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Management following resuscitation from cardiac arrest: recommendations from the 2003 Rocky Mountain Critical Care Conference

[Conduite à tenir après la réanimation post-arrêt cardiaque : recommendations de la conférence du Rocky Mountain Critical Care 2003]

Dean D. Bell, MD^*, Peter G. Brindley, MD, David Forrest, MD, Osama Al Muslim, MD and David Zygun, MD

^* From the Departments of Anesthesia and Medicine, University of Manitoba, Winnipeg, Manitoba;
the Division of Critical Care Medicine, University of Alberta, Edmonton, Alberta;
the Department of Medicine, University of British Columbia, Vancouver, British Columbia;
the Division of Critical Care, University of Western Ontario, London, Ontario; and
¶ the Department of Critical Care, University of Calgary, Calgary, Alberta, Canada.

Address correspondence to: Dr. Dean D. Bell, GE706 Health Sciences Centre, 820 Sherbrook Street, Winnipeg, Manitoba R3A 1R9, Canada. Phone: 204-787-3112; Fax: 204-787-3069; E-mail: Dean1{at}mts.net

	Abstract

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Purpose: To propose a strategy for the management of patients admitted to critical care units after resuscitation from cardiac arrest.

Source: Prior to the conference relevant studies were identified via literature searches and brief reviews circulated on the following topics: glucose and blood pressure management; therapeutic hypothermia; prearrest outcome prediction; post-arrest outcome prediction; and management of myocardial ischemia. Two days were devoted to assessing evidence and developing a management strategy at the conference. Consensus opinion of conference participants [intensive care unit (ICU) physicians] was used when high grade evidence was unavailable. Additional literature searches and data grading were performed post-conference.

Principal findings: High grade evidence was lacking in most areas. Specific goals of treatment were proposed for: general care; neurologic care; respiratory care; cardiac care; and gastrointestinal care. There was adequate evidence to recommend therapeutic hypothermia for comatose patients who had witnessed ventricular fibrillation or ventricular tachycardia arrests. Conference participants supported extending therapeutic hypothermia to other presenting rhythms in selected circumstances. Additional goals included mean arterial pressure 80 to 100 mmHg, glucose 5 to 8 mmol·L^–1 using insulin infusions, and PaO₂ > 100 mmHg for the first 24 hr. Absent withdrawal to pain 72 hr after resuscitation should prompt consideration of palliative care. The level of evidence for other recommendations was low.

Conclusions: The proposed management strategy represents an approach to manage patients in the ICU following resuscitation from cardiac arrest. Most of the recommendations are based on low grade evidence. Additional research is needed to improve the evidence base. A standard post-arrest management strategy could help facilitate future research.

	Introduction

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THERE are clinical practice guidelines for management during cardiac resuscitation, but little has been written about post-resuscitation management. While proposals for brain-oriented extracerebral life support were developed by Safar and used in a randomized controlled trial of barbiturates in post-arrest patients,^1,2 the evidence for these recommendations was not well described. Safar’s recommendations included suggestions for routine use of corticosteroids, hyperventilation, and neuromuscular blockers. New ACLS 2000 guidelines have updated the section on post-arrest management but have less detail.³ In the current document the immediate goals of post-resuscitation care are: to optimize brain and other tissue perfusion; to transport the patient to an appropriately equipped critical care unit; to attempt to identify the precipitating causes of the arrest; and to institute therapy to prevent recurrence. The ACLS 2000 guidelines specifically recommend monitoring temperature and treating fever aggressively; avoiding hypoxemia and hypotension; avoiding sustained hypocapnia and ventilating to achieve normocarbia; and taking measures to optimize cerebral perfusion pressure.³ There are not many other specific aspects of care singled out. Recently, randomized controlled trials in cardiac arrest patients have documented improved outcome with induced hypothermia post-arrest.^4,5 Additional controlled trials are needed to improve care and outcome in this patient population. Additional trials will require development of a more detailed standardized post-arrest management protocol.

