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MR. S, 57, EXPERIENCED a foreign body airway obstruction and subsequent cardiac arrest while eating lunch at work. His coworkers called 911 and began CPR; an automated external defibrillator (AED) wasn't available. Paramedics responded to the scene, found Mr. S in pulseless ventricular tachycardia (VT), performed rapid defibrillation, ensured continued high-quality CPR, established peripheral venous access, administered I.V. epinephrine, and intubated him. Return of spontaneous circulation (ROSC) occurred after an estimated code time of 16 minutes. He arrived at the ED unresponsive in sinus bradycardia. His medical history includes hypertension and type 2 diabetes.
Mr. S may be a candidate for therapeutic hypothermia. Prompt intervention could help to reduce the potential for further neurologic decline. Understanding the link between the pathophysiology of cardiac arrest and the physiology underlying therapeutic hypothermia can facilitate the nursing management of this challenging patient.
Each year, nearly 383,000 out-of-hospital sudden cardiac arrests occur, and 88% of these occur at home.1 Only about 33% of those who experience an emergency medical services (EMS)-treated out-of-hospital cardiac arrest report symptoms within 1 hour of arrest. Fewer than 25% of EMS-treated out-of-hospital cardiac arrest victims have an initial rhythm of ventricular fibrillation (VF) or VT or have a shockable rhythm analyzed by an AED.2
Therapeutic hypothermia, a controlled reduction of core body temperature to 89.6[degrees] F to 93.2[degrees] F (32[degrees] C to 34[degrees] C), is used in patients who don't regain consciousness after ROSC following cardiac arrest. How does therapeutic hypothermia help the body? Cardiac arrest can result in global ischemia, direct cell damage, and cerebral edema, leading to a high rate of cerebral ischemia. Hypoxic brain injury directly results in neuronal damage and cerebral edema. The earliest rationale for the effects of hypothermia as a neuroprotectant was based on the slowing of cellular metabolism that results from a drop in body temperature. For every 1.8[degrees] F (1[degrees] C) drop in body temperature, cellular metabolism decreases by 5% to 7%.3 Consequently, hypothermia protects the brain and preserves neurologic functioning long term.
Direct cellular damage from cardiac arrest is related to decreased adenosine triphosphate (ATP) production. Cells need ATP for energy to move ions (electrolytes) through the cells. Without oxygen, cells can't produce ATP, leading to abnormal ion flux. Excess extracellular potassium can lead to further cardiac instability and dysrhythmias, and excess intracellular sodium causes cellular edema. In addition, excess intracellular calcium harms the cells' mitochondria, further suppressing ATP production.4
Research shows that a moderate decrease in temperature strengthens the cellular membrane and helps decrease abnormal ion flux. Thus, hypothermia creates an environment that prevents the influx of unwanted ions after the ischemic event. Therapeutic hypothermia appears to limit the trauma resulting from ischemia by moderating the disruption of cellular homeostasis caused by ischemia.5
Therapeutic hypothermia also is effective in reducing reperfusion injury. Several inflammatory immune responses occur during reperfusion to tissues after an ischemic event such as a cardiac arrest. Oxidative stress causes damage by releasing free radicals, and the inflammatory response can lead to increased intracranial pressure (ICP). An increase in ICP can lead to additional cellular injury and, at times, cell death. Finally, therapeutic hypothermia decreases overall cellular demand for oxygen by reducing metabolism. This further decreases the chain of events leading to reperfusion injuries.6
Therapeutic hypothermia for patients with ROSC after cardiopulmonary arrest has been found to result in positive patient outcomes. In 2010, the American Heart Association (AHA) revised its guidelines to recommend therapeutic hypothermia for any patient who had ROSC after cardiac arrest and was comatose.7
Selection criteria for therapeutic hypothermia vary by facility, so know the facility's inclusion and exclusion criteria. Rapid and proper identification of candidates is key to starting therapeutic hypothermia promptly.
Patients who are candidates for therapeutic hypothermia typically:
* are over age 18.
* are resuscitated from cardiac arrest with an initial rhythm of VF, pulseless VT, pulseless electrical activity, or asystole.
