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Therapeutic Hypothermia for Post-Cardiac Arrest Patients Lois Andrews, RN-BC, MSN, CCRN 10/10.

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Presentation on theme: "Therapeutic Hypothermia for Post-Cardiac Arrest Patients Lois Andrews, RN-BC, MSN, CCRN 10/10."— Presentation transcript:

1 Therapeutic Hypothermia for Post-Cardiac Arrest Patients Lois Andrews, RN-BC, MSN, CCRN 10/10

2  Objectives: 1. Describe the physiologic effects of hypothermia. 2. Identify the indications for hypothermia after cardiac arrest. 3. Identify the contraindications for instituting the hypothermia protocol. 4. Describe the process for initiating cooling and rewarming.

3 Historical Perspective

4 Hypothermia Defined  Mild hypothermia = ◦ C  Moderate = ◦ C  Severe = ◦ C

5 2005 Recommendation AHA & ILCOR Recommended inducing & maintaining for 12 to 24 hours, Therapeutic hypothermia (33°C) after ROSC in patients experiencing OHCA who remain comatose hours of after resuscitation & in whom the initial cardiac rhythm is VF.

6 2010 International Consensus Therapeutic hypothermia: Adult patients who are comatose (not responding in a meaningful way to verbal commands) with spontaneous circulation after out-of-hospital VF cardiac arrest should be cooled to 32–34°C for 12–24 h. Induced hypothermia might also benefit comatose adult patients with spontaneous circulation after OHCA from a non-shockable rhythm or in- hospital cardiac arrest.

7 Brain ischemia during cardiac arrest (Global vs Focal) Inflammation and injury Increased ICP Poor neurological outcome Pathophysiology of Post-Cardiac Arrest

8 Physiologic Effects of Hypothermia  Desired effects: Decreases the cerebral metabolic rate (1°C = 5-7%) Decreases the cerebral metabolic rate (1°C = 5-7%) Inhibits influx of Ca & glutamate accumulation Inhibits influx of Ca & glutamate accumulation Suppresses ischemia- induced inflammatory cytokines Suppresses ischemia- induced inflammatory cytokines Reduces disruptions in BBB & vascular permeability Reduces disruptions in BBB & vascular permeability

9 Physiologic Effects of Hypothermia  Potential adverse effects: Decreases heart rate Decreases heart rate Decreases phosphate and Decreases phosphate and potassium concentrations potassium concentrations Decreases gut motility Decreases gut motility Increases blood glucose concentrations Increases blood glucose concentrations Increases systemic vascular resistance Increases systemic vascular resistance Prolongs clotting times Prolongs clotting times May cause diuresis May cause diuresis May decrease the number and function of WBCs and platelets May decrease the number and function of WBCs and platelets

10 Hypothermia Protocol IS THE PATIENT A CANDIDATE FOR THERAPEUTIC HYPOTHERMIA?

11 Inclusion Criteria for Therapeutic Hypothermia  Cardiac arrest patient, post resuscitation with return of spontaneous circulation and persistent coma (GCS < 6)  Resuscitation time (time of collapse to return of spontaneous circulation) should be < 1 hour  Patient is intubated  Time from resuscitation to initiation of hypothermia < 6 hours (ideally, but up to 12)

12 Exclusion Criteria for Therapeutic Hypothermia  Absolute: (If the patient meets any of the below, he/she is not a candidate) DNR code status DNR code status Metastatic cancer or other terminal illness Metastatic cancer or other terminal illness Responds to verbal commands Responds to verbal commands Pregnancy Pregnancy Comatose baseline due to CNS depressing drugs or other possible cause Comatose baseline due to CNS depressing drugs or other possible cause Temperature < 30ºC (86ºF) Temperature < 30ºC (86ºF)

13 Relative Exclusion Criteria: (the physician may continue to order the Hypothermia Protocol based on the belief that the benefits outweigh the potential risk) Hemodynamic instability (MAP < 60mmHg) for more than 30 minutes post resuscitation Hemodynamic instability (MAP < 60mmHg) for more than 30 minutes post resuscitation Uncontrolled cardiac arrhythmias, multiple arrests/ pulseless periods Uncontrolled cardiac arrhythmias, multiple arrests/ pulseless periods Prolonged QT interval (> 0.45) Prolonged QT interval (> 0.45) Prolonged hypoxemia (SaO2 < 85%) for greater than 15 minutes after return of spontaneous circulation Prolonged hypoxemia (SaO2 < 85%) for greater than 15 minutes after return of spontaneous circulation Delay of greater than 15 minutes to initiation of BLS Delay of greater than 15 minutes to initiation of BLS Patients with known bleeding diathesis or with active ongoing bleeding Patients with known bleeding diathesis or with active ongoing bleeding Platelet count < 50,000/mL Platelet count < 50,000/mL Recent surgery (within 14 days) Recent surgery (within 14 days) Active sepsis Active sepsis Etiology of cardiac arrest thought to be caused by trauma or severe bleeding Etiology of cardiac arrest thought to be caused by trauma or severe bleeding

14 To be successful, the patient must be managed in three phases:  Cooling  Maintenance  Rewarming Background Information

15 LET’S GET STARTED!  Physician completes inclusion & exclusion criteria on page 1 of orders  As soon as decision is made to start hypothermia, begin sedation. NO SEDATION VACATION DURING COOLING PHASE.  Induction of hypothermia should begin as soon as possible after ROSC and can be quickly achieved with 30mL/kg or 2L of cold (4°C) IV fluid and packing the patient’s neck, axilla & groin with ice packs. (AHA 2010)