The topic of post-arrest management in critical care units was discussed at the 2003 Rocky Mountain Critical Care Conference in Vernon, British Columbia. The meeting was designed to focus upon three topics (post-arrest management, sepsis management, and improving safety and reducing harm in critical care) with an view towards development of management plans or future research. The post-arrest section was focused towards proposing an approach to post-arrest management based upon evidence or best clinical practice. It was apparent to the organizers of this section that high grade evidence was lacking for most aspects of management. To proceed, the organizing group divided the subject into the following areas prior to the meeting: glucose and blood pressure management (D.Z.); therapeutic hypothermia (O.A.M.); pre-arrest outcome prediction (P.G.B.); post-arrest outcome prediction (D.D.B.); and management of myocardial ischemia (D.F.). If a structured review or meta-analysis had been conducted on a topic they were included. One member (D.D.B.) functioned as coordinator. Group members conducted literature searches to find relevant material (randomized controlled trials, clinical trials, and meta-analyses or structured reviews), and reference lists of relevant papers were examined. At the end of this process each member of the organizing group produced a summary document that was circulated to other core members for review. The organizing group provided comments and included their reviews in the conference syllabus distributed at the meeting. When the meeting convened in Vernon, the reviews and studies were considered by the organizing group and other critical care physicians attending the conference. Intense discussion and review occurred over two days under the direction of a moderator who came from outside of the core group. The input of participants at the conference was used to generate a document outlining specific goals of treatment for: general care; neurologic care; respiratory care; cardiac care; and gastrointestinal (GI) care. These recommendations were presented and discussed at a final session of the conference by all attendees, including those who had been working in sepsis and error prevention workshops. Approximately 35 critical care physicians participated in the conference, and the consensus was that the findings should be submitted for publication. After the conference adjourned the recommendations were reviewed by the core group to help with grading the evidence. Additional literature searches were conducted at this stage to clarify evidence grades. Grading was done using a system modified from Sackett.⁶ The grading system employed is shown in Table I. There were issues deciding how to handle important positive randomized controlled trials outside of the post-arrest population. These studies were considered, but were not granted A or B grades unless they included post-arrest patients, or unless post-arrest patients were probable to accrue the same benefit as the general intensive care unit (ICU) population. Conference participants believed that data from these trials must be considered in developing their recommendations, despite low numbers of post-arrest patients. The final evidence grade and supporting data for treatment goals of post-arrest patients are outlined below.

	General recommendations (Table II)

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Acetaminophen has been used as an antipyretic for many years, and has greater antipyretic efficacy than aspirin in volunteers receiving iv endotoxin.¹² No evaluation of acetaminophen vs NSAIDs for treatment of pyrexia has been performed in critically ill patients. Indeed, the entire concept of treating fever in ICU patients without cerebral injury has been questioned.^13,14 NSAID administration produces greater temperature decrements and longer duration of antipyresis than acetaminophen in studies in febrile children,¹⁵ and was also associated with faster resolution of fever in patients with malaria.¹⁶ In a nonrandomized open label trial in febrile cancer patients iv propacetamol (acetaminophen) had lower antipyretic efficacy than an NSAID (iv diclofenac).¹⁷ Two randomized trials have evaluated acetaminophen in stroke patients and reported small decreases in core body temperature even in normothermic patients.^18,19 Acetaminophen may modestly promote hypothermia < 36.5°C or prevent hyperthermia > 37.5°C.¹⁵ Unfortunately, the clinical significance of this effect appears small. Pharmacologic antipyresis with acetaminophen and/or NSAID in post-cardiac arrest patients requires more study, however, ongoing use of these medications was recommended until additional data are available (Grade E).

