Managing acute respiratory decompensation in the morbidly obese

Abstract

Morbid obesity adversely affects respiratory physiology, leading to reduced lung volumes, decreased lung compliance, ventilation perfusion mismatch, sleepdisordered breathing and the impairment of ventilatory control, and neurohormonal and neuromodulators of breathing. Therefore, morbidly obese subjects are at increased risk of various pulmonary complications that can present either acutely or chronically. Respiratory failure is one of the most common pulmonary complications related to morbid obesity. Both acute hypoxaemic and hypercapnic respiratory failure are more common among obese patients. The management pathway of respiratory failure depends, to a large extent, on the underlying cause, primarily due to the diversity of the underlying triggering diseases, the pathophysiology and the prognosis associated with each disease. Morbidly obese patients with hypoventilation have an increased risk of acute hypercapnic respiratory failure. Early diagnosis of this disorder and the application of non-invasive ventilation in this group of patients have been shown to improve respiratory parameters, decrease the need for invasive mechanical ventilation and improve survival.Invasive ventilation remains the last life-saving procedure in patients with respiratory failure who do not respond to non-invasive measures. However, due to the abnormal respiratory physiology in obese patients, special precautions are required during intubation, mechanical ventilation and weaning.

Effectiveness of non-invasive ventilation in acute respiratory failure of obese patients: a brief narrative review

“…[23][24][25][26] Several modes have been implemented: continuous positive airway pressure (CPAP), bilevel positive airway pressure (Bi-PAP), pressure support ventilation, assisted pressure control ventilation (APCV), Bi-PAP-spontaneoustimed (ST) with volume assured pressure support. 3,13,19,20,22,[25][26][27] More recently the so called highintensity ventilation (APCV with high rate back-up) has demonstrated encouraging results in terms of PaCO 2 reduction and mortality. 28 The setting of ventilator is very important because the delay in the reduction of PaCO 2 may be due to: -Inadequate level of inspiratory (IPAP) or expiratory (EPAP) pressure: in obese patients IPAP should range from 12 to 30 H 2 O or greater and EPAP from 8 to 12 cm H 2 O.…”

“…3 Oxygen therapy must be added if the patient continues to desaturates despite high positive airway pressure. 3,7,25 A back-up rate is mandatory because central apneas commonly occur. 3 -Inadequate duration of NIV: the obese patients as previously explained require longer NIV therapy than non-obese patients especially during the night; their apneas or hypoventilation worsen during hours of sleep.…”

“…9,17,20,22,25 This is due to the strict and more aggressive monitoring needed for these patients. 3,10,25,26 The most used ventilators have been NIV platform ventilators or ICU ventilators. In a study, a home ventilator was also used in Bi-PAP-ST or CPAP mode.…”

Bicarbonate Level for Early Diagnosis of Obesity Hypoventilation Syndrome: Still Defining Boundaries—Reply

“…OHS is a serious disorder associated with increased morbidity and mortality. 10 Therefore, early recognition is essential to prevent complications. Thus, we conclude that studies addressing the characteristics of OHS subjects and practical diagnostic tests should be performed in obese subjects.…”

Progressive Care of Obese Patients

“…Pulmonary conditions associated with obesity include obesity hypoventilation syndrome, obstructive sleep apnea, and respiratory failure. 8 Obesity hypoventilation syndrome is defined as a triad of obesity, daytime hypoventilation, and sleep-disordered breathing in the absence of alternative diagnoses and is accompanied by daytime hypercapnia and hypoxemia. 9 The syndrome is characterized by obesity (BMI ≥ 30) with awake arterial hypercapnia (PaCO 2 > 45 mm Hg).…”