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Presentation on theme: "JULIE M. WATERS RN MS CCRN CLINICAL NURSE EDUCATOR FOR CRITICAL CARE PROVIDENCE HEALTH CARE MARCH 2015 Hitting the Target: Does Temperature Management."— Presentation transcript:

1 JULIE M. WATERS RN MS CCRN CLINICAL NURSE EDUCATOR FOR CRITICAL CARE PROVIDENCE HEALTH CARE MARCH 2015 Hitting the Target: Does Temperature Management Matter After Cardiac Arrest?

2 What do they have in common?

3 Hit the target every time

4 Objectives Describe the impact of thermoregulation in patients after cardiac arrest Discuss the current state of targeted temperature management in cardiac arrest patients Identify key principles in the clinical management of patients receiving targeted temperature management

5 Cardiac Arrest - Dismal Cardiac Arrest ≈300K Hospital Discharge ≈60K Long Term Recovery ≈30K 80% Mortality 50% Neuro Injury

6 Cardiac Arrest - Management Major Goals:  Determine and treat the cause of the cardiac arrest  Etiology determines therapy  Minimize brain injury  Manage cardiovascular dysfunction  Manage problems resulting from global ischemia and reperfusion injury

7 Baseline Neurological Exam Determine the likely cause, possible clinical course, and need for interventions  Neurological injury is the most common cause of death in patients with out-of-hospital cardiac arrest Consider Targeted Temperature Management for: Patients who can not follow commands or demonstrate purposeful movement

8 Definitions for today….. Controlled Normothermia  36-37.5°C Temperature Control  No higher than 36°C Therapeutic Hypothermia  Decrease core temp to 32-34°C Targeted Temperature Management (TTM)  Maintaining body temp 33-36°C

9 Historical Perspective Ancient Greece – Hippocrates 1812 Napoleon’s soldiers 19 th Century “Russian Method of Resuscitation”

10 Early Methods of Cooling Make use of the environment Pack in ice

11 Problems with Early Hypothermia Goal was deep hypothermia (30  C) Duration of cooling varied widely (from 2-10 days) ICUs didn’t exist, monitoring was limited Cooling methods weren’t very reliable  1945: positive effects of TH in severe head injury  1950: improved neuro function in cardiac surgery with TH  Then …………..........

12 OutcomeHypothermia (n = 43) Normothermia (n = 34) Discharge to home or a rehab facility 39% (21/43)26% (9/34) Mortality*51%68% * Did not reach statistical significance

13 OutcomeHypothermia (n = 137) Normothermia (n = 138) Positive Neurological Recovery 55% (75/136)39% (54/137) Mortality at 6 months41%55%


15 2010 Updated AHA Guidelines

16 WHY?.........Ischemia Perman et al. Clinical Applications of Targeted Temperature Management. Chest 2014; 145(2):386-393.

17 Abnormal Electrical Depolarization Blood-Brain Barrier Disruption Free Oxygen Radical Formation Neurotransmitter Release Increased Levels of Excitotoxins Destabilized Cell Membranes Mitochondrial Failure Slide A. Lawrence 2015 Neuronal Damage

18 Increased temp in the neurologically injured brain or ischemic/anoxic brain… Cellular Derangements Cellular Damage Cell Death

19 Ischemic Brain Injury Injury occurs within 4-6 minutes without perfusion Initial insult followed by a cascade of events Damage occurs from hours to days Can be re-triggered by new ischemia All processes are temperature dependent  Stimulated by fever  Mitigated by hypothermia

20 Possible Mechanisms of Action Reduction of cerebral metabolic demand   6-8% for every 1  decrease in temp  Reduced 0 2 and glucose needs more closely match reduced blood flow  Less CO 2 and lactate production

21 Ischemic cell  Oxygen & glucose  ATP Disruption of Na-K ATP pump  Excitatory Neurotransmitters (glutamate)  Calcium Influx  Degradation enzymes (carpase, lipase) Cellular Apoptosis Mitochondrial Dysfunction X J. Dirks 2013

22 Reperfusion Injury (Inflammatory Response) ↑ Vascular Permeability (edema) Disruption of Blood-brain Barrier Activation of Coagulation Microthrombi formation Cellular Hyperactivity  Temperature in brain X J. Dirks 2013