Additional information is also needed regarding the technique, rapidity, and duration of inducing hypothermia after resuscitation. Recent trials have administered sedative and neuromuscular blocking agents during the hypothermia interval.^l4,15,20,21 Neuromuscular blockade is given to prevent shivering during hypothermia. Modest hypothermia has been induced in un-intubated stroke patients without resorting to the use of neuromuscular blockade or sedation.²² Hypothermia has also been induced with endovascular cooling during primary percutaneous coronary interventions in acute myocardial infarction without requiring neuromuscular blockade.²³ Shivering was prevented in these studies by administration of iv meperidine alone or in combination with oral buspirone. Meperidine and buspirone administration was studied in human volunteers made hypothermic with an infusion of 4°C iv fluid, and significantly reduced the shivering threshold while causing little sedation or respiratory toxicity.²⁴ Intravenous meperidine administration inhibits shivering and decreases the rewarming rate in hypothermic human volunteers.²⁵ The administration of sedative infusions and neuromuscular blockers during hypothermia can complicate neurologic assessment in post-arrest patients, and may not be necessary if meperidine administration successfully inhibits shivering. Studies need to be conducted to determine if neuromuscular blockade is essential during therapeutic hypothermia following cardiac arrest.

Multiple techniques of hypothermia induction have been published including: application of ice packs;⁵ surface cooling with cooled forced-air,^4,20 or circulating water blankets;^18,19 infusion of 4°C iv fluids;^26–28 immersion in cold water;²⁹ specialized endovascular cooling devices;^21,30,31 and cardiopulmonary bypass.³² No trials comparing hypothermia techniques in cardiac arrest patients have been published. A small trial comparing forced-air vs circulating water cooling blankets in febrile critically ill adults recommended forced air cooling.³³ A small trial in anesthetized volunteers found that bladder and gastric lavage were ineffective, forced-air and circulating water cooling resulted in cooling rates around 1.6°C·hr^–1, and greatest cooling occurred with ice-water immersion (9.7°C·hr^–1).²⁷ A retrospective review found endovascular cooling was superior to cooling blankets for rapid induction of hypothermia in subarachnoid hemorrhage patients.²⁸ At present, there is insufficient evidence to make definitive recommendations among techniques to induce therapeutic hypothermia after cardiac arrest. Comparative studies of techniques or combinations of techniques are required. Given the costs of equipment being marketed for therapeutic hypothermia, cost effectiveness and cost utility studies are also needed.

The ACLS 2000 guidelines recommend normalization of magnesium and potassium levels in the post-arrest period³⁴ (Grade E). It is clear that routine magnesium administration is not indicated in patients presenting with ST-elevation myocardial infarction.³⁵ Magnesium ions act as cerebral vasodilators and non-competitive antagonists of the N-methyl-D-aspartate receptor and have been studied as a neuroprotective agent in human stroke.^36,37 At present, evidence is insufficient to support routine magnesium administration for neuroprotection in post-arrest patients.

The recommendation to replace lines that may have been placed when adherence to aseptic technique cannot be ensured comes from the ACLS 2000 guidelines and Centers for Disease Control guidelines^3,38 (Grade E). ACLS 2000 guidelines also suggest searching for complications of cardiopulmonary resuscitation such as rib fractures, pneumothorax, and pericardial tamponade in resuscitated post-arrest patients³ (Grade E).

The final recommendation in this section advocates routine administration of prophylaxis to prevent venous thromboembolism in ICU patients. Venous thromboembolism prevention has been extensively reviewed, and guidelines were published by the American College of Chest Physicians (ACP) in 2001.³⁹ ACP guidelines support routine prophylaxis in patients admitted to ICU following cardiac arrest. (Grade A for general ICU patients, no specific data for post-arrest patients, but benefit should be applicable to post-arrest patients).

