Elizabeth Sinz

Part 8: Adult Advanced Cardiovascular Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

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.

Part 1: Executive Summary 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

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.

Part 12: Cardiac Arrest in Special Situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

This section of the 2010 AHA Guidelines for CPR and ECC addresses cardiac arrest in situations that require special treatments or procedures beyond those provided during basic life support (BLS) and advanced cardiovascular life support (ACLS). We have included 15 specific cardiac arrest situations. The first several sections discuss cardiac arrest associated with internal physiological or metabolic conditions, such as asthma (12.1), anaphylaxis (12.2), pregnancy (12.3), morbid obesity (12.4), pulmonary embolism (PE) (12.5), and electrolyte imbalance (12.6). The next several sections relate to resuscitation and treatment of cardiac arrest associated with external or environmentally related circumstances, such as ingestion of toxic substances (12.7), trauma (12.8), accidental hypothermia (12.9), avalanche (12.10), drowning (12.11), and electric shock/lightning strikes (12.12). The last 3 sections review management of cardiac arrest that may occur during special situations affecting the heart, including percutaneous coronary intervention (PCI) (12.13), cardiac tamponade (12.14), and cardiac surgery (12.15). Asthma is responsible for more than 2 million visits to the emergency department (ED) in the United States each year, with 1 in 4 patients requiring admission to a hospital.1 Annually there are 5,000 to 6,000 asthma-related deaths in the United States, many occurring in the prehospital setting.2 Severe asthma accounts for approximately 2% to 20% of admissions to intensive care units, with up to one third of these patients requiring intubation and mechanical ventilation.3 This section focuses on the evaluation and treatment of patients with near-fatal asthma. Several consensus groups have developed excellent guidelines for the management of asthma that are available on the World Wide Web: ### Pathophysiology The pathophysiology of asthma consists of 3 key abnormalities: Complications of severe asthma, such as tension pneumothorax, lobar atelectasis, pneumonia, and pulmonary edema, can contribute to fatalities. Severe asthma exacerbations are commonly associated with …

Part 1: Executive Summary

Mary Fran Hazinski, Co-Chair*; Jerry P. Nolan, Co-Chair*; John E. Billi; Bernd W. Böttiger; Leo Bossaert; Allan R. de Caen; Charles D. Deakin; Saul Drajer; Brian Eigel; Robert W. Hickey; Ian Jacobs; Monica E. Kleinman; Walter Kloeck; Rudolph W. Koster; Swee Han Lim; Mary E. Mancini; William H. Montgomery; Peter T. Morley; Laurie J. Morrison; Vinay M. Nadkarni; Robert E. O’Connor; Kazuo Okada; Jeffrey M. Perlman; Michael R. Sayre; Michael Shuster; Jasmeet Soar; Kjetil Sunde; Andrew H. Travers; Jonathan Wyllie; David Zideman

Part 1: Executive summary: 2015 American Heart Association guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care

Publication of the 2015 American Heart Association (AHA) Guidelines Update for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) marks 49 years since the first CPR guidelines were published in 1966 by an Ad Hoc Committee on Cardiopulmonary Resuscitation established by the National Academy of Sciences of the National Research Council.1 Since that time, periodic revisions to the Guidelines have been published by the AHA in 1974,2 1980,3 1986,4 1992,5 2000,6 2005,7 2010,8 and now 2015. The 2010 AHA Guidelines for CPR and ECC provided a comprehensive review of evidence-based recommendations for resuscitation, ECC, and first aid. The 2015 AHA Guidelines Update for CPR and ECC focuses on topics with significant new science or ongoing controversy, and so serves as an update to the 2010 AHA Guidelines for CPR and ECC rather than a complete revision of the Guidelines. The purpose of this Executive Summary is to provide an overview of the new or revised recommendations contained in the 2015 Guidelines Update. This document does not contain extensive reference citations; the reader is referred to Parts 3 through 9 for more detailed review of the scientific evidence and the recommendations on which they are based. There have been several changes to the organization of the 2015 Guidelines Update compared with 2010. “Part 4: Systems of Care and Continuous Quality Improvement” is an important new Part that focuses on the integrated structures and processes that are necessary to create systems of care for both in-hospital and out-of-hospital resuscitation capable of measuring and improving quality and patient outcomes. This Part replaces the “CPR Overview” Part of the 2010 Guidelines. Another new Part of the 2015 Guidelines Update is “Part 14: Education,” which focuses on evidence-based recommendations to facilitate widespread, consistent, efficient and effective implementation …

Inducible nitric oxide synthase is an endogenous neuroprotectant after traumatic brain injury in rats and mice

