Survival rates for sudden cardiac arrest are dismal. In 2004, survival rates to hospital discharge were 8.4% for all cardiac arrests and 17.7% for ventricular-arrhythmia cardiac arrests.
In December 2005, to improve survival rates, the American Heart Association (AHA) published resuscitation recommendations for using mild hypothermia. These recommendations apply when an unconscious adult has spontaneous circulation after an out-of-hospital cardiac arrest and the initial rhythm is ventricular fibrillation (VF) or ventricular tachycardia (VT). Cooling may also be beneficial for other arrhythmias and in-hospital cardiac arrests.
Chilly reception for new therapy
But adoption of the recommendations has been slow, despite clinical evidence supporting them and 2003 recommendations from the International Liaison Committee on Resuscitation (ILCOR). Some 18 months after the ILCOR statement, a survey found that only 25% of institutions had adopted the new resuscitation guidelines.
Why the chilly reception? In part, it’s because therapeutic hypothermia runs counter to what we’ve all been taught in nursing school and medical school—that is, to warm a cold patient. Also, implementing this new therapy isn’t simple. But it is doable. And taking the lead in helping the various disciplines through the process can be rewarding.
At Hoag Hospital, we researched therapeutic hypothermia and embraced the decision to adopt the guidelines. We reached consensus on a protocol and trained our medical and nursing staff.
Making the case for change
The first step in developing a protocol for therapeutic hypothermia is to prove the need for it in your institution. We did that by analyzing the care, processes, and outcomes for patients with cardiac arrest. To access information on cardiac arrests, we ran database queries on ICD-9 code 427.5 and associated diagnosis-related groups.
We included critical care and hospital length-of-stay and condition on discharge in our report. You can retrieve this data from the National Registry for Cardiopulmonary Resuscitation database. For functional neurologic outcomes, you can complete a simple chart review using the Cerebral Performance Category scale, the scale used in many studies to describe “good” and “poor” outcomes. In the pre-hospital setting, the most commonly used tool for evaluating neurologic function is the Glasgow Coma Scale.
Our report demonstrated a need for improvement, so we put together a multidisciplinary team with a shared vision to develop the protocol and lead the change in our hospital. Nurses on the team included a critical care clinical nurse specialist and an emergency department clinical nurse specialist. Also on the team were intensivists (including a critical care intensivist and a neurology intensivist) as well as cardiologists and emergency medical specialists. In retrospect, we should have included emergency medical services personnel. The critical care intensivist, who understood the process and could articulate the benefits of the therapy, acted as our champion.
Developing the protocol
One of our most important decisions was selecting the method for cooling the patient. At our institution, we typically used water blankets and ice. Traditional water blankets are relatively inexpensive, but initiating cooling and maintaining temperature are difficult, so patient management requires more nursing time and effort.
We needed a system that was safe and could reduce temperature quickly, maintain our goal temperature consistently, and rewarm gradually. After reviewing the available products, we decided on the noninvasive Arctic Sun® Temperature Management System, which uses three-layer cooling pads to provide automatic control with rapid cooling, tight control during maintenance, and gradual rewarming.
In developing our protocol, we focused on these main areas:
Indications and recommendations
- Indicated for VF or VT
- Recommended for pulseless electrical activity or asystole
- Age 18 or older
- Cardiac arrest with a return of spontaneous circulation (ROSC). Initial arrhythmia should be noted.
- Persistent coma (defined as not following commands, no speech, no purposeful movement to noxious stimuli, no eye opening) 15 to 30 minutes after resuscitation. Includes abnormal reflexes, such as decorticate or decerebrate posturing.
- Known down time of < 1 hr preferred. Unknown down time may be cause for exclusion.
Exclusion criteria (absolute)
- Certain reasons for coma, such as drug overdose or status epilepticus– Patient awakening with return of normal mental status 15 to 30 minutes after resuscitation
- Terminal illness, such as stage IV cancer
Exclusion criteria (relative)
- Coagulopathy before arrest (for example, a patient taking warfarin or a patient who has an International Normalized Ratio (INR) > 2.0 and an activated partial thromboplastin time (APTT) > 1.5 control).
- Persistent shock, defined as systolic blood pressure < 90 mm Hg or mean arterial pressure (MAP) < 65 mm Hg after resuscitation with fluids or vasopressors
- Bradycardia, defined as heart rate < 60 beats per minute
- Refractory VF
- Thrombocytopenia, defined as platelet count of < 50,000 x 10-6/L
- Don’t delay hypothermia therapy because of concurrent cardiac interventions such as percutaneous coronary intervention.
- Initiate the hypothermia protocol within 4 hours of ROSC.
- If the > 70 mm Hg MAP goal isn’t met after a 2-L infusion of crystalloid or colloid equivalent, infuse dopamine 5 to 20 mcg/kg/minute p.r.n.