23 Other Benefits of Hypothermia Reduction in intracranial pressure Suppression of epileptic activity Improved tolerance of recurrent ischemia


25 Design of Study International trial - 939 unconscious adults after OHCA targeting either 33°or 36° Blind study - between 2010-2013 36 ICUs across 10 countries in the EU and AUS All patients were sedated and ventilated and had feedback cooling devices All patients had 72 hrs of temp intervention post ROSC to prevent fever


27 Summary of Findings How can this be?

28 Considerations All had good post arrest care, 2/3 had angiography, strict rules outlined for prognostication and withdrawal of care The population included OHCA primary cardiac arrest patients with all rhythms (shockable and nonshockable)  80% were Vfib/Vtach and 20% PEA/Asystole 73% of patients received bystander CPR

29 December 2013

30 State of the Therapy All Comatose Post-Arrest Patients Active control of patient’s temp between 32-36°C Active avoidance of fever

31 TTM Recommendations - Patient Specific? 36°C33°C Duration: 24 hours Uncomplicated patient with some motor response Patient with loss of motor response or brainstem reflex No malignant EEG patterns Malignant EEG patterns No evidence of cerebral edema on CT CT changes suggestive of cerebral edema Rittenberger JC UpToDate: Post-Cardiac Arrest Management in Adults. Last updated 2/2015

32 Questions to be Answered  What is the optimal temperature?  TTM trial was neutral  33C based on extensive lab evidence and 2 RCTs  What is the optimal duration?  What is the optimal injury measurement for post- arrest?  We can’t tell who will have significant post-arrest injury currently  How should we tailor therapy to each patient?  Different presenting rhythms: VF/VT vs PEA/Asystole  Different length of down time  Severity of presenting illness or comorbidities Only get one shot to modify neurological injury

33 Indications and Contraindications Indications  ANY patient not following commands after cardiac arrest Contraindications  Advanced directive against aggressive therapy Considerations  Active noncompressible bleeding (36°C)  Nielsen trial showed no statistically significant differences in adverse events between 33°C and 36°C

34 Phases of TTM 1. Induction 2. Maintenance 3. Rewarming 4. Controlled Normothermia

35 Induction Temperature Measurement  Core Temp  2 Sites  Registered Temp + Lag Time = Overshoot

36 Site of Temperature Measurement Variation from Core Temperature Average Lag Time Best Practice: Advantage Disadvantage  Pulmonary Artery Catheter Gold Standard  Complex insertion Esophagus <0.1 ⁰ C 5 mins (range 3-10) Most rapid and accurate reflection of gold standard  Temp fluctuates according to depth of probe, accurate placement is key Bladder <0.2 ⁰ C 20 mins (range 10-60) Easy insertion, low risk dislodgement  Accuracy influenced by low U.O., Long lag time, movement of sensor Rectum <0.3 ⁰ C 15 mins (range 10-40) Easy insertion  High risk of dislocation, influenced by stool in rectum, long lag time

37 Rapid Induction is Key at 33 °C 35-38 ⁰ C 33.5 ⁰ C FASTFAST ICED SALINE ICE PACKS MEDS COOLING PADS Target Temp 36°C  If < 36°C: Controlled rewarm at 0.25°C/ hour

38 Infusion of Ice-Cold Fluids Rapidly infuse 30ml/kg (1-3L) of cold (4 ◦ C) isotonic saline via pressure bag  ↓ Body temp > 2 ◦ C per hour  1L of fluids over 15 minutes can ↓ body temp ≈ 1.0 ◦ C Caution in patients with:  Heart failure  Severe renal dysfunction  Pulmonary edema If clinically indicated – make the volume cold

39 Conventional Cooling Adequate although tricky Disadvantages Lack of feedback loop makes maintenance difficult High incidence of over cooling Extreme nursing vigilance required Effect of temperature fluctuations and excessive hypothermia on patient outcomes is unknown

40 Surface Cooling Thermostatically Controlled Devices  Disadvantages  Cover patient’s surface area 40-90%  Risk skin lesions  Advantages  Easy and fast time to administration  Nurse-driven protocols

41 Core Cooling Intravascular Cooling Devices  Disadvantages  Time and expertise to initiate therapy  Risk of catheter-related thrombosis  Advantages  Rapid cooling rates  Reliable maintenance of core temperature

42 Intravascular VS Surface Cooling Findings: comparable in terms of cooling effectiveness and automatic temperature feedback control Study  Time to device deployment were comparable  No significant differences in survival to final hospital discharge with good neurological function  No difference in rate of shivering  No device specific injuries were noted TФmte O, et al. A comparison of intravascular and surface cooling techniques in comatose cardiac arrest survivors. Crit Care Med 2011; 39(3):443-449.

