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KEY POINTS

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  • While some data suggest a decrease in the number of asthmatics requiring intubation and mechanical ventilation in recent years, all aspects of the management of severe asthma should be mastered by the intensivist, including optimizing mechanical ventilation in the face of large increases in airway resistance and propensity for dynamic hyperinflation.

  • Severe asthma exacerbation is defined by several, but not necessarily all, of the following features: dyspnea at rest, upright positioning, inability to speak in phrases or sentences, respiratory rate >30 breaths per minute, use of accessory muscles of respiration, pulse >120 beats/min, pulsus paradoxus >25 mm Hg, peak expiratory flow rate <50% predicted or personal best, hypoxemia, and eucapnia or hypercapnia.

  • Altered mental status, paradoxical respirations, bradycardia, a quiet chest, and absence of pulsus paradoxus from respiratory muscle fatigue identify imminent respiratory arrest.

  • Airway wall inflammation, bronchospasm, and intraluminal mucus cause progressive airflow obstruction. Fewer patients develop sudden-onset asthma from a more pure form of bronchospasm.

  • Airflow obstruction causes ventilation-perfusion inequality, lung hyperinflation, and increased work of breathing.

  • Oxygen, β-agonists, and systemic corticosteroids are first-line treatments. Second-line treatments include ipratropium bromide, magnesium sulfate, leukotriene modifiers, theophylline, inhaled steroids, and heliox.

  • Noninvasive ventilation is potentially useful in hypercapnic patients not requiring intubation.

  • Postintubation hyperinflation decreases right heart preload and results in tamponade physiology. This may present as tachycardia, hypotension, and even cardiac arrest. A ventilator strategy that lowers lung volume decreases these potential complications.

  • Treating airflow obstruction and prolonging the expiratory time during mechanical ventilation decreases lung hyperinflation. Expiratory time is prolonged by lowering minute ventilation and increasing inspiratory flow rate.

  • Deep sedation allows for safe and effective mechanical ventilation in most intubated patients. Paralysis increases the risk of complications.

  • Patient education, environmental control measures, and use of controller agents help prevent future exacerbations.

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Asthma is characterized by wheezing, dyspnea, cough, hyperreactive airways, airway remodeling, and reversible airflow obstruction.1 In the United States, it has a prevalence of just over 8.0% and is responsible for approximately 1.75 million emergency department (ED) visits, 450,000 hospitalizations and 3500 deaths.2 Underestimation of severity, poor communication between the health care provider and the patient, and failure to use a controller agent all contribute to morbidity and mortality.3-7 While some studies indicate the incidence of respiratory failure secondary to status asthmaticus requiring intubation and mechanical ventilation is falling,8 it is essential the intensivist become familiar with the full spectrum of acute asthma, be able to determine the stage and progression of this process, learn means to halt the progression of this syndrome, and to sustain patients who require mechanical ventilation safely until underlying airway disease responds to treatment.

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The objective of this chapter is to review the pathophysiology, assessment, and management of patients with severe asthma exacerbation, which is signaled by many, but not necessarily all of the following features: resting dyspnea, upright positioning, monosyllabic speech, respiratory rate >30 bpm, accessory muscle use, pulse >120/min, pulsus paradoxus >25 mm Hg, peak expiratory flow rate <40% of predicted or personal best, minimal or no relief from short-acting β-agonists, hypoxemia, and eucapnia or hypercapnia.1 Altered ...

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