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Prehospital Therapeutic Hypothermia Post Cardiac Arrest

Prehospital Therapeutic Hypothermia Post Cardiac Arrest. Amy Gutman MD ~ EMS Medical Director prehospitalmd@gmail.com / www.teaems.com. INTRODUCTION. Therapeutic Hypothermia (TH) is an evidence based intervention improving neurologic outcomes & decreasing mortality in cardiac arrest patients

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Prehospital Therapeutic Hypothermia Post Cardiac Arrest

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  1. Prehospital Therapeutic Hypothermia Post Cardiac Arrest Amy Gutman MD ~ EMS Medical Director prehospitalmd@gmail.com / www.teaems.com

  2. INTRODUCTION • Therapeutic Hypothermia (TH) is an evidence based intervention improving neurologic outcomes & decreasing mortality in cardiac arrest patients • Recommended by AHA (2010) & ALS Taskforce of International Liaison Committee (ILCOR) in 2003 as a prehospital intervention • Why cool patients? • Lower brain temperature in the 1st 24 hours after ROSC has positive effects on survival & neurologic recovery • Mild hypothermia reduces cerebral metabolic demand, decreasing damage from inflammatory responses occurring after restoration of cerebral perfusion • One large study showed that for every hour delay to onset of cooling, mortality increased by 20%!

  3. OBJECTIVES • Definition of Therapeutic Hypothermia (TH) • Pathophysiology of Hypothermia & Cerebral Reperfusion Injury • Indications, Contraindications, Adverse Reactions • Protocol Basics

  4. OOHCA EPIDEMIOLOGY • 295,000 OOHCA annually in the US • 88% at home / out-of-hospital • 23% VF • 31% Bystander CPR • Median survival all rhythms 8%, VF 21% • Prior to hypothermia the best EMS systems had a 18% survival to hospital discharge (34% VT/VF) • After hypothermia some systems (i.e. Portland ME) increased survival to 30% overall (55% PEA / asystole) with a 58% survival to discharge in VT/VF subgroup

  5. TH NOT JUST FOR OOHCA • Today we review Therapeutic Hypothermia in OOHCA, but TH has many other clinical applications: • Hepatic encephalopathy • Near hanging • Neonatal asphyxia • Elevated ICP, all causes • Severe SAH with cerebral edema

  6. AHA & ILCOR POSITION STATEMENTS • Unconscious VF OOHCA adults with ROSC should be cooled to 32-34°C for 12-24 hrs • Possiblebenefit for other rhythms or in-hospital cardiac arrest • Post-resuscitation treatment: • Induced hypothermia • Prevention of hyperthermia • Tight glucose control • Preventing hypocapnia • Maintaining elevated MAP

  7. AHA / ACC / ILCOR RECOMMENDATIONS FOR OOHCA CARE

  8. RECENT CHANGES IN CPR / CCR • Effective uninterrupted compressions • Decreased emphasis on ventilation, slower ventilatory rates • ETCO2 to for airway confirmation & to guide resucitation • IO for easy / rapid access • Emphasis on post-resuscitative “neurological salvage”

  9. WHY DO PATIENTS DIE AFTER OOHCA? • 10% Refractory dysrhythmias • 25% Low cardiac output states • 10% Infection / sepsis, coagulopathy • 35% Post Resuscitation Encephalopathy (PRE) • AKA “Cardiac Arrest Associated Brain Injury “CAABI” • Largest contributor to post resuscitation deaths & poor neurologic outcomes • Series of events beginning immediately following ROSC & brain reperfusion • Therapeutic hypothermia interventions aimed at reducing PRE effects improve patient outcomes, hence the concept of “neurological salvage”

  10. APOPTOSIS • Cells “pre-programmed” to die after damage / ischemic injury • The more cells die, the more ischemia occurs due to anaerobic metabolism • Anaerobic metabolism causes increased brain cell hyperexitability which worsens brain ischemia • Brain ischemia leads to cerebral edema, causing more cells death • Blood brain barrier disrupted during hypoperfusion / resuscitation causing fluid influx into brain, worsening edema & increasing ischemia • Therapeutic Hypothermia decreases apoptosis, therefore decreasing cerebral injury (“neuroprotective”)

