《心肺复苏指南》参考资料（英文版）Part 7.5：Postresuscitation Support

Flew randomized controlled clinical trials deal specifically inprovement in gas exchange do not ensure survival and with supportive care following cardio-pulmonary- functional recovery. Significant myocardial stunning and cerebral resuscitation(CPCR) from cardiac arrest. Neverthe- hemodynamic instability can develop,

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Part 7.5: Postresuscitation Support F lew randomized controlled clinical trials deal specifically inprovement in gas exchange do not ensure survival and with supportive care following cardio-pulmonary- functional recovery. Significant myocardial stunning and cerebral resuscitation(CPCR) from cardiac arrest. Neverthe- hemodynamic instability can develop, requiring vasopressor less, postresuscitation care has significant potential to im- support. Most postresuscitation deaths occur during the first prove early mortality caused by hemodynamic instability and 24 hours. 6,7 multi-organ failure and later mortality/morbidity resultin Ideally the patient will be awake, responsive, and breathin from brain injury. This section summarizes our evolving spontaneously. Alternatively the patient may initially be understanding of the hemodynamic, neurologic, and metabol- comatose but have the potential for full recovery after ic abnormalities encountered in patients who are resuscitated postresuscitation care. 3 Indeed, up to 20% of initially coma- from cardiac arrest tose survivors of cardiac arrest have been reported to have Initial objectives of postresuscitation care good l-year neurologic outcome. The pathway to the best Optimize cardiopulmonary function and hospital postresuscitation care of all initial survivors is not completely known, but there is increasing interest in identi- sion, especially perfusion to the brain Transport the victim of out-of-hospital cardiac arrest to the fying and optimizing practices that can improve outcome. 9 hospital emergency department(ED) and continue care Regardless of the patient's initial status, the provider should support adequate airway and breathing, administer supple an appropriately equipped critical care unit Try to identify the precipitating causes of the arrest mentary oxygen, monitor the patients vital signs, establish or Institute measures to prevent recurrence verify existing intravenous access, and verify the function of any catheters in place. Institute measures that may improve long-term, neurolog ally intact survival The clinician should assess the patient frequently and treat abnormalities of vital signs or cardiac arrhythmias and Improving postresuscitation Outcomes request studies that will further aid in the evaluation of the Postresuscitation care is a critical component of advanced life patient. It is important to identify and treat any cardiac support. Patient mortality remains high after return of spon- electrolyte, toxicologic, pulmonary, and neurologic precipi- taneous circulation(ROSC) and initial stabilization. Ultimate tants of arrest. The clinician may find it helpful to review the H's and Ts mnemonic to recall factors that may contribute to prognosis in the first 72 hours may be difficult to determine, 2 cardiac arrest or complicate resuscitation or postresuscitation yet survivors of cardiac arrest have the potential to lead care: hypovolemia, hypoxia, hydrogen ion(acidosis), hyper-/ normal lives. -5 During postresuscitation care providers hypokalemia, hypogl ycemia, hypothermia; toxins, tamponade should(1)optimize hemodynamic, respiratory, and neuro-(cardiac), tension pneumothorax, thrombosis of the coronary logic support;(2)identify and treat reversible causes of rrest; and (3)monitor temperature and consider treatment for or pulmonary vasculature, and trauma. For further inform disturbances of temperature regulation and metabolism. The tion see Part 10: " Special Resuscitation Situations first sections below discuss initial stabilization and tempera- After initial assessment and stabilization of airway, venti- lation, and circulation, transfer the patient to a special care ture/metabolic factors that may be relevant to improving unit for observation, continuous monitoring, and further ation outcome, particularly in the critically ill survivor. Subsequent sections highlight organ-specific eval- therapy. Personnel with appropriate training and resuscitation uation and support equipment must accompany the patient during transport to the special care unit. Return of Spontaneous Circulatin The principal objective of postresuscitation care is the re- Temperature Regulation establishment of effective perfusion of organs and tissue. Induced Hypothermia After ROSC in the out-of-hospital or in-hospital setting, the Both permissive hypothermia(allowing a mild degree of provider must consider and treat the cause of the arrest and hypothermia >33C [91.5.F] that often develops sponta the consequences of any hypoxemic/ischemic/reperfusion ously after arrest) and active induction of hypothermia may injury. In most cases the acidemia associated with cardiac play a role in postresuscitation care. In 2 randomized clinical arrest improves spontaneously when adequate ventilation and trials(LOE 1: LOE 2)induced hypothermia( cooling within perfusion are restored. But restoration of blood pressure and minutes to hours after ROSC) resulted in improved outcome in adults who remained comatose after initial resuscitation from out-of-hospital ventricular fibrillation(VF) cardiac ar- (Circulation. 2005: 000: IV-84-IV-88) o 2005 American Heart Associa rest. Patients in the study were cooled to 33C(915F) or to the range of32cto34°C(89.6°Fto93.2°F)4forl2to24 This special supplement to Circulation is freely available at http://www.circulationaha.org hours. The Hypothermia After Cardiac Arrest(HACA)study included a small subset of patients with in-hospital cardiac DOI: 10.1161/CIRCULATIONAHA. 105.166560 arrest IV-84

Part 7.5: Postresuscitation Support Few randomized controlled clinical trials deal specifically with supportive care following cardio-pulmonarycerebral resuscitation (CPCR) from cardiac arrest. Nevertheless, postresuscitation care has significant potential to improve early mortality caused by hemodynamic instability and multi-organ failure and later mortality/morbidity resulting from brain injury.1 This section summarizes our evolving understanding of the hemodynamic, neurologic, and metabolic abnormalities encountered in patients who are resuscitated from cardiac arrest. Initial objectives of postresuscitation care are to ● Optimize cardiopulmonary function and systemic perfusion, especially perfusion to the brain ● Transport the victim of out-of-hospital cardiac arrest to the hospital emergency department (ED) and continue care in an appropriately equipped critical care unit ● Try to identify the precipitating causes of the arrest ● Institute measures to prevent recurrence ● Institute measures that may improve long-term, neurologically intact survival Improving Postresuscitation Outcomes Postresuscitation care is a critical component of advanced life support. Patient mortality remains high after return of spontaneous circulation (ROSC) and initial stabilization. Ultimate prognosis in the first 72 hours may be difficult to determine,2 yet survivors of cardiac arrest have the potential to lead normal lives.3–5 During postresuscitation care providers should (1) optimize hemodynamic, respiratory, and neurologic support; (2) identify and treat reversible causes of arrest; and (3) monitor temperature and consider treatment for disturbances of temperature regulation and metabolism. The first sections below discuss initial stabilization and temperature/metabolic factors that may be relevant to improving postresuscitation outcome, particularly