Cardiopulmonary Changes

Obesity increases the demands on the cardiopulmonary system. The effects of obesity and pregnancy on the respiratory and cardiovascular systems are summarized in Table 49.1 and Table 49.2 . As energy expenditure increases proportionate to the increase in body mass, oxygen consumption and carbon dioxide (CO ₂ ) production also increase proportionate to the increase in work performed. Minute ventilation is increased owing to the elevated respiratory demand, except in the 5% to 10% of obese patients with Pickwickian syndrome, who display a reduced sensitivity to CO ₂ . Obesity affects the body’s ability to meet these demands by changing pulmonary mechanics, altering lung volumes, and impairing oxygen consumption.

Obesity increases the weight of the chest wall; thus, greater energy expenditure is required during ventilation to move this mass. Morbidly obese patients in comparison with lean controls expend a disproportionately high percentage of total oxygen consumption on respiratory work, even during quiet breathing. The weight gain during pregnancy further increases the work of breathing. In obese individuals, frequent shallow respirations may represent a more efficient breathing pattern than large tidal volumes. This pattern of frequent shallow respirations contrasts to the increased tidal volumes that typically accompany pregnancy.

Greater abdominal weight restricts diaphragm movement, especially in the supine or Trendelenburg position, thus encouraging smaller tidal volumes. Functional residual capacity (FRC) decreases at the expense of expiratory reserve volume and may be less than closing capacity. Both chest wall and lung compliance decrease, but airway resistance increases as a result of reduction in lung volumes.

Pulmonary diffusion typically remains normal in most women with morbid obesity. Decreased chest wall compliance and greater abdominal weight promote airway closure in the dependent portion of the lung. Ventilation preferentially occurs in the more compliant, nondependent portion of the lung. In contrast, pulmonary blood flow preferentially occurs in the dependent portion of the lung, resulting in ventilation-perfusion mismatch and hypoxemia. Consistent with the positional deterioration of lung volumes, oxygenation worsens in obese individuals in the supine and Trendelenburg positions.

Blood volume and cardiac output are increased, the latter owing to increases in both stroke volume and heart rate. Both preload and left ventricular afterload are increased; these changes result in both eccentric and concentric left ventricular hypertrophy. Among morbidly obese pregnant women, left atrial size, left ventricular thickness, interventricular septal thickness, and left ventricular mass are increased compared with nonobese pregnant women. The increase in heart rate limits the time for diastolic filling, thus diastolic relaxation is impaired. Pulmonary blood volume increases in proportion to increases in cardiac output and total blood volume. Pulmonary hypertension can occur and may be position dependent. A BMI of 30 kg/m ² or more is associated with a threefold higher incidence of hypertension during pregnancy than a BMI less than 30 kg/m ² . Aortocaval compression of the great vessels in the supine position may be greater in obese parturients, particularly those with a large fat panniculus.

Gastrointestinal Changes

It is unclear whether obesity in pregnancy is associated with an increase in gastric volume and a decrease in gastric pH. Roberts and Shirley reported that gastric volumes aspirated from obese laboring women undergoing cesarean delivery were significantly higher than those obtained from lean controls. Studies in the general surgical population, however, reported conflicting results; some confirmed these findings and others reported no difference in gastric volume and pH in obese compared with lean patients.

Similarly, data regarding gastric emptying in the obese population are conflicting; studies have reported delayed, unchanged, or more rapid rates of gastric emptying in obese subjects compared with lean subjects. In a nonobstetric obese population, Maltby et al. reported that drinking 300 mL of clear fluid 2 hours before surgery had no effect on gastric fluid volume and pH compared with fasting after midnight. Similarly, Wong et al. found that gastric emptying in obese, nonlaboring term pregnant volunteers was not delayed after ingestion of 300 mL of water compared with ingestion of 50 mL of water. The gastric volume returned to baseline 60 minutes after ingestion of water.

Both gastroesophageal reflux and hiatal hernia are more common in obese than in nonobese patients. Obesity is also associated with a higher risk for difficult airway management, which is a known risk factor for aspiration. Therefore, it seems likely that morbidly obese patients are at higher risk for pulmonary aspiration of gastric contents.

