Uteroplacental blood flow is directly related to maternal blood volume and arterial pressure. Support of maternal blood volume and oxygenation is the best way to prevent fetal hypoxia. With this principle in mind, a detailed understanding of cardiac arrest physiology is important. A full discussion of fetomaternal physiology can be found in Chap..99, but several points are discussed and put in perspective here.
The maternal cardiovascular system undergoes dramatic changes. Cardiac output increases to 30 to 45 percent above baseline levels by the twentieth week of gestation and remains at that level until delivery. In addition, the mean arterial blood pressure gradually falls throughout the first two trimesters of pregnancy and returns to baseline levels by term. This change is a result of decreased resistance in the pulmonary and uteroplacental circulations. The uteroplacental mass increases and requires 10 percent of systemic blood volume by term, compared to a baseline 2 percent. By the second half of pregnancy, the uteroplacental vascular bed functions as a passive low-resistance system, with flow determined by maternal perfusion pressure. Thus, in a state of cardiac compromise, uterine blood flow is greatly diminished. The addition of vasopressors with a- and b-adrenergic effects can cause significant vasoconstriction, decreasing uterine blood flow even further.
By the twentieth week of pregnancy, the enlarged uterus mechanically compresses the great vessels in the pelvis, particularly when the patient is in the supine position. As a result of decreased venous return from compression of the inferior vena cava, cardiac output is reduced 10 to 30 percent during spontaneous circulation (Fig, 12-1). Administration of medications through intravenous sites in the infradiaphragmatic vessels, such as the femoral or saphenous veins, is also compromised because of poor venous flow. These vascular sites are therefore not recommended for intravenous access in the resuscitation of a pregnant patient greater than 20 weeks' gestation. Aortal compression also occurs, causing diminished distal blood flow. The untoward effects of great vessel compression are worsened in the setting of maternal hypotension and uterine contractions, leading to an even more pronounced decrease in uteroplacental blood flow.
FIG. 12-1. Changes in maternal heart rate, stroke volume, and cardiac output during pregnancy with the gravida in the supine and lateral positions. (From Barclay ML, in Pearlman MD, Tintinalli JE (eds): Emergency Care of the Woman, McGraw-Hill, 1998.)
Pregnancy also alters the respiratory system. A state of partially compensated respiratory acidosis develops during the first trimester of pregnancy due to progesterone-stimulated hyperventilation. The resulting decrease in serum bicarbonate levels and P co2 makes the woman less able to buffer a state of acidosis from hypotension or cardiac arrest. In addition, the decreased functional residual capacity (FRC) and increased maternal oxygen consumption and basal metabolic rate during pregnancy, results in more rapid onset of anoxia with respiratory arrest. Arterial oxygen content drops three times more quickly in pregnant than in nonpregnant patients.4 Rapid resumption of respiration, whether mechanical or spontaneous, is essential to minimize hypoxic damage. Progesterone also increases gastric emptying time and decreases lower esophageal sphincter tone, making the gravid patient prone to aspiration. This is another reason to initiate endotracheal intubation early.
Fetal physiology appears to be protective of severe hypoxia. There are several reports of fetal survival when delivery occurred more than 20 min after maternal cardiac arrest in patients receiving cardiopulmonary resuscitation (CPR). The trauma literature indicates that absence of maternal vital signs for greater than 20 min renders emergency cesarean section futile. It is unclear whether CPR plays a role in potential fetal survival beyond 20 min. The fetal oxyhemoglobin dissociation curve is shifted to the left relative to the maternal oxyhemoglobin dissociation curve because of the greater affinity of hemoglobin F for oxygen. Thus, at any partial pressure of oxygen, fetal hemoglobin will bind oxygen more strongly, resulting in greater saturation. Fetal P o2 does not fall significantly unless maternal P o2 falls below 60 mmHg.5 Below this level, only slight decreases in maternal P o2 will result in significant decreases in fetal P o2. In addition, there is a higher concentration of fetal hemoglobin in fetal erythrocytes than maternal hemoglobin in maternal erythrocytes, and the fetus exists in a physiologically acidemic state relative to the mother, which allows preferential oxygen transfer at the fetal tissue level. Acidemia favors a rightward shift of the oxyhemoglobin dissociation curve. Thus, a greater amount of oxygen is supplied to fetal tissues.
Fetal cardiac output protects against hypoxia with increases in umbilical blood flow and placental gas exchange. Fetal blood flow is then preferentially redistributed to vital tissues. As a result, fetuses exposed to short periods of maternal hypoxia may not suffer neurologic damage.
Resuscitation of a pregnant patient can become a chaotic event. Particularly in major centers, there may be other specialists involved, including pediatricians, neonatologists, anesthesiologists, obstetricians, and possibly others. These specialists have unique skills and experience that will help in the resuscitation. However, many of the specialists are poorly versed in emergency medicine and advanced cardiac life support (ACLS) protocols. It is particularly important that the team leader of the resuscitation take strict control of the events and the order in which they occur. The other specialists involved should not be allowed to deviate from the proper process. The team leader for such resuscitations may be decided by hospital policy. If such a policy does not exist, then typically the emergency physician must be the director of the resuscitation and take firm control.
Was this article helpful?