[Physiological cardiovascular adaptation in pregnancy--its significance for cardiac diseases].
Stroke volume and heart rate rise at the very beginning of a pregnancy and decline after birth, over the course of months. Arterial blood pressure is lowered, plasma volume is increased while central venous pressure stays constant during pregnancy. The rise in cardiac output in early pregnancy can be induced quantitatively by oestrogen. The pregnancy-induced rise in cardiac output is based on the fairly general remodelling of the cardiovascular system. In a process of development, many portions of the cardiovascular system undergo programmed dilation (expansion): There is a programmed dilation of the heart, of the aorta, of the resistance vessels of the kidney and the resistance vessels of the placenta, and a programmed dilation of the venous system. All the changes favour the perfusion of the pregnant body. Cardiac dilation increases directly stroke volume, aortic dilation increases the susceptance (Windkessel function) of the aorta, the peripheral dilation increases the vascular conductance, and the venous dilation raises blood volume. Since the vascular conductance increase by peripheral dilation is higher than the increase in stroke volume, arterial pressure drops and evokes, via the baroreceptor reflex, an increase in heart rate; the increase in cardiac output occurs to an equal extent by an increase in stroke volume and an increase in heart rate. Compression of the caval vein by the pregnant uterus increases peripheral venous pressure and possibly slows down blood flow in the limbs. Increase in cardiac output means a burden for the heart, especially when associated with increase in heart rate. In this condition, cardiac energy expenditure is increased while oxygen supply is decreased. The rise in energy expenditure by an increase in flow rate is especially high for turbulent flow conditions at stenotic valves. In addition, there is an increased risk of arterial rupture by arterial remodelling and an increased risk of thrombosis by deceleration of venous blood flow velocity. Thus, the cardiovascular adaptation to pregnancy means an increased cardiovascular risk which may, on the basis of a basic cardiac disease, lead to cardiac failure.
Moll
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Institut für Physiologie, Universität Regensburg, Universitätsstr. 31 93053 Regensburg.
D000222:Adaptation, Physiological / Q000502:physiology; D001810:Blood Volume / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D007231:Infant, Newborn; D009206:Myocardium / Q000378:metabolism; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology