Therapeutic Hypothermia Post Cardiac Arrest

Prepared and Presented by: Cameron Schmidt MS RN Clinical Teacher Critical Care Education

Introduction
Clinically induced hypothermia is an evidence based intervention strategy that can improve the neurologic outcome of unconscious patients post sudden cardiac arrest

Introduction
Brain temperature during the first 24 hours after resuscitation from Cardiac Arrest may have significant effect on survival and neurologic recovery

Goals
The goal is to obtain a core temperature of 32-34 degrees C. Our Goal:33 degrees C (91.4 F) within 6 hours of the onset of cardiac arrest and to maintain core temperature of 32-34 degrees C for 24 hours, as this may decrease chances of death and increase chance of neurologic recovery

 Mild to moderate states of Hypothermia have been found to have a neuroprotective mechanism within the brain that can improve a patients outcome S/P Cardiac arrest

 Therapeutic Hypothermia provides several brain preserving effects, however it also has associated complications that require attentive Nursing Care and Interventions to prevent complications from therapy.

Pathophysiology and Adverse Effects

Cardiac Arrest Decreased perfusion (BP) Decreased Cerebral Oxygen delivery (causing neurological deficit) Cerebral Hypoxia Cerebral Edema Ischemia (Brain releases enzymes and experience intracellular ion changes that damage cellular mitochondria)

Pathophysiology Cont
APOPTOSIS (pre-programmed cellular death) Anaerobic Metabolism occurs Increased Calcium Increased hyper excitability in the brain cells Exacerbation of Hypoxemic state Cellular Death Increased Cerebral edema

Pathophysiology Cont
Blood Brain Barrier is Disrupted during low perfusion states Influx of fluid Worsening of Cerebral Edema

 Hypothermia slows neuroexcitory processes, stabilizing the influx of Ca, limiting cellular death and reducing disruption in the blood Brain Barrier therefore decreasing cerebral edema

 Apoptosis can last up to 48 hours after initial insult, which may explain why Therapeutic hypothermia is Neuroprotective.

 Cooling patients limits the negative effects from hypoxemia Inducing mild hypothermia slows cerebral metabolism, decreasing Cerebral metabolic rate by 5-7%(20-28% reduction in cerebral metabolism when pt is cooled to 33C) for each degree Centigrade reduction in body temperature

Other Pathophysiology
Therapeutic hypothermia suppresses ischemia induced inflammatory reactions Neutrophil and macrophage function decrease at temperature <35 degrees C Therefore. Decreased Cerebral edema.

Complications/Adverse Effects
There is a risk of infection due to changes in WBC function Mild Hypothermia induces insulin resistance and hyperglycemia results which increases risk of infection (Pulmonary and wound infections are the most common)
VAP oral care will be implemented

Complications Cont
Mild hypothermia causes mild bleeding from platelet dysfunction, may cause mild coagulopathies. Lab analysis of coagulation studies may not accurately report alterations in function because tests are usually performed on patients with body temps of 37 C therefore..
Nurses must observe for alterations in coagulation (delayed clotting)

Complications
Fluid and Electrolyte shifts occur during induction of hypothermia Mild Diuresis can occur with initiation of cooling
U/O replacement will be ordered on admission. Type and amount will be individualized on the order form

Hypothermia decreases Cardiac Output by 25% causing mild acidosis and increased serum lactate levels.
Lactate levels are drawn on admission and will be ordered prn.

Complications
Electrolytes shift because of changes in cellular membranes with ischemia and states of cellular acidosis (decreased MG, K, Ca Mg is Neuroprotective)
Labs will be drawn Q6hoursx24H (BMP,PT/PTT, CA, Mg, Po4, CBC diff)

Shivering
The bodys natural response to cold The goal of cooling is to decrease VO2 therefore prevention of shivering is essential Use sedatives and NMBAs
These will be ordered on the pre-printed order form

Shivering
Use shivering Scale Shivering Increase VO2 40-100% Early signs of shivering:
Decreased SVO2 Increased RR Facial Tensing Noise on EKG Palpation of muscle fasculations of face or chest Treat with sedatives and NMBAs

Shivering Scale
0- No Shivering 1- One or more of the following
Piloerection Peripheral vasoconstriction Peripheral cyanosis without other causes, but with visible muscular activity 2- Visible muscular activity confined to 1 muscle group 3- Visible muscular activity confined to 2 muscle groups 4- Gross Muscular activity involving the entire body If score is >2 for >5 minutes.Notify MD

