Pulmonary

Preoperative evaluation of obese patients reveals that 85% have exertional dyspnea and some degree of orthopnea. Periodic breathing, especially when sleeping, may also be present.

Obese patients tend to develop some degree of thoracic kyphosis and lumbar lordosis because of a protuberant abdomen. In addition, the layers of fat on the chest and abdomen reduce the bellows action of the thoracic cage. The overall lung-thorax compliance is reduced and thus leads to increased elastic resistance of the system. Usually the diaphragm is elevated, and the total work of breathing is increased as a result of the deposition of abdominal fat. Because of these factors, the oxygen cost of breathing is threefold or greater than normal, even at rest.

The primary respiratory defect of obese patients is a marked reduction in the expiratory reserve volume. The reason for the decrease in expiratory reserve volume and other lung volumes is that the obese patient is unable to expand the chest in a normal fashion. As a result, diaphragmatic movement must account for the changes in lung volume to a much greater extent than thoracic expansion does. As discussed previously, the diaphragmatic movement is moderately limited by the anatomic changes of obesity, which account for the decreased lung volumes.

In the obese patient, the functional residual capacity may be less than the closing capacity in the sitting and supine positions; therefore the dependent lung zones may be effectively closed throughout the respiratory cycle. Consequently, inspired gas is distributed mainly to the upper or nondependent lung zones. The resulting mismatch of ventilation to perfusion produces systemic arterial hypoxemia. The hypoventilation and ventilation-perfusion abnormalities that contribute to systemic arterial hypoxemia also contribute to retention of carbon dioxide and thus lead to hypercarbia.

In the general population, undiagnosed obstructive sleep apnea (OSA) is common in obese patients despite awareness that increased abdominal girth is a significant risk factor. Reportedly more than 70% of patients undergoing weight loss surgery have been clinically diagnosed with sleep apnea.⁴ OSA can occur in patients with redundant pharyngeal tissue. Obstructive sleep apnea is characterized by excessive episodes of apnea (approximately 10 seconds), apneic episodes occurring more than five times per hour, and a 50% reduction in airflow or a reduction sufficient to lead to a 4% decrease in oxygen saturation during sleep as a result of a partial or complete upper airway obstruction. Clinically significant apnea episodes of more than five episodes in 1 hour or 30 per night result in hypoxia, hypercapnia, systemic and pulmonary hypertension, and cardiac arrhythmias. In obese patients with OSA, there is an increased risk of difficult intubations as well as postextubation complications.⁴

Cardiovascular

Thirty pounds of fat are estimated to contain 25 miles of blood vessels, and the increased body mass in obesity leads to increased oxygen consumption and carbon dioxide production. It is not surprising that the cardiac output and the total blood volume are increased in the obese state. This increase in cardiac output is a result of an increase in stroke volume rather than an increase in heart rate; the latter usually remains normal.

The transverse cardiac diameter has been shown to be greater than normal in approximately two thirds of obese patients. A linear relationship seems to exist between cardiac diameter and body weight.

Obesity has been suggested to predispose one to electrocardiographic changes. The Q-T interval is often prolonged, and the QRS voltage is reduced because of the increased distance between the heart and the electrodes. Finally, the likelihood of ventricular arrhythmias is increased in the obese patient. These arrhythmias are believed to be a result of myocardial hypertrophy, hypoxemia, coronary artery disease, and fatty infiltration of the conducting and pacing systems.

A positive correlation exists between an increase in body weight and increased arterial pressure. Hypertension is a known risk factor for the development of coronary artery disease. A weight gain of 28 lb (12.75 kg) can increase the systolic and diastolic blood pressure by 10 and 7 torr, respectively. Systemic hypertension is tenfold more likely in the obese patient. The increase in blood pressure is probably caused by the increased cardiac output.

Chronic heart failure, although uncommon, can occur in persons with long-standing morbid obesity with or without hypertension. It is usually characterized by high output and biventricular dysfunction, with the left ventricle predominating. Clinically, heart failure can be difficult to diagnose because pedal edema may be chronically present.

Cerebral blood flow in obese persons does not differ significantly from that in persons of normal weight. Oxygen uptake of the brain remains normal in the obese person; however, the fraction of the total body oxygen represented in the cerebral metabolism is less than normal, because the total body oxygen requirement is increased. Although the kidneys of obese subjects weigh more than those of nonobese counterparts, renal blood flow is the same as or slightly lower than that of patients of normal weight.

Psychological