Jose G Cabanas MD MPH FACEP Paul R Hinchey MD MBA FACEP Office of the Medical Director AustinTravis County EMS System AustinTravis County EMS Approximately 12 million citizens 1100 square miles ID: 389253
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Slide1
Resuscitation and Post Resuscitation Care
Jose G. Cabanas, MD MPH FACEP
Paul R. Hinchey, MD MBA FACEP
Office of the Medical Director
Austin-Travis County EMS SystemSlide2
Austin/Travis County EMS
Approximately 1.2 million citizens, 1,100 square miles,
120
k
EMS calls
per year
1,000 cardiac
arrests
responses per
year
14 Fire Departments (1,500
FF’s
,)
EMS Transport Agency (400 Paramedics)
EMS
Systems are judged by their cardiac arrest resuscitation rates
Most large cities are 5-7%
King
Cnty
Wa
35-45%
Wake
Cnty
NC
38-42%
Austin 38%Slide3
Why are we talking about Cardiac Arrest Resuscitation?Slide4
Philosophy of Five
Time Dependent
Acute MI (STEMI)
Acute Stroke
Trauma / Surgical Emergency
Intervention Dependent
Cardiac Arrest
Respiratory Distress
Sophisticated providers/systems understand the differenceSlide5
Time Dependent
These conditions can not be definitively treated in the pre-hospital environment
Requires specialized intervention only available in the hospital
Outcomes are
improved by early access to definitive intervention
Goal is
recognition
and
short scene intervalSlide6
Intervention Dependent
Initial treatment can be delivered in
prehospital
environment
Outcomes linked to
prehospital
interventions
Goal is
identification
and
initiation of
treatment
Scene intervals are NOT criticalSlide7
Updates in Out-of-Hospital Resuscitation and Post Resuscitation CareSlide8
Objectives
Describe the importance of continuous compressions and controlled ventilations
Discuss what to do with the airway/drugs
Acknowledge the difficulty of performing continuous compressions and the need for a scripted process
Discuss importance of on-scene post ROSC stabilization
Describe role of resuscitation centers
Identify questions for the futureSlide9
Why do we worry about CA
Represents < 1% of our calls but…
> 70% of CA arrests occur outside the hospital
Definitive management of cardiac arrest is in the prehospital environment Slide10
“Stated succinctly, if ACLS care in the field cannot resuscitate the victim, ED care will not resuscitate the victim.”-
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (Part 7.2: Management of Cardiac Arrest)Slide11
Priorities in OOHCA Changed
Emphasis on compression
Limit interruptions from ANYTHING
Goal is to maximize % of time in compressions
Single D-fib every two minutes
Precharge monitor before break
Follow d-fib immediately by compressions
Decreased importance of ventilations
Fewer number of breaths
Each delivered more slowlySlide12
So if you had to push a car, would you push a few feet and stop….. only to start again a few minutes later?Slide13Slide14
So how important are compressions?Slide15
Compression fraction article
Circulation 2009Slide16
If compressions are the most important therapy when do you move the patient…..Slide17
Prehospital
Emergency Care 2011;15(1):106Slide18
Results (Pre-Feedback)
N = 108 % (25
th
, 75
th
)
Scene Correct Rate%
Median:
44.8
(9.54, 59.6)
Mean: 38.49 CI (33.2, 43.78)
Transport Correct Rate%
Median:
11.16
(5.83, 39.32)
Mean: 23.16 CI (18.35, 27.97)
Scene Correct Depth%
Median:
40.94
(15.96, 73.29)
Mean: 45.06 CI (38.76, 51.37)
Transport Correct Depth%
Median:
8.88
(2.62, 49.01)
Mean: 26.37 CI (20.12, 32.63)Slide19
Results (Post-Feedback)
N = 35 % (25
th
, 75
th
)
Scene Correct Rate%
Median:
48.16
(14.68, 62.36)
Mean: 43.6 CI (34.61, 52.59)
Transport Correct Rate%
Median:
19.0
(9.52, 60.22)
Mean: 32.78 CI (23.21, 42.33)
Scene Correct Depth%
Median:
75.73
(36.23, 95.07)
Mean: 66.86 CI (56.57, 77.16)
Transport Correct Depth%
Median:
14.0
(4.78, 90.78)
Mean: 42.04 CI (27.98, 56.11)Slide20
