after Cardiac Arrest Ankur A Doshi MD FACEP Post Cardiac Arrest Service UPMC Presbyterian Presenter Disclosure Information Ankur A Doshi MD FACEP ED and Hospital Care Can Improve Survival ID: 816441
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Slide1
ED and Hospital Care Can Improve Survival after Cardiac Arrest
Ankur A. Doshi, MD FACEP
Post Cardiac Arrest Service
UPMC Presbyterian
Slide2Presenter Disclosure Information
Ankur A. Doshi, MD FACEP
ED and Hospital Care
Can Improve Survival after Cardiac Arrest
2
FINANCIAL DISCLOSURE:
Employer: University of Pittsburgh/UPMC
Grants/Research Support: Pittsburgh Emergency Medicine Foundation
Slide3Learning objectivesDiscuss immediate steps shown to improve outcomes for patients with ROSC after cardiac arrest in the ED
List proven in-hospital medical therapies for post-cardiac arrest patients
Compare Targeted Temperature Management (TTM) with Induced Therapeutic Hypothermia (ITH)
Slide4What we won’t coverTreatment during cardiac arrest
Detailed
neuroprognostication
Seizure evaluation and treatmentOther therapies not yet proven to have benefit post-arrest
Slide5The good news
Girotra
2012 – GWTG Data
Daya
2013 – ROC Data
Slide6Opportunities
Langhelle
, 2003
% Survival (1 month) for OOHCA bystander witnessed and cardiac etiology
Herlitz, 2006
Slide7What therapies can improve survival from cardiac arrest?
Blood pressure control / perfusion
Ventilator management (O2 and CO2)
Temperature managementTertiary careCardiac catheterizationDelayed neuroprognostication
Post-discharge planning
Slide82015 Post-Arrest Guidelines
Early Coronary Angiography
Hemodynamic Goals
Targeted Temperature ManagementSeizure Detection and ManagementVentilation and OxygenationPrognosticationOrgan Donation
8
Slide9Blood pressure management
Slide10Anoxic injury impairs cerebral autoregulation
“Pressure passive”
Mean arterial pressure (mmHg)
50
100150Cerebral blood flow (ml/100g/min)Normal
0
50
100
Absent
Slide11Hemodynamic goals
Kilgannon
.
Crit
Care Med, 2014Beylin. Int Care Med, 2013MAP > 80 mmHg
Slide12Ventilation and oxygenation
Slide13Brain tissue hypoxia is bad and common
O
2
delivery/diffusion impairedPerivascular edemaMenon.
Crit Care Med, 2004
Slide14Is hyperoxia bad?
Drives oxidative injury, ROS generation,
etc
Hyperoxia is common Some OBSERVATIONAL data associate extreme hyperoxia with worse outcomes
Kilgannon. JAMA, 2010ExposureAdjusted OR
(95% CI)
Arterial oxygen (per hour)
Severe
hyperoxia
(
>
300mmHg)
0.83 (0.72 – 0.98)
Moderate hyperoxia (101-299mmHg)
1.01 (0.96 – 1.05)
Normoxia
(60-100mmHg)
1.01 (0.97 – 1.06)
Hypoxia (<60mmHg)
0.74 (0.47 – 1.16)
Slide15Oxygenation goalsMeasure PaO
2
In vivo
PaO2 5 mmHg lower per 1oCNormoxia (PaO
2 100-200)Significant hyperoxia is (probably) bad and frequentBrain tissue hypoxia is (probably) bad and often quite severe
Slide16Carbon dioxide goals
PaCO
2
40mmHg (temp corrected)
Slide17Carbon dioxide goals
PaCO
2
40mmHg (temp corrected)Observational data
Roberts. Circ, 2013 Schneider. Resus, 2013
Slide18Temperature management
Slide19Slide20Hypotherm
(%)
Normotherm
(%)
RR
[95% CI]
P value
NNT
Favorable neurologic recovery
at discharge
HACA
75/136
(55%)
54/137
(39%)
1.40
[1.08-1.81]
0.006
6.4
Bernard
21/43
(49%)
9/34
(26%)
2.65
[1.02-6.88]
0.046
4.5
Favorable neurologic recovery at
6 months
HACA
71/136
(52%)
50/137
(36%)
1.44
[1.11-1.76]
0.009
7.0
HACA. NEJM, 2002
Bernard. NEJM, 2002
Slide21950 patients, 36 ICUs in Europe and AustraliaGCS <8 after OHCA due to “presumed cardiac” etiology, regardless of rhythm (except exclude
unwitnessed
asystolic arrests)
Slide22Nielsen. NEJM, 2013.
Slide23Temps in RCTs
Slide2433ºC
37ºC
32-
34ºC
37ºC33ºC36ºCOutcomes in RCTsTTM results in good outcomes (50-60% survival)
Slide25What does the data tell us?TTM is another way of performing temperature management
Anywhere 33
deg
– 36 deg
C is reasonableDOING NOTHING IS NOT AN OPTION!
Slide26Tertiary care
Slide27Systems of Care
A comprehensive, structured, multidisciplinary system of care should be implemented in a consistent manner for the treatment of post–cardiac arrest patients
(Class I, LOE B).
AHA Guidelines 2010
Slide28Volume matters
Callaway.
Resuscitation
, 2013
Slide29Volume ~ Survival
Hospitals treat an average of 17 / year
Callaway.
Resuscitation
, 2013
Slide30Tertiary center effect
Survival different for first 5 days
More intensive cardiac AND ICU interventions
Søholm
. Circ Cardiovasc Qual Outcomes, 2015
Slide31Tertiary centers in CA
N=7,725 OOHCA cases adjusted for all covariates
OR (good neurological recovery) compared to non-STEMI center at
STEMI center (>40 cases/yr) 1.32 (1.06-1.64)STEMI center (<40 cases/yr)
1.63 (1.35-1.97)Mumma. Am Heart J, 2015
Slide32Pittsburgh outcomes
N=987 persons discharged from 7 hospitals.
Link to National Death Index to determine survival time.
Center 1 has a dedicated post-arrest service line with >250 patients per year
Slide33Cardiac catheterization
Slide34Non ST Elevation
60% survival;
86% with favorable neurological function
Kern.
JACC, 2012
Slide35Reynolds. Resuscitation, 2014
Slide36Delayed neuroprognostication
Slide37Time to awakening
Grossestreuer
.
Resuscitation
, 2013
Slide38Why do patients die after CA?
2,137 non-survivors after OHCA
Largest cause of in-hospital death was WLST for “neurological” reasons (61.2%)
Callaway. Resuscitation, 2014
Slide39When do patients die?
151 ROC research hospitals across North America
Elmer. Resuscitation, 2016
Slide40Prognostication
Delay neuro-prognostication for 72 hours
Slide41Post-discharge planning
Slide42Anxiety and depression
Anxiety in 24% of survivors
Depression in 13%
Slide43Cognitive Function
Cognitive dysfunction in 50%
Slide44Long term function
Cerebral Performance Category
Modified Rankin
Scale
Reintegration to Normal Living Index
Raina. Biomed Research International, 2015
Slide45Summary of in-hospital careBP
MAP > 80
Vent
PaCO2 ~ 40Normoxia (PaO2 100-200)TTM33-36 deg C for 24 hr
Tertiary centerCardiac catheterization “early”Delay neuroprognostication > 72 hrsFunctional recovery takes 12 monthsWatch for depression / anxiety / cognitive deficits