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Brain Resuscitation
1.
2. A previously healthy 44-year-old woman collapses at work
after complaining of chest tightness
– 3 min: bystander CPR initiated
– 7 min: defibrillation provided by bystanders using an
automated external defibrillator (AED)
– 9 min: EMS arrives, intubation performed
• Pulse present
• Generalized seizure activity noted
• Lorazepam 2 mg administered
– In the ED
•
•
•
•
Does not open eyes or follow commands
Extensor motor response to pain
Pupils minimally reactive at 3 mm
Corneal and weak gag reflexes present
2
3. •
•
•
•
Triage of the cardiac arrest survivor
Best outcome after ROSC
Role of therapeutic hypothermia
Performing therapeutic hypothermia
– How to cool
– Managing the complications of therapy
• Outcome and prognosis
3
6. • AT BEST - standard
closed-chest CPR
generates 20% to 30%
normal cardiac output
• 20% normal CBF is
required to maintain
neuronal viability
6
7. CBF with a GOOD CPR is
inversely proportional to arrest time
– CPR in 2 min à CBF to 50% normal
– CPR after 5 min à CBF 28% normal
– CPR after 10 min à CBF = 0%
7
9. Seder. Cause of death in patients surviving out of
hospital cardiac arrest but dying during hospitalization.
Proceedings of the American Thoracic Society 2007;
4:A792.
Oddo. Effect of the implementation of a therapeutic
hypothermia protocol on neurological outcome after outof-hospital VF/VT arrest. Crit Care Med. 2006;34:1865.
13. With Low flow (10-15% of NBF)
• 15 sec à LOC
• 1 minà cessation of brainstem function (agonal
respirations, fixed pupils)
• 4-5 min à depletion of glucose and ATP
(anaerobic metabolism)
• 4-6 min à irreversible damage
• Tolerate ~15 min of ischemia for total brain
damage
NBF= Normal Blood Flow
14
16. • “No flow” affects the
most metabolically
active areas of brain
– Cortex
– Basal ganglia
– Cerebellum
• “Low flow” affects the
watershed areas
between vascular
territories
17
24. Cardiac assessment
– Rhythm stabilization
– BP stabilization
– Evaluation and
treatment of the
underlying cause of the
cardiac arrest
– Consideration of urgent
coronary angiography
and revascularization
Neurological assessment
– Severity of HIE
– CT head to rule out
intracranial bleed
– Institution of therapeutic
hypothermia
– EEG monitoring if
appropriate
– Maintenance of
adequate cerebral blood
flow
25
29. 1. Good Cerebral Performance : Conscious, alert, able to work and lead a
normal life. May have minor psychological or neurological deficits
2. Moderate Cerebral Disability : Conscious. sufficient cerebral function for
part-time work in sheltered environment or independent activities of daily life
(dressing, traveling by public transportation, and preparing food).
3. Severe Cerebral Disability : Conscious. Dependent on others for daily
support because of impaired brain function (in an institution or at home with
exceptional family effort).
4. Coma/Vegetative State : Not conscious. Unaware of surroundings, no
cognition. No verbal or psychological interactions with environment.
5. Death : Certified brain dead or dead by traditional criteria.
Booth. JAMA. 2004;291:870.
30
32. • Australian randomized clinical
trial conducted 1996-1999
• Randomized on alternating days
to TH or routine care
• TH: good outcome 49%, routine
care good outcome: 26%
(p=0.046)
33
34. • “Unconscious adult patients with ROSC after
OHCA should be cooled to 32°C to 34°C
(89.6°F to 93.2°F) for 12 to 24 hours when the
initial rhythm was VT/VF
• “Similar therapy may be beneficial for patients
with non-VF arrest out of hospital or for inhospital arrest
”
• In-hospital arrest
35
Circulation 2010;111:IV-84-IV-88
36. Clinical criteria for therapeutic hypothermia
– <8 hr since ROSC.
– Encephalopathy is present (unable to follow verbal
commands)
– no life-threatening infection or bleeding.
– Aggressive care is warranted and desired by the
patient or the patient’s surrogate decision-maker.
