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Increased progesterone levels associated with pregnancy are presumed to increase the production of nitric oxide and prostacyclin. This is coupled with a decreased response to catecholamines and angiotensin, resulting in vasodilation. The subsequent decrease in systemic vascular resistance (SVR) is demonstrated by a decrease in blood pressure. Increased levels of relaxin, responsible for increased tissue elasticity, may lead to aortic dilation, especially in patients with connective tissue disorders. A parturient’s plasma volume increases partly, as a response to increased water and sodium retention, from increased renin levels. Table 54.1 summarizes the major cardiovascular changes.
Cardiac output | Increase 50% (plateaus by 28 weeks) |
---|---|
During labor | Additional 30%–40% increase |
Immediately postpartum | 75% increase above prelabor value |
48 hours postpartum | At or below prelabor value |
2 weeks postpartum | 10% above prepregnant value (returns to normal by 12–24 weeks postpartum) |
Stroke volume | Increase 25% (between 5 and 8 weeks) |
Heart rate | Increase 25% (increases 15% by end of first trimester) |
Mean arterial pressure | Decrease 15 mm Hg (normal by second trimester) |
Systemic vascular resistance | Decreases 21% |
Pulmonary vascular resistance | Decreases 34% |
Central venous pressure | No change |
Uterine blood flow | 10% maternal cardiac output (600–700 mL/min at term) |
The most notable increase in CO (see Table 54.1 ) is achieved immediately postpartum, as a result of autotransfusion during uterine contractions. This physiological change is one of the most important changes and can potentially be life threatening in patients with pulmonary hypertension or stenotic valvular lesions. Anatomically, the increase in blood volume results in ventricular hypertrophy, as demonstrated by an enlarged cardiac silhouette on chest x-ray. A new grade I–II systolic murmur can often be heard on physical examination. By the second half of pregnancy, the third heart sound can frequently be detected on auscultation, with a fourth heart sound heard in up to 16% of patients.
Table 54.2 summarizes the hematological changes during pregnancy. Relative to the nonpregnant state, plasma volume increases by 55% and total blood volume increases by 45% (1000–1500 mL). Red cell volume increases by 30%, which is offset by the increase in plasma volume, resulting in a dilutional anemia. The average hemoglobin and hematocrit is 11.6 g/dL and 35.5%, respectively. Maternal anemia occurs as a result of iron deficiency, particularly when the hemoglobin and hematocrit levels fall below 10 g/dL and less than 30%, respectively. Parturients may also experience a noninfectious leukocytosis with a concomitant decrease in cell-mediated immunity. Parturients are known to have an increased risk of developing viral infections, presumably from altered immunity from pregnancy.
Plasma volume | Increases 55% by term (15% by end of first trimester) |
Red blood cell volume | Increases 30% |
Blood volume | Increases 45% |
Hemoglobin | Decrease 15% by midgestation (≈ 11.6 g/dL) |
Platelet count | No change or decrease |
PT and PTT | Decreased |
Fibrinogen | Increased |
Fibrinolysis | Increased |
Factors I, VII, VIII, IX, X XII | Increased |
Pregnancy is associated with a hypercoagulable state as a result of increased activity of coagulation factors, particularly I, VII, VIII, IX, X, and XII, with a concomitant decrease in activity of anticoagulant factors, such as protein S and acquired activated protein C resistance. Accordingly, parturients are at increased risk for thrombotic events (e.g., deep venous thrombosis and pulmonary embolism). This is counterbalanced by increased fibrinolysis as a consequence of decreased levels of factors XI and XIII, which normally act as antifibrinolytics. There is increased platelet consumption, which is counterbalanced by increased platelet production. As a result, the platelet count is usually normal, although thrombocytopenia (platelet count < 150,000/mm 3 ) can occur in 7.6% of women, and 0.9% of patients can have a platelet count less than 100,000/mm 3 . Thrombocytopenia in pregnancy can also occur in pathological conditions, specifically with preeclampsia or with h emolysis, e levated l iver enzymes, and l ow p latelet count (HELLP) syndrome.
Parturients experience a cephalad displacement of the diaphragm, in addition to an increase in the anteroposterior diameter of the chest wall during pregnancy. These anatomic changes cause a decrease in functional residual capacity (FRC). Minute ventilation significantly increases in pregnant women because of increased oxygen consumption ( Table 54.3 ). The upper airway becomes more edematous with significant capillary engorgement, secondary to increased intravascular volume. The airway mucosa is often friable and prone to bleeding with manipulation or trauma.
Minute ventilation | 50% increase (can go up to 140% of prepregnancy values in the first stage of unmedicated labor and up to 200% in the second stage) |
Alveolar ventilation | 70% increase |
Tidal volume | 40% increase |
Oxygen consumption | 20% increase |
Respiratory rate | 15% increase |
Dead space | No change |
Lung compliance | No change |
Residual volume | 29% decrease |
Vital capacity | No change |
Total lung capacity | 5% decrease |
Functional residual capacity | 15%–20% decrease |
FEV1 | No change |
The decrease in FRC, coupled with an increase in oxygen consumption, significantly increases the risk of rapid desaturation with apnea. Airway edema associated with pregnancy further complicates managing the airway, where the risk of difficult/failed intubation is increased eight-fold. Therefore because of the combined risk of difficult intubation and the risk of rapid desaturation with apnea, it is extremely important to ensure adequate and effective preoxygenation, proper ramp positioning (see Chapter 49 , “Obesity and Sleep Apnea”), and the availability of other equipment (e.g., flexible scope).
Given the rise in minute ventilation, pregnant women develop a respiratory alkalosis ( Table 54.4 ). Hyperventilation during active labor further contributes to the preexisting metabolic disturbance and is the second most important physiological change during labor, as it can result in uterine vasoconstriction and decreased placental perfusion, hypoxemia, and fetal distress.
pH | PaO 2 | PaCO 2 | HCO 3 | |
---|---|---|---|---|
Pregnant | 7.41–7.44 | 85–109 mm Hg | 27–33 mm Hg | 21–27 mmol/L |
Nonpregnant | 7.35–7.45 | 60–100 mm Hg | 35–45 mm Hg | 24 mmol/L |
The expanding uterus displaces the stomach cephalad, resulting in incompetence of the lower gastroesophageal sphincter (GES) and increased intragastric pressure. Increased progesterone levels also decrease the tone of the lower GES. These changes place parturients at higher risk for reflux, regurgitation, and aspiration on both induction and emergence from anesthesia. Therefore all pregnant laboring patients are considered to have a full stomach and are managed accordingly (e.g., rapid sequence induction and intubation, cricoid pressure).
Renal plasma flow, glomerular filtration rate (GFR), and creatinine clearance increase by the fourth month of gestation. Blood urea nitrogen (BUN) and creatinine are decreased; normal values in pregnancy are 6 to 9 and 0.4 to 0.6 mg/dL, respectively. Glycosuria up to 10 g/dL and proteinuria up to 300 mg/dL is not abnormal. Urinary stasis contributes to the frequency of urinary tract infections seen in pregnancy.
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