Nitric oxide (NO) derived from the inducible isoform of NO synthase (iNOS) is an inflammatory product implicated both in secondary damage and in recovery from brain injury. To address the role of iNOS in experimental traumatic brain injury (TBI), we used 2 paradigms in 2 species. In a model of controlled cortical impact (CCI) with secondary hypoxemia, rats were treated with vehicle or with 1 of 2 iNOS inhibitors (aminoguanidine and L-N-iminoethyl-lysine), administered by Alzet pump for 5 days and 1.5 days after injury, respectively. In a model of CCI, knockout mice lacking the iNOS gene (iNOS–/–) were compared with wild-type (iNOS+/+) mice. Functional outcome (motor and cognitive) during the first 20 days after injury, and histopathology at 21 days, were assessed in both studies. Treatment of rats with either of the iNOS inhibitors after TBI significantly exacerbated deficits in cognitive performance, as assessed by Morris water maze (MWM) and increased neuron loss in vulnerable regions (CA3 and CA1) of hippocampus. Uninjured iNOS+/+ and iNOS–/– mice performed equally well in both motor and cognitive tasks. However, after TBI, iNOS–/– mice showed markedly worse performance in the MWM task than iNOS+/+ mice. A beneficial role for iNOS in TBI is supported.

Part 16: Education, Implementation, and Teams 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Optimizing the links in the Chain of Survival improves outcomes and saves lives. The use of evidence-based education and implementation strategies will allow organizations and communities to strengthen these links in the most effective and efficient manner.

Part 12: Education, Implementation, and Teams

Note From the Writing Group: Throughout this article, the reader will notice combinations of superscripted letters and numbers (eg, “Precourse Preparation”). These callouts are hyperlinked to evidence-based worksheets, which were used in the development of this article. An appendix of worksheets, applicable to this article, is located at the end of the text. The worksheets are available in PDF format and are open access.

Part 14: Education 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

Cardiac arrest is a major public health issue, with more than 500 000 deaths of children and adults per year in the United States.1–3 Despite significant scientific advances in the care of cardiac arrest victims, there remain striking disparities in survival rates for both out-of-hospital and in-hospital cardiac arrest. Survival can vary among geographic regions by as much as 6-fold for victims in the prehospital setting.4,5 Significant variability in survival outcomes also exists for cardiac arrest victims in the hospital setting, particularly when the time of day or the location of the cardiac arrest is considered.6 Inconsistencies in performance of both healthcare professionals and the systems in which they work likely contribute to these differences in outcome.7 For out-of-hospital cardiac arrest victims, the key determinants of survival are the timely performance of bystander cardiopulmonary resuscitation (CPR) and defibrillation for those in ventricular fibrillation or pulseless ventricular tachycardia. Only a minority of cardiac arrest victims receive potentially lifesaving bystander CPR, thus indicating room for improvement from a systems and educational point of view. For in-hospital cardiac arrest, the important provider-dependent determinants of survival are early defibrillation for shockable rhythms and high-quality CPR, along with recognition and response to deteriorating patients before an arrest. Defining the optimal means of delivering resuscitation education to address these critical determinants of survival may help to improve outcomes from cardiac arrest. Resuscitation education is primarily focused on ensuring widespread and uniform implementation of the science of resuscitation (eg, the Scientific Statements and Guidelines) into practice by lay and healthcare CPR providers. It aims to close the gap between actual and desired performance by providing lay providers with CPR skills and the self-efficacy to use them; supplementing training with in-the-moment support, such as dispatch-assisted CPR; improving healthcare professionals’ ability …

Quinolinic Acid Is Increased in CSF and Associated With Mortality After Traumatic Brain Injury in Humans

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 (37°C) treatments for 24 hours. Oth-erwise, patients received standard neurointensive care. Quinolinic acid was measured by mass spectrometry. Univariate and multivariate analyses were used to compare CSF quinolinic acid concentrations with age, gender, GCS, time after injury, mortality, and treatment (hypothermia versus normothermia). Quinolinic acid concentration in CSF increased maximally to 463 ± 128 nmol/L (mean ± SEM) at 72 to 83 hours after TBI. Normal values for quinolinic acid concentration in CSF are less than 50 nmol/L. Quinolinic acid concentration was increased 5-to 50-fold in many patients. There was a powerful association between time after TBI and increased quinolinic acid (P < 0.00001), and quinolinic acid was higher in patients who died than in survivors (P = 0.003). Age, gender, GCS, and treatment (32°C versus 37°C) did not correlate with CSF quinolinic acid. These data reveal a large increase in quinolinic acid concentration in CSF after TBI in humans and raise the possibility that this macrophage-derived excitotoxin may contribute to secondary damage.