Sodium nitroprusside enhanced cardiopulmonary resuscitation (SNPeCPR) improves vital organ perfusion pressures and carotid blood flow in a porcine model of cardiac arrest

Introduction: Sodium nitroprusside enhanced CPR (SNPeCPR) is a novel CPR method that includes a potent vasodilator, active compression-decompression CPR, an inspiratory impedance threshold device and abdominal binding. SNPeCPR has been shown to improve vital organ flow and functional survival outcomes compared to standard CPR methods in animals. We hypothesize that one of the main effects of SNPeCPR mediated increase in cardiac output during prolonged resuscitation is profound pulmonary artery vasodilation. Methods: After electrically induced VF was left untreated for 3 min, 20 (44-48Kg) pigs were randomized to receive SNPeCPR (10) or standard CPR (10) for a total of 30 min; the first 10 minutes were BLS CPR followed by twenty minutes of ACLS. During ACLS, animals were given IV SNP (1mg bolus) or standard epinephrine (0.5mg) q5 min until ROSC or 45 min total CPR. Shocks were delivered after 30 minutes of CPR at 300J. If ROSC was achieved, animal was monitored until 4-hour endpoint. Ventilations were provided with 10ml/kg at 10/min with a mechanical ventilator. Initially during CPR, room air was used and FiO2 was adjusted q5 minutes to maintain O 2 %saturation &gt 92% based on ABG. Lactic acid was also measured. Aortic, right atrial, and coronary artery pressures and carotid blood flow were recorded continuously. A-a oxygen gradient was measured with standard technique. Results: SNPeCPR animals documented a significantly higher mean CPP, lower lactic acid and 3x higher carotid blood flow over 30 minutes compared to standard CPR as previously documented. A-a oxygen gradient was dramatically increased in the SNPeCPR and coincided with a decreased lactate level (see Figure 1). Discussion: SNPeCPR causes profound pulmonary vasodilation and increases flow through non-ventilated lung areas. Despite that, the overall increase in forward flow leads to higher minute O 2 delivery and improved tissue perfusion. SNPeCPR should be used with 100% oxygen in the first human clinical trial.

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Abstract 114: Effect of Body Position on Intracranial Pressure and Carotid Blood Flow During Extracorporeal Cardiopulmonary Resuscitation

Circulation ◽

10.1161/circ.142.suppl_4.114 ◽

2020 ◽

Vol 142 (Suppl_4) ◽

Author(s):

Yaël Levy ◽

Rocio Fernandez ◽

Fanny Lidouren ◽

Matthias Kohlhauer ◽

Lionel Lamhaut ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Arrest ◽

Intracranial Pressure ◽

Cardiopulmonary Resuscitation ◽

Body Position ◽

Spontaneous Circulation ◽

Systemic Hemodynamics ◽

Body Tilt ◽

Whole Body ◽

Extracorporeal Cardiopulmonary Resuscitation

Introduction: Extracorporeal cardiopulmonary resuscitation (E-CPR) using extracorporeal membrane oxygenation (ECMO) is widely proposed for the treatment of refractory cardiac arrest. Hypothesis: Since cerebral autoregulation is altered in such conditions, body position may modify hemodynamics during ECPR. Our goal was to determine whether a whole body tilt-up challenge (TUC) could lower intracranial pressure (ICP) as previously shown with conventional CPR, without deteriorating cerebral blood flow (CBF). Methods: Pigs were anesthetized and instrumented for the continuous evaluation of CBF, ICP and systemic hemodynamics. After 15 min of untreated ventricular fibrillation they were treated with 30 min of E-CPR followed by sequential defibrillation shocks until resumption of spontaneous circulation (ROSC). ECMO was continued after ROSC to target a mean arterial pressure (MAP) >60 mmHg. Animals were maintained in the flat position (FP) throughout protocol, except during a 2 min TUC of the whole body (+30°) at baseline, during E-CPR and after-ROSC. Results: Four animals received the entire procedure and ROSC was obtained in 3/4. After cardiac arrest, E-CPR was delivered at 29±2 ml/kg/min to maintain a MAP of 57±8 mmHg in the FP. CBF was 28% of baseline and ICP remain stable (12±1 vs 13±1 mmHg during ECPR vs baseline, respectively). Under baseline pre-arrest conditions TUC resulted in a significant decrease in ICP (-63±7%) and CBF (-21±3%) versus the FP, with no significant effect on systemic hemodynamics. During E-CPR and after ROSC, TUC markedly reduced ICP but CBF remained unchanged vs the FP (Figure). Conclusion: During E-CPR whole body TUC reduced ICP without lowering CBF compared with E-CPR flat. Additional investigations with prolonged TUC and selective head and thorax elevation during E-CPR are warranted.

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