How about ventilations?Slide21
Importance of controlled Ventilation
Normal inspiration is negative pressure
Encourages blood return to the chest
Artificial ventilation is positive pressure
Reduces blood return to the chest
The faster the ventilation rate the higher the mean
intrathoracic
pressure
Higher MIP reduces cerebral emptying and reduces blood return to the heartSlide22
Survival in hyperventilationSlide23
STOP Hyperventilating
Telling providers not to hyperventilate is ineffective
High adrenaline situation
Tendency to ventilate faster and faster
Requires conscious effort to slow rates
Need constant reminder
Timing device
Goal directed ventilationSlide24
How to Deliver Ventilations
Goal is to oxygenate primarily and ventilate as a secondary consideration
Must provide continuous uninterrupted compressions
Traditional method is endotracheal intubation but increases interruption in compresions
So is this a paradigm that needs to be challenged?Slide25
Interrupt CPR…not ME
100 Cardiac Arrests
CPR interruptions 2* (1-9)
1
st
ETI interruption 46.5 s* (7-221 s)
Total all ETI interruption 109.5 s* (13-446 s)
1/3 > 1 min; ¼ > 3 min
ETI Interruptions 23% of all
* Indicates median values reported
Wang et
al Ann
Emerg
Med. 2009Slide26
But an advanced airway is a better airway…..Slide27
Advanced Airway Management
Advantages
No mask seal required
Easier to do
Less manpower
Allows continuous compressions
Disadvantage
Requires interruption of compressions
Easier to hyperventilate (rate and volume)
Doesn’t provide better ventilation/oxygenationSlide28
173 LMA vs 200 BVM by paramedics
No difference in median:
Pa
CO
2
52.9 v 55.3 (p=0.06)
Pa
O
2
64.6 v 71.9 (p=0.056)
There is no MAGIC to these devicesSlide29
Retrospective analysis of OOHCA
1,294 Cardiac Arrests
79% received intubation
10% BVM
4%
Combitube
/EOA
After adjusting for age, bystander CPR, witnessed arrest and initial rhythm
OR for BVM
vs
Advanced airway was 4.5Slide30
What is best vascular access?
Goal is vascular access by any means that does not interrupt compressions
Preferably rapid reliable access that does not detract from other tasks
Based on assumption that the drugs do anything….more on this later
IO access can be achieved in < 10 sec but which site should be used?Slide31
88 Cardiac arrest
56 (65.9%) used
tibial
site first
Initial success rate 89.7%
3 (5.8%) dislodged
18 (34%) used
humerus
first
Initial success rate 60%
6(33%) dislodged
Overall success rates
Tibia 84.5%
Humerus
40%Slide32
So what about the drugs?
Most recent quandary
Standard of care is currently being challenged
Will be a major change in management in your career
Who will make the first step…Slide33
851 patients with OOHCA randomized to:
418 given IV drugs
433 given no drugs
Primary outcome hospital discharge
Also looked at:
Hosp admission with ROSC
Neuro outcome at discharge
Survival at 1 yearSlide34Slide35
Recent epi
studySlide36
Running the Arrest
CA is not the most diagnostically challenging condition so thought to be “EASY”
EXECUTION is anything but…
Conflicting interests of multiple tasks and the need for continuous uninterrupted compressions and infrequent occurenceSlide37
This is harder to do than you thinkSlide38
Task Interruptions
Airway interventions and IVs
Ventilations
Pulse checks
Rhythm analysis
Defibrillation
Changing compressors
Patient movementSlide39
We have limited awareness of task time in complex processes….so these interruptions should be engineered and choreographed to minimize their impact…..Slide40
>20 second pause for defibrillation. Appears that a ventilation was given before the compressions resumed. Compressions resume 10 seconds after shock delivery.Slide41
Long pause for ventilations. Then short sequence of compressions during defib charging. Compressions resumed approximately 5 seconds after shock 1 delivered.Slide42
Why engineer the process?