in the critically ill survivor. Subsequent sections highlight organ-specific evaluation and support. Return of Spontaneous Circulation The principal objective of postresuscitation care is the reestablishment of effective perfusion of organs and tissue. After ROSC in the out-of-hospital or in-hospital setting, the provider must consider and treat the cause of the arrest and the consequences of any hypoxemic/ischemic/reperfusion injury. In most cases the acidemia associated with cardiac arrest improves spontaneously when adequate ventilation and perfusion are restored. But restoration of blood pressure and improvement in gas exchange do not ensure survival and functional recovery. Significant myocardial stunning and hemodynamic instability can develop, requiring vasopressor support. Most postresuscitation deaths occur during the first 24 hours.6,7 Ideally the patient will be awake, responsive, and breathing spontaneously. Alternatively the patient may initially be comatose but have the potential for full recovery after postresuscitation care.3 Indeed, up to 20% of initially comatose survivors of cardiac arrest have been reported to have good 1-year neurologic outcome.8 The pathway to the best hospital postresuscitation care of all initial survivors is not completely known, but there is increasing interest in identifying and optimizing practices that can improve outcome.9 Regardless of the patient’s initial status, the provider should support adequate airway and breathing, administer supplementary oxygen, monitor the patient’s vital signs, establish or verify existing intravenous access, and verify the function of any catheters in place. The clinician should assess the patient frequently and treat abnormalities of vital signs or cardiac arrhythmias and request studies that will further aid in the evaluation of the patient. It is important to identify and treat any cardiac, electrolyte, toxicologic, pulmonary, and neurologic precipitants of arrest. The clinician may find it helpful to review the H’s and T’s mnemonic to recall factors that may contribute to cardiac arrest or complicate resuscitation or postresuscitation care: hypovolemia, hypoxia, hydrogen ion (acidosis), hyper-/ hypokalemia, hypoglycemia, hypothermia; toxins, tamponade (cardiac), tension pneumothorax, thrombosis of the coronary or pulmonary vasculature, and trauma. For further information see Part 10: “Special Resuscitation Situations.” After initial assessment and stabilization of airway, ventilation, and circulation, transfer the patient to a special care unit for observation, continuous monitoring, and further therapy. Personnel with appropriate training and resuscitation equipment must accompany the patient during transport to the special care unit. Temperature Regulation Induced Hypothermia Both permissive hypothermia (allowing a mild degree of hypothermia 33°C [91.5°F] that often develops spontaneously after arrest) and active induction of hypothermia may play a role in postresuscitation care. In 2 randomized clinical trials (LOE 13; LOE 24) induced hypothermia (cooling within minutes to hours after ROSC) resulted in improved outcome in adults who remained comatose after initial resuscitation from out-of-hospital ventricular fibrillation (VF) cardiac arrest. Patients in the study were cooled to 33°C (91.5°F)3 or to the range of 32°C to 34°C (89.6°F to 93.2°F)4 for 12 to 24 hours. The Hypothermia After Cardiac Arrest (HACA) study3 included a small subset of patients with in-hospital cardiac arrest. (Circulation. 2005;000:IV-84-IV-88.) © 2005 American Heart Association. This special supplement to Circulation is freely available at http://www.circulationaha.org DOI: 10.1161/CIRCULATIONAHA.105.166560 IV-84

Part 7.5: Postresuscitation Support Iv-85 A third study(LOE 2) o documented improvement in during or after resuscitation from cardiac arrest. 14 metabolic end points (lactate and Oz extraction) when over, several studies have documented worse tose adult patients were cooled after ROSC from outcome in humans with fever after cardiac arrest hospital cardiac arrest in which the initial rhythm and ischemic brain injury (LOE 7 extrapolated from stroke pulseless electrical activity(PEA)/asystole victims). Thus, the provider should monitor the patient In the HACA and Bernard studies, only about 8% of temperature after resuscitation and avoid hyperthermia. patients with cardiac arrest were selected for induced hypo- thermia(ie, patients were hemodynamically stable but coma- Glucose Control This highlights the importance of identif ying the sube v). The postresuscitation patient is likely to develop electrolyte tose after a witnessed arrest of presumed cardiac etiology) abnormalities that may be detrimental to recovery. Although patients who may most benefit. Although the number of many studies have documented a strong association between patients who may benefit from hypothermia induction is high blood glucose after resuscitation from cardiac arrest and limited at present, it is possible that with more rapid and poor neurologic outcomes (Loe 421,22: LOE 59.22-26: LO controlled cooling and better insights into optimal target 627), they did not show that control of serum glucose level temperature, timing, duration, and mechanism of action, such alters outcome cooling may prove more widely beneficial in the future. A A prospective randomized study by van den Berghe (Oe recent multicenter study in asphyxiated neonates showed that 1)8 did show that tight control of blood glucose using insulin hypothermia can be beneficial in another select population. reduced hospital mortality rates in critically ill patients who Complications associated with cooling can include coagu- required mechanical ventilation. The study did not specifi- opathy and arrhythmias, particularly with an unintentional cally focus on postresuscitation patients, but the effect of drop below target temperature. Although not significantly blood glucose control on outcome is compelling. The study higher, cases of pneumonia and sepsis increased in the documented not only improved survival but decreased mor hypothermia-induction group3.4 Cooling may also increase tality from infectious complications, a common problem in the postresuscitation setting Most clinical studies of cooling have used external cooling In comatose patients, signs of hypoglycemia are less echniques(eg, cooling blankets and frequent applications of apparent, so clinicians must monitor serum glucose closely to ice bags)that may require a number of hours to attain target avoid hypoglycemia when treating hyperglycemia. On the temperature. More recent studies 3 suggest that internal cool- basis of findings of improved outcomes in critically ill ing techniques(eg, cold saline, endovascular cooling cathe patients when glucose levels are maintained in the normal ter)can also be used to induce hypothermia. Providers should range, it is reasonable for providers to maintain strict glucose continuously monitor the patient's temperature during control during the postresuscitation period. Additional study is needed, however, to identify the precise blood glucose In summary, providers should not actively rewarm hemo- concentration that requires insulin therapy, the target range of dynamically stable patients who spontaneously develop a blood glucose concentration, and the effect of tight glucose mild degree of hypothermia(33C [91.5FD after resusci- control on outcomes of patients after cardiac arrest. ation from cardiac arrest. Mild hypothermia may be benefi cial to neurologic outcome and is likely to be well tolerated Organ-Specific Evaluation and Support without significant risk of complications. In a select subset of After ROSC patients may remain comatose or have decreased patients who were initial y comatose but hemodynamically responsiveness for a variable period of time. If spontaneous stable after a witnessed vF arrest of presumed cardiac breathing is absent or inadequate, mechanical ventilation via etiology, active induction of hypothermia was beneficial. 