Page 1838 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 130: The Obesity Epidemic and Critical Care 1307

mechanisms. First, obesity increases the risk of coronary atheroscle- patients exhibiting relatively normal pulmonary function but some
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rosis by inducing several risk factors in parallel. For example, obesity patients experiencing more significant effects. 16-18 In general, abnor-
is associated with hypertension, insulin resistance, dyslipidemia, and malities accrue as the BMI increases, and with increases in thoracic
coagulation abnormalities, which separately and collectively promote and abdominal (eg, central) adiposity. The most predictable effect of
the development of cardiovascular disease. Impaired fibrinolysis and obesity is a decrease in the functional residual capacity (FRC) caused
systemic inflammation are suggested by the frequent elevation of by the mass load of adipose tissue around the rib cage and abdomen
plasminogen activator inhibitor I, fibrinogen, and interleukin-6 and and in the visceral cavity. In extremely obese patients, the FRC may
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C-reactive protein levels. The metabolic syndrome in particular repre- little exceed the residual volume, predisposing to small airway closure
sents a cluster of risk factors for atherosclerosis. 11 and atelectasis, particularly in the dependent areas of the lung. In
There are other, more direct mechanisms through which obesity addition, the overall compliance of the respiratory system is reduced,
causes heart disease. Obesity may impair cardiac function through mildly so in simple obesity and to as low as 45% of normal in patients
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chronic pressure and volume overload. Cardiac output is increased with OHS. This has historically been thought to be due to a combina-
in obesity as a result of increased extracellular volume and increased tion of reduced lung compliance and reduced chest wall compliance.
blood flow to most tissue beds. This increased cardiac output is associ- Conceivably, the former may arise from some combination of dependent
ated with increased preload and cardiac dilation, with the subsequent airway closure and increased surface tension related to breathing
development of eccentric left ventricular hypertrophy. This chronic at low lung volumes, and from increased thoracic blood volume.
volume-overloaded state, when combined with increased left ventricu- Studies of chest wall compliance have yielded conflicting results.
lar afterload from concurrent hypertension, may result in marked left However, it is likely the case that, while the configuration of the
ventricular hypertrophy. Over time, left ventricular hypertrophy leads pressure-volume curve of the chest wall is relatively normal, chest and
to impaired ventricular filling and diastolic heart failure. Systolic heart abdominal adiposity impose an inspiratory threshold load to breathe.
failure may result from ischemic heart disease, microvascular disease from In other words, while the initiation of the breath requires more effort,
diabetes mellitus, longstanding hypertension, or, in severe, longstanding once this threshold is surpassed chest wall compliance is normal. 19
obesity, a decrease in mid-wall fiber shortening and ejection fraction. 12 Airway function may be abnormal in some patients with obesity. 20,21
Pulmonary hypertension with right ventricular hypertrophy and There is some evidence that airway resistance is increased beyond that
dilation may accompany obesity. Frequently, the pathogenesis is multi- expected from a reduction in airway caliber due to reduced lung volume. In
factorial: for instance, due to the combination of diastolic heart failure addition, the effects of bronchoconstriction on expiratory flow limitation
and untreated sleep disordered breathing. Importantly, uncomplicated and airway closure may be more pronounced in obesity as a consequence
obstructive sleep apnea alone results in only mild pulmonary hyperten- of smaller lung volumes and airway caliber. Whether obesity is itself associ-
sion. The clinical implication of this is that the clinician who encounters ated with increased airway hyperresponsiveness is controversial.
a patient with moderate to severe pulmonary hypertension is obligated
to search for causes in addition to obstructive sleep apnea. Occult Pulmonary Function: The most frequent abnormality in pulmonary
diastolic dysfunction and chronic thromboembolic disease should be function in obesity is a decrease in the expiratory reserve volume
considered. The so-called “overlap syndrome” describes the relatively attributable to cephalad displacement of the diaphragm by adipose
common presentation of the patient who has both obstructive sleep tissue. In extremely obese individuals and in those with the OHS, total
apnea and chronic obstructive pulmonary disease, a condition that lung capacity and vital capacity may be reduced. In such patients, the
may lead to severe pulmonary hypertension. Cor pulmonale may also residual volume actually may be increased relative to total lung capac-
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develop in patients with the obesity hypoventilation syndrome (OHS). ity because of small airway closure and gas trapping. This is supported
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This poorly understood disorder is associated with daytime hypercap- by the finding of larger total lung capacity by body box plethysmogra-
nia and hypoxemia, with the latter arising from alveolar hypoventila- phy than by helium dilution. Similarly, spirometry is typically normal
tion and poor ventilation of the basal lung due to airway closure and in simple obesity, whereas severely obese individuals or those with
atelectasis. Hypercapnia and hypoxemia elicit pulmonary vasoconstric- the OHS may exhibit reductions in the forced expiratory volume in
tion. Eventually, this may lead to vascular remodeling with resulting 1 second and in the forced vital capacity, although the ratio of these
irreversible pulmonary hypertension and cor pulmonale. Individuals with two variables is preserved or even increased.
the OHS usually, but not always, have coexisting obstructive sleep apnea. Why do some individuals exhibit diminished pulmonary function and/
Interestingly, patients with cardiovascular disease who are overweight or the OHS, whereas comparably overweight individuals may be little
and obese tend to have better outcomes than patients with who are not. affected? Some, but not all, data suggest that the distribution of body fat
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There are many potential explanations for this so-called “obesity paradox,” may be an important determinant of pulmonary function; simply put,
including the possibility that patients who develop cardiovascular adipose tissue that is more centrally located is more likely to negatively
disease through obesity-related mechanisms may develop more mild influence pulmonary function. There may also be differences in respira-
forms of disease. tory muscle strength between patients with simple obesity and those with
What are the clinical implications of this susceptibility? First, the inten- the OHS, with the latter exhibiting relatively decreased inspiratory muscle
sivist caring for the extremely obese patient should have a high index of strength. Weakness may be considered absolute, a result of mechanical dis-
suspicion for the presence of ischemic heart disease from coronary artery advantage from diaphragm malposition, and relative, when the increased
or microvascular disease. Second, abnormal cardiac function, diastolic work of breathing from extreme obesity is considered (see below).
or systolic, may be present, even if other risk factors for heart disease are
absent. Particular sensitivity to changes in intravascular volume may result. Gas Exchange: Extreme obesity causes closure of small peripheral air-
ways in the dependent regions of the lung, resulting in mismatching
Third, pulmonary hypertension and right ventricular failure should be
suspected when obstructive lung disease and/or daytime hypoxemia or of ventilation and perfusion. The result may be a widened alveolar to
arterial oxygen gradient and mild to moderate hypoxemia that worsens
hypercapnia are present. The diagnosis of these conditions is complicated
by poor sensitivity of physical examination and transthoracic echocardiog- in the supine position. Severe hypoxemia may be present in individuals
with the OHS because of the additional contribution of hypoventilation.
raphy in extremely obese individuals. In selected patients, transesophageal
echocardiography or invasive hemodynamic monitoring may be necessary. The diffusing capacity for carbon monoxide is typically normal or even
elevated when indexed to alveolar volume.
■ PULMONARY EFFECTS Control of Breathing: Ventilatory drive is increased in simple obesity
Mechanics of the Respiratory System: The effect of obesity on pulmo- as assessed by the mouth occlusion pressure and diaphragm electrical
nary function varies considerably between individuals, with most activity in response to carbon dioxide inhalation. In contrast, mouth

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