Induced Hypothermia in Post-Cardiac Arrest Patients

Brandon Wilding, MD FACEPIdaho Emergency Physicians

Saint Alphonsus Regional Medical Center

Boise, Idaho

Historical Trivia,Name the Disease:

• “…skin black as ink, ulcers, difficult respiration, rictus of the limbs, teeth falling out and perhaps most revolting of all, a strange plethora of gum tissue sprouting out of the mouth, which immediately rotted and lent the victim’s breath an abominable odour.”

Name the Disease (Cont.):

• Affected early maritime explorers. • Vasco da Gama: 100 of 160 men died from

it while rounding the Cape of Good Hope en-route to India in 1499.

• Magellan lost 80% of his crew to it in 1520.• British Commodore George Anson had

1,300 out of 2,000 men die from it during the 1740’s.

Name the Disease(Cont.):

• Bleeding of the gums• Loose teeth• Halitosis• Hemmorhage into the

gums and skin

Name the Disease (Cont.):

• Poor wound healing• Anemia• Poor energy• If untreated, death

Answer:Scurvy

• Easily prevented and treated.

• Treatment was discovered in 1601 by Lancaster. Sailors on one ship drank 3 tsp lemon juice daily and had ZERO deaths. Other 3 ships had 110 of 278 (40%) die from scurvy by midway point.

• Where were the IRB and oversight committees?

• Why didn’t someone throw them some lemons?

Scurvy Timeline

• 1601 First conclusive experiment• 1747 Citrus again found to be curative by

Captain Cook’s physician James Lind• 48 years later British Navy ordered citrus in

all diets.• 70 years after that, in 1865, British Board of

Trade adopted the diet. 264 years after 1st conclusive experiment, 118 years after 2nd.

Fascinating, but is there any relevance?

• Unfortunately yes. Newton’s First Law applies to us. (An object in motion remains in motion until acted upon by some outside force) btw: I did that from memory…..

• Physicians/ health care teams (and paramedics) at rest tend to stay at rest until acted upon by a force.

Induced Hypothermia Post Cardiac Arrest with ROSC

• In 2002, the New England Journal published two well designed studies1,2 showing dramatically improved outcomes when patients are actively cooled after resuscitation from V. Fib or Pulseless V. Tach.

• This led to an advisory statement by the ILCOR that such patients should be cooled.

• 1. Bernard S. et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. NEJM 2002, Feb 21; 346(8): 557-563.

• 2. The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. NEJM 2002, Feb 21; 346(8): 549-556.

What does “improved outcomes” mean?

• More patients surviving to exist in persistent vegetative states is not an improved outcome.

• Both studies showed improved neurologic outcomes, not just improved mortality.

Historical Perspective

• Initial studies in 1930’s and 1940’s promising.

• Clinical trials in 50’s and 60’s discontinued because of side effects and uncertain benefits.

• Key: Profound hypothermia (< 30°C (86°F) ) was used in most of these studies.

• 1. Rosomoff HL, Safar P. Management of the comatose patient. Clin Anesth 1965; 1: 244-258.• 2. Rosomoff HL, et al. Brain reaction to experimental injury after hypothermia. Arch Neurol 1965; 13: 337-345.• 3. Lazorthes G, Campan L. Moderate hypothermia in the treatment of head injuries. Clin Neurosurg 1964; 12:293-299.• 4. Hamby WB. Intracranial surgery for aneurysm: effect of hypothermia upon survival. J. Neurosurg 1963: 20: 41-45.

Australian Study*

• Australian Study– 77 Patients (34 normothermia and 43 hypothermia)

– Pseudorandomization: odd vs even days

– Inclusion Criteria:• Initial rhythm V Fib

• ROSC but comatose

– Exclusion Criteria:• Men <18 yrs

• Women <50 yrs

• SBP <90 despite Epinephrine drip

• Non cardiac causes of coma (ie. CVA, head trauma, OD)

* Bernard S. et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. NEJM 2002, Feb 21; 346(8): 557-563.