* are hemodynamically stable (with or without vasopressor administration).
* are endotracheally intubated and mechanically ventilated.
* arrive at the facility within 6 hours of cardiac arrest and are pulseless for less than 60 minutes.
* have a Glasgow Coma Scale score less than 8 after ROSC.
Therapeutic hypothermia isn't appropriate for patients who are pregnant, patients who have do-not-resuscitate or do-not-intubate orders, patients with significant trauma or uncontrolled bleeding, patients who've recently had surgery, and patients with severe bradycardia, minimal premorbid cognitive status, or intracranial hemorrhage.8,9
The cooling methods used in therapeutic hypothermia are evolving, with new techniques introduced each year.
Noninvasive methods include ice packs, fans, alcohol baths, and cooling blankets not attached to automatic temperature control modules.10 Studies have found these cooling methods extremely effective in reducing body temperature. However, they can be labor-intensive, and maintaining the target temperature of 89.6[degrees] F to 93.2[degrees] F can be difficult.11 The patient's temperature must be closely monitored via an esophageal, bladder, pulmonary artery, or rectal temperature probe, and interventions regulated to achieve and maintain the target temperature.10 In some instances, this may require 1:1 nursing care. Because of the lack of specific guidelines, these noninvasive cooling methods also place a burden on nursing judgment.
Recent advancements in noninvasive cooling methods have helped decrease the labor intensity and risks involved with therapeutic hypothermia. Examples include gel pads that are placed on the patient's skin to cover about 40% of the body. Water circulates through the pads using a negative pressure system, minimizing the risks of leaks compared with other devices. The pads and a patient temperature source are connected to a console that automatically adjusts water temperature to achieve and maintain the target temperature.10 This system is generally well tolerated and can achieve temperature control with less complexity than most invasive methods. However, pitfalls of this device include high costs and potential for rare but serious skin complications such as skin breakdown secondary to peripheral vasoconstriction.11
A cold water immersion system using a portable suit has been shown to cool human-sized swine to 91.4[degrees] F (33[degrees] C) within 45 minutes.11 A continuous flow of water is cycled over the patient and through a pump, drawing heat off the body in a much more rapid process than gel pads or cooling blankets. As the patient reaches the target temperature, the water is drained off the patient and the suit discarded. The patient will remain cool for another 12 to 24 hours.
Risks of this system include unrecognized electrolyte shifts, intrinsic dangers of defibrillating a patient immersed in water, and potential for overcooling. Also, the suit is used only for induction; it has no mechanism for maintaining target temperature, so other methods must be used to maintain and rewarm patients.11
A drawback to all noninvasive external cooling methods is that they're less efficient in reducing the temperature of target organs such as the brain and the heart.12
Invasivemethods provide rapid induction of hypothermia and are very efficient at cooling target organs. One method involves administration of large volumes of ice-cold (39.2[degrees] F [4[degrees] C]) I.V. fluids such as 0.9% sodium chloride solution, lactated Ringer's solution, and albumin. The typical infusion is 30 to 40 mL of fluid per kilogram of body weight over 30 to 60 minutes. Large volumes of intravascular fluids are contraindicated in patients with pulmonary edema or chronic renal failure.12
Specialized machines using a closed-loop central venous access device (CVAD) inserted into the femoral vein also can be used for invasive cooling. Cold water circulates through balloons on the catheter tip, cooling the blood. These systems have been used extensively to cool cardiac arrest patients and the research suggests they provide excellent control throughout therapeutic hypothermia (see Phases of therapeutic hypothermia).11
Benefits of systems using a CVAD include the ability to administer vasopressors and caustic medications, monitor central venous pressure, and obtain specimens for intermittent central venous oxygen saturation (ScvO2) analysis. Drawbacks include the delay in starting therapeutic hypothermia while the specialized catheter is placed; risks of catheter-related injury, infection, or thrombosis; and the inability to place this catheter in certain settings such as an ambulance. Although invasive methods such as these systems can be expensive compared to noninvasive methods, the cost may be offset by the decrease in nursing time and complications, and improved patient outcomes.11
The principal role of the induction nurse is to initiate, and often complete, this phase. If induction occurs in the ED, patients are quickly transferred to the ICU for continued care.
