Morbidly obese patients have an increased work of breathing due to reduced chest wall compliance associated with the accumulation of fat on the chest wall, diaphragm, and abdomen. There is some contribution from obesity-related respiratory muscle dysfunction. Decreases in functional residual capacity (FRC) and ERV are the most commonly reported abnormalities of pulmonary function in obese subjects.8 Decreased respiratory compliance leads to decreased FRC, vital capacity (VC), and TLC. These parameters are significantly lower in individuals with upper body fat distribution (central obesity). The reduction in FRC is due to decreased ERV. Reduction in ERV is due to encroachment of abdominal contents on the diaphragm, decrease in respiratory system compliance by chest wall fat, and impairment of respiratory muscle strength. ERV is the most sensitive indicator of the effect of obesity on pulmonary function testing. Each kilogram of weight gained results in approximately a 26 mL reduction in VC.9 RV remains normal. Decreased FRC can result in lung volumes below closing capacity during normal tidal ventilation leading to small airway closure, V/Q mismatch, right-to-left shunting, and hypoxemia (Fig. 23-1). Anesthesia worsens the situation such that up to a 50% reduction in FRC occurs in the obese anesthetized patient compared with 20% in the nonobese. Reduction in FRC impairs the ability of the obese patient to tolerate even minimal periods of apnea; hence the rapid desaturation after induction of anesthesia despite adequate preoxygenation.
Effects of obesity, positioning, and anesthesia on lung volumes. CC, closing capacity; CV, closing volume; FRC, functional residual capacity; RV, residual volume. [Reprinted with permission from Ogunnaike BO, Whitten CW. Anesthesia and obesity. In: Barash PG, Cullen BF, Stoelting RK, et al., eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott, Williams, & Wilkins, 2009:1232].
Obesity increases total oxygen consumption and carbon dioxide production even at rest. This is due to the metabolic activity of excess body fat and increased workload on supportive tissues. Basal metabolic activity in relation to body surface area is usually within normal limits, and an increase in minute ventilation usually maintains normocapnia. The increase in minute ventilation requires an increase in oxygen consumption because most obese patients retain their normal response to hypoxemia and hypercapnia. Morbidly obese patients do extra work to maintain their augmented ventilation; therefore they have to dedicate a high percentage of their total oxygen utilization to perform respiratory work even during regular respiration.10 Dynamic lung volumes, including the forced expiratory volume in 1 second (FEV1) and the forced vital capacity (FVC) both, decline with increasing body mass, resulting in an unchanged ratio of FEV1 to FVC. Significant hypoxemia is attributed in part to the closure of dependent airways within the range of normal tidal ventilation. Substantial weight loss results in gas exchange improvement as evidenced by an increase in Pao2. Morbid obesity is associated with a reduction in forced expiratory flow during midexpiratory phase and maximum voluntary ventilation (MVV) while the diffusing capacity remains normal.11 MVV, an index of respiratory muscle strength, is decreased in extreme obesity. Respiratory muscle efficiency is suboptimal in obese patients. Inefficiency is suggested by a sharper increase in oxygen consumption during exercise when compared with nonobese patients. Supine position reduces FRC due to cephalad displacement of the diaphragm. This effect is exaggerated in the obese, leading to a further reduction in FRC, further small airway closure, and increased work of breathing. Clinically significant increases in intrapulmonary shunting and oxygen consumption have been documented in obese patients while changing from a sitting to a supine position. Chest wall and lung compliance are both decreased by fat accumulation on the thorax and abdomen. Increased pulmonary blood volume, which is part of an overall increase in total blood volume, partially explains the decreased lung compliance. Chronic hypoxemia causes polycythemia, which contributes to the increased blood volume. Morbidly obese patients breathing room air have lower arterial oxygen tensions (Pao2) than that predicted for similar-age nonobese subjects in both sitting and supine positions. Chronic hypoxemia can eventually lead to pulmonary hypertension and cor pulmonale.
