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Mr. A, 60, who has a history of coronary artery disease (CAD), suffers cardiac arrest while riding in a car with a friend. His friend drives him to a nearby fire station, where paramedics quickly begin CPR and attach Mr. A to an automated external defibrillator. After being defibrillated twice for ventricular fibrillation (VF), he's stabilized. The paramedics transport him to a nearby medical center.
On arrival, Mr. A experiences a -second cardiac arrest, requiring defibrillation and endotracheal intubation. Although he's in normal sinus rhythm with a pulse, he remains comatose and the decision is made to utilize -therapeutic (also known as induced) hypothermia.
ACCORDING TO 2010 American Heart Association (AHA) data, out-of-hospital cardiac arrest affects up to 295,000 people each year in the United States. Less than 7% survive; of those who do, up to two-thirds suffer neurologic impairment.1,2 Many of these patients don't have the resources for the type of care they need and may potentially live the rest of their lives in extended-care facilities.
Therapeutic hypothermia (TH) may help prevent or minimize neurologic impairment in certain patients after cardiac arrest.3 This article takes a look at when TH is used and how to care for patients who are undergoing this intervention.
TH involves decreasing the body's core temperature in an attempt to protect the brain from neurologic injury after a cardiac arrest. Cooling interrupts the injury to the brain. The 2010 AHA Guidelines for CPR and Emergency Care and the International Liaison Committee on Resuscitation recommend TH for comatose adult patients with return of spontaneous circulation (ROSC) after out-of-hospital VF cardiac arrest.2,3 They also recommend that TH be considered for comatose adult patients with ROSC after in-hospital cardiac arrest of any initial rhythm or after out-of-hospital cardiac arrest with an initial rhythm of pulseless electrical activity (PEA) or asystole. The guidelines recommend cooling patients who meet the above criteria to 32[degrees] C to 34[degrees] C (89.6[degrees] F to 93.2[degrees] F) for 12 to 24 hours.2,3
The mechanism of injury as a result of cardiac arrest occurs due to the connection between ischemia and reperfusion. Ischemia/reperfusion (I/R) injuries involve the lack of blood flow (oxygen and nutrients) to an area of the body and the associated events that occur once that blood flow is restored. The brain is subject to I/R injury as well. I/R injuries cause an inadequate supply of oxygen and -glucose, forcing the cells into anaer-obic metabolism. Loss of adenosine -triphosphate (ATP) and acidosis also inhibit the mechanisms that normally deal with excessive intracellular calcium in addition to failure of sodium/potassium pumps without adequate ATP. Excess calcium influx into the cells results in mitochondrial dysfunction and the release of other intracellular enzymes, which lead to the excess production of glutamate, an excitatory neurotransmitter. This permanent, prolonged cellular state of excitation leads to cellular death.4
During TH, cellular metabolism and oxygen demand slow while maintaining an adequate level of ATP.5 ATP is crucial to stabilize the cell because it serves to maintain normal calcium, sodium, potassium, and acid/base balance to prevent the eventual cycle that leads to cell death.4
Besides ion pump disturbances and neuroexcitability, free radical production plays a role in I/R injury. Free radicals increase in the post-arrest state and can oxidize and damage numerous cellular components. Although the brain normally has mechanisms that effectively fight against these compounds, the production is so high during the post-arrest phase that the brain becomes overwhelmed. As body temperature is lowered, free radical production decreases in a linear fashion, allowing the cell to repair itself rather than suffer permanent damage or death.4
After ischemia and during reperfusion, the body releases proinflammatory mediators (tumor necrosis factor-alpha, interleukin-1, macrophages, and neutrophils) starting around 1 hour and lasting up to 5 days after injury. These inflammatory mechanisms overwhelm the already injured cells and result in cellular death. Destructive effects of the inflammatory cascade are significantly slowed below 35[degrees] C (95[degrees] F), making TH an effective way to combat the injury caused by the arrest.5
Initiating TH with ROSC decreases free radical production, inflammatory pathways, cellular apoptosis, and nec-r-osis to prevent neurologic injury once oxygenated blood flow is restored to the brain.6
Mr. A is evaluated for the most likely cause of his cardiac arrest. Family members provide his history of CAD. The cardiology team is consulted and Mr. A is taken to the cardiac catheterization lab. The patient undergoes angioplasty and stenting of his left anterior descending coronary artery and his ejection fraction is down to 25% (from 45%, 2 years prior by records). He is in cardiogenic shock. An intra-aortic balloon pump and a pulmonary artery catheter are placed and he's transported to the cardiac ICU.
