Presentation on theme: "Cómo Morimos Bryan E. Bledsoe, DO, FACEP"— Presentation transcript:
1Cómo Morimos Bryan E. Bledsoe, DO, FACEP The George Washington University Medical Center
2How We Die Bryan E. Bledsoe, DO, FACEP The George Washington University Medical Center
3How We DieLife is pleasant. Death is peaceful. It is the transition that is troublesome.Isaac Asimov
4How We DieEstimated 500,000 deaths each year attributable to cardiac arrest.
5How We DieRegardless, the resuscitation rate remains < 5% and has changed little in the last 40 years.
6History of Resuscitation 1740—The Paris Academy of Sciences officially recommended mouth-to-mouth resuscitation for drowning victims.1767—The Society for the Recovery of Drowned Persons became the first organized effort to deal with sudden and unexpected death.
7History of Resuscitation 1891—Dr. Friedrich Maass performed the first equivocally documented chest compression in humans.
8History of Resuscitation 1903—Dr. George Crile reported the first successful use of external chest compressions in human resuscitation.1904—The first American case of closed-chest cardiac massage was performed by Dr. George Crile.
9History of Resuscitation 1947—Claude Beck developed first defibrillator and first human saved with defibrillation.
10History of Resuscitation 1954—James Elam was the first to prove that expired air was sufficient to maintain adequate oxygenation.
11History of Resuscitation 1956—Peter Safar and James Elam invented mouth-to-mouth resuscitation.
12History of Resuscitation 1957—The United States military adopted the mouth-to-mouth resuscitation method to revive unresponsive victims.
13History of Resuscitation 1960—CPR was developed. The American Heart Association started a program to acquaint physicians with closed-chest cardiac resuscitation and became the forerunner of CPR training for the general public.
14History of Resuscitation 1963—Cardiologist Leonard Scherlis started the American Heart Association's CPR Committee, and the same year, the American Heart Association formally endorsed CPR.
15History of Resuscitation 1965—J. Frank Pantridge converted an ambulance into a mobile coronary care unit with a portable defibrillator and recorded ten pre-hospital resuscitations.50% long-term survival rate.
16History of Resuscitation 1966—The National Research Council of the National Academy of Sciences convened an ad hoc conference on cardiopulmonary resuscitation to establish standardized training and performance standards for CPR.
17History of Resuscitation 1972—Leonard Cobb held the world's first mass citizen training in CPR in Seattle, Washington called Medic 2. He helped train over 100,000 people the first two years of the programs.
18History of Resuscitation 1979—The first automated external defibrillators (AEDs) became available, further extending the concept of pre-hospital care.
19History of Resuscitation 1981—A program to provide telephone instructions in CPR began in King County, Washington. Dispatcher-assisted CPR is now standard care for dispatcher centers throughout the United States.
20How We DieWe now know a great deal more about the pathophysiology of sudden death—especially ventricular fibrillation.
21How We Die Three Phase Model: Electrical Phase Circulatory Phase Metabolic Phase
23Electrical Phase Adequate oxygen content in myocardium. Adequate energy substrates (ATP).Near-normal pH.No myocardial ischemia.No myocardial infarction.
24Electrical Phase Early defibrillation a Class I recommendation. Survival rates approach 50%.
25Electrical PhaseMost effective treatment during electrical phase is rapid defibrillation.
26Circulatory Phase Inadequate oxygen content in myocardium. Inadequate energy substrates (ATP).Acidosis.Possible myocardial ischemia.No myocardial infarction.
27Circulatory PhaseDEFIBRILLATION IN THE GLOBALLY ISCHEMIC HEART MAY BE DETRIMENTAL!
28Circulatory PhaseChest compressions and tissue oxygen delivery take precedence over defibrillation.Initial therapy should be chest compressions and ventilations followed by defibrillation.Defibrillation usually delayed by 1-3 minutes.
29Circulatory PhaseAnimals allowed to fibrillate for 1,3,5, or 9 minutes prior to defibrillation.Immediate defibrillation optimal when performed in 3 minutes or less.