37
37. INDUCTION
• Rapidly bring the temperature to 32°-34°C
• Sedate with propofol or midazolam during TH
• Paralyze to suppress heat production
MAINTENANCE
• Maintain the goal temperature at 33°C
• Standard 24 hours
• Suppress shivering
DE-COOLING (REWARMING)
• Most dangerous period: hypotension, brain swelling,
• Goal is to reach normal body temperature over 12-24 hours
• Stop all sedation when normal body temperature is achieved
38
38. • Cold fluid
– 30 cc/kg LR or 0.9% NS over 30 minutes
• 2.0°-2.5°C temperature reduction
• EXPOSE THE PATEINT
• Monitor core temperature
– Bladder, esophagus, or central venous/pulmonary arterial
• Ice packs and cooling mats
– Effective, but difficult to control rate of temperature
change
Overcooling is dangerous
39
39. External (surface cooling)
systems
• Hydrogel heat exchange pads
• Cold water circulating
through plastic “suit”
• Cold water immersion –
awaiting safety data
Invasive (catheter-based)
systems
• Heat exchange catheter in
SVC or IVC
• Plastic or metallic heatexchange catheter
Holzer. New Engl J Med 2010;363:1256-64
40
40. INDUCTION
•
•
•
Traditional cooling
– Inexpensive and available
– Effective
– Very high incidence of
overcooling
Noninvasive cooling devices
– Safe – no insertion, lots of clinical
experience
– Effective, unless patients very
heavy
– Expensive
Invasive cooling devices
– Most effective at tight
temperature control
– Better for heavy patients
– Insertion dangers: thrombosis,
infection, placement-related
injury
– Expensive
Hoedemaekers. Crit Care. 2007;11:R91.
MAINTENANCE
41
41. • More bleeding
complications
• More infections
• But…a strong trend
toward lower mortality
Wolfrum. Crit Care Med. 2008;36:1780-1786.
42
42. • Maintain physiological homeostasis
– Adequate blood pressure and cerebral perfusion
– Head Position “ NO EVIDENCE YET ABOUT ELEVATION “
– Normal glucose level (100-140)
– Normal electrolytes
– Recognize and treat seizures
– Suppress shivering
– Adequate sedation TO IMMOBILIZ
– Adequate oxygenation
– Optimal volume status and cardiac output
43
43. At 24 hours after initiation of cooling, initiate rewarming
to a target temperature of 36.5° C at a rate of 0.15°/hr.
• Vasodilation causes hypotension
– May require several liters IVF replacement
• More shivering during this phase
• Increased ICP and decreased CPP
– Maintain adequate MAP!
• Watch for hyperkalemia
– Can be problematic in patients with renal failure
Discontinue paralytics at the onset of warming. Control
shivering with sedation, narcotics, and surface counter
Warming - Lighten sedation as tolerated as rewarming
44
progresses-.
44. • Discontinue endovascular temperature control
device after 48hours. (May use the device to
maintain normothermia after rewarming is
complete until it is removed.)
• Remove or minimize sedation to allow
neurologic evaluation before 72 hours to allow
the best possible clinical prognostication at
that time point. Neurology consultation
recommended.
45
45. •
•
•
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INFECTION ( High incidence of pneumonia)
COAGULOPATHY (Mild platelet dysf. and prolonged PT, aPTT)
HYPOKALEMIA (K+ may drop upto 1mg/dL during induction )
ARRHYTHMIA
– Almost all patients have asymptomatic bradycardia
– VT/VF: no significant increase with therapeutic hypothermia
• If VT/VF, verify no overcooling or hypokalemia
• DECREASED DRUG METABOLISM
– At least a 7-8% decrease per degree below 36°C
• Shivering
46
46. • Incidence of pneumonia 30%-50%
• Neutrophil oxidative killing, T-cell function
impaired at low temperature
• Fever and inflammation exacerbate brain
injury
• When pneumonia or aspiration is suspected,
consider:
– Cefuroxime 1500 mg x 2 doses, or
– Ampicillin/sulbactam x 3 days
Sirvent. Am J Respir Crit Care Med. 1997;155:1729.
Aquarolo. Intensive Care Med. 2005;31:510.
47
47. • systemic metabolic rate
– ↑CO2 production
– ↑ O2 consumption
• cerebral oxygen consumption
Prevent shivering with sedation
and nondepolarizing paralytic e.g.
Vecuronium bolus 0.1mg/kg prn
BSAS >2.
Bolus in ED. Bolus or drip in ICU
Badjatia. Metabolic impact of shivering during therapeutic temperature modulation: the Bedside Shivering Assessment Scale .
48
Stroke, 2008, In Press.
48. Up to 50% patients have abnormal
movements
– Myoclonus (Marker of severe brain
injury & poor prognosis)
– Seizures (↑cerebral oxygen
demand by 300% to 400%)
EEG of OHCA survivor with multiple generalized
epileptiform discharges discovered after
therapeutic hypothermia
• Convulsive seizures
• Nonconvulsive seizures ( 20%, need
continuous EEG
49
Hovland. Resuscitation. 2006;68:143. |
Claassen. Neurology. 2004;62:1743.