Obstructive sleep apnea (OSA) is defined as a cessation of airflow for more than 10 seconds 5 or more times per hour of sleep despite continuous respiratory effort against a closed glottis in combination with a decrease in arterial oxygen saturation of greater than 4% (Fig. 23-2). Obstructive sleep hypopnea is a decrease in airflow of more than 50% for more than 10 seconds, 15 or more times per hour of sleep; it is usually associated with snoring and arterial oxygen desaturation greater than 4%. The upper airway resistance syndrome is characterized by arousal in response to increased upper airway resistance without an elevated apnea-hypopnea index (AHI). AHI is the total number of apneas and hypopneas per hour and used to quantify the severity of OSA.12 The AHI is the total number of apneas and hypopneas per hour. An AHI index higher than 30 signifies severe OSA; values of 5 to 15 and 16 to 30 define mild and moderate OSA, respectively. The total arousal index (AI) is the total number of arousals per hour. The sum of the AHI and total AI is known as the respiratory disturbance index.13
Pattern of oxygen saturation in a patient with severe sleep apnea. The vertical lines below the oxygen saturation values indicate respiratory disturbances. Episodes of snoring are shown. Patient is in supine position. [Reprinted with permission from Flemons WW. Obstructive sleep apnea. N Engl J Med. 2002;347:498.]
Predisposing factors to OSA include male gender, middle age, and obesity. Alcohol consumption or night sedation worsens the situation. BMI higher than 30 kg/m2 and collar size more than 16.5 in correlate with severe OSA. Resulting physiologic abnormalities include hypoxemia, hypercapnia, and generalized (pulmonary and systemic) vasoconstriction. Secondary polycythemia due to recurrent hypoxemia increases the risk of cerebrovascular and ischemic heart disease. Right ventricular failure is a potential consequence of chronic hypoxic pulmonary vasoconstriction. Electrocardiogram (ECG) pattern of right ventricular hypertrophy or echocardiographic evidence of hypofunction may be seen. Initially, respiratory acidosis occurs only during sleep with return to normal homeostasis when awake. Hypoxemia during apnea can lead to bradycardia, long sinus pauses, second-degree heart block, and ventricular dysrhythmias with markedly increased severity if arterial oxygenation decreases below 60%. The higher incidence of nocturnal angina and myocardial infarction in OSA patients may be explained by the increased incidence of arrhythmias in these patients. Activation of the sympathetic nervous system occurs in response to hypoxemia due to apneic and hypopneic events, which may explain the increased incidence of hypertension in obese OSA patients. As obesity worsens, pharyngeal area decreases due to adipose tissue deposition into pharyngeal tissues including the uvula, tonsils, tonsillar pillars, tongue, aryepiglottic folds, and the lateral pharyngeal walls where it is most pronounced, correlating well with the severity of OSA (Fig. 23-3). Weight loss improves the pharyngeal and glottic function of patients with OSA.14 The upper airway can be compressed externally by superficially located fat masses that increase the pharyngeal extraluminal pressure. This situation is evidenced by a significantly larger neck in the obese patient with OSA when compared to those without OSA and the fact that the severity of OSA correlates better with larger neck circumference than with general obesity.
Airway obstruction during sleep apnea. [Reprinted with permission from Benumof JL. Obstructive sleep apnea in the adult obese patient: implications for airway management. J Clin Anesth. 2001;13:144.]
Central depressant anesthetic drugs (benzodiazepines, opioids, and induction agents such as thiopental and propofol) reduce the action of pharyngeal dilator muscles in obese OSA patients causing pharyngeal collapse. Precurarizing doses of muscle relaxants and nitrous oxide also reduce their action. Addition of opioids will depress ventilation and result in poor response to the ensuing hypoxemia and hypercapnia. OSA is associated with difficult mask ventilation and difficult laryngoscopy, which when combined with decreased FRC and reduced oxygen stores requires anticipation and preparation for an airway emergency.
