- The cardiovascular system undergoes significant changes during pregnancy. These are adaptations that the body makes to meet increased metabolic demands of the mother and the fetus and provide adequate uteroplacental circulatory for fetal development and growth. Preeclampsia, intrauterine growth retardation, and other signs of maternal and fetal hemodynamic problems can occur if there are not enough hemodynamic changes. A maternal inability or inability to adapt to these physiological shifts can reveal underlying cardiac disease. This is what some refer to as pregnancy nature’s stress tester. In North America, maternal mortality is highest due to cardiovascular disease during pregnancy. 1 This article will review the normal cardiovascular physiology for pregnancy in order to give clinicians a foundation for understanding how cardiovascular disease can affect the mother and the fetus, and how they might need to adjust their medical care decisions.
Maternal Hemodynamic Changes
Vasodilation occurs in pregnancy. As early as 5 weeks, the systemic vasodilation occurs in pregnancy. This occurs before full placentation and the development of the uteroplacental circulatory system.2 It begins at 5 weeks.3 (Figure 1 ). This decrease can be anywhere from 35% to 40% below the baseline. Postpartum systemic vascular resistance rises to levels that are near-pregnant. Postpartum, systemic vascular resistance rises to near-pregnancy levels. This causes a decrease in serum creatinine and urea levels.7
Figure 1. A longitudinal study of detailed hemodynamics was done on 54 women who had normal pregnancies, and then at 6, 23, 33 and 33 weeks during pregnancy, and 16 weeks after birth. The radial artery waveforms of 54 women were obtained using a high-fidelity micromanometer. A central waveform was created with a validated central function. Mean arterial pressure (MAP), was calculated with integrated software. The cardiac output (CO), which was measured using a noninvasive and validated inert gases rebreathing method, was evaluated. Peripheral vascular resistance (PVR), was calculated using the formula PVR=MAP(mm Hg)x80/CO/L/min. It is shown that PVR and CO are in a reciprocal relationship during pregnancy. The preconception stage sees CO rise and fall to the second trimester. It then drops to preconception levels 16 weeks after birth. After a significant fall in the PVR (a 19% drop) during the second trimester, there was an increase in the third trimester. The return to preconception levels occurred 16 weeks later. Based on data from Mahendru and colleagues.3
The cardiac output rises throughout pregnancy.8 Therefore, invasive measuring techniques are not often used during pregnancy. Echocardiography is used most frequently to evaluate hemodynamics in pregnancy. To avoid any positional variation, cardiac output measurements are typically taken with the mother in the left-lateral decubitus position. The first trimester is when cardiac output is at its highest.9 There is much debate about whether or not cardiac output plateaus or increases. In a normal, singleton pregnancies, the cardiac output can increase by up to 45% within 24 weeks.10
Both echocardiography and cardiac magnetic imaging estimate cardiac output in pregnancy similarly. Comparative study of 34 healthy pregnant women, with images taken during the third trimester, at least 3 months after delivery, showed that both methods demonstrated an increase left ventricular end diastolic volume and an increase left ventricular mass. However, transthoracic echocardiography consistently underestimated these values.11
A twin pregnancy has a 15% higher cardiac output than a singleton. There is also a significant increase in left atrial diameter, which is consistent with volume overload. The stroke volume gradually increases in pregnancy up to the end of the second trimestre, and then it stays constant or declines later in the pregnancy.
There is a decrease of arterial pressures during pregnancy, including diastolic and systolic bloodpressures (DBP), mean arterial, and central SBP. The DBP and the mean arterial pressure both decrease during pregnancy more than the SBP. The second trimester sees arterial pressures drop to a nadir (averaging 5-10 mm Hg lower than baseline). However, these changes are more common in the early stages of pregnancy and emphasize the importance to compare hemodynamic measurements with preconceptional values. The third trimester is when arterial pressures rise and then return to preconception levels after birth. The third trimester sees blood pressure rise and return to preconception levels. These studies used different methods to assess blood pressure (automated oscillometric devices and finger arterial pressure using the volume clamp method).15 This may explain the differences in the data. Also, there are significant ethnic differences in blood pressure levels during pregnancy.
Figure 2. A longitudinal study of detailed hemodynamics was done in 54 women who had normal pregnancies. The data was collected at six, 23, 33 and 33 weeks respectively during pregnancy, and sixteen weeks after delivery. The nondominant group was able to measure blood pressure using an automated, validated measuring device. The nadir was reached in the second trimester. However, most of the decrease occurred in early pregnancy. There was an increase in blood pressure in the third and fourth trimesters. The following table shows the mean arterial, diastolic and systolic blood pressures. There are significant differences. Figure based on Mahendru and colleagues’ data.
