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CASES OF NOTE |
Corresponding author: Mary Kay Bader, RN, Mission Hospital, 27700 Medical Center Rd, Mission Viejo, CA 92691-6426 (e-mail: Badermk{at}aol.com).
Abstract
Cessation of circulation during cardiac arrest causes critical end-organ ischemia. Although the neurological consequences of cardiopulmonary arrest can be catastrophic, an aggressive "push fast and push hard" resuscitation technique maintains blood flow until the return of spontaneous circulation. However, reperfusion to the cerebrum leads to cellular chaos and further neurological injury. Use of moderate hypothermia after cardiac arrest mediates these cellular and chemical processes, reducing the impact of the arrest and reperfusion phenomena. A 43-year-old man had 2 asystolic arrests with 20 minutes of cardiopulmonary resuscitation as a result of massive, multiple pulmonary emboli. After the cardiac arrest, the patient was comatose and posturing. The 2005 American Heart Association guidelines for cardiopulmonary resuscitation were used along with moderate hypothermia in an attempt to minimize the neurological consequences of the cardiopulmonary arrest and to optimize the patient’s outcome.
Once a return of spontaneous circulation occurs, care after resuscitation includes interventions to minimize the neurological sequelae of the cardiopulmonary arrest. Instituting hypothermia within 60 minutes may reduce the effect of the cardiopulmonary arrest on the brain. Mild hypothermia (33°C–34°C) is used to diminish the catastrophic neurological derangement associated with ischemic-anoxic brain injury after cardiac arrest. The brain uses approximately one-fifth of the cardiac output to meet its metabolic needs. In cardiac arrest, inadequate oxygen and glucose limit production of adenosine triphosphate (ATP). ATP production becomes severely limited within 2 minutes after circulatory arrest, and ion pumps that require ATP to maintain ionic gradients fail. Failure of the ion pumps results in cellular efflux of potassium and influx of sodium and calcium, causing cellular edema, terminal depolarization, and, eventually, cellular death.12
| Mild hypothermia diminishes neurological derangement associated with brain injury after cardiac arrest.
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Hypothermia decreases the brain’s metabolic rate by approximately 20% to 25%, minimizing the ATP depletion in damaged tissue12; however, this reduction is inadequate to completely explain the neuroprotective qualities of hypothermia. Most likely, hypothermia results in other beneficial mechanisms that lead to additional neuroprotection, such as decreasing the amounts of excitatory neurotransmitters and mitigating release of inflammatory cytokines and production of free radicals that lead to necrosis and apoptosis.12
The neuroprotective effects of hypothermia in ischemic brain injury after cardiac arrest were first demonstrated in animal models and have now been shown in human clinical trials.3,4 In a study of 77 patients who experienced cardiac arrest and received hypothermia, Bernard et al3 reported a survival advantage associated with good neurological outcomes in 49% of the patients treated with hypothermia compared with 26% of the control group treated without hypothermia. In a second study4 with 273 patients, 55% of patients treated with hypothermia experienced good neurological outcomes versus 39% of the control group. In this case report, we highlight the impact of the new CPR recommendations of the American Heart Association that focus on the use of hypothermia to limit neurological injury.
| Hypothermia decreases the brain’s metabolic rate by 20% to 25%, and may reduce adverse inflammatory processes.
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Case Report
A 43-year-old man arrived in the emergency department in extremis with no palpable blood pressure, tachycardia, and cyanosis (oxygen saturation, 64%). He had fractured his leg 10 days earlier, and it was immobilized with a splint. The day before admission, he had flown on an airplane while returning from a business trip. Within minutes of arrival in the emergency department, he was intubated and given intravenous fluids, but he had a pulseless arrest for 6 minutes with return of circulation after CPR. Pulmonary embolism was suspected, and he was given systemic tissue plasminogen activator. He remained hypotensive while receiving infusions of vasopressors, and arterial blood gas analysis showed a pH of 6.97, a PaCO2 of 70 mm Hg, and a PaO2 of 72 mm Hg. His wife arrived in the emergency department and explained that he had experienced deep vein thrombosis in a lower extremity 3 years before and had been treated with warfarin for a short time. Two family members were known to have hypercoagulable protein abnormalities.
