Presentation is loading. Please wait.

Presentation is loading. Please wait.

Cómo Morimos Bryan E. Bledsoe, DO, FACEP

Similar presentations

Presentation on theme: "Cómo Morimos Bryan E. Bledsoe, DO, FACEP"— Presentation transcript:

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

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

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

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

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

6 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.

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

8 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.

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

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

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

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

13 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.

14 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.

15 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.

16 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.

17 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.

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

19 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.

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

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

22 Phases of Cardiac Arrest
Electrical Phase minutes Circulatory Phase minutes Metabolic Phase > 10 minutes

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

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

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

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


28 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.

29 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.

30 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:

31 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:

32 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:

33 Circulatory Phase Seattle: Subgroup analysis:
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:

34 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):A1823

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

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

37 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.

38 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.

39 The Metabolic Phase Induced-hypothermia may be the answer for patients in the metabolic phase.

40 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:

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

42 The Metabolic Phase

43 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

44 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

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

46 So What Does This All Mean?

47 So What Does This All Mean?

48 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:

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

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

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

52 > 10 Minute Down Time

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

54 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

55 Induced-Hypothermia

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

57 What 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.

58 2005 AHA Recommendations

59 Chain of Survival

60 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.

61 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):

62 Summary Questions? This presentation available at:

Download ppt "Cómo Morimos Bryan E. Bledsoe, DO, FACEP"

Similar presentations

Ads by Google