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The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.

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C ardiac arrest occurs in a wide variety of settings, from the unanticipated event in the out-of-hospital setting to anticipated arrests in the intensive care unit. Outcome from cardiac arrest is a function of many factors including the willingness of bystanders to perform cardiopulmonary resuscitation (CPR), the ability of rescuers to integrate knowledge and psychomotor skills, the quality of performance delivered by individual rescuers and teams, and the efficiency and effectiveness of post-cardiac arrest care.The Chain of Survival is a metaphor used to organize and describe the integrated set of time-sensitive, coordinated actions necessary to maximize survival from cardiac arrest. The use of evidence-based education and implementation strategies can optimize the links of that chain.Strengthening the Chain of Survival in the prehospital setting requires focus on prevention and immediate recognition of cardiac arrest, increasing the likelihood of high-quality bystander CPR and early defibrillation, and improving regional systems of care. In the hospital setting, organized efforts targeting early identification and prevention of deterioration in patients at risk can decrease the incidence of cardiac arrest. The challenge for resuscitation programs is twofold: to ensure that providers acquire and maintain the necessary knowledge, skills, and team behavior to maximize resuscitation outcome; and to assist response systems in developing, implementing, and sustaining an evidence-based Chain of Survival.Maximizing survival from cardiac arrest requires improvement in resuscitation education and the implementation of systems that support the delivery of high-quality resuscitation and postarrest care, including mechanisms to systematically evaluate resuscitation performance. Well-designed resuscitation education can encourage the delivery of high-quality CPR. In addition continuous quality improvement processes should close the feedback loop and narrow the gap between ideal and actual performance. Community-and hospitalbased resuscitation programs should systematically monitor cardiac arrests, the level of resuscitation care provided, and outcomes. The cycle of measurement, benchmarking, feedback, and change provides fundamental information necessary to optimize resuscitation care and maximize survival.This chapter reviews key educational issues that affect the quality of resuscitation performance and describes major implementation and team-related issues shown to improve outcomes. The information is organized into four major categories: willingness to perform CPR, educational design, improving resuscitation quality, and issues related to implementation and outcomes.While Willingness to PerformWithout immediate initiation of CPR, most victims of cardiac arrest will die. Bystander CPR can significantly improve survival rates from cardiac arrest, 3 but recent evidence indicates that only 15% to 30% of victims of out-of-hospital arrest receive CPR before EMS arrival. 4 Strategies to increase the incidence of bystander-ini...

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Summary:We tested the hypothesis that quinolinic acid, a tryptophan-derived N-methyl-D-aspartate agonist produced by macrophages and microglia, would be increased in CSF after severe traumatic brain injury (TBI) in humans, and that this increase would be associated with outcome. We also sought to determine whether therapeutic hypothermia reduced CSF quinolinic acid after injury. Samples of CSF (n = 230) were collected from ventricular catheters in 39 patients (16 to 73 years old) during the first week after TBI, (Glasgow Coma Scale [GCS] < 8). As part of an ongoing study, patients were randomized within 6 hours after injury to either hypothermia (32°C) or normothermia (3rC) treatments for 24 hours. Oth erwise, patients received standard neurointensive care. Quino linie acid was measured by mass spectrometry. Univariate and multivariate analyses were used to compare CSF quinolinie acid concentrations with age, gender, GCS, time after injury, Abbreviations used: GCS, Glasgow Coma Scale; NMDA, N-methyl D-aspartate; TBI, traumatic brain injury. 610 mortality, and treatment (hypothermia versus normothermia). Quinolinie acid concentration in CSF increased maximally to 463 ± 128 nmollL (mean ± SEM) at 72 to 83 hours after TBl. Normal values for quinolinic acid concentration in CSF are less than 50 nmollL. Quinolinie acid concentration was increased 5-to 50-fold in many patients. There was a powerful association between time after TBI and increased quinolinie acid. (P < 0.00001), and quinolinic acid was higher in patients who died than in survivors (P = 0.003). Age, gender, GCS, and treat ment (32°C versus 37°C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinie acid con centration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.

A large and progressive increase in the macrophage-derived neurotoxin quinolinic acid is seen following severe TBI in children. The increase is strongly associated with increased mortality. Increased CSF quinolinic acid concentration on admission in children with shaken infant syndrome could reflect a delay in presentation to medical attention or age-related differences in quinolinic acid production. These findings raise the possibility that quinolinic acid may play a role in secondary injury after TBI in children and suggest an interaction between inflammatory and excitotoxic mechanisms of injury following TBI.