Maternal Cardiovascular, Respiratory, and Renal Adaptation to Pregnancy

Blood Volume

An increase in plasma volume begins at 6 to 8 weeks’ gestation, reaching a maximal volume of 4700 to 5200 mL at 32 weeks, an increase of 45% (1200 to 1600 mL) above nonpregnant values. ^, The mechanism of this plasma volume expansion is unclear but may be related to nitric oxide–mediated vasodilation, which induces the renin-angiotensin-aldosterone system and stimulates sodium and water retention, protecting from hemodynamic instability after blood loss. Because maternal hypervolemia is present with hydatidiform mole, it is unlikely that the presence of a fetus is necessary for this volume expansion to occur.

Red blood cell mass increases by 250 to 450 mL, an increase of 20% to 30%, by term compared with prepregnancy values. This rise reflects increased production of red blood cells rather than prolongation of red blood cell life. Placental chorionic somatomammotropin, progesterone, and perhaps prolactin are responsible for increased erythropoiesis, which increases maternal demand for iron by 500 mg during pregnancy. In addition, 300 mg of iron is transferred from maternal stores to the fetus, and 200 mg of iron is required to compensate for normal daily losses during pregnancy, making the total requirement approximately 1000 mg. Erythrocyte 2,3-diphosphoglycerate concentration increases in pregnancy, lowering the affinity of maternal hemoglobin for oxygen. This facilitates dissociation of oxygen from hemoglobin, enhancing oxygen transfer to the fetus.

Because plasma volume increases disproportionately to the increase in red blood cell mass, physiologic hemodilution occurs, resulting in a mild decrease in maternal hematocrit, which is maximal in the middle of the third trimester. This may have a protective function by decreasing blood viscosity to counter the predisposition to thromboembolic events in pregnancy and may be beneficial for intervillous perfusion.

Anatomic Changes

Histologic and echocardiographic studies indicate that ventricular wall muscle mass and end-diastolic volume increase in pregnancy without an associated increase in end-systolic volume or end-diastolic pressure. ^, Ventricular mass increases in the first trimester, whereas end-diastolic volume increases in the second and early third trimesters. ^, This increases cardiac compliance (resulting in a physiologically dilated heart) without a concomitant reduction in ejection fraction, implying that myocardial contractility must also increase. This is supported by studies of systolic time intervals in pregnancy ^, and echocardiographic demonstration of a decreased ratio of the load-independent wall stress to the velocity of circumferential fiber shortening. An echocardiographic study of left ventricular function during pregnancy suggested that changes in long-axis performance occur earlier than changes in transverse function, resulting in eccentric hypertrophy. ^, Authors have used a sphericity index to describe the geometry of the ventricular chambers as a predictor of ventricular function. Left atrial diameter, volume, and function increase in parallel with the rise in blood volume starting early in pregnancy and continuing into the third trimester. ^, Recently, small studies have investigated the effect of maternal obesity on cardiac structure and function using newer technologies such as speckle tracking echocardiography, which may be more sensitive in detecting subclinical myocardial changes. ^, Some of these suggest left ventricular hypertrophy and diastolic dysfunction, indicating early diastolic strain compared to women with normal body mass index.

A general softening of collagen occurs in the entire vascular system, associated with hypertrophy of the smooth muscle component. This results in increased compliance of capacitive (predominantly elastic wall) and conductive (predominantly muscular wall) arteries and veins that is evident as early as 5 weeks of amenorrhea.

Cardiac Output

Cardiac output, the product of heart rate and stroke volume, is a measure of the functional capacity of the heart. Cardiac output may be calculated by invasive heart catheterization, using dye dilution or thermodilution, or by noninvasive methods such as impedance, bioreactance cardiography, and echocardiography. Limited data have been obtained from normal pregnant women by means of an invasive method. M-mode echocardiography and Doppler studies have demonstrated good correlation with thermodilution methods. These validation studies have not been performed in healthy pregnant women, and reports are limited to critically ill patients. In contrast, thoracic electrical bioimpedance, which is influenced by intrathoracic fluid volume, hemoglobin, and chest configuration (all of which change in pregnancy), has had poor correlation with thermodilution techniques, with underestimation of cardiac output during pregnancy. ^{, ,}

Cardiac output increases by 30% to 50% during pregnancy, ^{, , , , ,} and half of this increase occurs by 8 weeks of gestation. A small decline in cardiac output at term results from a decrease in stroke volume. ^, Compared with nulliparous women, parous women (without a history of preeclampsia or small for gestational age) have a significantly higher median cardiac output and cardiac index as a result of higher median stroke volume, heart rate, and left ventricular outflow diameter and lower total vascular resistance. However, in parous women with prior history of preeclampsia or small for gestational age, unfavorable hemodynamic adaptation with abrupt decline in cardiac output and increase in peripheral vascular resistance is noted in the second half of pregnancy. In normal twin gestations, maternal cardiac output increases to an even greater extent from the midtrimester of pregnancy.

