Cardiovascular and Endocrinologic Changes Associated with Pregnancy

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158 Cardiovascular and Endocrinologic Changes Associated with Pregnancy

Marie R. Baldisseri

Fundamental to the management of a critically ill pregnant woman is a thorough knowledge of the physiologic changes that occur during gestation and immediately after delivery. Clinicians must have a clear understanding of the extent of these changes, which occur in all pregnant women, to appropriately treat the critically ill patient whose additional pathology complicates the altered metabolic homeostasis and hemodynamics of the normal pregnant state. It is important to recognize that these physiologic changes add a level of complexity to diagnosis and management in the critically ill pregnant woman. The normal physiologic changes of pregnancy may alter the presentation of a disease process or illness during pregnancy, as well as alter interpretation of clinical and diagnostic examination findings in the pregnant woman. Subsequently, the endpoints of treatment can be significantly different than those for nonpregnant patients.

Some of the physiologic changes associated with pregnancy occur early in the normal course of gestation, whereas others occur during the middle or later stages. To render the most effective care of critically ill pregnant patients, the clinician must be aware of the timing of important physiologic changes. They affect almost all organ systems to varying degrees, depending in part on the gestational age of the fetus. Hemodynamic, metabolic, hormonal, and structural changes all occur during pregnancy and allow for the natural growth and development of the fetus. The pregnant woman adapts remarkably well to these changes, as does the fetus, allowing the two to coexist without harm to the other. However, if the pregnant woman is ill, either from a preexisting underlying disease process or from a new process that occurs during the pregnancy, the normal physiologic adaptive mechanisms of pregnancy can be insufficient to maintain the normal healthy union between mother and fetus. Depending on the severity of the underlying process or new illness, the hemodynamic ramifications to the pregnant woman and her fetus can be devastating and life threatening.

image Cardiovascular Changes in Pregnancy

Cardiovascular and blood volume changes are among some of the more dramatic changes that occur in pregnancy (Table 158-1). These changes are primarily adaptive mechanisms, allowing the pregnant woman to accommodate her additional metabolic needs as well as those of the fetus during gestation and immediately after delivery. Cardiac output is significantly increased during pregnancy by as much as 50% compared with nonpregnant values. Cardiac output is further increased in twin pregnancies and multiple gestations.1,2 The dramatic rise in cardiac output is seen as early as the first 6 to 8 weeks of pregnancy. After the 10th week, cardiac output is increased by 1 to 1.5 L/min and reaches a maximum value by approximately the 20th to 24th week of gestation. The early increase in cardiac output is primarily due to a significant increase in stroke volume. However, stroke volume decreases as the pregnancy advances because of aortocaval compression by the uterus and the pressure of the fetal presenting part on the common iliac vein. Caval compression occurs because the large, gravid uterus rests on the vena cava, effectively decreasing venous return to the heart and therefore decreasing ventricular preload. In the latter half of pregnancy, a progressive increase in the maternal heart rate by 15 to 20 beats/min is primarily responsible for maintaining the elevated cardiac output. The additional increase in cardiac output before labor and delivery is caused by a further increase in heart rate. Resting cardiac output either is maintained or decreases slightly as term approaches.3

TABLE 158-1 Normal Hemodynamic Changes During Pregnancy

image

Influence of Body Position

Venous return is further compromised with changes in body position, particularly if the pregnant patient is supine. As a result, cardiac output can be diminished by as much as 25% to 30%. The effects of changes in body position are most obvious in the latter half of pregnancy when the fetal size and gravid uterus can effectively tamponade the vena cava. This phenomenon is exaggerated in women with poorly developed venous collaterals. With compression of the vena cava in the supine position, these women exhibit signs of severe hypoperfusion (hypotension and bradycardia), a phenomenon described as the supine hypotensive syndrome of pregnancy. Symptoms quickly resolve after the patient is repositioned to the left lateral recumbent position.4 Cardiac output can decrease by 30% to 40% in patients with this syndrome. This vasovagal phenomenon underscores the influence of maternal body position on the hemodynamic alterations occurring in pregnancy.