Australian Study

Methods:• Cooling initiated by EMS

using ice packs• Intubated, sedated,

paralyzed in ER.• Lytics if indicated.• All got ASA, Lido drip,

Versed and vecuronium.• Most got PA catheter.• Goal 33° C (91.4°F) for 12

hours• Passive rewarming for 6

hours, then active.

• Results:– 49% treatment vs 26%

control had good outcome.

– Discharge to home or rehab center vs death or long term nursing home.

– Odds Ratio: 5.25 (P= 0.01)

– Mortality: treatment group 51% vs 68%, but not significant (P=0.145).

European Study*

• 273 Patients (136 hypothermia vs 137 control)

• Randomized to hypothermia (32 to 34° C = 89.6-93.2°F) for 24 hours vs normothermia.

• Inclusion criteria:– Witnessed arrest, ROSC, comatose

– Initial rhythm V Fib or pulseless VT

– 18-75 yrs old

– 5 to 15 min from collapse to first attempted resuscitation, and < 60 min from collapse to return of pulse.

* The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. NEJM 2002, Feb 21; 346(8): 549-556.

European Study*

• Exclusion criteria:– Temp <30° C (86°F) on admission

– Pregnancy

– Terminal illness before arrest

– Hypoxia < 85% lasting > 15 minutes after ROSC

– MAP < 60 mmHg for > 30 min after ROSC

– Cardiac arrest after arrival of EMS

– Known pre-existing coagulopathy

* The Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. NEJM 2002, Feb 21; 346(8): 549-556.

European Study

Methods:• Intubated, sedated,

paralyzed and cooled in ER then maintained.

• Used cooling blankets and ice packs (105 min to initiation on average)

• Goal 32° to 34° for 24 hours from initiation.

• Passive re-warming for 8 hours

• Results:– Good neuro outcome

within 6 months: • Live independently and

hold part-time job.

– Good neuro outcome risk ratio 1.40

• NNTT = 6

– Mortality risk ratio 0.74

• NNTT = 7

Mild Therapeutic Hypothermia to Improve Neurologic Outcome after Cardiac Arrest

Mild Therapeutic Hypothermia to Improve Neurologic Outcome after Cardiac Arrest

Clearly the survival is not a short term phenomenon

Holzer, et al1.

• Meta-analysis including these two trials and another for patients resuscitated from PEA or asystole and cooled for 4 hours2.

• Neurologic recovery was improved and independent of method of cooling.

• Number needed to treat 4 – 13.

• 1. Holzer M, et al. Hypothermia for neuroprotection after cardiac arrest: Systemic review and individual patient data meta-analysis. Crit Care Med, 2005; 33(2): 414-418.

• 2. Hachimi-Idrissi w, et al. Mild hypothermia induced by a helmet device: a clinical feasibility study. Resuscitation, 2001; 51(3): 275-281.

ILCOR Advisory Statement

“Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32° to 34°C for 12 to 24 hours when the initial rhythm was ventricular fibrillation.”“Such cooling may also be beneficial for other rhythms or in-hospital cardiac arrest.”

• International Liaison Committee on Resuscitation. Therapeutic hypothermia after cardiac arrest – An advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Circulation 2003; 108: 118-121.

Why does it work?Theoretical Basis:

• Global ischemia: <5% baseline perfusion for 5-30 minutes.

• If re-perfused within 30 min, there is selective neuronal death.

• Polderman1 reported that, “virtually all animal experiments report clear and unmistakable protective effects of hypothermia if applied quickly”.

• 1. Polderman KH. Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: Indications and evidence. Int Care Med 2004, Apr; 30(4): 556-575.

Theoretical Basis for Hypothermia

• Slow cerebral metabolism

• Reduce apoptosis (programmed cell death)

• Blunt excitatory neurotoxicity

• Modulate immune response

Why does it work?Theoretical Basis:

• Slowed cerebral metabolism.– Decreased 5 to 7% for each degree Centigrade

reduction in body temperature.

– Decrease core temperature 4°C = 20-28% reduction in cerebral metabolism.

– Protective effects appear to be much greater than explained by this mechanism alone1,2.

