Near-Fatal Asthma

By Mark D. Siegel, MD, FCCP

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Mechanical Ventilation

Dynamic Hyperinflation

Most of the dangers of mechanical ventilation relate to dynamic hyperinflation (DHI) caused by severe airway obstruction.^55,56,58 In contrast to patients without obstruction who exhale to functional residual capacity (FRC) between breaths, patients with NFA may have insufficient time to reach FRC, especially when the minute volume (E) is high (Fig 3). As a result, the end exhalation volume gradually rises until a new equilibrium, FRC', is reached.

DHI has two major consequences: hemodynamic compromise and barotrauma. Hemodynamic compromise is caused by high intrathoracic pressure, which in turn leads to (1) decreased venous return; (2) pulmonary vascular compression and increased right ventricular afterload; (3) decreased left ventricular preload caused by right ventricular dilation and shift of the intraventricular septum towards the left; and (4) external compression of the heart by the hyperinflated lungs.

The goal of mechanical ventilation, in addition to ensuring oxygenation, is to minimize DHI. Unfortunately, the severity of DHI and the risks it entails are difficult to quantify and do not correlate well with the physical examination or chest radiograph findings. Instead, pressures measured at the airway opening are generally used, particularly the plateau pressure (Ppl), the peak airway pressure (Ppk), and intrinsic positive end-expiratory pressure (autoPEEP).

The Ppl, measured during an end-inspiratory breath hold, essentially equates with the elastic recoil pressure of the respiratory system (Pel), which is directly related to the degree of lung inflation and inversely related to respiratory system compliance. A Ppl of approximately 30 to 35 cm H₂O has been invoked, particularly in patients with the acute respiratory distress syndrome, as a threshold pressure beyond which lung overdistention may occur.⁵⁹ Few data show a clear correlation between Ppl and complications in patients with asthma, however.⁵⁵ Additionally, Ppl can be measured accurate only in a patient who is breathing passively, and thus it is impossible to measure in those who are actively inhaling or exhaling.

The Ppk measurement represents the sum of elastic recoil pressure and pressure related to airway resistance:

Ppk = Pel + Pr

The Pr is the product of the inspiratory flow rate and airway resistance (Raw):

Pr = flow rate x Raw

Pr is insignificant in normal individuals in whom Raw is negligible. In patients with high Raw, however, Pr can be significant. In fact, the difference between the Ppk and Ppl is a helpful way to measure Pr and is useful for detecting a response to therapy.

Some caveats must be considered, however, when interpreting the Pr. First, in addition to reflecting changes in Raw, the Pr also reflects changes in the set inspiratory flow rate, so that changes may reflect differences in ventilator settings rather than the patient's mechanics. An increase in the inspiratory flow rate can increase the Ppk dramatically. Thus, interpretation of the significance of the Ppk – Ppl difference must take the inspiratory flow rate into account. In general, Ppk correlates poorly with the risk of DHI-related complications,⁵⁵ probably because it overestimates the degree to which airway pressure is transmitted to the distal airways and alveoli, as airway pressure drops across areas of resistance in the larger airways (Fig 4).

Measurements of autoPEEP are frequently used to assess DHI.⁵⁵ AutoPEEP is measured by occluding the airway during an end-expiratory breath hold. The pressure measured reflects the Pel of the respiratory system at end exhalation. In normal individuals exhaling to FRC, this pressure should be 0 cm H₂O. However, in patients unable to exhale fully between breaths, expiratory flow continues and a persistent positive driving pressure can be detected. In NFA, however, autoPEEP reflects the degree of DHI only loosely, and may significantly underestimate DHI when airway occlusion occurs, eg, due to mucus plugging (Fig 5). Similarly, autoPEEP correlates poorly with response to treatment and the risk of complications.^55,60 As with the Ppl, autoPEEP can be measured only in relaxed patients.⁵

In contrast to these measurements, the volume at end inspiration, measured by inducing apnea and collecting exhaled gas in a spirometer over a 60-s period, correlates well with the risk of DHI-related complications.^55,56 Unfortunately, measurement of volume at end inspiration requires neuromuscular blockade and is not readily performed in most ICUs.

Although none of the measurements of DHI is perfectly sensitive or specific, the Ppl is probably most practical. A useful goal is to keep the Ppl < 25 cm H₂O if possible.^56,61 Whichever measure is used, however, it is essential to monitor patients for DHI-related complications such as shock or barotrauma. In hypotensive patients, improved hemodynamics occurring in response to lowering the Ve strongly suggests DHI.

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