2020 Volume 48 Issue 4 Pages 141-143
Several reports in the dental field have discussed post-hyperventilation apnea (PHA) during sedation. Here, we report the case of a 44-year-old woman with PHA who received dental treatment without experiencing apnea while under intravenous sedation with dexmedetomidine and hydroxyzine.
The patient had no history of hyperventilation and had never taken anxiolytics in her daily life. Initially, we used midazolam to sedate her. During treatment, the patient developed tachypnea, followed by tetany. After an additional 3 mg of midazolam, the patient developed apnea. We then initiated artificial ventilation using a bag-valve mask. Propofol was used during a second and third sedation, but she developed tachypnea during treatment and apnea after treatment. For a fourth sedation, we used hydroxyzine and dexmedetomidine. Hyperventilation and apnea did not occur during or after the treatment, and she could not recall any sensations during the treatment.
Hyperventilation reduces the partial pressure of arterial carbon dioxide, thereby decreasing respiratory stimulation from central chemoreceptors. As a result, PHA can develop because of the decrease in the ventilatory response. Drugs such as benzodiazepines and propofol may promote the development of PHA by inhibiting central chemoreceptor function and the behavioral respiratory control system. Dexmedetomidine can prevent hyperventilation attacks by its sympathetic depressant effect. When treating patients with hyperventilation syndrome, the possibility of apnea should be considered and the patients’ respiratory status should be monitored. To prevent the development of PHA, it is important to select drugs that minimize respiratory depression yet have a sufficient sedative ability, such as dexmedetomidine and hydroxyzine.