- If central venous pressure increases > 5 mm Hg in 5 minutes, temporarily discontinue an infusion or bolus of I.V. fluid.
Monitoring the patient
- Monitor laboratory values, especially those related to the common adverse effects of intracellular shifts of calcium, phosphorus, magnesium, and potassium. Obtain a basic metabolic panel, magnesium and ionized calcium levels, and prothrombin time, APTT, and INR every 6 hours.
- Monitor the patient’s phenytoin level daily.
- Glycemic control
- Venous thromboembolism (VTE) prophylaxis
- Stress ulcer prophylaxis
You can find sample protocols at a site created by the University of Chicago: http://hypothermia.uchicago.edu/.
Mr. Rudman’s cardiac arrest
Soon after developing our protocol, we had the opportunity to use it. Mr. Rudman, age 56, was admitted to the emergency department after experiencing a cardiac arrest. His wife and a bystander had initiated cardiopulmonary resuscitation (CPR). Called to the scene, the emergency response team used the guidelines for CPR and defibrillation. Mr. Rudman had a ROSC in less than 15 minutes.
On admission, he exhibited a persistent altered mental status—an upward left gaze, no spontaneous eye opening, and a delayed, abnormal limb flexion to central and peripheral noxious stimuli. He would not track, focus, nor blink to visual threat. His pupils were equal and reactive to light. At times, he was agitated, but he didn’t show purposeful movements. Nor did he follow verbal commands.
Mr. Rudman’s vital signs were relatively stable, with a MAP of more than 65 mm Hg. He was taken to the cardiac catheter lab for an angiogram, which showed multivessel coronary artery disease and a 100% occlusion of the right coronary artery.
Using our new protocol
When Mr. Rudman arrived intubated in the intensive care unit, the critical care intensivist decided to institute our new hypothermia protocol for neuroprotection. We inserted the temperature probe (incorporated into the Foley catheter) and connected it to the console of the Arctic Sun® Temperature Management System. To ensure the accuracy of the Foley temperature probe, we also took the patient’s temperature orally. Some facilities use other methods of monitoring temperature, including a rectal temperature probe and pulmonary catheter probe. Tympanic thermometers have been used but are less reliable.
We quickly applied the torso and leg hypothermia pads and turned the machine on in the automatic mode to achieve a temperature of 33º C (91.4º F).
For sedation, we administered midazolam I.V. For shivering, pain control, and sedation, we gave fentanyl and titrated the dose. We gave propofol and titrated the dosage to achieve a Sedation Agitation Scale of 1, defined as not arousable with minimal or no response to noxious stimuli. We also administered a loading dose of phenytoin for seizure prophylaxis and vecuronium intermittently p.r.n. to stop shivering.
To ensure patient safety, we instituted standard critical care protocols, including keeping the head of the bed at 30 degrees, starting VTE prophylaxis, and using stress ulcer prophylaxis. Before using low-molecular-weight heparin for VTE prophylaxis, we needed to rule out an intercerebral hemorrhage from the patient’s fall during cardiac arrest. So Mr. Rudman underwent computed tomography of the brain, which showed no evidence of acute or focal intercerebral abnormalities.
On alert for complications
The staff knew to notify the physician if shivering, seizures, hypotension (systolic blood pressure less than 90 mm Hg), or bradycardia (heart rate less than 60 beats per minute) developed. The risk of shivering is highest during induction and rewarming, and 5 minutes after cooling began, Mr. Rudman started shivering. We responded with vecuronium.
The possibility of aspiration during initial resuscitation and a resulting infection became an early concern, and we administered antibiotics based on our hospital’s antibiogram recommendations.
During therapeutic cooling, certain electrocardiogram changes, including the development of a J wave, may appear. Hypothermic J waves show as core body temperature decreases. Nonhypothermic J waves can occur in patients with electrolyte disturbances, cerebral brain injury, Prinzmetal’s angina, myocardial ischemia, VF, and Brugada syndrome. With hypothermia, a prolonged PR interval of more than 0.47 second and a prolonged QTc interval of more than 0.47 second often develop. Mr. Rudman had a PR interval of 0.22 second, but a QTc interval of 0.508 second. A small J wave appeared in lead V5.
Reaching and maintaining the temperature goal
Within 1½ hours of starting therapy, we reached our goal core body temperature of 33° C (91.4° F) without incident. Despite the time needed for the coronary angiogram, we were well within our protocol goal of achieving hypothermia within 6 hours of admission. We maintained Mr. Rudman at 33° C for 24 hours.
During the cooling phase and throughout the cool maintenance phase, Mr. Rudman’s heart rate dropped to between 40 and 50 beats per minute. Unless a patient has signs and symptoms of poor perfusion, such as hypotension or decreased urine output, bradycardia isn’t treated. Because Mr. Rudman was hypotensive, we added an I.V. infusion of dopamine, an inotropic, to maintain an acceptable MAP of more than 70 mm Hg. Keep in mind that a patient is at risk for hypotension during rewarming, as vasoconstriction reverses.