• 1. Milde LN. Clinical use of mild hypothermia for brain protection: a dream revisited. J. Neurosurg Anesth 1992; 4: 211-215.• 2. Small DL, et al. Biology of ischemic cerebral cell death. Prog Cardiovasc Dis, 1999; 42: 185-207.

Ischemic Neuron

P artia l

C o m p lete

R eco v ery N ecro s i s

M ito ch o n d ria l D ysfu n ctio n

R elease o f d es tru ctiv ein tracellu l ar en zym e s

A p o p to tic P ath w ay

N euron

Why does it work?Theoretical Basis:

• Apoptosis:– Cells have three options: become necrotic, recover or

enter apoptotic pathway (programmed cell death).

– Apoptosis involves mitochondrial dysfunction and release of destructive intracellular enzymes1,2,3.

– Hypothermia can prevent these two processes leading to apoptosis4,5,6.

• 1. Small DL, et al. Biology of ischemic cerebral cell death. Prog Cardiovasc Dis, 1999; 42: 185-207.• 2. Siesjo BK. Pathophysiology and treatment of focal cerebral ischemia: I. Pathophysiology. J. Neurosurg, 1992; 77: 169-184.• 3. Siesjo BK, et al. Calcium, excitotoxins, and neuronal death in brain. Ann NJ Acad Sci, 1989; 568: 234-251. • 4. Xu L, et al. Mild hypothermia reduces apoptosis of mouse neurons in vitro early in the cascade. J. Cereb Blood Flow Metab, 2002; 22: 21-28.• 5. Adachi M, et al. Combination effect of systemic hypothermia and caspase inhibitor administration against hypoxic-ischemic brain damage in neonatal

rats. Pediatr Res, 2001; 50: 590-595.• 6. Auer RN. Non-pharmacologic (physiologic) neuroprotection in the treatment of brain ischemia. Ann NY Acad Sci, 2001; 939: 271-282.

Why does it work?Theoretical Basis:

• Excitatory neurotoxicity1:– As neurons become ischemic, they cannot maintain

membrane potential, depolarize and release glutamate.

– Energy-requiring mechanisms of re-uptake are impaired.

– Surrounding neurons are stimulated longer than normal in an ischemic state, causing more damage.

– Hypothermia is believed to stabilize cell membranes and has been shown in animals to slow excitatory neurotoxicity2,3,4.

• 1. Siesjo BK, et al. Calcium, excitotoxins, and neuronal death in brain. Ann NJ Acad Sci, 1989; 568: 234-251.• 2. Busto R, et al. Small differences in intraischemic brain temperature critically dtermine the extent of ischemic neuronal injury. J. Cereb Blood Flow Metab, 1987; 7: 729-738.• 3. Globus M, et al. Glutamate release and free radical production following brain injury: effects of post-traumatic hypothermia. J Neurochem, 1995; 65: 1704-1711.• 4. Busto R, et al. Effect of mild hypothermia on ischemia-induced release of neurotransmitters and free fatty acids in rat brain. Stroke, 1989; 20: 904-910.

Why does it work?Theoretical Basis:

• Modulation of immune response and edema– Hypothermia suppresses release of inflammatory

cytokines (TNF-α and IL-1)1.– It also slows production of free radicals2.– Reduces disruptions of the blood-brain barrier3 ,

decreasing edema.• There is an animal study that challenges this4.

Showing no difference in serum inflammatory markers.

• 1. Kimura A, et al. Moderate hypothermia delays proinflammatory cytokine production of human peripheral blood mononuclear cells. Crit Care Med, 2002; 30: 1499-1502.• 2. Globus M, et al. Glutamate release and free radical production following brain injury: effects of post-traumatic hypothermia. J Neurochem, 1995; 65: 1704-1711.• 3. Huang ZG, et al. Biphasic opening of the blood-brain barrier following transient focal ischemia: effects of hypothermia. Can J Neurol Sci, 1999; 26: 298-304.• 4. Callaway CW, et al. Hypothermia after cardiac arrest does not alter serum inflammatory markers. Crit Care Med, 2008; 36(9):2698-9.

