You are on page 1of 48

Best Practices in

Resuscitation

Dr. K.S. Chew, MD, MMED


School of Medical Sciences, Universiti Sains Malaysia

Conflict of Interest
No conflict of interest to declare.

www.PresentationPro.com

Contents
What are NOT considered best practices
Recommendations from AHA consensus statement
2013
Post-cardiac arrest MAP are we hitting the right
target?
Therapeutic Hypothermia post-cardiac arrest
www.PresentationPro.com

What Are Not Really Best


Practices

Is Adrenaline Really Really Beneficial In


Cardiac Arrest?

Lin S et al. Resuscitation. 2014;85(6):732-40.


www.PresentationPro.com

Meta-Analysis (Lin et al, 2014)

Meta-analysis, 14 RCTs, 12,246 patients


P = OHCA patients
I = Standard dose adrenaline 1 mg q3min
C = various comparators
vs placebo (1), n = 534
vs high dose adrenaline (6), n = 6,174
vs vasopressin (1), n = 336
vs adrenaline + vasopressin (6), n = 5202

O = survival to hospital discharge (primary)


Lin S et al. Resuscitation. 2014;85(6):732-40.
www.PresentationPro.com

Standard
dose
adrenaline
vs
High dose
adrenaline
Lin S et al. Resuscitation. 2014;85(6):732-40.

Standard
dose
adrenaline
vs
Adre/Vaso
www.PresentationPro.com

Lin S et al. Resuscitation. 2014;85(6):732-40.

Results
Adrenaline* vs placebo (1), n = 534
No difference in survival or neuro outcome

Adrenaline vs high dose adrenaline* (6), n = 6,174


No difference in survival or neuro outcome

Adrenaline vs vasopressin (1), n = 336


No difference in ROSC, admit, survival or neuro outcome

Adrenaline vs adre + vasopressin (6), n = 5,202


No difference in ROSC, admit, survival or neuro outcome
* Higher ROSC, higher admission
www.PresentationPro.com

Historical Perspectives
Based on in-vitro, animal studies
1874, Pellacani - first to administer adrenal extract
to animals
1896, Gottlieb administered adrenal extract,
restored circulation after inducing hypotension
1906, Crile and Dolley the need of adrenaline to
restore aortic pressure
1963, Pearson and Reddings classic paper on
animal studies showed benefits of adrenaline
Am. Heart J. 1963 (66) 210214
www.PresentationPro.com

Authors Conclusion
There was no clear advantage of SDA over placebo, HDA,
adrenaline and vasopressin combination, or vasopressin
alone, in survival to discharge or neurological outcomes
after OHCA. There were improvements in rates of survival to
admission and ROSC with HDA over SDA and with SDA over
placebo. Thus, the efficacy of vasopressor use in OHCA
remains unanswered. Future trials are needed to determine
the optimal dose of adrenaline for OHCA.
*SDA = standard dose adrenaline;
HAD = high dose adrenaline

Lin S et al. Resuscitation. 2014;85(6):732-40.


www.PresentationPro.com

Will AHA/ ILCOR/ ERC, etc Strip Away


Adrenaline Too??

www.PresentationPro.com

Effect of Hyperoxia On Post-CA: A MetaAnalysis

Wang CH et al. Resuscitation. 2014;85(9):1142-8.


www.PresentationPro.com

Methods

10 studies, N = 32,993
No language limitation in article selection
P = Post-ROSC patients
I = Hyperoxia (PaO2 >300 mmHg)
C = Non-hyperoxia or Normoxia (60 300 mmHg)
O = In-hospital mortality (primary)

www.PresentationPro.com

In-Hospital Mortality

OR, 1.40; 95% CI, 1.021.93

Wang CH et al. Resuscitation. 2014;85(9):1142-8.


www.PresentationPro.com

Poor Neurological Outcome

Non-Hyperoxia

Hyperoxia

OR, 1.62; 95% CI, 0.873.02

www.PresentationPro.com

Avoid Too Much O2 In Ventilated Stroke


Patients

Rincon F et al. Crit Care Med 2014;42(2):387-396


www.PresentationPro.com

Methods
Prospective study
N = 2894 ventilated adult stroke
49% intracranial hemorrhage
32% subarachnoid hemorrhage
19% acute ischemic stroke