Because of the physiologic changes caused by hypothermia, collect baseline data so these changes can be monitored and addressed as needed. Baseline data should include vital signs, SpO2, 12-lead ECG, chest X-ray, arterial blood gas analysis, complete blood cell count, prothrombin time, international normalized ratio, partial thromboplastin time, basic metabolic panel, amylase, lipase, troponin, lactate, toxicology screen, blood cultures, urinalysis, urine culture, sputum cultures (if appropriate), and a pregnancy test for women of childbearing age. A head computed tomography scan should be obtained if intracranial bleeding is suspected.
Thoroughly assess the patient's neurologic status, skin integrity, and pain intensity.9 Pain assessment in unresponsive patients is challenging. Consider using bispectral index monitoring or electroencephalography (EEG) monitoring during therapeutic hypothermia.8,13 Although no standard guidelines exist for how to best assess and manage pain in these patients, I.V. sedation and analgesia are recommended.
All patients should be endotracheally intubated and have an orogastric or nasogastric tube, an indwelling urinary catheter, a CVAD or a minimum of two peripheral venous access devices, and a core temperature sensing device in place before induction can begin.8 Cooling should begin as soon as possible, the target temperature achieved within 4 hours of ROSC, and the temperature maintained for 12 to 24 hours from the start of induction.7 Because of the effects of hypothermia on the cardiac conduction system, an initial tachycardia, followed by bradycardia, is common. Don't let the patient's temperature fall below 89.6[degrees] F (32[degrees] C).
A heart rate of 40 to 45 beats/minute is considered ideal for a patient undergoing therapeutic hypothermia.5 Additional hypothermia-related ECG changes include a widened QRS complex, prolonged PR interval, and the development of Osborn waves (prominent J waves; see Making waves). These changes are often benign and don't require treatment. If necessary, the heart rate can be increased by rewarming the patient, transvenous or transcutaneous cardiac pacing, or by administering I.V. infusions such as dopamine or epinephrine.13
However, increasing the heart rate can decrease myocardial contractility. As long as the patient's core temperature is greater than 86[degrees] F (30[degrees] C), the overall risk of developing a cardiac dysrhythmia is low.5
At temperatures below 86[degrees] F (30[degrees] C), patients are more likely to develop life-threatening dysrhythmias that may be refractory to defibrillation or medications. Patients can develop atrial fibrillation (AF), which can progress to VF. If the patient becomes extremely bradycardic and chest compressions are performed, the patient can convert from a sinus rhythm to AF, VT, or even VF due to the increased irritability of the cold myocardium.
Monitor for physiologic changes associated with therapeutic hypothermia, such as shivering, the body's natural defensive response to cold. (Cold skin surface temperatures can reduce the shivering threshold by up to 20%.)14 Shivering interferes with therapeutic hypothermia by increasing oxygen consumption and energy expenditure, thereby raising body temperature.
