HYPOTHERMIA POST CARDIAC ARREST 2011

HYPOTHERMIA POST CARDIAC ARREST

2011

M. Nelson January 2011

OBJECTIVES

1. History

2. Pathophysiology

3. Changes & Side Effects During Hypothermia

4. Indications/Exclusions

5. Overview of the UOHI Protocol

HISTORY

The concept of induced hypothermia in medicine has ebbed and flowed through the years. Benson et al (1959) studied hypothermia post cardiac arrest in humans and showed decreased mortality. Lack of sufficient evidence kept hypothermia from general acceptance.Using mild hypothermia post cardiac arrest to preserve neurological function came to the forefront with the publishing of two landmark trials in the NEJM in 2002.

HISTORY

Both studies cooled out of hospital survivors of ventricular fibrillation and ventricular tachycardia arrests to 32°C-34°C for 12-24 hours. They showed decreased mortality and improved neurological function.

After these studies were published, ILCOR and AHA recommended the use of therapeutic hypothermia post cardiac arrest. The beneficial results of these studies have subsequently been supported by other studies.

HISTORY

Despite this evidence, the use of hypothermia is limited at best even though survival of out of hospital cardiac arrest is very poor. Less than ½ of the victims who develop ROSC and survive to hospital leave the hospital alive and, in most cases, the cause of death is anoxic brain injury.

CARDIAC ARREST – WHAT HAPPENS?

CARDIAC ARREST

ROSCDepletes ATP in

4 min. failure of Na/K and Ca

pumpscellular depolarization &

injury

ISCHEMIA

Lipolysis free fatty acidsfree oxygen radicalsApoptosis

Activates inflammatory

cascade – inflammatory

cytokines likely contribute to

cerebral edema

CEREBRAL BLOOD FLOW ALTERATION

1. first 5-30 minHyperemia2. then cerebral

hypoperfusion (about 50% of normal) for up to 12 hrs

Cerebral microvascular occlusions

from thrombi formed during arrestImpaired cerebral reflow


Brain injury occurs at 2 time points:

1. Ischemia which activates multiple inflammatory and proapoptotic pathways

&

2. Reperfusion which increases neuronal injury by alterations in blood flow autoregulation, production of reactive oxygen species and more excitotoxic injury


Reperfusion Injury

MANIFESTATIONS OF BRAIN INJURY

•Coma•Seizures•Myoclonus•Cognitive dysfunction•Persistent vegetative state•Secondary Parkinsonism•Cortical or spinal stroke•Brain death

HYPOTHERMIA – HOW DOES IT WORK?

The many processes that cause brain injury are temperature dependant – fever stimulates the destructive pathways and mild to moderate hypothermia can block or mitigate these processes.

PROTECTIVE EFFECTS OF MILD TO MODERATE HYPOTHERMIA.

HYPOTHERMIA – THE PROCEDURE

The process of hypothermia involves cooling a patient to a prescribed temperature (32-34°C), for a period of time (12-24 hours) and then allowing the patient to rewarm or decool gradually.

The goal temperature, how quickly to cool, how to cool, how long to stay at target temperature, how slow to rewarm, these remain moving targets as further research becomes available.


The 2005 American Heart Association guidelines regarding the use of hypothermia post cardiac arrest are summarized as follows:

•Unconscious patients with ROSC after out-of- hospital cardiac arrest should be cooled to 32-34°C from 12-24 hrs when the initial rhythm was VF (class lla)

•May be beneficial for patients with non VF arrest or in-hospital arrest (class llb)

•Hemodynamically stable patients post ROSC with spontaneous mild hypothermia should not be actively rewarmed


•Cardiac arrests from VF or VT have the most favorable results with hypothermia. Asystole and PEA are much less positive.

•Most of the literature suggests cooling to a temperature of 33°C and to remain at that temperature for 24 hours.

•Many animal studies have shown that starting cooling as soon as possible and attempting to reach target temperature quickly is the most effective procedure.