Creates uniformity:
Accurate assessment of outcomes
Linking specific interventions to outcomes
Baseline for future modification
In the process it:
Improves outcomes
Improves efficiency
Reduces errorsSlide43
Regional Variation in Incidence / Outcome
2008
11,898 cardiac arrests
2729 had initial rhythm of V-Fib / V-
Tach
.
954 (4.6% of total) were discharged alive.
Incidence of EMS-treated CA was 52.1 per 100 000
survival ranged from 3.0% to 16.3% (median of 8.4%)
Median ventricular fibrillation 12.6 per 100 000
survival ranged
from 7.7% to 39.9%, Slide44
So how do you control variabilitySlide45Slide46
Professional CA resuscitation
is to CPR ….
….what a pit crew
is to changing tiresSlide47
Pit Crew Model
Same name…many versions
CPR
Maximize compression fraction
Effective compression(rate/depth)
Provider fatigue
Controlled ventilations
Defib
Pre-charge @1:45
Emphasis on Shock/Don
’
t
’
shockSlide48
Current Goal:
Less than 10 second break
in every
2 minute cycle of CPRSlide49
Staying Alive or
Another One Bites the Dust?
Staying alive 103 bpm
30:2
100 compressions/min =18s for compressions
5 s break for ventilations every 30 compressions?
18 of every 23s in active compression is 78%
NOT counting other breaks in CPR
Pit Crew
Continuous compressions w/asynchronous ventilation
10s break every 2 min is 92%
5s break every 2 min is 96%Slide50
Typical example
(actually 40:2)
©2010 Paul R. HincheySlide51
Good example of ventilations at a rate of about 8-10 per minute.
©2010 Paul R. HincheySlide52
©2010 Paul R. HincheySlide53
So we went to the simulation lab and now it
’
s ALL choreographed….Slide54Slide55
BLS
&
ALSSlide56Slide57Slide58
©2010 Paul R. Hinchey
Need cpr checklistSlide59
Some ScenariosSlide60
Scenario 1
78 y/o Wal-Mart greeter suffers cardiac arrest in the front of a store:
Where do you work the cardiac arrest? Would this be different if it were in his house?
When do you begin transport to the hospital?
If unsuccessful when do you terminate the resuscitation?Slide61
Scenario 2
78 y/o Wal-Mart greeter has been resuscitated from CA and is being transported when he re-arrests:
What would you instruct your crews to do if they were 20 min out from the hospital?
What if they were 5 min out?Slide62
Scenario 3
78 y/o suffers CA at home. Wife does 2 min dispatcher directed CPR. Pt has ROSC and wakes up. Walks to couch. Crews find in CHF and treat appropriately w/meds and CPAP. FF ride w/crew to hosp. While pulling into ED bay pt goes into CA:
What do you want your crews to do?Slide63
Take Home Message
CA is not as easy as once thought
Pre-hospital providers must be the experts
Its all about compressions
Airway, drugs, etc are a big ?