Hemodynamic changes associated with a decrease in preload and, subsequently, a reduced cardiac output are less pronounced when the gravid uterus is minimally compressing the vena cava. This is optimally achieved by maintaining the pregnant woman with more than 20 weeks gestation in the full left lateral position whenever she is recumbent. Alternatives to this position, less optimal than the left lateral position but preferable to the supine position, are a left lateral tilt to 15 degrees or manual displacement of the gravid uterus. The latter maneuver of left uterine displacement can be performed by manually moving the uterus away from the midline to the left side when the patient is supine. This maneuver is particularly useful when performing cardiac compressions in a pregnant patient. In the supine position, the gravid uterus, which accounts for as much as 10% of the cardiac output, hinders successful resuscitation because of its adverse effects on intrathoracic pressure and venous return. Although hemodynamics are optimized in the left lateral position, it is difficult to achieve optimal chest compressions with the patient tilted all the way into the left lateral decubitus position. Acceptable alternatives are to perform cardiac compressions with the patient supine but with concurrent manual displacement of the uterus to the other side; it is also satisfactory to place a wedge under the right hip of the patient.5,6

Oxygen Consumption and Ventricular Performance

As cardiac output progressively increases, maternal oxygen consumption also increases. However, the increase in cardiac output is seen earlier than the rise in maternal oxygen consumption. Accordingly, the arteriovenous oxygen difference actually narrows early in pregnancy. The arteriovenous oxygen difference widens at the end of gestation. By term, there is a 20% increase in maternal oxygen consumption, mostly as a result of the increase in metabolic needs of the fetus. The increase in oxygen consumption is also a result of the increased work of ventilation during pregnancy, the increase in myocardial oxygen demand, and the increase in renal oxygen consumption. Oxygen extraction also gradually increases throughout gestation. The increase in cardiac output is probably the result of a combination of factors including increased uterine blood flow, increased maternal circulating blood volume (and hence ventricular preload), and possibly estrogen- and prolactin-induced augmentation of myocardial contractility. Ventricular dynamics are improved during pregnancy as a direct result of the action of steroid hormones on the pregnant myocardium. In animal models, estrogens have been shown to increase cardiac output and decrease peripheral vascular resistance.7 Echocardiographic studies performed in healthy pregnant women have demonstrated a decrease in the pre-ejection period of left ventricular systole but an increase in the left ventricular end-diastolic dimension.8–10 It may be that a combination of improved myocardial contractility and increased ventricular diastolic area may be responsible for increases in cardiac output during normal pregnancy.11

Hemodynamic Changes during Labor and Delivery

Although cardiac output remains relatively constant in the latter half of pregnancy, there is a significant increase during active labor and immediately after delivery. With each uterine contraction, cardiac output dramatically increases as an additional 300 to 500 mL of maternal blood volume from the uterus is returned to the heart. Cardiac output can rise to 50% greater than normal when the pregnant woman is pushing in the second stage of labor. The amount of blood returned to the heart is accentuated in the supine position. When the pregnant patient is supine, uterine contractions can cause a 25% increase in cardiac output, a 15% decrease in maternal heart rate, and a 30% to 35% increase in stroke volume. In the lateral recumbent position, the hemodynamic changes associated with uterine contractions are less pronounced; cardiac output and stroke volume may rise by only 6% to 7%, and there may be only a small change in maternal heart rate. Cardiac output may be preferentially diverted to the heart if there is partial obstruction of the abdominal aorta by the uterus during contraction.

The hemodynamic changes seen during labor and delivery are influenced by anesthetic and analgesic techniques. The increase in cardiac output is less if caudal anesthesia is used.12,13 Within the first 20 to 30 minutes after delivery of the fetus and placenta, there is an even greater increase in cardiac output, because blood is no longer diverted to the uteroplacental vascular bed. Approximately 500 mL is redirected to the maternal circulation in the so-called autotransfusion effect of pregnancy. This effect can cause cardiac output to increase by 60% to 80% after aortocaval compression is removed and blood volume is increased. Most of the physiologic changes of pregnancy resolve and revert to normal within several days after delivery. Cardiac output returns to normal within 2 weeks to 3 months after delivery as sodium and water balances normalize.