Nursing Care of the Hypothermic Patient

RNs must provide vigilant surveillance over the patients changing physical condition

Nursing Care Cont

The RNs knowledge of Pathophysiology will require assessment of the following:
Prevention of rewarming during the cooling phase Electrolyte imbalances Arrhythmia recognition Prevention of infection Skin Care Pain/ Sedation management

 Prior to initiating hypothermia:

Perform a complete skin assessment Assess response to pain Perform baseline Neurological exam: This is essential to allow for comparison after therapies, as well as some patients wakeup prior to cooling thus Therapeutic Hypothermia would not be an option

 Once target temperature is reached, temperature needs to be maintained within target range (3234 degrees C) Temperature must be constantly monitored. Gaymar Mediterm III does this for you. It becomes a big thermometer!! Ensure cool air is not lost when performing nursing functions that may require removal of garments(this should be avoided at all cost) Must remove ice packs so temperature does not fall below 33c (20-25 minutes of application according to ECMC orders) Excessive cooling or overshooting the target temperature(<33C) puts the patient at risk for Moderate Hypothermia with significant complications
Gaymar Mediterm III when set, will maintain set point temp

Sedation
Monitor for effective analgesia and sedation without oversedating ( Pain Scale, SAS Scale) This maximizes patient comfort Benzodiazepines are effective sedative agents and inhibit neurotransmitters on the brain and decrease cerebral VO2
Lorazepam or midazolam drips

Propofol

Pain
Fentanyl and Morphine are preferred

Train of Four (TOF)

Must be established before initiating NMBA therapy Due to Peripheral Vasoconstriction during hypothermia, it may be difficult for ongoing TOF monitoring
If this occurs titrate NMB to prevent shivering

Hypothermia changes drug metabolism and pharmacokinetics Dosing of sedation, pain and NMBAs may need to be decreased DC NMBAs at the beginning of rewarming

Cardiac Complications
As temperature decreases, CO and SV decrease. SVR and BP increase in response to vasoconstriction Sinus Bradycardia is a common finding with cooling related to hypothermic myocardial depression. It is refractory to Atropine Risk of Dysrhythmias during MODERATE cooling is higher (<32C)

Cardiac Complications Cont

Skin will be pale and Pedal Pulses are often difficult to assess Osborne waves are seen in lateral precordial waves (V5, V6) Osborne Wave- a positive deflection notch on the down stroke of the QRS complex(at the junction between the QRS complex and the ST segment) Occurs due to delayed closing of the transient outward K current channels Not unique only to hypothermia, can also be seen with autonomic dysreflexia, hypercalcemia and cerebral injury

Osborne Wave

Additional Cardiac Changes

Wide QRS ST elevations or depressions T wave inversion QT prolongation These are caused by ischemia or acidosis and can occur for days after rewarming

Hyperglycemia
Due to insulin resistance Associated with increased infection Associated with increased incidence of Renal failure Insulin requirements are higher than normal to maintain normal glucose levels.
Sliding Insulin scale will be ordered

Electrolytes
Alterations are due to extracellular ion shifts Fluxuations in K, Mg, Ca occur Mg levels are treated to maintain normal to high levels due to its role mitigating neurological injuries
If Mg <1.7, MD may order 2 grams Magnesium Sulfate

K levels will drop during cooling and rise during rewarming

K will not be replaced unless K is <3 during the cooling phase

Immune Response/Hematologic
WBC decrease blood cultures may be ordered Cooling masks normal response to fever Platelets decrease
MD may order platelets if platelets <30,000 MD may order FFP (Vitamin K if on Coumadin) to correct INR>2

Hemoconcentration occurs due to loss of plasma through changes in vascular permeability and cold Diuresis For every 1 C decrease in temperature, the HCT increases by about 2%.
MD may order PRCs if hemoglobin is<10

Renal
Cold induced Diuresis due to decreased reabsorbtion of solute in the loop of henle Resistance to ADH If CO decreases too drastically, GFR will decrease.
If GFR decreased<30 ml/min Cisatricurium will be used as the NMB agent and Famotidine will be given Q24h instead of Q 12h

Conclusion
Hypothermia is evidenced-based practice proven to improve neurological outcomes of some unconscious cardiac arrest patients. Early interventions with hypothermic therapy offers a realistic approach to preventing severe neurological deficits post cardiac arrest. Critical Care and ED nurses that are knowledgeable in the management of patients during clinically induced hypothermia therapy can positively impact patient care and prevent adverse neurologic complications from sudden cardiac arrest, as well as prevent complications associated with this therapy.