If you want to do this well you must have universally understood goals and plan Slide64
Post Resuscitation CareSlide65
Post-Cardiac Arrest Syndrome
Post-cardiac arrest brain injury
Responsible for 68% of deaths of patients who survived to ICU admission (Lever, 2004)
Post-cardiac arrest myocardial dysfunction
LV dysfunction, myocardial stunning, cardiogenic shock
Systemic ischemia/reperfusion injury
Inflammatory response, impaired vasoregulation, oxygen delivery and utilization, resulting in hypotension / MSOF
Persistent precipitating pathology
STEMI, Toxic Ingestion, Hypoxia, Hemorrhage, etc. Slide66
Phases of Post-Cardiac Arrest SyndromeSlide67
Post-Resuscitation Care
Goals of Post-Arrest Care
Maintain Hemodynamic Stability
Preserve the Brain
Avoid hyperventilation
Prevent re-arrest
Elements of Post-Care include
Vasopressor titration
Therapeutic Hypothermia
Early Cardiac Catheterization
Sedation
Glucose and Electrolyte ManagementSlide68
Post Cardiac Arrest Care
The first 20 minutes after ROSC is the Immediate Phase of Post Cardiac Arrest Syndrome
Patients in these phases may be critically ill and benefit by immediate treatment AT SCENE:
This is a better strategy for patient survival than rapid movement to the vehicle and rapid transport delaying or deferring key interventions
Failure to initiate immediate aggressive treatment may result in re arrest of patient or increased morbidity Slide69
1,199 Cardiac Arrests
ROSC in 27.4%
Rearrest in 36%
Time to rearrest
Median 3.1 min (1.6-6.3)Slide70
Post-Resuscitation Care
Focus should be on restoring perfusion
Perfuse the myocardium
Perfuse the brain
Fluids and pressors for MAP >90
Remove the ITD
Initiate hypothermia
Obtain 12 lead EKG
THEN move the patientSlide71Slide72
Barriers in Post-Cardiac Arrest Care
Post– cardiac arrest patients are treated by multiple teams of providers
Variation in post-cardiac arrest treatment and patient outcome between institutions.
Limited reliability of early prognostication (<72 hours after arrest)Slide73
The science behind the cooling
Han Solo frozen in Carbonite – Star Wars Episode V (1980)Slide74
Journal Iowa Medical Society,
November
1964 Slide75
Therapeutic Hypothermia
HACA
2002
Bernard 2002
Idrissi 2001Slide76
ILCOR Advisory Statement
Unconscious adult patients with ROSC after out-of-hospital VF cardiac arrest should be cooled to 32°C - 34°C for 12 - 24 hours
Possible benefit for other rhythms or in-hospital cardiac arrestSlide77
Editorial Comments
“The reason hypothermia has not become the standard of care for post-resuscitation is simple. Emergency and EMS physicians have failed to make it so.”
Mennegazzi and Callaway, PEC 2005Slide78
“The Future”
720j Defibrillation?
Hands on Defibrillation?
Intra-arrest cooling?
Mechanical CPR and AC/DC CPR?
Regional Receiving Facilities?Slide79
Knowledge Gaps
Impact of Prehospital Cooling in Outcomes?
Continuous temperature in the Field?
Rate of Cooling?
Target? How Long?
Urban vs. Rural EMS?
ALS Vs BLS?
How do we train Providers?Slide80
Take Home Message
Resuscitation is not over with ROSC
Post-Cardiac Arrest Patients need to be treated with a high sense of urgency.
Patients should receive hypothermia specially if initial rhythm was VF/VT.
Hypothermia is not a substitute for other key components in the Chain of SurvivalSlide81
Take Home Message
Post
-resuscitation/cardiac specialty hospitals
should
receive patients directly from the field or in prompt
transfer
Coordination between EMS, EM, ICU, and Cardiology is a must!!
Engage all stakeholders in your system
Management of Cardiac Arrest is evolving rapidly!! EMS Medical Directors must keep upSlide82Slide83
Questions?Slide84
Out-of-Hospital Initiation of Therapeutic Hypothermia with Cold Saline Improves Survival in Patients with Return of Spontaneous Circulation in the Field.
