Near-Fatal Asthma

By Mark D. Siegel, MD, FCCP

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Mechanical Ventilation

Ventilation Strategies

Ventilation strategies designed to minimize DHI improve outcome in patients with NFA.^53,55,56,62 Since Darioli and Perret's landmark article in 1984, the mortality rate among asthmatics requiring mechanical ventilation has dropped precipitously. As long as oxygenation is adequate, most patients do well when ventilation goals are relaxed, even if hypercapnia ensues.⁶³

In general, an initial E of < 115 mL/kg (eg, with a VT of 8 to 10 mL/kg and a respiratory rate of 11 to 14 breaths/min) is unlikely to cause excessive hyperinflation.^55,61 In contrast to COPD, positive end-expiratory pressure is generally not useful in asthma and may increase lung volume.^64,65 Some suggest that a combination of synchronized intermittent mandatory ventilation with pressure-support ventilation may be less likely to cause hyperinflation than assist-control ventilation in spontaneously breathing patients.⁵ In sedated, paralyzed patients, ventilator mode is unimportant.

The chief goal of mechanical ventilation is to minimize DHI by ensuring sufficient expiratory time (TE). Ways to increase TE include (1) increasing the inspiratory flow rate to decrease inspiratory time, (2) decreasing the respiratory rate, and (3) decreasing the VT.

An increased TE can be achieved much more effectively with the latter two interventions (Fig 6). Although an increase in the inspiratory flow rate generally decreases the inspiratory/expiratory (I:E) ratio, the absolute increase in TE tends to be modest when the E is low. Concerns that an increase in the IFR can worsen hyperinflation by inducing hyperventilation are not supported by recent data in COPD.⁶⁶

Decreases in E have a more dramatic impact on the degree of hyperinflation than changes in inspiratory flow rate (Fig 6, Fig 7).⁵⁸ At low E, increases in inspiratory flow rates do not ameliorate hyperinflation significantly, even with substantial decreases in the I:E ratio. In contrast, decreases in the E, effected by decreasing either respiratory rate or VT, can have a dramatic impact on DHI by substantially increasing TE (Fig 7).

Decreases in E predictably increase the PaCO₂, although, because dead space may decrease, the rise in PaCO₂ may be smaller than expected.⁵ Hypercapnia must be considered a necessary consequence of protective ventilation techniques, not a goal itself. Hypercapnia is generally well tolerated, in part due to an extensive regulatory system, including intracellular buffers, which mitigate against decreases in the intracellular pH.⁶³

Side effects of hypercapnia include cerebral vasodilation and edema, decreased myocardial contractility, systemic vasodilation, and pulmonary vasoconstriction.^5,63 If possible, the PaCO₂ should be maintained at < 90 mm Hg and acute increases should be avoided.^5,63 Exogenous bicarbonate is generally unnecessary.

Permissive hypercapnia is potentially dangerous in patients with intracranial lesions (eg, large strokes or mass lesions) who may develop intolerable increases in intracranial pressure.⁶³ In addition, the intracellular acidosis associated with hypercapnia may be tolerated poorly by patients with underlying myocardial dysfunction. The risks of hyperinflation need to be weighed against the significant risks of hypercapnia in these populations.⁶³

Patients generally require heavy sedation and sometimes neuromuscular blockade to minimize the ventilatory response to hypercapnia.^5,67 Various regimens are potentially effective, although a combination of a narcotic (eg, fentanyl) and a benzodiazepine (midazolam or lorazepam) or propofol should be adequate. As patients improve, it is important to try continuously to increase ventilation towards normal, moving expeditiously to extubation when safe.

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