Coagulation Changes

Obesity is associated with a higher risk for thromboembolic complications. Venous thromboembolism is a leading cause of direct maternal mortality. In the United Kingdom, 54% of women who died from thromboembolic complications in 2009 to 2013 were overweight or obese.

Obesity is associated with changes in coagulation, venous stasis, and endothelial injury that contribute to the pathogenesis of venous thromboembolism. For instance, adipose tissue secretes the following: (1) adipokines such as plasminogen activator inhibitor-1 (PAI-1), which results in impaired fibrinolysis; (2) leptin, which promotes platelet aggregation; and (3) interleukin-6, which stimulates the liver to produce coagulation factors. C-reactive protein levels are also elevated in obese women, leading to platelet activation. Venous stasis is compounded in obese women by increased intra-abdominal pressure, which leads to increased iliofemoral venous pressure. Obesity was shown to be associated with endothelial dysfunction in the nonpregnant population. Therefore, all risk factors that contribute to the pathogenesis of thromboembolic complications are likely to be exacerbated by obesity. The risk is further increased by reduced mobility, comorbidities such as preeclampsia, and an increased frequency of operative delivery.

Endocrine Changes

Gestational diabetes and diabetes mellitus occur more frequently in obese patients. The pathologic process is attributed to the following: (1) peripheral insulin resistance as a result of augmentation of free fatty acids by visceral obesity, (2) increased proinflammatory cytokine levels, (3) relative gonadotropin resistance, and (4) a low sex hormone–binding globulin concentration, which leads to hyperandrogenism and decreased insulin sensitivity. The concentration of adiponectin, an adipokine with insulin-sensitizing properties, is also decreased in obesity, which leads to decreased insulin sensitivity.

Sleep Apnea

Obesity is a significant risk factor for obstructive sleep apnea (OSA), which is characterized by repeated episodes of complete or partial upper airway collapse, leading to hypoxemia and hypercarbia. Those repeated periods of hypoxemia and reoxygenation lead to significant endocrine and metabolic disturbances, which result in an increased risk for hypertension, myocardial infarction, stroke, diabetes, and metabolic syndrome. It is estimated that 15% to 20% of obese pregnant women have OSA.

The changes of pregnancy may both worsen and protect against OSA. For instance, weight gain and estrogen-induced hyperemia and edema of nasal mucosa might promote OSA, whereas sleeping in the lateral position, reduced rapid eye movement (REM) sleep, and the progesterone-induced increase in minute ventilation might protect against it.

OSA may adversely affect maternal and neonatal outcomes. A large inpatient database study showed that pregnant women with OSA are at increased risk for preeclampsia, eclampsia, cardiomyopathy, and pulmonary embolism, and are five times more likely to die in the hospital during a pregnancy or delivery admission than women without OSA. These differences were unchanged after controlling for obesity, but the associations with preeclampsia and severe cardiovascular complications were stronger in obese women. The association between OSA and increased risks for preeclampsia and gestational diabetes were confirmed in a large prospective study involving 3705 women.

Some studies have examined the impact of maternal OSA on perinatal outcomes. A 2014 meta-analysis reported an association between sleep-disordered breathing and low birth weight, neonatal intensive care unit admission, fetal growth restriction, and a 1-minute Apgar score less than 7.

Other Comorbidities

Obesity is associated with an increased risk for a number of disease states compared with lean controls ( Table 49.3 ). These comorbidities complicate the care of obese parturients.

Maternal and Fetal Complications

Obesity results in greater use of health care resources. Chu et al. reported that obese pregnant women receive significantly more prenatal tests, ultrasonographic examinations, medications, and prenatal visits with a physician, and they are at greater risk for having a high-risk pregnancy, cesarean delivery, and prolonged hospitalization than pregnant women of normal weight.

Obesity is associated with a significantly increased incidence of maternal, fetal, and neonatal complications. These include a higher risk for spontaneous abortion (miscarriage), thromboembolic complications, gestational diabetes, hypertensive disorders of pregnancy, dysfunctional labor, shoulder dystocia, operative vaginal delivery, cesarean delivery, postpartum hemorrhage, wound infection, fetal macrosomia, fetal congenital anomalies, stillbirth, and neonatal death ( Table 49.4 ).

TABLE 49.4

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