Controlling shivering is of paramount importance and should begin with nonpharmacologic measures: apply surface counterwarming to the patient's face, hands, and feet. If this is ineffective, quickly proceed to more aggressive pharmacologic interventions as prescribed. Meperidine, an opioid, is often the drug of choice to reduce shivering; its antishivering effects may be enhanced by concurrent administration of buspirone or dexmedetomidine. A magnesium sulfate infusion causes vasodilation and can decrease shivering. Propofol can also reduce shivering by decreasing vasoconstriction. If these drugs are ineffective, neuromuscular blockers such as vecuronium may be prescribed to inhibit the vasomotor response to the shivering reflex elicited in the central nervous system.14
If a patient needs drugs to control shivering, monitor for adverse drug effects. Magnesium and buspirone may lower BP; dexmedetomidine may exacerbate bradycardia; and meperidine and vecuronium may lower the seizure threshold, putting a population already predisposed to seizure activity at even higher risk. Patients undergoing therapeutic hypothermia who are receiving neuromuscular blockers should be monitored via continuous EEG to observe for seizure activity that might otherwise go undetected.14
Be aware that therapeutic hypothermia may decrease the body's ability to clear many commonly used drugs, including norepinephrine, morphine, phenytoin, propofol, midazolam, vecuronium, and nitrates. Healthcare providers may be able to achieve the desired patient response with lower doses than might otherwise be required.13
Insulin resistance is associated with hypothermia, so closely monitor the patient's blood glucose levels and administer insulin infusions as prescribed for optimal glycemic control.9 Diuresis and associated electrolyte shifts (particularly reductions in potassium, phosphorus, and magnesium) also are common, making volume and electrolyte replacement critical nursing interventions.8 Measure the patient's urine output at least every 2 hours and administer ongoing fluid therapy to replace the volume lost through cold-induced diuresis. Closely monitor the patient's vital signs along with CVP and ScvO2 to monitor perfusion and fluid status.9
Supportive care should also include ensuring skin integrity and providing venous thromboembolism prophylaxis. Patients who are paralyzed or heavily sedated are at risk for eye injury such as corneal abrasion. Follow the facility's policy for eye care. Also follow evidence-based practice for preventing ventilator-associated pneumonia, including elevating the head of the bed 30 degrees unless contraindicated, providing continuous subglottal suctioning, and performing comprehensive oral hygiene.15,16
Rewarming should be started 24 hours after the start of cooling, and should be done slowly, usually over 6 to 12 hours, to prevent the hypotension and rapid shifts in fluid volume and electrolytes associated with vasodilation. The patient's potassium and glucose levels will likely start to rebound during this phase, so expect possible decreases in blood glucose and ensure that all potassium-containing fluids have been stopped.7 Discontinue neuromuscular blockade once the patient's temperature is greater than 96.8[degrees] F (36[degrees] C), after which sedation can be weaned as well.9
Determining neurologic outcomes in patients who undergo therapeutic hypothermia after cardiac arrest is challenging. The medications used for sedation and neuromuscular blockade during therapeutic hypothermia can make clinical assessment unreliable. Diagnostic testing such as magnetic resonance imaging, EEG, and somatosensory evoked potentials are also used.17
The American Academy of Neurology reports that patients who exhibit absent corneal, pupillary, and motor responses, or who have extensor posturing 72 hours after rewarming, have a poor clinical prognosis. Delaying neurologic prognostication until at least 72 hours after rewarming is recommended by the AHA and the International Liaison Committee on Resuscitation.18
Nursing care of families is essential during their loved one's critical illness. Frequent nurse-family meetings can help to acknowledge the family's suffering and vulnerability, as well as giving families an opportunity for honest, sensitive communication about the patient and ongoing interventions.19
Mr. S was considered a good candidate for therapeutic hypothermia, which was initiated in the ED. After being rapidly cooled, he was transferred to the ICU. On day 3, he was awake and responding to simple commands. On day 4, Mr. S was extubated. He demonstrated some mild neurologic deficits (extremity weakness and slowed speech) and was discharged to a rehabilitation facility on day 10.
Therapeutic hypothermia for select patients experiencing ROSC after cardiac arrest is a valid intervention in which nurses play a vital role. Understanding the physiologic basis for therapeutic hypothermia, as well as the responsibilities related to patient care, are the keys to achieving optimal patient outcomes.
Induction: During this phase, the patient's temperature is brought down to the target temperature.
Maintenance: This is the longest phase of therapeutic hypothermia, lasting 12 to 24 hours, during which the patient is maintained at the target temperature.
Rewarming: During this phase, the patient is returned to normothermia.
