Severe Asthma Management

Vol. 12 •Issue 3 • Page 43
Severe Asthma Management

Aggressive Intervention Key to Preventing Last Resort of Mechanical Ventilation

When treating patients with severe asthma, there’s one clear cut way to reduce the morbidity and mortality of those on mechanical ventilation: Don’t ventilate them in the first place. To do that, you must recognize the at-risk asthmatic patients before they even progress to the point of respiratory failure and then aggressively intervene.

But even if a patient requires intubation and mechanical ventilation, successful outcomes still can be reached. Monitor constantly, and stick to a management strategy that focuses on reducing and keeping airway and alveolar pressures as low as appropriately possible.


More than 5,000 deaths from asthma occur yearly in the United States, and while many times these deaths occur within a hospital setting like the intensive care unit, they’re often iatrogenic and preventable.1

Before appropriate and timely intervention can be implemented in the ICU for these patients with severe asthma, we need to first identify who the severe asthmatic is. This is a patient who:

• has continuous symptoms, including frequent nighttime indicators

• has had a number of exacerbations in the past

• has a one-second forced expiratory volume and/or peak expiratory flow < 60 percent predicted

• whose PEF fluctuates as much as 30 percent from baseline.

Those at an increased risk of dying include patients who have escalating corticosteroid use prior to their hospital visit, a short duration of symptoms (about three days), or had prior asthma-related hospitalizations (more than three). Increased mortality risk also includes those patients with a long duration of hospitalization (about four days), a history of prior intubations, or those who are nonadherent or have psychological difficulties.

Other risk factors should be kept in mind. Most asthma deaths occur in urban areas, for instance, and there may be genetic variations that predispose subgroups of asthmatics to a higher risk of mortality. Asthmatics who have died or are at high risk for death have polymorphisms at the 589 position of the IL-4 gene.2


Once patients with severe asthma have been identified, a number of measures can be taken to manage them properly to prevent respiratory failure. For starters, supplemental oxygen should be administered if room air oxygen saturation (quickly determined by a pulse oximeter) is less than 90 percent. Adequate doses of short-acting beta2-agonists should be given immediately, and inhalation of ipratropium bromide as an adjunct to beta2-agonists can be useful.

Continuous nebulization or frequent intermittent nebulizations has significant benefits.3 In the emergency setting, a 1.25 mg or 2.5 mg administration of isomeric levalbuterol appears to have superior advantage compared to 2.5 mg or 5 mg of racemic albuterol.4

Systemic corticosteroids also should be given promptly. Because of its slow onset of action, don’t prescribe theophylline early on unless the patient is already taking it and blood levels are known.

The administration of adequate intravenous fluids can be useful to help expectorate mucus, and intravenous magnesium sulfate has its proponents.5 Additional adjuncts that have been advocated include helium-oxygen (heliox) mixtures that reduce the airway turbulence.6 Not much strong evidence exists to confirm the effectiveness of heliox in asthma, but if desperate measures are needed because of impending respiratory failure, then it’s reasonable to consider its use.

If heliox is used, be certain there’s adequate administration of oxygen. Mixtures of 70 percent helium to 30 percent oxygen or 60 percent helium to 40 percent oxygen would be safe concentrations to start with.


If patients with progressive and unrelenting bronchoconstriction are unresponsive to these acute interventions, they’re likely to wind up in respiratory failure. Like one domino falling into another, a probable mechanism leading to this scenario is that bronchospasm impedes gas emptying, which causes hyperinflation. Alveolar pressure increases, which in turn will lead to a further load on a diaphragm that’s already struggling to move air at the higher volumes, thus further increasing the work of breathing. This induces muscle fatigue, and the eventual consequence is respiratory failure.

Hypotension also may occur as a result of similar mechanisms, such as the dynamic hyperinflation and an increase in intrinsic PEEP, which influences and reduces cardiac output. Also producing comparable outcomes are rapid respiratory rates with high tidal volumes, which are associated with a shortened gas emptying time due to airway obstruction. Additionally, watch for arrhythmias that may occur because of hypoxemia, hypotension, or either respiratory or metabolic acidosis. Lastly, barotrauma, particularly pneumothorax, can be a disastrous predicament due to the mechanisms outlined above. This may occur spontaneously or may be the result of overly aggressive resuscitator ventilation with a bag-valve mask.