  11. POST-RESUSCITATIVE ENCEPHALOPATHY (PRE) • PRE characterized by metabolic & hemodynamic derangements similar to severe sepsis • Initial hypoperfusion “insult” followed by ROSC hyperperfusion • Key characteristic is the loss of cerebral autoregulation causing cerebral inflammation / edema, cerebral vasoconstriction, vascular “sludging” / clotting, and a mismatch in supply & demand of metabolic resources • Cell injury from O2 free radical formation, inflammatory cascade & glutamate mediated cell death • PRE leads to Post Resuscitative Syndrome (PRS)

  12. POST-RESUSCITATION SYNDROME (PRS) • Apoptosis can last >48 hrsafter initial ischemic events • Controlled TH neuroprotectiveby inhibiting inflammatory cascade occurring secondary to apoptosis & cerebral reperfusion • Neutrophil & macrophage functions slow <35C • Decreases cerebral metabolic demands 7% for each temp degree • Maintains blood-brain-barrier patency decreasing cerebral edema from toxic lipomembranousprotein & fluid influxes PRS

  13. TH IS NOT A “NEW” CONCEPT! Anesthesia and Analgesia 1959;38 (6): 423

  14. HYPOTHERMIA DEFINITIONS • Mild • 89.6-95°F (32-35°C) • Moderate • 82.4-89.5°F (28-32°C) • Severe • <82.4°F(28°C) • Induced or “Therapeutic” • Active body cooling to below normal levels part of a multifaceted approach to optimizing neurologic resuscitation

  15. So why doesn’t EVERY OOHCA patient receive TH? • Survey of 2,248 EM MDs, intensivists & cardiologists (UK, US, Finland) • 74% US & 64% of non-US MDs never use hypothermia • Only 34% of US intensivists used hypothermia • Rationale? • Not enough data for non-VF arrests • Not “mandatory” in ACLS guidelines (“recommended”) • Technically difficult

  16. CLINICAL STUDIES • Bernard SA. “Treatment of comatose survivors of OOHCA with induced hypothermia.” NEJM 2002 • 77 patients • 43 hypothermia, 34 normothermia • 49% hypothermic pts with good outcomes vs 26% normothermic pts • “Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest.” Hypothermia After Cardiac Arrest Study Group. NEJM 2002 • Multi-center trial with 275 patients • 137 hypothermia, 138 normothermia • 55% hypothermic pts with good outcomes vs 39% normothermicpts • Bernard SA, et al. Induced hypothermia using large volume, ice-cold IVF in comatose survivors of OOHCA: a preliminary report. Resuscitation 2003 • 22 OOHCA, comatose adults • LR at 4°C at 30ml/kg over 30 min via peripheral IV to obtain & maintain temp at 33°C • Median temp decreased 1.6°C, median MAP increased 10 mmHg • No adverse outcomes

  17. Wake Forest EMS Study 2011

  18. EBM META-ANALYSIS OF TH BENEFITS Polderman. Lancet 2008, 371:1955-1969

  19. METANALYSIS Summary of Studies Neurologic 50% vs 14% Neurologic 23% vs 7% Survival 50% vs23% Survival 54% vs 33% Neurologic 49% vs 26% Neurologic 55% vs 39% Survival 48% vs 32% Survival 59% vs 45%

  20. “NNT?” NUMBER NEEDED TO TREAT • Average number of patients who need to be treated to prevent one additional bad outcome • The Bernard meta-analysis study showed the NNT for OOHCA patients was 6 • Aspirin therapy in myocardial infarction NNT = 25 • Beta blocker in myocardial infarction NNT = 42 • Cardiac catherization vs thrombolytics = 15 6

  21. WHAT ABOUT NON-VF OOHCA PATIENTS? • Non-VF OOHCA patients receiving TH • Though evidence growing that TH may have benefits in these patients, there is still no AHA / ILCOR recommendation for TH in non-VF OOHCA • It’s unclear if data from VF pts (a very different type of patient than an asystolic or PEA patient) can be extrapolated to non-VF OOHCA • Do potential benefits outweigh risks?

