Presentation on theme: "HYPOTHERMIA POST CARDIAC ARREST 2011"— Presentation transcript:
1 HYPOTHERMIA POST CARDIAC ARREST 2011 M. Nelson January 2011
2 OBJECTIVES History Pathophysiology Changes & Side Effects During HypothermiaIndications/ExclusionsOverview of the UOHI Protocol
3 HISTORYThe 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.
4 HISTORYBoth studies cooled out of hospital survivors of ventricular fibrillation and ventricular tachycardia arrests to 32°C-34°C for 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.
6 HISTORYDespite 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.
7 CARDIAC ARREST – WHAT HAPPENS? ROSCDepletes ATP in 4 min. failure of Na/K and Ca pumpscellular depolarization & injuryCEREBRAL BLOOD FLOW ALTERATIONfirst 5-30 minHyperemiathen cerebral hypoperfusion (about 50% of normal) for up to 12 hrsISCHEMIAActivates inflammatory cascade – inflammatory cytokines likely contribute to cerebral edemaLipolysis free fatty acidsfree oxygen radicalsApoptosisCerebral microvascular occlusionsfrom thrombi formed during arrestImpaired cerebral reflowADDITIONAL NEURON DEATH
8 CARDIAC ARREST – WHAT HAPPENS? Brain injury occurs at 2 time points:Ischemia which activates multiple inflammatory and proapoptotic pathways&Reperfusion which increases neuronal injury by alterations in blood flow autoregulation, production of reactive oxygen species and more excitotoxic injury
9 CARDIAC ARREST – WHAT HAPPENS? Reperfusion Injury
10 MANIFESTATIONS OF BRAIN INJURY ComaSeizuresMyoclonusCognitive dysfunctionPersistent vegetative stateSecondary ParkinsonismCortical or spinal strokeBrain death
11 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.Other reasons for TH: severe traumatic brain injury, stroke, hepatic failure, spinal chord injury, and MI(in heart hypo may decrease area of injury, promote epicardial flow, myocardial O2 demand, and preserve intracellular high energy phosphate stores.
12 PROTECTIVE EFFECTS OF MILD TO MODERATE HYPOTHERMIA. Critical Care Medicine. Therapeutic Temperature Management: State of the Art in the Critically Ill. 37(7) Supplement:S186-S202, July 2009.DOI: /CCM.0b013e3181aa5241
13 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.
14 HYPOTHERMIA – THE PROCEDURE 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 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
15 HYPOTHERMIA – THE PROCEDURE 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.
16 HYPOTHERMIA – THE 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.
17 THE OTTAWA EXPERIENCE In 2008, the stats for Ottawa (pop.~ 900,000): 400 VSA patients in field due to cardiac arrest61% had “cease resuscitation” order39% were transported to the ED18% continued resuscitation efforts in ED14% were admitted to hospital8% survived to dischargeJustin Maloney
19 HYPOTHERMIA – CHANGES & SIDE EFFECTS Hypovolemia: from cold diuresis which can result in hypotensionCardiovascular changes: BP, CVP, mixed venous saturation; HR, COECG 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)HR is the factor most related to cardiac output (25-40% with TH). Generally, in metabolic rate is =or than the in CO.Myocardial contractility dependent on the HR – if HR allowed to with T, systolic function usually (may have mild diast. dysfcn. If artificially HR myocardial contractility decreases significantly.CVP usually. systemic arterial resistance, slight in BP from vasoconstriction (but not in cerebral arteries) – this would theoretically help those patients who develop SIRSARRHYTHMIAS: don’t allow to go below 30. myocardium at deep hypo is less responsive to antiarrhythmics
20 HYPOTHERMIA – CHANGES & SIDE EFFECTS Hypocoagulation/risk of bleeding: thrombocytopeniaShivering: warming, O2 consumption, metabolic demands and intracranial pressureRisk of Infections: inflammatory response is suppressed by coolingHyperglycemia: Hypothermia suppresses insulin release and causes insulin resistanceSkin Problems: from vasoconstriction, immobilization and immune suppression
21 HYPOTHERMIA – CHANGES & SIDE EFFECTS Lab Changes: amylase, liver enzymes, lactate, ketonic acid, and glycerol; WBC & platelets; mild hematocrit; mild acidosisProlonged Drug Clearance: Delays metabolism & clearance of sedatives, NMBAs, anticonvulsants, & analgesics
22 INDICATIONSCardiac Arrest Patients with less than 30 minutes down timeDown time is defined as time of cardiac arrest to initiation of ACLSCardiac arrest patients who are not responding appropriately to verbal commandsHemodynamically stableVT, VF; consider PEA & Asystole
