1. Therapeutic Hypothermia for Post-Cardiac Arrest Patients
Lois K. Andrews, RN-BC, MS, CCRN
April 3, 2011

2. Objectives
Review the historical background of hypothermia use in medicine.
Describe the physiologic effects of hypothermia.
Identify the indications for hypothermia after cardiac arrest.
Identify the contraindications for instituting the hypothermia protocol.
Describe the patient care required during cooling and rewarming.

3. The Problem 310,000 experience sudden cardiac death in the US yearly
265,100 EMS-treated out of hospital cardiac arrests in the US
40% of those resuscitated have ROSC
Survival to discharge of OHCA %
Less than 10% of survivors regain former lifestyles
There is a wide variation in the reported incidence of and outcome for out-of-hospital cardiac arrest. These differences are due in part to differences in definition and ascertainment of cardiac arrest data, as well as differences in treatment after the onset of
cardiac arrest.
Each year, either out of hospital or in the ED, approximately 310,000 people in the United States experience
sudden cardiac death (American Heart Association, 2008). An additional 375, ,000 people are resuscitated each year (Maramattom & Wijdicks, 2005}.
Approximately 40% of those resuscitated will have a return of spontaneous circulation (Maramattom &C Wijdicks, 2005). Although they survive the arrest, some still have negative repercussions from the physiological responses that occur as a result of the arrest state.
The number of resuscitated patients who achieve spontaneous circulation remains poor, however. Research shows that the overall
survival-to-discharge after out-of-hospital cardiac arrest is about 5 per cent and of those admitted to intensive care units (ICUs), only between 25 and 40 per cent survive until discharge with conventional therapy (Pell 2003).
Moreover, less than 10 per cent of survivors regain their former lifestyles, primarily because of disabilities caused by hypoxic brain damage. Many people require constant care and some cannot return to gainful activity because of severe memory problems or cognitive impairment (Thompson and Damian 2007).

4. Historical Background Information
Hippocrates
Napoleon’s Surgeon
1950’s
1960’s
1980
2002
2010
Historical use of Hypothermia
Hypothermia used by Egyptians, Greeks & Romans5
Hippocrates – advocated packing wounded pts in ice & snow to reduce hemorrhage
Napoleon’s surgeon Genral Baron Larrey observed injured soldiers who became hypothermic & were put closer to the fire died more rapidly than those who remained hypothermic
1930’ & 1940’s – cases of successful resuscitation of drowning victims, hypothermic, after prolonged asphyxia
1945 – 1st published case study of pts with severe head injury
1950’s – during intracerebral aneurysm surgery & during complete circulatory arrest – intracardiac operations without blood
1960’s – clinical trials by Rosomoff – ischemic brain injury - ↑side effects (<30°C)
1980’s – moderate hypothermia (32-35°C) = benefits without side effects
In 1955, open heart surgery was performed at the NIH Clinical Center using hypothermia. The patient was placed in a bed of ice to lower the total body temperature so that body tissues used very little oxygern. This permitted interuption of the blood flow for a brief period so that some procedures could be performed. This technique preceded the advent of the heart-lung machine, which today takes over the job of pumping blood during heart surgery.
Short history of the National Institute of Health

5. 2002 Studies Stringent inclusion criteria – VF/VT
Fewer deaths & disability in both studies
6 month mortality decreased from 55% to 41% in European study, NNT = 6
In Australian study, mortality decreased from 68% to 51% and 49% of survivors were reported to have a favorable neurological outcome

6. 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.
Based on 2 studies, one in Europe and one in Australia, both published in the same issue of The New England Journal of Medicine in 2002
International Liaison Committee on Resuscitation

7. 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.
2010 International Consensus on Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care Science Resuscitation October supplement
It is now clear that organized post-cardiac arrest care with emphasis on protocols for optimising cardiovascular and neurological care, including therapeutic hypothermia, can improve survival to hospital discharge among victims who achieve ROSC after cardiac arrest.22,53,54 Although it is not yet possible to determine the individual effect of many of these therapies, it is clear that this “bundle of care” can improve outcome. Therapeutic hypothermia has been shown independently to improve outcome after adult witnessed out-of-hospital VF cardiac arrest and after neonatal hypoxic-ischaemic insult. Since 2005, two nonrandomised studies with concurrent controls indicated possible benefit of hypothermia after cardiac arrest from other initial rhythms in-hospital and out-of-hospital,55,56 and other studies with historic controls have shown benefit for therapeutic hypothermia after out-of-hospital all-rhythm cardiac arrests in adults.22,57–6