43 Thermoregulatory Defenses  Behavioral  Autonomic  Vasoconstriction  Shivering Normal……………. 37°C Vasoconstriction…..36.5°C Shivering…..…….35.5°C Below shivering…..34°C Threshold **Still see shivering at 36°C

44 Shivering ↑ heat production by 600% ↑ oxygen consumption 2-3x ↑ CO2 production 2-3x ↑ metabolic rate 2-5x Linked to ↑ risk of morbid cardiac events Impedes induction of TTM and eliminates possible neuroprotective benefits

45 Who is likely to shiver? >60% patients undergoing TTM experience shivering Young Males Low Magnesium levels <1.7mg/dL Patients with a difficult-to-extinguish shivering response had a higher odds of neurological intact survival

46 How to assess for shivering Early detection  Observe for piloerection  Palpation of the mandible for vibrations  Identifying ECG artifact  Resistance to cooling

47 Objective Indicators Look for increase in patient’s temp Look at water temp What does it indicate the patient is doing?

48 Bedside Shivering Assessment Scale* ScoreDefinition 0None: no shivering noted on palpation of the masseter, neck, or chest wall 1Mild: shivering localized to the neck and/or thorax only 2Moderate: shivering involves gross movement of the upper extremities (in addition to neck and thorax) 3Severe: shivering involves gross movements of the trunk and upper and lower extremities *Badjatia N et al, Metabolic impact of shivering during therapeutic temperature modulation: Stroke 2008; 39:3242-3247. Goal is BSAS ≤ 1

49 How to combat shivering: Pharmacological & Nonpharmacological

50 Surface Warming Skin temperature influences at least 20% of the shivering threshold Works by countering the feedback loop from the skin temp to the hypothalamus Effective adjunct in suppressing the shivering reflex Air-circulating blanket Insulation of cutaneous thermoregulators on face, hands and feet

51 Pharmacological Goal: Pharmacological induction of thermal tolerance Avoid a cooling-related stress response through pharmacological impairment Combination of drugs to prevent excessive toxicity Vasodilation with sedation & analgesia Sedation is important Monitor efficacy and potency due to decreased metabolism and elimination of drugs

52 Miscellaneous Drugs Acetaminophen  Inhibits cyclooxygenase-mediated prostaglandin synthesis  650-1000mg Q 4-6 H (IV/PO/PR) Buspirone  Acts on 5-HTLA receptor; lowers shiver threshold  20-30mg PO Q 8 H Magnesium Sulfate  Peripheral vasodilation & Facilitates the cooling process  Decreased time to goal temperature  Possible direct neuroprotective effects  500mg – 1 gm/hr to reach goal Mg level 3-4mg/dL

53 Opioids  FENTANYL o 25-50 mcg/hr IV  MORPHINE  MEPERIDINE  25-50mg IV Q 1 H  One of the most effective anti-shivering drugs  Lowering of the seizure threshold?????  Caution in renal failure

54 Sedation  Dexmedetomidine  Dose 0.2-1.5mcg/kg/hr (off-label)  Bradycardia & Hypotension  Propofol  50-75 mcg/kg/min  Anti-seizure effect  Hypotension  Midazolam/Benzodiazepines  2-10 mg/hr  Complicates neuro evaluation  Less hypotension

55 Paralytics Muscles may stop – Brain is still working  Advantages  Very effective; quickest method to stop shivering  Help achieve goal temp quickly  Do not cause hypotension  Considerations  May not be able to detect seizure activity  Consider continuous EEG  ↑ risk of critical illness polyneuromyopathy  May mask incomplete sedation  Only use as long as needed…….stop/restart  TOF does NOT correlate in TH

56 Combination Agents  Buspirone & Meperidine  Buspirone & Dexmedetomidine  Dexmedetomidine & Meperidine Benefit from combination therapy- Whether methods or drugs