3.4 3 an endotracheal tube or other advanced airway device may be Thus, unconscious adult patients with ROSC after out-of- required Hemodynamic status may be unstable with abnor hospital cardiac arrest should be cooled to 32C to 34.C malities of cardiac rate, rhythm, systemic blood pressure, and (89.6F to 93.2 F) for 12 to 24 hours when the initial rhythm organ perfusion was vF(Class IIa). Similar therapy may be beneficial for linicians must prevent, detect, and treat hypoxemia and patients with non-VF arrest out of hospital or for in-hospital hypotension because these conditions can exacerbate brain arrest(Class Ilb). injury. Clinicians should determine the baseline postarrest status of each organ system and support organ function as Hyperthermia needed After resuscitation, temperature elevation above normal can The remainder of this chapter focuses on organ-specific create a significant imbalance between oxygen supply and measures that should be provided in the immediate postresus- citation period either frequent use of antipyretics or"controlled normother mia"with cooling techniques) have directly examined the Respiratory System effect of temperature control immediately after resuscitation. After ROSC patients may exhibit respiratory dysfunction Because fever may be a symptom of brain injury, it may be Some patients will remain dependent on mechanical ventila difficult to control it with conventional antipyretics. Many tion and will need an increased inspired concentration of studies of brain injury in animal models, however, show oxygen. Providers should perform a full physical examination exacerbation of injury if body/brain temperature is increased and evaluate the chest radiograph to verify appropriate

A third study (LOE 2)10 documented improvement in metabolic end points (lactate and O2 extraction) when comatose adult patients were cooled after ROSC from out-ofhospital cardiac arrest in which the initial rhythm was pulseless electrical activity (PEA)/asystole. In the HACA3 and Bernard4 studies, only about 8% of patients with cardiac arrest were selected for induced hypothermia (ie, patients were hemodynamically stable but comatose after a witnessed arrest of presumed cardiac etiology). This highlights the importance of identifying the subset of patients who may most benefit. Although the number of patients who may benefit from hypothermia induction is limited at present, it is possible that with more rapid and controlled cooling and better insights into optimal target temperature, timing, duration, and mechanism of action, such cooling may prove more widely beneficial in the future.11 A recent multicenter study in asphyxiated neonates showed that hypothermia can be beneficial in another select population.12 Complications associated with cooling can include coagulopathy and arrhythmias, particularly with an unintentional drop below target temperature. Although not significantly higher, cases of pneumonia and sepsis increased in the hypothermia-induction group.3,4 Cooling may also increase hyperglycemia.4 Most clinical studies of cooling have used external cooling techniques (eg, cooling blankets and frequent applications of ice bags) that may require a number of hours to attain target temperature. More recent studies13 suggest that internal cooling techniques (eg, cold saline, endovascular cooling catheter) can also be used to induce hypothermia. Providers should continuously monitor the patient’s temperature during cooling.3,4 In summary, providers should not actively rewarm hemodynamically stable patients who spontaneously develop a mild degree of hypothermia (33°C [91.5°F]) after resuscitation from cardiac arrest. Mild hypothermia may be beneficial to neurologic outcome and is likely to be well tolerated without significant risk of complications. In a select subset of patients who were initially comatose but hemodynamically stable after a witnessed VF arrest of presumed cardiac etiology, active induction of hypothermia was beneficial.3,4,13 Thus, unconscious adult patients with ROSC after out-ofhospital cardiac arrest should be cooled to 32°C to 34°C (89.6°F to 93.2°F) for 12 to 24 hours when the initial rhythm was VF (Class IIa). Similar therapy may be beneficial for patients with non-VF arrest out of hospital or for in-hospital arrest (Class IIb). Hyperthermia After resuscitation, temperature elevation above normal can create a significant imbalance between oxygen supply and demand that can impair brain recovery. Few studies (with either frequent use of antipyretics or “controlled normothermia” with cooling techniques) have directly examined the effect of temperature control immediately after resuscitation. Because fever may be a symptom of brain injury, it may be difficult to control it with conventional antipyretics. Many studies of brain injury in animal models, however, show exacerbation of injury if body/brain temperature is increased during or after resuscitation from cardiac arrest.14 –17 Moreover, several studies have documented worse neurologic outcome in humans with fever after cardiac arrest (LOE 3)18 and ischemic brain injury (LOE 7 extrapolated from stroke victims18). Thus, the provider should monitor the patient’s temperature after resuscitation and avoid hyperthermia. Glucose Control The postresuscitation patient is likely to develop electrolyte abnormalities that may be detrimental to recovery. Although many studies have documented a strong association between high blood glucose after resuscitation from cardiac arrest and poor neurologic outcomes (LOE 421,22; LOE 59,22–26; LOE 627), they did not show that control of serum glucose level alters outcome. A prospective randomized study by van den Berghe (LOE 1)28 did show that tight control of blood glucose using insulin reduced hospital mortality rates in critically ill patients who required mechanical ventilation. The study did not specifically focus on postresuscitation patients, but the effect of blood glucose control on outcome is compelling. The study documented not only improved survival but decreased mortality from infectious complications, a common problem in the postresuscitation setting. In comatose patients, signs of hypoglycemia are less apparent, so clinicians must monitor serum glucose closely to avoid hypoglycemia when treating hyperglycemia. On the basis of findings of improved outcomes in critically ill patients when glucose levels are maintained in the normal range, it is reasonable for providers to maintain strict glucose control during the postresuscitation period. Additional study is needed, however, to identify the precise blood glucose concentration that requires insulin therapy, the target range of blood glucose concentration, and the effect of tight glucose control on outcomes of patients after cardiac arrest. Organ-Specific Evaluation and Support After ROSC patients may remain comatose or have decreased responsiveness for a variable period of time. If spontaneous breathing is absent or inadequate, mechanical ventilation via an endotracheal tube or other advanced airway device may be required. Hemodynamic status may be unstable with abnormalities of cardiac rate, rhythm, systemic blood pressure, and organ perfusion. Clinicians must prevent, detect, and treat hypoxemia and hypotension because these conditions can exacerbate brain injury. Clinicians should determine the baseline postarrest status of each organ system and support organ function as needed. The remainder of this chapter focuses on organ-specific measures that should be provided in the immediate postresuscitation period. Respiratory System After ROSC patients may exhibit respiratory dysfunction. Some patients will remain dependent on mechanical ventilation and will need an increased inspired concentration of oxygen. Providers should perform a full physical examination and evaluate the chest radiograph to verify appropriate Part 7.5: Postresuscitation Support IV-85