Blood Volume Changes

The changes in maternal blood volume during pregnancy are dramatic. Plasma volume increases by 30% to 50% by the end of gestation. This value is increased in the multigravida patient compared with primigravidas, but the exact mechanism responsible for this effect is unclear. The increase in blood volume can be as high as 70% with twin pregnancies. An increase of 10% to 15% in blood volume is seen as early as the seventh week of gestation. Blood volume is maximal at 30 to 34 weeks, after which the value plateaus until term.14 Ventricular filling pressures do not increase despite the large increases in plasma volume.15 This is most likely the result of concurrent decreases in systemic and pulmonary vascular resistance.

The increase in blood volume is a striking adaptive mechanism that permits additional blood flow to the uterus and other maternal organs, in particular the kidneys. Uterine blood flow increases to 100 mL/min by the end of the first trimester and reaches 1200 mL/min at term. Both sodium and water retention contribute to the increase in plasma volume. Total body water increases by approximately 6.5 to 8 L. Most of this increase is seen in the extracellular space and is preferentially distributed in the lower extremities. The total increase in body water includes approximately 3.5 L of amniotic fluid, placental fluid, and water in the fetus. The maternal blood volume increases by 1 to 2 L. Red blood cell (RBC) mass accounts for only 300 to 400 mL of the increase in total blood volume.

Plasma renin and aldosterone levels are elevated during pregnancy despite expansion of the maternal blood volume. Activation of the renin-angiotensin-aldosterone system may result from the concomitant decrease in peripheral vascular resistance and the increase in vascular capacitance seen as early as the first 6 weeks of pregnancy.2 Both estrogens and progesterone increase aldosterone levels, increasing sodium and water retention.16 At 12 weeks of gestation, atrial natriuretic peptide levels also increase, most likely in response to the increase in plasma volume.

The increase in blood volume is an adaptive mechanism that provides some level of protection for the inevitable blood loss that accompanies delivery of the fetus and placenta. Average blood loss during vaginal delivery is 500 mL; average blood loss during cesarean delivery is approximately 1000 mL. Although providing some degree of protection from peripartum blood loss, the increased plasma volume associated with pregnancy also can lull the clinician into a false sense of security. A pregnant woman can lose up to 35% of her blood volume before the usual signs of hypovolemia and acute hemorrhage are obvious. Although the pregnant woman may appear to have stable vital signs up to this point, the fetus may be severely compromised and deprived of adequate maternal blood flow. Tachycardia, hypotension, and other signs of hemodynamic instability are late manifestations of a significant deficit in maternal blood volume.

Physiologic Anemia of Pregnancy

Accompanying the increase in blood volume is an increase in RBC mass stimulated by increased circulating levels of erythropoietin. The RBC mass increases during the second trimester and continues to increase progressively throughout the pregnancy. However, the increase of 15% to 20% in RBC mass is disproportionate to the 30% to 50% increase in blood volume. As a result, the hematocrit decreases, resulting in the “physiologic hemodilutional anemia” of pregnancy. Hemodilution is most notable during the 30th to 34th gestational weeks. The hemoglobin concentration can decrease by as much as 9%. In the second trimester, the hemoglobin level can decrease to 11 to 12 g/100 mL, compared with the normal nonpregnant value of 13 to 14 g/100 mL. The decrease in blood viscosity associated with the anemia of pregnancy allows for decreased resistance to blood flow and facilitates placental perfusion. The hematocrit decreases until the end of the second trimester but increases later in the pregnancy, when the increase in RBC mass is proportionate to the increase in plasma volume. The hematocrit stabilizes at that point or even increases slightly as term approaches.

The degree of change in RBC mass during pregnancy depends in part on whether iron is supplemented. With the increase in RBC mass, there is a need for additional iron to prevent the development of iron-deficiency anemia. Maternal requirements for iron can increase to 5 to 6 mg/d. The fetus uses iron from maternal stores to prevent fetal anemia, but the presence of significant maternal iron-deficiency anemia has been shown to result in a higher incidence of fetal complications, including preterm labor and late spontaneous abortions.17

Renal Blood Flow During Pregnancy

Under the influence of circulating hormones, there is a preferential redistribution of blood flow to the uterus, breast, and kidneys during pregnancy. Each kidney increases in length and weight, and the renal pelvis and ureters dilate. The glomerular filtration rate (GFR) increases by 50%, and renal blood flow increases by 25% to 50%. Changes in GFR and renal blood flow occur by the sixth week of gestation. The increase in renal blood flow plateaus early in pregnancy and remains unchanged or decreases slightly as term is approached. Urine flow and sodium excretion are increased and are influenced by position, especially in late pregnancy. Flow rates and the sodium excretion rate are significantly higher in the lateral recumbent position compared with the supine position. Concentrations of serum creatinine and blood urea nitrogen are reduced proportionately to the increase in GFR. Glycosuria may also occur during pregnancy as a result of the increase in GFR and impaired tubular reabsorption of glucose.

