Introduction: The Importance of Maternal Health and Fetal VulnerabilityEdit
Fetal health parallels maternal health during gestation. Normal fetal development highly depends on the ability of the maternal cardiovascular system to provide sufficient oxygen and nutrients. If the mother has impaired cardiac function or significant vascular redistribution to areas other than the utero-placento-fetal complex, the supply of oxygen and nutrients to the fetus, as well as the capacity for waste and heat removal will be compromised. Furthermore, treatment and diagnostic workup of maternal heart disease may also jeopardize fetal development or viability.
Physiologic Cardiovascular and Respiratory Changes During Gravity and ParturitionEdit
The primary determinant of cardiac output is the oxygen requirement of peripheral tissues: during pregnancy the maternal VO2 increases to levels greater than 30% of the values before pregnancy. Stroke volume and heart rate therefore increase throughout pregnancy, elevating the cardiac output by more than 40%; cardiac output reaches its zenith at approximately the 20th week of gestation. This may be compounded by the concomitant fall in total peripheral resistance which also peaks at 20 weeks of gestation (maintenance of stable mean arterial pressure would require the increase in cardiac output). Left ventricular preload, however, is compromised later in pregnancy due to fetal compression of the inferior vena cava, reducing venous return from the lower extremities. The normal change in blood pressure during pregnancy includes a drop (with a nadir at approximately the 20th week of gestation) of 10-15mmHg, followed by a subsequent rise to baseline values at parturition. Positional changes, especially the supine position, can result in supine hypotensive syndrome of pregnancy, a condition which can be relieved by placement of a thin pillow underneath the right buttocks whilst the mother is in the supine position.
The mechanism of increased cardiac output during pregnancy may be caused by fluid overload (over 5 L of total body water gained.) This increase may be partially mediated by sodium retention, which begins as early as 6 weeks post-conception. Marked increases in activity of the renin-angiotensin-aldosterone system result in sodium retention. A consequence of this increase in fluid volume (most is extracellular, e.g. plasma volume) is a decrease in hematocrit to as low as 30%. Increases in cardiac stroke volume (although without change in ejection fraction) may be an intrinsic cardiac adaptation to pregnancy which increases cardiac output: this is likely due to a primary cardiac remodeling process. The maternal vasculature contributes to increased cardiac output via increased venous capacitance (we will discuss the contribution of this change to maternal thromboembolic risk,) tone, and arterial compliance4.
During labor, cardiac output increases with each subsequent uterine contraction due to a muscle pump effect on venous return and an increase in heart rate. Note that the administration of anaesthesia (epidural or general) will reduce the cardiac output. Postpartum, the cardiac output reaches approximately 10L/min1. This level of output reverts to nonpregnant levels within weeks postpartum.
Total Peripheral Resistance and Blood Flow RedistributionEdit
The total peripheral resistance in the pregnant woman decreases markedly. This may be the result of progesterone, increased diversion of blood from the arterial to the venous system as a result of the placental "arterio-venous shunt," and/or a decreased vascular responsiveness to vasopressors such as angiogensin II. Failure of the pregnant female's vascular system to decrease responsiveness to systemic vasopressors leads to pre-eclampsia.
|Summary: Potential Etiologies of Decreases in Total Peripheral Resistance During Pregnancy|
|Placental Arterio-Venous Shunt|
|Decreased vascular responsiveness to vasopressors.|
The most obvious redistribution of blood flow that occurs with pregnancy is the increase in vascular supply to the pregnant uterus (increase from 100mL/min to approximately 1200mL/min at full term.2, 3)
The venous pressure in the pregnant female increases, especially in the lower limbs. This may manifest as varicose veins, hemorrhoids, and thromboembolic events. The mechanism of increased lower limb venous pressure is likely due to aorto-caval compression and the placental arterio-venous shunt.
During pregnancy, blood volume increases 40-50%. This increase is comprised of a 40-50% increase in plasma volume and a 30-40% increase in red blood cell (RBC) volume. The increase in RBC volume is not as large in magnitude as the increase in plasma volume. This may be due to the high concentrations of sex steroids and atrial natriuretic peptide, and constant activation of the renin-angiotensin-aldosterone system.
White blood cell (WBC) count increases, with normal values reaching as high as 20,000/mL.
|In evaluating inflammatory/infectious disease with the white blood cell count, differential analysis is more valuable than total WBC count. Pregnant females may have leukocyte counts in the 15,000 range. Thus, when assessing for preterm delivery indications, fever is a much better predictor of delivery requirement.|
Estrogen is known to stimulate hepatic protein synthesis. This results in greater levels of circulating factors II, VII, IX, X, and proteins C & S.
During pregnancy, lung capacities do not change with the exception of residual volume decreasing approximately 20%. Tidal volume increases in parallel with minute ventilation, which is greater than non-pregnant levels by 40-50% (arterial blood gas analysis does in fact demonstrate compensated respiratory alkalosis).