Aminophylline in bradyasystolic cardiac arrest: a randomised placebo-controlled trial.

BACKGROUND: Endogenous adenosine might cause or perpetuate bradyasystole. Our aim was to determine whether aminophylline, an adenosine antagonist, increases the rate of return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest. METHODS: In a double-blind trial, we randomly assigned 971 patients older than 16 years with asystole or pulseless electrical activity at fewer than 60 beats per minute, and who were unresponsive to initial treatment with epinephrine and atropine, to receive intravenous aminophylline (250 mg, and an additional 250 mg if necessary) (n=486) or placebo (n=485). The patients were enrolled between January, 2001 and September, 2003, from 1886 people who had had cardiac arrests. Standard resuscitation measures were used for at least 10 mins after the study drug was administered. Analysis was by intention-to-treat. This trial is registered with the ClinicalTrials.gov registry with the number NCT00312273. FINDINGS: Baseline characteristics and survival predictors were similar in both groups. The median time from the arrival of the advanced life-support paramedic team to study drug administration was 13 min. The proportion of patients who had an ROSC was 24.5% in the aminophylline group and 23.7% in the placebo group (difference 0.8%; 95% CI -4.6% to 6.2%; p=0.778). The proportion of patients with non-sinus tachyarrhythmias after study drug administration was 34.6% in the aminophylline group and 26.2% in the placebo group (p=0.004). Survival to hospital admission and survival to hospital discharge were not significantly different between the groups. A multivariate logistic regression analysis showed no evidence of a significant subgroup or interactive effect from aminophylline. INTERPRETATION: Although aminophylline increases non-sinus tachyarrhythmias, we noted no evidence that it significantly increases the proportion of patients who achieve ROSC after bradyasystolic cardiac arrest.

Tissue plasminogen activator in cardiac arrest with pulseless electrical activity.

BACKGROUND: Coronary thrombosis and pulmonary thromboembolism are common causes of cardiac arrest. We assessed whether the administration of tissue plasminogen activator (t-PA) during cardiopulmonary resuscitation would benefit patients with cardiac arrest and pulseless electrical activity of unknown or presumed cardiovascular cause. METHODS: Patients who were older than 16 years of age and who had more than one minute of pulseless electrical activity that was unresponsive to initial therapy outside the hospital or in the emergency department were eligible. Patients were randomly assigned to receive 100 mg of t-PA or placebo intravenously over a 15-minute period in a double-blind fashion. Standard resuscitation was then continued for at least 15 minutes. The primary outcome was survival to hospital discharge. RESULTS: During the study period, 1583 patients with cardiac arrest were treated and 233 patients were enrolled (117 in the t-PA group and 116 in the placebo group). The characteristics of the patients in the two groups were similar. One patient in the t-PA group survived to hospital discharge, as compared with none in the placebo group (absolute difference between groups, 0.9; 95 percent confidence interval, -2.6 to 4.8; P=0.99). The proportion of patients with return of spontaneous circulation was 21.4 percent in the t-PA group and 23.3 percent in the placebo group (absolute difference between groups, -1.9; 95 percent confidence interval, -12.6 to 8.8; P=0.85). CONCLUSIONS: We found no evidence of a beneficial effect of fibrinolysis in patients with cardiac arrest and pulseless electrical activity of unknown or presumed cardiovascular cause. Our study had limited statistical power, and it remains unknown whether there is a small treatment effect or whether selected subgroups may benefit.

Prospective time study derivation of emergency physician workload predictors.