lV-86 Circulation December 13, 2005 endotracheal tube depth of insertion and identify cardiopul- dysfunction 7 that can last many hours but may improve with monary complications of resuscitation. Providers should ad- vasopressors. 38 Cardiac biomarker levels may be increased in just mechanical ventilatory support based on the patients association with global ischemia caused by absent or de blood gas values, respiratory rate, and work of breathing. As creased coronary blood flow during cardiac arrest and CPR. the patients spontaneous ventilation becomes more efficient, Increased cardiac biomarkers may also indicate acute myo- the level of respiratory support may be decreased until cardial infarction as the cause of cardiac arrest spontaneous respiration returns. If the patient continues to Hemodynamic instability is common after cardiac ar require high inspired oxygen concentrations, providers should d early death due to multi-organ failure is associated with determine if the cause is pulmonary or cardiac and direct care a persistently low cardiac index during the first 24 hours after cordingly resuscitation(LOE 5).6.39 Thus, after resuscitation clinicians Debate exists as to the length of time patients who require should evaluate the patients electrocardiogram, radiographs ventilatory support should remain sedated. To date there is and laboratory analyses of serum electrolytes and cardiac little evidence to guide therapy. One observational study biomarkers. Echocardiographic evaluation within the first 24 (LOE 3)29 found an association between use of sedation and hours after arrest is useful to guide ongoing management 5.40 development of pneumonia in intubated patients during the One large case series(LoE 5)6 of patients resuscitated designed to investigate sedation as a risk factor for either cant early but reversible myocardial dysfunction and low time there is inadequate data to recommend for or against the cardiac output, followed by later vasodilation. The hemody use of a defined period of sedation or neuromuscular block namic instability responded to fluid administration and vaso- ade after cardiac arrest( Class Indeterminate). Use of neuro- measure blood pressure accurately and to determine the most muscular blocking agents should be kept to a minimum because these agents preclude thorough neurologic assess appropriate combination of medications to optimize blood ments during the first 12 to 72 hours after ROSC. 2 flow and distribution. The provider should titrate volume Sedation may be necessary to control shivering during administration and vasoactive(eg, norepinephrine), inotropic hypothermia. If shivering continues despite optimal sedation, (eg, dobutamine), and inodilator (eg, milrinone) drugs as neuromuscular blockade may be required in addition to deep needed to support blood pressure, cardiac index, and systemic sedation perfusion. The ideal target blood pressure or hemodynamic parameters associated with optimal survival have not been ntilatory Parameter established Sustained hypocapnea(low PCo2) may reduce cerebral blood Both cardiac arrest and sepsis are thought to involve flow 30-31 After cardiac arrest, restoration of blood flow multi-organ ischemic injury and microcirculatory dysfunc results in an initial hyperemic blood flow response that lasts tion. Goal-directed therapy with volume and vasoactive drug to 30 minutes, followed by a more prolonged period of low administration has been effective in improving survival from blood flow. 2. During this latter period of late hypoperfu- sepsis. I The greatest survival benefit is due to a decreased sion, a mismatch between blood flow(oxygen delivery) and incidence of acute hemodynamic collapse, a challenge also oxygen requirement may occur. If the patient is hyperventi- seen in the postresuscitation setting Data extrapolated from a lated at this stage, cerebral vasoconstriction may further study of goal-directed therapy for sepsis(LOE 14 for sepsis: decrease cerebral blood flow and increase cerebral ischemia LOE 7 [extrapolated] for cardiac arrest) suggests that provid- There is no evidence that hyperventilation protects the ers should try to normalize oxygen content and oxygen brain or other vital organs from further ischemic damage after transport. cardiac arrest. In fact, Safar et al34 provided evidence that Relative adrenal insufficiency may develop following the stress of cardiac arrest, but the use of early corticosteroid tilation may also generate increased airway pressures and supplementation in such patients to improve either hemody augment intrinsic positive end-expiratory pressure(so-called amics or outcome is unproven and requires further "auto PEEP"), leading to an increase in cerebral venous and intracranial pressures. 5.36 Increases in cerebral venous pres Although sudden cardiac arrest may be precipitated by sure can decrease cerebral blood flow and increase brain cardiac arrhythmia, it is unclear if antiarrhythmics are bene ischemia ficial or detrimental in the postresuscitation period. Thus, In summary, no data supports targeting a specific arterial there is insufficient evidence to recommend for or against Pacoz level after resuscitation from cardiac arrest. But data prophylactic administration of antiarrhythmic drugs to pa- extrapolated from patients with brain injury supports venti- tients who have survived cardiac arrest from any cause. It lation to normocarbic levels as appropriate. Routine hyper ventilation is detrimental( Class IID) antiarrhythmic drug that was associated with RosC(Class Indeterminate). Also, given the cardioprotective effects of Cardiovascular System B-blockers in the context of ischemic heart disease, the use of Both the ischemia/reperfusion of cardiac arrest and electrical B-blockers in the postresuscitation setting seems prudent if defibrillation can cause transient myocardial stunning and there are no contraindications. 9

endotracheal tube depth of insertion and identify cardiopulmonary complications of resuscitation. Providers should adjust mechanical ventilatory support based on the patient’s blood gas values, respiratory rate, and work of breathing. As the patient’s spontaneous ventilation becomes more efficient, the level of respiratory support may be decreased until spontaneous respiration returns. If the patient continues to require high inspired oxygen concentrations, providers should determine if the cause is pulmonary or cardiac and direct care accordingly. Debate exists as to the length of time patients who require ventilatory support should remain sedated. To date there is little evidence to guide therapy. One observational study (LOE 3)29 found an association between use of sedation and development of pneumonia in intubated patients during the first 48 hours of therapy. The study, however, was not designed to investigate sedation as a risk factor for either pneumonia or death in patients with cardiac arrest. At this time there is inadequate data to recommend for or against the use of a defined period of sedation or neuromuscular blockade after cardiac arrest (Class Indeterminate). Use of neuromuscular blocking agents should be kept to a minimum because these agents preclude thorough neurologic assessments during the first 12 to 72 hours after ROSC.2 Sedation may be necessary to control shivering during hypothermia. If shivering continues despite optimal sedation, neuromuscular blockade