A prediction model for out-of-hospital cardiopulmonary resuscitation.

BACKGROUND: We created a prediction model to be used in cardiopulmonary resuscitation (CPR) attempts as a decision tool to omit futile CPR attempts and to save resources. METHODS: In this post hoc analysis, we assessed predictive parameters for neurological recovery after successful CPR. The original study was designed as a blinded, randomized, prospective, controlled, multicenter clinical trial. RESULTS: We identified 1166 prehospital cardiac arrest patients being treated with advanced cardiac life support. Seven hundred eighty-six of 1166 patients (67.4%) died at the scene and 380 of 1166 (32.6%) were brought to the hospital. Two hundred sixty-five of 1166 patients (22.7%) died in the hospital. One hundred fifteen of 1166 (9.8%) were discharged from the hospital and 92 of the 115 patients (80%) could be followed-up. Good cerebral performance was regained by 54% of discharged patients (50 of 92 patients). In 46% of patients (42/92), unconsciousness or severe disability remained. Ventricular fibrillation was more likely to have occurred in patients with good neurological recovery (42/50 = 84.0%), whereas asystole was more likely in patients with poor neurological recovery (9/42 = 21.4%). A score was developed to predict the probability of death using logistic regression analysis. Predicting death in the hospital revealed a sensitivity of 99.8% (953/955), but only a specificity of 2.9% (3/104; threshold 0.5). Predicting survival until discharge from the hospital revealed a sensitivity of 99% (103/104), but only a specificity of 8% (72/955; threshold 0.99). A receiver operating characteristic curve yielded an area under the curve of 0.795 (0.751-0.839) at a confidence interval of 95%. CONCLUSION: For out-of-hospital patients with cardiac arrest, parameters documented in the field did not allow accurate prediction of hospital survival.

Influence of ventilation strategies on survival in severe controlled hemorrhagic shock.

OBJECTIVE: To investigate the effect of different ventilation settings on hemodynamic stability in severe controlled hemorrhagic shock. DESIGN: Prospective, randomized, controlled animal study. SETTING: Research laboratory in a university hospital. SUBJECTS: Approximately 35-45 kg domestic pigs. INTERVENTIONS: Twenty-four domestic pigs were bled 45 mL/kg (estimated 65% of their calculated blood volume) and then ventilated with either 0 cm H2O positive end-expiratory pressure and a respiratory rate of 14 ventilations/min (positive end-expiratory pressure 0 respiratory rate 14), or with 5 cm H2O positive end-expiratory pressure, a respiratory rate of 28 ventilations/min, and a tidal volume reduced by half (positive end-expiratory pressure 5 respiratory rate 28), or with 5 cm H2O positive end-expiratory pressure and a respiratory rate of 14 ventilations/min (positive end-expiratory pressure 5 respiratory rate 14). After 1 hr study phase surviving animals, received fluid resuscitation and were monitored for further 1 hr. MEASUREMENTS AND MAIN RESULTS: Pulmonary variables, hemodynamic variables, and short-term survival. There were no significant differences in mean arterial blood pressure and cardiac index after hemorrhage. After 20 mins of different ventilation strategies mean arterial blood pressure was 40 +/- 3 mm Hg in the positive end-expiratory pressure 0 respiratory rate 14 group, vs. 24 +/- 6 mm Hg the positive end-expiratory pressure 5 respiratory rate 28 group (p < 0.05) vs. 19 +/- 3 mm Hg in the positive end-expiratory pressure 5 respiratory rate 14 group (p < 0.01). Cardiac index was 65 +/- 5 mL/min/kg in the positive end-expiratory pressure 0 respiratory rate 14 group vs. 37 +/- 5 mL/min/kg in the positive end-expiratory pressure 5 respiratory rate 28 group(p < 0.01) and 20 +/- 3 mL/min/kg in the positive end-expiratory pressure 5 respiratory rate 14 group (p < 0.01). Mean airway pressure and positive end-expiratory pressure correlated strongly with mean arterial blood pressure and cardiac index. None of the positive end-expiratory pressure 0 respiratory rate 14 animals died in the study phase, whereas six of seven positive end-expiratory pressure 5 respiratory rate 28 animals, and all seven positive end-expiratory pressure 5 respiratory rate 14 animals died. CONCLUSIONS: In this porcine model of severe hemorrhagic shock, reduction of positive end-expiratory pressure was the most important ventilation strategy component influencing hemodynamic stability. Reducing mean airway pressure by decreasing tidal volumes and increasing respiratory rates seemed to have less influence on cardiopulmonary function and survival than 0 cm H2O positive end-expiratory pressure.