ACLS 2015 Updates - The Malaysian Perspective

Advanced Cardiac Life
Support Updates 2015
(The Malaysian Perspective)
K.S. Chew, MD, MMED
School of Medical Sciences, Universiti Sains Malaysia

Conflict of Interest
•  No conflict of interest to declare.

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Effect of Hyperoxia On Post-CA: A Meta-
Analysis
Wang CH et al. Resuscitation. 2014;85(9):1142-8.

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)

In-Hospital Mortality
OR, 1.40; 95% CI, 1.02–1.93

Poor Neurological Outcome
OR, 1.62; 95% CI, 0.87–3.02
HyperoxiaNon-Hyperoxia

Why Too Much Oxygen is Bad?
Cornet AD et al. Critical care. 2013;17(2):313

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.

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

Oxygen Use During Cardiac Arrest
•  Observational study
•  145 OHCA
•  PaO2 level and CPR outcomes
•  Results:
–  PaO2 <61 mmHg: 18.8% survival to hosp adm
–  PaO2 61 – 300 mmHg: 50.6% survival to hosp adm
–  PaO2 > 300 mmHg: 83.3% survival to hosp adm
–  No statistical difference in overall neurologic survival
Spindelboeck W, Schindler O, Moser A et al. Increasing arterial oxygen partial pressure during
cardiopulmonary resuscitation is associated with improved rates of hospital admission.
Resuscitation. 2013;84(6):770-5.

Authors’ Conclusion
We describe a significantly increased rate
of hospital admission associated with
increasing PaO2. We found that the
previously described potentially harmful
effects of hyperoxia after return of
spontaneous circulation were not
reproduced for PaO2 measured during
CPR.

AHA 2015 Guidelines
•  When supplementary oxygen is available, it may be
reasonable to use the maximal feasible inspired
oxygen concentration during CPR.
•  Evidence for possible detrimental effects of
hyperoxia in the immediate post-cardiac arrest
period should not be extrapolated to CPR context

AHA 2015 Guidelines
Post-CPR:
•  When resources are available to titrate FiO2, it is
reasonable to decrease FiO2 when SaO2 is 100%
provided the SaO2 is maintained at 94% or greater.

Theoretical Background
Adrenaline:
•  Alpha-adrenergic effect: vasoconstriction
•  Increase coronary perfusion pressure
•  Increase cerebral perfusion pressure
•  Beta-adrenergic effect: ? controversial
•  Increase myocardial work
•  Reduced subendocardial perfusion

Is Adrenaline Really Beneficial In Cardiac
Arrest?
Lin S et al. Resuscitation. 2014;85(6):732-40.

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)

Standard
dose
adrenaline
vs
High dose
adrenaline

Standard
dose
adrenaline
vs
Adre/Vaso

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

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.

AHA 2015 Recommendations
•  Standard-dose epinephrine (1 mg every 3 to 5
minutes) may be reasonable for patients in cardiac
arrest (Class IIb, LOE B-R).
•  High-dose epinephrine is not recommended for
routine use in cardiac arrest (Class III: No Benefit,
LOE B-R).

How early should adrenaline be given?
•  IHCA
•  N = 25095, non-shockable rhythms.
•  Adjusted OR (survival to discharge):
–  OR = 1.0 for 1-3 min (reference group)
–  OR = 0.91 (95% CI 0.82 to 1.00; P=0.055) for 4-6 min
–  OR = 0.74 (95% CI 0.63 to 0.88; P<0.001) for 7-9 min
–  OR = 0.63 (95% CI 0.52 to 0.76; P<0.001) for >9 min
Donnino MW, Salciccioli JD, Howell MD, Cocchi MN, Giberson B, Berg K, et al. Time to
administration of epinephrine and outcome after in-hospital cardiac arrest with non
shockable rhythms: retrospective analysis of large in-hospital data registry. BMJ
2014;348:g3028.

OHCA setting
•  Shockable rhythm:
–  Cantrell et al (2013)
•  ROSC achiever: shorter scene arrival-to-first adrenaline than
non-ROSC (8.1 vs. 9.8 min, p < 0.01)
•  Non-shockable rhythm
–  Goto et al (2013), N = 209577
•  improved 1-month survival; adrenaline <9 min, EMS-initiated
CPR vs adrenaline >10 min
–  Nakahura et al (2012), N = 212228
•  improved survival to discharge; adrenaline<10 min, EMS-initiated
CPR vs no adrenaline
–  Koscik et al (2013), N = 686
•  improved ROSC in adrenaline <10 min, PEA

•  For initial non-shockable rhythm: It may be
reasonable to administer adrenaline as soon as
feasible after the onset of cardiac arrest (Class IIb,
LOE C-LD).
•  For initial shockable rhyhtm: There is insufficient
evidence to make a recommendation as to the
optimal timing of adrenaline, particularly in relation
to defibrillation

Amiodarone vs Placebo (ARREST study)
•  Compared to placebo, amiodarone has better
survival to adm (44% vs. 34%, P =0.03); adjusted
OR 1.6 (95% CI: 1.1 to 2.4). No difference in
survival to discharge and survival with good neuro
(not powered)
Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, et al. Amiodarone
for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med
1999;341(12):871-8.

