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Intensive CareIntensive CareManagement from the ExpertsManagement from the Experts
Dr. David Seder Maine Medical CenterDr. David Seder Maine Medical CenterDr William Parham ANW Intensivist ProgramDr William Parham ANW Intensivist Program
Dr Lisa Kirkland ANW Intensivist ProgramDr Lisa Kirkland ANW Intensivist Program
Dr. Michael Mooney Program Director and ModeratorDr. Michael Mooney Program Director and Moderator
ObjectivesObjectivesReview the anticipated impact of therapeutic hypothermia onReview the anticipated impact of therapeutic hypothermia on cardiac output measurements
Describe the intravenous fluid infusion process for lowering body temperature
Discuss use of short-acting sedation and paralytics for therapeutic hypothermia
Summarize the induction, maintenance and rewarming phases of h i h h itherapeutic hypothermia
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Neurological Resuscitation after Cardiac Arrest
David Seder MDMaine Medical Center
Managing the patient during Induction, Maintenance, and Rewarming…
Maine Medical CenterDirector of Neurocritical Care
Disclosures
• No financial conflictsALL li ti• ALL applications described are off-label!
• Grant support from MMC NSI and MRC http://www.neurocriticalcare.org
http://www.hypothermianetwork.com/INTCAR.htm
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Crit Care Med 2009;37 (Suppl):S211-S222.
Epidemiology of OHCA• Cardiac arrest is common
– 295,000 OHCA per year in US295,000 OHCA per year in US• 23% VF• 31% Bystander CPR
– Median survival all rhythms 7.9%, VF 21%– Best EMS systems: ie: Seattle 1998-2001 (resuscitated)
• 17.5% survival to hospital discharge • 34% VT/VF subgroup
IHCA adults: 19% (despite 95% witnessed or monitored)– IHCA adults: 19% (despite 95% witnessed or monitored)• Mortality among patients surviving to be hospitalized
– Ontario 72% (1994-2002)– Taipei 75% (2003-4)– Goteborg 68% (2003-5)– Rochester 65% (1998-2001) Circulation 2010;Jan 26:e12-13
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Is the cup half empty?• Nationally, the survival
rate of OHCA is < 8%rate of OHCA is 8%• Half of patients who
survive to be hospitalized die in the hospital
• Half of those who are discharged from thedischarged from the hospital have neurological disability
• Why bother?
…or half full?• 40% of MMC OHCA
survivors have GNOsurvivors have GNO• 55-60% with VT/VF &
without shock have GNO
• A statewide program in Az of bystander CPR, CCR, and hypothermia l d t t i li fled to a tripling of OHCA survival!
• These patients have a chance
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Northern Hypothermia Network
Acta Anaesthesiol Scand. 2009 Aug;53(7):926-34
Acta Anaesthesiol Scand. 2009 Aug;53(7):926-34
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• 37 centers, 7 countries
NHN CA outcomes
• 986 patients received TH after CA 2004-2008
• 26% CPC 1-2 among asystole/PEA
Acta Anaesthesiol Scand. 2009 Aug;53(7):926-34
Factors associated with survival
Acta Anaesthesiol Scand. 2009 Aug;53(7):926-34
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From what do “survivors” die…?