may be required in addition to deep sedation. Ventilatory Parameters Sustained hypocapnea (low PCO2) may reduce cerebral blood flow.30 –31 After cardiac arrest, restoration of blood flow results in an initial hyperemic blood flow response that lasts 10 to 30 minutes, followed by a more prolonged period of low blood flow.32,33 During this latter period of late hypoperfusion, a mismatch between blood flow (oxygen delivery) and oxygen requirement may occur. If the patient is hyperventilated at this stage, cerebral vasoconstriction may further decrease cerebral blood flow and increase cerebral ischemia and ischemic injury. There is no evidence that hyperventilation protects the brain or other vital organs from further ischemic damage after cardiac arrest. In fact, Safar et al34 provided evidence that hyperventilation may worsen neurologic outcome. Hyperventilation may also generate increased airway pressures and augment intrinsic positive end-expiratory pressure (so-called “auto PEEP”), leading to an increase in cerebral venous and intracranial pressures.35,36 Increases in cerebral venous pressure can decrease cerebral blood flow and increase brain ischemia. In summary, no data supports targeting a specific arterial PaCO2 level after resuscitation from cardiac arrest. But data extrapolated from patients with brain injury supports ventilation to normocarbic levels as appropriate. Routine hyperventilation is detrimental (Class III). Cardiovascular System Both the ischemia/reperfusion of cardiac arrest and electrical defibrillation can cause transient myocardial stunning and dysfunction37 that can last many hours but may improve with vasopressors.38 Cardiac biomarker levels may be increased in association with global ischemia caused by absent or decreased coronary blood flow during cardiac arrest and CPR. Increased cardiac biomarkers may also indicate acute myocardial infarction as the cause of cardiac arrest. Hemodynamic instability is common after cardiac arrest, and early death due to multi-organ failure is associated with a persistently low cardiac index during the first 24 hours after resuscitation (LOE 5).6,39 Thus, after resuscitation clinicians should evaluate the patient’s electrocardiogram, radiographs, and laboratory analyses of serum electrolytes and cardiac biomarkers. Echocardiographic evaluation within the first 24 hours after arrest is useful to guide ongoing management.5,40 One large case series (LOE 5)6 of patients resuscitated following out-of-hospital cardiac arrest documented significant early but reversible myocardial dysfunction and low cardiac output, followed by later vasodilation. The hemodynamic instability responded to fluid administration and vasoactive support.6 Invasive monitoring may be necessary to measure blood pressure accurately and to determine the most appropriate combination of medications to optimize blood flow and distribution. The provider should titrate volume administration and vasoactive (eg, norepinephrine), inotropic (eg, dobutamine), and inodilator (eg, milrinone) drugs as needed to support blood pressure, cardiac index, and systemic perfusion. The ideal target blood pressure or hemodynamic parameters associated with optimal survival have not been established. Both cardiac arrest and sepsis are thought to involve multi-organ ischemic injury and microcirculatory dysfunction. Goal-directed therapy with volume and vasoactive drug administration has been effective in improving survival from sepsis.41 The greatest survival benefit is due to a decreased incidence of acute hemodynamic collapse, a challenge also seen in the postresuscitation setting. Data extrapolated from a study of goal-directed therapy for sepsis (LOE 141 for sepsis; LOE 7 [extrapolated] for cardiac arrest) suggests that providers should try to normalize oxygen content and oxygen transport. Relative adrenal insufficiency may develop following the stress of cardiac arrest, but the use of early corticosteroid supplementation in such patients to improve either hemodynamics or outcome is unproven and requires further evaluation.42 Although sudden cardiac arrest may be precipitated by cardiac arrhythmia, it is unclear if antiarrhythmics are beneficial or detrimental in the postresuscitation period. Thus, there is insufficient evidence to recommend for or against prophylactic administration of antiarrhythmic drugs to patients who have survived cardiac arrest from any cause. It may be reasonable, however, to continue an infusion of an antiarrhythmic drug that was associated with ROSC (Class Indeterminate). Also, given the cardioprotective effects of -blockers in the context of ischemic heart disease, the use of -blockers in the postresuscitation setting seems prudent if there are no contraindications.9 IV-86 Circulation December 13, 2005

Part 7.5: Postresuscitation Support 1v-87 Central Nervous System S umma Iry A healthy brain and a functional patient are the primary goals The postresuscitation period is often marked by hemodyna of cardio-pulmonary-cerebral resuscitation. Following ic instability as well as laboratory abnormalities. This is also ROSC, after a brief initial period of hyperemia cerebral blood a period for which promising technological interventions flow is reduced(the "no-reflow phenomenon")as a result of such as controlled therapeutic hypothermia are being evalu- microvascular dysfunction. This reduction occurs even when ated. Every organ system is at risk during this time, and patients may ultimately develop multi-organ dysfunction. A Neurologic support for the unresponsive patient should complete discussion of this topic is beyond the scope of this include measures to optimize cerebral perfusion pressure by chapter. The goal of the postresuscitation period is to manage maintaining a normal or slightly elevated mean arterial the patient's vital signs and laboratory abnormalities and pressure and reducing intracranial pressure if it is elevated. support organ system function to increase the likelihood of Because hyperthermia and seizures increase the oxygen intact neurologic requirements of the brain, providers should treat hyperther- mia and consider therapeutic hypothermia. Witnessed sei- References zures should be promptly controlled and maintenance anti I. Safar P. Resuscitation from clinical death: pathophysiologic limits and convulsant therapy initiated( Class Ila). Because of a paucity therapeutic potentials. Crir Care Med. 1988: 16: 923-941 of data, routine seizure prophylaxis is a Class Indeterminate Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient dead vegetative, or severely neurologically impaired? Assessing outcome for recommendation at present. comatose survivors of cardiac arrest. JAMA. 2004: 291: 870-879 3. Hypothermia After Cardiac Arrest Study Group. Mild therapeutic hypo- Prognostic Factors thermia to improve the neurologic outcome after cardiac arrest. N Engi The period after resuscitation is often stressful to medical 4. Bernard SA, Gray Tw, Buist MD, Jones BM, Silvester W, Gutteridge G, staff and family members as questions arise about the Smith K. Treatment of comatose survivors of out-of-hospital cardiac patient's ultimate prognosis. Ideally a clinical assessment, boratory test, or biochemical marker would reliably predict 5. Bunch TJ. White RD. Gersh BJ. Meverden RA, Hodge do, Ballman Kv utcomes of out-of- outcome during or immediately after cardiac arrest. Unfortu- Hammill SC, Shen WK, Packer DL. Long hospital cardiac arrest after successful early defibrillation. N Engl J Med. nately no such predictors are available. Determination of 2003:348:2626-2633 6. Laurent I, Monchi M, Chiche JD, Joly LM, Spaulding C, Bourgeois B be difficult, and coma scores may be less predictive than Cariou A, Rozenberg A, Carli P, Weber S, Hainaut JF. Reversible individual motor and brainstem reflexes found in the first 12 myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol. 2002: 40: 2110-2116. to 72 hours after arrest. 