Jose G. Cabanas MD, MPH / Brent Myers MD, MPH
Wake County EMS SystemSlide85
Authors
Brent Myers MD, MPH, Wake EMS/
WakeMed
Jose G. Cabanas, MD, Wake EMS/
WakeMed
Ryan Lewis, MS, EMT-P, Wake EMS
Valerie De
Maio
, MD
MSc
,
WakeMed
Graham
Synder
, MD,
WakeMed
Gay
Beneveides
, MD,
WakeMed
Robert Denton, MD, Rex Healthcare
Daniel
Licastese
, RN, Rex Healthcare
Robert Lee, MS MA,
WakeMedSlide86
Disclosure
This Project was supported by the SAEMS EMS
Physio
-Control Award (2008)Slide87
Objective
To determine the impact on survival of a standard post-resuscitation care protocol that includes
prehospital
initiation of therapeutic hypothermia in patients with return of spontaneous circulation (ROSC) in the field.Slide88
Methods
Observational cohort
“Before and after” – Introduction of Therapeutic Hypothermia for patients with
prehospital
ROSC
Post-resuscitation patients are selectively transported to one of 2 high volume PCI centers
Wake County NC - pop. 897,000
April 2005 through December 2008Slide89
Cardiac Arrest Response
All calls receive EMD from a single, high-volume center
Fire first response with AED and compressions
Paramedic response with transport ambulances (2)
Supervisory response at paramedic levelSlide90
Protocol Revision
[Apr 2005-Oct 2006]: Continuous compressions, controlled ventilations
[Oct 2006-Dec 2008]: Induced Hypothermia after ROSCSlide91
Criteria for Induced Hypothermia
ROSC after cardiac arrest not related to trauma or hemorrhage
Age 16 years or greater
Female without obviously gravid uterus
Initial temperature >34 C
Patient with advanced airway (no RSI)
Patient remains comatose without purposeful response to painSlide92
Data Collection
All EMS records are maintained in an electronic database
Records with any of the following characteristics are reviewed to determine if cardiac arrest occurred:
EMS Patient Disposition = cardiac arrest
CPR procedure is recorded
Defibrillation is recorded
Induced Hypothermia ProcedureSlide93
Inclusion Criteria
All adult patients resuscitated from out of hospital cardiac arrest (OHCA) prior to hospital arrival, regardless of initial rhythm, were included if they had ROSC in the field.Slide94
Age less than 16
Obvious traumatic origin of arrest
EMS witnessed arrest
Arrest not in EMS control
Prison facilities
Out-of-system intercept
Arrests under direction of non-EMS physician
Exclusion CriteriaSlide95
Outcome Measures
Discharge from hospital (
primary
)
Neurologically intact survival was defined as CPC 1 or 2 at time of hospital discharge.
2 blinded physician reviewers from each hospital independently assigned CPC scores based on patient discharge recordsSlide96
Included Patients / Phase
All Phases
N=640
Before (17 Months)
227
After (26 Months)
413Slide97
Before After
(n=227) (n=413)
Mean age (yrs)
66
64
Male sex
62%
60%
Bystander witnessed arrest
45%
32%
Bystander CPR
38%
39%
Mean Response (
mins
)
5.6
5.6
Initial rhythm VF/VT
35%
38%
NOTE: no statistically significant difference between study periods
Patient and EMS CharacteristicsSlide98
Multivariate Odds of
Neuro
Intact Survival
Factor
Odds
95% CI
Age
0.97
0.96-0.98
Bystander CPR
1.44
.94-2.19
Vfib
8.58
5.5-13.1
Hypothermia (After)
1.95
1.23-3.09Slide99
Survival to Hospital Discharge for All Rhythms
NOTE: statistically significant difference p value <0.0163Slide100
Survival to Hospital Discharge for All Rhythms
*Difference in overall survival was significant with a p-value of 0.0163Slide101
Percent of Survivors Neurologically Intact
NOTE: no statistically significant difference between study periodsSlide102
Limitations
Protocol-driven pre- and post-resuscitation cardiac arrest care
Hawthorne effect
Intention-to-treat analysisSlide103
Conclusion
Out-of-hospital standard post-resuscitation care protocol that includes induced hypothermia for all patients with ROSC significantly improved survival to hospital discharge in this EMS systemSlide104
www.wakeems.comSlide105
Wake County EMS
Annually 70,000+ 911 calls (700 OHCA)
Providers: 1,500
BLS
, 225 ALS, 17
APPs
Tiered response incl. dispatch assisted CPR, first responder apparatus and paramedic supervisor to high acuity calls
Serve 7 hospitals of 3 health care systems, incl. 2 PCI capable facilities
Annual protocol updates in April
Utstein
style data collection templateSlide106
Survival to Discharge – VF/VT
NOTE: no statistically significant difference between study periodsSlide107
Optimizing Neurologic Resuscitation
Mild Induced Hypothermia (IH)
Decrease metabolic demand
4,5,6,7
Inhibits inflammatory cascade
12,14,15
IH is time sensitive
8,11,14,15
Hemodilution
12,13
Normal saline dilution as part of hypertensive reperfusion strategy
Hypertensive reperfusion
Use of vasopressors to target MAP of 90Slide108
Circulation 2007Slide109
Standardized post resuscitation bundle:
Cardiac catheterization
Therapeutic hypothermia
Hemodynamic maintenance
Ventilator management
Electrolyte/glucose control
PrognosticationSlide110
Outcome –CPC 1 or 2
Control period 15/58 (26%)
Treatment period 34/61(56%)
OR 3.61 (CI 1.66-7.84, p=0.001)Slide111
Induced Hypothermia
Do NOT delay starting IH
If patient meets inclusion criteria start cooling
Do not worry about rewarming Slide112Slide113
?Slide114
So if compressions are the MOST important intervention for a successful resuscitation what is our airway management device of choice in a cardiac arrest?