Are there benefits to delayed cooling?

• The sooner a patient is cooled, the better, but even when delayed for a few hours, mild hypothermia has been shown to have some benefit in animal models of global ischemia or cardiac arrest1,2.

• Safar P. Resuscitation of the ischemic brain. In: Albin MS, ed. Textbook of neuroanesthesia: with neurosurgical and neuroscience perspectives. New York: McGraw-Hill, 1997: 557-93.

• Hickey RW. Et al. Delayed, spontaneous hypothermia reduces neuronal damage after asphyxial cardiac arrest in rats. Crit Care Med 2000; 28: 3104-06.

Risks of Hypothermia

• Major risks: cardiac arrhythmias, infection and coagulopathy1,2.

– These risks are increased the longer hypothermia is maintained.

– They increase more with lower temperatures, especially below 30°C.

– Temperature overshoot is a common occurrence3.

• 1. Dripps RD, ed. The physiology of induced hypothermia: proceedings of a symposium, 28-29 October 1955. Washington D.C.: National Academy of Sciences, 1956.

• 2. Tisherman SA, et al. Therapeutic hypothermia in traumatology. Surg Clin North Am 1999: 79: 1269-89.• 3. Merchant RM, et al. Unintentional temperature overshoots are common during therapeutic hypothermia after cardiac arrest: P85. Circulation 2005;

111(20): e327.

Risks of Hypothermia

• Temperature overshoot was common in a small study of 12 patients.– 8 patients were < 32° for > 6 hrs.

– 4 were < 31° for > 4 hrs.

– 2 were < 30° for > 2 hrs.

– 3 patients survived to discharge, but none cooled below 31° survived.

• Merchant RM et al. Unintentional temperature overshoots are common during therapeutic hypothermia after cardiac arrest: P85. Circulation 2005; 111(20): e327.

Risks of Hypothermia

• Even mild hypothermia can induce: shivering (increased metabolism), hypothermia-induced polyuria, electrolyte disorders, hypovolemia and hypotension1,2.

• Seen predominantly in the initial phase of cooling.• Fortunately, these are easily managed, but must be

monitored.

• 1. Polderman KH, et al. Hypothermia. J Neurosurg 2001; 94: 853-858.• 2. Polderman KH, et al. Hypophosphatemia and hypomagnesemia induced by cooling in patients with severe head injury. J Neurosurg

2001; 94: 697-705.

Potential Side Effects & Frequency

High Probability Coagulopathy

Hypovolemia (increased diuresis)

Electrolyte disorders

Insulin resistance, secretion

Low Probability Manifest bleeding

Airway infections (with prolonged hypothermia)

Wound infections (vasoconstriction & transient immune supp.)

Myocardial ischemia

Rare Manifest pancreatitis

Intracerebral bleeding

Other Risks/ Unknowns

• Australian and European studies had strict exclusion criteria.

• Patients in cardiogenic shock were excluded.

• What are the effects on these patients?

• Should we apply it in such patients?

Induced Hypothermia is Underutilized

• A survey1 published in 2005 showed only 13% of respondents were using hypothermia.

• Substantial selection bias with 19% response rate, mostly from academic and tertiary referral centers.

• 1. Abella B. et al. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation 2005; 64: 181-186.

Induced Hypothermia is Underutilized

• 1. Abella B. et al. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation 2005; 64: 181-186.

New ACLS Guidelines

• Unconscious adult patients with ROSC after out-of-hospital 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)1.

• Circulation 2005; 112: IV-84 – IV-88.

Underutilization was predictable

• Cabana1 reported in JAMA that barriers to compliance with practice guidelines fall into certain categories:– Knowledge:

• Unaware of existence or unfamiliar with details.

– Attitudes: • Lack of motivation (inertia of previous practice), disagree with

guidelines or don’t feel they can do it.

– External barriers: • Patient refusal. • Lack of: time, resources, reimbursement, clear consensus or

systemic support.

