mitral stenosis Mitral stenosis Aortic insufficiency Aortic insufficiency Aortic insufficiency, mitral insufficiency Aortic insufficiency Aortic stenosis Aortic stenosis Aortic stenosis S.E. valves S.E. valves Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis Pulmonic stenosis “Predominant tCriteria $Postmitral &Starr
lesion of New
York
listed Heart
class?
Fetal weight (Gm.)
Weeks’ gestation at delivery
I I
2,540 2,848
42 41
I I
3,345 1,786 3,005
43 34 40
2,650 3,062 3,045 2,565 2,183 2,325 3,430 2,637 2,551 3,045 4,026 3,245 3,629 3,260 2,722 2.580
40 40 38 41 38 35 39 40 40 40 40 40 40 40 40 40
II II II II I I II II I I I II II I I I I
first. Association.
commissurotomy.
Edwards
aortic
valve.
women appears to change. Table VII compares the data from three studies of hemodynamic responses to exercise in normal pregnant patients. The table lists cardiac output, heart rate, and stroke volume as values in excess of those obtained in the same group of patients in the nonpregnant state. The
rise in cardiac output recorded by Guzman and Caplar? in responseto an exercise load of 150 k.p.m. for 4 minutes was quite similar to that found by the authors7 and did not increase with advancing pregnancy. The heart rate responsewas similar in all three studies and, in contrast with cardiac output, showed a progressive increase as pregnancy continued. Therefore, in normal women, with advancing gestation, the increase of cardiac output with exercise was achieved more and more by an increase in heart rate, and the stroke volume response to exercise became less as pregnancy advanced. It should be noted, however, that, according to our data, the stroke volume was higher at all stagesof gestation when compared to that of the nonpregnant individuals.
All of our pregnant cardiac patients showed an increase in cardiac output during some cardiac reserve. exercise, indicating None of the mothers encountered any diiculty attributable to their cardiac disease during pregnancy, labor, or delivery. However, several infants were born prematurely by weight or gestational age, and several more were small, even though delivered at term (Table VIII). These findings suggest that the mother with valvular heart disease, even of Class I or II severity, may have a sufficiently limited blood flow and oxygen supply to her fetus that its proper growth and development are impaired. This suggestion can be found in the analyses by Niswander and associates5of the charts of 327 pregnant women with heart disease.The incidence of birth weight I 2,000 grams was 6.1 per cent, 2,001 to 2,500 grams, 11.9 per cent, and 2 2,501 grams, 82.0 per cent. This is comparable to our figures for 21 patients of 4.8, 14.3, and 80.9 per cent, respectively. These are all quite different from those of the contol group of Niswander and associ-
Volume Number
113 1
Responses of heart patients
ates5 If the birth weights of the 12 infants delivered at 40 weeks’ gestation are analyzed, the mean weight is 3,034 grams. This is much lower than the mean birth weight reported by Babson and colleagues1 for a white middle-class population in Oregon of 3,534 grams for boys and 3,389 grams for girls. Maternal deaths due to heart disease have been reduced strikingly in the past 50 years. In our care of pregnant cardiac patients, perhaps more thought and effort should be directed toward improvement of the uterine environment for fetal growth and development. This might be accomplished by such
to pregnancy
and exercise
59
measures as : ( I ) restricting maternal physical activity; (2) stressing proper maternal posture, with avoidance of abdominal compression and the supine position; (3) maximizing the oxygen-carrying capacity of the blood by prompt and continued iron supplementation; (4) avoiding sodium restriction and the use of oral diuretics which limit the normal rise of maternal blood volume and may thereby limit cardiac output and uterine blood flow; (5) using graded elastic stockings to prevent venous pooling in the lower extremities, thus augmenting venous return.
REFERENCES
1. 2. 3. 4.
Babson, S. C., Behrman, R. E., and Lessel, R.: Pediatrics 45: 937, 1970. Bruce, R. A., and Johnson, W. P.: Clin. Obstet. Gynecol. 4: 665, 1961. Guzman, C. A., and Caplan, R.: AM. J. OBSTET.GYNECOL. 108:600,1970. Ihrman, K.: Acta Sot. Med. Ups. 65: 335, 1960.
5.
6. 7.
Niswander, K. R., Berendes, H., Deutschberger, J., Lipko, N., and Westphal, M. C.: AM. J. OBSTET. GYNECOL. 98: 871, 1967. Robbe, H.: Acta Obstet. Gynecol. Stand. 38: 1, 1959. Ueland, K., Novy, M. J., Peterson, E. N., and Metcalfe, P.: AM. J. OBSTET. GYNECOL. 104: 856, 1969.