The big chill: Improving the odds after cardiac arrest
RN/Thomson AHC Home Study Program
The big chill: Improving the odds after cardiac arrest
CE credit is no longer available for this article. (Expired May 2007)
Originally posted May 2005
By Patty Calver, RN, BSN, Theresa Braungardt, RN, BSN, Nicole Kupchik, RN, BSN, CCRN, Andrew Jensen, RN, BSN and Cynthia Cutler, RN , BA
The authors all work at Harborview Medical Center in Seattle. Ms. Calver is a clinical manager of quality improvement, Ms. Braungardt is a nurse manager in the medical and neurosurgical ICU, Ms. Kupchik and Ms. Cutler are assistant nurse managers in the CICU, and Mr. Jensen is a CICU staff nurse. The authors have no financial relationships to disclose.
Mild hypothermia has been standard practice with bypass surgery for years, but recent studies show that it has benefits after cardiac arrest, too.
When 53-year-old construction worker Bob Howard collapsed at home, his panicked wife called 911 and then tried frantically to revive him. After the ambulance arrived, paramedics resuscitated Mr. Howard, but he remained comatose.
Emergency physicians suspected that Mr. Howard may have suffered anoxic brain injury, but told his wife that further damage might be prevented with the help of a new treatment: They recommended cooling his body temperature to 91.4° F (33° C) in hopes of decreasing cerebral oxygen demand and reducing the likelihood of permanent brain damage.
The medical team stabilized Mr. Howard in the ED and with his wife's approval, initiated the hospital's non-traumatic cardiac arrest hypothermia protocol. The patient was placed on a ventilator and monitored in the ICU. After 24 hours, he was slowly rewarmed with blankets.
Mr. Howard woke up 36 hours later and was taken off the ventilator. He suffered no permanent brain damage, and his cardiac function was fully restored.
Mr. Howard was lucky. He received prompt on-site care and was taken to a facility much like Harborview Medical Center in Seattle, where we work, that had a protocol for therapeutic hypothermia following cardiac arrest. Though the treatment has been used since the 1950s to protect the brain from the effects of global ischemia during cardiopulmonary bypass surgery, it is anything but commonplace following cardiac arrest. But that is changing.
Studies back an approach that can help many
Cardiac arrest kills more than 90% of its victims before they reach the hospital, causing more than 300,000 deaths in the United States each year.1 Its onset is sudden and dramatic, typically related to ventricular tachycardia (VT), ventricular fibrillation (V fib), or both. Brain death can occur in four to six minutes.2
Cardiac arrest is often reversible if treated within a few minutes with CPR and an electric shock to the heart. The increasing availability of portable defibrillators can help, but defibrillation must be used immediately. Even after a successful resuscitation, the brain may suffer reperfusion injury from chemical reactions that occur when the blood starts to flow again.2,3
Recent landmark studies in Australia and Europe, however, show that inducing mild hypothermia—to a target range of 89.6° - 93.2° F (32° - 34° C) for 12 - 24 hours—can prevent brain damage and often save lives. The idea itself, however, has been a long time coming. The successful use of therapeutic hypothermia following cardiac arrest was reported in the late 1950s, but it waned because of uncertain benefits and difficulties with its use.4 But research continued, animal studies began to show progress, and then the results of the Australian and European studies were published in 2002.
In the Australian study, half of the 43 patients treated with hypothermia—91.4° F (33° C) for 12 hours—were discharged alive, compared to about a third of the 34 patients who received standard care.5 In the European study, more than half of the 136 hypothermic patients had a "favorable neurological outcome" at six months—meaning they were living independently—compared with less than 40% of the 137 patients who were given standard care. The European patients were cooled to 89.6° - 93.2° F (32° - 34° C) for up to 24 hours. 6
So how, exactly, does therapeutic hypothermia benefit these patients? Here's what we know:
When a patient is resuscitated, reperfusion sets off a series of chemical reactions that can continue for up to 24 hours, possibly causing significant inflammation in the brain. Inducing mild hypothermia decreases intracranial pressure, the cerebral metabolic rate, and the brain's demand for oxygen consumption. In addition, it is thought to suppress many of the chemical reactions associated with reperfusion injury, including free radical production, excitatory amino acid release, and calcium shifts, which can in turn lead to mitochondrial damage and apoptosis.4,7 The end result: Patients have a better chance of recovering with their neurological function intact.