	Neurologic recommendations (Table III)

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Many of these recommendations are generalized from other types of cerebral injury. It is well accepted that hypoxia, hypotension, and ongoing seizures are bad for the injured brain.⁴⁰ Some post-arrest patients will develop cerebral edema and raised intracranial pressure.⁴¹ The recommendation to elevate the head of the bed and maintain central position reflects the standard approach in head injured patients and is advocated in the ACLS 2000 guidelines³ (Grade C). Head elevation has not been prospectively studied in cardiac arrest patients, but is a reasonable extrapolation from head injury studies. It may also help with patients intubated for long periods as head of bed elevation has been recommended to decrease ventilator-associated pneumonia in intubated patients.⁴²

Sedation use in post-arrest patients has not been studied. The European hypothermia study employed sedation with infusions of fentanyl and midazolam and used neuromuscular blockers during the hypothermia period.⁴ There are no human data to suggest that post-resuscitation administration of sedative agents improves outcome from anoxic or traumatic brain injury. A large trial of barbiturate therapy in cardiac arrest survivors was negative.² Routine administration of neuromuscular blockers complicates clinical neurologic examination and is not universal practice. Propofol has seen increasing use in neuroanesthesia for head injured patients and is frequently used to sedate ICU patients. It has been studied in the treatment of head injured intubated patients and shown to be safe, although not associated with better outcomes than morphine.⁴³ Its inclusion acknowledges the increasingly common use of propofol in intensive care units for short-term sedation of critically ill adults, but also acknowledges a paucity of data. Daily interruption of sedation has been studied in critically ill patients and was associated with decreased time of mechanical ventilation and time in the ICU.⁴⁴ This intervention has not been studied in post-arrest patients, however the principle of minimizing sedation to allow assessment of neurologic status and ability to breathe should apply to this population (Grade B).

The management protocol for post-arrest patients who are seizing follows evidence-based recommendations for therapy in standard sources.⁴⁵ There are no specific studies in post-arrest patients to consider, but no reason to deviate from standard seizure treatment recommendations (Grade A). There are no evidence based recommendations for treatment of myoclonus in post-arrest survivors. There are data suggesting that myoclonic status epilepticus in post-anoxic coma arises from lethal damage to neurons.⁴⁶ Wijdicks et al. studied 40 patients with myoclonus status after cardiac resuscitation and concluded that it should be considered an agonal phenomenon indicating devastating neocortical damage.⁴⁷ There is a syndrome of post-hypoxic myoclonus (Lance-Adams syndrome) where myoclonus can be initiated by action or auditory or painful stimuli. This has a much better prognosis and has been treated with clonazepam.^48–50 Animal data suggest the pathogenesis of post-hypoxic myoclonus may involve activation of glutamate neurotransmission,⁵¹ and serotonin receptors have also been implicated.⁵² Animal models have tested new anticonvulsants (riluzole and lamotrigine) and reported antimyoclonic and neuroprotective effects.^52,53 Propofol has also been recommended based on anecdotal evidence.⁵⁴ The recommendations made for clonazepam or valproic acid are clearly not based on high grade evidence (Grade E). Treatment of myoclonus after cardiac arrest is an area where trials are needed. Treatment with any agent is difficult and often unsuccessful.

There are two published structured reviews on post-arrest prognostication using clinical criteria.^55,56 Both concur that accurate prediction can only occur after 72 hr have elapsed from return of spontaneous circulation (ROSC). Motor response to pain at the 72-hr interval predicted poor outcome if the patient did not move or exhibited extensor or flexor posturing. Recently a structured review of clinical examination in comatose patients following cardiac arrest found useful likelihood ratios (LR) for four clinical signs 24 hr after ROSC.⁵⁷ The four signs at 24 hr were absent corneal reflexes [LR 12.9; 95% confidence interval (CI) 2.0–68.7], absent pupillary response (LR 10.2; 95% CI 1.8–48.6), absent withdrawal response to pain (LR 4.7; 95% CI 2.2–9.8), no motor response (LR 4.9; 95% CI 1.6–13.0). Absent motor response to pain 72 hr after ROSC was also found to predict death or poor outcome (LR 9.2; 95% CI 2.1–49.4) The review by Booth and colleagues estimated 77% pre-test probability of poor neurologic outcome in comatose post-arrest survivors.⁵⁷

