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Extreme obesity presents unique cardiorespiratory challenges in the intensive care unit and frustrates the delivery of routine care.
Extreme obesity leads to a variety of cardiovascular diseases through diverse mechanisms. Therefore, a high index of suspicion for their presence is warranted in the critically ill patient.
Many patients with extreme obesity suffer from varying degrees of pulmonary hypertension. Potential etiologies include the obesity hypoventilation syndrome, the “overlap syndrome” of coexisting obstructive sleep apnea and chronic obstructive pulmonary disease, chronic venous thromboembolic disease, and left heart failure. Diastolic dysfunction is common and may contribute to this pathology.
Although simple obesity has relatively minor effects on pulmonary function, extreme obesity may be associated with reductions in forced vital capacity, forced expiration volume in 1 second, and total lung capacity. Arterial hypoxemia may be present, particularly in the supine position.
Unrecognized sleep-disordered breathing in the critically ill patient may contribute to cardiopulmonary failure. It may also confer increased sensitivity to sedatives and narcotics.
An increased risk of venous thromboembolism in obesity merits an aggressive approach to prophylaxis.
Intraabdominal pressure is elevated in obesity, placing the patient at increased risk for the abdominal compartment syndrome.
Extreme obesity is associated with a significant increase in the percentage of oxygen consumption attributable to the work of breathing. This decreased respiratory reserve results in a predisposition to the development of respiratory failure even after trivial insults.
Atelectasis is common in the extremely obese postoperative patient and, along with sleep-disordered breathing, may lead to respiratory failure. The early use of noninvasive ventilation in the high-risk postoperative patient may prevent the development of respiratory failure.
Intubation of the extremely obese patient may be technically challenging because of poor visibility of the glottis and decreased oxygen stores in alveoli from a reduced functional residual capacity.
Extremely obese patients should be ventilated in the upright or semi-upright position to improve respiratory system compliance and reduce the work of breathing. Positive end-expiratory pressure between 8 and 15 cm H2O may be necessary to prevent atelectasis.
Because the compliance of the respiratory system is reduced in extreme obesity, a high plateau pressure does not necessarily indicate alveolar overdistention. When using low tidal volume ventilation in the management of the acute respiratory distress syndrome, a plateau pressure of 35 to 40 cm H2O may be acceptable in some patients.
Ultrasound guidance may be useful in establishing vascular access in the extremely obese patient.
Numerous unpredictable alterations in pharmacokinetics have been described in obesity. Reference to published guidelines for individual drugs and close monitoring of clinically available serum drug levels are recommended.
Nutritional support in the form of carefully balanced hypocaloric enteral regimens is recommended.
Interestingly, while obesity is associated with increased all-cause mortality, the preponderance of evidence suggests that ICU outcomes are not worse in the obese critically ill patient.
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An ever-increasing percentage of the inhabitants of developed countries is obese or overweight. This trend includes men ...