Improving handoffs in the emergency department.

Patient handoffs at shift change are a ubiquitous and potentially hazardous process in emergency care. As crowding and lengthy evaluations become the standard for an increasing proportion of emergency departments (EDs), the number of patients handed off will likely increase. It is critical now more than ever before to ensure that handoffs supply valid and useful shared understandings between providers at transitions of care. The purpose of this article is to provide the most up-to-date evidence and collective thinking about the process and safety of handoffs between physicians in the ED. It offers perspectives from other disciplines, provides a conceptual framework for handoffs, and categorizes models of existing practices. Legal and risk management issues are also addressed. A proposal for the development of handoff quality measures is outlined. Practical strategies are suggested to improve ED handoffs. Finally, a research agenda is proposed to provide a roadmap to future work that may increase knowledge in this area.

Comparison of linear-stochastic and nonlinear-deterministic algorithms in the analysis of 15-minute clinical ECGs to predict risk of arrhythmic death.

OBJECTIVE: Comparative algorithmic evaluation of heartbeat series in low-to-high risk cardiac patients for the prospective prediction of risk of arrhythmic death (AD). BACKGROUND: Heartbeat variation reflects cardiac autonomic function and risk of AD. Indices based on linear stochastic models are independent risk factors for AD in post-myocardial infarction (post-MI) cohorts. Indices based on nonlinear deterministic models have superior predictability in retrospective data. METHODS: Patients were enrolled (N = 397) in three emergency departments upon presenting with chest pain and were determined to be at low-to-high risk of acute MI (>7%). Brief ECGs were recorded (15 min) and R-R intervals assessed by three nonlinear algorithms (PD2i, DFA, and ApEn) and four conventional linear-stochastic measures (SDNN, MNN, 1/f-Slope, LF/HF). Out-of-hospital AD was determined by modified Hinkle-Thaler criteria. RESULTS: All-cause mortality at one-year follow-up was 10.3%, with 7.7% adjudicated to be AD. The sensitivity and relative risk for predicting AD was highest at all time-points for the nonlinear PD2i algorithm (p 100 (p 11.4 (p

Risk stratification for arrhythmic death in an emergency department cohort: a new method of nonlinear PD2i analysis of the ECG.

Heart rate variability (HRV) reflects both cardiac autonomic function and risk of sudden arrhythmic death (AD). Indices of HRV based on linear stochastic models are independent risk factors for AD in postmyocardial infarction (MI) cohorts. Indices based on nonlinear deterministic models have a higher sensitivity and specificity for predicting AD in retrospective data. A new nonlinear deterministic model, the automated Point Correlation Dimension (PD2i), was prospectively evaluated for prediction of AD. Patients were enrolled (N = 918) in 6 emergency departments (EDs) upon presentation with chest pain and being determined to be at risk of acute MI (AMI) >7%. Brief digital ECGs (>1000 heartbeats, approximately 15 min) were recorded and automated PD2i results obtained. Out-of-hospital AD was determined by modified Hinkle-Thaler criteria. All-cause mortality at 1 year was 6.2%, with 3.5% being ADs. Of the AD fatalities, 34% were without previous history of MI or diagnosis of AMI. The PD2i prediction of AD had sensitivity = 96%, specificity = 85%, negative predictive value = 99%, and relative risk >24.2 (p ≤ 0.001). HRV analysis by the time-dependent nonlinear PD2i algorithm can accurately predict risk of AD in an ED cohort and may have both life-saving and resource-saving implications for individual risk assessment.

Adenosine A1 antagonism attenuates beta-adrenergic-resistant sudden hypoxic cardiac insufficiency.

OBJECTIVES: In states such as hypoxia, shock, and cardiac arrest, compromised systemic oxygenation or perfusion appears to induce cardiac insufficiency that can be resistant to beta-adrenergic drugs. Elevated levels of adenosine may mediate such beta-adrenergic-resistant cardiac insufficiency via the adenosine A(1) receptor (A(1)AdoR). The objective of this study was to test the hypothesis that selective A(1)AdoR antagonism attenuates hypoxic cardiac insufficiency more efficaciously than beta(1)-adrenergic agonism or nonselective adenosine antagonism. METHODS: Rats were paralyzed and ventilated to a pCO(2) level of 35-40 mm Hg. Ten minutes before hypoxia (inspired o(2) concentration = 5%), rats were treated intravenously with one of the following: 0.1 mg/kg BG-9719 (n = 9), 10 mg/kg NPC-205 (n = 10; BG-9719 and NPC-205 are selective A(1)AdoR antagonists, with durations of action of 30-60 minutes and 60-90 minutes, respectively), 10 mg/kg aminophylline (n = 12), 5 microg/kg/min dobutamine (n = 11), or control solutions. These drug doses maximized survival duration in dose-response studies. RESULTS: Before hypoxia, cardiac work was increased more by aminophylline and dobutamine than by BG-9719. Mean (+/-SEM) duration of survival (in minutes) after hypoxia increased from <13 (control solutions) to 13.8 (+/-1.4) (dobutamine), 20.0 (+/-1.6) (aminophylline), 31.7 (+/-4.6) (BG-9719), and 40.5 (+/-7.5) (NPC-205) (p < 0.0001). Heart rate and dP/dt decreased rapidly after hypoxia, but decreases were attenuated with BG-9719 and NPC-205 compared with dobutamine (p < 0.05) and tended toward attenuation with aminophylline. CONCLUSIONS: BG-9719 and NPC-205 improved survival duration, heart rate, and left ventricular contractility during hypoxia more efficaciously than dobutamine and possibly aminophylline. Selective A(1)AdoR antagonists warrant further study as alternatives to beta-adrenergic agonists in hypoxia, shock, and cardiac arrest, in which compromised systemic perfusion or oxygenation impairs cardiac output.