Increased maternal cardiac output is caused by an increase in both stroke volume and heart rate. Stroke volume is primarily responsible for the early increase in cardiac output, ^, probably reflecting the increase in ventricular muscle mass and end-diastolic volume. Stroke volume declines toward term and may not have the capacity to respond to any further increase in preload in the third trimester. ^, In contrast, maternal heart rate, which increases from 5 weeks’ gestation to a maximal increment of 15 to 20 beats/min by 32 weeks’ gestation, is maintained ( Fig. 9.1 ). ^{, ,} Therefore in the late third trimester, maternal heart rate is primarily responsible for maintaining cardiac output.

Maternal posture significantly affects cardiac output. Turning from the left lateral recumbent to the supine position at term can result in a decrease in cardiac output by 25% to 30%. This is the result of aortocaval compression by the gravid uterus, which diminishes venous return from the lower extremities, decreasing stroke volume and cardiac output. ^, Although most women do not become hypotensive with this maneuver, up to 8% demonstrate supine hypotensive syndrome, which presents as a sudden drop in blood pressure, bradycardia, and syncope. This may result from inadequacy of the paravertebral collateral blood supply in these women, because symptomatic supine hypotensive syndrome does not appear to be associated with a decrease in baroreceptor response. This physiologic supine hypotension may affect cardiac hemodynamic parameters and dimensions as measured by cardiac magnetic resonance imaging; therefore patients having serial studies should be imaged in a consistent position. Changes in maternal position may have less effect on cardiac output in women who are overweight or obese.

The physiologic increase in cardiac output has a selective regional distribution. Uterine blood flow increases 10-fold to between 500 and 800 mL/min, a shift from 2% of total cardiac output in the nonpregnant state to 17% at term. Renal blood flow increases significantly (by 50%) during pregnancy, as does perfusion of the breasts and skin. ^, There does not appear to be any major alteration in blood flow to the brain or liver.

Blood Pressure

Arterial blood pressure decreases in pregnancy beginning as early as the seventh week. This early decrease probably represents incomplete compensation for the decrease in peripheral vascular resistance by the increase in cardiac output. Intraarterial measurements of diastolic pressures may be 15 mm Hg lower than manual determinations, whereas they may be significantly higher than automated cuff diastolic measurements. When measured in the sitting or standing positions, systolic blood pressure remains relatively stable throughout pregnancy, whereas diastolic blood pressure decreases by a maximum of 10 mm Hg at 28 weeks and then increases toward nonpregnant levels by term. In contrast, when measured in the left lateral recumbent position, both systolic and diastolic blood pressures decrease by 5 to 10 mm Hg and 10 to 15 mm Hg, respectively, below nonpregnant values. This nadir occurs at 24 to 32 weeks’ gestation and is followed by a rise toward nonpregnant values at term ( Fig. 9.2 ). Because diastolic pressures decrease to a greater extent than systolic pressures do, there is a slight increase in pulse pressure in the early third trimester. Arterial blood pressures are approximately 10 mm Hg higher in the standing or sitting position than in the lateral or supine position; consistency in position during successive blood pressure measurements is essential for the accurate documentation of a trend during pregnancy. Pregnant women who are obese have higher systolic, diastolic, and mean arterial pressures but lower resting heart rates. Additionally, women with obesity do not show the normal decline in blood pressure between the first and second trimesters of pregnancy and have greater increases in blood pressure between the second and third trimesters.

Systemic Vascular Resistance

Systemic vascular resistance is calculated by the following equation:

Systemic vascular resistance decreases from 5 weeks of pregnancy as a result of the vasodilatory effect of progesterone and prostaglandins and the low-resistance uteroplacental circulation. ^{, ,} It has been proposed that increased production of endothelium-derived relaxant factors, such as nitric oxide, initiates vasodilation and a drop in systemic vascular resistance. ^, This decrease in systemic vascular tone may be the primary trigger for increasing heart rate, stroke volume, and cardiac output in the first few weeks of pregnancy. ^, The fall in systemic vascular resistance is paralleled by an increase in vascular compliance, which reaches a nadir at 14 to 24 weeks’ gestation and then rises progressively toward term. ^,

Venous Vascular Bed

Venous compliance increases progressively during pregnancy as a result of the relaxant effect of progesterone or endothelium-derived relaxant factors on blood vessel smooth muscle or as a result of altered elastic properties of the venous wall. This results in a decrease in flow velocity and leads to stasis. Therefore pregnant women are more sensitive to autonomic blockade, which results in further venous pooling, decreased venous return, and a fall in cardiac output, which may result in a sudden decrease in arterial blood pressure.