Critical Care Management of Severe Asthma Exacerbations

Abstract

Severe asthma exacerbations, including near-fatal asthma (NFA), have high morbidity and mortality. Mechanical ventilation of patients with severe asthma is difficult due to the complex pathophysiology resulting from severe bronchospasm and dynamic hyperinflation. Life-threatening complications of traditional ventilation strategies in asthma exacerbations include the development of systemic hypotension from hyperinflation, air trapping, and pneumothoraces. Optimizing pharmacologic techniques and ventilation strategies is crucial to treat the underlying bronchospasm. Despite optimal pharmacologic management and mechanical ventilation, the mortality rate of patients with severe asthma in intensive care units is 8%, suggesting a need for advanced non-pharmacologic therapies, including extracorporeal life support (ECLS). This review focuses on the pathophysiology of acute asthma exacerbations, ventilation management including non-invasive ventilation (NIV) and invasive mechanical ventilation (IMV), the pharmacologic management of acute asthma, and ECLS. This review also explores additional advanced non-pharmacologic techniques and monitoring tools for the safe and effective management of critically ill adult asthmatic patients.

Keywords: asthma; bronchospasm; dynamic hyperinflation; extracorporeal life support; mechanical ventilation; non-invasive ventilation.

Figure 1

Air trapping and dynamic hyperinflation during asthma exacerbations. During acute asthma exacerbations, air trapping and dynamic hyperinflation occur as the respiratory rate increases due to reduced exhalation time. Residual volume and end-expiratory volume increase while inspiratory reserve volume decreases.

Figure 2

Effect of air trapping and hyperinflation on the pressure–volume curve in status asthmaticus. A well-controlled asthmatic patient without exacerbation will have a normal-appearing pressure–volume loop (green curve). In status asthmaticus, bronchoconstriction, dynamic hyperinflation, and air trapping occur, leading to decreased lung compliance and the requirement of higher peak pressures in order to reach the desired tidal volume, resulting in a “bird beaking” pattern. Additionally, the curve is shifted to the right, representing intrinsic positive end-expiratory pressure (PEEP) secondary to air trapping (blue curve).

Figure 3

Campbell diagram of the normal lung at tidal breathing. Lung recoil is plotted against chest recoil. The loop demonstrates one breath from functional residual capacity in the direction of the arrows. The red shaded area demonstrates the work done against resistance and the grey shaded area demonstrates the work done against the elastic recoil of the lung and chest wall.

Figure 4

Campbell diagram of the lung of a subject in severe asthma exacerbation. Lung recoil is plotted against chest recoil. The loop demonstrates one breath from functional residual capacity in the direction of the arrows, here occurring at a higher volume. The red arrow represents intrinsic PEEP. The red shaded area demonstrates the work done against resistance and the grey shaded area demonstrates the work done against elastic recoil of lung and chest wall. Here, the blue shaded area represents the work done to overcome intrinsic PEEP.

Figure 5

Inspiratory to expiratory time during mechanical ventilation in acute asthma. (A) Mechanical ventilation with respiratory rate set to 24 breaths per minute in patients with acute asthma. The I:E ratio is close to 1:1, and the volume waveform does not quite reach the baseline before the next breath starts. This will lead to air trapping, auto-PEEP, and dynamic hyperinflation. (B) The same patient but with respiratory rate set to 14 breaths per minute. The I:E ratio is ~1:5, and the volume waveform clearly returns to baseline before the next breath is initiated; this will prevent air trapping, auto-PEEP, and dynamic hyperinflation. I:E: inspiratory to expiratory. PEEP: positive end-expiratory pressure.