Cardiac output increases as a result of increases in both heart rate and stroke volume (Fig. 4). The acceleration of heart rate is evident a few weeks earlier than the increase in stroke volume and continues to increase gradually until term. The acceleration of heart rate is probably driven by the combined effects of increased venous return, increased blood volume, and decreased arterial pressure. Venous return is increased as a result of decreased arteriolar resistance and increased blood volume (see below). Although increased compliance of the great veins accommodates the increase in volume with little change in central venous pressure, stretch receptors in the walls of the vena cava and right atrium are nevertheless activated and send afferent signals to the vasomotor center, which responds with sympathetic stimulation of the sinoatrial node. This classical Bainbridge reflex (see Chapter 14) accelerates heart rate without increasing arteriolar tone. Decreased activation of baroreceptors in accordance with the decline in arterial pressure probably results in additional impetus to heart rate through decreased vagal inhibitory tone. Studies of baroreceptor reflex responses indicate that parasympathetic input to the heart is diminished in pregnant women. It is also
likely that hormones of pregnancy act directly at the level of the vasomotor center in the brain to adjust regulatory set-points.
Stroke volume increases steadily in the first half of pregnancy and thereafter remains constant until late in the third trimester, when it falls somewhat. It may be recalled (see Chapter 13) that stroke volume is determined by cardiac contractility, diastolic volume (preload), and aortic pressure (afterload). Compliance of the heart and aorta increases because of changes in physical properties of the extracellular matrix, a phenomenon called remodeling. Such remodeling is thought to occur in response to the high circulating levels of estrogens and progesterone. Increased compliance lowers resistance to ventricular filling and results in increased diastolic volume without a corresponding increase in pressure. Indeed, pregnancy produces a mild increase in heart size without a change in thickness of the ventricular walls. Increased aortic distensibility coupled with decreased peripheral resistance reduce afterload. Because the ejection fraction remains relatively constant throughout pregnancy, end diastolic volume increases and heart size is increased. Myocardial contractility per se is little changed, but force and speed of ventricular contraction increase in accordance with the Frank-Starling relationship (see Chapter 13).
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