Cardiovascular adaptation

Cardiovascular changes during pregnancy are summarized in Table 1..

Table 1 Cardiovascular and respiratory adaptation to pregnancy

Peripheral vasodilatation occurs early in pregnancy, probably mediated by endothelium-dependent factors. These include nitric oxide synthesis upregulated by estradiol and possibly vasodilatory prostaglandins (prostaglandin 12). To compensate for the consequent fall in systemic vascular resistance, cardiac output increases by 40 per cent during pregnancy. This is achieved via an increase in both stroke volume and heart rate, and begins early in gestation ( Robson,et al 1989), so that by

8 weeks the cardiac output has already increased by 20 per cent. The maximum cardiac output is found at about 20 to 28 weeks. There is a minimal fall at term. An increase in stroke volume is possible because of the early increase in ventricular wall muscle mass and end-diastolic volume (but not end-diastolic pressure) seen in pregnancy. The heart is physiologically dilated and myocardial contractility is increased. Although stroke volume declines towards term, the increase in maternal heart rate (15-20 beats/min) is maintained, thus preserving the increased cardiac output. As well as the absolute increase in cardiac output, there is also significant redistribution with a marked increase in uteroplacental flow. Differences in the effects of pregnancy hormones on endothelium-derived mechanisms and vascular reactivity may underlie this redistribution (,Welne.Le,t,,al, 1995). Standardization of cardiac output by correcting for body surface area and using a cardiac index is not justified since the correlation between cardiac output and body surface area is poor in pregnancy ( V§n,„,„OPP§D„,„§,Lat 1995).

Towards term, maternal position has a profound effect upon the hemodynamic profile of both the mother and the fetus. In the supine position, pressure of the gravid uterus on the inferior vena cava causes a reduction in venous return to the heart and a consequent fall in stroke volume and cardiac output. Turning from the lateral to the supine position may result in a 25 per cent reduction in cardiac output. Therefore pregnant women should be nursed in the left or right lateral position wherever possible. If the mother has to be kept on her back, the pelvis should be rotated so that the uterus drops forward and both cardiac output and uteroplacental blood flow are optimized.

Blood pressure is directly proportional to systemic vascular resistance and cardiac output. In early pregnancy, before the increase in cardiac output can adequately compensate for the fall in systemic vascular resistance, blood pressure begins to decrease. Indeed, it is likely that vasodilation is the primary change in the circulation in pregnancy. Blood pressure continues to decrease in the first and second trimesters of normal pregnancy until the nadir in systolic and diastolic blood pressure is reached by about 24 to 28 weeks' gestation. From then on there is a steady rise to prepregnant levels until term. Because phase V (disappearance) of Korotkoff sounds may be audible at zero cuff pressure in pregnancy, it has been traditionally recommended in the United Kingdom that phase IV (muffling) should be taken as the diastolic reading. In fact phase V is more reproducible ( ShennaD„,et,al, 1996) and correlates better with intra-arterial measurements of diastolic blood pressure.

Since a blood pressure measured using phase V as the diastolic is lower than one measured using phase IV, hypertension defined using phase V will be more severe and therefore is more closely related to outcome. In the third trimester the blood pressure should be taken with the woman sitting or lying on her side with a 30° tilt. The upper arm (when using a cuff) should be at the same level as the heart.

Although both blood volume and stroke volume increase in pregnancy, pulmonary artery wedge pressure and central venous pressure do not increase significantly. Pulmonary vascular resistance, like systemic vascular resistance, decreases significantly in normal pregnancy. This is probably why women with fixed pulmonary vascular resistance and pulmonary hypertension (e.g. Eisenmenger's syndrome) tolerate pregnancy so poorly. Although there is no increase in the pulmonary artery wedge pressure, serum colloid osmotic pressure is reduced, making pregnant women particularly susceptible to pulmonary edema. Intrapartum and postpartum hemodynamic changes

Labor is associated with a further increase in cardiac output (15 per cent in the first stage and 50 per cent in the second stage). Following delivery there is an immediate rise in cardiac output owing to the relief of inferior vena caval obstruction and contraction of the uterus which empties blood into the systemic circulation. Venous return and stroke volume are increased further by transfer of fluid from the extravascular space. Women with cardiovascular compromise are most at risk of pulmonary edema during the second stage of labor and the immediate postpartum period. Cardiac output has nearly returned to normal 2 weeks after delivery, although some pathological changes (e.g. hypertension in pre-eclampsia) may take much longer (see below).

Blood pressure usually falls immediately after delivery, although it tends to rise subsequently reaching a peak 3 to 4 days postpartum. A considerable number of previously normotensive women may become transiently hypertensive following delivery. The explanation for this phenomenon may be related to return of normal vascular tone and a period of vasomotor instability while normal non-pregnant vasoregulation is re-established. This is of particular relevance for women who develop hypertension or pre-eclampsia since, although delivery theoretically 'cures' the problem, there may be a period of postpartum deterioration and some manifestations may take several weeks to resolve. Women with hypertension in pregnancy often require antihypertensive drugs postpartum.

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