Cause of Death in OHCA
Cause of death in IHCAOHCA
HIECardiac
HIE
Cardiac
3 d
68%
9%
23%51%
26%
23%
MOSF 3rdMOSF
Laver. Intensive Care Med 2004;30:2126
Mechanisms of brain injury in circulatory arrest
• Primary Injury:– “Energy failure” due to ATP depletion
• Secondary injury:– Loss of transcellular electrolyte gradients
• Ca+, Na+, Cl- enter, K+ exits cell• Water follows Na+ into cells causing cytotoxic edema6-72h– Lipid peroxidases damage membranes
– Neurotransmitter release causes excitotoxicity– Activation of apoptotic pathways– Microvascular thrombosis– Reperfusion injury
6-72h
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Other secondary injury…• Uncontrolled seizure activity• Hypotension hypoperfusion• Hypotension, hypoperfusion
– Postresuscitation syndrome– ICP crisis– Autoregulatory failure
• Fever• Re-arrest• Hypoxia• Derangements of glucose
metabolism
Neurology 2008;72:744
The hours after ROSC
• Mediators of cerebral blood flow after CA:Changes in blood viscosity– Changes in blood viscosity
– Sludging of erythrocytes– Development of platelet aggregates
• Heavy concentrations in post-ischemic tissue beds
– Imbalance of the coagulation system– Endothelial flapsp– Compression by swollen glial cells– Increased cerebral vascular tone and
resistanceResuscitation 2003;58:337
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Cardiac arrest associated brain injury “CAABI”
• “No flow” affects the most metabolicallymost metabolically active areas of brain– Cortex– Basal ganglia– Cerebellum
• “Low flow” affects the• Low flow affects the watershed areas between vascular territories
75 yo man OHCA 4-2010• Unwitnessed arrest• VF on EMS arrival• VF on EMS arrival• 35 minutes CPR
and resuscitation• Therapeutic
hypothermia• 108h after ROSC,108h after ROSC,
GCS 4• CMO at family
request
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Pseudolaminar necrosis
Shrunken eosinophilic neuron (anoxic neuron) is the hallmark of HIE
necrosis
http://www.neuropathologyweb.org/chapter2/chapter2aHIE.html
Rationale for temperature modulation after brain injury
• Hypothermia drives “Death Spiral”
fatally injured cells away from lysis and toward apoptosis
• Hypothermia drives marginally injured cells away from apoptosis and t dtoward recovery
• Intracellular calcium mediates injury and most apoptotic pathways
Crit Conn 2008;7(4):16
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Anesthesia and Analgesia 1959;38 (6): 423
Anesthesia and Analgesia 1959;38 (6): 423
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Clinical evidence for TH after CA
• Largest RCT of TH in OHCA survivorsOHCA survivors– 275 patients
randomized to TH or routine care
– Europe 1996-2001• Absolute 16% increase
in chance of a goodin chance of a good neurological outcome
• Absolute 14% decrease in 6 month mortality
N Engl J Med 2002;346:549-56
Clinical evidence for TH after CA
N Engl J Med 2002;346:549-56
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Clinical evidence for TH after CA
• Australian Randomized clinicalRandomized clinical trial conducted 1996-1999
• Randomized on alternating days to TH or routine careor routine care
• TH: good outcome 49%, routine care good outcome: 26% (p=0.046)
New Engl J Med 2002; 346:557-63
Nonrandomized data
Polderman. Lancet 2008, 371:1955-1969.
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Lausanne
• 55 VT/VF OHCA treated with TH 2002treated with TH 2002-2004
• Compared to historical controls 1999-02
• Similar DT, severity of , yillness
• CPC 1-2: 56% vs. 26% pre-TH
Effect of the implementation of a therapeutic hypothermia protocol on neurological outcome after out-of-hospital VF/VT arrest
-Crit Care Med 2006;34:1865
Japan• 400 patients with
variable i l t ti fimplementation of TH
• Developed model to isolate the interaction between use of TH and outcomes at different timeat different time points.
• No benefit of TH in DT < 15 minutes.
Crit Care. 2010 Aug 16;14(4):R155
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What are the risks of TH?• More infections
– LungLung• Trends toward
more bleeding*• Electrolyte shifts• Clinically
insignificantinsignificant bradycardia
• Changes in drug metabolism
HCASG. NEJM 2002;346:549-56
Skeptic’s arguments
• 3300 patients d i HACA
• Many non–TH ti tscreened in HACA
to enroll 275 over 6 years– Does not reflect “real
world” experience
patients were allowed to develop fever– Unfair comparitor?
• Single multicenter– Most commonly
managed patients not included
Single multicenter RCT should not set standard of care
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TTM Trial
• European trial of TH (33C) TN
• Multinational trialTH (33C) vs TN (36.5C) in CA survivors
• Niklas Neilsen PI• (INTCAR founder)
• Do we need to “prove” the efficacy of TH, again?
• What are the consequences of a• (INTCAR founder) consequences of a poorly designed or inconclusive trial result?
2005 AHA ACLS Guidelines• “Unconscious adult patients with ROSC after out-of-
hospital cardiac arrest should be cooled to 32°C tohospital cardiac arrest 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 VF (Class IIa).”
• “Similar therapy may be beneficial for patients with non-VF arrest out of hospital or for in-hospital arrest (Class IIb).”
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Only 10% patients with OHCA will meet RCT criteria for TH
•The decision to
Risks
initiate TH is usually based on clinical judgement of risk and benefit, not on proof!