Certain inclusion and exclusion criteria are used to determine if TH should be used after cardiac arrest (see Is TH right for my patient?). This varies by facility. It's important to regain ROSC as quickly as possible, preferably within that 1-hour window of the arrest because the longer that ischemic period persists, the more damage is being done and the likelihood for a favorable outcome decreases.3 TH should be initiated no later than 10 hours after ROSC to achieve the desired effects.7
TH is an intensive intervention that can result in complications such as depressed myocardial function, dysrhythmias, coagulopathy, immunosuppression, fluid and -electrolyte imbalances, and slowed drug metabolism.4 It's important that TH doesn't preclude or interfere with the ability of the patient to be taken to the cardiac catheterization lab as was demonstrated with Mr. A.
TH can be used in combination with immediate coronary angiography and/or percutaneous coronary intervention. Combining the two essential therapies hasn't been shown to increase cardiac or neurologic risks.7 Many cardiac arrests result from a coronary artery occlusion, so evaluation and treatment of the causative factor is still the highest priority.8 Depending on the type of device used, cooling may continue during the cardiac catheterization. Ice packs placed in the axilla or cold I.V. fluids as appropriate may be another option if time and patient presentation permit.
Upon admission to the cardiac ICU, Mr. A's hemodynamic status is closely monitored while he reaches the goal temperature of 33 C (91.4[degrees]F) at 18:30, just 3 hours after arrival to the ED. At this time, he's receiving vasopressor support to maintain his mean arterial pressure and continuous infusions of anxiolytic, analgesic, and paralytic agents (paralytics are sometimes used to control shivering). Mr. A's lab results, such as serial coagulation profiles and basic metabolic panels, are monitored frequently to assess for -complications. He remains at his goal temperature of 33[degrees] C (91.4[degrees] F) with the assistance of an external cooling device until 18:30 the following evening, at which time the device is set to rewarm at 0.3[degrees] C per hour.
Initial cooling begins with an infusion of iced isotonic fluid of 0.9% sodium chloride or lactated Ringer's solution (30 mL/kg) and placement of ice packs to the groin, axillae, and around the head. Various mechanisms for cooling are available, ranging from the use of iced, wet sheets and fans to invasive and noninvasive commercially available devices.
Invasive devices available involve the insertion of a central venous catheter that cools the patient from within via a cold balloon or the circulation of cold saline. External devices involve the placement of pads or blankets on the patient that are prechilled. One such external device utilizes gel pads that transfer heat from the patient to the pads, which are thermostatically controlled from a patient-regulated feedback and cool the patient at set rates noninvasively.9 Whichever method is used, the patient's core body temperature is best continuously monitored by pulmonary artery catheter, a bladder catheter-temperature probe (in nonanuric patients), or an esophageal probe.3 Axillary and oral temperatures are inadequate for measurement of core temperature changes, especially -during active manipulation of temperature for TH.
Patients undergoing TH require close BP monitoring and continuous cardiac monitoring for dysrhythmias. Advanced hemodynamic monitoring may or may not be appropriate depending on the patient's condition, but TH alone doesn't necessarily require pulmonary artery catheter placement. These patients usually benefit from the placement of a central venous catheter and an arterial line for continuous BP monitoring.
A known complication of TH is bleeding risk. For every 1[degrees] C drop in temperature, coagulation-factor function decreases by 10%, and body temperature below 34[degrees] C (93.2[degrees] F) adversely affects the coagulation cascade. This is particularly important for patients with invasive lines in terms of the timing of the line placement, subsequent monitoring of the lines, and any arterial sheath removal following -cardiac catheterization. Institute bleeding precautions and monitor the vascular access insertion sites.
