Patients with acute severe asthma breathe close to their total lung capacity; this may be further increased by mechanical ventilation (Figure below: Lung volumes during spontaneous breathing and mechanical ventilation in patients with severe asthma. During spontaneous breathing, inspiration and expiration are near the total lung volume (TLC) and occur above the total lung volume during mechanical ventilation. After mechanical ventilation to deliver tidal volume (VT), the prolonged expiratory time expels the high gas volume produced by dynamic hyperinflation (VDHI); however, the lung volume at the end remains well above normal FRC because gas is trapped behind the obstructed airway (Vtrap)). During mechanical ventilation, dynamic hyperinflation occurs when there is insufficient time to fully exhale the tidal volume during the expiratory phase, resulting in increased end-expiratory lung volume and auto-PEEP.
In subsequent breaths, the progressive increase in lung volume leads to improved expiratory flow due to higher elastic retraction and increased airway diameter, which allows the entire tidal volume to be exhaled (below). Although dynamic hyperinflation may be an adaptive process that enhances expiratory flow, it can lead to severe hypotension and barotrauma, a life-threatening complication resulting from extreme alveolar hyperinflation.
Monitoring of respiratory mechanics is therefore important and a common method of monitoring is to assess airway pressure (as shown below, proximal airway pressure during end-inspiratory and end-expiratory airway obstruction. After end-inspiratory obstruction, airway pressure initially falls rapidly, secondary to airway resistance, followed by a gradual fall in pressure due to gas redistribution and tissue resistance).
In persistent asthma, the goal of controlled hypoventilation is a peak airway pressure (Ppeak) of less than 50 cmH2O. However, Ppeak is highly dependent on inspiratory flow-resistance characteristics and may not accurately reflect the degree of overinflation. When inspiratory flow is high, asthmatics typically have a Ppeak above 50cmH2O, but their risk of air pressure injury may be negligible. In addition, the inconsistency of the change in Ppeak with the reduced response to dynamic hyperinflation following prolonged expiratory time may be due to increased airway resistance as lung volume decreases. (see below, peak airway pressure, plateau pressure and auto-PEEP at respiratory rates of 18, 12 and 6 breaths/min during mechanical ventilation in severe asthma. ppeak did not decrease with prolonged expiratory time). pplat may be a better parameter for monitoring lung hyperinflation in persistent asthma.
Pplat may be a better parameter to monitor hyperinflation of the lungs in persistent asthma. Patients with severe airflow obstruction usually have near normal respiratory compliance and dynamic hyperinflation leads to an increase in Pplat. At a constant tidal volume, changes in the degree of dynamic hyperinflation from bronchodilators or altered expiratory times can be inferred from changes in Pplat. Because Pplat provides an estimate of maximum alveolar pressure, it may (in theory) help to predict the risk of alveolar rupture. However, it should be noted that Pplat represents the average end-inspiratory alveolar pressure and that some lung units will have higher maximum alveolar pressures (see the diagram below, which shows the effect of different degrees of airway obstruction on end-expiratory alveolar volume and pressure. The schematic below shows the expected distribution of tidal volumes when pressure is applied during mechanical ventilation in the presence of uneven airway obstruction). The safe threshold for Pplat in the asthmatic state is not well defined, but 25 to 30 cmH2O is the upper acceptable limit.
When measured by end-expiratory airway obstruction, autoPEEP provides an estimate of mean end-expiratory alveolar pressure. The expected level of autoPEEP in persistent asthma has rarely been reported, but two studies found mean values of 15 and 10 cmH2O, respectively. usually, changes in autoPEEP are closely related to changes in Pplat, and either (or both) may be useful in tracking the degree of dynamic hyperinflation. Sometimes, patients with persistent asthma who have radiological evidence of hyperinflation and Pplat may have low autoPEEP measurements when ventilating at very low respiratory rates, which can promote airway closure and thus prevent accurate assessment of end-expiratory alveolar pressure. autoPEEP should always be measured during passive expiration, as forceful expiration usually leads to autoPEEP s gross overestimation and dynamic overinflation, which may lead to unnecessary restrictions on minute ventilation.
(Tip: for drugs to facilitate intubation) 1. ketamine does not cause respiratory depression or hypotension but may increase laryngeal reflexes and excessive upper airway manipulation predisposes to laryngospasm. 2. isoproterenol reduces airway resistance after intubation compared with etomidate or sodium thiopental. 3. etomidate causes less hypotension than propofol and may be a better alternative for haemodynamically unstable patients. In fact, many of the drugs used to facilitate intubation reduce vascular tone and this, combined with the sudden reduction in venous return due to lung hyperinflation, may lead to post-intubation hypotension. 4. Post-intubation hypotension, severe and difficult to treat.
Controlled hypoventilation with permissive hypercapnia was first proposed as a ventilator strategy for the treatment of severe asthma. In short, the rationale behind this approach is that the risk of hypercapnia is smaller than the significantly increased lung volume.
In severe asthma, three key factors determine the degree of increase in end-expiratory volume during mechanical ventilation: expiratory resistance, tidal volume and expiratory time. The ventilator settings that have the greatest impact on the severity of hyperinflation are tidal volume, respiratory rate and inspiratory flow rate. Minute ventilation volume is the most important determinant of dynamic hyperinflation (see below, effect of minute ventilation (̇VE) and inspiratory flow rate (VI) on dynamic hyperinflation during mechanical ventilation in severe asthma), and the degree of dynamic hyperinflation is similar for a given minute ventilation volume, regardless of the specific combination of respiratory rate and tidal volume. The degree of hyperinflation became apparent as the minute ventilation rate increased from 10 to 16 and 26 litres/min; at the highest minute ventilation rate, hypotension and barometric injury occurred.