Amiodarone vs Lidocaine (ALIVE)
•  Compared to lidocaine, amiodarone has better
survival to adm (22.8% vs. 12%, P =0.009); OR
2.17 (95% CI: 1.21 to 3.83). No difference in
survival to discharge and survival with good neuro
Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared
with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med 2002;346(12):
884-90.

Does anti-arrhythmics really improve
survival to discharge?
•  Wait for the results of ALPS trial in early 2016!

•  Amiodarone may be considered for VF/pVT that is
unresponsive to CPR, defibrillation, and a
vasopressor therapy (Class IIb, LOE B-R).
•  Lidocaine may be considered as an alternative to
amiodarone for VF/pVT that is unresponsive to
CPR, defibrillation, and vasopressor therapy (Class
IIb, LOE C-LD).

“…none (of the antiarrhythmics) have yet
been proven to increase long term
survival or survival with good neurologic
outcome. Thus establishing vascular
access to enable drug administration
should not compromise the quality of CPR
or timely defibrillation, which are known to
improve survival.”

AHA 2015 Recommendations on
Ultrasound Use
Ultrasound (cardiac or noncardiac )may be
considered during the management of
cardiac arrest, although its usefulness has
not been well established (Class IIb, LOE C-
EO). If a qualified sonographer is present and
use of ultrasound does not interfere with the
standard cardiac arrest treatment protocol,
then ultrasound may be considered as an
adjunct to standard patient evaluation (Class
IIb, LOE C-EO).

Why Therapeutic Hypothermia?
1.  reduce the cerebral metabolic rate for oxygen
(CMRO2) (6% for q1°C reduction in brain
temperature >28°C)
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.

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

Historical Perspective
•  The Hypothermia after Cardiac Arrest Study Group
study – OHCA with ROSC: 32-34ºC over 24 hours
(n=137) improved functional recovery at discharge
(55% vs 39%; NNT = 6), lower 6-mo mortality rate
vs with normothermic patients (41% vs 55%)
(NNT=7)
•  In Bernard et al, 77 OHCA with ROSC: hypothermia
(33°C for 12 hours) vs normothermia: Good neuro
at discharge in 49% of hypothermic patients vs 26%
normothermic

Therapeutic Hypothermia – Colder Is Not
Better
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 36°C, instead of
allowing fever to develop in patients who have been
resuscitated after cardiac arrest.”

New therapy in cardiac
arrest:
Combo of adrenaline-
vasopressin-steroids?

Post-resuscitation as sepsis-like?
•  During and after CPR, it has been found that there
are
–  activation of blood coagulation
–  platelet activation with formation of thromboxane A2 and
–  alteration of soluble E-selectin and P-selectin

•  Four phases post-resuscitation:
1. First 24 hrs - microcirculatory dysfunction from
multifocal hypoxia leading to rapid release of toxic
enzymes & free radicals into CSF and blood
2. 1 to 3 days - cardiac function & systemic function
improved, but increased intestinal permeability
predisposes to sepsis syndrome and MODS
3. Days later – serious infection, patient declines
rapidly
4. Death

Vasopressin-Steroids-Adrenaline

Vasopressin
•  Non-survivors of CPR have lower plasma
vasopressin level compared to those who survived
•  Vasopressin acts directly on V1 receptors on
vascular contractile elements
•  In cardiac arrest, vasopressin is released as
adjunct vasopressor to adrenaline

Steroids
•  Cardiac arrest – lower cortisol levels during and
after CPR
•  ROSC is associated with increased plasma
cytokine elevation, endotoxemia, coagulopathy,
adrenal insufficiency resulting in post-resus shock
•  Steroids may be beneficial to improve
hemodynamics and reduce intensity of post-resus
SIRS and MODS

Vasopressin-steroids-epinephrine (VSE)
Mentzelopoulus et al (2013)
•  P = In-hospital cardiac arrest
•  I = VSE
•  C = saline-placebo
•  O = ROSC for > 20 min
•  = Survival to discharge with good neuro

VSE vs control
•  VSE – higher ROSC > 20 min (83.9% vs 65.9%;
OR, 2.98; 95%CI, 1.39-6.40; P = 0.005)
•  VSE – higher survival to discharge with good neuro
(CPC score of 1 or 2) (13.9% vs 5.1%; OR, 3.28;
95%CI, 1.17-9.20; P = 0.02).
•  Post-resus shock: VSE – higher survival to
discharge with good neuro (21.1% vs 8.2%; OR
3.74; 95% CI 1.20 – 11.62; p = 0.02), improved
hemodynamics; less oran dysfunction
Post-resus shock: sustained post-resus shock >4 hours or required >50% increase of
vasopressor to maintain MAP>70 mmHg post-resus

ACLS 2015 Updates - The Malaysian Perspective

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