Changes in Blood Pressure and Vascular System

Arterial blood pressure decreases as early as the sixth week of pregnancy; the lowest diastolic pressures are recorded during the second trimester. By the eighth week of gestation, diastolic blood pressure decreases by approximately by 10%. Diastolic pressure reaches a nadir at 16 to 24 weeks and is typically 5 to 10 mm Hg less than normal. After the 16th gestational week, blood pressure progressively increases and is back to baseline by term. With the increase in venous return associated with uterine contractions and the additional factors of pain, anxiety, and stress during labor and delivery, an increase in blood pressure usually occurs during this time. The decrease in blood pressure during pregnancy is associated with a significant decrease in peripheral vascular resistance. The decrease in arteriolar tone is influenced by several factors, including hormonal changes that induce vasodilatation and lack of responsiveness to the pressor effect of angiotensin II.18 There is evidence for blood vessel remodeling in pregnancy, leading to increased venous compliance.19,20 During pregnancy, circulating levels of numerous endogenous procoagulant and anticoagulant proteins change, leading to a hypercoagulable state. As a consequence, the risk of venous thrombosis increases during pregnancy. The reported incidence is 0.7 cases per 1000 women, and this rate increases threefold to fourfold in the postpartum period.21

The treatment of choice for severe hypotension resulting from acute hemorrhage, sepsis, or other critical illness during pregnancy is (ideally) aggressive fluid resuscitation. However, in cases of fluid-unresponsive hypotension, vasopressors must be used to prevent detrimental consequences to both the mother and fetus as a result of inadequate uterine blood flow secondary to hypotension. Most vasopressors increase maternal blood pressure at the expense of fetal blood flow, inducing vasoconstriction of the uterine vessels. There are few human studies of these agents in pregnant women. However, animal studies animals indicate that ephedrine and dopamine increase uterine blood flow to the uteroplacental circulation while at the same time increasing maternal blood pressure.22

Structural Remodeling of the Heart

The heart is dramatically remodeled during the first few weeks of pregnancy. There is enlargement of all four chambers. The valvular annular diameters increase, as does the thickness of the left ventricular wall. End-diastolic volume increases, although end-diastolic pressure remains unchanged.10,20 Chamber enlargement, particularly of the left atrium, may be a predisposing factor for supraventricular and atrial arrhythmias. Nonspecific ST-T wave changes may also be found in asymptomatic pregnant woman.

As the uterus enlarges and the diaphragm elevates, the heart is rotated upward and to the left. The apical impulse on physical examination is heard best over the fourth intercostal space, lateral to the midclavicular line. Left axis deviation is seen on the electrocardiogram as a result of the rotation of the heart. Because of the displacement of the heart, pregnant women may appear to have cardiomegaly on the chest radiograph. In addition, lung markings may be more prominent, suggesting vascular congestion. These changes can be similar to those seen in patients with heart disease. Even in women with no underlying cardiac pathology, the normal physiologic changes of pregnancy can result in signs and symptoms that are difficult to differentiate from those associated with cardiac disease. Symptoms such as fatigue, decreased exercise tolerance, peripheral edema, palpitations, chest pain, dyspnea, and orthopnea are common complaints as pregnancy advances.

New murmurs often appear during pregnancy. Systolic flow murmurs and a third heart sound are common but are soft. Mild pulmonic and tricuspid regurgitation occurs in more than 90% of healthy pregnant woman.23,24 One-third of pregnant women have evidence of clinically insignificant mitral regurgitation. Diastolic, pansystolic, and late systolic murmurs are rare in normal pregnancy and may indicate underlying heart disease. Bruits originating from the internal mammary artery and venous hums with diastolic components are common during pregnancy. These findings can initially confuse the diagnosis of a more serious underlying cardiac illness.

