Joshua Diamond and William Schweickert

Background/Epidemiology

Worldwide at least 1 billion people are overweight, and more than 300 million are obese. The United States is experiencing an epidemic of obesity. The national health surveys conducted in 2009-2010 estimated more than one third of the adult U.S. population (about 78 million) as obese and virtually guarantee the presence of obese patients in the intensive care unit (ICU). The critically ill obese patient presents unique challenges that must be understood and anticipated to ensure optimal delivery of care (Table 29.1).

Respiratory Effects of Obesity

Obesity produces a wide range of effects on the respiratory system. The magnitude of these effects depends on three factors:

The most commonly encountered pulmonary function change is a decrease in the expiratory reserve volume (ERV), ascribed to the cephalad displacement of the diaphragm by adipose tissue (Figure 29.1). Other frequent changes include increases in the ratio of the forced expiratory volume in one second (FEV₁) to the forced vital capacity (FVC; ratio: FEV₁/FVC). As obesity becomes extreme, lung volumes can become more deranged with low total lung capacity (TLC), vital capacity (VC), and functional residual capacity (FRC). As expected, the respiratory system compliance is decreased, from the mechanical effects of the adipose tissue on the thoracic cage (chest wall restriction), and also on lung compliance from the reduced FRC with dependent atelectasis. Interestingly, residual volume (RV) may be increased relative to TLC (i.e., RV/TLC ratio), reflecting a reduction in small airway caliber and susceptibility to premature airway closure, precipitating gas trapping. Furthermore, evidence implicates increased rates of asthma in the obese population.

The respiratory system derangements produced by obesity are exacerbated by the supine position of a critically ill patient. The maximal displacement of the diaphragm and added weight of the chest cause peripheral airway closure in dependent lung regions (atelectasis), resulting in mismatch of ventilation and perfusion. This ventilation/perfusion () mismatch creates a widened alveolar to arterial oxygen gradient (PAo₂-Pao₂), along with typically mild to moderate hypoxemia. Severe hypoxemia may be present, however, in individuals with the obesity hypoventilation syndrome (as a result of the additional contribution of hypoventilation; see Chapter 80) or in the postoperative patient (especially following thoracic and upper abdominal surgeries; see Chapter 90). Even severe hypoxemia may present with a relatively unremarkable chest radiograph, or perhaps minimal basilar atelectasis.

An elevated work of breathing predisposes obese patients with critical illness to respiratory failure. At baseline, obese patients have a high oxygen consumption (O₂), although oxygen consumption per kilogram is somewhat reduced given the relatively low metabolic rate of adipose tissue. Furthermore, the fraction of oxygen consumption related to the work of breathing is very high, from highly inefficient respiratory muscle function. Therefore, morbidly obese patients should be viewed as manifesting chronic ventilatory failure in which relatively small additional increases in O₂ or carbon dioxide production (CO₂) (i.e., from sepsis or respiratory compensation for metabolic acidosis) precipitate acute hypercapnic respiratory failure (Chapter 1).

Cardiovascular Effects of Obesity

The circulatory derangements attributed to obesity can be quite difficult to appreciate. The usual markers of volume status (neck vein assessment, precordial impulse, distal pulses), chest radiographs, electrocardiograms, and even blood pressure measurements (appropriate cuff sizing) can all be limited. Therefore, maintain a high clinical suspicion for ventricular dysfunction and pulmonary hypertension.

Cardiac output is increased in obesity from increased extracellular volume and blood flow to most tissue beds, mediating increased preload and cardiac dilation. This chronic volume-overload state, either in isolation or combined with increased left ventricular afterload from concurrent systemic hypertension, may result in marked left ventricular hypertrophy, further impairing ventricular filling and resulting in diastolic heart failure.

Systolic dysfunction may also result from this chronic pressure overloaded state (long-standing hypertension) or from ischemic heart disease. The risk of death from cardiovascular disease rises steeply above a BMI of 30 kg/m². Obesity increases the risk of coronary and other atherosclerosis from a myriad of parallel risk factors including hypertension, insulin resistance, and dyslipidemia.

Pulmonary hypertension with right ventricular hypertrophy and dilation may accompany obesity. When not caused by left ventricular failure, pulmonary hypertension in obese patients typically arises from sustained hypercapnia and hypoxemia (because of obesity hypoventilation [Chapter 80] or concomitant chronic obstructive pulmonary disease), eliciting pulmonary vasoconstriction. Absent effective therapy (weight loss, nocturnal invasive or non-invasive ventilation, supplemental oxygen), such pulmonary hypertension can produce cor pulmonale.

Other Organ System Manifestations

Obesity is associated with progressive renal insufficiency. Microalbuminuria combined with increased renal blood flow and elevated glomerular filtration rate are frequently present in obesity, subsequently leading to glomerular sclerosis in a manner analogous to diabetes. Beyond the direct effects of obesity on the kidney, concomitant diabetes and hypertension account for a significant proportion of cases of end-stage renal disease in this population.

The hepatobiliary system endures damages as well. Obesity is a well-established risk factor for cholesterol gallstones, increasing the likelihood of biliary sepsis and gallstone pancreatitis. Multiple studies reveal obese subjects have ultrasonographic evidence of fatty liver, and 30% of these patients have documented nonalcoholic steatohepatitis (NASH) that may progress to cirrhosis. The degree of obesity parallels the likelihood for both fatty liver and NASH.

Implications for Management