CARDIOVASCULAR CHANGES IN PREGNANCY

Oestrogen and progesterone mediated relaxation of
vascular smooth muscle in pregnancy cause vasodilatation
reducing the peripheral vascular resistance by 20%.
Consequently systolic and diastolic blood pressures fall.
Areflex increase in heart rate by 25% together with a 25%
increase in stroke volume, results in a 50% increase in
cardiac output. During labour cardiac output may increase
further by up to 45%. Cardiac contractility remains
unchanged. The rise in cardiac output is facilitated by
anatomical changes, namely left ventricular hypertrophy
and dilatation.
In the supine position the gravid uterus can compress the
inferior vena cava. This will reduce venous return to the
heart resulting in a decrease of cardiac output, maternal
blood pressure and placental perfusion. The descending
aorta can also be compressed by the uterus causing a
reduction in uterine blood flow. Aortocaval compression
must be considered as a cause of maternal hypotension
from the end of the 1st trimester onwards, though it
typically occurs after 20 weeks gestation