Title:
Toxic inhalation with hydrogen cyanide prompts a significant increase of mean pulmonal
arterial pressure in an animal model.
Purpose of the study
Toxic smoke inhalation contains mainly two major toxic gases carbonmonoxide (CO) and hydrogen cyanide (HCN) leading to hypoxia of cells [1,2]. We investigated the effect of multiple mixture of gases on pulmonal arterial blood pressure during intoxication in a smoke inhalation pig model.
Materials and methods
With approval by local authorities an intoxication model for pigs (25-35kg) with anaesthesia, intubation and instrumentation including a pulmonal arterial catheter was used.  Smoke intoxication was simulated by controlled ventilation in a closed circuit with: t=0min (no toxic gases), t=5min air with CO=1500ppm (parts per million) over 5 minutes, t=10min air with CO=750ppm and HCN=500ppm over 5minutes, t=15min air with HCN=1000ppm until cardiac arrest occurred. The mean pulmonal arterial pressure (mPAP) was recorded from t=0min until t=30min. Analysis with Wilcoxon-Test compared to Baseline. Results as median (25/75%percentiles).
Results
Cardiac arrest occurred in all pigs in a median time of 38min(25.5/48.5), so that 16 of 24 animals could be included until t=30min. t=0min 21mmHg(17/23), t=5min 21mmHg(19/30), p=0.1680; t=10min 37mmHg(33/43), p=<0.0001; t=15min 36mmHg(33/41), p=<0.0001; t=20min 31 mmHg(29/34), p=0.0003; t=25min 27mmHg(21/31), p=0.0259; t=30min 22mmHg(19/25), p=0.3745.
Conclusions
Hydrogen cyanide inhalation caused an early and significant increase of mPAP. During prolonged intoxication and shortly before cardiac arrest occured mPAP decreased to baseline levels. Further investigations are needed to investigate the effects of hydrogen cyanide on pulmonary vascular tree in detail.

Toxic inhalation with hydrogen cyanide prompts a significant increase of mean pulmonal arterial pressure in an animal model.