A significant number of patients with OSA are undiagnosed, which poses various perioperative challenges for the anesthesiologist. The STOP questionnaire, the initial portion of the STOP-BANG scoring model (Table 23-4), is a concise and easy-to-use screening tool for OSA. Incorporating BMI, age, neck size, and gender with the STOP questionnaire (STOP-BANG scoring model) significantly increases screening sensitivity especially for patients with moderate to severe OSA.15
Table 23-4 STOP-BANG Scoring Mode ||Download (.pdf)
Table 23-4 STOP-BANG Scoring Mode
|1.||Snoring||Do you snore loudly (louder than talking or loud enough to be heard through closed doors)?|
|2.||Tired||Do you often feel tired, fatigued, or sleepy during the daytime?|
|3.||Observed||Has anyone observed you stop breathing during sleep?|
|4.||Blood Pressure||Do you have or are you being treated for high blood pressure?|
|5.||BMI||BMI more than 35 kg/m2?|
|6.||Age||Age >50 y?|
|7.||Neck Circumference||Neck circumference >40 cm?|
Questions 1-4 represent the STOP questionnaire
- High risk of OSA: answering yes to 2 or more questions
- Low risk of OSA: answering yes to fewer than 2 questions
Questions 1-8 together make up the STOP-BANG Scoring Model
- High risk of OSA: answering yes to 3 or more items
- Low risk of OSA: answering yes to fewer than 3 three items
Obesity-hypoventilation syndrome (OHS) is a combination of obesity and chronic hypoventilation that ultimately results in pulmonary hypertension and cor pulmonale.14 It can also be defined as a combination of obesity (BMI >30 kg/m2) and awake arterial hypoxemia (Paco2 >45 mm Hg) in the absence of known causes of hypoventilation. OHS is seen in up to 10% of morbidly obese patients. Clinical features are similar to those seen with OSA including excessive daytime somnolence, fatigue, and morning headaches. In addition, there is daytime hypercapnia and hypoxemia that are associated with pulmonary hypertension and right-sided congestive heart failure (cor pulmonale), resulting in substantial morbidity and mortality.16
OHS patients have an increased sensitivity to the respiratory depressant effects of general anesthetics. Episodes of central apnea from progressive desensitization of respiratory centers to hypercapnia are initially limited to sleep but eventually leads to a progressive reliance on hypoxic drive for ventilation. Pickwickian syndrome,17 characterized by obesity, hypersomnolence, hypoxia, hypercapnia, right ventricular failure, and polycythemia, is the end result of OHS. Chronic daytime hypoxemia may be a better predictor of pulmonary hypertension and cor pulmonale than the presence and severity of OSA.18 There is a strong correlation between increasing BMI (>40 kg/m2) and the likelihood of developing OHS.19 Many obese patients with OHS also have OSA, but the reverse is not always true, suggesting that OHS is an autonomous disease.20
Arterial blood gas (ABG) analysis should be obtained in any morbidly obese patient with unexplained hypoxemia or features of cor pulmonale because pulse oximetry detects oxyhemoglobin desaturation without consideration for the presence of hypercapnia. This results in inappropriate treatment with supplemental oxygen alone that does not reverse the hypoventilation.15 ABG confirms the presence of daytime hypercapnia and usually reveals compensated respiratory acidosis and hypoxemia. Elevated bicarbonate level is consistent with chronic hypercapnia.
Treatment of OHS with weight reduction, tracheostomy, or nocturnal positive-pressure support improves daytime hypercapnia and hypoxia without changing the abnormal ventilatory responses.