• Infections• Bleeding• Need for
sedation
Benefits• Strongly neuroprotective
• Decreased mortality• Better neurological
outcomeN Engl J Med 2002;346:549-56
TH after Cardiac Arrest
• Clinical criteria for therapeutic hypothermiaNo more than 8 hours have elapsed since the– No more than 8 hours have elapsed since the return of spontaneous circulation.
– Encephalopathy is present, typically defined as the patient being unable to follow verbal commands.
– There is no life-threatening infection or bleeding.– Aggressive care is warranted and desired by the
patient or the patient’s surrogate decision-maker• Terminal underlying disease• Impending cardiopulmonary collapse
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The Devil’s in the details…
How to cool…
Baltimore, 1955 Portland, Maine, 2006
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Basics of Therapeutic Hypothermia
• There are 3 phases of treatment:– InductionInduction
• Rapidly bring the temperature to 32-34C• Sedate with propofol or midazolam during TH• Paralyze to suppress heat production
– Maintenance• maintain the goal temperature at 33C• Standard 12-24 hours (optimal duration is unknown)• Suppress shiveringpp g
– De-cooling (rewarming)• Most dangerous period: hypotension, cerebral edema, seizures• Goal is to reach normal body temperature over 12-24h• Stop all sedation when normal body temperature is achieved
Induction: how to cool• Monitor core temperature
– Bladder esophagus or central venous/pulmonary– Bladder, esophagus, or central venous/pulmonary arterial
• Cold fluid– 30cc/kg LR or 0.9%NS over 30 minutes
• 2-2.5C temperature reduction– No adverse cardiovascular results
Rare to cause pulmonary edema– Rare to cause pulmonary edema• Ice packs and cooling mats
– Effective, but difficult to control rate of temperature change
– Overcooling is dangerous
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Induction: how to cool
• Commercial cooling devicesSer o mechanism aries temperat re of– Servo mechanism varies temperature of circulating water or air (prevents overcooling)
– External (surface cooling) systems• Hydrogel heat exchange pads• Cold water circulating through plastic “suit”• Cold water immersion – awaiting safety datag y
– Invasive (catheter based) systems• Heat exchange catheter in SVC or IVC• Plastic or metalic heat-exchange catheter
Cold IVF• Polderman 2005
– 110 patients, 2-3L over 50’Bernard 2003
- 22 patients 30cc/kg LR at 4°C 30 i 3 °C 33 8°C
p ,– 36.9°C to 34.6°C, MAP
increased by 15mmHg, no pulmonary edema
over 30 min: 35.5°C to 33.8°CImprovements in MAP, renal function, no pulmonary edema
Polderman. Crit Care Med 2005;33:2744Bernard. Resuscitation 2003;56:9
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Cold IVF
• 2-3L of Ringers or Saline at 4C decreases gbody temperature– No effect on LVEF by echo– Improved hemodynamic indices
Kim. Circulation 2005;112:715
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Induction – How I do it• Examine and place BIS
monitor• Monitor and replace
potassium ando to• Give 30-40cc/kg IVF at
4ºC over 30 minutes –LR or NS– Pressure bag, not IV
pump• Sedate and paralyze
potassium and magnesium
• Antibiotics, usually• Ventilate to a normal
pH, and PaO2>110M i t i MAP 80
p ythe patient
• Apply a commercial cooling device
• Maintain a MAP > 80• CVC, Arterial
catheter, CO/CI/SVV device
Comparison of cooling methods• Traditional cooling
– inexpensive & available– Effective
INDUCTION
– Very high incidence overcooling
• Noninvasive cooling devices– Safe – no insertion, lots of
clinical experience– Effective, unless patients very
heavy– Expensive
• Invasive cooling devicesMAINTENANCE
Invasive cooling devices– Most effective at tight
temperature control– Better for heavy patients– Insertional dangers:
thrombosis, infection, placement-related injury
– ExpensiveCrit Care 2007;11:R91
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Outcomes with Surface vs Endovascular Cooling
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Utility of the Medivance Arctic Sun for TH after Cardiac Arrest
• Effective at Induction80% within 4h– 80% within 4h
– 90% within 6h– 100% within 9h– 2 pts got adjuvant cooling:
• ice or fluids
• Effective at maintenanceEffective at maintenance– 96.7% of the maintenance
phase was spent in the target temperature range
Jarrah. Neurocrit Care 2009;11:S23