49. • BLOOD GLUCOSE CONTROL
- normoglycemia and mild insulin-induced hypoglycemia have been shown to improve
neurologic function after focal and global ischemia.
- insulin itself have a neuronal growth factor–like effect that may theoretically also be
neuroprotective
- BUT BECAUSE OF THE RISK OF HYPOGLYCEMIA POST ARREST 144-180 mg/dL
• BLOOD PRESSURE MANIPULATION
– Map ≥ 65 mmHg
– Normovolemic hemodilution of hematocrit to 20-25% - promotes
homogenous cerebral perfusion
– Anticoagulation with low-molecular weight heparins
– Low-dose thrombolytics to prevent microvascular fibrinolytic clotting
• SpO2 CONTROL
≥ 94%, Quantitative waveform capnography 35-45 mmHg.
50
50. • EEG
•
– Nonconvulsive seizure activity is common
– Continuous EEG preferred
– Sedation with propofol/midazolam will
suppress
Bispectral index (Verify no awareness
during hypothermia)
• Systemic oxygen utilization
(Maintain SvO2 > 60%)
• Brain oxygen extraction
(maintain SjvO2 > 55%)
• Intracranial pressure
(↑ ICP in 25% survivors, CPP< 50 in 56%)
• Intracranial metabolism
( brain glu OR cerebral lactate/pyruvate ratio )
Gueugniaud. Resuscitation. 1990;20:203.
Gueugniaud. Resuscitation 1991;17:392.
Lemiale. Resuscitation. 2008;76:17.
51
Intensive Care Med. 1991;17:392-398.
51. • Neuro exam (24 h, 72 h, 7 day )
• Serum markers
- Neuron-specific enolase
- S100B protein
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•
•
•
EEG
Somatosensory evoked potentials (SSEPs)
Myoclonic status epilepticus
MRI
“Current indicators of prognosis are derived from patients not treated
with hypothermia ”
Wijdicks. Neurology. 2006;67:203.
52
52. • Drugs that build up
during hypothermia may
confound prognosis!
• Verify that sedation,
analgesia, and paralytics
are no longer present!
Wijdicks. Neurology. 2006;67:208.
53
56. • 125 patients randomized
to prehospital vs ED
cooling
• Good outcome in VT pts
cooled in the field
– 20/29 vs 10/22 (P=0.15)
• No safety concerns
• Average temp at ED
arrival differed by only
1ÂşC
57
Circulation. 2007;115(24):3064-70.
58. • Cardiac Arrest
• Hepatic encephalopathy with cerebral
edema
• Near hanging
• Neonatal asphyxia
• Elevated ICP, all causes
• Severe (Hunt and Hess IV-V) SAH with
cerebral edema
59
59. •
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Hydrogen peroxide
Iron (from Fenton reaction)
Activated neutrophils
Clotting derangement
Mannitol increases cerebral blood flow
and is a good free-radical scavenger, but
optimal doses have not been determined
Etomidate is a carboxylated imidazole that
depresses cerebral metabolism without
cardio-toxicity, but no human studies exist
confirming its usefulness
Corticosteroids have been shown to
stabilize vascular membranes, prevent
astrocyte swelling, and improve
intracranial compliance, no CLINICAL
benefit has been shown
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•
•
•
•
•
Catalase
Superoxide dismutase
Deferoxamine
Antineutrophil antibody
Heparins, thrombolytics
Allopurinol
• HYPERTENSIVE FLUSH
– 1 to 5 minutes of MAP >130 mm
Hg
– Flushes toxins out of cerebral
circulation
60
61. • Therapeutic hypothermia urgently initiated
– Sedated with propofol, paralyzed with vecuronium
– Cooled to 33°C over 4 hr using cold mat and ice packs
– Rewarmed after 18 hr
• No further seizure activity
• Coronary angiography revealed spontaneous LAD dissection
– Conservative management with antiplatelet therapy
• Discharged with short-term memory deficits and emotional
lability
• Cognitively normal at 6 months after ROSC
62
62. • Neuronal injury is a dynamic process that
continues for hours or days after an
ischemic insult to the brain.
• Hypotension, hypoperfusion, and hypoxia
must be avoided during brain
resuscitation.
• Hyperthermia, hyperglycemia, and
seizures should be treated
• promptly during brain resuscitation.
• Comatose survivors of out-of-hospital
cardiac arrest should be rapidly cooled in
the ED and maintained at 33° C in an ICU
setting for 12 to 24 hours after
resuscitation.
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