….more on this laterSlide115
Ventilation vs Oxygenation
Oxygenation is delivery of oxygen to RBC and tissues
Oxygenation determined by two things:
FiO
2
(
% inspired O
2
)
Pressure of gas (CPAP or PEEP)
Ventilation is the elimination of CO
2
Ventilation is determined by two things:
Tidal volume
Ventilatory rateSlide116
Why is this important?
Cells require oxygen to make energy
Inability to oxygenate the tissue is quickly fatal
Exchanging carbon dioxide is NOT!
If forced to make the choice between oxygenation and CO2 exchange
CHOOSE OXYGENATION!Slide117
So why does that matter?
If oxygenation has nothing to do with ventilation why do we ventilate patients at rates > 30 breaths per minute?
Who cares…..if breathing 12 times a minute is good 30 times a minute MUST be better right?Slide118
….what is our airway management device of choice in a cardiac arrest?Slide119
The device that allows us to
oxygenate
the patients brain and myocardium and causes the…
LEAST interruption in compressionsSlide120
Objective
Describe the importance of:
Prehospital resuscitation
Continuous compression
Controlled ventilatory rates
Describe the value and limitations of advanced airway management adjuncts
List the critical components of cardiac arrest managementSlide121
Pit Crew CPR
Went to simulation to design highly scripted process that allows intervention without interruption
Tasks assigned to positions rather than individuals because individuals changeSlide122
OOHCA What matters!
For first 2 cycles concentrate on
compressions
Get on the chest as quick as possible
Compress hard and fast (do NOT exceed 120)
Minimize interruptions
If on monitor compress up to delivery of shock
Resume compressions immediately regardless of pulse or rhythm
BVM
ONLY
Control ventilation (use your blinky light)Slide123
OOHCA What matters!
After 2 cycles (4 min) place King Airway
Don’t stop compressions!
ETI only if unsuccessful with BIAD
Place gastric tube via KING or OG/NG
Control your ventilations
Recheck tube with each patient movementSlide124
OOHCA What matters!
Continue resuscitation
Rhythm/Pulse check
only
at 2 min
Change compressor q 1 min regardless of fatigue
Run checklist to assure overlooked errors
Careful consideration of causes
Do NOT move the patient unless:
You are in potential danger
You are in a public place
Other situation not suitable to leave the bodySlide125
Pre-hospital providers must be the experts in cardiac arrest resuscitation!Slide126
0
2
4
6
8
10
12
14
16
18
20
Arrest Time (min)
SHOCK
CCC
HYPO?
Electric
Circulatory
Phase
Etapa metabólica
What we know?
Metabolic PhaseSlide127
BackgroundSlide128
Inertia…..
it’s not just for cars anymore!
Blood
Inertia?
Berg et al. Resuscitation 2001Slide129
What is Post-Cardiac Arrest Syndrome?
Unique / complex combination of pathophysiological processes, which include:
Post–cardiac arrest brain injury,
Post–cardiac arrest myocardial dysfunction
Systemic ischemia/reperfusion response.
