Inhaled short acting bronchodilators are the mainstay of treatment of an asthma exacerbation. Most commonly, inhaled short acting beta-2 agonists such as albuterol, levalbuterol, or salbutamol are employed. These medications target the underlying physiologic cause of respiratory failure, bronchospasm. They do not, however, treat the underlying inflammatory insult which causes bronchospasm. Albuterol is the most commonly used short acting bronchodilator in the United States. In the most serious cases, it can be used as a continuous nebulized inhaled solution. No data exists in regards to withholding short acting bronchodilators during an asthma exacerbation and equipoise does not exist for such study given the presumed obvious benefit. A meta-analysis showed no advantage of continuous administration of beta agonists, as compared to intermittent administration, in acute asthma [3]. Likewise, a controlled trial in the subset of severe asthma failed to show benefit of continuous beta agonists as compared to treatments every 20 min followed by treatments every hour [4]. For the even smaller subset of life threatening asthma, no prospective data exists in adults to our knowledge.

Addition of inhaled short acting anticholinergic medications to administration of short acting beta agonists improve pulmonary mechanics [5] as well as decrease admission rates [6] in patients with severe asthma, and are recommended by a panel of experts [7]. No data exists in patients receiving mechanical ventilation, though use of anticholinergic may theoretically decrease hypersecretion of mucus and mucus plugging, a finding common in fatal asthma [8].

Corticosteroids are administered during an asthma exacerbation to decrease the inflammation that leads to bronchospasm. Meta-analysis has shown a benefit of steroid therapy in adults with acute asthma [9]. No good data exist for the optimal dose of corticosteroids, but 2 mg/kg of methylprednisolone or †he equivalent is recommended by an expert panel [7]. In a randomized trial, no benefit was demonstrated with high dose (500 mg methylprednisolone) versus standard dose (100 mg methylprednisolone) corticosteroids [10].

Arterial blood gases are monitored during status asthmaticus in the spontaneously breathing patient. In a patient with adequate respiratory reserve during an asthma exacerbation, an arterial blood gas typically shows respiratory alkalosis. A normal pH and partial pressure of carbon dioxide with a high work of breathing, respiratory acidosis, or normalization of the pH after an initial respiratory alkalosis are all harbingers of impending respiratory embarrassment, and escalation of support with adjunctive treatments and/or invasive mechanical ventilation should be initiated.

Strategies for asthmatic patients on mechanical ventilation hinge on the avoidance of hyperventilation, or air trapping, as illustrated in our case. Indeed, hypotensive and mechanical complications are related to the volume of gas enclosed in the thorax above functional residual capacity (FRC) at end exhalation [2] (please see section “Monitoring for Hyperinflation”). Entrapment of supra-physiologic gas volumes is best avoided by allowing for full exhalation of tidal volumes and return to FRC. Unfortunately, with severe airway obstruction the exhalation time required to fully empty the lung to FRC can be extremely prolonged. To allow full exhalation, clinicians can either decrease the tidal volume of the inspired breath, or allow additional time for exhalation. In other words, maximization of expiratory time is key. Whatever isn’t inspiratory time is expiratory time.

To this end, clinicians can decrease tidal volume in order to decrease the air volume that needs to be exhaled, or decrease the respiratory rate, which increases the time of exhalation. Adjustment of the ratio of inspiratory time to expiratory time by adjusting the flow rate (i.e. 60–100 L/min) or shape (accelerating to square) also increase the amount of exhalation time, however the incremental benefit as compared to decreasing the respiratory rate is minimal at low tidal volumes [11]. Increased flows can also increase spontaneous respiratory rates in some mechanically ventilated patients, which would outweigh any incremental benefit [12]. As a starting setting, a minute ventilation of 10 L per minute or less and a respiratory rate of 10–14 breaths/minute are reasonable [13]. Vigilant monitoring for the efficacy of ventilator settings is needed and is discussed in the section “Monitoring for Hyperinflation”.

During permissive hypoventilation, hypercarbia often develops as the minute ventilation provided is not adequate to eliminate the produced carbon dioxide. In a patient with spontaneous respiration on the ventilator, hypercarbia will often lead to an increased respiratory rate, which may be detrimental (see ventilator strategies). Often, deep sedation or paralysis is needed to allow for permissive hypercapnia (or permissive hypoventilation). Elevation in carbon dioxide on arterial blood gas should be tolerated, with a goal arterial blood pH above 7.15 [14]. If the pH drops below 7.15, sodium bicarbonate or THAM infusions can be utilized. Minute ventilation can be increased cautiously if there is no significant hyperinflation. If life-threatening changes in pH continue, further strategies include deeper sedation or paralysis to minimize carbon dioxide production by muscular tissues. In the rare case that these treatments are inadequate, extracorporeal life support (ECLS) can be utilized for CO₂ removal (see evidence contour).

Respiratory causes of death from status asthmaticus often stem from circulatory collapse or mechanical complications of invasive mechanical ventilation, which are typically caused by air trapping and pneumothorax respectively. Avoidance of these complications requires monitoring for hyperinflation. Indeed, the volume of trapped air above functional residual capacity (FRC) at end exhalation correlates with risk for pneumothorax and hypotension (see Fig. 23.1) [2]. However, measuring this volume in clinical practice is difficult due to lack of familiarity with the technique needed (see Fig. 23.2 for full discussion).

Plateau pressure, Auto-PEEP, and analysis of flow volume curves are used as surrogates to directly measuring the entrapped air volume above FRC. Interestingly, plateau pressure and Auto-PEEP did not correlate with barotrauma or hypotensive complications in a single study of mechanically ventilated asthmatic patients [2], despite having some correlation with end inspiratory lung volume (VEi) [15]. However, monitoring of these parameters is advocated by experts as a surrogate for direct measurement of trapped air volume, with goals being auto-PEEP as low as possible and plateau pressures less than 30 cm H₂O [11, 16].