• Moderate hypoglycemia– 18% vs 2%
• No mortality diff (33%
• 90 patients with OHCA – VF arrest and TH randomized– 72-108mg/dl
108 144mg/dl difference (33% vs35%)
– 108-144mg/dl• Hypoglycemia defined
as <54mg/dl
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Measurement of Blood Glucose
• MMC prospectively enrolled 12 CA survivors and12 CA survivors and measured concurrent AG, VG, FBG
• Mean glucose values higher during TH
• >20% discrepancy FBG vsAG in 5% when T>36C andAG in 5% when T>36C, and 17% when T<34%
• FBG values uniformly higher than AG values
Maintenance: How I do it• Surface cooling for most patients with bladder
or esophageal temperatureor esophageal temperature• Intravascular cooling if they need a CVC,
have skin problems, or if I have extra time• cEEG• CO/CI and preload monitoring
MAP 80• MAP > 80• Bispectral index when paralyzed to make
sure they’re “out”
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Five patients who were not out
• 5/204 awoke during TH after CA
• All witnessed arrests– 0-1 minute low flow– 13-24 minutes No flow
• “BIS1” = BIS after first dose of NMBdose of NMB
• BIS1: 43,52,54,52,63• All were receiving
propofol and/or fentanyl
De-cooling• Vasodilation causes hypotension
– May require several liters IVF increased– May require several liters IVF, increased vasopressors
• More shivering• Inflammation increases at higher temperature
– “post-resuscitation” syndrome• Increased ICP• Watch for hyperkalemia
– Primarily in renal failure• SEIZURES
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Patients do not like to rewarm, even if you call it “decooling”.
Shivering
• Drives up systemic metabolic ratemetabolic rate– Increased CO2 production– Increased O2 consumption– Major cardiac stressor
• Drives up cerebral oxygen consumptionconsumption– Favors ischemia
• Uncomfortable
Stroke. 2008 Dec;39(12):3242-7.
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BIS monitor can be used to quantify shivering
• EMG dB fromp=0.001 EMG dB from BIS monitor correlated with the validated BSAS
• EMG power CC -0.38
pcorrelates with rate of cooling
May. Crit Care Med 2009;37 (12 Supp); A467
EMG BSAS
Shiverplots
12345
2030405060
BSA
S
G P
ower
(dB
) * **
*
-10
010
22:5
50:
131:
312:
494:
075:
256:
438:
019:
1910
:37
11:5
513
:13
14:3
116
:30
17:4
819
:06
20:2
421
:42
23:0
0
EMG
Time
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Shiverplots
60
70
80
• Each additional “shivering episode” associated with 35% increase in odds of GNO
0
10
20
30
40
50
70
80
odds of GNO
0
10
20
30
40
50
60
Management of shivering• Neuromuscular blockade
– Vecuronium bolus 0 1mg/kg prn BSAS>2– Vecuronium bolus 0.1mg/kg prn BSAS>2– Cisatricurium in renal failure
• Propofol• Alpha blockade
– Dexmedetomidine infusion or clonidine• Scheduled acetaminophen, buproprionp , p p• Meperidine or fentanyl• Focal counterwarming• Magnesium infusion (serum level 3-4mg/dl)
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Sedation and analgesia during therapeutic hypothermia
• Comfort• Antiepileptic effects• Antiepileptic effects• HCASG
– Midaz 0.125mg/kg/hr– Fentanyl 2mcg/kg/hr– Pancuronium 0.1 mg/kg
q2h
• 70kg man/32h• 70kg man/32h– 280mg midazolam– 4480mcg fentanyl– 224 mg pancuronium
– That’s a lot of drugs!New Engl J Med 2002;346:549Crit Care Med 2006;34:1865
Drug metabolism during hypothermia: what do we know?
• Propofol concentrations 30% higher at 34ºC than 37ºC (healthy volunteers)
• Fentanyl concentrations ↑ 5%/↓ºC• (healthy swine)
Pharmacotherapy 2009;28:102Anesth Analg 1995;80:1007Anesthesiology 1999;91:A444
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Sedation
• Deep, antiepilepticantiepileptic sedation, or
• Light sedation with cEEG, or
• BIS-guided sedationsedation
Seizures prior to therapeutic hypothermia
• 19-34% incidence overall• Myoclonic status epilepticus traditionally
associated with 100% mortality• NCSE present, less common due to
absence of NMBPatients rarely received propofol or BDZ• Patients rarely received propofol or BDZ
-Ann Neurol 1994; 35:239–243-Neurology 1988; 38:401–405-Intensive Care Med 2006; 32:836–842
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• 19 children cEEG x72h during TH after CA
• 9 (47%) seized• 6/9 NCSE• 7/9 generalized• 8/9 during late TH or
rewarming periodsrewarming periods• 6 (32%) had SE
What do the seizures mean?
