best practices in resuscitation

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.

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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


What Are Not Really Best Practices

Is Adrenaline Really 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

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


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.

Will AHA/ ILCOR/ ERC, etc Strip Away Adrenaline Too??


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


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

OR, 1.40; 95% CI, 1.021.93

Poor Neurological Outcome


OR, 1.62; 95% CI, 0.873.02

Hyperoxia Non-Hyperoxia

Avoid Too Much O2 In Ventilated Stroke Patients


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

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


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

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.


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%


AVOID Study


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

AVOID Study

P = STEMI patients*, symptoms

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


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.

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.

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.

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??


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

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.



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.


Therapeutic Hypothermia Colder Is Not Better


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

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.

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: 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.


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


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.



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!


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)


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?


Thank You For Your Attention

best practices in resuscitation

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