• Cabana M. et al. Why don’t physicians follow clinical practice guidelines? JAMA 1999, Oct 20; 282 (15): 1458-1465.

Delay in Implementation was predictable

• Berwick1 published an article in JAMA characterizing the innovation and adoption of technology.

• Berwick D. Disseminating innovations in health care. JAMA 2003, Apr 16; 289 (15): 1969-1975.

Proposed ACLS Algorithm

• Shock

• CPR (Epi)

• Shock

• CPR (Amio)

• Shock

• Pulse?

• Ice, Ice baby…

Specifics

• V. Fib or Pulseless V. Tach.• Return of pulse, but comatose.• Intubate, sedate, paralyze, “foleyize”

(bladder temp) and ice.• Goal 32° to 34° for 12-24 hours.• Allow passive re-warming after that for six

hours, then if needed gentle active re-warming.

Details, details, details.

• Methods vary: cooling blanket using air or solutions, ice packs, helmet device1, central catheters2.

• Ice cold IV fluids have proven very effective and rapid at inducing hypothermia3,4,5. (This is where we live).

• 1. Hachimi-Idrissi W, et al. Mild hypothermia induced by a helmet device: a clinical feasibility study. Resuscitation, 2001; 51(3): 275-281.• 2. Mack WJ, et al. Ultrarapid, convection-enhanced intravascular hypothermia: a feasibility study in non-human primate stroke. Stroke 2003; 34(8): 1994-1999.• 3. Polderman K, et al. Induction of hypothermia in patients with various types of neurologic injury with use of large volumes of ice-cold intravenous fluid. Crit

Care Med, 2005, 33(12): 2744-51.• 4. Bernard S, et al. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of hospital cardiac arrest: a preliminary report.

Resuscitation 2003, 56: 9-13.• 5. Rajek A, et al. Core cooling by central venous infusion of ice-cold (4° C and 20° C) fluid. Anesthesiology 2000, 93(3): 629-37.

Cooling helmet

• Re-usable helmet device, kept in freezer and changed every hour.

• Frigicap

Cooling Blanket Device

• Cooling blanket device covering back, abdomen and thighs.

• (Arctic Sun)

Cooling catheter

• This is one of the commercially available cooling catheters.

Chilled IVF Protocols

• Polderman Study1: 1500 mL of IVF at 4-6° C infused over 30 minutes, followed by 500 cc boluses as needed to obtain temp of 33.5° C. Maintained with external methods. (134 patients).

• Target temp achieved in 60 min.• Adverse events:

– 8 cases of mild pulmonary edema required increased PEEP to maintain PO2.

• Do not have long term outcome data (survival etc.)

• 1. Polderman K, et al. Induction of hypothermia in patients with various types of neurologic injury with use of large volumes of ice-cold intravenous fluid. Crit Care Med, 2005, 33(12): 2744-51.

Chilled IVF Protocols

• Bernard study1: 30mL/ kg ice-cold IVF infused over 30 min in 22 patients that survived out of hospital cardiac arrest.

• Results: 8/ 14 with V Fib survived to discharge, 2/ 8 with PEA or asystole survived to discharge. All deaths occurred after re-warming.

• Historical controls cooled 0.3 to 0.9° C per hour. This study decreased temp by 1.6° C in 30 min.

• Deaths attributed to severe neurologic injury and unrelated to IVF protocol.

• 1. Bernard S, et al. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-of hospital cardiac arrest: a preliminary report. Resuscitation 2003, 56: 9-13.

Immediate Prehospital Hypothermia feasible and safe

• French study1 using large volume ice cold infusion. Found it to be feasible and safe.

• 41% treatment vs. 18% of control had admission temp less than 35°C.

• Not associated with pulmonary edema.• Study showed no significant long term morbitity or

mortality. (In fact slightly worse good outcome)

• Hammer L, et al. Immediate prehospital hypothermia protocol in comatose survivors of out-of hospital cardiac arrest. Am J Emerg Med 2009, Jun; 27(5): 570-3.

Pre Hospital Induced Hypothermia Rarely Used1

• Questionnaire from attendees at National Association of EMS Physicians at the national conference Jan 2007.