At the conference, participants determined that motor response to pain at 72 hr was the best supported clinical predictor. Therapeutic hypothermia can complicate using motor response to pain for prediction, especially if sedation and neuromuscular blockade are employed. These concerns resulted in recommendations for short-acting sedatives and neuromuscular blockers, and consideration of inducing therapeutic hypothermia without sedation/paralysis if possible (Grade E). If physicians are confident that sedatives and neuromuscular blockers are not confounding the neurologic examination, lack of motor response to pain 72 hr after ROSC should prompt consideration of withdrawal of life support and institution of palliative care (Grade D). The usual caveats of medications, temperature, and other disease processes beside central nervous system damage must be considered before applying this prediction rule. The best original studies on the topic were published between 1985–1995.^58,59 The age of the data suggests additional studies would be useful, given changes in practice and technology since that time.

Routine computed tomography (CT) scanning cannot be supported in post-arrest patients with anoxic cerebral damage (Grade E). There are no trials indicating that CT imaging adds to clinical assessment unless stroke, bleeding or trauma is suspected on the basis of history or clinical examination. There are preliminary reports that magnetic resonance imaging (MRI) can be used to determine the prognosis of patients with diffuse cerebral anoxia.^60,61 The role of MRI in post-arrest patients is an exciting approach which should be integrated into future research.

Systematic reviews of outcome prediction in comatose patients post-arrest have concluded that somatosensory evoked potentials (SSEP) are the best diagnostic method for predicting outcome^55,56 (Grade C). New research should evaluate SSEP in larger samples to determine the utility and value of the technique. Routine electroencephalograms were not supported by the results of the published reviews, but should be used if ongoing seizure activity is suspected.⁵⁵

Outcome measurements beyond mortality are important for resuscitation research. Guidelines for reporting data from both out-of-hospital and in-hospital resuscitation attempts (Utstein style) have been developed by an international process.^62,63 The use of the Glasgow outcome scoring system is recommended for reporting results of resuscitation research^64,65 (Grade E). This system records cerebral performance category (CPC) and overall performance category (OPC) at intervals to determine degree of impairment after cardiac arrest. Additional, more sensitive, instruments should also be employed, but CPC and OPC represent the minimum outcome dataset for resuscitation research.

	Respiratory recommendations (Table IV)

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In 1986 Safar proposed maintaining PaO₂ over 100 mmHg and using minimal positive end-expiratory pressure (PEEP) after ROSC.^1,2 The evidence for this recommendation is not clear, and recent ACLS 2000 revisions have not specified PaO₂ goals.³ There are data from animal studies showing worse central nervous system outcomes and higher levels of oxidized cerebral lipids in dogs resuscitated and maintained at FIO₂ ^1.0 for at least one hour post-resuscitation.^66,67 There do not appear to be any human data to consider on the topic. The proposal to maintain PaO₂ over 100 mmHg for the first 24 hr reflects common practice in ICU and physician comfort (Grade E). Studies are needed to determine if this approach is harmful. The PEEP recommendation also reflects common practice and animal data that repeated opening and closing of alveoli and normal tidal volumes may be harmful in the setting of acute lung injury⁶⁸ (Grade E).

There is controversy about the efficacy of buffers in the management of lactic acidosis.⁷⁰ ACLS 200 guidelines have de-emphasized the use of buffers during resuscitation except in the setting of known or suspected hyperkalemia.³⁴ Buffer infusion has been shown to treat non-anion gap metabolic acidosis produced by infusion of normal saline solutions.⁷¹ Buffer infusion was also employed for pH correction during a recent trial of low tidal volumes in the management of Acute Respiratory Distress Syndrome.⁷² Given these ongoing uses of buffering agents in intensive care patients, it appears reasonable to suggest their use for specific indications in post-arrest management (Grade E). Physicians and nurses must ensure that improvement of oxygen delivery takes precedence over infusion of buffers when facing unresolving lactic acidosis post-resuscitation.

