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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Oxygen Use

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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

Hyperoxia Non-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.


Adrenaline

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

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

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


Anti-arrhythmic Drugs

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).

Therapeutic Hypothermia

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 www.PresentationPro.com

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

Thank You For Your Attention

acls 2015 updates - the malaysian perspective

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