Intrathoracic Pressure Regulator During Continuous-Chest-Compression Advanced Cardiac Resuscitation Improves Vital Organ Perfusion Pressures in a Porcine Model of Cardiac Arrest

Demetris Yannopoulos, MD; Vinay M. Nadkarni, MD; Scott H. McKnite, BS; Anu Rao, MD; Kurt Kruger, BS; Anja Metzger, PhD; David G. Benditt, MD; Keith G. Lurie, MD

From the Departments of Cardiology (D.Y.), Cardiac Arrhythmia Center, Cardiovascular Division (D.G.B., K.G.L.), Department of Medicine (A.R., D.G.B.), and Department of Emergency Medicine and Internal Medicine (K.G.L.), University of Minnesota, Minneapolis (D.Y.); Department of Anesthesia and Critical Care Medicine, Children’s Hospital of Philadelphia, Philadelphia, Pa (V.M.N.); Minnesota Medical Research Foundation, Hennepin County Medical Center, Minneapolis (S.H.N.); and Advanced Circulatory Systems Incorporation, Eden Prairie, Minn (K.K., A.M.).

Reprint requests to Keith G. Lurie, MD, Minneapolis Medical Research Foundation, 914 S 8th St, 3rd Floor, Minneapolis, MN 55404. E-mail klurie@advancedcirculatory.com

Received December 19, 2004; de novo received February 7, 2005; revision received April 14, 2005; accepted April 25, 2005.

Background— A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled –10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest.

Methods and Results— In protocol 1, 20 pigs (weight, 30±0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O₂) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO₂ values were measured (mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman’s repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer’s exact test was used for survival. Significance was set at P<0.05. Vital organ perfusion pressures and end-tidal CO₂ were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour survival was 100% with ITPR-CPR and 10% with STD-CPR (P=0.001). Arterial blood pH was significantly lower and PaCO₂ was significantly higher with ITPR- CPR in protocol 1. Arterial oxygen saturation was 100% throughout the study in both protocols. PaCO₂ and PaO₂ remained stable, but metabolic acidosis progressed, as expected, throughout the 15 minutes of CPR in protocol 3.

Conclusions— Compared with STD-CPR, use of ITPR-CPR improved hemodynamics and short-term survival rates after cardiac arrest.