Introduction: Following cardiac arrest (CA), ventilation with the noble gas Argon after ROSC has been shown to improve hemodynamic and neurologic outcome in rats and pigs. We recently found a pronounced vasodilatory effect of inhaled Argon on pulmonary vessels in an isolated lung model and an antiarrhythmic effect in isolated hearts.
Hypothesis: We hypothesized that the vasodilatory effect of Argon leads to higher pulse pressure during CPR in vivo.
Methods: After 10 min of ventricular fibrillation, 10 intubated and isoflurane-anesthetized female pigs were randomized to receive CPR with standard (S-CPR, 30% O2, 70% N2, n=5) or Argon inhalation (30% O2, 70% Argon, n=5). All groups received 0.5 mg of epinephrine at minute 3 of CPR and defibrillation (200J) after 4 min. After baseline measurements, arterial blood pressure was measured continuously with the onset of chest compressions, and blood gases were taken after ROSC. Data are mean ± standard deviations. Statistics: Unpaired student’s t-test (two-tailed), α .05.
Results: Argon animals had a significantly higher pulse pressure (62.3±8.2 vs 40.4±8.7 mmHg). Mean arterial pressure was not different (46.3±6.6 vs 44.1±4.6 mmHg), due to a higher systolic pressure (89.7±6.0 vs 71.3±10.5 mmHg) and a trend towards lower diastolic pressures. Although the rate of ROSC was not significantly different (Argon 5/5 vs S-CPR 4/5), blood gases after ROSC with Argon inhalation showed a trend towards a better oxygenation (SaO2 95±5 vs 89±7 %). As previously seen in vitro, the antiarrhythmic effect of Argon was confirmed by a lower number of shocks prior to ROSC (1.6±0.89 vs 5.0±3.5).
Conclusion: These findings suggest that, the noble gas argon, when given as a post-conditioning agent immediately at the beginning of CPR, leads to improved hemodynamics as evidenced by higher developed pulse pressure and better oxygenation.