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HEMODYNAMIC CHANGES DURING PREGNANCY, DELIVERY AND POSTPARTUM
PERIOD
Pregnancy and childbirth require significant adaptation of the cardiovascular system in the mother to cope
with the increased metabolic demands of the mother and fetus. The various hemodynamic changes that
occur during pregnancy in normal women are highlighted in Figure 1A. The usual pattern of hemodynamic
adaptation to pregnancy is attenuated in women with CHD . Moreover, these hemodynamic alterations
[16]
can sometimes have deleterious effects on the mother with CHD as well as on the developing fetus.
Plasma volume and cardiac output reach a maximum of 40%-50% above baseline at 32 weeks of gestation,
while 75% of this increase occurs by the end of first trimester. These are then maintained at the same level
throughout the pregnancy. The increase in cardiac output is initially achieved by an increase in stroke
volume in the first half of pregnancy and a gradual increase in heart rate after this period [17,18] . The heart size
increases while ventricular function is preserved. In women with CHD, ventricular adaptation to pregnancy
may be suboptimal and can result in impaired uteroplacental flow and suboptimal fetal outcome .
[19]
There is generally a minor change in systolic blood pressure (BP), but there is a fall in diastolic BP due to
hormone-induced vasodilation. Diastolic BP reaches a minimum of 10 mmHg below baseline in the second
trimester of pregnancy and returns to pre-pregnancy levels by term [17,18] . In the third trimester, BP can
decrease due to the compression of the inferior vena cava by the enlarged uterus, especially in the right
decubitus position or while lying supine. Since the fall in BP is primarily due to the fall in systemic vascular
resistance, it is likely to aggravate the right-to-left shunt in cyanotic CHD.
Patients with CHD are at higher risk of arrhythmias due to intrinsic conduction abnormalities, residual
hemodynamic problems, and operative scars, and they are further burdened by the tachycardia and volume
overload due to pregnancy . The occurrence of tachyarrhythmias or failure to adequately increase heart
[20]
[21]
rate can cause decompensation and adverse outcomes . The incidence of arrhythmias was ~2% in one of
the largest registries of pregnant CHD patients . The fragility of the arterial wall increases during
[22]
pregnancy due to increased serum levels of estrogen and relaxin. This is an adaptive response during
pregnancy but can result in formation of ascending aortic aneurysms or even dissection of aorta in
predisposed women, e.g., women with bicuspid aortic valve, coarctation of aorta, and Marfan syndrome [23,24] .
The red blood cell counts increase by 20%-30%, and the increased plasma volume causes relative anemia.
There is a hypercoagulable state in late pregnancy due to an increase in vitamin K-dependent clotting factor
and a reduction in free protein S. This is of particular concern in pregnant women with prosthetic heart
valves, atrial fibrillation, preexisting ventricular dysfunction, or uncorrected CHD. In contrast to the 0.1%
risk of thromboembolism risk in normal pregnancy , the rate of thromboembolism was found to be 1.2%
[25]
in those with CHD as per a recent multicentric registry . Other obstetric issues such as hypertensive
[22]
disorders of pregnancy, preeclampsia, or multiple pregnancies further increase the risk of maladaptation to
hemodynamic needs and thus the risk of cardiovascular complications in susceptible patients .
[3,5]
Further changes in hemodynamics occur at the time of labor and delivery. Cardiac output and other
hemodynamic parameters fluctuate markedly with each uterine contraction . The changes during normal
[17]
labor are shown in Figure 1B. The BP and cardiac output increase during labor and post-partum. Volume
shifts at the time of delivery is poorly tolerated by women with some CHD where cardiac output is highly
dependent on preload . After delivery, the cardiac output and heart rate start decreasing as early as 24 h
[20]
after delivery.