Setting: 131 U.S. adult ICUs


Primary outcome: in-hospital mortality
Definition - Hyperoxia: PaO2 >300 mmHg
Hypoxia: PaO2<60 mmHg
www.PresentationPro.com

Rincon F et al. Crit Care Med 2014;42(2):387-396


www.PresentationPro.com

Results
Mortality was highest in the hyperoxia group
compared with the normoxia group (OR 1.7, 95%
CI 1.3-2.1;p < 0.0001) and the hypoxia group (OR
1.3; 95% CI 1.11.7]; p < 0.01.

www.PresentationPro.com

Summary thus far


Meta-analysis by Wang CH et al (2014) on post-CA
with ROSC: Hyperoxia is bad! Worse survival to
discharge

In Rincon et al (2014), for ventilated stroke patients,


Hypoxia bad
Hyperoxia worse!
Normoxia good
Aim SaO2 92-94%
www.PresentationPro.com

AVOID Study

Stub D et al. Am Heart J. 2012;163(3):339-45


www.PresentationPro.com

AVOID Study

P = STEMI patients*, symptoms <12 hours


I = 8L/min Oxygen via Face Mask
C = No Supplemental Oxygen (unless SaO2<94%)
O = Cardiac enzymes over first 72 hours (CK, Trop
I) to evaluate infarct size

* Excluded if SaO2<94%, altered mental status

www.PresentationPro.com

Why Too Much Oxygen is Bad?

Cornet AD et al. Critical care. 2013;17(2):313


www.PresentationPro.com

Mechanisms of Injury of Hyperoxia


Hyperoxia leads to generation of reactive oxygen
species
This decreases the bioavailability of nitric oxide and
results in vasoconstriction.

Hyperoxia results in closure of K+ATP channels,


inducing vasoconstriction
Ischemia ! fall intracellular ATP !induce opening of K+
channels ! hyperpolarization of the vasc sm ms cells !
vasodilation
In hyperoxia ! the closure of K+ channels !
vasoconstriction.
www.PresentationPro.com

Mechanisms of Injury of Hyperoxia


Hyperoxia induce vasoconstriction by acting directly
on L-type Ca2+ channels
Hyperoxia increases releases of angiotensin II
AT II promotes endothelin-1 release ! vasoconstriction.

Hyperoxia increases 20-hydroxyeicosatetraeonic


acid (20-HETE)
20-HETE is an arachidonic acid metabolite and a potent
vasoconstrictor

www.PresentationPro.com

www.PresentationPro.com

What Are The Best


Practices

What Are The Best Practices Are Really The


Known Basic Stuffs

Morrison LJ et al. Circulation. 2013;127(14):1538-63.


www.PresentationPro.com

Best Practices
Prevention of cardiac arrest: early identification of
deteriorations of vital signs or symptoms
Minimize interruptions in chest compression
Optimizes quality of depth of chest compression
Avoid hyperventilation
Early defibrillation
Debriefing and learning
Education, training, practice
Morrison LJ et al. Circulation. 2013;127(14):1538-63.
www.PresentationPro.com

Emphasis on Prevention: Be vigilant.


Fuhrmann et al (2008) in an observational study of
surgical and medical wards shows that 1 out of 5
patients developed abnormal vital signs and this
group of patients had a 3-fold increase in 30 days
mortality. More than 50% of these abnormal vital
signs went unnoticed by the nursing staffs
Be vigilant IHCA is frequently preceded by
clinical deterioration as evidenced by symptoms
and vital signs abnormalities (Smith et al, 1998)
Smith et al. Resuscitation. 1998;37(3):133-7.
Fuhrmann et al. Resuscitation. 2008;77(3):325-30.
www.PresentationPro.com

Post-cardiac Arrest: What Should The MAP


Be?
Current recommendation: target mean arterial
pressure (MAP) >65 mm Hg and mixed venous
oxygen saturation (SvO2) >70%
Based on hemodynamic goals for sepsis
Maybe cerebral autoregulation differ between
sepsis and cardiac arrest??

www.PresentationPro.com

Post-cardiac Arrest: What Should The MAP


Be?

Ameloot K et al. Resuscitation. June 2015 e-pub ahead of print.