2 7. Negovsky VA. The second step in resuscitation--the In a meta-analysis (Loe 1) bilateral absence of cortical 7 response to median nerve somatosensory-evoked potentials 8. A randomized clinical study of cardiopulmonary-cerebral resuscitation design, methods, and patient characteristics. Brain Resuscitation Clinical predicted poor outcome in normothermic patients who were Trial I Study Group. Am J Emerg Med. 1986: 4: 72-86. comatose for at least 72 hours after hypoxic-ischemic insult. 9. Skrifvars MB, Pettila V, Rosenberg PH, Castren M. A multiple logist A case report also documents the usefulness of this evalu- regression analysis of in-hospital factors related to survival at six months ation. Therefore, median nerve somatosensory-evoked poten- n patients resuscitated from out-of-hospital ventricular fibrillation. Resuscitation. 2003: 59: 319-328 tials measured 72 hours after cardiac arrest can be used to 10. Hachimi-ldrissi S Corne L, Ebinger G, Michotte Y, Huyghens L Mild predict neurologic outcome in patients with hypoxic-anoxid induced by a helmet device: a clinical feasibility study coma Resuscitation. 2001: 51: 275-281 A recent meta-analysis(LOE 1)of ll studies involving 11. Nolan JP, Morley PT, Hoek TL, Hickey RW. Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advancement Life 1914 patients documented 5 clinical signs that were found to Support Task Force of the International Liaison Committee on Resusci- strongly predict death or poor neurologic outcome, with 4 of tation. Resuscitation. 2003: 57: 231-235. the 5 predictors detectable at 24 hours after re 12. Shankaran S. Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, Fanaroff AA, Poole WK, Wright LL, Higgins RD, Fine Absent corneal reflex at 24 hours N. Carlo WA, Duara S, Oh w, Cotten CM, Stevenson DK. Stoll BJ Lemons JA, Guillet R, Jobe AH. Whole-body hypothermia for neonates Absent pupillary response at 24 hours th hypoxic-ischemic encephalopathy. N Engl J Med. 2005:353: Absent withdrawal response to pain at 24 hours No motor response at 24 hours 13. Bernard S, Buist M, Monteiro O, Smith K Induced hypothermia using Large volume ice-cold intravenous fluid in comatose survivors of out-of esponse at 72 hours hospital cardiac arrest: a preliminary report. Resuscitation. 2003 56: 9-13 14. Hickey RW, Kochanek PM, Ferimer H, Alexander HL, Garman RH, An electroencephalogram performed >24 to 48 hours after Graham SH. Induced hyperthermia exacerbates neurologic neuronal his resuscitation has also been shown to provide useful predictive tologic damage after asphyxial cardiac arrest in rats. Crit Care Med. information(LOE 547-50)and can help define prognosis 2003:31:531-535 15. Dietrich WD, Busto R, Halley M, Valdes L The importance of brain temperature in alterations of the blood-brain barrier following cerebral Other Complications schemia. J Neuropathol Exp Neurol. 1990: 49: 486-497 Sepsis is a potentially fatal postresuscitation complication. 51 16. Dietrich WD, Busto R, Valdes I, Loor Y. Effects of normothermic versus Patients with sepsis will benefit from goal-o therapy mild hyperthermic forebrain ischemia in rats. Stroke. 1990: 21 Renal failure 52 and pancreatitis, while often 17. Kim Y, Busto R, Dietrich WD, Kraydieh S berg Md d be diagnosed and evaluated 3.53 postischemic hyperthermia in awake rats worsens the histopath

Central Nervous System A healthy brain and a functional patient are the primary goals of cardio-pulmonary-cerebral resuscitation. Following ROSC, after a brief initial period of hyperemia cerebral blood flow is reduced (the “no-reflow phenomenon”) as a result of microvascular dysfunction. This reduction occurs even when cerebral perfusion pressure is normal.43,44 Neurologic support for the unresponsive patient should include measures to optimize cerebral perfusion pressure by maintaining a normal or slightly elevated mean arterial pressure and reducing intracranial pressure if it is elevated. Because hyperthermia and seizures increase the oxygen requirements of the brain, providers should treat hyperthermia and consider therapeutic hypothermia. Witnessed seizures should be promptly controlled and maintenance anticonvulsant therapy initiated (Class IIa). Because of a paucity of data, routine seizure prophylaxis is a Class Indeterminate recommendation at present. Prognostic Factors The period after resuscitation is often stressful to medical staff and family members as questions arise about the patient’s ultimate prognosis. Ideally a clinical assessment, laboratory test, or biochemical marker would reliably predict outcome during or immediately after cardiac arrest. Unfortunately no such predictors are available. Determination of prognosis based on initial physical examination findings can be difficult, and coma scores may be less predictive than individual motor and brainstem reflexes found in the first 12 to 72 hours after arrest.2 In a meta-analysis (LOE 1)44 bilateral absence of cortical response to median nerve somatosensory-evoked potentials predicted poor outcome in normothermic patients who were comatose for at least 72 hours after hypoxic-ischemic insult. A case report46 also documents the usefulness of this evaluation. Therefore, median nerve somatosensory-evoked potentials measured 72 hours after cardiac arrest can be used to predict neurologic outcome in patients with hypoxic-anoxic coma. A recent meta-analysis (LOE 1) of 11 studies involving 1914 patients2 documented 5 clinical signs that were found to strongly predict death or poor neurologic outcome, with 4 of the 5 predictors detectable at 24 hours after resuscitation: ● Absent corneal reflex at 24 hours ● Absent pupillary response at 24 hours ● Absent withdrawal response to pain at 24 hours ● No motor response at 24 hours ● No motor response at 72 hours An electroencephalogram performed 24 to 48 hours after resuscitation has also been shown to provide useful predictive information (LOE 547–50) and can help define prognosis. Other Complications Sepsis is a potentially fatal postresuscitation complication.51 Patients with sepsis will benefit from goal-directed therapy. Renal failure52 and pancreatitis, while often transient, should be diagnosed and evaluated.3,53 Summary The postresuscitation period is often marked by hemodynamic instability as well as laboratory abnormalities. This is also a period for which promising technological interventions such as controlled therapeutic hypothermia are being evaluated. Every organ system is at risk during this time, and patients may ultimately develop multi-organ dysfunction. A complete discussion of this topic is beyond the scope of this chapter. The goal of the postresuscitation period is to manage the patient’s vital signs and laboratory abnormalities and support organ system function to increase the likelihood of intact neurologic survival. References 1. Safar P. Resuscitation from clinical death: pathophysiologic limits and therapeutic potentials. Crit Care Med. 1988;16:923–941. 2. Booth CM, Boone RH, Tomlinson G, Detsky AS. Is this patient dead, vegetative, or severely neurologically impaired? Assessing outcome for comatose survivors of cardiac arrest. JAMA. 2004;291:870 – 879. 3. 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. 4. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557–563. 5. Bunch TJ, White RD, Gersh BJ, Meverden RA, Hodge DO, Ballman KV, Hammill SC, Shen WK, Packer DL. Long-term outcomes of out-ofhospital cardiac arrest after successful early defibrillation. N Engl J Med. 2003;348:2626 –2633. 6. Laurent I, Monchi M, Chiche JD, Joly LM, Spaulding C, Bourgeois B, Cariou A, Rozenberg A, Carli P, Weber S, Dhainaut JF. Reversible myocardial dysfunction in survivors of out-of-hospital cardiac arrest. J Am Coll Cardiol. 