• 145 (59%) attendees completed survey (34 US states, 3 Canadian provinces, 1 European country)

• 9/ 145 (6.2%) have protocols using ice packs or cold IV fluids.

• Only 1 in 8 had cooled more than 10% of eligible patients

• 1. Suffoletto BP, et al. Use of prehospital-induced hypothermia after out-of-hospital cardiac arrest: A survey of the National Associatioin of Emergency Medical Services physicians. Prehosp Emerg Care 2008, Jan-Mar; 12(1): 52-6.

Barriers to Pre Hospital Induced Hypothermia1

• Overburden with other tasks• Short transport times• Lack of refrigeration equipment• Receiving hospitals failure to continue therapy• Lack of guidelines specifically addressing prehospital

cooling• 62% correctly identified 32-34° C as correct target

temp.

• 1. Suffoletto BP, et al. Use of prehospital-induced hypothermia after out-of-hospital cardiac arrest: A survey of the National Associatioin of Emergency Medical Services physicians. Prehosp Emerg Care 2008, Jan-Mar; 12(1): 52-6.

Prehospital Initiation of Hypothermia Feasible & Safe1

• 63 patients randomized to cooling• 49 patients received 500-2000 mL of 4° C normal

saline before hospital arrival.• Mean temp decrease of 1.24° C vs. mean temp

increase of 0.10° C in control.• No association found with adverse consequences

in BP, pulse, Pox, pulmonary edema or re-arrest.

• 1. Kim F, et al. Pilot randomized clinical trial of prehospital induction of mild hypothermia in out-of-hospital cardiac arrest patients with a rapid infusion of 4° C normal saline. Circulation 2007, 115(24): 3064-70.

Prehospital Initiation of Hypothermia Feasible & Safe1

• Non significant trend toward awakening and discharge alive from hospital in VF patients.

• These results less reliable because treatment groups not maintained once in hospital.

• Initial rhythm of PEA or asystole had a lower proportion discharged alive vs. control (6% vs. 20%). Small sample needs further validation.

• 1. Kim F, et al. Pilot randomized clinical trial of prehospital induction of mild hypothermia in out-of-hospital cardiac arrest patients with a rapid infusion of 4° C normal saline. Circulation 2007, 115(24): 3064-70.

Proposed Hypothermia Protocol

Duration of Pulselessness Predicts Outcome

• Oddo, et al found that a key predictor of outcome was length of pulselessness1.– 65.7% of patients with ROSC ≤ 25 min

survived.– 3.1% of those with ROSC > 25 min survived.

• This emphasizes the importance of teamwork. The success of the ICU depends upon EMS and the ER.

• 1. Oddo M, et al. Early predictors of outcome in comatose survivors of ventricular fibrillation and non-ventricular fibrillation cardiac arrest treated with hypothermia: A prospective study. Crit Care Med 2008; 36: 2296-2301.

What about STEMI arrests?

• One study shows that it is feasible and safe to apply mild hypothermia to STEMI arrest patients1.

• Time from STEMI to balloon was not increased (it was in fact decreased, but likely confounded).

• 1. Wolfrum S, et al. Mild therapeutic hypothermia in patients after out of hospital cardiac arrest due to acute ST-segment elevation myocardial infarction undergoing immediate percutaneous coronary intervention. Crit Care Med 2008; 36(6): 1780-86.

Case Report: Cocaine induced Cardiac Arrest1

• 28 year old woman• 30 minutes before EMS activation had encounter

with police for suspected crack cocaine distribution.

• Patient chewed on then swallowed what she claimed were breath mints.

• Taxi driver called EMS, patient had vomited and became unresponsive.

• Fuller ET, et al. Therapeutic hypothermia in cocaine-induced cardiac arrest. Ann Emerg Med 2008; 51: 135-137

Case Report: Cocaine induced Cardiac Arrest

• Upon EMS arrival: V. Fib arrest• Defibrillated, CPR, intubated, then

epinephrine and atropine.• Return to pulse, but comatose.• Asystole en route to hospital, epi, atropine

and transcutaneous pacing.• In ER, pulseless with monitor of sinus

rhythm = PEA.