Cardiac Disease and Pregnancy

In women with significant cardiac pathology, the hemodynamic aberrations associated with pregnancy can be life threatening. The incidence of significant cardiac disease in pregnancy is less than 2% but is increasing.25,26 Advances in medical therapy and in cardiac surgery have allowed female cardiac patients to survive to childbearing age and to have successful term pregnancies.27 For women with severe cardiac problems such as pulmonary hypertension, Eisenmenger’s syndrome, severe mitral stenosis, or Marfan syndrome (in which the risk of aortic dissection is high during pregnancy), the physiologic changes of pregnancy can increase both maternal and fetal morbidity and mortality by transiently or permanently worsening the underlying heart disease.28 Increases in blood volume, stroke volume, cardiac output, and heart rate and the decrease in systemic vascular resistance are poorly tolerated by pregnant women with severe underlying cardiac disease. Maternal mortality is less than 1% for patients with less severe cardiac problems, but it increases to 50% if pregnancy is associated with the presence of underlying primary pulmonary hypertension or cyanotic disorders such as Eisenmenger’s syndrome.29,30

Approximately 90% of pregnant women with cardiac disease are rated as New York Heart Association (NYHA) functional class I or class II. These patients tolerate the hemodynamic changes of pregnancy and can be managed well with medical therapy, although the incidence of heart failure and arrhythmias tends to be higher in this group of patients.31 The 10% of pregnant patients with NYHA functional class III or IV heart disease account for 85% of cardiac deaths.32 Fetal morbidity and mortality are increased in these patients, and there is a higher incidence of prematurity, miscarriage, and intrauterine growth retardation.33 Cardiac telemetry, fetal monitoring, and hemodynamic monitoring are usually necessary for these high-risk patients during labor and delivery and, because of the large changes in intravascular volume after delivery, during the first few postpartum days.

image Endocrine and Metabolic Changes in Pregnancy

There are numerous endocrine and metabolic alterations during pregnancy, many of which are directly attributable to hormonal signals originating from the fetoplacental unit. Maternal adaptations to hormonal changes that occur during pregnancy directly influence the growth and development of the fetus and placenta. In pregnancy, there is also a change in the normal hormonal feedback mechanisms that control the synthesis and release of hormones. As with cardiac disease, the presentation of endocrine and metabolic disorders may be difficult to differentiate from the normal hypermetabolic state of pregnancy.

Hypothalamic and Pituitary Alterations

As in the nonpregnant state, the hypothalamic-pituitary axis is responsible for regulating many aspects of metabolism. Circulating levels of most of the releasing hormones of the hypothalamus increase during pregnancy because of increased production by the placenta rather than increased production and release by the hypothalamus. The target organ of the hypothalamus, the pituitary gland, undergoes remarkable structural and metabolic changes in pregnancy. Its size increases almost threefold secondary to estrogen stimulation. Gonadotropin and growth hormone production decrease during pregnancy. However, synthesis of ACTH, prolactin, and thyroid-stimulating hormone (TSH) increases.

Free and bound cortisol levels are increased in pregnancy, even though circulating ACTH concentrations are elevated. These changes suggest that the normal negative feedback loop between ACTH and cortisol concentrations is altered in the pregnant state.34 Free plasma cortisol concentrations may be two to three times higher than normal at term. Diurnal variation of cortisol is blunted but maintained throughout pregnancy. The clinical signs of weakness, peripheral edema, glucose intolerance, and weight gain associated with Cushing’s disease are sometimes difficult to differentiate from the clinical features of normal gestation. The symptoms of Cushing’s disease are exacerbated by pregnancy but often resolve after delivery. Improved outcomes are seen with surgical therapy intrapartum, if pituitary or adrenal tumors are discovered during the course of the pregnancy.35,28 In normal pregnancy, cortisol release may not be suppressed with a low intravenous dose (1 mg) of dexamethasone. An 8-mg dose of dexamethasone is usually needed to suppress cortisol secretion if a tumor is present. In patients with occult adrenal insufficiency, a life-threatening adrenal crisis may be precipitated by the stress of labor and delivery. During pregnancy, the signs and symptoms may be vague and nonspecific, but with the stress of labor, these symptoms are exaggerated. The clinical diagnosis is made in conjunction with laboratory evidence of a low cortisol level or even a low-normal level and no increase in the plasma cortisol concentration with an ACTH stimulation test. Immediate treatment with stress doses of hydrocortisone is indicated in these patients.

