Obesity and ARDS

Abstract

The obesity pandemic continues, with rising prevalence reported throughout the world. In the United States, recent data show that more than twothirds of US citizens are either obese or overweight (BMI . 25 kg/m 2 ). Approximately 33% of adults in the United States are obese (BMI . 30 kg/m 2 ), and in some areas of the country the prevalence of obesity reaches . 40%. 1 In Europe, obesity prevalence varies by country but ranges from 9% to 30%, and is steadily increasing. 2 All of these statistics emphasize the importance of obesity and related conditions in patient care. Even in a state of relative health, obesity has major effects on cardiopulmonary physiology. ARDS continues to be both prevalent and very morbid, with an estimated age-adjusted incidence of 86.2 per 100,000 patient years, and reported in-hospital mortality of nearly 40%. 3 Data from the 2009 infl uenza A(H1N1) pandemic suggested that patients who are obese represent a unique patient population in ARDS. Among patients with severe or fatal 2009 infl uenza A(H1N1), rates of severe and morbid obesity (BMI . 35 kg/m 2 and . 40 kg/m 2 , respectively) were fi ve to 15 times higher than the general population. 4 , 5 This fi nding, with other data, suggests a potential link between ARDS and obesity, and at a minimum demonstrates that when critical illness is coincident with obesity, there are additional considerations for dis ease mechanism, management, and prognosis. 6 Such inpatients are often challenging to manage due to issues including line placement, transportation, drug dosing , and imaging ( Table 1 ). Changes in Baseline PhysiologyEven without the additional pathophysiology of ARDS, patients who are obese experience a number of changes in their physiology compared with lean control subjects. Some of the baseline alterations in respiratory mechanics of the patient who is obese include a decrease in total lung capacity (TLC), functional residual capacity (FRC), and vital capacity (VC) as well as increases in pleural pressure and upper and lower airway resistance.The decreased TLC, FRC, and VC are due to an overall decrease in respiratory system compliance, which in turn is secondary to increased weight of the chest wall and increased abdominal pressure from

Early severe acute respiratory distress syndrome: What’s going on? Part I: pathophysiology

“…[Thus, focal ARDS in a morbidly obese patient requires: a) from a physiological point of view, a low PEEP (5−10 cm H 2 O) to reopen the dependent atelectasis itself [87] (Fig. 2 in [87]); and b) from a practical point of view, a high PEEP to withstand the high IAP [120,121]. In this specific setting, a high PEEP takes precedence over a low PEEP].…”

Successful Use of Early Percutaneous Dilatational Tracheotomy and the No Sedation Concept in Respiratory Failure in Critically Ill Obese Subjects

“…3 Obese patients often suffer from obstructive sleep apnea, obesity hypoventilation, ARDS, hypertension, ischemic heart disease, hyperlipidemia, and type 2 diabetes mellitus. 1,4,5 Respiratory physiology in obese patients is characterized by reduction of tidal volume, expiratory reserve volume, residual volume, total lung capacity, functional residual capacity, vital capacity, FEV 1 , FVC, lung compliance, chest wall compliance, maximum voluntary ventilation, maximum oxygen consumption, diffusing lung capacity for carbon monoxide, upper and lower airway resistance, and increased pleural pressure and work of breathing with unchanged FEV 1 /FVC. 1,[4][5][6] Function of the diaphragm is hampered in obesity due to increased intraabdominal pressure, which additionally contributes to limited compliance of the respiratory system and decreased static and dynamic lung volumes.…”

“…1,4,5 Respiratory physiology in obese patients is characterized by reduction of tidal volume, expiratory reserve volume, residual volume, total lung capacity, functional residual capacity, vital capacity, FEV 1 , FVC, lung compliance, chest wall compliance, maximum voluntary ventilation, maximum oxygen consumption, diffusing lung capacity for carbon monoxide, upper and lower airway resistance, and increased pleural pressure and work of breathing with unchanged FEV 1 /FVC. 1,[4][5][6] Function of the diaphragm is hampered in obesity due to increased intraabdominal pressure, which additionally contributes to limited compliance of the respiratory system and decreased static and dynamic lung volumes. 1,[4][5][6] Further, pleural pressure is increased in obese patients, resulting in reduced transpulmonary pressure, and thereby enables collapse of airways and lung parenchyma and generation of atelectasis.…”

“…1,[4][5][6] Function of the diaphragm is hampered in obesity due to increased intraabdominal pressure, which additionally contributes to limited compliance of the respiratory system and decreased static and dynamic lung volumes. 1,[4][5][6] Further, pleural pressure is increased in obese patients, resulting in reduced transpulmonary pressure, and thereby enables collapse of airways and lung parenchyma and generation of atelectasis. 1 Atelectasis diminishes lung volume and subsequently the area for gas exchange.…”

“…1,[4][5][6] Further, pleural pressure is increased in obese patients, resulting in reduced transpulmonary pressure, and thereby enables collapse of airways and lung parenchyma and generation of atelectasis. 1 Atelectasis diminishes lung volume and subsequently the area for gas exchange. 1 However, prone position performed in ARDS patients to reduce atelectasis and to improve arterial oxygenation can be applied in obese patients safely.…”