23 EXCLUSIONS Unwitnessed cardiac arrest with no CPR 15 minutes More than 30 minutes from arrest to ACLSRefractory shock despite treatment with IV fluids and vasopressorsPersistent or repeated episodes of cardiac arrhythmiasRefractory hypoxia (O2 sat less than 85% for more than 15 min despite adequate ventilation)Severe coagulopathy with evidence of bleeding
24 METHODS OF COOLING Ice Packs Cooled IV fluids (4°C) Trans Nasal Evaporative CoolingCommercial Surface Cooling Intravascular Cooling CoolingMethods aimed at convection and conduction to T.Older pt tend to cool faster:less effective temp regulationYounger patients need more opiates and sedativesObese patients will take more time to cool
25 UOHI PROTOCOL Patient Selection STEMI versus non STEMI Blood Work Baseline assessment including VS, Neuro, Skin, RASS, TOFInsert nasopharyngeal temperature probe, oral gastric tube & foley catheterCentral Venous Access & arterial lineEnsure second temperature source: foley, PA line, tympanic
26 UOHI PROTOCOL Set target temperature to 33°C IV Sufentanil & IV PropofolNeuromuscular blockade with IV Cisatacurium to maintain TOF at 2:4 and to suppress shiveringMaintain target temperature at 33°C for 24 hoursTemperature, VS, NVS (pupils), TOF q1h – maintain MAP of ≥ 65Bedside Shivering Assessment Scale
27 UOHI PROTOCOL Monitor for frostbite q2h & prn Counterwarming as needed Routine blood work: ABGs, K, Mg, glucoseIV/SC Heparin, IV Insulin, Artificial tears eye ointmentAfter 24 hours at target temperature, begin rewarming or “decooling”Use Arctic Sun to warm 0.25°C per hourDiscontinue NMBA at start of warmingRapid rewarming post cardiac surgery has been shown to jugular venous O2 sat indicating brain hypoxia – less jug desats are seen with slower rewarming
28 UOHI PROTOCOLMaintain temperature 37°C for 48 hours after rewarming has begunContinue sedation & analgesia till temperature is 36°C and TOF is 4:4When TOF is 4:4, wean analgesiaWean sedation lastHyperthermia (T≥ 37.5°C) in the first 72 hours of ROSC is independently associated with a poor outcome regardless of the cause. Even with a mild T, more severe derangements of cerebrovascular reactivity has been seen
30 CHANGES & SIDE EFFECTS SHIVERING Happens on induction at T of 35.5 and generally stops when temperature is than 33.5Older 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 bodyShivering in the awake patient can O2 consumption by between %Shivering has been linked to morbid cardiac events & adverse outcome if occurs in post op phase.
31 CHANGES & SIDE EFFECTS SHIVERING To 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 NMBAPros- very effective, does not cause hypotensionCons- Brain continues to try to make body shiver, may mask seizures, prolonged paralysis risk of polyneuropathyMust make sure patients are sufficiently sedated when using NMBA.Loss of protective effect of hypo can be lost if patients are not adequately sedated (with or without NMBA)
32 CHANGES & SIDE EFFECTS SHIVERING Bedside Shivering Assessment Scale 0: None – no shivering1: Mild – localized to neck/thorax, may onlybe seen on ECG2: Moderate – intermittent involvement ofupper extremities +/- thorax3: Severe – generalized shivering or sustainedupper extremity shiveringMaintain Normal Magnesium Level
33 CHANGES & SIDE EFFECTS CARDIOVASCULAR Hypotension We 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.
34 CHANGES & SIDE EFFECTS ELECTROLYTE DISORDERS & HYPERGLYCEMIA Potassium & phosphate shift intracellularly during cooling and extracellularly during warmingMagnesium for shiveringIV Insulin continuous infusion is used frequently for glucoseHYPOCOAGULATION/BLEEDINGThis has not been an issue for us even with the STEMI patients on Plavix and possibly IV Heparin
35 CHANGES & SIDE EFFECTS INFECTION About 50% of our patients have developed pneumonia due to ?aspiration, VAPUse rotation mode of the Total Care Bed, HOB at least 30 degrees, chlorhexidine mouthwashWe do not use prophylactic antibioticsSKIN PROBLEMSPads are easy to get on & off to checkPositioning/rotation
36 CHANGES & SIDE EFFECTS PROLONGED DRUG CLEARANCE May also have renal or hepatic dysfunction from prolonged cardiac arrest affecting metabolism & elimination for ? Amount of timeUse minimal doses for desired effectChoice of drugs – which is best?
37 SEIZURESSome form of continuous EEG monitoring is suggested especially if NMBA are used.The other option is Bispectral IndexMonitoring.
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