The increased morbidity and mortality of obesity is largely due to cardiovascular problems, including hypertension, ischemic heart disease, cardiac failure, cardiomyopathy, arrhythmias, dyslipidemia, and sudden cardiac death.21 Total blood volume is increased in the obese, but it is less than that in nonobese individuals when compared on a volume-to-weight basis (50 mL/kg compared with 70 mL/kg). Most of the extra blood volume supplies adipose tissue. Excess adiposity requires an increase in cardiac output to parallel the increase in oxygen consumption, leading to a systemic arteriovenous oxygen difference that remains normal or slightly above normal. Cardiac output increases with increasing weight (20-30 mL/kg of excess adipose tissue) because of ventricular dilatation and an increase in stroke volume. Left ventricular dilatation results in increased left ventricular wall stress leading to eccentric hypertrophy that leads to reduced left ventricular compliance, impairment of left ventricular filling (diastolic dysfunction) elevation of left ventricular end diastolic pressure (LVEDP), and eventual pulmonary edema. The dilated left ventricle has a limited capacity to hypertrophy, so when left ventricular wall thickening fails to keep pace with dilatation, systolic dysfunction ("obesity cardiomyopathy") results with eventual biventricular failure (Fig. 23-4). Obese subjects compensate by using cardiac reserve, especially in the presence of hypertension. Systemic vascular resistance (SVR) is usually within normal limits in morbidly obese patients, suggesting that hypertension and obesity can coexist with a normal SVR.
Interrelationship of cardiovascular and pulmonary sequelae of obesity. LV, left ventricle; OHS, obesity hypoventilation syndrome; OSA, obstructive sleep apnea; RV, right ventricle. [Reprinted with permission from Ogunnaike BO, Whitten CW. Anesthesia and obesity. In: Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 6th ed. Philadelphia, PA: Lippincott, Williams, & Wilkins; 2009:1234.]
Obesity accelerates atherosclerosis; however, because of reduced mobility, morbidly obese patients appear asymptomatic in the face of significant cardiovascular disease; symptoms such as angina or exertional dyspnea only occur during periods of significant physical activity.22 Cardiac output rises faster in response to exercise in the morbidly obese and is often associated with a rise in left ventricular end-diastolic pressure and pulmonary capillary wedge pressure. Increase in cardiac output during exercise is achieved by increases in heart rate without a concomitant increase in stroke volume or ejection fraction but with an increase in filling pressures. Similar changes occur during the perioperative period. With the exception of renal and splanchnic blood flows that increase with obesity, organ blood flow does not change significantly because the additional cardiac output is diverted to perfuse excess fat. Blood volume and cardiac output are approximately twice the values predicted for those with ideal body weight, but when it is normalized for body surface area, it is within normal limits or slightly below normal. Chronically increased cardiac output and blood volume may cause the SVR to increase over time. A high SVR and high preload combination may lead to an early left ventricular dysfunction and congestive heart failure.
Obesity is an independent risk factor for ischemic heart disease and eventual heart failure and is strongly associated with central (android) distribution of fat. Angina may actually be a direct symptom of obesity because a significant number of obese patients with angina do not have demonstrable coronary artery disease.23 The risk of heart failure increases by 5% for men and 7% for women for every increment of 1 kg/m2 in BMI.24 Coronary blood flow reserve in obese patients is limited because of ventricular mass and metabolic demands of the myocardium. Intraoperative cardiac failure can occur from rapid intravenous fluid administration (indicating left ventricular diastolic dysfunction), negative inotropy of anesthetic agents, or pulmonary hypertension precipitated by hypoxia or hypercapnia.
Cardiac arrhythmias can be precipitated by fatty infiltration of the conduction system, hypoxia, hypercapnia, electrolyte imbalance, coronary artery disease, increased circulating catecholamines, OSA, and myocardial hypertrophy. ECG findings frequently seen in morbidly obese patients include low QRS voltage, multiple criteria for left ventricular hypertrophy (LVH) and left atrial enlargement, and T-wave flattening in the inferior and lateral leads.25 In addition, there is a leftward shift of the P-wave, QRS complex, and T-wave axes, lengthening of the corrected QT interval, and prolonged QT interval duration. Echocardiography usually shows an increased cardiac output, increased LVEDP, and LVH in otherwise healthy obese subjects.
