Presentation on theme: "HYPOTHERMIA POST CARDIAC ARREST 2011 M. Nelson January 2011."— Presentation transcript:
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 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 ROSC Depletes ATP in 4 min. failure of Na/K and Ca pumps cellular depolarization & injury ISCHEMIA Lipolysis free fatty acids free oxygen radicals Apoptosis Activates inflammatory cascade – inflammatory cytokines likely contribute to cerebral edema CEREBRAL BLOOD FLOW ALTERATION 1.first 5-30 min Hyperemia 2.then cerebral hypoperfusion (about 50% of normal) for up to 12 hrs Cerebral microvascular occlusions from thrombi formed during arrest Impaired cerebral reflow
CARDIAC ARREST – WHAT HAPPENS? 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
CARDIAC ARREST – WHAT HAPPENS? 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.
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 ° 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
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.
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.
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)
HYPOTHERMIA – CHANGES & SIDE EFFECTS Hypocoagulation/risk of bleeding: thrombocytopenia Shivering: warming, O 2 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
HYPOTHERMIA – CHANGES & SIDE EFFECTS 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 time Down 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 (O 2 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 Selection 2.STEMI versus non STEMI 3.Blood Work 4.Baseline assessment including VS, Neuro, Skin, RASS, TOF 5.Insert nasopharyngeal temperature probe, oral gastric tube & foley catheter 6.Central Venous Access & arterial line 7.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 less Counterwarming: can help to lower the shivering threshold by countering the feedback loop from the skin temperature to the hypothalmic thermoregulation centre; focal or body
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 NMBA Pros - very effective, does not cause hypotension Cons - Brain continues to try to make body shiver, may mask seizures, prolonged paralysis risk of polyneuropathy
CHANGES & SIDE EFFECTS SHIVERING Bedside Shivering Assessment Scale 0: None – no shivering 1: Mild – localized to neck/thorax, may only be seen on ECG 2: Moderate – intermittent involvement of upper extremities +/- thorax 3: Severe – generalized shivering or sustained upper extremity shivering Maintain Normal Magnesium Level
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 rewarming Ensure adequate fluid volume prior to rewarming Arrhythmias Bradycardia, bradycardia and more bradycardia Usually we have not needed to treat; if have BP or MAP, or urine output, will treat with IV Dopamine If want PA line & hemodynamics need to use iced injectate.
CHANGES & SIDE EFFECTS 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
CHANGES & SIDE EFFECTS 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
CHANGES & SIDE EFFECTS 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.
FAVORITE ARTICLES Bernard, 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), Geocadin, R.G., et al. (2008). Management of brain injury after resuscitation from cardiac arrest. Neurologic Clinics 26, Hirsch, K.G., et al. (2009). Management of brain injury after cardiac arrest. Continuum Lifelong Learning Neurology 15(3), ILCOR Consensus Statement (2008). Post-cardiac arrest syndrome. Circulation 118, 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), 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