Cardiopulmonary arrest causes blood. Cases of Note KEEPING COOL: A CASE FOR HYPOTHERMIA AFTER CARDIOPULMONARY RESUSCITATION

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1 Cases of Note Cases of Note features peer-reviewed case reports and case series that document clinically relevant findings from critical and high acuity care environments. Cases that illuminate clinical diagnoses and management issues in the treatment of critically and acutely ill patients and include discussion of the patient s experience with the illness or intervention are encouraged. Proposals for future Cases of Note articles may be ed to ajcc@aacn.org. KEEPING COOL: A CASE FOR HYPOTHERMIA AFTER CARDIOPULMONARY RESUSCITATION By Mary Kay Bader, RN, MSN, CCNS, CCRN, CNRN, Michael Rovzar, MD, Laurie Baumgartner, RN, MSN, ACNP, BC, CNS, CCRN, Robert Winokur, MD, Jon Cline, MD, and George Schiffman, MD 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. (American Journal of Critical Care. 2007;16:636, ) Cardiopulmonary arrest causes blood flow to the brain to cease, a situation that leads to depletion of brain oxygen stores within 20 seconds, resulting in irreversible brain damage if circulation is not restored. 1-4 Cardiopulmonary resuscitation (CPR) with chest compressions provides some blood flow to the brain but is often delayed and may be ineffective. 5-9 The 2005 evidence-based guidelines 10,11 of the American Heart Association emphasize a push fast and push hard chest compression technique and care after resuscitation that includes moderate hypothermia to reduce potentially devastating end-organ injury and optimize outcomes. 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 (33ºC-34ºC) is used to diminish the catastrophic neurological derangement associated with ischemicanoxic brain injury after cardiac arrest. The brain uses approximately one-fifth of the cardiac output to Continued on page AJCC AMERICAN JOURNAL OF CRITICAL CARE, November 2007, Volume 16, No. 6

2 Mild hypothermia diminishes neurological derangement associated with brain injury after cardiac arrest. Hypothermia decreases the brain s metabolic rate by 20% to 25%, and may reduce adverse inflammatory processes. Cases of Note Continued from page 636 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 Hypothermia decreases the brain s metabolic rate by approximately 20% to 25%, minimizing the ATP depletion in damaged tissue 12 ; 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 al 3 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 study 4 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 About the Authors Mary Kay Bader is a neuro/critical care clinical nurse specialist, Michael Rovzar is a physician in the Department of Medicine, Laurie Baumgartner was (at the time this manuscript was written) a clinical nurse specialist in the cardiac intensive care unit and telemetry, Robert Winokur is medical director of emergency services, Jon Cline is an emergency physician, and George Schiffman is a pulmonary intensivist at Mission Hospital, Mission Viejo, California. Corresponding author: Mary Kay Bader, RN, Mission Hospital, Medical Center Rd, Mission Viejo, CA ( Badermk@aol.com). new CPR recommendations of the American Heart Association that focus on the use of hypothermia to limit neurological injury. 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 PaCO 2 of 70 mm Hg, and a PaO 2 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. Sixty minutes after return of circulation, moderate hypothermia was implemented and managed by the unit s advanced practice nurses. The goal temperature of 33ºC was achieved within 4 hours of initiating cooling and was maintained for 18 hours. Rewarming of the patient occurred during a 24-hour period without adverse events. Although the patient s recovery was complicated by the subsequent development of pulmonary infarcts, prolonged mechanical ventilation, and mediastinal and rectus sheath hematomas that required blood transfusions, he was discharged 3 weeks later with no neurological impairment. Six weeks after the cardiopulmonary arrest, he returned to work full-time with no apparent neurological deficits. 632 AJCC AMERICAN JOURNAL OF CRITICAL CARE, November 2007, Volume 16, No. 6

3 A B Figure Angiograms show a large thrombus in right iliac vein (A) and pulmonary emboli (B). 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, hypo - thermia 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 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 Table 1 Inclusion/exclusion criteria for moderate hypothermia Inclusion criteria 1.1 Cardiac arrest with a return of spontaneous circulation (may include noncardiac causes such as pulmonary embolism) 1.2 Unresponsive or not following commands after cardiac arrest 1.3 Witnessed arrest with a down time of less than 60 minutes Exclusion criteria 2.1 Pregnancy 2.2 Core temperature less than 35.0ºC after cardiac arrest 2.3 Age less than 18 years or greater than 85 years 2.4 Existing do-not-resuscitate status 2.5 End-stage terminal illness 2.6 Chronic renal failure 2.7 Sustained refractory ventricular arrhythmias 2.8 Severe bradycardia without a temporary pacemaker 2.9 Active bleeding, gastrointestinal bleeding, or intracerebral hemorrhage 2.10 Traumatic full arrest 2.11 Shock 2.12 Persistent hypotension, defined as a mean arterial pressure less than 60 mm Hg despite adequate intravenous fluid replacement (central venous pressure >6 mm Hg) and stable levels of vasopressors 2.13 Comatose state or severe neurological dysfunction (eg, dementia) before cardiac arrest 2.14 Awake and responsive to verbal commands after cardiac arrest 2.15 Platelet count less than 50 x 10 3 /µl or known coagulopathy (international normalized ratio >3.0) 2.16 Acute myocardial infarction while undergoing intervention in catheterization laboratory 2.17 Drug intoxication AJCC AMERICAN JOURNAL OF CRITICAL CARE, November 2007, Volume 16, No

