Acute Asthma Management

Epidemiology

As many as 65% of adults with asthma have chronic and persistent symptoms, and up to 50% of adults with asthma meet criteria for uncontrolled asthma at any given time. It is not surprising, then, with increasing rates of disease and increasing disease severity that so many of these patients require critical care services.

Pathophysiology

See Allergic Asthma for more details on the pathophysiology of chronic asthma. Essentially, it is a disease of the distal airways characterized by bronchoconstriction, mucus hypersecretion, and intense cellular infiltration/inflammation. Poorly controlled chronic asthma leads to airway remodeling which can lead to an irreversible state of poor control.

Status asthmaticus is a severe asthma attack that does not respond to immediate and consecutive bronchodilator therapy. Near-fatal asthma refers to persistent status asthmaticus that ultimately requires ventilatory support.

Several issues in severe asthma attacks:

• Severe V-Q mismatch, leading to deranged ventilation and oxygenation
• Air trapping secondary to decreased absolute and relative expiratory time which leads to decreased venous return, reduced effective Vt, and increased likelihood of barotrauma

Outcomes

In the USA, for hospital admissions with a primary diagnosis of asthma, 10.1% were admitted to intensive care units (ICUs) and 2.1% were intubated.

A patient’s inability to markedly improve peak expiratory flow rates with aggressive bronchodilator therapy is the best predictor of asthma-associated morbidity, and a prior near-fatal asthma exacerbation is the best predictor of mortality.

Clinical Manifestations

1. Wheezing (nonspecific) and silent chest (late and severe presentation).
2. Hyperventilation - the PCO2 should be low. A normal or near-normal PaCO2 in a patient with tachypnea is an ominous sign and requires immediate attention.
3. Clinical work of breathing is increased (accessory muscle use, tripoding, diaphoresis, tachycardia, tachypnea).
4. The ECG can show acute right heart strain which generally resolves with control of airflow obstruction.

Management

Inhaled Therapies

1. Oxygen - maintain SpO2 92% or above. Note that inhaled bronchodilators can cause transient hypoxemia due to shunt physiology but this effect is mostly noted in children. Consider using heated humidified oxygen to avoid bronchoconstriction induced by dried air.
2. Inhaled SABAs are the cornerstone of rescue treatment in severe asthma exacerbations.
   1. Initial therapy is albuterol 2.5-5 mg nebulized q20 minutes x 3 doses; then 2.5 to 10 mg q1-4 hours as needed, or 10-15 mg/hr continuously.
   2. MDI beta-agonists (e.g. Ventolin) have been shown to be equally efficacious and cheaper in cost and resource utilization than the nebulized equivalents. The downsides of this are that the patient needs to be able to cooperate and use the spaced, and the dose is increased. 4 puffs of albuterol by MDI with spacer are equivalent to 2.5 mg of nebulized albuterol
3. Inhaled SAMAs are mostly effective as an additive adjunct to inhaled beta-agonists (they attenuate bronchodilation). Combination therapy generally does not provide benefit after the first 24 hours.
   1. Initial dose is ipratropium 0.5 mg nebulized q20 minutes x 3 doses; then every 2-4 hours as needed.
   2. The onset of ipratropium is slow (20-90 minutes)
4. Heliox is a mixture of helium and oxygen (mostly helium). This transitions airflow to a laminar state, reducing airway pressures and improving flow through distal bronchioles. This may be a useful treatment in very severe exacerbations.

Systemic Therapies

1. Corticosteroids - there are no proven differences in long-term outcomes between IV and PO steroids, but IV forms have a faster onset of action. Every severe asthma exacerbation should be treated with steroids. The current recommended dose is approximately methylprednisolone 40-80 mg/d IV in 1-2 divided doses until PEF reaches 70% of predicted or personal best. Higher doses are NOT more effective, IV is not superior, and treatment durations are 3-10 days without a need for a taper.
2. IV MgSO4 works be inhibiting calcium channels, reducing smooth muscle bronchoconstriction and reducing airway parasympathetic tone. Relatively contraindicated in renal insufficiency. The onset of action is between bronchodilators and steroids. A Cochrane meta-analysis concluded that use of IV magnesium sulfate improves pulmonary function and decreases hospital admissions in acute severe asthma, particularly in patients with severe exacerbations. Therefore, consider MgSO4 2g IV x 1 for all asthma exacerbations in hospital.

Mechanical Ventilation of Asthma

Indications for Mechanical Ventilation

2% of asthmatics admitted to hospital require intubation, and 10% require ICU admission. Impending respiratory failure should trigger pre-emptive intubation and ventilation:

1. Central cyanosis
2. altered mentation
3. paradoxical breathing
4. refractory hypercarbia/hypoxemia - an elevated PaCO2 indicates an FEV1 < 25% predicted
5. silent chest

Managing the Vent

• MV is not a curative therapy for patients with acute asthma
• vent settings need to maximize expiratory time, reduce air trapping, and avoid barotrauma
  • avoid excessive tidal volumes and respiratory rates
  • trend the plateau pressure as a surrogate measure of auto-PEEP
• the best strategy currently is likely mild permissive hypercarbia for brief periods to facilitate reduced air trapping and improved venous return
• What are the recommended initial vent settings?
  • Vt 6-8 mL/kg IBW
  • RR 10-14 with increased expiratory time (square inspiratory waveform, 1:3 to 1:5)
  • minute ventilation < 8-12 L/min
  • SpO2 > 90%
  • controlled ventilation in these patients invariable requires heavy sedation and analgesia, +/- neuromuscular blockade (see below)
  • There is no rule for SIMV, and pressure control ventilation is discouraged because of fluctuating high airway resistance and intrinsic PEEP

Neuromuscular Blockade

Avoid NBMAs as much as possible. If used, target TOF to 1-2 twitches. Cisatracurium (Nimbex) is preferred due to its method of elimination (Hoffman elimination).

NIV

The role of NIV is not clear in acute asthma. If used, start with support of 8/5 and increase IPAP by 2 cm H2O every 15 minutes to a goal to reduce the respiratory rate to <25 breaths per minute.

References

1. Parrillo Critical Care Medicine