  22. TH METABOLIC CHANGES • Slows cerebral metabolism rate by 20-28% when patient cooled to 33C • 5-7% reduction for each degree lowered temp • Decreased O2 consumption & CO2 production • Stabilizes glucose levels • Decreases myocardial demans

  23. TH CARDIOVASCULAR CHANGES • Decreased CO & SV • Increased SVR & SBP • Response to vasoconstriction • Sinus bradycardia • Response to myocardial depression • Refractory to atropine • High risk of arrhythmias in moderate cooling (<32C) • Osborne waves • Positive deflection notch at junction between QRS complex & ST segment • Due to delayed K+ closing Osborn Waves

  24. PRIOR TO INITIATING TH • Indications, contraindications • Primary & secondary assessment • Baseline neuro exam essential to allow for comparison when patients are wakened • Pain/ Sedation management

  25. EXAMPLES OF CHECKSHEETS

  26. INDICATIONSOnly ~10% Patients with OOHCA Meet TH Criteria • >18 years old • ROSC post cardiac arrest • Unresponsive (GCS<8) • No purposeful movements • Brainstem reflexes / posturing movements may be present • Secured airway with adequate ventilation (ETI preferred) • SBP ≥90mmHg (MAP >80) spontaneously or with vasopressors • SpO2 >85% • Glucose >50mg/dl • Destination hospital must have ability to continue hypothermia

  27. CONTRAINDICATIONS / EXCLUSIONS • Cardiac instability / refractory arrhythmia • Cannot maintain SBP >90mm Hg (MAP >80) despite IVF & vasopressors • Active bleeding / history of coagulopathy or thrombocytopenia • Thrombolytic &/or fibrinolytics do not preclude use of hypothermia • Pregnancy • Trauma patients • Environmental hypothermia or initial temperature <32°C • Unclear why, but these patients actually have worse outcomes

  28. ADVERSE EFFECTS • Always a risk:benefit question in ALL interventions • One large meta-analysis study found no significant differences in complication rates in normothermic& hypothermic groups except for infections (i.e. sepsis, pneumonia) • Most common: • Respiratory alkalosis • Neutropenia, sepsis & increased pneumonia risk • Altered clotting cascade & platelet function (coagulopathy) • Arrhythmias rarely significant if core temp maintained >30°C • Electrolyte shifts • Potassium intracellular shift with induction, extracellular shifts with warming • Sodium, Calcium, Magnesium metabolism abnormalities • Fluid shifts with cooling (diuresis) & re-warming (hypovolemia) • Changes in drug metabolism, ½ lives & elimination

  29. 3 PHASES TO INDUCE HYPOTHERMIA • Induction (EMS / ED) • Rapidly bring temp to 32-34C • Sedate • Paralyze to suppress heat production • Maintenance (ED / CCU / ICU) • Goal temp 33C for 12-24 hours (optimal duration unknown) • Suppress shivering • Rewarming (CCU / ICU) • Most dangerous period: hypotension, cerebral edema, seizures common • Goal is to reach “normal” core temp over 12-24h • Sedation stopped when “normal” core temp achieved Portland, ME 2006

