Cуmo Morimos

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 lt 5
  and has changed little in the last 40 years.

6
History of Resuscitation

• 1740The Paris Academy of Sciences officially
  recommended mouth-to-mouth resuscitation for
  drowning victims.
• 1767The Society for the Recovery of Drowned
  Persons became the first organized effort to deal
  with sudden and unexpected death.

7
History of Resuscitation

• 1891Dr. Friedrich Maass performed the first
  equivocally documented chest compression in
  humans.

8
History of Resuscitation

• 1903Dr. George Crile reported the first
  successful use of external chest compressions in
  human resuscitation.
• 1904The first American case of closed-chest
  cardiac massage was performed by Dr. George Crile.

9
History of Resuscitation

• 1947Claude Beck developed first defibrillator
  and first human saved with defibrillation.

10
History of Resuscitation

• 1954James Elam was the first to prove that
  expired air was sufficient to maintain adequate
  oxygenation.

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History of Resuscitation

• 1956Peter Safar and James Elam invented
  mouth-to-mouth resuscitation.

12
History of Resuscitation

• 1957The United States military adopted the
  mouth-to-mouth resuscitation method  to revive
  unresponsive victims.

13
History of Resuscitation

• 1960CPR 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

• 1963Cardiologist 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

• 1965J. 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

• 1966The 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

• 1972Leonard 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

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

19
History of Resuscitation

• 1981A program to provide telephone instructions
  in CPR began in King County, Washington. Dispatche
  r-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 deathespecially
  ventricular fibrillation.

21
How We Die

• Three Phase Model
• Electrical Phase
• Circulatory Phase
• Metabolic Phase

22
Phases of Cardiac Arrest

• Electrical Phase 0 - 4 minutes
• Circulatory Phase 4 - 10 minutes
• Metabolic Phase gt 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.

27
Circulatory Phase

• DEFIBRILLATION IN THE GLOBALLY ISCHEMIC HEART MAY
  BE DETRIMENTAL!

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.
• gt 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. 19808157-163

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. 199285281-287

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 199322235-239

33
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 19992811182-1188

34
Circulatory Phase

• Oslo
• gt 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. 2002106 (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 2002346549-556

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. 200584341-346

49
What Does This All Mean?

• EMS arrival lt 4 minutes after collapse

Immediate defibrillation
Bystander CPR not as important during this phase.
50
What Does This All Mean?

• EMS arrival less than gt4 but lt10 minutes after
  collapse

CPR defibrillation
Bystander CPR VERY important during this phase.
51
What Does This All Mean?

• EMS arrival gt 10 minutes after collapse

?
52
gt 10 Minute Down Time
53
Induced-Hypothermia

• Dandenong Hospital, Melbourne, VIC
• 30 mL/kg cold (4- 8 C) lactated Ringers
  administered in ED after out-of-hospital
  resuscitation by paramedics.

54
Induced-Hypothermia

• Patients n22
• Age 70 (55-75)
• Cause of Arrest
• Cardiac21
• TCA OD1
• Rhythm
• V-fib14
• Asystole4
• PEA4

• EMS Call 2 minutes
• Response 8 minutes
• EMS arrival to ROSC 16 minutes
• Collapse to ROSC 26 minutes
• ROSC to infusion73 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. 2003569-13

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.
  2002288(23)3035-3038

62
Summary

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