Case Report: Cocaine induced Cardiac Arrest

• Regained pulse with CPR, epi, atropine

• Initial labs– ABG: pH 6.53, pCO2 87, HCO3 7.2 (23-37)

and lactate 24.9 (0.50 to 2.20).

• Initial temp 35.8° C (96.4° F).

• Two more episodes PEA, recovered with CPR, epi, vasopressin, then norepi infusion.

Case Report: Cocaine induced Cardiac Arrest

• EKG showed wide QRS with large R’ in aVR (usually tricyclic, also massive cocaine OD)

• Gastric lavage produced large quantity of apparent crack cocaine

• Sodium bicarb infusion.

• Urine Tox screen + cocaine, - tricyclics

Case Report: Cocaine induced Cardiac Arrest

Case Report: Cocaine induced Cardiac Arrest

Case Report: Cocaine induced Cardiac Arrest

Case Report: Cocaine induced Cardiac Arrest

• Outcome– Extubated 48 hours– Mild deficit in short-term memory and

orientation– Discharged to police custody on day 6.

St Alphonsus Experience

Numbers treated• 23 patients treated

since Oct 2006• Most recent 1/10/2008

• 9 Deaths• 9 Home with good

prognosis• D/C to SNF, tertiary

care center or home with hospice 4

• 1 yet to receive disposition

Conclusion

• It works (improved mortality and neurologic outcomes).

• We are doing it.• It is relatively inexpensive.• It can safely be initiated in the prehospital

setting and decreases time till cool.• Protocol has been proposed. (We have one

now!)

Other Indications for Therapeutic Hypothermia

• Whole body hypothermia is used to reduce the risk of death or disability in infants with moderate or severe hypoxic-ischemic encephalopathy1,2,3,4.

• Some experts predict hypothermia will prove beneficial in stroke patients and it is being investigated currently5,6.

• It is used extensively intraoperatively.• It is being investigated for intestinal ischemia in animal

models (poor rats). It was found to decrease mortality and limit area of damage7.

• 1. Shankaran, S. et al. Whole body hypothermia for neonates with hypoxic-ischemic encephalopathy. NEJM 2005; 353: 1574-1584.• 2. Higgins, RD. Hypoxic ischemic encephalopathy and hypothermia: a critical look. Obstet Gynecol. 2005; 106(6): 1385-1387.• 3. Gunn AJ, et al. Therapeutic hypothermia: from lab to NICU. J Perinat Med 2005; 33(4): 340-346.• 4. Rutherford MA, et al. Mild hypothermia and the distribution of cerebral lesions in neonates with hyopoxic-ischemic encephalopathy.

Pediatrics 2005; 116(4): 1001-1006• 5. Schwab, S Therapy of severe ischemic stroke: breaking the conventional thinking. Cerebrovasc Dis 2005; 20(2): 169-178.• 6. De Keyser,J, et al. Neuroprotection in acute ischemic stroke. Acta Neurol Belg.2005; 105(3): 144-148.• 7. Stefamutti G. Crit Care Med 2008; 36(5): 1564-72.

ACP Induced Hypothermia Protocol

INCLUSION CRITERIA

• ROSC - Neuro exam 5 minutes after ROSC shows NO purposeful pain response

• Age >16 (Adult)• Temp > 34 C • Intubated (Intubate if indicated)• SBP > 90mmHg

ACP Induced Hypothermia Protocol

EXCLUSION CRITERIA

• DNR/POST, or other Advanced Driective

• Obvious Pregnancy

• Obvious Traumatic Arrest • Obvious Terminal Illness (Hospice patients?)

ACP Induced Hypothermia Protocol

Procedure

Assess & Document Pupillary response Neuro Assessment

Airway Control: 

 Intubate as needed Ventilate to ETCO2 of

35mmHg Do not hyperventilate!

