part 1 union hospital, inc. emergency department

Part 1Union Hospital, Inc.

Emergency Department

Newsweek July 2007

New York Times Dec 2008

Historical Perspective of HypothermiaHypothermia for

clinical purposes has ancient roots, used by Egyptians, Greeks, and Romans

Hippocrates advocated packing wounded patients in snow and ice to reduce hemorrhage

1950’s Hypothermia was utilized for intracranial aneurysm clipping and for cardiac surgery during circulatory arrest

1960’s Clinical trials with hypothermia (30 degrees Celsius or lower) were discontinued because of the side effects, uncertain benefits, and management problems

Historical Perspective of Hypothermia1980’s Animal studies

showed benefits of mild (32-35 degrees Celsius) hypothermia rather than moderate or deep hypothermia (less severe side effects)

1997 first human study by Dr. Bernard with mild hypothermia

Two landmark studies in 2002.

55% in the hypothermia group had favorable neurologic outcome within six months compared to 39% in normothermic group.

49% hypothermia vs 29% normothermia DC to home or rehab

Recommendations2010 ILCOR (2010

International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations)

2010 AHA guidelines for Post Resuscitation Induced Hypothermia

The StudiesThe Studies-1. Bernard SA, Gray TW Treatment of comatose survivors

of out-of-hospital cardiac arrest with induced hypothermia NEJM 2002;346:557-563, Australia

Results: 49% vs 26%, hypo vs normo, had a “good outcome”- as defined by discharge to home or rehab

2. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest NEJM 2002;346:549-556 Austria

Results: 55% vs 39%, hypo vs normo, had a CPC-cerebral performance category score of “good recovery” or “moderate disability”

Epidemiology of Cardiac ArrestApproximately 450,000 people

experience Sudden Cardiac Arrest (SCD) every year

95% of patients that have experienced SCD died before they reach the hospital

PathophysiologyBrain loses oxygen stores within 20 secondsDamage starts 4-6 minutes after the heart

stopsGlucose and adenosine triphosphate stores

deplete (brain energy)Membrane depolarizationCalcium influxesGlutamine is releasedAcidosis and edema develop

Ischemia may persist for several hours after resuscitation (re-perfusion injury)

CoolingCooling inhibits the process of cell

destruction (apoptosis) caused by traditional resuscitation during reperfusion.

When a patient is resuscitated, reperfusion sets off a series of chemical reactions that continue for up to 24 hrs, possibly causing significant inflammation in the brain.

Why make them Cool?↓ Free Radical production↓ ICP ↓ Cerebral metabolic rate ↓ Brains demand for 02 consumption Prevents mitochondrial damage and

apoptosis Better chance of recovery with neurological

function intact.

CardiovascularBradycardiaSlight increase in

blood Pressure (10mmHG)

Mild arrhythmias Increased PR intervalIncreased QT intervalWidened QRS

Increased Systemic Vascular Resistance

Increased Central Venous Pressure

Decreased Cardiac Output

Hematologic

ThrombocytopeniaImpaired platelet

functionLeukopeniaImpaired Leukocyte

functionIncreased PT/PTT

Gastrointestinal

Impaired Bowel Function

Decreased GI motility/ Ileus

Mild Pancreatitis (increased amylase)

Increased liver enzymes

Pharmacokinetics

Altered clearance of medicationsClearance is slowed

having a prolonged effect

Keep this in mind when re-warming.

GeneralBody attempts to

maintain homeostasisShiveringPeripheral

vasoconstrictionDecreased

circulation to skin

MetabolismIncreased fat

metabolism with increased production of glycerol, free fatty acids, ketonic acids, lactate

Metabolic acidosisDecreased oxygen

consumptionDecrease CO2

production

NeurologicDecreased metabolic rate 5-7 % for each 1

degree CDecreased Cerebral Blood Flow

(vasoconstriction)Decreased Magnesium- associated with

worse outcomes. MayCause Cerebral and Coronary

Vasoconstriction

Endocrine

Increased epinephrine, Nor epinephrine, and Cortisol levels

Hyperglycemia due to decreased insulin sensitivity and decreased insulin levels

Renal

DiuresisRenal Tubular

DysfunctionElectrolyte loss (K,

MG, Ca, Phos)

Mechanics of CoolingPassive Cooling

Ineffective have to wait on temperature to decrease to 33◦ Celsius

Active CoolingConvection

Air Cooling Blanket Therma cool Bair Hugger

Conduction Ice packs Cold Blankets

Infusion Cold NS infusion (2L

over 4 hours)

Exclusion CriteriaPregnancyAge less than 18 years of ageKnown terminal illness/ Do Not ResuscitateHead TraumaComatose state prior to cardiac arrestComa for reasons other than cardiac arrest, such as

drug overdose or seizureActive bleedingCore temp less than 86° F on admissionActive infection requiring antibiotics at time of

admission (systemic infection/sepsis)

Inclusion CriteriaCardiac arrest defined as absence of pulse requiring

chest compressions regardless of location or presenting rhythm with return of spontaneous circulation (ROSC).

Coma (does not follow verbal commands, no eye opening, no purposeful response to noxious stimuli) - Prior to sedation. Brainstem reflexes and pathologic posturing are permissible.

Time down less than 60 minutes.Systolic Blood Pressure (SBP) > 90 mmHg and Mean

Arterial Pressure (MAP) > 60 with or without the use of vasoactive medications.

Intubated and ventilated via bag valve mask or mechanical ventilator.

Initial temperature greater than 86° F.Confirmation of ICU Bed assignment.

MonitoringVital Signs Q 15 min X 1

hour, then hourly.

Core Temperature Q15 min until target reached then hourly.

Continuous ECG monitoring.

BIS Monitoring

Glasgow Coma Scale hourly.

FSBS hourly.

I & O hourly.

Assess skin Q2 hour.

Obtain patient weight.

Complications of HypothermiaPneumonia RiskVentilator DependencyDecreased WBC / BM

SuppressionDecreased Inflammatory

cytokinesElevated Glucose

Miscellaneous ComplicationsDoes NOT significantly increase metabolic

acidosisor Lactate levelsWill often cause mild HYPOTENSION, use

Pressorsto maintain MAP > 80 for cerebral perfusion

(90 – 100)Drug Metabolism slowed significantly(Propofol / Fentanyl / Verapamil / Propanolol)

ShiveringIncreases O2 Consumption between 40 – 100%Shivering responses occur primarily between 30 –

35 CSedation and anesthesia to halt shivering also

increasePeripheral Blood FlowIf you paralyze, you can’t screen for seizuresBuspirone (Buspar) 30mg PO q 8hrs / hold for SCr

> 1.7Fentanyl 75mcg IVUse Paralytics as second line

The Future is in Our Hands