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Post cardiac arrest ICU care
1. Patients resuscitated after prolonged cardiac arrest will
develop post cardiac arrest syndrome
2. Out-of-hospital cardiac arrest survivors should be considered
for urgent PCI unless the cause of cardiac arrest was clearly
non-cardiac or continued treatment is considered futile.
3. Interventions may impact on neurological outcome:
especially targeted temperature management.
4. Comatose survivors: prediction of the final outcome in the
first few days may be unreliable.
Post-cardiac arrest syndrome
• Post-cardiac arrest brain injury – coma and seizures.
• Post-cardiac-arrest myocardial dysfunction – can be
severe and usually recovers after 48-72 hours.
Post-cardiac arrest syndrome
• Post-cardiac arrest brain injury – coma and seizures.
• Post-cardiac-arrest myocardial dysfunction – can be
severe and usually recovers after 48-72 hours.
• Systemic ischaemia/reperfusion response –
reperfusion can cause apoptosis effecting all organ
systems.
Post-cardiac arrest syndrome
• Post-cardiac arrest brain injury – coma and seizures.
• Post-cardiac-arrest myocardial dysfunction – can be
severe and usually recovers after 48-72 hours.
• Systemic ischaemia/reperfusion response –
reperfusion can cause apoptosis effecting all organ
systems.
• Persisting precipitating pathology – coronary artery
disease is the commonest precipitating cause after
OHCA.
Early coronary reperfusion
PROCAT

Parisian Region Out of hospital Cardiac ArresT

Registry
Dumas F. Circ
Cardiovasc Interv
2010;3:200-7

714 OHCA admitted to ICU
714 OHCA admitted to ICU

No obvious extra-cardiac cause
No obvious extra-cardiac cause
(n = 435)
(n = 435)

STEMI
STEMI
N = 134 (31%)
N = 134 (31%)

Other ECG
Other ECG
N = 301 (69%)
N = 301 (69%)

≥ coronary lesion
≥ coronary lesion
N = 128 (96%)
N = 128 (96%)

≥ coronary lesion
≥ coronary lesion
N = 176 (58%)
N = 176 (58%)

Successful PCI
Successful PCI
N = 99 (74%)
N = 99 (74%)

Successful PCI
Successful PCI
N = 78 (26%)
N = 78 (26%)

Successful angioplasty independent predictor survival OR 2.06 (1.16 to 3.66)
ECG criteria for selection of AMI
in OHCA patients (n = 165)

Sensitivity (%)
(CI)

Specificity
(%) (CI)

ST-elevation (n = 70)

88 (77 – 95)

84 (75 – 90)

ST-elevation and/or depression (n = 96)

95 (86 – 99)

62 (52 – 72)

100 (94 – 100)

46 (36 – 56)

As above + LBBB or
nonspecific QRS complexes (n = 116)

Angiographic AMI in 60 (36%) patients

Resuscitation 2011;82:1148-53
PCI after cardiac arrest
ST elevation vs. no ST elevation

Radsel P. Am J Cardiol
2011;108:634-8

%

Dumas F. Circ Cardiovasc Interv
2010;3:200-7
Cronier P. Crit Care
2011;15:R122-9
Mooney MR. Circulation
2011;124:206-14

Kern KB. JJ Am Coll Cardiol Intv 2012;5:597-605
Kern KB. Am Coll Cardiol Intv 2012;5:597-605
Mechanisms of ischemia/reperfusion injury.

Levitsky S Circulation 2006;114:I-339-I-343

Copyright © American Heart Association
Enteral nutrition

Insulin

Cooling

Inotropes

Defibrillator

Ventilation
Pacing

IABP
Mode of death after admission to
ITU following cardiac arrest

126 (62%) deaths out
of 206 admissions

Laver S. Intensive Care Med 2004; 30:2126-8
Laver S. Intensive Care Med 2004; 30:2126-8
Improving neurological outcome
after cardiac arrest
•
•
•
•
•

Controlled re-oxygenation
Cerebral perfusion
Glucose control
Control of seizures
Targeted temperature
management
Airway and breathing with
controlled re-oxygenation
In-hospital mortality n (%) [95% CI]*

*P<0.001

hyperoxia vs. normoxia and
hyperoxia vs. hypoxia
Circulation 2011;123:2717-2722
Intensive care registry studies
• High FiO2 surrogate marker of illness severity
•
•
•
•