Adenosine A1 antagonism attenuates atropine-resistant hypoxic bradycardia in rats.

OBJECTIVES: To test the following hypotheses: Hypoxia induces bradycardia and hemodynamic compromise that are resistant to atropine but responsive to selective antagonism of the adenosine A1 receptor (A1AdoR). The mechanism for such attenuation is independent of the vagus nerve. METHODS: Ten minutes after sham or actual bilateral cervical vagotomy, paralyzed ventilated rats were made hypoxic (5% fractional inspired oxygen, continued until death). Five minutes after beginning hypoxia, intravenous treatment with BG-9719, a selective A1AdoR antagonist (0.1 mg/kg); atropine (0.1 mg/kg); BG-9719 vehicle; or saline was initiated. These drug doses were based on pilot studies. Of the eight treatment groups (eight possible combinations of vagotomy status and drug/vehicle treatment), n = 8 in all except nonvagotomized, vehicle-treated rats (where n = 7). RESULTS: Heart rate and left ventricular contractility decreased rapidly with hypoxia. Atropine had minimal effects in prolonging survival (from mean +/- SEM of 15.5 +/- 2.1 minutes to 20.2 +/- 2.5 minutes, p = 0.94) and attenuating posthypoxic decreases in heart rate (p = 0.89) and contractility (p = 0.83) compared with saline. BG-9719 prolonged survival, however, from 14.4 +/- 1.9 minutes (with vehicle treatment) to 37.2 +/- 6.8 minutes (p < 0.001). Survival, heart rate, and contractility were preserved with BG-9719 compared with atropine and vehicle (p < 0.05, all comparisons). Vagotomy prevented the effects of BG-9719 on survival prolongation (p = 0.003), heart rate (p = 0.01), and contractility (p < 0.001) but did not affect those outcomes in saline-treated rats. CONCLUSIONS: Survival, heart rate, and contractility were better preserved with BG-9719 than atropine. A1AdoR selective antagonism, possibly because of its multiple mechanisms for attenuating hypoxic cardiac insufficiency, resulted in better hemodynamic and clinical outcomes. That attenuation seems to have a component of vagal mediation.

The relative utility of cardiac troponin I, creatine kinase-MBmass, and myosin light chain-1 in the long-term risk stratification of patients with chest pain.

BACKGROUND: Sensitive and specific cardiac markers convey important short-term prognostic information about patients with an acute coronary syndrome. There are, however, few data assessing their value as long-term predictors. HYPOTHESIS: The aim of the current study was to assess the relative value of three such markers and clinical characteristics in determining the long-term prognosis of patients with chest pain. METHODS: Cardiac troponin I (cTnI), myosin light chain-(MLC-1), and creatine kinase-MBmass levels were obtained on admission (0 h) and at 4, 8, 16, and 24 h in 208 patients with chest pain. Eligible subjects were determined, at the time of hospital admission, to be at >7% risk of acute myocardial infarction (MI), but without new ST-segment elevation on their presenting electrocardiogram. Follow-up was performed a median of 28 (range 1-46) months later. The primary study endpoint was death or nonfatal MI, subsequent to the index admission. RESULTS: Cardiac TnI levels > or = 0.2 ng/ml (odds ratio [OR] 1.93, 95% confidence interval [CI] 1.09-3.40) and MLC-1 levels > or = 1 ng/ml (OR 3.24, 95% CI 1.83-5.73) were both significant predictors of death or MI during long-term follow-up; MLC-1 was, however, the only independent biochemical predictor (OR 2.11,95% CI 1.14-3.93). CONCLUSIONS: Both cTnl and MLC-1 predict the long-term outcome of patients with chest pain, but, in this cohort, MLC-1 proved to be a better predictor of mortality and nonfatal acute MI.

Biochemical and clinical predictors of long-term outcome in patients with nonspecific chest pain and nondiagnostic electrocardiograms.