1. American Heart Association. CPR statistics. 2011. http://www.heart.org/HEARTORG/CPRAndECC/WhatisCPR/CPRFactsandStatistics_UCM_3075. [Context Link]
2. Roger VL, Go AS, Lloyd-Jones DM, et al. Heart disease and stroke statistics-2011 update: a report from the American Heart Association. Circulation. 2011;123(4):e18-e209. [Context Link]
3. Kammersgaard LP, Jorgensen HS, Rungby JA, et al. Admission body temperature predicts long-term mortality after acute stroke: the Copenhagen Stroke Study. Stroke. 2002;33(7):1759-1762. [Context Link]
4. Huether SF, McCance KL. Understanding Pathophysiology. 5th ed. St. Louis, MO: Elsevier Mosby, Inc.; 2012. [Context Link]
5. Polderman KH, Herold I. Therapeutic hypothermia and controlled normothermia in the intensive care unit: practical considerations, side effects, and cooling methods. Crit Care Med. 2009;37(3):1101-1120. [Context Link]
6. Lampe JW, Becker LB. State of the art in therapeutic hypothermia. Annu Rev Med. 2011;62:79-93. [Context Link]
7. Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: post cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Care. Circulation. 2010;122(18 suppl 3):S768-S786. [Context Link]
8. Therapeutic Hypothermia Protocols. Hospital of the University of Pennsylvania post-cardiac arrest care pathway. Perelman School of Medicine, University of Pennsylvania. 2012. http://www.med.upenn.edu/resuscitation/hypothermia/protocols.shtml. [Context Link]
9. Hypothermia protocol for resuscitated cardiac arrest. John Dempsey Hospital, Department of Nursing, University of Connecticut Health Center. 2010. http://nursing.uchc.edu/unit_manuals/emergency_dept/docs/Hypothermia%20Protocol%. [Context Link]
10. McKean S. Induced moderate hypothermia after cardiac arrest. AACN Adv Crit Care. 2009;20(4):342-353. [Context Link]
11. Seder DB, Van der Kloor TE. Methods of cooling: practical aspects of therapeutic temperature management. Crit Care Med. 2009;37(suppl 7):S211-S222. [Context Link]
12. Lee R, Asare K. Therapeutic hypothermia for out-of-hospital cardiac arrest. Am J Health-Syst Pharm. 2010;67(15):1229-1237. [Context Link]
13. Deckard M, Ebright P. Therapeutic hypothermia after cardiac arrest: what, why, who, and how. Amer Nurse Today. 2011;6(7):23-28. [Context Link]
14. Presciutti M, Bader MK, Hepburn M. Shivering management during therapeutic temperature modulation: nurses' perspective. Crit Care Nurse. 2012;32(1):33-42. [Context Link]
15. American Association of Critical-Care Nurses. Ventilator-associated pneumonia. 2009. http://www.aacn.org/wd/practice/content/vap-practice-alert.pcms?menu=practice. [Context Link]
16. American Association of Critical-Care Nurses. Oral care for patients at risk for ventilator-associated pneumonia. 2010. http://www.aacn.org/wd/practice/content/oral-care-practice-alert.pcms?menu=pract. [Context Link]
17. Blondin NA, Greer DM. Neurologic prognosis in cardiac arrest patients treated with therapeutic hypothermia. Neurologist. 2011;17(5):241-248. [Context Link]
18. Perman SM, Kirkpatrick JN, Reitsma AM, et al. Timing of neuroprognostication in post cardiac arrest therapeutic hypothermia. Crit Care Med. 2012;40(3):719-724. [Context Link]
19. Nelms T, Eggenberger SK. The essence of the family critical illness experience and nurse-family meetings. J Fam Nurs. 2010;16(4):462-486. [Context Link]
Bernard S. Hypothermia after cardiac arrest: expanding the therapeutic scope. Crit Care Med. 2009;37(suppl 7):S227-S233.
Dumas F, Grimaldi D, Zuber B, et al. Is hypothermia after cardiac arrest effective in both shockable and nonshockable patients? Insights from a large registry. Circulation. 2011;123(8):877-886.
Sagalyn E, Band RA, Gaieski DF, Abella BS. Therapeutic hypothermia after cardiac arrest in clinical practice: review and compilation of recent experiences. Crit Care Med. 2009;37(suppl 7):S223-S226.
Wartenberg KE, Mayer SA. Use of induced hypothermia for neuroprotection: indications and application. Future Neurol. 2008;3(3):325-361.
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