Because of cold diuresis, our patient’s urine output increased dramatically during the entire cooling period, and we maintained adequate fluid resuscitation to keep pace.
We also ensured adequate electrolyte replacement during the cooling and maintenance phases because of the expected intracellular shifts of calcium, phosphorus, magnesium, and potassium. Hypokalemia is common during cooling, but you should stop a potassium infusion during rewarming because hyperkalemia may occur as potassium exits the cells.
We also checked Mr. Rudman’s skin every 4 hours to ensure adequate skin perfusion. And we monitored his blood glucose level. Our target was a level of less than 120 mg/dl, and we used the Critical Care Intensive I.V. insulin protocol. Since we treated this patient, the Society of Critical Care Medicine has recommended an allowance of up to 150 mg/dl.
We did not observe seizures, but subclinical seizures are always a possibility. During the maintenance period, the patient had an electroencephalogram, which showed no seizure activity. Mr Rudman’s daily phenytoin levels were therapeutic, ranging from 10 to 14 mcg/ml.
Rewarming the patient
After maintaining Mr. Rudman at 33° C (91.4° F) for 24 hours, we gradually rewarmed him, increasing his core body temperature 0.5° to 1º C per hour. When he reached the target temperature of 36.5° C (97.7° F), we began rapid weaning from sedative and analgesic infusions. Several hours later, he opened his eyes and followed simple commands. We weaned him from the ventilator, using a rapid-weaning protocol.
Although Mr. Rudman had a short-term memory deficit, he could move his arms and legs, and his neurologic function was intact. He had amnesia regarding the entire event and the entire day before admission. On the fourth day of his hospitalization, he underwent four-vessel coronary bypass graft surgery. On the seventh day, he was discharged: He was awake, alert, and oriented, with no significant neurologic deficit.
We were deeply moved by our first experience with therapeutic hypothermia. The long wait to learn the outcome of our new protocol created a great deal of suspense for the staff and the family, and a bond developed between them.
When Mr. Rudman woke up and realized what had happened, he was grateful for his second chance, and we were profoundly affected by his recovery—and by the possibility of saving others with this new therapeutic approach to cardiac arrest. With his recovery, we knew that we’d established a safe, effective protocol that would save more lives.
Abella BS, Rhee JW, Huang KN, Vanden Hoek TL, Becker LB. Induced hypothermia is underused after resuscitation from cardiac arrest: a current practice survey. Resuscitation. 2005; 64:181-186.
Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-563.
Brain Resuscitation Clinical Trial I Study Group. A randomized clinical study of cardiopulmonary-cerebral resuscitation: design, methods, and patient characteristics. Am J Emerg Med. 1986;4:72-86.
Cummins RO, Chamberlain DA, Abramson NS, Allen M, Baskett PJ, Becker L, et al. Recommended guidelines for uniform reporting of data from out-of-hospital cardiac arrest: the Utstein Style. A statement for health professionals from a task force of the American Heart Association, the European Resuscitation Council, the Heart and Stroke Foundation of Canada, and the Australian Resuscitation Council. Circulation. 1991;84:960-975.
Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346:549-556.
Part 7.5: Postresuscitation Support. Circulation. 2005:000:IV-84-IV-88. Available at: http://circ.ahajournals.org/cgi/reprint/CIRCULATIONAHA.105.166560v1.pdf. Accessed May 31, 2007.
Rea TD, Eisenberg MS, Sinibaldi G, White RD. Incidence of EMS-treated out-of-hospital cardiac arrest in the United States. Resuscitation. 2004;63:17-24.
White L. Therapeutic hypothermia to improve postresuscitation outcomes from sudden cardiac arrest. Curr Emerg Cardiac Care. 2006;17(2):6-7.
Kirsten Pyle, RN, CCRN, is Critical Care Clinical Outcomes Coordinator, Quality Management; Ginger Pierson, MSN, RN, CCRN, CNS, is a Cardiovascular Clinical Nurse Specialist, Coronary Care Unit/ Cardiovascular Intensive Care Unit; Deborah Lepman, BS, RN, MPH, CEN, is the Department Director, Coronary Care Unit/ Cardiovascular Intensive Care Unit/Sub-Intensive Care Unit; and Molly Hewett, MS, BSN, RN, CCRN, is Assistant Vice President, Neurologic Intensive Care Unit. The authors work at Hoag Memorial Hospital Presbyterian, Newport Beach, California. Pyle has received an educational grant from Medivance for presentations on therapeutic hypothermia; the other authors do not have any financial arrangements or affiliations with any corporations offering financial support or educational grants for continuing nursing education activities.