BACKGROUND: There are few data assessing the relative value of clinical factors and sensitive cardiac markers in determining the long-term prognosis of patients with chest pain. Likewise, little information exists about the long-term outcome of patients with chest pain who have negative markers of myocardial cell necrosis. This study addresses these issues in a cohort of patients with nonspecific chest pain and nondiagnostic electrocardiograms (ECGs). METHODS: Eligible subjects (n = 501) had experienced >15 minutes chest pain at rest during the previous 24 hours, but were found to be at low-risk for acute myocardial infarction (AMI) by means of a well-validated clinical algorithm. Cardiac troponin I, creatine kinase MB(mass), myoglobin, and myosin light chain-1 were collected at presentation and 3, 6, and 12 hours later. Patients were observed for a median of 31 months. The composite end point was death or AMI subsequent to the index admission. RESULTS: Cardiac troponin I was the best single biochemical predictor of outcome (risk ratio 2.34, 95% CI 1.31-4.17, P =.004), but was of less independent prognostic value than age and an abnormal presenting ECG. It was also inferior to a combination strategy, using all 4 markers tested (risk ratio 2.37, 95% CI 1.44-3.91, P <.001). Fifty of 428 patients (12%) with a cardiac troponin I level < or =0.2 ng/mL and 25 of 287 patients (9%) without elevation of any marker tested sustained an adverse event during follow-up. CONCLUSIONS: Cardiac troponin I is the most useful single biochemical predictor of long-term outcome, but the best determinants are age, an abnormal presenting ECG, and an "any marker positive" strategy. Patients without elevated cardiac markers have an adverse event rate of approximately 10% in the subsequent 31 months.

Post hoc mortality analysis of the efficacy trial of diaspirin cross-linked hemoglobin in the treatment of severe traumatic hemorrhagic shock.

BACKGROUND: The efficacy trial of diaspirin cross-linked hemoglobin (DCLHb) in traumatic hemorrhagic shock demonstrated an unexpected mortality imbalance, prompting a three-step review to better understand the cause of this finding. METHODS: Patients were enrolled in this DCLHb hemorrhagic shock study using 28-day mortality as the primary endpoint. Mortality data were primarily analyzed using the TRISS method and a nonblinded clinical review, followed by an independent Pennsylvania Trauma Outcome Study (PTOS)-derived probability of survival analyses. Finally, a trauma expert conducted a blinded clinical review of cases incorrectly predicted by these PTOS analyses. RESULTS: More of the DCLHb patients predicted to survive using TRISS actually died than in the control subgroup (24% vs. 3%, p < 0.002). Nonblinded clinical review noted that 72% of the patients who died had prior traumatic arrest, a presenting Glasgow Coma Scale score of 3, or a base deficit > 15 mEq/L. DCLHb patients predicted to survive using PTOS also more often died than did control patients (30% vs. 8%, p < 0.04). Blinded clinical review determined that 94% of the deaths were clinically justified. Both the TRISS and the PTOS models gave an adjusted mortality relative risk of 2.3, similar to the unadjusted risk data. CONCLUSION: Mortality analysis in this shock study involved both clinical case reviews and mortality prediction models. Despite the observation that nearly all of the deaths were clinically justified, the TRISS and PTOS models demonstrated excess unpredicted deaths in the DCLHb subgroup. A combined process, using both mortality prediction models and clinical case reviews, is useful in trauma studies that use a mortality endpoint.

Elevated soluble P-selectin levels are associated with an increased risk of early adverse events in patients with presumed myocardial ischemia.

BACKGROUND: Cell adhesion molecules (CAMs) play a pivotal role in the interactions between leukocytes, platelets, and vascular endothelium. Soluble CAMs (sCAMs) are shed from cell surfaces and reflect cellular activation. Elevated levels of sCAMs have been reported in the acute coronary syndromes. We hypothesized, therefore, that sCAMs might prove of prognostic value in patients with acute chest pain presumed to be the result of myocardial ischemia. METHODS: One hundred twenty-six consecutive patients with chest pain, thought clinically to represent myocardial ischemia, were studied prospectively. Soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin) and P-selectin (sP-selectin) levels were assayed at presentation, as were cardiac troponin I (cTnI) and creatine kinase-MB(mass) (CK-MB(mass)). The primary study end point was the occurrence of a serious cardiac event (SCE) during the index admission or the subsequent 3 months. RESULTS: sP-selectin and cTnI levels were significantly higher among patients who had an early SCE (P =.006 and P <.001, respectively). Both remained independently predictive (P <.001) in a multivariate regression equation. The other independent predictor was a history of vascular disease (P <.05). No other markers were significant predictors of early outcome. CONCLUSION: Elevated sP-selectin levels, but not those of other sCAMs, are predictors of early adverse events in patients with chest pain presumed caused by myocardial ischemia. Their utility in predicting the outcome of individual patients is, however, limited.

Clinical Policy for Procedural Sedation and Analgesia in the Emergency Department.

[American College of Emergency Physicians: Clinical policy for procedural sedation and analgesia in the emergency department. Ann Emerg Med May 1998;31:663-677.].

Clinical Policy for the Initial Approach to Patients Presenting With Acute Blunt Trauma.

[American College of Emergency Physicians: Clinical policy for the initial approach to patients presenting with acute blunt trauma. Ann Emerg Med March 1998;31:422-454.].