  30. One of the best Hypothermia protocols available is from Wake County EMS All of Wake’s protocols are high-quality, evidence-based & FREE to reference on-line TH PROCEDURE • Institute rapid cooling with core temp goal 33°C • Core temp monitoring with a core temp rectal or nasal probe • Acutely cool with either: • Cold (4°C) LR IVF (2 L over 30 mins) +/- ice packs BL to neck, axillae, groin • If ice-cold fluids unavailable, apply ice packs BL to neck, axillae & groin • If pt begins shivering, administer midazolam* 0.1mg/kg in 2 mg increments slow IVP with maximum single dose 5 mg • Document vitals, initial GCS, pupillary response, brief neurological exam • Transport to facility that can maintain hypothermia intervention • If post-arrest ECG indicates STEMI, call med control to discuss ED STEMI bypass • Do not allow core temperature to drop below 33°C *Consider reducing by 50% if >70 years

  31. SOME SYSTEMS USE WEIGHT-BASED DOSING

  32. ED / CRITICAL CARE TH INDICATIONS • Less time-dependent than prehospital criteria but data shows that the earlier TH started, the better the outcomes • In some non-evidence-based protocols, TH can be started up to 8 HOURS post ROSC! • Encephalopathy present • Defined as patient unable to follow verbal commands • No life-threatening infection • No active bleeding or coagulopathy • Aggressive care warranted & desired by patient or decision-maker (i.e. no terminal underlying disease, DNR / DNI or Hospice)

  33. ED / CCU / ICU HYPOTHERMIA PROTOCOL Crit Care Med 2009;37:S211-S222

  34. ED / CCU / ICU EXTERNAL COOLING DEVICES • Many commercially available devices • External “surface cooling” systems commonly 1st devices utilized while internal devices prepped or patient being stabilized • Servo mechanism varies temp of circulating water / air temp to prevent overcooling • Hydrogel heat exchange pads • Cold water circulates through plastic suit or pads • RhinoChillTM is a unique device that cools the brain through the nose!

  35. ED / CCU / ICU INTERNAL COOLING DEVICES • Invasive (catheter based) systems cool the body via circulation of temperature controlled saline in central or vena cava IV lines • Heat exchange catheter in SVC or IVC (plastic or metallic heat-exchanger) • Bladder, esophagus, or central venous/pulmonary arterial line monitoring

  36. COLD SALINE / ICE STORAGE • Target IVF temp 36-39°F (2-4 °C) • Maintain base IVF stock at 45°F • Many systems use Engel’s Model 15 Freezer (~400$) • 14 quart capacity • Maintains temps 1-40F • 3.9 Amp Draw on 12V System • Fits on floorboard of SUV • Easier to store ice-packs than ice

  37. THOMAS CHILLCORE TMTHERAPEUTIC HYPOTHERMIA INDUCTION KIT ($1K) • Enables immediate scene TH induction • Keeps IVFs at temps as low as 20˚F in ambient temps of 120˚F • Maintains constant set temp +/- 1˚ • Stores 4L IVF • 3L if stored with Thomas RSI Drug case • Interior LCD light for low visibility areas • Exterior Dimensions: 19.2 x 15.2 x 7.3 • Interior: 11.5 x 9.5 x 3.25 • Durable plastic case with standard 12v vehicle power standard, optional 110v *In ambient temperatures up to 120˚ F

  38. SHIVERING • Natural response to cold in order to maintain core temperature • Signs in unconscious patient w/ROSC • Decreased SVO2 • Increased RR • ECG noise • Muscle fasciculations / tremors • Increases systemic metabolic rate • Increases systemic and cerebral VO2 & O2 consumption 40-90% • Increased CO2 production • Major cardiac stressor

  39. SHIVERING MANAGEMENT • Sedation • Midazolam / Versed • Neuromuscular blockade • Vecuronium • Analgesia • Fentanyl, morphine • Alpha blockade • Clonidine, dexmedetomidine • Antipyretics • Tylenol rectally • Focal counterwarming • Magnesium infusion

  40. POST-ROSC BLOOD PRESSURE GOALS • Retrospective review of 1,234 patients in the Brain Resuscitation Clinical Trials (BRCT) II and III databases CritCare Med 1999;27(S):A29 • Higher SBP at 5, 10, 20& 60 mins associated with good neurological outcome (controlling for age, gender, arrest time, CPR time & comorbidities) • 2 episodes SBP <100mmHg in 1st 6 hrs associated with 3 times greater chance of dying • Cerebral perfusion concerns balanced against risks to the heart • Blood pressure can be titrated to specific hemodynamic endpoints, or to directly measured CNS targets (i.e. MAP)