In preparation for lactation, circulating prolactin levels progressively increase to about 10 times normal during the course of pregnancy, secondary to stimulation of the anterior pituitary by placental estrogens and progesterone. The dramatic increase in plasma prolactin concentration may lead to an increase in size of preexisting pituitary adenomas larger than 1 cm.36 Symptoms resulting from an increase in prolactin secretion usually subside within 6 weeks after delivery if the patient is not breastfeeding.

TSH secretion is transiently decreased in the first trimester, but circulating TSH concentrations are usually increased by term. Circulating levels of thyroxine (T4) and triiodothyronine (T3) increase as a result of a twofold estrogen-stimulated increase in the synthesis of thyroxine-binding globulin. Levels of free (dialyzable) T4 and free T3 are unchanged. The thyroid gland does not increase in size, despite the increase in production of thyroid hormones. Pregnant women who obtain sufficient dietary iodine (more than 200 µg daily) have no untoward complications from the changes in thyroid function.37,38

Posterior pituitary hormones are altered in pregnancy. Circulating oxytocin levels increase, but the vasopressin concentration remains essentially unchanged. Plasma osmolality decreases by 5 to 10 mOsm/kg, suggesting that the threshold for secretion of vasopressin decreases during gestation. Although vasopressin levels remain unchanged, some women develop transient diabetes insipidus during pregnancy.39

Changes in Glucose Metabolism

Early in pregnancy, glucose metabolism is influenced primarily by increased levels of estrogens and progesterone, which induce pancreatic β-cell hyperplasia and increased insulin secretion. Glucose metabolism is primarily controlled by placental hormones later in the pregnancy in response to the increased nutritional and metabolic demands of the fetus. Circulating glucose and insulin levels fluctuate widely depending on the nutritional state of the mother. Morning fasting levels of glucose can decrease to less than 55 mg/dL. Fasting blood glucose levels decrease by 10% to 20% because of increased peripheral glucose utilization, decreased hepatic glucose production, and increased consumption of glucose by the fetus.

Pregnant women with diabetes mellitus experience more hypoglycemic episodes in the first trimester, because hepatic gluconeogenesis is decreased during this period. Insulin secretion increases during pregnancy. There is a relative state of insulin resistance, as evidenced by postprandial maternal hyperglycemia.40 Normally, women adapt to the state of relative insulin resistance during pregnancy. However, those women with marginal pancreatic reserve or preexisting insulin resistance due to obesity may not produce sufficient insulin, leading to the development of gestational diabetes mellitus. Pregnant women with preexisting diabetes mellitus require as much as 30% more insulin than before pregnancy. There is a close correlation between maternal blood glucose levels and glucose uptake and utilization by the fetus, because glucose crosses the placental barrier. Poor maternal glucose control worsens fetal morbidity. For patients with preexisting insulin-dependent diabetes mellitus, fetal and neonatal mortality rates have decreased significantly, from 65% to between 2% and 5%, as a result of implementing strict metabolic glucose control with insulin.41

Lipid metabolism is accelerated in pregnancy, and the circulating concentrations of triglycerides and cholesterol increase. Increased production of triglycerides allows for maternal consumption while sparing glucose for use by the fetus.42 Lipolysis is stimulated in adipose tissue, and there is a release of glycerol and fatty acids that decreases maternal glucose utilization, additionally sparing glucose for the fetus.