Dysrhythmias are a potential complication of the hypothermic state and should be anticipated. Sinus bradycardia generally follows as temperatures drop below 35.5[degrees] C (95.9[degrees] F), with a progressive decrease in heart rate as temperature continues to decline. This decline results from a decrease in repolarization of sinoatrial node cells.8 ECG changes include a prolonged PR interval, widened QRS complex, and a prolonged QT interval. This bradycardia usually doesn't require treatment depending on the patient's hemodynamic response; if deemed necessary, however, isoproterenol or dopamine may be administered. Atropine isn't effective in the hypothermic state.8
If the heart rate doesn't drop in conjunction with the temperature, the patient may not be sedated adequately. Atrial fibrillation may also occur, as well as recurrent pulseless ventricular tachycardia and VF. This is generally seen when temperatures are lower than target for TH (less than 30[degrees] C [86[degrees] F]), which further supports close monitoring of the patient. BP management and support may be required through the use of vasopressors and/or volume replacement.8 The vasoconstrictive effect of hypothermia results in an increase in systemic vascular resistance, increasing the potential for a slight increase in BP (10 mm Hg). Most of these patients will also develop a systemic inflammatory response syndrome (SIRS) and subsequent decreased vascular tone.8 The individual response from each patient is difficult to predict and must be closely monitored.
Throughout rewarming, vasodilatation may occur, causing hypotension and further adjustments to the treatment plan. Assess for the development of seizure activity and initiate seizure precautions.10 Continuous EEG monitoring and a neurology consult early on may be appropriate if the patient develops seizure activity.
Because of the changes in temperature, assess patients and control any shivering they may experience. Shivering is the body's natural response to being cold, but it's contrary to the goal of TH.11 Wrapping the patient's hands, feet, and head in blankets can create the sensation of warmth and diminish the shiver response. Patients may respond to magnesium, clonidine, dexmedetomidine, and meperidine.11 Administering paralytic agents can also control shivering.6 Paralytics are administered simultaneously with analgesics and anxiolytics, and are titrated to eliminate shivering.
Bispectral index (BIS) monitoring can directly monitor the patient's level of consciousness and help ensure an adequate level of anesthesia. BIS monitoring noninvasively measures electrical brain activity and reports a score that's correlated with level of sedation or level of anesthesia.
Monitor lab test results frequently with an emphasis on serum electrolytes. This is partly due to "cold diuresis," which requires significant attention to fluid status and the replacement of fluids and electrolytes as indicated.6 During hypothermia, potassium is lost with cold-induced diuresis, as well as shifts of potassium from the extracellular fluid (ECF) compartment to the intracellular fluid (ICF) compartment. During rewarming, hypokalemia will be partially corrected as potassium shifts from the ICF to ECF compartment. As a result, the repletion of potassium during the cooling phase should be done judiciously expecting that upon warming, the levels will rise to some degree. Magnesium and phosphorus are also impacted and should be replaced because they're also lost with diuresis. Preventing hypomagnesemia may help decrease the incidence of dysrhythmias.6
Glucose is also affected by the hypothermic state and levels tend to rise. Aggressive management of hyperglycemia is encouraged to prevent adverse neurologic outcomes associated with hyperglycemia.6 Follow coagulation profile results to assess bleeding risk.
Monitor the patient's white blood cell count to help assess for infection.6 Hyperglycemia will also increase infection risk. Also, if the cooling device requires more energy to keep the patient cold, this may indicate that the patient is fighting a higher temperature, which may be a cause for concern.
Monitor temperature-corrected arterial blood gas results as the patient's clinical status requires.7 -Verify with the hospital lab to determine at what temperature the blood gas sample must be labeled as a temperature-corrected sample, which alters the results of the gases significantly if the test isn't done correctly.