Healthcare groups provide their support
In 2003, in response to the landmark study findings, the American Heart Association (AHA) endorsed the use of therapeutic hypothermia following cardiac arrest and the International Liaison Committee on Resuscitation (ILCOR), an umbrella group of specialists worldwide, issued a recommendation supporting its use.4
ILCOR's endorsement applied to use of this therapy only after resuscitation from out-of-hospital cardiac arrest due to V fib—the only specifications the research addressed. But the committee did raise the possibility of using induced hypothermia for patients with other causes of cardiac arrest and for in-hospital cardiac arrests.4
According to the ILCOR recommendations, cooling should be initiated as soon as possible after return of spontaneous circulation, but appears to be helpful even if delayed four to six hours. Many critical care clinicians routinely sedate and ventilate the lungs of comatose survivors of cardiac arrest for at least 12 - 24 hours, so application of therapeutic hypothermia over this period would be possible. Careful monitoring of temperature is important because of complications such as dysrhythmia, infection, and coagulopathy, which are likely to increase if the core temperature falls considerably below 89.6° F (32° C).4 Patients should be rewarmed slowly to avoid rebound hyperthermia—the literature recommends that the body be rewarmed at 1° - 2° F ( 0.5° - 1° C) every hour.8
However, despite the backing of ILCOR and the AHA, therapeutic hypothermia has yet to be broadly incorporated into emergency medical practice, suggests a recent national survey of 265 physicians in emergency medicine, critical care, and cardiology.1 Researchers found that more than three-quarters of respondents had not used hypothermia following cardiac arrest.
Their reasons were revealing: Many said there wasn't enough data to support its use. Others found cooling methods to be technically too difficult or slow. Still others noted that this therapy hadn't been incorporated into advanced cardiovascular life support (ACLS) protocols. In fact, the ACLS guidelines, published by the AHA, were last revised in 2000, before there was sufficient evidence to recommend the procedure.4
Teaching hospitals like ours have taken the lead
Our hospital has been using induced hypothermia since 2002, as have other major teaching hospitals nationwide.9 This approach is standard care at our medical center for post-cardiac arrest patients who are brought in asystolic, with V fib, pulseless VT, or pulseless electrical activity. Patients are resuscitated en route to the ED and transferred to the cardiac catheterization lab if the arrest is the likely result of coronary artery occlusion, or brought to the ICU if the arrest appears to have other causes.
The optimal timing for inducing hypothermia is still being studied, but it's believed that if resuscitation is delayed by 15 minutes, hypothermia would have little impact, because the severe brain damage that occurs cannot be reversed.
The active cooling process begins by placing a water-filled cooling blanket, set at 50° F (10° C), beneath the patient. For greatest effectiveness, the blanket must span more than 50% of the body surface area. Ice packs are added to the axilla, groin, and front and back of the neck, and a forced cool air blanket is draped over the patient.
At our center, we cool patients to 91.4° F (33° C) for up to 24 hours. An esophageal probe, which provides continuous monitoring of core temperature, is inserted through the mouth into the esophagus to the level of the heart, and then connected to an external monitoring device.
The cooling blankets and ice packs, however, may take up to six hours to lower the patient's temperature. What's more, cool air surrounding the body is lost each time the blanket is lifted for routine nursing care.
As a result, we're looking into a newer cooling method: a non-invasive device called the Medivance Arctic Sun, which uses pads that adhere to the skin to circulate cooled water. The pads are applied with a gel to the thighs, trunk, and back, leaving vital areas in the groin, neck, and chest exposed for lines, procedures, and elimination. A computer monitors the patient's temperature and automatically cools or warms the circulating water as needed.
At other facilities, cooling catheters inserted via a central vein into the superior vena cava, or femoral vein into the inferior vena cava, are being used. These include Radiant Medical's Set Point and the Alsius Corp.'s Cool Line. These catheters are similar in size to a dialysis catheter and use ice-cold fluid circulating in a closed circuit from an external refrigerator or pump, which effectively cools the blood.10
Nursing support is vital to therapy
In addition to the usual monitoring, critical care nurses' knowledge of potential complications associated with therapeutic hypothermia is essential.
Among them: Cooling shifts potassium into the cells, causing low serum potassium, while warming shifts potassium back into the serum. Potassium levels that are too high or low can cause lethal dysrhythmias. We replace potassium to keep levels within normal parameters and have not had a problem with hyperkalemia during rewarming.
Blood pressure also must be monitored carefully: It typically remains elevated during hypothermia as a result of peripheral vasoconstriction. More important to watch for is a drop during the warming phase. Medication is needed if the BP drops to less than 90 mm Hg systolic or the mean arterial pressure falls below 60.
Hypothermia is known to increase clotting time and to decrease platelets, putting patients at risk for thrombocytopenia or coagulopathy. It may also mask infection by causing neutropenia. Therefore, bleeding times, partial thromboplastin time (PTT), prothrombin time (PT), and international normalized ratio (INR) and CBC counts must be checked regularly during both the cooling and rewarming phases of treatment. Hypothermic patients are also at risk for aspiration and aspiration pneumonia, so good pulmonary hygiene and routine turning is essential.