Key Points

1 Normal pregnancy is associated with numerous physiologic changes that affect almost all maternal organ systems.
2 Hemodynamic, metabolic, hormonal, and structural changes that occur during pregnancy are adaptive mechanisms for maintaining a healthy homeostasis between the mother and the fetus.
3 Maternal hemodynamic alterations and poor fetal outcome can occur if the physiologic adaptive mechanisms are insufficient to maintain the normal homeostasis between the mother and the fetus.
4 The physiologic changes occur at different stages throughout the pregnancy.
5 The normal physiologic changes of pregnancy may alter the presentation of a maternal disease process, confound the diagnosis, or alter the endpoints of treatment.
6 Cardiac output is increased significantly, up to 50% above prepartum values, by the 24th week of gestation. The value then plateaus until term. During labor and delivery, cardiac output is further increased with uterine contractions and the “auto-transfusion” effect of increased preload after delivery of the fetus and placenta.
7 The increase in cardiac output early in pregnancy is primarily caused by an increase in blood volume. Later in pregnancy, an increase in the heart rate by 15 to 20 beats/min is mainly responsible for the increase in cardiac output. Improved myocardial contractility may account in part for an improvement in cardiac output in pregnancy.
8 Maternal body position directly affects cardiac output and stroke volume. In the supine position, the gravid uterus causes aortocaval compression and decreased preload. An extreme manifestation of this effect is the “supine hypotensive syndrome” of pregnancy.
9 After the 20th week of gestation, pregnant women should not be placed supine but rather in the left lateral recumbent position, which maximizes maternal hemodynamics. During cardiac resuscitation, the pregnant patient should be placed in this position, or manually displace the uterus to the left.
10 Left ventricular end-diastolic volume is increased during pregnancy, but filling pressures are relatively unchanged; this may reflect the decrease in afterload caused by a decrease in systemic and pulmonary vascular resistance.
11 Blood volume increases by 30% to 50% by the end of gestation. However, red blood cell mass increases by only 15% to 20%, creating the “physiologic anemia” of pregnancy.
12 A pregnant woman can lose up to 35% of her blood volume before tachycardia and hypotension occur as a result of acute hemorrhage or severe hypovolemia.
13 Blood flow is increased to many organs during pregnancy, especially to the breasts, uterus, and kidneys. Renal blood flow increases by 25% to 50%, and the glomerular filtration rate increases by up to 50%, with a decrease in the plasma creatinine and blood urea nitrogen concentrations.
14 A decrease in the diastolic blood pressure by 10% is seen in the second trimester, secondary to the decrease in systemic vascular resistance. By the end of pregnancy, blood pressure levels should increase to prepartum values.
15 Blood vessel remodeling and changes in the coagulation system during pregnancy, including an increase in most clotting factors, makes the pregnant woman hypercoagulable and more susceptible to venous thromboembolism throughout pregnancy and in the postpartum period.
16 Remodeling of the heart causes enlargement of all four chambers. The pregnant woman may be more susceptible to supraventricular and atrial arrhythmias because of left atrial enlargement.
17 Systolic ejection murmurs and a third heart sound can commonly be heard during pregnancy. Diastolic, pansystolic, and late systolic murmurs should prompt the clinician to look for an underlying cardiac problem.
18 Pregnant patients with mild to moderate cardiac disease usually tolerate the hemodynamic changes of pregnancy. Those patients with pulmonary hypertension and right-to-left shunts have mortality rates as high as 50%.
19 There are numerous endocrine and metabolic alterations during pregnancy that primarily affect the hypothalamus, pituitary, and adrenal glands. As with cardiac disease, the presentation of a patient with endocrine and metabolic disorders may be difficult to differentiate from the normal hypermetabolic state of pregnancy.
20 Both corticotropin (ACTH) and cortisol levels are elevated in pregnancy. Cushing’s syndrome can be exacerbated by pregnancy. Acute adrenal crisis may be precipitated by the stress of labor and delivery. The treatment is immediate glucocorticoid administration.
21 In preparation for lactation, prolactin levels are increased 10-fold throughout the pregnancy as a result of estrogen and progesterone stimulation. This increase in prolactin may increase the size of pituitary adenomas and precipitate symptoms during the pregnancy.
22 Thyroid hormones are increased during pregnancy as a result of increased synthesis of thyroxine-binding globulin. Free levels are unchanged. Despite the complex thyroidal changes that occur during pregnancy, pregnant women have no untoward complications if their daily iodine intake is sufficient.
23 Transient diabetes insipidus can develop during pregnancy, secondary to a state of vasopressin resistance.
24 Large fluctuations in glucose and insulin levels are seen in pregnancy, depending on the nutritional state of the mother. Fasting glucose levels can decrease by 10% to 20%.
25 During pregnancy, there is increased insulin secretion, with a relative state of insulin resistance.
26 Obese women with insulin resistance and women with marginal pancreatic reserve can develop gestational diabetes mellitus.
27 Fetal and neonatal mortality rates are low if strict metabolic glucose control with insulin therapy is maintained.
28 Maternal lipid metabolism is increased during pregnancy, allowing for increased glucose utilization by the fetus.