	Cardiac recommendations (Table V)

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Blood pressure goals after resuscitation were set by Safar in 1986.¹ Routine insertion of an arterial line in patients with brain injury post-resuscitation is recommended to measure blood pressure, facilitate arterial blood gas sampling, follow glucose levels when using insulin infusions, and to closely monitor patients receiving therapeutic hypothermia (Grade E). In the early post-arrest period, cerebral blood flow may be significantly decreased^73–75 and the cerebral autoregulatory curve right-shifted.^76,77 Therefore, hypotension (mean arterial pressure < 80 mmHg) should be scrupulously avoided. A mean arterial pressure range of 80 to 100 mmHg is recommended in post-arrest patients, with higher pressures targeted in chronically hypertensive patients with shifted autoregulatory curves (Grade D).

In 1992 the American Heart Association ACLS guidelines included the concept of a "cardiovascular triad" of conducting system, myocardium, and vascular system to conceptualize treatment of hypotension and shock during the first hour of resuscitation.⁸² Using this approach hypotension mechanisms are: rate problems, pump problems, or volume problems. The use of repeated titrated volume infusion (250–500 mL aliquots of normal saline) followed by sympathomimetic therapy (norepinephrine, dopamine) if volume infusion is unsuccessful, is suggested for restoration of systolic blood pressure⁸² (Grade E). The use of pulmonary artery catheters in ICU patients has generated controversy.^83–85 Despite this, the 2000 ACLS guidelines target systolic blood pressure over 100 mmHg and cardiac index > 2.5 L·min^–1·m² using dobutamine as the first line agent for low cardiac index once systolic blood pressure exceeds 100 mmHg.³ Poor left ventricular (LV) function has been found during the post-resuscitation period in humans surviving out-of-hospital cardiac arrest.⁸⁶ Animal studies support the use of dobutamine to manage post-resuscitation LV systolic and diastolic dysfunction.⁸⁷ Human outcome data in post-arrest patients are lacking, but maintenance of adequate forward cardiac output with inotropic support is recommended over emphasis on blood pressure goals only (Grade E). Given positive results reported from early goal-directed hemodynamic resuscitation in septic shock,⁸⁸ similar strategies should be studied during resuscitation of patients following cardiac arrest.

Acute coronary syndrome has been studied extensively and practice guidelines established by the American College of Cardiology (ACC) and the American Heart Association (AHA) for unstable angina and non-ST segment elevation myocardial infarction were updated in 2002.⁸⁹ The ACC/AHA also published guidelines in 1999 for the management of patients with acute ST elevation myocardial infarction.⁹⁰ In addition the ACLS 2000 guidelines outline management plans for resuscitated patients with acute coronary syndromes.⁹¹ These existing guidelines are the basis for recommendations to administer aspirin, beta blockers, and anticoagulants or other antiplatelet agents when acute coronary syndrome or myocardial infarction are diagnosed. The working group felt ACC/AHA guidelines should be followed when post-arrest patients have evidence of an acute coronary syndrome (Grade A). There is evidence supporting an immediate aggressive invasive strategy in patients resuscitated from out-of-hospital cardiac arrest.⁹² Application of a standardized protocol of revascularization and electrophysiologic testing in survivors of cardiac arrest has been reported to be associated with excellent long-term outcomes.⁹³ One group has reported a small trial where a clinical prediction rule was evaluated to aid triage decisions about use of an invasive strategy in post-arrest patients.⁹⁴ This approach requires further validation.