First 60 min post ROSC data is missed
Duration and timing of hyperoxia unknown
Impact of therapeutic hypothermia?
Need large prehospital RCT
Targeted oxygen therapy after return
of spontaneous circulation
• “…as soon as arterial blood
oxygen saturation can be
monitored reliably… titrate
the FiO2 to maintain the
arterial blood oxygen
saturation in the range of 94
-98%.”
Target Temperature Management
After Cardiac Arrest (TTM) Trial
• RCT out-of-hospital cardiac arrest – all rhythms
(n = 950)
• 33oC versus 36oC for 24 h
• Neurological evaluation 72 h after rewarm
• Primary outcome – mortality at 6 months
• Finished recruiting
• NCT01020916
Nielsen N. Am Heart J 2012;163:541-8
Target Temperature Management the TTM trial
Clinicaltrials.gov: NCT01020916
www.ttm-trial.org
info@ttm-trial.org
Results embargoed-17th Nov to be presented at the AHA

Target Temperature Management after out-of-hospital cardiac arrest-a
randomized, parallel-group, assessor-blinded clinical trial rationale and design.
Am Heart J. 2012;163(4):541-8
Therapeutic hypothermia
after cardiac arrest
An Advisory Statement by the ALS Task Force of the
International Liaison Committee on Resuscitation (ILCOR)

• Unconscious adult patients with spontaneous
circulation after out of hospital cardiac arrest
should be cooled to 32-34oC for 12-24 hours
when the initial rhythm was VF
• For any other rhythm, or cardiac arrest in
hospital, such cooling may also be beneficial
Knowledge gaps

What rhythms?
When to start cooling?
What technique?
How long?
A

B
Cerebral resuscitation
•

Sedation
– propofol, fentanyl
– Clearance of many drugs is reduced by a third at 34 oC

•

Cerebral perfusion
– Autoregulation is impaired after cardiac arrest
– Aim to maintain a normal mean arterial pressure for that
particular patient.

•

Seizures or myoclonus or both occur in about 24% of those who
remain comatose and cooled after cardiac arrest
– Conazepam, sodium valproate, levetiracetam

•

Blood glucose
– 4-10 mmolL-1
Prognostication
Prognostication
• Therapeutic hypothermia invalidates previous
“standards”
• May reflect a direct effect of hypothermia on
progress of neurological recovery and/or the
residual effects of sedatives and opioids (larger
doses: longer to clear)
SSEPs
36 patients with absent N20 – 2 good recoveries

Leithner C. Neurology 2010;74:965-9
When should neurological prognostication be
carried out?

• Since induced hypothermia changes the
conditions for the clinical neurological
examination, there is good reason to
postpone the final assessment of hypothermia
treated patients to at least 72 h after
normothermia, which corresponds to
approximately 4.5 days after the arrest.
Prognostication
•
•
•
•
•
•

Findings at the clinical neurological examination
Neurophysiological methods (EEG/SSEP)
Clinical and electrographic seizures
Diagnostic imaging (CT/MRI)
Biochemical markers
Recommended routine for prognostication
Early: During first 24 h or before onset of rewarming (24 h). Late: After the first 24 h or after rewarming has been
initiated.
1: Good support in the literature and goodreliability. 2: Good support in the literature, but moderate reliability. 3: Some
support in the literature and limited reliability.
Early: During first 24 h or before onset of rewarming (24 h). Late: After the first 24 h or after rewarming has been
initiated.
1: Good support in the literature and goodreliability. 2: Good support in the literature, but moderate reliability. 3: Some
support in the literature and limited reliability.
ICU care for cardiac arrest survivors

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ICU care for cardiac arrest survivors