The ultimate goal of severe asthma management is to prevent deterioration to respiratory failure and to avoid intubation and mechanical ventilation because of the associated increased morbidity and mortality, for as close to 13 percent of asthmatics on mechanical ventilation die.7

But many times, ventilation is inevitable. In some studies, mechanical ventilation was needed in up to 50 percent of hospitalized patients, and its average duration was about three days.8 Early recognition of possible candidates for mechanical ventilation is important to improving the chance of a successful outcome.

Ventilation candidates exhibit several signs and symptoms. Look for patients who have a change in their baseline sensorium, either becoming more agitated or somniferous, and patients who have altered baseline vital signs. These would include patients who have worsening tachycardia, those who are becoming hypotensive, or those who are demonstrating oxygen desaturation.

In the end, if the patient requires intubation and mechanical ventilation, use as large an endotracheal tube size as feasible to help lower airway resistance. Lowering airway resistance, plus continuous monitoring, is key for the successful management of the intubated patient. Otherwise, a dire consequence could be severe barotrauma.

An especially critical period to watch for with this condition is just after intubation, during resuscitator ventilation, or within the first several hours after the patient has been initially placed on the ventilator. The likely scenario leading to barotrauma starts with the tendency to administer larger tidal volumes or more rapid rates of ventilation when high airway resistance is met. Because of this, ventilator settings should be employed that would lower airway resistance and keep intrinsic PEEP < 15 cm H2O pressure. Increasing the inspiratory flow rates to allow more exhalation time (to decrease the inhalation-exhalation ratio), or applying small amounts of external PEEP, are strategies that can be used to minimize intrinsic PEEP.9

If these measures aren’t possible and intrinsic PEEP worsens, then the likelihood of barotrauma is high. At this point, prophylactic insertion of chest tubes has been advocated, though a less extreme approach would be to implement low tidal volumes of 5 cc/kg to 8 cc/kg, or allow respiratory rates below 15 breaths.10 This hypoventilatory strategy could result in hypercapnia and acidemia, so infusion of bicarbonate may be needed if the pH falls below 7.2. It also may be needed if there’s myocardial depression, arrhythmias, hypotension or central nervous system changes from elevated intracranial pressures.

Medications are essential to help lower airway resistance. In addition to bronchodilators, sedation with or without the use of muscle relaxants may help lower airways resistance. Ketamine and/or inhalational anesthetics may be attempted in severe cases that don’t respond to conventional management.

Weaning and eventual extubation should commence as soon as possible and when appropriate. A turning point to be aware of is when the peak airway pressures start to fall below 30 cm H2O, intrinsic PEEP is minimal, and hypercarbia improves. Delaying extubation when this window of opportunity is available unfortunately may provoke further bronchospasm and prolong dependence on the ventilator.


In addition to mechanical ventilation, other intervention options are available. Noninvasive ventilation (continuous positive airway pressure or bilevel positive airway pressure) has shown benefits in some studies, and bronchoscopic lavage to remove airway mucus can be helpful but risky in an unstable patient.11 Extracorporeal membrane oxygenation is extreme but also could provide temporary benefit when other strategies fail.12 Inhaled anesthetics (e.g. halothane) have limited benefit.

However, not recommended at all are inhaled long-acting beta2-agonists that have a slow onset of action; beta2-agonists given intravenously that can enhance the risk of cardiotoxicity (e.g., terbutaline or epinephrine); or inhaled corticosteroids, which are ineffective compared with systemic corticosteroids for the near fatal asthmatic.

Whatever the treatment, aggressive and timely intervention to prevent the asthmatic patient from reaching a severe state is foremost to reducing morbidity and mortality. If the patient should progress to respiratory failure, be watchful and quick to take action.


Board certified in allergy/immunology, pulmonary and critical care medicine, Dr. Barbers is a specialist in asthma and lung transplantation. He’s a professor of medicine in the division of pulmonary and critical care medicine at the Keck School of Medicine, University of Southern California, Los Angeles. He’s also director of the USC Adult Asthma and Allergy Center.

For a list of references, please call John Crawford at (610) 278-1400, ext. 1499, or visit

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