Gestation is coupled with considerable physiological changes. The association between obesity and pregnancy can result in further limitation of parturient physiological reserve. In the presence of obesity, comorbidities may represent an additional risk for parturient outcome.
In the pregnant woman, cardiovascular changes are due to increased oxygen demand and include an augmented cardiac output, blood volume expansion and reduced systemic vascular resistances. During labor, cardiac output increases further and the immediate postpartum uterine contractions are responsible for an additional increase with a peak in cardiac output by as much as 75% above predelivery values.
Excess weight also results in a proportional rise of cardiac output. Every 100 g of fat increases cardiac output by 30-50 ml/min. Increased cardiac output combined with normal peripheral vascular resistance leads to systemic hypertension. Mild-to-moderate hypertension is seen in most morbidly obese patients. The increased left ventricular wall stress caused by increased stroke volume and the resultant ventricular dilation leads to cardiac hypertrophy. However, the extent of cardiovascular pathological changes secondary to obesity is dependent on the duration of obesity and its severity.
In moderately overweight parturients, the incidence of hypertension and toxemic syndromes are 2.0-3.7- and 1.5-1.9-times higher, respectively, than in control subjects. In obese women, the incidence of hypertension is multiplied by a factor of 2.2-21 and that of toxemia by a factor of 1.2-9.7. Obese women have a two- to five-fold higher incidence of preeclampsia during pregnancy, yet the therapeutic principles and management of these pathological conditions does not vary significantly from that of nonobese pregnant women.
The aortocaval compression in supine position by the enlarged uterus during the second half of gestation may lead to hypotension that can compromise uteroplacental blood flow and place the parturient at increased risk of cardiovascular collapse. This syndrome is greatly exacerbated in the obese patient, when large fat panniculi may further compress the great vessels. Two cases of sudden death in nonpregnant, morbidly obese patients have been attributed to supine position and consequent circulatory changes.
During pregnancy, progesterone stimulation of the respiratory center in the brainstem and relaxation of the airway smooth muscle, with consequent decrease of airway resistance, concur in reducing some of the negative effects of obesity on the respiratory system.
In obese patients, functional residual capacity is significantly reduced due to a decrease in expiratory reserve volume. There may be some improvement in respiratory function in an obese patient who becomes pregnant by amelioration, or at least by any additional reduction of functional residual capacity, as is the case in normal-weight parturients. However, the supine and, especially, the Trendelenburg position considerably worsen the lung volumes of obese parturients. Arterial blood-gas analysis demonstrates much more-frequent oxygen desaturation compared with nonobese parturients, stressing the importance of adequate preoxygenation before induction of general anesthesia.
The ventilatory stimulating effect of progesterone and, in the later part of pregnancy, tendency to sleep on the side, can offer some protective effect on obstructive sleep apnea. Obstructive sleep apnea is not uncommon in the obese parturient, leading to an increased risk of systemic and pulmonary hypertension, coronary artery disease, cardiac arrhythmias and oxygen desaturation, which can result in fetal hypoxia and poor fetal growth.
Anemia appears to occur less often in severely obese pregnant women than in normal-weight women.
Obesity further increases the risk of glucose intolerance and insulin resistance, while the incidence of gestational diabetes mellitus in parturients with a BMI of greater than 30 or weight greater than 150% of ideal bodyweight, is 1.4- to 20-fold higher than in normal-weight subjects.[35,36]
Obesity is associated with significant changes in body composition and function that may alter the pharmacodynamics and pharmacokinetics of various drugs, leading to increased volume of distribution for lipophilic medications and to lower volume of distribution for hydrophilic ones, particularly when administered according to total bodyweight.
Expert Rev of Obstet Gynecol. 2009;4(3):313-319. © 2009 Expert Reviews Ltd
Cite this: Pathophysiological and Perioperative Features of Morbidly Obese Parturients - Medscape - May 01, 2009.