However, many centres have had positive results even when the initiation of cooling and attainment of target temperature have been delayed. This suggests that hypothermia should be inclusive rather than exclusive and that other factors, such as age, likely play a role.

THE OTTAWA EXPERIENCE

In 2008, the stats for Ottawa (pop.~ 900,000):

•400 VSA patients in field due to cardiac arrest•61% had “cease resuscitation” order•39% were transported to the ED•18% continued resuscitation efforts in ED•14% were admitted to hospital•8% survived to discharge

Justin Maloney

HYPOTHERMIA – CHANGES & SIDE EFFECTS

•Hypovolemia: from cold diuresis which can result in hypotension

•Cardiovascular changes: BP, CVP, mixed venous saturation; HR, CO

•ECG changes: Bradycardia, PR & QT intervals, wide QRS complex; arrhythmias when temp 30°C (a.fib at 30°C, VT/VF at 28°C)

•Electrolyte disorders: K, Mg, P, Ca (risk of hyperkalemia in warming)


•Hypocoagulation/risk of bleeding: thrombocytopenia

•Shivering: warming, O2 consumption, metabolic demands and intracranial pressure

•Risk of Infections: inflammatory response is suppressed by cooling

•Hyperglycemia: Hypothermia suppresses insulin release and causes insulin resistance

•Skin Problems: from vasoconstriction, immobilization and immune suppression


•Lab Changes: amylase, liver enzymes, lactate, ketonic acid, and glycerol; WBC & platelets; mild hematocrit; mild acidosis

•Prolonged Drug Clearance: Delays metabolism & clearance of sedatives, NMBAs, anticonvulsants, & analgesics

INDICATIONS •Cardiac Arrest Patients with less than 30 minutes down timeDown time is defined as time of cardiac arrest to initiation of ACLS

•Cardiac arrest patients who are not responding appropriately to verbal commands

•Hemodynamically stable•VT, VF; consider PEA & Asystole

EXCLUSIONS

•Unwitnessed cardiac arrest with no CPR 15 minutes

•More than 30 minutes from arrest to ACLS•Refractory shock despite treatment with IV fluids and vasopressors

•Persistent or repeated episodes of cardiac arrhythmias

•Refractory hypoxia (O2 sat less than 85% for more than 15 min despite adequate ventilation)

•Severe coagulopathy with evidence of bleeding

METHODS OF COOLING

Ice Packs Cooled IV fluids (4°C)

Trans Nasal Evaporative Cooling

Commercial Surface Cooling Intravascular Cooling Cooling

UOHI PROTOCOL

1. Patient Selection2. STEMI versus non STEMI3. Blood Work4. Baseline assessment including VS, Neuro,

Skin, RASS, TOF 5. Insert nasopharyngeal temperature probe,

oral gastric tube & foley catheter6. Central Venous Access & arterial line7. Ensure second temperature source: foley, PA

line, tympanic

UOHI PROTOCOL

8. Set target temperature to 33°C

9. IV Sufentanil & IV Propofol

10.Neuromuscular blockade with IV Cisatacurium to maintain TOF at 2:4 and to suppress shivering

Maintain target temperature at 33°C for 24 hours

1. Temperature, VS, NVS (pupils), TOF q1h – maintain MAP of ≥ 65

2. Bedside Shivering Assessment Scale

UOHI PROTOCOL

3. Monitor for frostbite q2h & prn

4. Counterwarming as needed

5. Routine blood work: ABGs, K, Mg, glucose

6. IV/SC Heparin, IV Insulin, Artificial tears eye ointment

After 24 hours at target temperature, begin rewarming or “decooling”

1. Use Arctic Sun to warm 0.25°C per hour

2. Discontinue NMBA at start of warming

UOHI PROTOCOL

3. Maintain temperature 37°C for 48 hours after rewarming has begun

4. Continue sedation & analgesia till temperature is 36°C and TOF is 4:4

5. When TOF is 4:4, wean analgesia

6. Wean sedation last

CHANGES & SIDE EFFECTS

SHIVERING•Happens on induction at T of 35.5 and generally stops when temperature is than 33.5