The frequent repositioning combined with skin care is important because decreased circulation and peripheral capillary vasoconstriction can lead to skin breakdown. It may be necessary to pad bony prominences and the back of the head. Patients should also be monitored for minor frostbite of the fingers and toes.
Shivering, the body's attempt at maintaining homeostasis, is a major concern because it generates heat and impairs the ability to achieve and maintain the target temperature. We record shivering every hour and PRN on a shiver scale, a tool we devised to rate the severity of shivering in hypothermic patients. Shivering is assessed at four levels: 0-no shivering; 1-mild shivering (face and jaw fasciculations); 2-peripheral shivering; and 3-severe shivering (uncontrolled rigors).
At first, we responded by medicating the patient with meperidine (Demerol) and diazepam (Valium). We've since found that administering a neuromuscular blocking agent in conjunction with sedation leads to a rapid decrease in temperature and prevents shivering. Our orders now include a continuous vecuronium (Norcuron) drip.
Following successful hypothermic treatment and rewarming, patients are transferred out of critical care when they are extubated, require little oxygen, and are hemodynamically stable. They may go to a stepdown unit, such as telemetry, if they need further monitoring for dysrhythmia or an adjustment in their heart medication.
Induced hypothermia is a promising method to save lives. However, despite strong data supporting its use, many more questions remain to be answered —including how to best cool patients, how long they should be chilled, whether paramedics should be taught to initiate the procedure, and when it's too late to help.7 Another controversial issue is whether findings from animal experiments and published clinical studies are enough to extend the use of therapeutic mild hypothermia to patients who remain comatose after cardiac arrest from any rhythm, after in-hospital cardiac arrest, and after cardiac arrest in children.
In the meantime, induced hypothermia has been studied with promising results in patients with severe stroke and with variable results in patients with severe head injury.5 Given its potential—and its recent success with cardiac arrest patients—nurses will need to stay abreast of the latest research on this therapeutic option. It's fairly safe to say that as time goes by, our use of therapeutic hypothermia is likely to expand. The question is: Will you be ready?
1. Abella, B. S., Rhee, J. W., et al. (2005). Induced hypothermia is underused after resuscitation from cardiac arrest: A current practice survey. Resuscitation, 64(2), 181.
2. American Heart Association. "About sudden death and cardiac arrest." 2005. www.americanheart.org/presenter.jhtml?identifier=604 (31 Jan. 2005).
3. University of Washington, Harborview Medical Center. "Frequently asked questions." 2005. www.uwmedicine.org/Facilities/Harborview/Overview/Research/Hypothermia/FAQ.htm (17 Mar. 2005).
4. Nolan, J. P., Morley, P. T., et al. (2003). Therapeutic hypothermia after cardiac arrest: An advisory statement by the Advanced Life Support Task Force of the International Liaison Committee on Resuscitation. Circulation, 108(1), 118.
5. Bernard, S. A., Gray, T. W., et al. (2002). Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med, 346(8), 557.
6. The Hypothermia After Cardiac Arrest Study Group (2002). Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med, 346(8), 549.
7. American Heart Association. "American Heart Association outlines 'chilling' plan to prevent brain damage after cardiac arrest." 2003. www.americanheart.org/presenter.jhtml?identifier=3013397 (31 Jan. 2005).
8. Massachusetts General Hospital Stroke Service. "Hypothermia after cardiac arrest—guideline of care." 2004. http://neuro-oas.mgh.Harvard.edu/stopstroke/hypothermia.htm (4 Feb. 2005).
9. McNeil, D. G. (2003, July 8). Chill therapy is endorsed for some heart attacks. The New York Times, p. A1.
10. Bernard, S. A., & Buist, M. (2003). Induced hypothermia in critical care medicine: A review. Crit Care Med, 31(7), 2041.
Physiologic effects of hypothermia
Mild hypothermia not only reduces intracranial pressure, but it also decreases the cerebral metabolic rate—and thus the brain's demand for oxygen. In fact, for each 1° C decrease in temperature, there is a 6% - 7% decrease in the cerebral metabolic rate. In addition, maintaining a temperature of 89.6° - 93.2° F (32° - 34° C) for 12 - 24 hours does the following:
- Decreases heart rate
- Decreases phosphate and potassium concentrations
- Decreases gut motility
- Increases blood glucose concentrations
- Decreases phosphate and potassium concentrations
- Increases systemic vascular resistance
- Increases the solubility of gases in the blood
- Prolongs clotting times
- May increase the risk of aspiration pneumonia
- May cause diuresis
- May act as an anticonvulsant
- May decrease the number and function of white blood cells and platelets
Source: Bernard, S. A., & Buist, M. (2003). Induced hypothermia in critical care medicine: A review. Crit Care Med, 31(7), 2041.