Ileus is common during hypothermia. As prescribed, convert medications typically administered via an enteral tube to I.V. whenever possible due to the slowing of gastric motility during cooling.8
During your patient assessment, ensure adequate family support. Offer clergy support or child-life specialists if children are involved. Provide explanations in understandable terms and printed information as appropriate.
Mr. A is rewarmed at a rate of 0.3[degrees] C per hour. Ten hours later, when his temperature returns to 36[degrees] C (96.8[degrees] F), the sedatives, analgesia, and paralytics are discontinued. Within the next 24 hours Mr. A slowly wakes up and although still mechanically ventilated, he begins following simple commands. He's weaned from the mechanical ventilator, extubated, and given supplemental oxygen via nasal cannula. Mr. A is alert, responds to verbal commands appropriately, and demonstrates no evidence of neurologic impairment. Two days later, Mr. A undergoes placement of an implantable cardioverter defibrillator. He's discharged to home just 8 days after suffering sudden cardiac arrest.
The optimal duration of TH isn't fully understood. It's suggested that 24 hours is a reasonable goal, although protocols differ among various facilities.3 Once cooling is complete, the patient should slowly rewarm to normothermia.12
Regardless of the cooling method used, rewarming should occur at 0.3[degrees] C to 0.5[degrees] C per hour.5 Commercial intravascular cooling devices and external gel-pad devices can be set to slowly increase core body temperature per hour and help control the process and avoid complications of rapid rewarming, such as dangerous electrolyte shifts and rebound hyperthermia. During this time, monitor lab values and be aware that serum potassium will likely increase and glucose will likely decrease. Once the rewarming goal temperature is reached, discontinue paralytics, sedation, and analgesia as prescribed.
Neurologic outcomes in patients who've undergone TH may not be predictable initially after rewarming; it may take several days for a meaningful neurologic assessment.8 Gradual neurologic improvement may occur over the first several days of waking up, from mild disorientation to being fully alert and oriented. Each patient will experience a different level of neurologic recovery, and predicting the end result is difficult. This can be very frustrating for patients and their families, so provide support as needed.
Patients with a successful neurologic outcome will continue treatment related to the underlying cause of the cardiac arrest. The patient may be a candidate for an implantable cardioverter defibrillator to prevent a future cardiac event.
Teach patients about lifestyle cha-nges they can make to help prevent the progression of atherosclerosis and CAD. Discuss the importance of basic life-support training with the family.
If the patient isn't demonstrating signs of neurologic improvement 72 hours after rewarming and discontinuation of neuromuscular block agents, the goals of therapy, long-term outcomes, and the patient's and family's wishes are important to discuss. Brain death determination should be sought judiciously with a full neurologic evaluation.10 This is often difficult because the family has just spent several days in hopeful anticipation that TH would result in the return of their loved one to the prearrest state. No final decisions need to be made at this point because it may take up to 7 days for results to be seen. Be transparent and honest with the family in preparation for a positive or unfavorable outcome.
The use of TH in patients after cardiac arrest can help them avoid brain damage and other serious complications. Knowing how to closely monitor patients undergoing TH can help ensure the best possible outcomes.
* pulseless VT or VF
* unresponsive after ROSC
* between ages 18 and 75.
Unresponsiveness includes inability to follow commands, lack of speech, no eye opening, and no purposeful movement to noxious stimuli. Positive brain reflexes and posturing are permissible. Patients experiencing other pulseless arrests, such as PEA and asystole may be candidates at the discretion of the attending physician, although further research is required in addressing these patient populations.
* return of consciousness
* terminal state
* preexisting comatose state
* major trauma
* recent major surgery
* medically refractory cardiogenic shock
* continued hemodynamic instability.
Sources: Anderson R. Ask the experts. Crit Care Nurse. 2007;27(5):61-62; Oddo M, Schaller MD, Feihl I, Ribordy V, Liaudet L. From evidence to clinical practice: effective implementation of therapeutic hypothermia to improve patient outcome after cardiac arrest. Crit Care Med. 2006;34(7):1865-1873.
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