DON’T FORGET!! the unresolved pathological process that caused the cardiac arrest.Slide130
Post-Cardiac Arrest Syndrome
High mortality of cardiac arrest patients after ROSC is due to multiple organ system dysfunction
Cardiac Arrest etiology
Duration of cardiac arrest and no flow
Reperfusion injury after ROSC Slide131
Post-Cardiac Arrest Brain Injury
Pathophysiology
Impaired Cerebral Autoregulation
Cerebral Edema
Clinical Manifestations
Coma, Seizures, Myoclonus
Vegetative State, Brain Death, Strokes
Potential Treatments
Therapeutic Hypothermia
Early Hemodynamic Optimization
Ventilation/ Oxygenation Slide132
Did Rate Change with Feedback?
Independent Variables (Not Paired)
Scene
Kruskal-Wallis Test
P = 0.25
Transport
Kruskal-Wallis Test
P = 0.39*Slide133
Post-Cardiac Arrest Myocardial Dysfunction
Pathophysiology
Global Hypokinesis
ACS
Clinical Manifestations
Reduced Cardiac Output (Low BP)
Dysrhythmias
Cardivascular Collapse
Potential Treatments
Early Revascularization (AMI)
Hemodynamic OptimizationSlide134
Systemic Ischemia/ Reperfusion Response
Pathophysiology
Systemic Inflammatory Response
Increased Coagulation
Adrenal Suppression
Key Potential Treatments
Temperature Control
Hemodynamic Optimization
Glucose Control
Treat Cause of ArrestSlide135
Aha statement
Post-Resuscitation Recommendations
Induced hypothermia
Prevention of hyperthermia
Tight glucose control
Prevent hypocapnia
Maintain elevated MAPSlide136
Therapeutic Hypothermia
The protective effects of hypothermia
induction have been suggested since
the time of Hippocrates, who
advocated packing bleeding patients
in
snow.
Baron Larrey, Napoleon’s Battle surgeon during the invasion of Russia had noted that soldiers that were left in the snow had improved survival than those treated with blankets and warm drinks.
Slide137
History of Hypothermia and Cardiac Arrest
Williams et al -Annals of Surgery, Volume 4 #3 September 1958 Slide138
Why Induced Hypothermia?
Pre-hospital ROSC
1
45%(38%) of v-fib arrests
37% (22%)of all cardiac arrests
Discharge
1
12%(10%)
Post Resuscitation Deaths
3
10% die due to recurrent dysrhythmias
30% die to due to cardiovascular collapse
40% die due to PRESlide139
Mechanisms of Hypothermia
In the normal brain, hypothermia reduces the cerebral metabolic rate for oxygen (CMRO2) by 6% for every 1°C reduction in brain temperature
It is thought to suppress many of the chemical reactions associated with reperfusion injury. (free radical
, excitatory
amino acid release, and calcium shifts, which can in turn lead to mitochondrial damage and apoptosis
Steen PA, Newberg L, Milde JH, et al. Hypothermia and barbiturates: individual and combined effects on canine cerebral
oxygen consumption.
