Best Practices In Resuscitation
Content
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 Redding’s classic paper on
animal studies – showed benefits of adrenaline
– Am. Heart J. 1963 (66) 210–214
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, 1.02–1.93
Wang CH et al. Resuscitation. 2014;85(9):1142-8.
www.PresentationPro.com
Poor Neurological Outcome
Non-Hyperoxia
Hyperoxia
OR, 1.62; 95% CI, 0.87–3.02
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 1.1–1.7]; 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 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.
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 32-34ºC 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 (33°C 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 36°C over 28 hours then gradual
rewarming 0.5°C/hour to 37°C
• C = cooling to 33°C over 28 hours then gradual
rewarming 0.5°C/hour to 37°C
• 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 36°C, 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 we’ve already known
High quality compression
Don’t 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 36°C is just as good as 33°C
• The beneficial effect may be due to the prevention
of post-CA hyperthermia rather than the cool 33°C
per se
• Therapeutic hypothermia may be de-emphasized in
the new AHA Guideline?
www.PresentationPro.com
Thank You For Your Attention
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 Redding’s classic paper on
animal studies – showed benefits of adrenaline
– Am. Heart J. 1963 (66) 210–214
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, 1.02–1.93
Wang CH et al. Resuscitation. 2014;85(9):1142-8.
www.PresentationPro.com
Poor Neurological Outcome
Non-Hyperoxia
Hyperoxia
OR, 1.62; 95% CI, 0.87–3.02
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 1.1–1.7]; 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 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.
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 32-34ºC 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 (33°C 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 36°C over 28 hours then gradual
rewarming 0.5°C/hour to 37°C
• C = cooling to 33°C over 28 hours then gradual
rewarming 0.5°C/hour to 37°C
• 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 36°C, 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 we’ve already known
High quality compression
Don’t 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 36°C is just as good as 33°C
• The beneficial effect may be due to the prevention
of post-CA hyperthermia rather than the cool 33°C
per se
• Therapeutic hypothermia may be de-emphasized in
the new AHA Guideline?
www.PresentationPro.com
Thank You For Your Attention