Mild to moderate hypertension is common in obese patients. There is a 3 to 4 mm Hg increase in systolic and a 2 mm Hg increase in diastolic arterial pressure for every 10 kg of weight gained. SVR is usually within normal limits, suggesting that hypertension and obesity can coexist with a normal SVR. Their expanded blood volume causes an increased cardiac output with a lower calculated SVR for the same level of arterial blood pressure. The renin-angiotensin system has been implicated in the hypertension of obesity. Increases in circulating levels of angiotensinogen, aldosterone, and angiotensin-converting enzyme occur. With obesity, most tissues have normal to increased level of sympathetic nervous system activity. An increased basal level of sympathetic activity predisposes to insulin resistance, dyslipidemia, and hypertension.26 Obesity-induced insulin resistance enhances the pressor activity of norepinephrine and angiotensin II.27 Hyperinsulinemia further activates the sympathetic nervous system causing sodium retention and contributing to the hypertension of obesity.28 Hypertension causes concentric hypertrophy of the ventricle in normal weight individuals but causes eccentric dilatation in obese subjects.29 The combination of obesity and hypertension causes left ventricular wall thickening and a larger heart volume and therefore increased likelihood of cardiac failure (Fig. 23-5).
Adaptation of the heart to obesity and hypertension. [Reprinted with permission from Messerli FH. Cardiovascular effects of obesity and hypertension. Lancet. 1982;1:1165.]
A hypofibrinolytic and hypercoagulable state predisposes the obese patient to cardiovascular disease. Obese patients have higher levels of fibrinogen (a marker for the inflammatory process of atherosclerosis) factor VII, factor VIII, von Willebrand factor, and PAI-1 produced by adipose tissue.30 Increased fibrinogen, factor VII, factor VIII, and hypofibrinolysis due to increased PAI-1 levels are associated with hypercoagulability and an increased risk of coronary artery disease. High factor VIII coagulant activity levels are associated with increased cardiovascular mortality. Visceral (abdominal) fat is associated with increased levels of PAI-1, factor VIII, and von Willebrand factor. Endothelial dysfunction induced by insulin increases von Willebrand factor and factor VIII levels, predisposing to fibrin formation.
Gastric volume and acidity are increased, hepatic function altered, and drug metabolism adversely affected by obesity. A significant number of fasted morbidly obese patients have gastric volumes in excess of 25 mL and gastric pH less than 2.5, which are the generally accepted volume and pH indicative of high risk for pneumonitis in the event of regurgitation and aspiration. Gastric emptying can be delayed in obese patients because of increased abdominal mass that causes antral distension, gastrin release, and a decrease in pH with parietal cell hypersecretion. However, emptying may be faster, with high-energy content intake such as fat emulsions, but RV is increased because of their larger gastric volume (up to 75% larger). Accelerated gastric emptying induces hunger and frequent eating by reducing the negative feedback satiety signal produced by the presence of nutrients inside the stomach, thus precipitating a feeling of hunger and shortening the interval between consecutive meals.31
An increased incidence of hiatal hernia and gastroesophageal reflux (GERD) increases aspiration risk. Fasting nonpremedicated, nondiabetic obese surgical patients who have no significant gastroesophageal pathology are not more likely to have high-volume, low pH gastric contents than lean patients at the time of general anesthetic induction after routine preoperative fasting.32 They should follow the same guidelines as nonobese patients and be allowed to drink clear liquids (up to 300 mL) until 2 hours before elective surgery, a quantity that has been shown not to affect gastric pH and volume at induction of anesthesia adversely.33 One mechanism of increased risk of GERD is via mechanical factors whereby abdominal obesity increases intragastric pressure, increasing the frequency of transient lower esophageal sphincter relaxation and/or formation of hiatal hernia. A greater than 3.5 kg/m2 increase in BMI is associated with a 2.7-fold increase in risk for developing new reflux symptoms.34 The combination of hiatus hernia, GERD, and delayed gastric emptying, coupled with increased intra-abdominal pressure and a high volume-low pH gastric content, increases the incidence of severe pneumonitis should aspiration occur.
