Mild Therapeutic Resuscitative Hypothermia

Edward M. Omron MD, MPH

Critical Care Service

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

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

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.

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).

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.

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

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.

Physiological Effects of Cooling

When a patient is cooled,pCO2, pO2 decrease, andpH increases, measured atthe patient’s temperature.

At 37ºC in Machine: 7.35 / 45 / 100At 33ºC in Patient: 7.41 / 40 / 90

Blood Gases and Temperature

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)

As you cool the patient, vasoconstriction will decrease effective vascular volume.- Diuresis- Lose potassium- Lose phosphate- Potassium shifts intracellularlyAs 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)

Electrolyte and Fluid Shifts

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

• 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

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

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

Questions?