•Older people tend to shiver lessCounterwarming: can help to lower the shivering threshold by countering the feedback loop from the skin temperature to the hypothalmic thermoregulation centre;

focal or body


SHIVERINGTo Block Or Not To Block: We have routinely

used NMBA; problem has been that the TOF becomes unreliable so more difficult to titrate; Sedation and analgesia are needed even without NMBA

Pros- very effective, does not cause hypotensionCons- Brain continues to try to make body shiver, may

mask seizures, prolonged paralysis risk of polyneuropathy


SHIVERING

Bedside Shivering Assessment Scale

0: None – no shivering

1: Mild – localized to neck/thorax, may onlybe seen on ECG

2: Moderate – intermittent involvement of upper extremities +/- thorax

3: Severe – generalized shivering or sustainedupper extremity shivering

Maintain Normal Magnesium Level

CHANGES & SIDE EFFECTSCARDIOVASCULAR

HypotensionWe have not seen cold diuresis, hypotension has generally been due to cardiogenic shock prior to induction and vasodilation on rewarmingEnsure adequate fluid volume prior to rewarmingArrhythmiasBradycardia, bradycardia and more bradycardiaUsually we have not needed to treat; if have BP or MAP, or urine output, will treat with IV DopamineIf want PA line & hemodynamics need to use iced injectate.


ELECTROLYTE DISORDERS & HYPERGLYCEMIA•Potassium & phosphate shift intracellularly during cooling and extracellularly during warming

•Magnesium for shivering• IV Insulin continuous infusion is used frequently for glucose

HYPOCOAGULATION/BLEEDING•This has not been an issue for us even with the STEMI patients on Plavix and possibly IV Heparin


INFECTION•About 50% of our patients have developed pneumonia due to ?aspiration, VAP•Use rotation mode of the Total Care Bed, HOB at least 30 degrees, chlorhexidine mouthwash•We do not use prophylactic antibiotics

SKIN PROBLEMS•Pads are easy to get on & off to check•Positioning/rotation


PROLONGED DRUG CLEARANCE

May also have renal or hepatic dysfunction from prolonged cardiac arrest affecting metabolism & elimination for ? Amount of time•Use minimal doses for desired effect•Choice of drugs – which is best?

SEIZURES

Some form of continuous EEG monitoring is suggested especially if NMBA are used.

The other option is Bispectral Index

Monitoring.

QUESTIONS?

FAVORITE ARTICLESBernard, S. (2009). Hypothermia after cardiac arrest. Critical Care

Medecine 37(7Suppl.), S227-S233.Chamorro, C.,et al. (2010). Anesthesia and analgesia protocol during

therapeutic hypothermia after cardiac arrest: A systemic Review. Anesthesia and Analgesia 110(5), 1328-1335.

Geocadin, R.G., et al. (2008). Management of brain injury after resuscitation from cardiac arrest. Neurologic Clinics 26, 487-506.

Hirsch, K.G., et al. (2009). Management of brain injury after cardiac arrest. Continuum Lifelong Learning Neurology 15(3), 100-120.

ILCOR Consensus Statement (2008). Post-cardiac arrest syndrome. Circulation 118, 2452-2483.

Polderman, K.H., et al. (2009). Therapeutic Hypothermia and controlled normothermia in the intensive care unit: Practical considerations, side effects, and cooling methods. Critical Care Medicine 37(3), 1101-1120

Polderman, K.H. (2009). Mechanism of action, physiological effects, and complications of hypothermia. Critical Care Medicine 37(7 Suppl.), S186-S202

Seder, D.B. (2009). Methods of cooling: Practical aspects of therapeutic temperature management. Critical Care Medicine 37(7 Suppl.), S211-S222

HYPOTHERMIA POST CARDIAC ARREST 2011

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