57 *Seder DB et al, CCM 2009; 37(7):S211-S222

58 Columbia Anti-Shivering Protocol StepInterventionDose 0BaselineAcetaminophen Buspirone Magnesium Sulfate Skin Counterwarming 650-100mg Q 4-6 h 30mg Q 8 h 0.5-1 mg/h IV (Goal 3-4 mg/dl) 43 ⁰ C/MAX Temp 1Mild Sedation Dexmedetomidine OR Opioid 0.2-1.5 mcg/kg/h Fentanyl starting dose 25mcg/h Meperidine 50-100mg IM or IV 2Moderate Sedation Dexmedetomidine AND Opioid Doses as above 3Deep Sedation Propofol50-75 mcg/kg/min 4NMBVecuronium0.1mg/kg IV Choi HA et al. NeuroCrit Care 2011; 14:389-394. 5.1% of patients 18% of patients

59 November 2013

60 Physiological Impact of Hypothermia Patients require ICU care to:  Maintain hemodynamic stability  Ensure adequate oxygenation  Correct fluid/electrolyte derangements  Prevent complications (infection or bleeding)  Deliver safe, controlled cooling and re-warming  Manage shivering

61 Immunologic: Impaired leukocyte function Cutaneous vasoconstriction Increased risk of infection if hypothermia maintained >24 hrs Systemic Effects of Hypothermia

62 Hematologic: Depressed clotting enzyme reactions Impaired platelet function Mild coagulopathy, possible bleeding Systemic Effects of Hypothermia

63 Hemodynamic Slight increase in contractility (mild hypothermia) then decrease (moderate-deep) TH not associated with increased need for vasopressor support  CO =  demand

64 Typical EKG Changes Bradycardia Prolonged PR, QRS, QTc Osborne waves (a dome or hump occurring at the R-ST junction (J point) on the ECG) From: Krantz MJ, Lowery CM. “Giant Osborne Waves in Hypothermia” N Engl J Med 2005; 352:184 Bradycardia usually well tolerated 33°C

65 Systemic Effects of Hypothermia “Cold Diuresis”: Electrolytes: Vasoconstriction increases venous return Intracellular shifts of electrolytes during temperature manipulation  renal losses due to tubular dysfunction Hypovolemia Loss of electrolytes (potassium, magnesium, phosphate) 33°C

66 Metabolic: Decreased cellular metabolism   O 2 & glucose consumption   fat metabolism   CO 2 production  insulin sensitivity ABGs:  O 2,  CO 2, acidosis Glucose: Goal 140-180 mg/dL Systemic Effects of Hypothermia

67 Induction Phase Rapid identification and implementation Rapidly cool to 33°C If <36°C – controlled rewarm at 0.25°C/hr

68 Maintenance Phase  Maintain target temperature for 24 hours Monitor EKG changes Maintain fluid status Watch for infection Monitor for bleeding Electrolyte monitoring Monitor for skin breakdown Avoid hyperglycemia

69 Rewarming Phase Rapid rewarming can negate the benefits of TTM Controlled rate of rewarming to 37°C  ≤0.5°C / hour  Most suggest 0.25°C / hour Monitor for  Electrolyte abnormalities  Cerebral edema  Seizures  Shivering

70 Controlled Normothermia Phase  Fever during the first 72 hours after ROSC has been associated with poor outcome  For patients unable to follow commands: maintain normothermia (<37.5°C) for an additional 48 hours after rewarming

71 Rebound fevers after therapy stopped

72 Neuroprognostication Drug clearance is decreased so sedatives may be present 48-72 hours Decisions regarding withdrawal of care must be delayed until adequate clinical exam can be performed Patient’s temperature must be at 35˚C before declaration of brain death can be made 72 hours

73 Summary  TTM has been shown to improve outcomes in patients after cardiac-arrest  TTM is considered the standard of care for comatose survivors after cardiac-arrest (VF/VT)  TTM is best implemented as a protocol-driven therapy  Shivering must be controlled  Stratifying patients based on organ system dysfunction may be the way to determine 33 vs 36

74 33°C 36°C What is my target temperature?

75 Questions? “The odds of hitting your target go up dramatically when you aim at it.” M. Pancoast


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