Obesity is associated with a shortened life expectancy, particularly in severely obese younger individuals.8 This section summarizes important physiologic derangements associated with obesity, with an emphasis on those germane to the care of the morbidly obese critically ill patient.
The risk of death from cardiovascular disease rises steeply above a BMI of 30 kg/m2.9 There are several mechanisms through which obesity can cause cardiovascular disease. First, obesity increases the risk of coronary atherosclerosis by inducing several risk factors in parallel. For example, obesity is associated with hypertension, insulin resistance, dyslipidemia, and coagulation abnormalities, which separately and collectively promote the development of cardiovascular disease.
There are other mechanisms through which obesity causes heart disease. Obesity may impair cardiac function through chronic pressure and volume overload.10 Cardiac output is increased in obesity as a result of increased extracellular volume and increased blood flow to most tissue beds. This increased cardiac output is associated with increased preload and cardiac dilatation, with the subsequent development of eccentric left ventricular hypertrophy. This chronic volume-overloaded state, when combined with increased left ventricular afterload from concurrent hypertension, may result in marked left ventricular hypertrophy. Over time, left ventricular hypertrophy leads to impaired ventricular filling and diastolic heart failure. Systolic heart failure may result from ischemic heart disease, microvascular disease from diabetes mellitus, longstanding hypertension, or, in severe, longstanding obesity, a decrease in mid-wall fiber shortening and ejection fraction.9
Pulmonary hypertension with right ventricular hypertrophy and dilation may accompany obesity. When not caused by left ventricular failure, pulmonary hypertension in these patients typically arises from conditions that cause nocturnal and diurnal hypoxemia. A relatively common presentation of this problem is that of the patient with obstructive sleep apnea who has coexisting chronic obstructive pulmonary disease. Cor pulmonale may also develop in patients with the obesity hypoventilation syndrome (OHS). This poorly understood disorder is associated with daytime hypercapnia and hypoxemia, with the latter arising from alveolar hypoventilation and poor ventilation of the basal lung due to airway closure and atelectasis. Hypercapnia and hypoxemia elicit pulmonary vasoconstriction. Eventually, this may lead to vascular remodeling with resulting irreversible pulmonary hypertension and cor pulmonale. Individuals with the OHS frequently, but not always, have coexisting obstructive sleep apnea.
Plasminogen activator inhibitor I and fibrinogen levels are elevated in most patients with obesity, suggesting a role for hypercoagulability and impaired fibrinolysis in cardiac and cerebrovascular diseases. Elevated proinflammatory cytokines, for example, interleukin 6 and C-reactive protein, potentially indicate the presence of a low-grade inflammatory state in this condition.9
What are the clinical implications of this susceptibility to such a range of cardiovascular disorders? First, the intensivist caring for the morbidly obese patient should have a high index of suspicion for the presence of ischemic heart disease from coronary artery or microvascular disease. Second, abnormal cardiac function, diastolic or systolic, may be present, even if other risk factors for heart disease are absent. Particular sensitivity to changes in intravascular volume may result. Third, pulmonary hypertension and right ventricular failure should be suspected when obstructive lung disease and/or daytime hypoxemia or hypercapnia are present. The diagnosis of these conditions is complicated by poor sensitivity of physical examination and transthoracic echocardiography in morbidly obese individuals. In selected patients, transesophageal echocardiography or invasive hemodynamic monitoring may be necessary.
Mechanics of the Respiratory System
The effect of obesity on pulmonary function varies considerably between individuals, ranging from trivial to profound impairment, but generally increases in severity with the BMI.11,12 The overall compliance of the respiratory system is reduced, mildly so in simple obesity and as low as 45% of normal in patients with OHS. Some studies have suggested that decreased chest wall compliance from the mechanical effect of adipose tissue on the thoracic cage is the principal cause of this abnormality, whereas other investigators have implicated reduced lung compliance as an additional factor, probably from a decrease in functional residual capacity. Airway resistance has been found to be increased, and a reduction in mid to late expiratory flows has been noted; because the ratio of forced expiratory volume in 1 second (FEV1) to forced vital capacity (FVC) is typically normal or even elevated in obesity, a reduction in small airway caliber is likely responsible.
