During cardiopulmonary resuscitation, adequate coronary perfusion pressure is essential for establishing return of spontaneous circulation. Current American Heart Association guidelines recommend standardized interval administration of epinephrine for patients in cardiac arrest. The objective of this study was to compare short-term survival using a hemodynamic directed resuscitation strategy versus chest compression depth-directed cardiopulmonary resuscitation in a porcine model of cardiac arrest.
Randomized interventional study.
Preclinical animal laboratory.
Twenty-four 3-month-old female swine.
After 7 minutes of ventricular fibrillation, pigs were randomized to receive one of three resuscitation strategies: 1) Hemodynamic directed care (coronary perfusion pressure-20): chest compressions with depth titrated to a target systolic blood pressure of 100 mm Hg and titration of vasopressors to maintain coronary perfusion pressure greater than 20 mm Hg; 2) Depth 33 mm: target chest compression depth of 33 mm with standard American Heart Association epinephrine dosing; or 3) Depth 51 mm: target chest compression depth of 51 mm with standard American Heart Association epinephrine dosing. All animals received manual cardiopulmonary resuscitation guided by audiovisual feedback for 10 minutes before first shock.
Forty-five–minute survival was higher in the coronary perfusion pressure-20 group (8 of 8) compared to depth 33 mm (1 of 8) or depth 51 mm (3 of 8) groups; p equals to 0.002. Coronary perfusion pressures were higher in the coronary perfusion pressure-20 group compared to depth 33 mm (p = 0.004) and depth 51 mm (p = 0.006) and in survivors compared to nonsurvivors (p < 0.01). Total epinephrine dosing and defibrillation attempts were not different.
Hemodynamic directed resuscitation targeting coronary perfusion pressures greater than 20 mm Hg during 10 minutes of cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest improves short-term survival, when compared to resuscitation with depth of compressions guided to 33 mm or 51 mm and standard American Heart Association vasopressor dosing.
1Department of Pediatrics, St. Louis Children’s Hospital, Washington University in St. Louis School of Medicine, St. Louis, MO.
2Department of Anesthesiology and Critical Care Medicine, The Children’s Hospital of Philadelphia, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
3Department of Anesthesiology and Critical Care Medicine, Bloomberg Children’s Center, Johns Hopkins Hospital, Johns Hopkins University School of Medicine, Baltimore, MD.
4Department of Emergency Medicine, The Hospital of the University of Pennsylvania, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA.
* See also p. 2817.
Supported, in part, by the Russell Raphaely Endowed Chair Funds at The Children’s Hospital of Philadelphia.
Supported, in part, by the Russell Raphaely Endowed Chair Funds at The Children’s Hospital of Philadelphia and the Laerdal Foundation for Acute Care Medicine. Dr. Friess was supported by the National Institute of Neurological Disorders and Stroke (K08). Dr. Sutton was supported by the National Institute of Child Health and Human Development (K23) and a research grant from Laerdal Foundation. Dr. Weiland III received funding from NIH. Dr. Becker has consulted for Philips Health Care, given expert testimony for various attorneys, received payment for lectures from Philips Medical Systems, received travel reimbursements from the American Heart Association, and has a patent from the University of Pennsylvania Technology Transfer. He has received grant support from Philips Medical Systems, Stavanger, Betheseda, Cardiac Science, BeneChill Inc., Zoll Medical Corp, PhysioControl, Medtronic Foundation, and Abbott Point of Care. The remaining authors have disclosed that they do not have any potential conflicts of interest.
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