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Cardiovascular and endocrinologic changes associated with pregnancy
Fundamental to the management of a critically ill pregnant woman is a detailed knowledge of the normal physiologic changes that occur during gestation and immediately after delivery. Some of these physiologic adaptations are from the hormonal changes associated with pregnancy, and others are to support the mother and the growing fetus. Clinicians must have a good understanding of the extent of these changes, which occur in all pregnant women, to appropriately diagnose and treat critically ill patients whose additional pathology complicates the distinct 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 baseline physiologic changes of pregnancy often alter the presentation of a disease process or illness that presents during pregnancy, and they can unmask a previously silent disease process of the woman. The normal physiologic maternal adaptations will change the interpretation of clinical and diagnostic examination findings in the pregnant woman. Subsequently, the endpoints of treatment can be significantly different from those for nonpregnant patients. To detect early signs of deterioration in a critically ill pregnant patient, modified early obstetric warning score (MEOWS) charts have been introduced in some obstetric centers. ,
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 healthy pregnant woman adapts remarkably well to these changes, as does the fetus, allowing the two to coexist symbiotically without harm to the other. However, if the pregnant woman is ill, either from a preexisting underlying disease process or from a new pathologic process that occurs during the pregnancy, the normal physiologic adaptive mechanisms of pregnancy are often 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.
Cardiovascular changes in pregnancy
Cardiovascular and blood volume changes are among some of the more significant changes that occur in pregnancy ( Table 131.1 ). These changes are primarily adaptive mechanisms, allowing the pregnant woman to accommodate her additional metabolic needs in addition to 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 increased by 15% in twin pregnancies and in multiple gestations. An increase in cardiac output is seen as early as the first 6–8 weeks of pregnancy. A series of meta-analyses of singleton pregnancies found that cardiac output peaks during the early third trimester: 1.5 L/min (31%) above nonpregnant values. Cardiac output can increase by 75% by the end of the third trimester. The early increase in cardiac output is primarily the result of 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, decreasing venous return to the heart and therefore effectively decreasing ventricular preload. In the latter half of pregnancy, a progressive increase in the maternal heart rate by 15–20 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. ,
TABLE 131.1
Normal Hemodynamic Changes During Pregnancy
| Physiologic Parameter | Term Pregnancy | Labor and Delivery | Postpartum |
|---|---|---|---|
| Cardiac output | Increases 30%–50% | Increases 50% | Increases 60%–80% within 15–20 min |
| Blood volume | Increases 30%–50% | Additional 300–500 mL with each contraction | Decreases to baseline |
| Heart rate | Increases by 15–20 beats/min | Increase depends on stress and pain relief | Decreases to baseline |
| Blood pressure | Decreases by 5–10 mm Hg in midpregnancy | Increase depends on stress and pain relief | Decreases to baseline |
| Systemic vascular resistance | Decreases | Increases | Decreases to baseline |
| Oxygen consumption | Increases by 20% | Increases with stress of labor and delivery | Decreases to baseline |
| Red blood cell mass | Increases by 15%–20% | — | — |
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%–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, the abdominal aorta, and the iliac arteries. 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. Cardiac output can decrease by 30%–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 decreases in preload and cardiac output are less pronounced when the gravid uterus is minimally compressing the vena cava, which is optimally achieved by maintaining the pregnant woman at greater than 20 weeks’ gestation in the left lateral position when 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 best in the left lateral position, it is difficult to achieve optimal chest compressions with the patient in this 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 firm wedge under the right hip of the patient. ,
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 maternal increased work of ventilation during pregnancy, maternal increase in myocardial oxygen demand, and maternal 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. Echocardiographic studies performed in healthy pregnant women have demonstrated a decrease in the preejection period of left ventricular systole but an increase in the left ventricular end-diastolic dimension. 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.
Hemodynamic changes during labor and delivery
Although cardiac output remains relatively constant in the third trimester, there is a significant increase during active labor and immediately after delivery. With each uterine contraction, cardiac output dramatically increases as an additional 300–500 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%–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%–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. , Within the immediate 20–30 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 increase cardiac output by 60%–80% after aortocaval compression is removed and blood volume is increased. Many 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.
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