2002;40:2110 –2116. 7. Negovsky VA. The second step in resuscitation—the treatment of the ‘post-resuscitation disease.’ Resuscitation. 1972;1:1–7. 8. A randomized clinical study of cardiopulmonary-cerebral resuscitation: design, methods, and patient characteristics. Brain Resuscitation Clinical Trial I Study Group. Am J Emerg Med. 1986;4:72– 86. 9. Skrifvars MB, Pettila V, Rosenberg PH, Castren M. A multiple logistic regression analysis of in-hospital factors related to survival at six months in patients resuscitated from out-of-hospital ventricular fibrillation. Resuscitation. 2003;59:319 –328. 10. Hachimi-Idrissi S, Corne L, Ebinger G, Michotte Y, Huyghens L. Mild hypothermia induced by a helmet device: a clinical feasibility study. Resuscitation. 2001;51:275–281. 11. Nolan JP, Morley PT, Hoek TL, Hickey RW. Therapeutic hypothermia after cardiac arrest: an advisory statement by the Advancement Life Support Task Force of the International Liaison Committee on Resuscitation. Resuscitation. 2003;57:231–235. 12. Shankaran S, Laptook AR, Ehrenkranz RA, Tyson JE, McDonald SA, Donovan EF, Fanaroff AA, Poole WK, Wright LL, Higgins RD, Finer NN, Carlo WA, Duara S, Oh W, Cotten CM, Stevenson DK, Stoll BJ, Lemons JA, Guillet R, Jobe AH. Whole-body hypothermia for neonates with hypoxic-ischemic encephalopathy. N Engl J Med. 2005;353: 1574 –1584. 13. Bernard S, Buist M, Monteiro O, Smith K. Induced hypothermia using large volume, ice-cold intravenous fluid in comatose survivors of out-ofhospital cardiac arrest: a preliminary report. Resuscitation. 2003;56:9 –13. 14. Hickey RW, Kochanek PM, Ferimer H, Alexander HL, Garman RH, Graham SH. Induced hyperthermia exacerbates neurologic neuronal histologic damage after asphyxial cardiac arrest in rats. Crit Care Med. 2003;31:531–535. 15. Dietrich WD, Busto R, Halley M, Valdes I. The importance of brain temperature in alterations of the blood-brain barrier following cerebral ischemia. J Neuropathol Exp Neurol. 1990;49:486 – 497. 16. Dietrich WD, Busto R, Valdes I, Loor Y. Effects of normothermic versus mild hyperthermic forebrain ischemia in rats. Stroke. 1990;21: 1318 –1325. 17. Kim Y, Busto R, Dietrich WD, Kraydieh S, Ginsberg MD. Delayed postischemic hyperthermia in awake rats worsens the histopathological Part 7.5: Postresuscitation Support IV-87

/V-88 Circulation December 13, 2005 transient focal cerebral ischemia. Stroke. 1996: 2 36. Ligas JR, Mosiehi F. Epstein MAF. Occult positive end-expiratory 2274-2280: discussion 2281 pressure with different types of mechanical ventilators. J Crit Care 18. Zeiner A. Holzer M, Sterz F, Schorkhuber W, Eisenburger P, Havel C, Kliegel A, Laggner AN. Hyperthermia after cardiac arrest is associated 37. Weaver WD, Cobb LA, Copass MK, Hallstrom AP. Ventricular defibrin- with an unfavorable neurologic outcome. Arch Intern Med. 2001: 161 comparative trial using 175-J and 320-J shocks. N Engl J Med. 82:307:110l-l1106 19. Hajat C, Hajat S. Sharma P. Effects of poststroke pyrexia on stroke 38. Vasquez A, Kern KB. Hilwig Rw, Heidenreich J, Berg RA, Ewy GA. outcome:a meta-analysis of studies in patients. Stroke. 2000: 3 Optimal dosing of dobutamine for treating post-resuscitation left ventric- ular dysfunction. Resuscitation. 2004: 61: 199-207. 20. Mullner M, Sterz F, Binder M, Schreiber W. Deimel A, Laggner AN. 39. Mullner M, Domanovits H, Sterz F, Herkner H, Gamper G, Kurkciyan L lood glucose concentration after cardiopulmonary resuscitation Laggner AN. Measurement of myocardial contractility following suc ery in human cardiac arrest sur- cessful resuscitation: quantitated left ventricular systolic function utilising vivos. J Cereb Blood Flow Metab. 1997: 17: 430-436 anghelle A, Tyvold Ss, Lexow K, 40. Spaulding CM, Joly LM, Rosenberg A, Monchi In-hospital factors associated with improved outcome after out-of- F, Carli P. Immediate coronary angiography in survivors of out-of hospital cardiac arrest: a comparison between four regions in Norway hospital cardiac arrest. N Engl J Med. 1997: 336: 1629-1633 Resuscitation. 2003: 56: 247-263 41. Rivers E,, Nguyen B, Havstad S, Ressler J. Muzzin A, Knoblich B, 22. Calle PA, Buylaert WA, Vanhaute OA Glycemia in the post-resuscitation Peterson E, Tomlanovich M. Early goal-directed therapy in the treatment period. The Cerebral Resuscitation Study Group. Resuscitation. 1989 of severe sepsis and septic shock. N Engl J Med. 2001: 345: 1368-1377 17(suppl): S181-S188: discussion S199-$206 42. Ito T, Saitoh D, Takasu A, Kiyozumi T, Sakamoto T, Okada Y. Serum 23. Mackenzie cf A review of 1oo cases of cardiac arrest and the relation of cortisol as a predictive marker of the outcome in patients resuscitated otassium, glucose, and haemoglobin levels to survival. West Indian Mee after cardiopulmonary arrest. Resuscitation. 2004: 62: 55-60 J.1975;24:39-45 43. Gisvold SE, Sterz F, Abramson NS, Bar-Joseph G, Ebmeyer U, Gervai 4. Longstreth WT Jr, Diehr P. Inui TS. awakening after H, Ginsberg M, Katz LM, Kochanek PM, Kuboyama K, Miller B, Obrist out-of-hospital cardiac arrest. N Engl 308:1378-1382 w. Roine Ro, Safar P, Sim KM, Vandevelde K, White RJ. Xiao F 25. Longstreth WT Jr, Inui TS. High cose level on hospital Cerebral resuscitation from cardiac arrest: treatment potentials. Crif Care rery after cardiac arm Neurol.1984:15:59-6 44. del Zoppo GJ, Mabuchi T. Cerebral microvessel responses to focal 26. Longstreth WT Jr, Copass MK, Dennis LK, Rauch-Matthews ME, Stark ischemia. J Cereb Blood Flow Metab. 2003: 23: 879-894 MS, Cobb LA. Intravenous glucose after out-of-hospital cardiopulmonar 45. Zandbergen EG, de Haan R, Stoutenbeek CP, Koelman JH, Hijdra A. ommunity-based random ischaemic coma. Lancet. 1998: 352: 1808-1812. Sheldon RA, Partridge JC, Fermiero DM. Postischemic hyperglycemia is 46. Rothstein TL. Recovery from near death following cerebral anoxia: a ca not protective to the neonatal rat brain. Pediatr Res. 1992: 32: 489-493. report demonstrating superiority of median somatosensory evoked 8. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, avorable outcome after cardiopul- Schetz M. Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive resuscitation. Resuscitation. 2004: 60- 335-341 itically ill patients. N Engl J Med. 2001: 34 w, Genoud D, Ho TW. Jallon P. Etiology, neurologic corre- 359-1367. lations, and prognosis in alpha coma. Clin Neurophysiol. 1999: 110: 29. Rello J, Diaz E, Roque M, Valles J. Risk factors for developing 205-213. pneumonia within 48 hours of intubation. Am J Respir Crit Care Med. 48. Ajisaka H. Early electroencephalographic findings in patients with anoxi 999:159:17421746. cephalopathy after cardiopulmonary Garnacho A Cerebral hemodynamic changes during sustained hypocap- 49. Bassetti C, Bomio F, Mathis J, Hess Cw. Early pr nia in severe head injur hyperventilation cause cerebral ischemia? cardiac arrest: a prospective clinical, electrophysiological, and bio- Acta Neurochir Suppl. 1998: 71: 1-4 chemical study of 60 patients. J Neurol Neurosurg Psychiatry. 1996: 61: 31. Yundt KD. Diringer MN. The use of hyperventilation and its impact on 610-615 mia in the treatment of traumatic brain injury. Crit Care 50. Berkhoff M. Donati F in.1997:13:163-184 praisal of its prognostic significance. Clin Neurophysiol. 2000; I 32. Wolfson SK Jr. Safar P. Reich H. Clark JM. Gur D. Stezoski w. Cook EE, Krupper MA Dynamic heterogeneity of cerebral hypoperfusion after 51. Dellinger RP. Carlet JM, Masur H, Gerlach H, Calandra T prolonged cardiac arrest in dogs measured by the stable xenon/CT tech Gea-Banacloche J. Keh D, Marshall JC. Parker MM. nique: a preliminary study. Resuscitation. 1992: 23: 1-20. erman JL, Vincent JL, Levy MM. Surviving s sc 33. Fischer M Hossmann KA. No-reflow after cardiac arrest. Intensive Care sidelines for management of severe sepsis and septic Crit Care Med.1995;:21:132-141 Med.2004:32:858-873. 34. Safar P, Xiao F, Radovsky A, Tanigawa K, Ebmeyer U, Bircher N, 52. Zeiner A, Sunder-Plassmann G, Sterz F, Holzer M, Losert H, Laggner Alexander H, Stezoski Sw. Improved cerebral resuscitation from cardiac AN. Muller M. The of mild therapeutic hypothermia on renal rest in dogs with mild hypothermia plus blood flow promotion. Stroke. function after car ary resuscitation in men. Resuscitation. 2004 996:27:105-113 60:253-261 65. Gottfried SB. Rossi A, Milic-Emili J Dynamic hyperinflation, intrinsic 53. Mattana J, Singhal PC Prevalence and determinants of acute renal failure PEEP, and the mechanically ventilated patient Crif Care Digest. 1986; following cardiopulmonary resuscitation. Arch Intern Med. 1993: 153 5:30-33 235-239

