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Excerpt
Dr. Reyes' comments concerning terbutaline are correct. In addition to terbutaline, this child was receiving continuous albuterol aerosols, 2% isoflurane (a potent bronchodilator), and epinephrine (1.2 micro g/kg/min). He had been receiving these drugs for several hours before the initiation of pressure support ventilation. The best PaCO2 that could be obtained was 150 torr (20.0 kPa). The child had tachycardia and was hypotensive, and it was not felt wise, or even potentially beneficial, to increase the terbutaline. The child was converted from pressure-limited intermittent mandatory ventilation to pressure-support ventilation. Within 20 mins, the PaCO2 decreased; within 2 hrs, the PaCO2 was <80 torr (<10.7 kPa).
Inhalational anesthetics, as well as ketamine, are bronchodilators. These therapies were begun before initiating pressure-support ventilation. Ventilation remained poor. Pressure-support ventilation was initiated, and, in all cases, a rapid decrease in PaCO2 was noted without altering the bronchodilator support. In this uncontrolled, retrospective study, it is impossible to be certain that pressure-support ventilation was solely responsible for the children's improvement. They may have finally responded to other forms of therapy, including steroids, bronchodilators, and anesthetics.
The purpose of this report [1] was to present the possibility of using pressure-support ventilation in children with status asthmaticus. Current dogma is that mechanically ventilated asthmatic patients require low rates, pressure control, and prolonged expiratory time. To provide this, these patients are invariably paralyzed. Paralysis removes their ability to exert forceful expiration and, I believe, contributes to air trapping and increased deadspace, thus worsening CO2 retention. My colleagues and I have used this mode of ventilation several times since the publication of this article [1]. Most recently, a 16-yr-old patient was transferred to us, intubated, paralyzed, and mechanically ventilated at a rate of 10 breaths/min, with a prolonged expiratory time. She had a PaCO2 of 150 torr (20.0 kPa). She had received fentanyl as sedation. Her neuromuscular blockade was reversed and she promptly resumed spontaneous ventilation with pressure-support ventilation. Within 10 mins, the PaCO2 was 48 torr (6.4 kPa). She was sedated solely with fentanyl and treated with continuous aerosolized beta agonists.
In our institution, pressure-support ventilation for intubated asthmatic patients has become routine. If necessary, patients are anesthetized, preferably with bronchodilating agents, such as ketamine and inhalational anesthesia. However, we are beginning to sedate with narcotics and benzodiazepines to enable the patients to tolerate intubation and establish regular respiration without being anesthetized.
Randall C.
