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Physiology of Pregnancy and Anesthetic Considerations

(Originally posted 23 March 1998 on About Anesthesiology)

Pregnancy is associated with changes in virtually every organ system. Subsequent labor and delivery also results in significant physiologic effects. The knowledge of these changes is important to the anesthesiologist who is managing the pregnant patient. This knowledge will allow proper selection of anesthetic techniques in an effort to maximize comfort and safety for both mother and fetus.

An increase in intravascular fluid volume begins in early pregnancy resulting in about a one liter expansion by term. Plasma volume increases out of proportion to red cell mass and this leads to what is commonly called the "physiologic anemia of pregnancy". Note that a hemoglobin less than 11 g/dl is still considered abnormal and is most likely associated with iron deficiency. This increase in volume will offset the approximate 500cc blood loss of a vaginal delivery (1000cc for cesarean section).

Cardiac output also increases early in pregnancy and remains elevated until after delivery. Normally, the cardiac output is approximately 40% higher than pre-pregnancy levels and this is due primarily to an increase in stroke volume (with lesser increases in heart rate). Labor can further increase cardiac output about 20% with each contraction. The highest cardiac output is seen early after delivery as the uterus contracts and returns intravascular volume from a low resistance reservoir.

Blood pressure does not increase in the normal pregnancy and, since cardiac output is increased, this reflects a decrease in systemic vascular resistance.

Supine hypotensive syndrome can be seen in near term patients and manifests as a decrease in blood pressure when in the supine position. This can result in diaphoresis, nausea, altered mental status, etc. The mechanism is compression of the inferior vena cava by the uterus which interferes with venous return to the heart.

It has also been shown that the uterus can compress the abdominal aorta. This, while it may not result in a symptomatic mother, can result in decreased uterine blood flow. Thus, it is routinely emphasized that the patient should remain in a lateral position (left uterine displacement can also be achieved with a pad under the right hip).

Changes are seen in the upper airway due to capillary engorgement of the mucosal linings. This can result in obstruction of nasal passages, increased likelihood of nosebleeding, smaller upper airway (requiring smaller endotracheal tubes) and the need for gentle instrumentation when intubating or suctioning.

Minute venitlation is increased early in pregnancy (approximately 50%) apparently due to an increased level of progesterone. As a result of this increase, resting PaCO2 is decreased to about 30mm Hg and PaO2 is increased slightly. The kidneys compensate for this to maintain a normal arterial pH and resting plasma bicarbonate levels decrease about 4 mEq/L.

Lung volumes also change, but not until about the middle of the second trimester. The enlarging uterus exerts upward pressure on the diaphragm and lungs, dsiplacing them. As a result, expiratory reserve volume, residual volume and functional residual capacity are all decreased approximately 20%.

The combination of a higher minute ventilation and a decreased FRC speeds the rate of denitrogenation, induction with inhalational agents, and emergence from inhalational anesthetics. There may also be a decrease in anesthestic requirements which contributes to the faster onset of anesthesia. Care must be taken since these patients lost consciousness sooner upon induction than non-pregnant patients.

The rate of desaturation with apnea is also increased due to the decrease in FRC (the increase in oxygen consumption near term also contributes to this phenomena). Therefore, preoxygenation is a must in these patients. Although it is commonly said that three full breaths of 100% oxygen is sufficient for denitrogenation, studies have shown that three minutes of 100% oxygen is probably better. In fact, some have suggested that as long as six minutes is required before preoxygenation is of any benefit to the fetus since that much time is required for maternal-fetal equilibirum.

Anesthestic requirements for inhalational agents are reduced 25-40% in animals at term. The sedative effect of progesterone may explain at least part of this effect. However, it is likely that the phenomena is multi-factorial. The important result is that levels of anesthetic that would not produce unconsciousness in nonpregnant patients may be sufficient for anesthesia in the pregnant patient.

There is a 35-50% decrease in dose requirements for epidural and subarachnoid anesthesia in the pregnant patient. This has been proposed to be due to multiple factors including:

  • Increased intra-abdominal pressure results in engorgement of the epidural veins. This reduces the size of the epidural space and may decrease the volume of CSF as well.
  • There may be a pumping effect of these veins that encourages the spread of local anesthetic.
  • Higher pressures may facilitate transfer of local anesthetic into the CSF.
  • The swollen veins may block escape of drugs through the nerve root foramina.
  • Exaggerated lumbar lordosis may contribute to cephalad spread.