8. Pathophysiology of Post-Cardiac Arrest
Brain ischemia during cardiac arrest
(Global vs Focal)
Inflammation and injury
Increased ICP
Poor neurological outcome
Necrosis & penumbra with focal ischemia, at normothermic complete by 24 hours
Global ischemia – selective neuronal death, more protracted, peaks approx 48hrs after injury
Ischemia -> decrease ATP: acidosis, K, Na & Ca channels don’t work = loss of Na, influx of Ca to cell, Na & K pumps fail
Proinflammatory mediators are released in large quantities following ischmia, especially during reperfusion in 1st hour

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

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

11. IS THE PATIENT A CANDIDATE FOR THERAPEUTIC HYPOTHERMIA?
Hypothermia Protocol

12. Inclusion Criteria for Therapeutic Hypothermia
Patient must meet BOTH criteria:
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
Time from resuscitation to initiation of hypothermia < 6 hours (Optimally, but up to 12 can be considered)
Patient is intubated
*no level of coma short of brain death precludes cooling.

13. Exclusion Criteria for Therapeutic Hypothermia
Absolute: (If the patient meets any of the below, he/she is NOT a candidate)
DNR code status
Metastatic cancer or other terminal illness
Responds to verbal commands
Pregnancy
Comatose baseline due to CNS depressing drugs or other possible cause
Temperature < 30ºC (86ºF)
Glascow Coma Scale (GCS) GREATER than 6
Baseline CNS depression eg. Drug intoxication, pre-existing coma
Updated per EPIC 10/30

14. Relative Exclusion Criteria
Hemodynamic instability (MAP < 60mmHg) for more than 30 minutes post resuscitation
Uncontrolled cardiac arrhythmias, multiple arrests/ pulseless periods
Significant pre-existing neurological Impairment
Extremes of age
Prolonged QT interval (> 0.45)
Prolonged hypoxemia (SaO2 < 85%) for greater than 15 minutes after return of spontaneous circulation
Delay of greater than 15 minutes to initiation of BLS
Patients with known bleeding diathesis or with active ongoing bleeding
Platelet count < 50,000/mL
Recent surgery (within 14 days)
Active sepsis
Etiology of cardiac arrest thought to be caused by trauma or severe bleeding
Initial rhythm = asystole
(the physician may continue to order the Hypothermia Protocol based on the belief that the benefits outweigh the potential risk)
Relative Exclusion Criteria: The following have been added: multiple arrests/pulseless periods; significant pre-existing neurological impairment; extremes of age; & initial rhythm = asystole.
Criteria checked with epic 10/30

15. Process of Therapeutic Hypothermia
The patient must be managed in three phases:
Cooling
Maintenance
Rewarming

16. Hypothermia Defined Mild hypothermia = 32-35◦C Moderate = 28- 32◦C
Severe = 20-28◦C

17. LET’S GET STARTED! Consider inclusion & exclusion criteria
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
Rapid infusion of cold (48°C) IV fluid – 30mL/kg or up to 2 L
AHA 2010: Rapid infusion of ice-cold IV fluid at 30mLkg−1 is a safe, feasible, and simple method for initially lowering core temperature
by up to 1.5 ◦C, as is application of ice packs.WhenIV fluids are used to induce hypothermia, additional cooling strategies will
be required to maintain hypothermia.
13In one study, A key finding is that infusion of up to 2 litres of cold (48C) intravenous fluid (0.9% saline or Ringer’s lactate) in the immediate post-ROSC phase is an effective and safe method of cooling and is not associated with significant complications or cardiovascular instability.
14Results from animal models suggest, however, that, if hypothermia is initiated as soon as possible after ROSC, its effectiveness can be increased (Abella et al 2004, Nozari et al 2006). In addition, Bernard et al (2003) has hypothesised that early, preferably pre-hospital, initiation of cooling can be of maximum benefit for patients.