• Are they markers for terrible and irreversibleterrible and irreversible brain injury?
• Are they causing active, ongoing injury?
• Should we treat?If h ?
MSE
• If so, how?
Neurology 2008;72:744
NCSE
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ICU care following CA
• Many techniques f f i TH
• Seizure detectionfor performing TH
• Electrolytes• Glucose
managementManagement of
• Antibiotics for aspiration or ALI
• Analgosedation• Medication dosing
• Management of shivering
• Perfusing BP
Hospital size and CA outcome
>109 000 patients>109,000 patients in the NIS
Intensive Care Med 2009;35(3):505-11
Mortality was lower at urban, teaching, and large hospitals
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CA volume vs outcomes• 4674 patients from 39
hospitalsp• Overall mortality was
56.8%– Not all patients comatose
• After adjusting for age and severity of illness, institutional mortality ranged from 46% to 68%ranged from 46% to 68%
• Annual case volume strongly associated with outcome
Resuscitation. 2009 Jan;80(1):30-4
Thank You!
Horstmann et al. Brain h i h f h fatrophy in the aftermath of
cardiac arrest. NEUROLOGY 2010;74:306-312
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1. Central Venous Pressures1. Central Venous Pressures
•• Managing MAP > 60 and CVP >8 Managing MAP > 60 and CVP >8
•• CO /Index frequency CO /Index frequency –– Value during hypothermia ?Value during hypothermia ?
•• Cardiac outputs on done upon arrival to ICU; what Cardiac outputs on done upon arrival to ICU; what Cardiac outputs on done upon arrival to ICU; what Cardiac outputs on done upon arrival to ICU; what should a protocol suggest to followshould a protocol suggest to follow
•• Cooling Cardiac output vs normal temp Cardiac Cooling Cardiac output vs normal temp Cardiac Output?Output?
2. Sedation vs Paralytics 2. Sedation vs Paralytics •• Shorter acting Sedation and use of Shorter acting Sedation and use of Shorter acting Sedation and use of Shorter acting Sedation and use of
Paralytics Paralytics
•• What about Versed, Precedex, Propofol ?What about Versed, Precedex, Propofol ?
•• Train of 4 monitoring, Train of 4 monitoring, D/C paralytic when temp back at 36. C vs 37.0 CD/C paralytic when temp back at 36. C vs 37.0 C
•• Consider bolus dosing vs continuous dripConsider bolus dosing vs continuous drip
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3. EEG Monitoring3. EEG Monitoring•• Continuous EEG monitoring Continuous EEG monitoring •• Continuous EEG monitoring Continuous EEG monitoring
•• (Neuro Prognostication)(Neuro Prognostication)••Practicality/BenefitsPracticality/Benefits
•• SeizuresSeizures
4. LINES4. LINES
•• IV Fluids and Line Placement IV Fluids and Line Placement
•• Order of events to utilize IV fluids to Order of events to utilize IV fluids to cool faster cool faster
•• Where is the best place to place lines Where is the best place to place lines ICU, Cath Lab or ED?ICU, Cath Lab or ED?
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5. Non Phamaceutical 5. Non Phamaceutical Interventions for shiveringInterventions for shivering
•• Shivering how do we control it?Shivering how do we control it?•• Shivering, how do we control it?Shivering, how do we control it?
•• What are some Non pharmaceutical What are some Non pharmaceutical interventions we can apply? interventions we can apply?
D h t d t i it h i t?D h t d t i it h i t?•• Do heated vent circuits have impact?Do heated vent circuits have impact?
6. Management of fever post 6. Management of fever post coolingcooling
•• How should we treat the “rebound How should we treat the “rebound •• How should we treat the rebound How should we treat the rebound fever” after cooling is stopped?fever” after cooling is stopped?
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7. Magnesium Levels 7. Magnesium Levels
•• Magnesium levels, importanceMagnesium levels, importance
•• Goal of magnesium level during THGoal of magnesium level during TH