  • 2.
  • 3.
  • 4.
  • 5.
  • 6.
  • 7. 1. Patients resuscitated after prolonged cardiac arrest will develop post cardiac arrest syndrome 2. Out-of-hospital cardiac arrest survivors should be considered for urgent PCI unless the cause of cardiac arrest was clearly non-cardiac or continued treatment is considered futile. 3. Interventions may impact on neurological outcome: especially targeted temperature management. 4. Comatose survivors: prediction of the final outcome in the first few days may be unreliable.
  • 8. Post-cardiac arrest syndrome • Post-cardiac arrest brain injury – coma and seizures. • Post-cardiac-arrest myocardial dysfunction – can be severe and usually recovers after 48-72 hours.
  • 9. Post-cardiac arrest syndrome • Post-cardiac arrest brain injury – coma and seizures. • Post-cardiac-arrest myocardial dysfunction – can be severe and usually recovers after 48-72 hours. • Systemic ischaemia/reperfusion response – reperfusion can cause apoptosis effecting all organ systems.
  • 10. Post-cardiac arrest syndrome • Post-cardiac arrest brain injury – coma and seizures. • Post-cardiac-arrest myocardial dysfunction – can be severe and usually recovers after 48-72 hours. • Systemic ischaemia/reperfusion response – reperfusion can cause apoptosis effecting all organ systems. • Persisting precipitating pathology – coronary artery disease is the commonest precipitating cause after OHCA.
  • 12. PROCAT Parisian Region Out of hospital Cardiac ArresT Registry Dumas F. Circ Cardiovasc Interv 2010;3:200-7 714 OHCA admitted to ICU 714 OHCA admitted to ICU No obvious extra-cardiac cause No obvious extra-cardiac cause (n = 435) (n = 435) STEMI STEMI N = 134 (31%) N = 134 (31%) Other ECG Other ECG N = 301 (69%) N = 301 (69%) ≥ coronary lesion ≥ coronary lesion N = 128 (96%) N = 128 (96%) ≥ coronary lesion ≥ coronary lesion N = 176 (58%) N = 176 (58%) Successful PCI Successful PCI N = 99 (74%) N = 99 (74%) Successful PCI Successful PCI N = 78 (26%) N = 78 (26%) Successful angioplasty independent predictor survival OR 2.06 (1.16 to 3.66)
  • 13. ECG criteria for selection of AMI in OHCA patients (n = 165) Sensitivity (%) (CI) Specificity (%) (CI) ST-elevation (n = 70) 88 (77 – 95) 84 (75 – 90) ST-elevation and/or depression (n = 96) 95 (86 – 99) 62 (52 – 72) 100 (94 – 100) 46 (36 – 56) As above + LBBB or nonspecific QRS complexes (n = 116) Angiographic AMI in 60 (36%) patients Resuscitation 2011;82:1148-53
  • 14. PCI after cardiac arrest ST elevation vs. no ST elevation Radsel P. Am J Cardiol 2011;108:634-8 % Dumas F. Circ Cardiovasc Interv 2010;3:200-7 Cronier P. Crit Care 2011;15:R122-9 Mooney MR. Circulation 2011;124:206-14 Kern KB. JJ Am Coll Cardiol Intv 2012;5:597-605 Kern KB. Am Coll Cardiol Intv 2012;5:597-605
  • 15.
  • 16. Mechanisms of ischemia/reperfusion injury. Levitsky S Circulation 2006;114:I-339-I-343 Copyright © American Heart Association
  • 18. Mode of death after admission to ITU following cardiac arrest 126 (62%) deaths out of 206 admissions Laver S. Intensive Care Med 2004; 30:2126-8 Laver S. Intensive Care Med 2004; 30:2126-8
  • 19. Improving neurological outcome after cardiac arrest • • • • • Controlled re-oxygenation Cerebral perfusion Glucose control Control of seizures Targeted temperature management
  • 20. Airway and breathing with controlled re-oxygenation
  • 21. In-hospital mortality n (%) [95% CI]* *P<0.001 hyperoxia vs. normoxia and hyperoxia vs. hypoxia
  • 23. Intensive care registry studies • High FiO2 surrogate marker of illness severity • • • • First 60 min post ROSC data is missed Duration and timing of hyperoxia unknown Impact of therapeutic hypothermia? Need large prehospital RCT
  • 24. Targeted oxygen therapy after return of spontaneous circulation • “…as soon as arterial blood oxygen saturation can be monitored reliably… titrate the FiO2 to maintain the arterial blood oxygen saturation in the range of 94 -98%.”
  • 25.
  • 26.
  • 27. Target Temperature Management After Cardiac Arrest (TTM) Trial • RCT out-of-hospital cardiac arrest – all rhythms (n = 950) • 33oC versus 36oC for 24 h • Neurological evaluation 72 h after rewarm • Primary outcome – mortality at 6 months • Finished recruiting • NCT01020916 Nielsen N. Am Heart J 2012;163:541-8
  • 28. Target Temperature Management the TTM trial Clinicaltrials.gov: NCT01020916 www.ttm-trial.org info@ttm-trial.org Results embargoed-17th Nov to be presented at the AHA Target Temperature Management after out-of-hospital cardiac arrest-a randomized, parallel-group, assessor-blinded clinical trial rationale and design. Am Heart J. 2012;163(4):541-8
  • 29. Therapeutic hypothermia after cardiac arrest An Advisory Statement by the ALS Task Force of the International Liaison Committee on Resuscitation (ILCOR) • Unconscious adult patients with spontaneous circulation after out of hospital cardiac arrest should be cooled to 32-34oC for 12-24 hours when the initial rhythm was VF • For any other rhythm, or cardiac arrest in hospital, such cooling may also be beneficial
  • 30. Knowledge gaps What rhythms? When to start cooling? What technique? How long? A B
  • 31. Cerebral resuscitation • Sedation – propofol, fentanyl – Clearance of many drugs is reduced by a third at 34 oC • Cerebral perfusion – Autoregulation is impaired after cardiac arrest – Aim to maintain a normal mean arterial pressure for that particular patient. • Seizures or myoclonus or both occur in about 24% of those who remain comatose and cooled after cardiac arrest – Conazepam, sodium valproate, levetiracetam • Blood glucose – 4-10 mmolL-1
  • 33. Prognostication • Therapeutic hypothermia invalidates previous “standards” • May reflect a direct effect of hypothermia on progress of neurological recovery and/or the residual effects of sedatives and opioids (larger doses: longer to clear)
  • 34.
  • 35. SSEPs
  • 36. 36 patients with absent N20 – 2 good recoveries Leithner C. Neurology 2010;74:965-9
  • 37.
  • 38. When should neurological prognostication be carried out? • Since induced hypothermia changes the conditions for the clinical neurological examination, there is good reason to postpone the final assessment of hypothermia treated patients to at least 72 h after normothermia, which corresponds to approximately 4.5 days after the arrest.
  • 39. Prognostication • • • • • • Findings at the clinical neurological examination Neurophysiological methods (EEG/SSEP) Clinical and electrographic seizures Diagnostic imaging (CT/MRI) Biochemical markers Recommended routine for prognostication
  • 40.
  • 41. Early: During first 24 h or before onset of rewarming (24 h). Late: After the first 24 h or after rewarming has been initiated. 1: Good support in the literature and goodreliability. 2: Good support in the literature, but moderate reliability. 3: Some support in the literature and limited reliability.
  • 42. Early: During first 24 h or before onset of rewarming (24 h). Late: After the first 24 h or after rewarming has been initiated. 1: Good support in the literature and goodreliability. 2: Good support in the literature, but moderate reliability. 3: Some support in the literature and limited reliability.

