Mild Therapeutic Resuscitative Hypothermia

1. Mild Therapeutic Resuscitative Hypothermia Edward M. Omron MD, MPH Critical Care Service

2. Introduction • Improving outcomes from sudden cardiac death is a healthcare and only 0-30% survive to discharge. • Mild resuscitative therapeutic hypothermia with basic neuro-critical care interventions may improve neurologic outcomes in survivors of cardiac arrest. • Basic neuro-critical care interventions • Airway Protection (Intubation and Mechanical Ventilation) • MAP >70 Hg or Cerebral Perfusion Pressure > 60 mm Hg • Treatment of cerebral edema if present • PCO2 arterial 30-35 mm Hg (not hyperventilation) • GI and DVT prophylaxis • Treatment of hyperglycemia (Glucose > 150 mg/dL) • Head of Bed to 30 degrees at all times

3. How does cooling work? • During cardiac arrest maintenance of cerebral perfusion and oxygen delivery is critical to neurologic outcome. • Hypothermia influences the entire cascade of destruction from ischemia, reperfusion injury, and cerebral edema • reduction in cerebral metabolism • reduction in vascular permeability and cerebral edema • reduction in immune response and inflammation

4. Clinical Studies • Two prospective, randomized clinical trials published in 2002, compared mild hypothermia (32 –24 Celsius) with normothermia in comatose survivors of out of hospital cardiac arrest. • Both studies demonstrated a decreased likelihood of death and improved neurologic recovery with hypothermia and basic neuro-critical care interventions.

5. How to Cool • Different cooling techniques are combined for optimal patient cooling. • Induction cooling is accomplished initially with ice-chilled crystalloid infusion and ice packs followed by a cooling blanket system. • Endovascular Cooling with Surface Cooling: • Initially, 10 – 30 ml/kg ice-cold (4 degrees Celsius) crystalloid solutions (Lactated Ringer’s or Normal Saline) over 30 minutes • Cooling apparatus (Blanketrol III) with the water temperature set to 93 degrees Fahrenheit (33 degrees Celsius).

6. Timing and Depth of Cooling • Cooling should be initiated after return of spontaneous circulation. The 2005 AHA ACLS guidelines recommend cooling patients to 32-34 Celsius for 12- 24 hours. • Place rectal, esophogeal probe or Foley catheter thermistor in the patient and connect to machine. • Desired core temperature is 93 degrees Fahrenheit (33 – 33.5 degrees Celsius) within 4 hrs of presentation to the intensive care unit (goal is within 2 hrs). • Maintain a core temperature of 93 degrees Fahrenheit (33 – 33.5 degrees Celsius) for 18 hrs.

7. Cooling Monitoring • Shivering which prevents achieving the target temperature is treated aggressively with paralytics and or demerol. • Mechanically ventilated patients are deeply sedated. • Midazolam (Versed) drip (0.5 mg/ml) 50 mg/100 ml NS -Initiate at 1 – 2 mg/hr • Fentanyl drip (5 mcg/ml) 500 mg/100 ml NS -Initiate at 0.5 mcg/kg/hr. • Atracurium (Tracrium) 0.3 – 0.5 mg/kg IVP as loading dose, followed by 8 – 14 mcg/kg/min continuous infusion with both Train of Four and BiSpectral Index (BIS) Monitoring options. • Train of 4 titrate 0 to 1 and BiSpectral Index < 60

8. Rewarming • After 18 hrs, begin warming the patient. • Set the cooling machine for a desired body temperature of 98.5 degrees Fahrenheit (37.5 degrees Celsius) with desired rate for warming at < 0.5 degrees/hr. • DO NOT ALLOW THE PATIENT TO SHIVER. Rebound hyperthermia is common and must be avoided.

9. Physiological Effects of Cooling

12. Blood Gases and Temperature When a patient is cooled, pCO2, pO2 decrease, and pH increases, measured at the patient’s temperature. At 37ºC in Machine: 7.35 / 45 / 100 At 33ºC in Patient: 7.41 / 40 / 90

13. Complications of Cooling • Hypovolemia (hypothermia induced diuresis) • Coagulopathy (impaired coagulation cascade and thrombocytopenia) • Electrolyte disorders (hypothermia induced diuresis, K, Mg, Ca) • Insulin resistance • Changes in drugs effects and metabolism (altered clearance of fentanyl, midazolam, and atracurium)

14. Electrolyte and Fluid Shifts As you cool the patient, vasoconstriction will decrease effective vascular volume. - Diuresis - Lose potassium - Lose phosphate - Potassium shifts intracellularly As you warm up, patient intravascular space expands, and potassium shifts out of cells Danger of hyperkalemia if you replaced potassium earlier (Abiki 2001; CCM 29: 1726-30; Zeiner 2004; Resuscitation 60: 253-61)

15. Case Review • 65 yo wm presented to IRMC s/p cardiact arrest secondary to ventricular fibrillation with return of spontaneous circulation within 60 minutes • GCS on admission E1, M1, V1 = 3T • PMH: St. Jude Aortic Valve for AS, CAD, EF 25% • Meds: Coumadin, Furosemide, monopril

16. Vital Signs and Labs • BP 122/72, HR 91, Temp 99 F, RR 26, Sat 99% • Vent Settings: PRVC TV 600 , Peep 0, FIO2 = 100%, set rate 14 • ABG: 7.47, 27, 484, 19.5 • Na 139, K 4, BUN 16, Creat 0.9 • INR 3.7 • WBC 9, Hematocrit 41 • Troponin and CPK 2000

17. Hospital Course • Hypothermia protocol initiated with cold saline and Blanketrol III set to 93 F • Clinical assessment initially revealed hypovolemia: crystalloid volume loading • MAP >70 mm HG (presumed increased ICP) • ABG at 4 hours • pH = 7.255, PCO2 59.4, PaO2 278 • Could not correct respiratory acidosis till paralysis initiated, train of four 0 to 1 and bispectral to 40

18. Hospital Course • First 6 hours • K = 2.8, repleted • P = 1.8 repleated • Lactic acid = 2 • INR > 5, corrected with FFP • WBC decreased to 2.7 • After 24 hours • CT Head, No Acute Intracranial Process • Paralysis stopped with slow neurologic recovery • Retroperitoneal Bleed recognized and treated

19. Questions?