16 LIFEFLIGHT OF MAINE: CRITICAL CARE TRANSPORT TEAM 3.2a NEUROPROTECTIVE INDUCED HYPOTHERMIA AFTER CARDIAC ARREST Procedure: A. Institute cooling as early as possible. Temp goal is 33°C. B. Sedate and paralyze the patient as per Protocol 2.3.; Veccuronium is preferred. Suppress shivering with neuromuscular blockade. C. Rapid IV infusion of ice cold (4°C). LR. Administer 30 ml/kg IVx1 dose over a period of 30 minutes immediately after neuromuscular blocking agent administered. Maximum of 2 liters LR during transport. D. Apply ice packs to patient’s neck, axilla, and inguinal area after patient is sedated and paralyzed and iced LR is administered IV. E. If patient shivering increase sedative and/or analgesia dose prior to increasing paralytic F. Monitor temperature via esophageal temperature probe –as time and mission allow. G. Consider turning on aircraft AC to assist with cooling enroute. H. Report to receiving tertiary care center.

17 In the ICU  Prior to initiation of cooling: Have initial labs drawn Have initial labs drawn Perform a thorough skin assessment Perform a thorough skin assessment Place temperature probe: PA, Foley or esophageal & rectal Place temperature probe: PA, Foley or esophageal & rectal Turn room thermostat to lowest setting during cooling and maintenance phase Turn room thermostat to lowest setting during cooling and maintenance phase Prepare for A-line and CVP line insertion. Prepare for A-line and CVP line insertion.  Ventilator circuit – no heating

18  Patients will be on the following protocols: Electrolyte replacements Electrolyte replacements Glycemic Control/Intensive insulin Glycemic Control/Intensive insulin Neuromuscular blockade Neuromuscular blockade  Correct potassium (goal of 3.5) PRIOR to onset of cooling therapy  Admitting MD to consult critical care intensivist (if applicable) to manage therapeutic hypothermia In the ICU

19 LAB and DIAGNOSTIC STUDIES Stat Portable Chest x-ray on admission Stat Portable Chest x-ray on admission Stat 12-lead EKG on admission Stat 12-lead EKG on admission Labs on admission: Complete Metabolic Panel, iCa, LFTs, amylase, lipase, CBC w/diff, PT/PTT/INR Labs on admission: Complete Metabolic Panel, iCa, LFTs, amylase, lipase, CBC w/diff, PT/PTT/INR Labs every 4hrs x 24hrs: Basic Metabolic Panel, magnesium, phosphorus, CBC w/diff, PT/PTT/INR Labs every 4hrs x 24hrs: Basic Metabolic Panel, magnesium, phosphorus, CBC w/diff, PT/PTT/INR Obtain one set of blood cultures 12 hours after onset of cooling (Hypothermia may mask infection) Obtain one set of blood cultures 12 hours after onset of cooling (Hypothermia may mask infection) During warming – BMP q 4 hrs During warming – BMP q 4 hrs

20 COOLING PHASE  Cool patient to a target temperature of 32º - 34º C (89.6º º F) within 6-12 hours of onset of arrest. Maintain at target temperature for 24 hours.  Monitor and record VS, CVP, cardiac rhythm and primary temperature q 30 min. until goal temp is achieved.  Correlate and record secondary temperature source q 2hours.  If unable to achieve target core temperature, consult MD

21 COOLING PHASE Shivering  Perform shivering assessment hourly throughout cooling phase (Palpate mandible to assess for shivering)  If shivering occurs during cooling phase, implement Critical Care Neuromuscular Blocker orders.  Preferred Neuromuscular blocking agents are Cisatracurium, Atracurium, or Vecuronium. (NO neuromuscular drug holiday during the cooling phase!)

22  PATIENT SHOULD REMAIN AT TARGET TEMPERATURE FOR 24 HOURS.

23 MAINTENANCE PHASE  Once target temp is achieved, monitor and record VS, CVP, cardiac rhythm and primary temperature hourly and PRN during maintenance.  Correlate and record secondary temperature every 2 hours  Assess skin every 2 hours for any signs of breakdown  If patient has recurring malignant dysrhythmias discontinue cooling, begin rewarming and notify MD.

24 REWARMING PHASE Active vs Passive  Should begin 24 hours after target temperature achieved  Proceed with rewarming slowly (0.5° - 1° C per hour) over 6-8 hours to prevent vasodilation, hypotension and rapid fluid & electrolyte shifts.  Draw BMP q 4 hrs, but DO NOT replace potassium during rewarming phase (shifts back into serum from cells)  Discontinue neuromuscular blockers once patient’s temperature >36ºC, but continue sedation until TOF = 4.  If shivering occurs, apply warm blankets or use Demerol  Do not permit hyperthermia in the first 24 hours after cooling.  Administer acetominophen for temp >37ºC (98.6ºF)  Once normothermic goal reached for 48 hours, consult MD for removal of unnecessary lines.

25 SNGH TH Patients

26 CONCLUSION  Cardiac arrest with widespread cerebral ischemia frequently leads to severe neurologic impairment. Induced hypothermia is a promising method that increases the rate of favorable neurologic outcome and reduces mortality.

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