Cómo Morimos Bryan E Bledsoe DO FACEP The

Cómo Morimos Bryan E. Bledsoe, DO, FACEP The George Washington University Medical Center

How We Die Bryan E. Bledsoe, DO, FACEP The George Washington University Medical Center

How We Die Life is pleasant. Death is peaceful. It is the transition that is troublesome. Isaac Asimov

How We Die Estimated 500, 000 deaths each year attributable to cardiac arrest.

How We Die Regardless, the resuscitation rate remains < 5% and has changed little in the last 40 years.

History 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.

History of Resuscitation 1891—Dr. Friedrich Maass performed the first equivocally documented chest compression in humans.

History 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.

History of Resuscitation 1947—Claude Beck developed first defibrillator and first human saved with defibrillation.

History of Resuscitation 1954—James Elam was the first to prove that expired air was sufficient to maintain adequate oxygenation.

History of Resuscitation 1956—Peter Safar and James Elam invented mouth-tomouth resuscitation.

History of Resuscitation 1957—The United States military adopted the mouthto-mouth resuscitation method to revive unresponsive victims.

History 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.

History 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.

History 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.

History 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.

History 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.

History of Resuscitation 1979—The first automated external defibrillators (AEDs) became available, further extending the concept of prehospital care.

History 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.

How We Die We now know a great deal more about the pathophysiology of sudden death— especially ventricular fibrillation.

How We Die Three Phase Model: Electrical Phase Circulatory Phase Metabolic Phase

Phases of Cardiac Arrest Electrical Phase Circulatory Phase Metabolic Phase 0 - 4 minutes 4 - 10 minutes > 10 minutes

Electrical Phase Adequate oxygen content in myocardium. Adequate energy substrates (ATP). Near-normal p. H. No myocardial ischemia. No myocardial infarction.

Electrical Phase Early defibrillation a Class I recommendation. Survival rates approach 50%.

Electrical Phase Most effective treatment during electrical phase is rapid defibrillation.

Circulatory Phase Inadequate oxygen content in myocardium. Inadequate energy substrates (ATP). Acidosis. Possible myocardial ischemia. No myocardial infarction.

Circulatory Phase DEFIBRILLATION IN THE GLOBALLY ISCHEMIC HEART MAY BE DETRIMENTAL!

Circulatory Phase Chest 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.

Circulatory Phase Animals allowed to fibrillate for 1, 3, 5, or 9 minutes prior to defibrillation. Immediate defibrillation optimal when performed in 3 minutes or less.

Circulatory Phase CPR + 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: 157 -163

Circulatory Phase In 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: 281 -287

Circulatory Phase In 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: 235 -239

Circulatory Phase Seattle: Standard immediate defibrillation: 24% survival 90 seconds CPR then defibrillation: 30% survival Subgroup analysis: Immediate defibrillation superior to 90 seconds CPR for first 3 minutes only. Cobb et al. JAMA 1999; 281: 1182 -1188

Circulatory 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): A 1823

The Metabolic Phase Effectiveness of both immediate defibrillation and CPR + defibrillation decrease rapidly. Survival rates poor.

The Metabolic Phase Tissue injury from global ischemic events and reperfusion cause circulating metabolic factors that cause injury in excess of local ischemia.

The Metabolic Phase Gut mucosa begins to malfunction secondary to ischemia. Translocation of gram-negative bacteria cause endotoxin and cytokine release. Both suppress myocardial function after defibrillation.

The Metabolic Phase Reperfusion 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.

The Metabolic Phase Inducedhypothermia may be the answer for patients in the metabolic phase.

The Metabolic Phase Induced-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 outcome Hypothermia Study Group NEJM 2002; 346: 549 -556

The Metabolic Phase Possible beneficial technologies: Correcting calcium-entry Correcting sodium alterations Preventing inflammation

The Metabolic Phase

The 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: Buffer Low calcium Increased potassium High-dextrose

The Metabolic Phase Whereas epinephrine may be beneficial during the circulatory phase, it may be detrimental during the metabolic phase. Epinephrine: Increases gut ischemia May lead to sepsis

So What Does This All Mean? This concept based on ventricular fibrillation. May be similar for trauma and hypoxia induced cardiac arrest.

So What Does This All Mean?

So What Does This All Mean? Vilke et al. The three-phase model of cardiac arrest as applied to ventricular fibrillation is a large, urban emergency medical services system. Resuscitation. 2005; 84: 341 -346

What Does This All Mean? EMS arrival < 4 minutes after collapse Immediate defibrillation Bystander CPR not as important during this phase.

What Does This All Mean? EMS arrival less than >4 but <10 minutes after collapse CPR + defibrillation Bystander CPR VERY important during this phase.

What Does This All Mean? EMS arrival > 10 minutes after collapse ?

> 10 Minute Down Time

Induced-Hypothermia Dandenong Hospital, Melbourne, VIC 30 m. L/kg cold (4˚- 8˚ C) lactated Ringer’s administered in ED after out-of-hospital resuscitation by paramedics.

Induced-Hypothermia Patients: n=22 Age: 70 (55 -75) Cause of Arrest: Cardiac=21 TCA OD=1 Rhythm: V-fib=14 Asystole=4 PEA=4 EMS Call: 2 minutes Response: 8 minutes EMS arrival to ROSC: 16 minutes Collapse to ROSC: 26 minutes ROSC to infusion: 73 minutes

Induced-Hypothermia

Induced-Hypothermia Survival (initial rhythm): V-fib: 8/14 (80%) Not v-fib: 2/8 (25%) Bernard et al. Resusc. 2003; 56: 9 -13

What about ventilations? Lay public can not or will not do mouthto-mouth in many cases. Adequate oxygen stores initially. Patient may gasp for a minute. May take away from effective chest compressions.

2005 AHA Recommendations

Chain of Survival

Summary 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.

Major Reference Weisfeldt ML and Becker LB. Resuscitation After Cardiac Arrest: A 3 Phase Time-Sensitive Model. Journal of the American Medical Association. 2002; 288(23): 3035 -3038

Summary Questions? This presentation available at: http: //www. bryanbledsoe. com