The patient was taken to the interventional radiology suite emergently and underwent pulmonary angiography. A large iliofemoral thrombosis and large-volume bilateral pulmonary emboli were found (see Figure
). Pulse-spray tissue plasminogen activator was administered directly into the pulmonary arteries. During infusion, the patient had another asystolic arrest that lasted 14 minutes. During both arrests, the resuscitation team administered 100 forceful chest compressions per minute, with members of the team rotating every 1 to 2 minutes. Blood pressures of 150 to 160 mm Hg systolic were recorded from the femoral artery catheter during the 14-minute arrest. Upon return of circulation, the patient remained unresponsive with extensor posturing.
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Discussion
This case illustrates the importance of coordinated implementation of the new American Heart Association CPR guidelines, rapid diagnosis and treatment of conditions such as massive pulmonary embolism, and the immediate use of hypothermia to prevent potential adverse neurological outcomes.
The positive outcomes of this case were most likely related to the rapid and effective multidisciplinary implementation of the new CPR guidelines in the emergency department. However, as noted earlier, successful resuscitation by itself is not enough. The guidelines also seek to ensure that devastating end-organ injury does not occur. To that end, hypothermia is provided, and in this case hypothermia contributed to the patient’s full neurological recovery.
The advanced practice nurses who implemented and managed the patient’s hypothermia used clearly written protocols that stated inclusion and exclusion criteria, how to start and stop the therapy, care priorities, and the management of electrolytes. The protocols used in this case were developed by a multidisciplinary team of physicians from emergency, cardiology, neurology, and critical care services, critical care advanced practice nurses, and a pharmacist. The team used information based on the literature, protocols from 2 leading academic hospitals, and a Web cast on inducing hypothermia after cardiac arrest.13–15
The criteria for selecting patients for treatment with therapeutic hypothermia (Table 1) are based on the risks of hypothermia and the outcomes expected on the basis of knowledge acquired during animal studies and human trials. Initiation of the hypothermia protocol should occur as soon as possible after spontaneous circulation is restored (Table 2). Studies in animals have indicated that improved outcomes are achieved with earlier cooling, although improved outcomes still occur with initiation of cooling up to 8 hours after the return of spontaneous circulation.4 Duration of hypothermia for at least 18 hours at a goal temperature of 33°C is important because rewarming too early diminishes the neuroprotective effect of cooling.
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). The patient usually shivers while the core temperature is being lowered. Interventions such as administration of sedatives, narcotics, or paralytic medications, as well as the use of adjunctive warming of extremities, can be used to diminish or eliminate shivering.
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Rewarming of the patient after 18 hours of hypothermia requires a gradual elevation of core temperature. The automatic mode of the cooling machine was used to ensure control of the process at the rate of 0.25°C/h. Electrocardiograms, vital signs, and pulse oximetry results were monitored every 30 minutes during rewarming. Observing for signs of hypovolemia was important because of the fluid shifts in the intravascular compartment and the vasodilatation. Levels of sodium, potassium, chloride, magnesium, phosphate, and calcium were measured every hour during rewarming to ensure stability of electrolyte levels. Once the patient’s body temperature reached 36°C, he was weaned off the neuromuscular agent and propofol. The cooling pads were kept on for 48 hours with the goal temperature of 37°C maintained to prevent rebound hyperthermia. Improved outcomes are seen even when hypothermia is started 8 hours after return of circulation.
Conclusion
This case highlights the potential usefulness of moderate hypothermia in the treatment of patients with cardiac arrest. The neurological consequences of the cardiac arrest were minimized and the patient’s good outcome was most likely the result of the CPR and hypothermia protocols used. Our experience suggests that open and continuous communication between physicians, ancillary staff, and nurses provides opportunity for more timely adjustments in the care plan and promotes safe and effective treatment.
FINANCIAL DISCLOSURES
None reported.
Now that you’ve read the article, create or contribute to an online discussion about this topic using eLetters. Just visit www.ajcconline.org and click "Respond to This Article" in either the full-text or PDF view of the article.
To learn more about induced hypothermia following cardiac arrest, visit http://ccn.aacnjournals.org and read the article by Kozik, "Induced Hypothermia for Patients With Cardiac Arrest: Role of a Clinical Nurse Specialist" (Critical Care Nurse, October 2007).
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