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 pH.
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 vfib, 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):A1823
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?
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 mL/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 3Phase Time-Sensitive Model. Journal of
the American Medical Association.
2002;288(23):3035-3038
Summary
Questions?
This presentation available at:
http://www.bryanbledsoe.com
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Cómo Morimos - Dr. Bryan E. Bledsoe