BACKGROUND: A reliable emergency department (ED) workload measurement tool would provide a method of quantifying clinical productivity for performance evaluation and physician incentive programs; it would enable health administrators to measure ED outputs; and it could provide the basis for an equitable formula to estimate ED physician staffing requirements. Our objectives were to identify predictors that correlate with physician time needed to treat patients and to develop a multivariable model to predict physician workload. METHODS: During 31 day, evening, night and weekend shifts, a research assistant (RA) shadowed 20 emergency physicians, documenting time spent performing clinical and non-clinical functions for 585 patient visits. The RA recorded key predictors including patient gender, age, vital signs and Glasgow Coma Scale (GCS) score, and the mode of arrival, triage level assigned, comorbidity and procedures performed. Multiple linear regression was used to describe the associations between predictor variables and total physician time per patient visit (TPPV), and to derive an equation for physician workload. Model derivation was based on 16 shifts and 314 patient visits; model validation was based on 15 shifts and 271 additional patient visits. RESULTS: The strongest predictor variables were: procedure required, triage level, arrival by ambulance, GCS, age, any comorbidity, and number of prior visits. The derived regression equation is: TPPV = 29.7 + 8.6 (procedure required [Yes]) - 3.8 (triage level [1-5]) + 7.1 (ambulance arrival) - 1.1 (GCS [3-15]) + 0.1 (age in years) - 0.05 (n of previous visits) + 3.1 (any comorbidity). This model predicted 31.3% of the variance in physician TPPV (F [12, 29] = 13.2; p < 0.0001). CONCLUSIONS: This study clarifies important determinants of emergency physician workload. If validated in other settings, the predictive formula derived and internally validated here is a potential alternative to current simplistic models based solely on patient volume and perceived acuity. An evidence-based workload estimation tool like that described here could facilitate ED productivity measurement, benchmarking, physician performance evaluation, and provide the substrate for an equitable formula to estimate ED physician staffing requirements.

A geospatial assessment of transport distance and survival to discharge in out of hospital cardiac arrest patients: Implications for resuscitation centers.

OBJECTIVES: National leaders have suggested that patients with an out of hospital cardiac arrest (OOHCA) may benefit from transport to specialized hospitals. We sought to assess the survival of OOHCA patients by transport distance and hospital proximity. METHODS: Prospective, cohort study of OOHCA patients in 11 Resuscitation Outcomes Consortium (ROC) sites across North America. Transport distance and hospital proximity was calculated using weighted centroid of census tract location by Geographic Information Systems (GIS). Patients were stratified into quartiles based on transport distance to the receiving hospital calculated via GIS. Descriptive statistics were used to describe characteristics by transport distance and to compare proximity to other hospitals. Multivariate logistic regression was used to evaluate the impact of transport distance on survival. RESULTS: 26,628 patients were identified, 7540 (28%) were transported by EMS and included in the final analysis. The median transport time was 6.3 min (IQR 5.4); the median transport distance being 2.4 miles (3.9 km). Most patients were taken to the closest hospital (71.7%; N=5412). However, unadjusted survival to discharge was lower for those taken to the closest compared to further hospitals (12.1% vs. 16.5%) despite similar patient characteristics. Transport distance was not associated with survival on logistic analysis (OR 1.00; 95% CI 0.99-1.01). CONCLUSIONS: Survival to discharge was higher in OOHCA patients taken to hospitals located further than the closest hospital while transport distance was not associated with survival. This suggests that longer transport distance/time might not adversely affect outcome. Further studies are needed to inform policy decisions regarding best destination post-cardiac arrest.

The effect of an education program on violence in the emergency department.

STUDY OBJECTIVE: We examine whether a specific educational effort reduces emergency department violence in the short term and quantify the amount of violence in the ED. METHODS: Cross-sectional prospective surveys were conducted at a tertiary referral center at baseline (1998) and at 3 and 6 months (1999) after the Prevention and Management of Aggressive Behavior Program (PMABP). ED staff on all shifts for 7 alternate days in a 2-week period were surveyed. We measured the total and mean number of physical and violent events per survey. A generalized estimating equation Poisson regression model examined the effect of the program on the numbers of physically and verbally violent events per shift per employee, after adjusting for other covariates. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. RESULTS: Physical violence events per survey at baseline, 3 months posttraining, and 6 months posttraining were 0.27, 0.10, and 0.21, respectively. The number of reported violent interactions at the same intervals were 49, 19, and 46 (adjusted OR 1.0, 0.35 [95% CI 0.15 to 0.84], and 0.79 [95% CI 0.48 to 1.40]), respectively. Verbal violence events per survey at baseline, 3 months posttraining, and 6 months posttraining were 0.85, 0.31, and 0.51, respectively. The number of reported interactions involving verbal violence at the same intervals were 154, 58, and 69 (adjusted OR 1.0, 0.31 [95% CI 0.21 to 0.46], and 0.47 [95% CI 0.33 to 0.66]), respectively. CONCLUSION: Violent events are frequent in the ED. Education programs may reduce the number of events at least temporarily but do not clearly reduce violence in the long term.