The most frequent abnormality in pulmonary function in obesity is a decrease in the expiratory reserve volume attributable to cephalad displacement of the diaphragm by adipose tissue. In severely obese individuals and in those with the OHS, total lung capacity and vital capacity may be reduced. In such patients, the residual volume may actually be increased relative to total lung capacity because of small airway closure and gas trapping. This is supported by the finding of larger total lung capacity by body box plethysmography than by helium dilution.13 Similarly, spirometry is typically normal in simple obesity, whereas severely obese individuals or those with the OHS may exhibit reductions in FEV1 and FVC, even though the ratio of these two variables is preserved or even increased.
Why do some individuals exhibit diminished pulmonary function and/or the OHS, whereas comparably overweight individuals may be little affected? Some, but not all, data suggest that the distribution of body fat may be an important determinant of pulmonary function; simply put, adipose tissue that is more centrally located is more likely to negatively influence pulmonary function. There are also important differences in respiratory muscle strength between patients with simple obesity and those with the OHS, with the latter exhibiting decreased inspiratory muscle strength. Weakness may be considered absolute, a result of mechanical disadvantage from diaphragm malposition, and relative, when the increased work of breathing from morbid obesity is considered (see below).
Morbid obesity causes closure of small peripheral airways in the dependent regions of the lung, resulting in mismatching of ventilation and perfusion.14 The result may be a widened alveolar to arterial oxygen gradient and mild to moderate hypoxemia that worsens in the supine position. Severe hypoxemia may be present in individuals with the OHS because of the additional contribution of hypoventilation. The diffusing capacity for carbon monoxide is typically normal and may be elevated when indexed to alveolar volume.
Ventilatory drive is increased in simple obesity as assessed by the mouth occlusion pressure and diaphragm electrical activity in response to carbon dioxide inhalation. In contrast, mouth occlusion pressure response to carbon dioxide is reduced in OHS compared to normal individuals and to patients with simple obesity. Diaphragm electrical activity in response to carbon dioxide is inappropriately low in OHS.
Perioperative and Other Pulmonary Considerations in Obesity
The reduced functional residual capacity associated with severe obesity encroaches on the closing capacity, the lung volume at which small airways in the lung bases begin to close. This places severely obese patients at significant risk for atelectasis in the perioperative period, particularly where upper abdominal or thoracic operations are concerned. Hypoxemia may result and may be marked in the setting of a relatively unremarkable chest radiograph. Pulmonary embolism should always be considered in the differential diagnosis of such patients. Treatment involves adequate analgesia, avoidance of oversedation, early mobilization, and vigorous pulmonary toilet. Sleep-disordered breathing may worsen in the postoperative period, thereby increasing the risk of respiratory failure. Early application of noninvasive ventilation may decrease the incidence of postoperative pulmonary complications. The risk of aspiration of gastric contents is generally felt to be increased in obesity, and efforts to minimize this occurrence should be taken at the time of intubation (see below).
Not surprisingly, the risk of obstructive sleep apnea increases significantly with obesity, to as high as 40% when the BMI exceeds 40 kg/m2. Patients who successfully lose a significant amount of weight, usually via surgical approaches to weight reduction, may exhibit significant improvements in lung volumes, gas exchange, and work of breathing, and sleep-disordered breathing may improve or even resolve.
An intriguing association between obesity and progressive renal insufficiency is becoming apparent.10,15 Obesity is associated with increased renal blood flow, glomerular filtration rate, and microalbuminuria. Glomerular hyperfiltration may subsequently lead to glomerular sclerosis in a manner analogous to diabetes, even in obese patients without this diagnosis. Several potential mechanisms for this process have been suggested, ranging from hyperleptinemia to insulin resistance to a chronic state of low-grade inflammation induced by obesity. Apart from the direct effects of obesity on the kidney, a significant proportion of cases of end-stage renal disease may be attributable to the diabetes and hypertension associated with obesity.
The risk of venous thromboembolism is greatly increased in obese patients (BMI >30 kg/m2). Inactivity, venous stasis, and hypercoagulability likely contribute to this risk. The risk of death from cancer is substantially increased in individuals with a BMI greater than 40 kg/m2.16