What are the physiologic changes during pregnancy and how do they impact on anesthesia?
Due to increased progesterone levels during the first trimester, minute ventilation is increased by almost 50% and remains at this level for the remainder of the pregnancy. The increase in minute ventilation leads to a decrease in arterial carbon dioxide tension (PaCO2) to approximately 30 mmHg. Arterial pH remains unchanged because of a compensatory increase in renal excretion of bicarbonate ions. At term, alveolar ventilation is increased by 70% because anatomic dead space does not change significantly during pregnancy. After the fifth month of pregnancy, the functional residual capacity, expiratory reserve volume, and residual volume are all decreased by about 20% because of the gravid uterus pushing on the diaphragm. Vital capacity is not appreciably changed from prepregnancy levels.
Anesthetic Implications Increased alveolar ventilation and decreased functional residual capacity lead to a more rapid uptake and excretion of inhaled anesthetics.
The decrease in functional residual capacity in conjunction with increases in cardiac output, metabolic rate, and oxygen consumption make the pregnant patient more susceptible to arterial hypoxemia during periods of apnea or airway obstruction.
Edema, weight gain, and increase in breast size may make intubation of the trachea technically difficult. An array of laryngoscope blades and handles and other emer-gency airway management equipment should be available. Capillary engorgement of the mucosal lining of the upper airway accompanies pregnancy. This mandates extreme care during manipulation of the airway and the use of a smaller-than-normal tracheal tube. The use of a nasal airway and nasotracheal intubation should be avoided.
Cardiac output is increased by 30–40% during the first trimester. This is primarily related to an increase in stroke volume (30%) and secondarily related to an increase in heart rate (15%). Cardiac output increases slightly further during the second trimester and lasts throughout the pregnancy.
Blood pressure normally decreases during pregnancy because of a 15% decrease in systemic vascular resistance. Near term, 10–15% of patients have a dramatic reduction in blood pressure in the supine position, often associated with diaphoresis, nausea, vomiting, pallor, and changes in cerebration. This is the “supine hypotensive syndrome” and is caused by compression of the inferior vena cava and aorta by the gravid uterus. Other manifestations of the syndrome are decreases in renal and uteroplacental blood flow from compression of the aorta. Displacing the uterus by tilting the patient on her left side can alleviate the symp-toms of this syndrome.
Intravascular volume is increased by 35% during pregnancy. Because plasma volume increases by a greater percentage than red blood cell volume (45% and 20% respectively) there is a relative anemia during pregnancy. Nevertheless, a hemoglobin concentration of less than 11 g/dL is considered abnormal.
Anesthetic Implications Increases in cardiac output will hasten the speed of intravenous inductions.
Due to increased progesterone levels, gastrointestinal tract motility is decreased by the end of the first trimester. The stomach, displaced upward by the enlarging uterus, eventually assumes a horizontal position further slowing stomach emptying. This also results in a change in position and function of the gastroesophageal sphincter. Anxiety, pain, and administration of opioids and anticholinergics will further slow gastric emptying. Gastrin production is increased during pregnancy (because the placenta produces gastrin) leading to an increase in acid production.
Anesthetic Implications The above changes in the gastro-intestinal system, by the end of the first trimester, place the pregnant patient at increased risk for aspiration of gastric contents. A nonparticulate antacid, H2 receptor blocker, and metoclopramide should be used to decrease the acidity and volume of the gastric contents. After the first trimester, all general anesthetics should be conducted with a rapid sequence induction, cricoid pressure, and tracheal intubation.
Tests of liver function (serum glutamic-oxaloacetic transaminase, lactic acid dehydrogenase, alkaline phos-phatase, and cholesterol) are commonly increased during pregnancy. These increases do not necessarily indicate abnormal liver function. Pseudocholinesterase activity declines by as much as 20% during the first trimester and remains fairly stable during the remainder of the pregnancy.
Anesthetic Implications Prolonged apnea is rarely a problem following a standard dose of succinylcholine. Similarly, prolonged activity of ester-linked local anesthetics has not been a problem.
Pregnancy does not significantly alter the lymphocyte count, but lymphocyte function is depressed, which can decrease maternal resistance to infection. The risk of upper respiratory infections is increased, which may complicate airway management during general anesthesia.
The platelet count decreases by about 20% during preg-nancy but is usually of no clinical significance. Circulating levels of coagulation factors increase significantly during pregnancy leading to the hypercoagulable state of pregnancy.
Anesthetic Implications The increased risk of upper air-way infections may complicate airway management during general anesthesia. Increased coagulability may predispose the pregnant patient to thromboembolic events including pulmonary embolism.
Renal blood flow (RBF) and glomerular filtration rate (GFR) are increased during the first trimester, leading to a rise in creatinine clearance and a fall in serum creatinine. During the third trimester, RBF and GFR decrease toward prepregnant levels because of compression of the aorta by the enlarging uterus. Due to progesterone, renal calyces and pelves dilate during the third month of pregnancy. During the third trimester, they dilate further because of ureteral compression. This dilatation may lead to stasis and urinary tract infections.
Anesthetic Implications Care should be taken not to over-hydrate the patient because urinary retention is common during spinal or epidural anesthesia, which may necessitate bladder catheterization and further predispose the patient to urinary tract infections.
The minimum alveolar concentration (MAC) for inhaled anesthetics is decreased by up to 40% during preg-nancy. This is related to a progesterone and endorphin effect. Compression of the inferior vena cava by the gravid uterus leads to dilatation of the azygos system and the epidural veins. Epidural venous engorgement decreases the size of the epidural and intrathecal spaces.
Anesthetic Implications The decrease in MAC along with an increase in alveolar ventilation places the pregnant patient at risk for anesthetic overdose. The decreased size of the epidural and intrathecal spaces as a result of epidural venous engorgement explains why the doses of drugs used during a major conduction block must be decreased. An alternative explanation is that progesterone may increase the sensitivity of nerve cells to local anesthetics since neuraxial drug requirements decrease prior to uterine enlargement.