Amiodarone is effective treatment of hemodynamically unstable ventricular tachycardia and ventricular fibrillation and has been recommended in the ACLS 2000 guidelines because of its broad antiarrhythmic spectrum and lesser negative inotropic effects compared to lidocaine⁹⁵ (Grade B). Implantable defibrillator insertion should be considered according to guidelines published by the ACC/AHA.⁹⁶

	GI recommendations (Table VI)

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Hyperglycemia is common following resuscitation from cardiac arrest and several studies have addressed the association of blood glucose concentration and neurologic outcome in humans following cardiac arrest.^97–102 Animal studies have demonstrated that insulin treatment can reduce ischemic necrosis and modify the structural and neurobehavioural consequences of cerebral ischemia in rats.^103,104 A recent study in critically ill patients admitted to surgical ICU demonstrated significant mortality benefit when glucose levels were clamped between 4.4 to 6.1 mmol·L^–1 using insulin infusion with administration of calories via iv glucose infusion or enteral/parenteral nutrition.¹⁰⁵ These findings suggest that hyperglycemia should be treated with insulin infusions following cardiac arrest (Grade D).

Infusion of glucose containing solutions or the provision of enteral or parenteral feeding was felt to be critical to prevent hypoglycemia in post-arrest patients, particularly when insulin infusions are used (Grade E). Caution must be exercised with infusion of hypotonic solutions as animal data suggest this can worsen cerebral edema and raise intracranial pressure.¹⁰⁷ Indeed, hypertonic resuscitation fluids have been reviewed in trauma, head injury, and sepsis and may offer outcome advantages over isotonic solutions.^108,109

Canadian clinical practice guidelines for nutrition support in mechanically ventilated ICU patients have been published recently.¹¹⁰ These guidelines favour enteral nutrition over parenteral nutrition and suggest initiation within 24 to 48 hr after ICU admission. There are no data to suggest the Canadian guidelines should not be adhered to in the management of post-cardiac arrest patients (Grade E).

Guidelines on stress ulcer prophylaxis have been published,¹¹¹ and a large randomized controlled trial in mechanically ventilated ICU patients was completed in Canada.¹¹² The recommendation for H₂ blocker or sucralfate administration comes from these sources. These studies have included small numbers of post-arrest patients, but the population has multiple known risk factors for stress ulceration. Despite the lack of specific trials in post-arrest populations this recommendation was assigned evidence Grade A. Proton pump inhibitors safely and efficaciously increase gastric pH in critically ill patients, but have not demonstrated superiority over H₂ blockers or sucralfate for prophylaxis in ICU patients. Their use is suggested only as an alternate to the other agents until additional data are obtained.

	Conclusion

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Each day patients are resuscitated from cardiac arrest and admitted to critical care units. Recent research has demonstrated improved outcomes with pre-arrest interventions (access to automated defibrillators),¹¹³ intra-arrest interventions (vasopressin for asystole),¹¹⁴ and post-arrest interventions (therapeutic hypothermia).^4,5 Only time will determine if these advances result in improved outcome outside of study populations. To date studies indicate that less than 20% of patients experiencing cardiac arrest are discharged from hospital.¹¹⁵

It is possible outcomes will improve if interventions from recent studies are adopted into clinical practice. Participants at the 2003 Rocky Mountain Critical Care Conference believe post-arrest management requires examination and standardization. This was felt to be particularly important to facilitate future research in cardiac arrest patients. It is apparent that many of the basic aspects of post-arrest care have never been tested in well-designed trials. There are exciting opportunities to test interventions and management strategies in post-arrest patients, which has the potential to improve care and outcome in the future.

	Acknowledgments

 
We thank Dr. Dan Roberts for moderating the session at the conference.

	Footnotes

 
The 2003 Rocky Mountain Critical Care Conference (February 19–22, 2003) was organized by the Continuing Medical Education Department and the Section of Critical Care of the University of Manitoba. Unrestricted grants to support the conference were obtained from Astra Zeneca and Lilly. No author reported a conflict of interest. Conference website: www.rmccc.ca

Accepted for publication May 31, 2004. Revision accepted December 13, 2004.

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