  41. DOCUMENTATION • Utstein data points • Indications, contraindications • Time of ROSC • Time of start of cooling procedure • Evaluation of cooling procedure • Notification of receiving center destination and alert

  42. CLINICAL PEARLS • Do not delay transport to cool • Can be done while en-route • Expose patient but try & maintain modesty • Appropriate airway & hemodynamic management • Don’t forget the basics & the bigger picture! • If patient re-arrests, discontinue cooling & treat per appropriate protocol • Obtain & maintain target core temperature between 32-34C • Temp should be monitored prior to initiation & at receiving ED prior to transfer of care • Excessive cooling puts patient at risk for significant complications

  43. TRANSPORT DECISIONS • OOHCA patients unstable by definition & should be transported to the nearest hospital that can continue TH • If STEMI…go to a STEMI center, otherwise, go to closet regional hospital • After adjusting for age & illness severity institutional mortality ranged from 46% to 68% • Annual case volume strongly associated with outcome

  44. REFERENCES • Santa Clara County EMS Training Module “Therapeutic Hypothermia-Chill Out!”. 2010 • Wake County EMS Training Module “Induced Hypothermia”. 2011. • Seder D. MMC Director of NeurocriticalCare. “Post-resuscitation care of the cardiac arrest survivor”. 2010. • Hypothermia After Cardiac Arrest (HACA) Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002; 346:549-56. • Bernard, SA et al. Treatment of comatose survivors of OOHCA with induced hypothermia. NEJM 2002; 346:557-63. • Yanagawa, Y, et al. Preliminary clinical outcome study of mild resuscitative hypothermia after OOHCA. Resuscitation 1998; 36:61-66. • Bernard, SA, et al. Clinical trial of induced hypothermia in comatose survivors of OOHCA. Ann EM. 1997;30:146-53. • Persse, DE et al. Managing the post-resuscitation patient in the field. PEC 2002;6:114-22. • AHA Position Statement. Part 7.5: Postresuscitation Support. Circulation 2005;112:84-88. • Kollmar, R. Early effects of acid-base management during hypothermia on cerebral infarct volume, edema, and cerebral blood flow in acure focal cerebral ischemia in rats. Anesthesiology 2002;97:868-74. • SterzF, et al. Hypertension with or without hemodilution after cardiac arrest in dogs. Stroke. 1990;21:1178-84. • Kuboyama K, et al. Delay in cooling negates beneficial effects of mild resuscitative hypothermia after cardiac arrest in dogs. Crit Care Med. 1993;21:1348-58. • Nolan, JP. 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. • RoherMJ. Effect of hypothermia on the coagulation cascade. Crit Care Med. 1992; 20: 1402-05. • Valerie CR. Hypothermia induced platelet dysfunction Ann Surg. 1987;205:175-81. • Holzer M. Hypothermia for neuroprotection after cardiac arrest: Systematic review and individual patient data meta-analysis. Crit Care Med 2005; 33:414-18. • Horstmann et al. Brain atrophy in the aftermath of cardiac arrest. Neurology 2010;74:306-312 • www.MIEMSS.org

  45. SUMMARYprehospitalmd@gmail.com / www.teaems.com • <50% patients with ROSC survive; very few survive neurologically intact • To improve OOHCA patients’ outcomes, prehospital & critical care clinicians must use an aggressive paradigm including therapeutic hypothermia & hemodynamic support • Therapeutic Hypothermia requires minimal training with few complications, though it has significant costs & is difficult to do well • Therapeutic Hypothermia ideally suited to EMS as it positively impacts patient outcomes & is extremely time sensitive • The impact of great prehospital care does not end at the ED door!

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