4 Table 2 Protocol for induction of hypothermia Initiating hypothermia (preferably within 60 minutes of arrest) 1.1 Anticipate need for blood pressure support. Goal for mean arterial pressure is >80 and <100 mm Hg. Use fluids to maintain euvolemia. Use vasopressors/vasoactive medications to increase mean arterial pressure once euvolemic. 1.2 Administer fentanyl 1-3 µg/kg per hour intravenously or morphine 2-4 mg intravenously per hour. 1.3 Start propofol infusion to achieve a score of -4 on the Richmond Agitation-Sedation Scale and/or a bispectral index of Place continuous temperature monitoring probe (Foley or rectal). 1.5 Apply pads to body and use the automatic mode on the cooling machine. 1.6 Set the desired target temperature to 33ºC, press Automatic, and begin cooling. 1.7 Note the time cooling is initiated on the critical care flow sheet. 1.8 If patient has myoclonic jerks or seizures before the start of cooling, administer loading dose of fosphenytoin (Cerebyx) 1000 mg intravenously and then 100 mg intravenously every 8 hours. 1.9 Monitor continuous or intermittent electroencephalogram as available. 2.0 Before induction of hypothermia: Administer an intravenous bolus of paralytic agent, with a goal of a train-of-4 of 1 of 4. Discontinue paralytics once goal temperature has been achieved. Redose as needed if shivering uncontrolled by other means. 2.1 Assess vital signs, electrocardiogram, peripheral oxygen saturation, end-tidal carbon dioxide, and presence of shivering every 15 minutes during induction of hypothermia, then every 30 minutes for 2 hours, and then every hour. 2.2 Goal core temperature of 33ºC to 34ºC should be obtained in 4 to 6 hours. Notify physician if unable to reach goal temperature within 6 hours. Maintain goal temperature for 18 hours or a total of 24 hours since initiation of hypothermia. 2.3 If patient s hemodynamic status is unstable at 33ºC to 34ºC, notify physician, stop cooling, and initiate rewarming. Table 3 Protocol for electrolyte management during hypothermia 1. During initiation of hypothermia, patients with normal renal function will experience diuresis, causing a potential loss of sodium, potassium, magnesium, phosphorus, and calcium. 1.1 Hypokalemia may exacerbate or cause ventricular arrhythmias. Severe hypokalemia may occur in hypothermic patients, which may represent a shift of potassium into the cell rather than a true loss. Sliding scale for potassium replacement: Administer 40 meq potassium chloride via intravenous infusion (for 4 hours if peripheral catheter or 2 hours if central catheter) for potassium levels <3.0 meq/l (mmol/l). Administer 80 meq potassium chloride via intravenous infusion (for 8 hours if peripheral catheter or 4 hours if central catheter) for potassium levels <2.0 meq/l and notify physician. 1.2 Hypomagnesemia may cause ventricular arrhythmias (torsades de pointes) and muscle and central nervous system irritability. Use sliding scale to replace magnesium if 1.8 mg/dl (to convert to millimoles per liter, multiply by ; normal is mg/dl). If magnesium <1.8 mg/dl, administer 2 g magnesium sulfate via intravenous infusion for 1 hour. 1.3 Elevated lactate levels indicate metabolic acidosis. Assess propofol use if metabolic acidosis is evident on arterial blood gas analysis. Assess for sepsis. 1.4 Use sliding scale to replace phosphorus if 2.0 mg/dl (to convert to millimoles per liter, multiply by 0.323; normal is mg/dl). If phosphorus <2.4 mg/dl, administer 12 mmol sodium phosphate via intravenous infusion for 3 hours. 1.5 Use sliding scale to replace calcium if ionized calcium is 4.0 mg/dl (to convert to millimoles per liter, multiply by 0.25; normal is mg/dl). If ionized calcium 4.0 mg/dl, administer 2 g calcium gluconate via intravenous infusion for 30 minutes. 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 33ºC is important because rewarming too early diminishes the neuroprotective effect of cooling. A written protocol scripting the process, including the monitoring and clinical interventions to be considered during the cooling phase, is essential. As temperature descends, vasoconstriction occurs and electrolytes shift from intravascular to intracellular compartments. Patients undergoing mild hypothermia must be closely monitored for changes in electrocardiographic findings, blood pressure, pulse, urine output, and neurological status. Potential electrocardiographic changes include arrhythmias, prolonged QT interval, and the occurrence of a j wave. Careful manipulation of fluids and electrolytes are needed to ensure a stable condition (Table 3). The patient usually shivers while the core temperature is being lowered. Interven tions 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. While the patient is in the hypothermic state, constant attention is required to maintain the temperature at 33ºC. System support includes interventions to prevent deep vein thrombosis and stress 634 AJCC AMERICAN JOURNAL OF CRITICAL CARE, November 2007, Volume 16, No. 6