Editor's Notes

  1. Angiography was performed in all patients - 60 had confirmed AMI Conclusion: In patients with OHCA without obvious non-cardiac causes, selection for coronary angiogram based on the combined criterion would detect all AMI and avoid the performance of the procedure in 30% of the patients, in whom coronary angiogram did not have a therapeutic role.
  2. A summary of the available data comparing outcomes after acute coronary angiography post– cardiac arrest among patients with and without ST-segment elevation is seen in Figure 4. Survival was 49% in those with ST-segment elevation after emergent coronary angiography and PCI and 45% in those without ST-segment elevation (p 0.72). Likewise, there was no difference in intact neurological function among survivors between those with and those without ST-segment elevation (79% vs. 82%; p 0.66).
  3. Figure 3. Mechanisms of ischemia/reperfusion injury. Putative mechanisms of the calcium and free radical hypotheses and inflammation in the generation of ischemia/reperfusion injury.
  4. Out-of-hospital VF arrest associated with AMI. Primary PCI. Alsius cooling, IABP, pacing, ventilation, inotropes, defibrillator NICO is missing
  5. Adrie has reported 60% neurological deaths after OHCA in JACC 2005 paper
  6. If you don’t get it right – this what you end up with!
  7. This follow up analysis shows that the relationship between oxygen tension and mortality is linear.
  8. Based on the information that we had at the time – including just the first Kilgannon study – this was the consensus for the ERC guidelines
  9. Visit by Peter Safar to Negovsky’s lab in 1963
  10. June 2013 – completion of primary endpoint
  11. Guidelines – probably should be doing this now