Normal gestation sees an increase in heart rate. Contrary to many other parameters, which reach their maximum changes in the second trimester of pregnancy, the heart rate gradually increases throughout the pregnancy, increasing by 10-20 bpm each month, and reaching its maximum rate during the third trimester. 3,4,12,17
While multiple cardiovascular parameters may be altered during pregnancy, myocardial contraction6 and left and right ventricular Ejection fractions don’t appear to change.11
Sympathetic Activity & Baroreceptors
The normal level of vasomotor sympathetic activity in a pregnancy is elevated,18 which is evident as early as the 10th weeks of pregnancy.22
Pregnancy Hormonal Changes
There is a correlation between higher levels of estrogen and progesterone, and vasodilation24. Certainly, both levels rise significantly during pregnancy. The corpus luteum produces relaxin, which circulates throughout pregnancy. It is detected in the luteal stage of the ovulatory cycles. If conception occurs, serum concentrations rise to a peak at the end of the first trimester and fall to an intermediate value throughout pregnancy.25 This hormone has been demonstrated to have an endothelium-dependent vasodilatory role in pregnancy that can influence small arterial resistance vessels.26 In a Swedish observational study of pregnant women, the effects of serum concentrations of progesterone, relaxin, and estradiol on arterial blood pressure were studied. Lower mean SBPs in the third and fourth trimesters were associated with higher serum levels of progesterone and relaxin. The mean SBPs in the second and third trimesters were lower for women who had DBPs greater than 90 mm Hg later in pregnancy.
In a normal pregnancy, there is substantial activation of the renin-angiotensin-aldosterone system. Early in pregnancy, there is an increase in activity in the renin–angiotensin/aldosterone system. Plasma volume increases begin at 6-8 weeks and gradually rise to 28-28 weeks. As estrogen production rises, so does renin substrate production (angiotensinogen).32,33 This activates the renin-angiotensin and aldosterone systems and keeps blood pressure stable. The second and third trimesters see an increase of exchangeable sodium by 500 mEq (20 mg/wk)34, and a net gain in 1000 mg.7 Relaxin stimulation during pregnancy also results in increased vasopressin secretion, drinking, and water retention. Plasma osmolality decreases despite an increase in exchangeable sodium. This is what causes hyponatremic high blood pressure (Table). Table. Progesterone, a powerful aldosterone antagonist, acts on the mineralocorticoid to prevent sodium retention36 and protect against hypokalemia. The activation of the mineralocorticoid receptor by maternal aldosterone seems to be necessary for trophoblast development and normal fetoplacental function.37 Levels of maternal plasma atrial natriuretic protein increase by 40% in the third trimester. They are also 1 1/2 times normal the first week after birth, which suggests a significant role for diuresis.38
BaselineFirst TrimesterSecond TrimesterThird Trimester
Neurohumoral | Sympathetic activity
Renin/angiotensin Plasma volume* || ||| |||| |||||
RBC changes RBC mass | || || (Autotransfusion)
Chamber sizes 4-Chamber enlargement
Aorta Increased Distensibility
BP stands for blood pressure. CO is cardiac output. HR stands for heart rate. LV stands for left ventricle. RBC stands red blood cell. SVR stands systemic vascular resistance. and
*A greater increase in plasma volume than the increase in RBC masses results in physiological anemia.
Plasma Volume and Red Blood Cell Mass
The effects of erythropoietin may be enhanced by placental lactogen. Normal pregnancy results in an increase in maternal erythropoietin levels. Red cell hemoglobin levels are lower in subclinical iron deficiency.42 Normal pregnancy has a decreased erythrocyte lifespan due to “emergency haploiesis” which is caused by elevated erythropoietin.43 Plasma volume expansion is directly related to fetal growth. Preeclampsia, other medical conditions and reduced plasma volume expansion have been linked to decreased plasma volume expansion. The blood volume rises rapidly in the first few weeks and continues to increase throughout the pregnancy. The blood volume increases vary from 20% to 100% over the pre-pregnancy levels, which are usually around 45%. Plasma volume expansion is not the only factor. Erythropoiesis can also increase red blood cell production by up to 40%. The plasma volume is proportional to the red blood cells mass. This results in hemodilution and “physiological anemia”. Hemoglobin levels as low at 11 g/dL are considered physiological.