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Chill Out!!. Therapeutic Hypothermia Post Cardiac Arrest. Prepared and Presented by: Cameron Schmidt MS RN Clinical Teacher Critical Care Education. Chill Out!!. Introduction.

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therapeutic hypothermia post cardiac arrest

Chill Out!!

Therapeutic Hypothermia Post Cardiac Arrest

Prepared and Presented by:

Cameron Schmidt MS RN

Clinical Teacher

Critical Care Education

Chill Out!!

  • Clinically induced hypothermia is an evidence based intervention strategy that can improve the neurologic outcome of unconscious patients post sudden cardiac arrest
  • Brain temperature during the first 24 hours after resuscitation from Cardiac Arrest may have significant effect on survival and neurologic recovery
  • The goal is to obtain a core temperature of 32-34 degrees C.Our Goal:33degrees 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
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 con t
Pathophysiology Con’t
  • 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 con t1
Pathophysiology Con’t
  • 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 metabolismwhen pt is cooled to33C) for each degree Centigrade reduction in body temperature
other pathophysiology
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
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 con t
Complications Con’t
  • 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)
  • 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.
  • 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)
  • The body’s natural response to cold
  • The goal of cooling is to decrease VO2 therefore prevention of shivering is essential
  • Use sedatives and NMBA’s
    • These will be ordered on the pre-printed order form
  • 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 NMBA’s
shivering scale
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
Nursing Care of the Hypothermic Patient
  • RN’s must provide vigilant surveillance over the patients changing physical condition
nursing care con t
Nursing Care Con’t
  • The RN’s 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 (32-34 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
  • 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
  • Fentanyl and Morphine are preferred
train of four tof
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 NMBA’s may need to be decreased
  • DC NMBA’s at the beginning of rewarming
cardiac complications
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 con t
Cardiac Complications Con’t
  • 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
additional cardiac changes
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
  • 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
  • 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
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 PRC’s if hemoglobin is<10
  • 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
  • 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.