18. 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.

19. ThermoSuit, a hypothermia water immersion system from Life Recovery Systems, HD, LLC, of Alexandria, LA,

20. LIFEFLIGHT OF MAINE INDUCED HYPOTHERMIA AFTER CARDIAC ARREST
Institute cooling as early as possible. Temp goal is 33°C.
Sedate and paralyze the patient as per Protocol 2.3.; Veccuronium is preferred. Suppress shivering with neuromuscular blockade.
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.
Apply ice packs to patient’s neck, axilla, and inguinal area after patient is sedated and paralyzed and iced LR is administered IV.
If patient shivering increase sedative and/or analgesia dose prior to increasing paralytic
Monitor temperature via esophageal temperature probe –as time and mission allow.
Consider turning on aircraft AC to assist with cooling enroute.
Report to receiving tertiary care center.

21. In the ICU Draw initial labs
Correct potassium (goal of 3.5) PRIOR to onset of cooling therapy
Patients will be on the following protocols:
Electrolyte replacements
Glycemic Control/Intensive insulin
Neuromuscular blockade
Obtain one set of blood cultures 12 hours after onset of cooling (Hypothermia may mask infection)
During warming – BMP q 4 hrs
Perform a thorough skin assessment
Place temperature probe: PA, Foley or esophageal & rectal
Turn room thermostat to lowest setting during cooling and maintenance phase
Prepare for A-line and CVP line insertion.
Ventilator circuit – no heating
(K, Mg, Phosphorous & Ca)
(Cooling shifts potassium into the cells, causing low serum potassium, while warming shifts potassium back into the serum)

22. 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

23. COOLING PHASE Shivering
Thermoregulatory reflex to hypothalmic set point
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. (NO neuromuscular drug holiday during the cooling phase!)
Cutaneous warming can be used (anterior surface)
Administration of Magnesium
(Shivering is a MAJOR concern because it generates heat and impairs the ability to achieve and maintain the target temperature.)
Range for shivering (37-35??)
difficult to achieving and maintaining goal temperature during shivering (1–3). This is an integrated thermoregulatory reflex triggered by a
core body temperature that is lower than the hypothalamic set point
, the shiver
found that by covering the entire anterior surface, sparing the neck and face, surface CW is beneficialing–vasoconstrictive response can be combated by altering the cutaneous response to changes in body temperature
Additional targeting of the cutaneous vasoconstrictive response, however, may
still be possible with the intravenous administration of magnesium. As seen in this study and previous assessments of
shivering (1), hypomagnesemia is a risk factor for not only baseline shivering but also response to surface CW. Magnesium at high doses reduces the shivering response or increases the rate of achieving mild hypothermia in healthy volunteers (26) and postoperative patients (27–29).

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

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

26. 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)

28. Sentara Norfolk General Hospital
SNGH’s Experience
Level I
Level I trauma centers have an organized trauma response and are required to provide total care for every
aspect of injury, from prevention through rehabilitation. These facilities must have adequate depth of resources
and personnel with the capability of providing leadership, education, research, and system planning
Virginia Trauma Center standards are based upon national standards put forth by the American College
of Surgeons and the American College of Emergency Physicians. The Virginia standards are reviewed
and updated based on changes in the national standards as well as the evolving needs of the Trauma
System in Virginia.
Sentara Norfolk General Hospital
Level I Trauma Center

29. Sentara’s Background Information
2007
2008
2009
2010 ?
VBEMS

30. SNGH TH Patients
2008 – total of 3 pts, 1 incomplete, 1 expired & 1 to SNF
2009 – 11 pt attempted, 2 incomplete, 7 expired, 1 SNF & 1 D/C home
2010 – 11 pts. 2 incomplete, 4 exp. 2 SNF(long-term unknown tx to NJ asDNR), 3 D/C
NNT in studies 6-7

31. Sentara Hospitals Combined Experience

32. SHH Combined Experience: Patients Treated

33. SHH Combined Experience: Survivors

34. 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.