Obesity is an independent risk factor for cardiovascular disease. Since adipose tissue needs perfusion, total blood volume and stroke volume will increase to perfuse additional body fat. Cardiac output (C.O.) increases by 0.1 L/min for each 1 kg addition in body weight.

Gradual accumulation of fat between fibers of heart muscle may cause myocyte degeneration and cardiac dysfunction. Lipotoxicity of the myocardium by free fatty acids may also cause apoptosis of lipid-laden cardiomyocytes and contribute to cardiomyopathy. Increased C.O., left ventricular hypertrophy (LVH), and LV diastolic dysfunction all predispose to heart failure. Diabetes mellitus (DM), hypertension (HTN), and coronary artery disease (CAD) are other factors that predispose these people to congestive heart failure.

Increased C.O. with normal peripheral resistance causes hypertension. For every 10 kg increase in body weight, there is 3–4 mmHg increase in systolic pressure and 2 mmHg increase in diastolic pressure. This increase is more prominent with abdominal obesity. Peripheral vascular resistance may also increase due to different substances released from adipocytes and sympathetic nervous system stimulation. Obese people with metabolic syndrome specially have higher risk of CAD. Left atrial (LA) dilation increases risk of atrial fibrillation (AF) in these patients. QT prolongation also occurs in 30 % of obese patients and risk of arrhythmia and sudden death also is higher.

Despite high C.O., ventricular filling pressures increase, while the pumping function of leg and calf muscles decreases. Both of these factors contribute to higher risk of deep vein thrombosis (DVT) in obesity. Byproducts of adipose tissue may also cause pro-thrombotic or hypercoagulable state.

Adipose tissue is metabolically active and O₂ consumption and CO₂ production will rise with obesity , as does the work of breathing. Chest wall compliance is decreased in obese people and expiratory reserve volume (ERV) and consequently functional residual capacity (FRC) is significantly reduced. FRC may fall below closing capacity and consequently during normal ventilation small airways may close. Total lung capacity (TLC) is also reduced. Supine position further decreases FRC and TLC. This often results in ventilation-perfusion mismatch. Decrease in FRC means quicker desaturation during periods of apnea and limited available time between induction of anesthesia and intubation. Postoperative atelectasis is more common in this group of patients due to decreased FRC and TLC. Obesity increases the work of breathing due to decrease in both chest wall compliance and decreased respiratory muscle strength. These may lead to dyspnea.

Obstructive sleep apnea (OSA) is more common in obese people and is characterized by frequent episodes of apnea and airway obstruction at night, snoring, fragmented sleep, and daytime sleepiness. It may be difficult to ventilate and intubate a patient with OSA. Repetitive sympathetic stimulation at night may be responsible for hypertension in these patients. About 70 % of people with OSA are obese and 40 % of obese people have OSA.

Hypoventilation of obesity ( Pickwickian syndrome) is respiratory failure in markedly obese patient characterized by somnolence, daytime hypercapnia (PaCO₂ >45), hypoxemia, polycythemia, pulmonary hypertension, and cardiac enlargement (cor pulmonale). Most of these patients also have OSA.

Fatty liver (fat accumulation in liver cells >10 % of liver weight) is very common in obese patients. Fat accumulation in liver cells may cause inflammation and wide spectrum of liver disease from simple fatty liver to cirrhosis. Abdominal obesity is also associated with higher risk of gastroesophageal acid reflux (GERD) and aspiration.

Obesity is associated with hyperlipidemia, hypertension, insulin resistance, and pro-inflammatory and pro-thrombotic states. Extra adipose tissue releases several products including nonsteroidal fatty acids (NSFA), cytokines, plasminogen activator inhibitor (PAI)-1, interleukin-6, and adiponectin. These products are responsible for metabolic complications and are associated with higher risk of coronary artery disease. Treatment should be targeted toward weight reduction. Figure 21.1 depicts common systemic manifestations of obesity.

Airway evaluation should be performed before bringing the patient to the operating room, and a fiberoptic intubation (FOI) cart should be available and ready in the OR if difficult intubation is anticipated. Occasionally awake FOI may be necessary. Investigation for co-morbidities, including sleep apnea, hypoventilation of obesity, hypertension, coronary artery disease, and diabetes mellitus, is advised. Intravenous access can be a challenge in obese patients, and central access may therefore be necessary.

If the procedure is being performed through a laparotomy, epidural anesthesia may improve postoperative pain control and respiratory status. Evaluation of the lumbar and thoracic spine area and the feasibility of epidural anesthesia should be addressed in preoperative evaluation. Nerve blocks may also be considered for surgery on extremities.

Availability of a bariatric operating table and availability of an appropriately sized bariatric hospital bed for the postoperative period should be addressed before bringing the patient to the operating room. It is also important to obtain an appropriately sized noninvasive blood pressure cuff for accurate measurement of blood pressure. If a cuff is too narrow blood pressure will be overestimated.

Obese patients should be preoxygenated with 100 % oxygen for at least 3 min before induction with their head and shoulders optimally positioned prior to intubation. It may be advisable to confirm ability to mask ventilate before administering any muscle relaxant. Discussion about difficult intubation can be found in Chap. 9, Airway Evaluation and Management. A rapid sequence induction (RSI) should be considered in patients with gastrointestinal reflux symptoms.

Positioning difficulties related to patient’s body habitus and risk of nerve injury should also be addressed with appropriate padding and positioning. Additional intravenous access, if necessary, should be established soon after induction and before the patient is prepped and draped. As a general rule, medications with weak or moderate lipophilicity can be dosed on the basis of lean body weight (LBW) , while highly lipophilic medications with high volume of distribution are usually dosed based on total body weight (TBW) . Fluid requirements are usually higher than expected. Sequential compression devices, stockings, and subcutaneous heparin or low-molecular-weight heparin (if not contraindicated by surgery) should be used to prevent deep venous thromboses (DVTs) .

Adequate pain management is important so that the patient can achieve deep breathing (helps prevent lung atelectasis) and early ambulation. Postoperative pain management in abdominal surgery may be achieved with either epidural anesthesia or patient-controlled analgesia (PCA) . Long-acting narcotics should be used judiciously due to concern for respiratory depression in patients with OSA. Epidural analgesia utilizing local anesthetic and possibly an opioid may be a good alternative to intravenous analgesia. DVT prophylaxis should be continued until the patient is able to ambulate.

CPAP (continuous positive airway pressure) or BIPAP (Bi-level positive airway pressure) should be considered for postoperative care in patients with OSA. Initiation of CPAP therapy in the recovery room and continuation overnight for prevention of post operative atelectasis has been advocated. Sometimes selected patients are left intubated postoperatively, particularly those who had a difficult intubation.

Any emergent surgery warrants full stomach precautions, and intraabdominal emergencies are associated with ileus and higher risk of aspiration – even if the patient had nothing to eat or drink for several hours. Signs and symptoms of ileus include nausea, vomiting, and abdominal distention. Some elective abdominal surgeries carry a higher risk of aspiration due to the nature of the disease, as in anti-gastrointestinal reflux surgery or surgery for achalasia. H2 blockers and sodium citrate are often administered before induction in patients at high risk for aspiration. However, metoclopramide is contraindicated in bowel obstruction.