Renal blood flow and glomerular filtration rate are increased during pregnancy but return to normal in the third trimester. There are no significant anesthetic considerations usually described as a result of these changes.

Plasma cholinesterase activity is decreased by approximately one-fourth as a result of pregnancy. This theoretically could prolong the duration of succinylcholine action but is rarely (if ever) of clinical significance. No other significant anesthetic considerations are usually described in relation to the hepatic system and pregnancy.

The changes in this system are important as they make the pregnant patient more prone to regurgitation and aspiration. Gastric emptying is prolonged in these patients both as an anatomic effect (the uterus pushes the pylorus up and back) and as a hormonal effect (progesterone decreased gastrointestinal motility). In addition, the uterus changes the angle of the gastroesophageal junctionand this leads to incompetence of the lower esophageal sphincter. Reflux and esophagitis is very common in pregnant patients and the incidence of silent regurgitation is theoretically increased.

Note that the administration of opioids for labor analgesia can also slow gastric emptying. The routine use of antacids to increased gastric pH is advocated by many. Other drugs are often considered such as histamine receptor antagonists (to decrease acid secretion) and metoclopramide (to increase lower esophageal sphinter tone and speed gastric emptying). Note that metoclopramide may not effectively reverse the decreased motility caused by opioids.

The placenta serves as the interface between mother and fetus allowing for the exchange of physiologically important substances including oxygen, carbon dioxide, waste products of metabolism, drugs, etc. Fetal blood travels from the fetal heart to the placenta by way of two umbilical arteries and returns (nutrient enriched and waste free) to the fetus by means of a single umbilical vein.

Uterine blood flow is one critical determinant of the proper functioning of the placenta and thus the health of the fetus. Uterine blood flow is not autoregulated and as a result the flow is proportional to uterine perfusion pressure (arterial pressure minus uterine venous pressure). Flow is also inversely related to uterine vascular resistance.

Blood flow is reduced by drugs or events that decrease perfusion pressure or increase vascular resistance. Although it is estimated that the flow can decrease by half before fetal distress is seen there may be unmeasurable fetal effects at higher levels of flow and there is little reserve in the fetus for reduced flow. Alpha agonist drugs can produce direct uterine vascular constriction and therefore are relatively contraindicated. (Ephedrine increased blood pressure without vasoconstriction and can thus increase flow - it is the drug of choice for treating maternal hypotension.) Uterine constriction can also occur with the pain of labor and therefore adequate anesthesia may actually improve fetal condition.

As far as anesthesia techniques it is likely that it is their effect in decreasing maternal blood pressure that results in deceased uterine flow rather than direct uterine effects that results in difficulties for the fetus. Thus, as long as blood pressure is maintained, there is little detrimental effect of one drug or technique versus another. Epidural anesthesia has been shown not to alter uterine blood flow as long as blood pressure is maintained.

Transfer of drugs from mother to fetus takes place at the level of the placenta mainly by diffusion. Thus, keeping maternal blood levels of drugs as low as possible is a major strategy for decreasing the amount of drug that reaches the fetus. In addition, since 75% of the blood in the umbilical vein travels to the liver, a large portion of drug can be metabolized before reaching vital fetal organs. Drug in the unbilical vein that travels via the ductus venosus to access the inferior vena cava will be diluted with blood from the lower extremities (which has no drug) and this further reduces concentration of drugs inthe fetal blood.

Two things work against this "safety feature": (1) fetal acidosis during times of distress causes increased perfusion of the heart and brain and thus increases delivery of drug to these important organs. (2) Fetal pH is lower than maternal pH and results in basic drugs (such as local anesthestics) becoming more ionized when they reach fetal circulation. This effectively traps them on the fetal side of the circulation since ionized molecules cannot easily cross the placenta. This also maintains a gradient for diffusion. This is known as "ion trapping" and can be quite a significant effect especially during times of fetal distress (pH gets even lower).


© 2002-2005 by Paul H. Ting and All Rights Reserved.
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