outcome of transient focal cerebral ischemia. Stroke. 1996;27: 2274 –2280; discussion 2281. 18. Zeiner A, Holzer M, Sterz F, Schorkhuber W, Eisenburger P, Havel C, Kliegel A, Laggner AN. Hyperthermia after cardiac arrest is associated with an unfavorable neurologic outcome. Arch Intern Med. 2001;161: 2007–2012. 19. Hajat C, Hajat S, Sharma P. Effects of poststroke pyrexia on stroke outcome: a meta-analysis of studies in patients. Stroke. 2000;31: 410 – 414. 20. Mullner M, Sterz F, Binder M, Schreiber W, Deimel A, Laggner AN. Blood glucose concentration after cardiopulmonary resuscitation influences functional neurological recovery in human cardiac arrest survivors. J Cereb Blood Flow Metab. 1997;17:430 – 436. 21. Langhelle A, Tyvold SS, Lexow K, Hapnes SA, Sunde K, Steen PA. In-hospital factors associated with improved outcome after out-ofhospital cardiac arrest: a comparison between four regions in Norway. Resuscitation. 2003;56:247–263. 22. Calle PA, Buylaert WA, Vanhaute OA. Glycemia in the post-resuscitation period. The Cerebral Resuscitation Study Group. Resuscitation. 1989; 17(suppl):S181–S188; discussion S199 –S206. 23. Mackenzie CF. A review of 100 cases of cardiac arrest and the relation of potassium, glucose, and haemoglobin levels to survival. West Indian Med J. 1975;24:39 – 45. 24. Longstreth WT Jr, Diehr P, Inui TS. Prediction of awakening after out-of-hospital cardiac arrest. N Engl J Med. 1983;308:1378 –1382. 25. Longstreth WT Jr, Inui TS. High blood glucose level on hospital admission and poor neurological recovery after cardiac arrest. Ann Neurol. 1984;15:59 – 63. 26. Longstreth WT Jr, Copass MK, Dennis LK, Rauch-Matthews ME, Stark MS, Cobb LA. Intravenous glucose after out-of-hospital cardiopulmonary arrest: a community-based randomized trial. Neurology. 1993;43: 2534 –2541. 27. Sheldon RA, Partridge JC, Ferriero DM. Postischemic hyperglycemia is not protective to the neonatal rat brain. Pediatr Res. 1992;32:489 – 493. 28. van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in the critically ill patients. N Engl J Med. 2001;345: 1359 –1367. 29. Rello J, Diaz E, Roque M, Valles J. Risk factors for developing pneumonia within 48 hours of intubation. Am J Respir Crit Care Med. 1999;159:1742–1746. 30. Ausina A, Baguena M, Nadal M, Manrique S, Ferrer A, Sahuquillo J, Garnacho A. Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia? Acta Neurochir Suppl. 1998;71:1– 4. 31. Yundt KD, Diringer MN. The use of hyperventilation and its impact on cerebral ischemia in the treatment of traumatic brain injury. Crit Care Clin. 1997;13:163–184. 32. Wolfson SK Jr, Safar P, Reich H, Clark JM, Gur D, Stezoski W, Cook EE, Krupper MA. Dynamic heterogeneity of cerebral hypoperfusion after prolonged cardiac arrest in dogs measured by the stable xenon/CT technique: a preliminary study. Resuscitation. 1992;23:1–20. 33. Fischer M, Hossmann KA. No-reflow after cardiac arrest. Intensive Care Med. 1995;21:132–141. 34. Safar P, Xiao F, Radovsky A, Tanigawa K, Ebmeyer U, Bircher N, Alexander H, Stezoski SW. Improved cerebral resuscitation from cardiac arrest in dogs with mild hypothermia plus blood flow promotion. Stroke. 1996;27:105–113. 35. Gottfried SB, Rossi A, Milic-Emili J. Dynamic hyperinflation, intrinsic PEEP, and the mechanically ventilated patient. Crit Care Digest. 1986; 5:30 –33. 36. Ligas JR, Mosiehi F, Epstein MAF. Occult positive end-expiratory pressure with different types of mechanical ventilators. J Crit Care. 1990;52:95–100. 37. Weaver WD, Cobb LA, Copass MK, Hallstrom AP. Ventricular defibrillation: a comparative trial using 175-J and 320-J shocks. N Engl J Med. 1982;307:1101–1106. 38. Vasquez A, Kern KB, Hilwig RW, Heidenreich J, Berg RA, Ewy GA. Optimal dosing of dobutamine for treating post-resuscitation left ventricular dysfunction. Resuscitation. 2004;61:199 –207. 39. Mullner M, Domanovits H, Sterz F, Herkner H, Gamper G, Kurkciyan I, Laggner AN. Measurement of myocardial contractility following successful resuscitation: quantitated left ventricular systolic function utilising non-invasive wall stress analysis. Resuscitation. 1998;39:51–59. 40. Spaulding CM, Joly LM, Rosenberg A, Monchi M, Weber SN, Dhainaut JF, Carli P. Immediate coronary angiography in survivors of out-ofhospital cardiac arrest. N Engl J Med. 1997;336:1629 –1633. 41. Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, Peterson E, Tomlanovich M. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345:1368 –1377. 42. Ito T, Saitoh D, Takasu A, Kiyozumi T, Sakamoto T, Okada Y. Serum cortisol as a predictive marker of the outcome in patients resuscitated after cardiopulmonary arrest. Resuscitation. 2004;62:55– 60. 43. Gisvold SE, Sterz F, Abramson NS, Bar-Joseph G, Ebmeyer U, Gervais H, Ginsberg M, Katz LM, Kochanek PM, Kuboyama K, Miller B, Obrist W, Roine RO, Safar P, Sim KM, Vandevelde K, White RJ, Xiao F. Cerebral resuscitation from cardiac arrest: treatment potentials. Crit Care Med. 1996;24(2 suppl):S69 –S80. 44. del Zoppo GJ, Mabuchi T. Cerebral microvessel responses to focal ischemia. J Cereb Blood Flow Metab. 2003;23:879 – 894. 45. Zandbergen EG, de Haan RJ, Stoutenbeek CP, Koelman JH, Hijdra A. Systematic review of early prediction of poor outcome in anoxicischaemic coma. Lancet. 1998;352:1808 –1812. 46. Rothstein TL. Recovery from near death following cerebral anoxia: a case report demonstrating superiority of median somatosensory evoked potentials over EEG in predicting a favorable outcome after cardiopulmonary resuscitation. Resuscitation. 2004;60:335–341. 47. Kaplan PW, Genoud D, Ho TW, Jallon P. Etiology, neurologic correlations, and prognosis in alpha coma. Clin Neurophysiol. 1999;110: 205–213. 48. Ajisaka H. Early electroencephalographic findings in patients with anoxic encephalopathy after cardiopulmonary arrest and successful resuscitation. J Clin Neurosci. 2004;11:616 – 618. 49. Bassetti C, Bomio F, Mathis J, Hess CW. Early prognosis in coma after cardiac arrest: a prospective clinical, electrophysiological, and biochemical study of 60 patients. J Neurol Neurosurg Psychiatry. 1996;61: 610 – 615. 50. Berkhoff M, Donati F, Bassetti C. Postanoxic alpha (theta) coma: a reappraisal of its prognostic significance. Clin Neurophysiol. 2000;111: 297–304. 51. Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, Gea-Banacloche J, Keh D, Marshall JC, Parker MM, Ramsay G, Zimmerman JL, Vincent JL, Levy MM. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med. 2004;32:858 – 873. 52. Zeiner A, Sunder-Plassmann G, Sterz F, Holzer M, Losert H, Laggner AN, Mullner M. The effect of mild therapeutic hypothermia on renal function after cardiopulmonary resuscitation in men. Resuscitation. 2004; 60:253–261. 53. Mattana J, Singhal PC. Prevalence and determinants of acute renal failure following cardiopulmonary resuscitation. Arch Intern Med. 1993;153: 235–239. IV-88 Circulation December 13, 2005

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