Effect of atropine on time to cardiac arrest in hypoxic bradycardia: a randomised cross-over study in a porcine apnoea model.

BACKGROUND

In profound hypoxia, including 'cannot intubate, cannot oxygenate' (CICO) situations, bradycardia may represent an oxygen-conserving reflex rather than a correctable pathology. We hypothesised that atropine would, by increasing heart rate and myocardial oxygen demand, hasten cardiac arrest in apnoea-induced hypoxic bradycardia.

METHODS

We performed a randomised, placebo-controlled, cross-over trial in intubated, anaesthetised pigs (n=8). Each animal underwent two episodes of apnoea-induced hypoxia separated by a 6-12-h stabilisation period. At the onset of hypoxia-induced bradycardia, 1 mg of atropine or placebo was administered in random order. Apnoea was maintained until 50 s after cardiac arrest, then mechanical ventilation was resumed, and standard cardiopulmonary resuscitation was initiated. The primary outcome was time from study-drug administration to cardiac arrest. Secondary outcomes included time to return of spontaneous circulation (ROSC), heart-rate response, oxygen-delivery indices, and brain tissue oxygen tension.

RESULTS

No statistically significant difference in time to cardiac arrest was detected: 142 seconds (95% Confidence interval [CI] 84-199) after atropine vs 138 seconds (95% CI 80-195) after placebo; mean difference 4 seconds (95% CI -33 to 41), P=0.803. In four animals, atropine shortened the time to arrest, and in four it prolonged it. No significant between-condition differences were observed in systemic haemodynamic, brain oxygenation, lactate concentrations, or time to ROSC.

CONCLUSIONS

In this porcine model of apnoea-induced hypoxic bradycardia, atropine neither delayed cardiac arrest nor improved oxygenation, perfusion, or resuscitation outcomes.

TRIAL REGISTRATION NUMBER: Open Science Framework (OSF), DOI: https://doi.org/10.17605/OSF.IO/492NY.