Annotated References

2005 2005 American Heart Association Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 10:8: cardiac arrest associated with pregnancy. Circulation. 2005;112:IV-150.

Recommendations and guidelines for CPR and ACLS drug administration in pregnancy are presented by the AHA. Evidence extrapolated from peri-arrest resuscitation scenarios indicated that ultrasound assessment undertaken by trained rescuers may help to identify intraabdominal hemorrhage as a cause of cardiac arrest in pregnancy in the hospital setting. Clinicians are advised to identify common and reversible causes of cardiac arrest in pregnancy during the resuscitation attempts. The use of abdominal ultrasound by a skilled operator should be considered in detecting pregnancy and possible causes of cardiac arrest in pregnancy, but this should not delay other treatments.

Clark SL, Cotton DB, Lee W, et al. Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol. 1989;161:1439.

This landmark paper presents central hemodynamic data obtained with the use of a pulmonary artery catheter during pregnancy and after delivery. Ten primigravidas patients in late pregnancy (between the 36th and 38th weeks of gestation) underwent pulmonary artery catheter and arterial catheter placement. These same patients were restudied with a pulmonary artery catheter at 11 to 13 weeks after delivery. All measurements were performed with the patient in the left lateral recumbent position. The authors found significant decreases in systemic vascular resistance, pulmonary vascular resistance, colloid oncotic pressure, and colloid oncotic pressure-pulmonary capillary wedge pressure gradient in the third-trimester measurements (P <.05). A significant rise in cardiac output and heart rate was seen in all patients before delivery (P <.05). No significant changes in pulmonary capillary wedge pressure, central venous pressure, left ventricular stroke work index, or mean arterial pressure were found. Although blood volume and preload are elevated in pregnancy and end-diastolic volume increases, there were no substantial increases in the filling pressures of the heart as measured by the pulmonary artery catheter, suggesting a decrease in afterload with the decrease in the systemic and pulmonary vascular resistance.

Snow V, Qaseem A, Barry P, et al. Management of venous thromboembolism: a clinical practice guideline from the American College of Physicians and the American Academy of Family Physicians. Ann Intern Med. 2007;146:204.

Recommendation 4: There is insufficient evidence to make specific recommendations for types of anticoagulation management of VTE in pregnant women. During pregnancy, women have a fivefold increased risk for VTE compared with nonpregnant women. Clinicians should avoid vitamin K antagonists in pregnant women, because these drugs cross the placenta and are associated with embryopathy between 6 and 12 weeks’ gestation, as well as fetal bleeding (including intracranial hemorrhage) at delivery. Neither LMWH nor unfractionated heparin crosses the placenta, and neither is associated with embryopathy or fetal bleeding.

Burt CC, Durbridge J. Management of cardiac disease in pregnancy. Contin Educ Anaesth Crit Care Pain. 2009;9:44.

This article is an excellent review of cardiac disease in pregnancy, focusing on the different causes of cardiac disease and their management in pregnancy. Cardiac disease is the most common cause of mortality in pregnancy and may present with cardiovascular decompensation during pregnancy, at the time of delivery, or immediately postpartum. The goals of therapy are: early risk assessment, optimization, regular monitoring for deterioration, planning of delivery, and surveillance for deterioration in the immediate postpartum period. Vaginal delivery with low-dose regional analgesia and careful fluid management is the preferred method of delivery and cesarean section deliveries should be reserved for obstetric indications.

Van De Velde M, De Buck F. Anesthesia for non-obstetric surgery in the pregnant patient. Minerva Anestesiol. 2007;73:235-240.

Surgery during pregnancy is relatively common. This review of the literature focuses on relevant issues such as maternal safety during nonobstetric surgery in pregnancy, teratogenicity of anesthetic drugs, avoidance of fetal asphyxia, prevention of preterm labor, the safety of laparoscopy, and the need to monitor the fetal heart rate and will finally give a practical approach to manage these patients.

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