Peculiar morphologic and biochemical abnormalities of the liver associated with obesity include fatty infiltration, inflammation, focal necrosis, and cirrhosis. Fatty infiltration reflects the duration rather than the degree of obesity. Histologic and liver function test abnormalities are relatively common in the obese, but clearance is usually not reduced. Abnormal liver function tests are seen in up to a third of obese patients who have no evidence of concomitant liver disease; increased alanine aminotransferase is most frequently seen. Despite these histologic and enzymatic changes, no clear correlation exists between routine liver function tests and the capacity of the liver to metabolize drugs.35 Hepatic decompensation can occur after Roux-en-Y gastric bypass (RYGB), which necessitates careful assessment for preexisting liver disease in candidates scheduled to undergo this procedure because of a high prevalence (63%) of nonalcoholic fatty liver disease (NAFLD) and cirrhosis.36 NAFLD is a group of liver abnormalities associated with obesity and insulin resistance. Hepatomegaly, elevated liver enzymes, and abnormal liver histology (including steatosis, steatohepatitis, fibrosis, and cirrhosis) are an intrinsic part of this disease.37 Up to 95% of morbidly obese patients have nonalcoholic steatohepatitis (NASH).38 NASH is an aggressive form of NAFLD that can progress to cirrhosis or hepatocellular carcinoma. The incidence of gallbladder disease, including cholelithiasis, is significantly increased in morbidly obese subjects; the relative risk appears to be positively correlated with increasing BMI.39 Abnormal cholesterol metabolism is partially to blame.
Renal, Endocrine, and Metabolic Systems
Impaired glucose tolerance in the morbidly obese is reflected by a high prevalence of type 2 diabetes mellitus due to the resistance of peripheral fatty tissues to insulin. A significant number of obese patients have an abnormal glucose tolerance test that predisposes them to wound infection and an increased risk of myocardial infarction.40 Exogenous insulin may be required perioperatively, to oppose the catabolic response to the stress of surgery, even in obese patients on oral hypoglycemic agents. Gastric bypass surgery improves or even cures type 2 diabetes mellitus by substantially improving insulin resistance through an unknown mechanism.41 Subclinical hypothyroidism occurs in about 25% of all morbidly obese patients.42 Thyroid stimulating hormone levels are frequently elevated, suggesting the possibility that obesity leads to a state of thyroid hormone resistance in peripheral tissues.43,44 Hypothyroidism should be considered in any obese patient who displays perioperative cardiovascular or respiratory instability. Hypoglycemia, hyponatremia, and impaired hepatic drug metabolism are other adverse consequences of hypothyroidism. Reduction in thyroxine requirements is seen with a decrease in BMI.45
Obesity is a major risk factor for end-stage renal disease and essential hypertension. It induces high blood pressure through increased renal tubular sodium reabsorption, impaired pressure natriuresis, and volume expansion due to the activation of the sympathetic nervous system and renin-angiotensin system, and by physical compression of the kidneys especially when visceral obesity is present. Chronic obesity results in increasing urinary protein excretion and gradual loss of nephron function that worsens with time and exacerbates hypertension. Obesity-related glomerular hyperfiltration decreases after weight loss, which decreases the incidence of overt glomerulopathy.46 Obesity-related glomerulopathy is defined as focal segmental glomerulosclerosis and glomerulopathy or glomerulopathy alone.
According to the International Diabetes Federation, diagnostic criteria for metabolic syndrome include central obesity (defined as WC >94 cm for men and >80 cm for women); plus any 2 of the following 4 factors: raised serum triglyceride, low serum high-density lipoprotein-cholesterol level, high blood pressure or treatment of previously diagnosed hypertension, and abnormal fasting plasma glucose or previously diagnosed type 2 diabetes mellitus.47 It is a cluster of metabolic abnormalities including diabetes (or prediabetes), abdominal obesity, and changes in cholesterol and high blood pressure. People with this syndrome have up to a 5-fold greater risk of developing type 2 diabetes mellitus (if not already present) and are also twice as likely to die from and 3 times more likely to have a heart attack or stroke compared with people without the syndrome.