Related Experiment Videos
The effect of chloral hydrate on genioglossus and diaphragmatic activity
Insights
Chloral hydrate (CH) may selectively depress genioglossus muscle activity, increasing the risk of upper airway obstruction in patients with obstructive sleep apnea (OSA). This finding suggests caution when using CH for sleep studies in OSA patients.
Area of Science:
- Anesthesiology
- Pulmonology
- Neurophysiology
Background:
- Obstructive sleep apnea (OSA) is a condition characterized by recurrent upper airway collapse during sleep.
- Chloral hydrate (CH) is a sedative-hypnotic agent sometimes used to facilitate sleep for diagnostic evaluations.
- A case of near-fatal airway obstruction following CH administration in an OSA patient prompted this investigation.
Observation:
- Genioglossus (GG) integrated electromyograms (I EMGs), reflecting upper airway muscle activity, were recorded in cats and rabbits.
- Diaphragmatic (DIA) I EMGs, reflecting respiratory drive, were also recorded.
- Animals received hypnotic doses of CH ranging from 200-1000 mg/kg.
Findings:
- CH significantly reduced peak, minimum, and phasic GG I EMGs in most animals.
- Average peak GG I EMG decreased to 37% of pre-CH levels.
- In contrast, CH did not significantly alter peak or phasic DIA I EMGs.
Implications:
- Hypnotic doses of CH may preferentially depress genioglossus muscle activity, compromising upper airway stability.
- This selective depression could increase the risk of life-threatening airway obstruction in susceptible individuals.
- CH may not be suitable for facilitating sleep in patients with suspected OSA due to this risk.
Abstract:
A child presented with obstructive sleep apnea (OSA) and a near-fatal airway obstruction and respiratory arrest shortly after receiving chloral hydrate (CH). We, therefore, hypothesize that CH might selectively depress upper airway maintaining muscles such as the genioglossus and so predispose to airway obstruction. Genioglossus (GG) and diaphragmatic (DIA) integrated electromyograms (I EMGs) were recorded in four cats and four rabbits before and after hypnotic doses of CH ranging from 200-1000 mg/kg. Results were similar in both species. Peak GG I EMG decreased within 10-20 min after CH in seven of eight animals. Average peak GG I EMGs were decreased from 100% before CH to as low as 37.0 +/- 27.2% (SD) after CH (P less than 0.001). Minimum GG I EMGs fell from 47.2 +/- 27.2% of peak values before CH to as low as 16.0 +/- 9.7% after CH (P less than 0.01). Phasic GG I EMGs decreased from 53.8 +/- 25.1% of peak control activity to as low as 20.6 +/- 24.6% after CH (P less than 0.05). By contrast, peak and phasic DIA I EMGs after CH were not significantly different from those before CH administration. We conclude that hypnotic doses of CH may preferentially depress GG activity as compared with DIA activity. Selective depression of airway-maintaining muscular contraction by CH may place susceptible patients at risk for life-threatening airway obstruction and may preclude the use of CH to facilitate sleep for polygraphic evaluations in patients suspected of having OSA.