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  • 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 (bpm), 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.
  • Severe exacerbations and death can occur in patients with mild asthma.
  • Airflow obstruction causes ventilation-perfusion inequality, lung hyperinflation, and increased work of breathing.
  • Oxygen, β agonists, and systemic corticosteroids are first-line treatments. Agents of debated efficacy include ipratropium bromide, magnesium sulfate, leukotriene modifiers, theophylline, inhaled steroids, and heliox.
  • Noninvasive ventilation is potentially useful in hypercapneic patients not requiring intubation.
  • Postintubation hyperinflation decreases preload to the right ventricle and may cause barotrauma, hypotension, or cardiac arrest. A ventilator strategy that lowers lung volume decreases complications.
  • Treating airflow obstruction and prolonging expiratory time decreases lung hyperinflation. Expiratory time is prolonged on the ventilator by lowering minute ventilation (even at the cost of hypercapnia) and increasing inspiratory flow rate.
  • Deep sedation allows for safe and effective mechanical ventilation in most intubated patients. Paralysis increases the risk of myopathy.
  • Patient education, environmental control, and pharmacotherapy are crucial to prevent exacerbations and death.

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Asthma is characterized by wheezing, dyspnea, cough, hyperreactive airways, and reversible airflow obstruction.1–3 In the vast majority of cases, the disease is managed uneventfully in the ambulatory setting. However, severe attacks and death can occur regardless of severity classification, and in some cases there is little warning before a terminal event.4 Deaths often occur outside the hospital; patients who have not arrested prior to emergency department (ED) arrival generally have a good prognosis.5 Underestimation of severity, a gap in communication between health care provider and patient, airway inflammation (even in mild disease), and failure to use inhaled corticosteroids all contribute to asthma morbidity and mortality.6–10

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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 bpm, use of accessory muscles of respiration, pulse >120/min, pulsus paradoxus >25 mm Hg, peak expiratory flow rate <50% predicted or personal best, hypoxemia, and eucapnia or hypercapnia.1 Altered mental status, paradoxical respirations, bradycardia, a quiet chest, and absence of pulsus paradoxus from respiratory muscle fatigue identify imminent respiratory arrest.1

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The objectives of this chapter are to review the pathophysiology of severe asthma exacerbations, discuss clinical assessment and differential diagnosis, assess pharmacologic treatment, and provide a ventilatory strategy for intubated patients. It is perhaps in this last area of acute severe asthma management that intensivists have made their greatest strides over the last two decades, with indirect evidence suggesting that current strategies ...

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