ACP Induced Hypothermia Protocol

Sedation and Paralytics

• Midazolam (Versed) – may be used to prevent shiveringIV, IO, IM: 0.5-5 mg, Max of 10mg

• Vecuronium (Norcuron): Use only when patient shivering is witnessed (to prevent heat production)

IV/IO/IM: 0.1mg/kg (usually 10mg) repeat PRN

• Administer Vecuronium only after ET Tube is secured and placement confirmed with SPO2 and continuous ETCO2 monitoring

(Get that waveform up!)

ACP Induced Hypothermia Protocol

Induced Hypothermia

• Establish a second IV if possible.

• Expose the patient while protecting modesty.

• Cold Packs to Groin, Axilla, and Neck (if accessible).

• Saline/Water soaked Sheet applied to trunk

• Chilled CrystalloidIV: 30 cc/kg fluid bolus to max of 2 liters

oInitiate cold saline bolus through up to (2) IV or I/O access points. oInfuse cold saline at 30ML/kg to max 2 liters

0.9 Normal Saline at near

freezing

WEIGHT (kg) Volume Max (mL)

30 900

35 1050

40 1200

45 1350

50 1500

55 1650

60 1800

> or = 65 2000

oTarget Mean Arterial Pressure (MAP: 90-100oCheck MAP on the LP-12 but monitor manually as well.

Systolic Diastolic Map

110 80 90

120 75-90 90-100

130 70-85 90-100

140 65-80 90-100

ACP Induced Hypothermia Protocol

Target Systolic Blood Pressure : 90 mmHg systolic

• Vasopressors: titrate to a blood pressure of 90 systolic if chilled saline does not maintain BP

• Cold saline is a strong vasoconstrictor. Watch blood pressures closely!

Dopamine infusion - IV: 2-20 mcg/kg/min.

Epinephrine infusion - IV: 2-10 mcg/min

• Ensure early notification to receiving facility for expeditious coordination of care.

ACP Induced Hypothermia Protocol

PHYSICIAN PEARLS:

• If vecuronium is administered, ensure versed is provided for patient sedation.

• To clarify: SBP > 90 mmHg systolic needed before initiation of cooling. Patients may require vasopressors to meet this inclusion criteria.

?????Where does it all go?????

The Thomas EMS “Chillcore Case”

The Thomas EMS “Chillcore Case”

• The “Covered” thingies….. Should not EVER be occluded!!!

• Occlusion will result in a rig burning to the ground. You will need to find a new job if that occurs…. I am almost 100% certain of this.

The Thomas EMS “Chillcore Case”

• The middle port between the 2 fans is where the power cord goes.

• 12V – plug and twist (similar to CPAP circuits). DO NOT JUST PULL THE PLUG!!!!!!!!!!!!!!

The Thomas EMS “Chillcore Case”

• NOTE: When the ChillCore Case is turned on, it will begin cooling (or warming) to the factory set default temperature of 35 degrees F. The default temperature can be adjusted by the end user.

• To adjust temperature, simultaneously hold down the pre-set button and push desired temperature button either higher or lower.

BATTERY LEVEL & MAINTENANCE

• The ChillCore Case displays the percent of battery level remaining either by looking at the LCD display or by simply pressing on the “Battery” Button on the control panel display. When the case is charging, and below a full charge, the battery symbol will flash.

• If battery display bars are not present, this is due to the battery falling below 9.4 Volts. Leave the case plugged into the power and you should start to see bars on the display within approximately 30 minutes.

• Prior to initial use, run the case and charge the batteries for a minimum of 8-10 hours before placing in service.

• If storing the ChillCore case for an extended period, you must plug in and run for 24 hours at least once per month.

• ChillCore contains Lithium Polymer batteries.

The Thomas EMS “Chillcore Case”

• The fluid has to be in contact with the cold plates as shown in the 2nd photo.

The Thomas EMS “Chillcore Case”

• Insulated pressure infuser with 1L NS already in place.

• For storage, the insulated infuser should cover all fluids and “tuck” under the sides of the internal compartment.

Conclusion #2

Eat yer oranges or be a scurvy dog.

Questions?