5 ulcers. Monitoring for arrhythmias, coagulopathies, fluid imbalances, infections, and electrolyte disturbances during induction, maintenance, and rewarming are required to prevent adverse effects of treatment. This close supervision and intense treatment often warrant assignment of additional nursing staff to the patient. In this case, 2 experienced intensive care nurses and 1 advanced practice nurse provided care during the 4-hour induction period. The patient remained under the care of 2 experienced critical care nurses for the full 24 hours of hypothermia. 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 0.25ºC/h. Electrocardiograms, vital signs, and pulse oximetry results were monitored every 30 minutes during rewarming. Observing for signs of hypovolemia was Improved outcomes are seen even when hypothermia is started 8 hours after return of circulation. 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 36ºC, he was weaned off the neuromuscular agent and propofol. The cooling pads were kept on for 48 hours with the goal temperature of 37ºC maintained to prevent rebound hyperthermia. 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. eletters Now that you ve read the article, create or contribute to an online discussion about this topic using eletters. Just visit and click Respond to This Article in either the full-text or PDF view of the article. SEE ALSO To learn more about induced hypothermia following cardiac arrest, visit and read the article by Kozik, Induced Hypothermia for Patients With Cardiac Arrest: Role of a Clinical Nurse Specialist (Critical Care Nurse, October 2007). REFERENCES 1. Safar P, Behringer W, Bottiger BW, Sterz F. Cerebral resuscitation potentials for cardiac arrest. Crit Care Med. 2002;30(4 suppl):s140-s Bernard S. Hypothermia for cardiac arrest. In: Mayer SA, Sessler DI, eds. Therapeutic Hypothermia. New York, NY: Marcel Dekker; 2005: Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346(8): Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med. 2002;346(8): Abella BS, Alvarado JP, Myklebust H, et al. Quality of cardiopulmonary resuscitation during in-hospital cardiac arrest. JAMA. 2005;293(3): Abella BS, Sandbo N, Vassilatos P, et al. Chest compression rates during cardiopulmonary resuscitation are suboptimal: a prospective study during in-hospital cardiac arrest. Circulation. 2005;111(4): Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incomplete chest wall decompression: a clinical evaluation of CPR performance by EMS personnel and assessment of alternative manual chest compression-decompression techniques. Resuscitation. 2005;64(3): Greingor JL. Quality of cardiac massage with ratio compression-ventilation 5/1 and 15/2. Resuscitation. 2002; 55(3): Liberman M, Lavoie A, Mulder D, Sampalis J. Cardiopulmonary resuscitation: errors made by pre-hospital emergency medical personnel. Resuscitation. 1999;42(1): American Heart Association. Part 4: Adult Basic Life Support. Circulation. 2005;112(suppl):IV-19 IV American Heart Association. Part 7.5: Postresuscitation care. Circulation. 2005;112(suppl I):IV-84 IV Yenari M, Wijman C, Steinberg G. Effect of hypothermia on cerebral metabolism, blood flow, and autoregulation. In: Mayer SA, Sessler DI, eds. Therapeutic Hypothermia. New York, NY: Marcel Dekker; 2005: Peabody MA. Therapeutic hypothermia after cardiac arrest: practical considerations for protocol development and implementation strategies [Web cast]. May 30, University of Chicago. Protocol for hypothermia after cardiac arrest. Emergency Resuscitation Center Web site. Updated December 2, Accessed August 1, Washington Hospital Center. Protocol for Critical Care Therapeutic Hypothermia. Updated August 2, Washington, DC: Washington Hospital Center; To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA Phone, (800) or (949) (ext 532); fax, (949) ; , reprints@aacn.org. AJCC AMERICAN JOURNAL OF CRITICAL CARE, November 2007, Volume 16, No