Anesthesiology. 1983;58:527–532.Slide140
Post
R
esuscitation
E
ncephalopathy
Initial insult from cardiac arrest
Period of luxuriant hyperperfusion
3
Cell injury
8,11
Oxygen free radical formation
Inflammatory cascade
Glutamate mediated cell death
Loss of autoregulation
Sludging and hypoperfusion
3,8,11
Perfusion/demand mismatch
8,11
Slide141
Wake EMS Experience…Slide142
Objective
To determine the impact on survival of a standard post-resuscitation care protocol that includes prehospital initiation of therapeutic hypothermia in patients with return of spontaneous circulation (ROSC) in the field.Slide143
Methods
Observational cohort
“Before and after” – Introduction of Therapeutic Hypothermia for patients with prehospital ROSC
Post-resuscitation patients are selectively transported to one of 2 high volume PCI centers
Wake County NC - pop. 897,000
April 2005 through December 2008Slide144
Cardiac Arrest Response
All calls receive EMD from a single, high-volume center
Fire first response with AED and compressions
Paramedic response with transport ambulances (2)
Supervisory response at paramedic levelSlide145
Protocol Revision
[
Apr 2005-Oct 2006]: Continuous compressions, controlled ventilations
[Oct 2006-Dec 2008]: Induced Hypothermia after ROSCSlide146
Criteria for Induced Hypothermia
ROSC after cardiac arrest not related to trauma or hemorrhage
Age 16 years or greater
Female without obviously gravid uterus
Initial temperature >34 C
Patient with advanced airway (no RSI)
Patient remains comatose without purposeful response to painSlide147
Data Collection
All EMS records are maintained in an electronic database
Records with any of the following characteristics are reviewed to determine if cardiac arrest occurred:
EMS Patient Disposition = cardiac arrest
CPR procedure is recorded
Defibrillation is recorded
Induced Hypothermia ProcedureSlide148
Inclusion Criteria
All adult patients resuscitated from out of hospital cardiac arrest (OHCA) prior to hospital arrival, regardless of initial rhythm, were included if they had ROSC in the field.Slide149
Age less than 16
Obvious traumatic origin of arrest
EMS witnessed arrest
Arrest not in EMS control
Prison facilities
Out-of-system intercept
Arrests under direction of non-EMS physician
Exclusion CriteriaSlide150
Outcome Measures
Discharge from hospital (
primary
)
Neurologically intact survival was defined as CPC 1 or 2 at time of hospital discharge.
2 blinded physician reviewers from each hospital independently assigned CPC scores based on patient discharge recordsSlide151
Included Patients / Phase
All Phases
N=640
Before (17 Months)
227
After (26 Months)
413Slide152
Before After
(n=227) (n=413)
Mean age (yrs)
66
64
Male sex
62%
60%
Bystander witnessed arrest
45%
32%
Bystander CPR
38%
39%
Mean Response (mins)
5.6
5.6
Initial rhythm VF/VT
35%
38%
NOTE: no statistically significant difference between study periods
Patient and EMS CharacteristicsSlide153
Survival to Hospital Discharge for All Rhythms
NOTE: statistically significant difference p value <0.0163Slide154
Survival to Hospital Discharge for All Rhythms
*Difference in overall survival was significant with a p-value of 0.0163Slide155
Percent of Survivors Neurologically Intact
NOTE: no statistically significant difference between study periodsSlide156
Limitations
Protocol-driven pre- and post-resuscitation cardiac arrest care
Hawthorne effect
Intention-to-treat analysisSlide157
Conclusion
Out-of-hospital standard post-resuscitation care protocol that includes induced hypothermia for all patients with ROSC significantly improved survival to hospital discharge in this EMS systemSlide158
Optimizing Neurologic Resuscitation
Mild Induced Hypothermia (IH)
Decrease metabolic demand
4,5,6,7
Inhibits inflammatory cascade
12,14,15
IH is time sensitive
8,11,14,15
Hemodilution
12,13
Normal saline dilution as part of hypertensive reperfusion strategy
Hypertensive reperfusion
Use of vasopressors to target MAP of 90Slide159
Is Earlier Better??
Nordmark
2005
20 Pigs Subjected to 8 minutes of V-fib followed by CPR
Randomized into 2 groups (hypothermia/control)
Hypothermic group received cold saline after 1 min in CPR
Conclusion:
“Inducing Therapeutic Hypothermia with a cold infusion seems to be an effective method that can be started during ongoing CPR”Slide160
Is Earlier Better??
Bernard
2008
Resuscitation
60 year-old female in cardiac arrest (37 minutes) due to pericardial tamponade
D/H Alert and Oriented
Conclusion:
“Treatment with a rapid Intravenous Infusion of large volume (40ml/kg), Ice-cold (4˚C) fluid during CPR induces mild hypothermia and may provide neurological protection
”Slide161
Is Pre-Hospital Cooling Safe??
Bruel
2008
The study was aimed to determine the safety and effectiveness of cooling patients while in ALS Support
The Median time
to reach mil hypothermia (<34˚C) after ROSC
was
16 minutes
Conclusion:
“The
infusion of 2 liters of Normal Saline at 4˚C in the field during ALS to induce mild hypothermia in resuscitated OHCA patients is safe, feasible and effective”