Available at: http://tinyurl.com/mue6yra
www.PresentationPro.com

Post-cardiac Arrest: What Should The MAP


Be?
What is the range of MAP and SvO2 values
associated with lower mortality and improved
cerebral perfusion (measured by near infrared
spectroscopy)?
Analyzed hemodynamic data measured
continuously during the first 24 hours of
resuscitation in 82 post-cardiac arrest patients in
Belgium.
Ameloot K et al. Resuscitation. June 2015 e-pub ahead of print.
Available at: http://tinyurl.com/mue6yra
www.PresentationPro.com

www.PresentationPro.com

Ameloot K et al. Resuscitation. June 2015 e-pub ahead of print.


Available at: http://tinyurl.com/mue6yra

Conclusions
As the authors have noted, it is hard to determine
from just this observational study whether these
parameters of MAP should guide interventions or
are merely prognostic.
But these data does support further studies of
maybe a relatively higher MAP should be targeted
after cardiac arrest.

www.PresentationPro.com

Therapeutic Hypothermia Colder Is Not


Better

Nielsen N et al. N Engl J Med. 2013;369(23):2197-206.


www.PresentationPro.com

Why Therapeutic Hypothermia?


1. reduce the cerebral metabolic rate for oxygen
(CMRO2) (6% for q1C reduction in brain
temperature >28C)
2. suppression of free radical production in
reperfusion injury
3. suppression of excitatory amino acids release,
and calcium shifts, which can in turn lead to
mitochondrial damage and apoptosis
Adverse effects: arrhythmias, infection, and
coagulopathy.
Nolan JP. et al. Circulation. 2003;108(1):118-21.
www.PresentationPro.com

Historical Perspective
2 studies in Feb 2002 NEJM show improved
survival and neurological outcomes with induction
of mild therapeutic hypothermia for survivors of
OHCA

www.PresentationPro.com

Historical Perspective
The Hypothermia after Cardiac Arrest Study Group
study OHCA with ROSC: cooling to 32-34C over
24 hours in ED (n=137) improved functional
recovery at discharge (55% vs 39%; NNT = 6) and
lower 6-mo mortality rate vs with normothermic
patients (41% vs 55%) (NNT=7)
In Bernard et al, 77 OHCA with ROSC randomized
to hypothermia (33C for 12 hours) or to
normothermia. Good neurologic outcome at
discharge in 49% of hypothermic patients vs 26% of
normothermic patients.
www.PresentationPro.com

What Temperature for Therapeutic


Hypothermia?
Intention-to-treat analysis
P = OHCA with ROSC >20 min, presumed cardiac
origin (N = 950 from 36 Australian and European
ICUs)
I = cooling to 36C over 28 hours then gradual
rewarming 0.5C/hour to 37C
C = cooling to 33C over 28 hours then gradual
rewarming 0.5C/hour to 37C
O = All-cause mortality (primary)
Excluded: unwitnessed aystole, intracranial causes
www.PresentationPro.com

Nielsen N et al. N Engl J Med. 2013;369(23):2197-206.

Nielsen N et al. N Engl J Med. 2013;369(23):2197-206.

Conclusion: Preventing Post-arrest


Hyperthermia?
No significant differences between the two
groups in overall mortality at the end of the trial or
in the composite of poor neurologic function or
death at 180 days.
..Nevertheless, it is important to acknowledge
that there may be a clinically relevant benefit of
controlling the body temperature at 36C, instead of
allowing fever to develop in patients who have been
resuscitated after cardiac arrest.
Nielsen N et al. N Engl J Med. 2013;369(23):2197-206.
www.PresentationPro.com

Summary
Not best practices:
Adrenaline Not shown to improve survival to
hospital discharge but give anyway. Higher chance
of ROSC than placebo.
High dose oxygen Bad! Higher risk of death!
Just aim for SaO2 92 94%
Oxygen is a drug. Not harmless!

www.PresentationPro.com

Summary

Best practices are what weve already known


High quality compression
Dont hyperventilate
Be vigilant. Look out for deterioration
What your mind do not consider, your eyes do not
see (availability bias)

www.PresentationPro.com

Summary
Post-CA MAP: We may need to be aiming higher
than 65 mmHg. Inconclusive yet.
Therapeutic hypothermia: aiming to bring down
slightly to 36C is just as good as 33C
The beneficial effect may be due to the prevention
of post-CA hyperthermia rather than the cool 33C
per se
Therapeutic hypothermia may be de-emphasized in
the new AHA Guideline?
www.PresentationPro.com

Thank You For Your Attention

You might also like