30Circulatory PhaseCPR + epinephrine resulted in better survival when performed after 5-9 minutes.> 5 minutes of cardiac arrest, immediate defibrillation resulted in 30% successful defibrillation and 0% ROSC.1 minute of CPR + epinephrine before defibrillation resulted in 70% conversion rate and 40% ROSC.Yakaitis et al. Crit Care Med. 1980;8:
31Circulatory PhaseIn animals with 7.5 minutes of untreated v-fib, 5 minutes of CPR + epinephrine was compared to immediate defibrillation.Significant improvement (64% vs. 21% survival) when compared to immediate defibrillation.Niemann et al. Resusc. 1992;85:
32Circulatory PhaseIn animals, 8 minutes of untreated v-fib treated with immediate defibrillation or CPR + drug cocktail (epinephrine, lidocaine, bretylium, propranolol) then defibrillation.77% versus 22% ROSC for the drug cocktail group.Menegazzi et al. Ann Emerg Med 1993;22:
33Circulatory Phase Seattle: Subgroup analysis: Standard immediate defibrillation: 24% survival90 seconds CPR then defibrillation: 30% survivalSubgroup analysis:Immediate defibrillation superior to 90 seconds CPR for first 3 minutes only.Cobb et al. JAMA 1999;281:
34Circulatory Phase Oslo: > 5 minutes after collapse, if CPR performed for 3 minutes prior to defibrillation.Survival to hospital discharge 22% vs. 4%1 year survival 20% vs. 4%Wik et al. Circ. 2002;106 (Suppl 2):A1823
35The Metabolic PhaseEffectiveness of both immediate defibrillation and CPR + defibrillation decrease rapidly.Survival rates poor.
36The Metabolic PhaseTissue injury from global ischemic events and reperfusion cause circulating metabolic factors that cause injury in excess of local ischemia.
37The Metabolic PhaseGut mucosa begins to malfunction secondary to ischemia.Translocation of gram-negative bacteria cause endotoxin and cytokine release.Both suppress myocardial function after defibrillation.
38The Metabolic PhaseReperfusion in this phase can contribute to cell death and diminished organ function independent of the adverse effects of ischemia.Key to survival during this phase appears to be control of injurious factors during reperfusion.
39The Metabolic PhaseInduced-hypothermia may be the answer for patients in the metabolic phase.
40The Metabolic PhaseInduced-hypothermia (34-32˚ C) have shown an improvement in neurologically-intact survival after out-of-hospital cardiac arrest.Patients cooled late in cardiac arrest:49% survival compared with 26%55% good neurological outcomeHypothermia Study Group NEJM 2002;346:
43The Metabolic Phase Metabolic-focused treatment Cardiopulmonary bypass Administration of metabolic therapies (similar to what is used in cardiac bypass procedures):Amino acid-enriched solution with:BufferLow calciumIncreased potassiumHigh-dextrose
44The Metabolic PhaseWhereas epinephrine may be beneficial during the circulatory phase, it may be detrimental during the metabolic phase.Epinephrine:Increases gut ischemiaMay lead to sepsis
45So What Does This All Mean? This concept based on ventricular fibrillation.May be similar for trauma and hypoxia induced cardiac arrest.
56Induced-Hypothermia Survival (initial rhythm): V-fib: 8/14 (80%) Not v-fib: 2/8 (25%)Bernard et al. Resusc. 2003;56:9-13
57What about ventilations? Lay public can not or will not do mouth-to-mouth in many cases.Adequate oxygen stores initially.Patient may gasp for a minute.May take away from effective chest compressions.
60Summary Try and know the phase your patient is in. Most EMS responses will arrive in the circulatory phase and 1-3 minutes of chest compressions are essential.Many new therapies coming down the line.
61Major ReferenceWeisfeldt ML and Becker LB. Resuscitation After Cardiac Arrest: A 3-Phase Time-Sensitive Model. Journal of the American Medical Association. 2002;288(23):
62SummaryQuestions?This presentation available at: