2010年CPR心肺复苏最新指南_PART_9_心脏骤停后治疗

ISSN: 1524-4539 Copyright © 2010 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online 72514 Circulation is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX DOI: 10.1161/CIRCULATIONAHA.110.971002 2010;122;S768-S786 Circulation Kronick Silvers, Arno L. Zaritsky, Raina Merchant, Terry L. Vanden Hoek and Steven L. Geocadin, Janice L. Zimmerman, Michael Donnino, Andrea Gabrielli, Scott M. Mary Ann Peberdy, Clifton W. Callaway, Robert W. Neumar, Romergryko G. for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Part 9: Post�Cardiac Arrest Care: 2010 American Heart Association Guidelines http://circ.ahajournals.org/cgi/content/full/122/18_suppl_3/S768 located on the World Wide Web at: The online version of this article, along with updated information and services, is http://www.lww.com/reprints Reprints: Information about reprints can be found online at journalpermissions@lww.com 410-528-8550. E-mail: Fax:Kluwer Health, 351 West Camden Street, Baltimore, MD 21202-2436. Phone: 410-528-4050. Permissions: Permissions & Rights Desk, Lippincott Williams & Wilkins, a division of Wolters http://circ.ahajournals.org/subscriptions/ Subscriptions: Information about subscribing to Circulation is online at by on October 19, 2010 circ.ahajournals.orgDownloaded from Part 9: Post–Cardiac Arrest Care 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Mary Ann Peberdy, Co-Chair*; Clifton W. Callaway, Co-Chair*; Robert W. Neumar; Romergryko G. Geocadin; Janice L. Zimmerman; Michael Donnino; Andrea Gabrielli; Scott M. Silvers; Arno L. Zaritsky; Raina Merchant; Terry L. Vanden Hoek; Steven L. Kronick There is increasing recognition that systematic post–cardiacarrest care after return of spontaneous circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is based in part on the publication of results of randomized controlled clinical trials as well as a description of the post–cardiac arrest syndrome.1–3 Post–cardiac arrest care has significant potential to reduce early mortality caused by hemo- dynamic instability and later morbidity and mortality from multiorgan failure and brain injury.3,4 This section summarizes our evolving understanding of the hemodynamic, neurologi- cal, and metabolic abnormalities encountered in patients who are initially resuscitated from cardiac arrest. The initial objectives of post–cardiac arrest care are to ● Optimize cardiopulmonary function and vital organ perfusion. ● After out-of-hospital cardiac arrest, transport patient to an appro- priate hospital with a comprehensive post–cardiac arrest treat- ment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. ● Transport the in-hospital post–cardiac arrest patient to an appropriate critical-care unit capable of providing compre- hensive post–cardiac arrest care. ● Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest. Subsequent objectives of post–cardiac arrest care are to ● Control body temperature to optimize survival and neuro- logical recovery ● Identify and treat acute coronary syndromes (ACS) ● Optimize mechanical ventilation to minimize lung injury ● Reduce the risk of multiorgan injury and support organ function if required ● Objectively assess prognosis for recovery ● Assist survivors with rehabilitation services when required Systems of Care for Improving Post–Cardiac Arrest Outcomes Post–cardiac arrest care is a critical component of advanced life support (Figure). Most deaths occur during the first 24 hours after cardiac arrest.5,6 The best hospital care for patients with ROSC after cardiac arrest is not completely known, but there is increasing interest in identifying and optimizing practices that are likely to improve outcomes (Table 1).7 Positive associations have been noted between the likelihood of survival and the number of cardiac arrest cases treated at any individual hospi- tal.8,9 Because multiple organ systems are affected after cardiac arrest, successful post–cardiac arrest care will benefit from the development of system-wide plans for proactive treatment of these patients. For example, restoration of blood pressure and gas exchange does not ensure survival and functional recovery. Significant cardiovascular dysfunction can develop, requiring support of blood flow and ventilation, including intravascular volume expansion, vasoactive and inotropic drugs, and invasive devices. Therapeutic hypothermia and treatment of the underly- ing cause of cardiac arrest impacts survival and neurological outcomes. Protocolized hemodynamic optimization and multi- disciplinary early goal-directed therapy protocols have been introduced as part of a bundle of care to improve survival rather than single interventions.10–12 The data suggests that proactive titration of post–cardiac arrest hemodynamics to levels intended to ensure organ perfusion and oxygenation may improve out- comes. There are multiple specific options for acheiving these goals, and it is difficult to distinguish between the benefit of protocols or any specific component of care that is most important. A comprehensive, structured, multidisciplinary system of care should be implemented in a consistent manner for the treatment of post–cardiac arrest patients (Class I, LOE B). Programs should include as part of structured interventions therapeutic hypothermia; optimization of hemodynamics and gas exchange; immediate coronary reperfusion when indi- cated for restoration of coronary blood flow with percutane- ous coronary intervention (PCI); glycemic control; and neu- rological diagnosis, management, and prognostication. Overview of Post–Cardiac Arrest Care The provider of CPR should ensure an adequate airway and support breathing immediately after ROSC. Unconscious The American Heart Association requests that this document be cited as follows: Peberdy MA, Callaway CW, Neumar RW, Geocadin RG, Zimmerman JL, Donnino M, Gabrielli A, Silvers SM, Zaritsky AL, Merchant R, Vanden Hoek TL, Kronick SL. Part 9: post–cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122(suppl 3):S768–S786. *Co-chairs and equal first co-authors. (Circulation. 2010;122[suppl 3]:S768–S786.) © 2010 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.110.971002 S768 by on October 19, 2010 circ.ahajournals.orgDownloaded from patients usually require an advanced airway for mechanical support of breathing. It may be necessary to replace a supraglot- tic airway used for initial resuscitation with an endotracheal tube, although the timing of replacement may vary. Methods for securing an advanced airway are discussed in Part 8.1: “Airway Management,” but several simple maneuvers deserve consider- ation. For example, rescuers and long-term hospital providers should avoid using ties that pass circumferentially around the patient’s neck, potentially obstructing venous return from the brain. They should also elevate the head of the bed 30° if tolerated to reduce the incidence of cerebral edema, aspiration, and ventilatory-associated pneumonia. Correct placement of an advanced airway, particularly during patient transport, should be monitored using waveform capnography as described in other sections of the 2010 AHA Guidelines for CPR and ECC. Oxygenation of the patient should be monitored continuously with pulse oximetry. Although 100% oxygen may have been used during initial resuscitation, providers should titrate inspired oxygen to the lowest level required to achieve an arterial oxygen saturation of �94%, so as to avoid potential oxygen toxicity. It is recognized that titration of inspired oxygen may not be possible immedi- ately after out-of-hospital cardiac arrest until the patient is transported to the emergency department or, in the case of in-hospital arrest, the intensive care unit (ICU). Hyperventilation or “overbagging” the patient is common after cardiac arrest and should be avoided because of potential adverse hemodynamic effects. Hyperventilation increases intrathoracic pressure and inversely lowers cardiac output. The decrease in PaCO2 seen with hyperventilation can also potentially decrease cerebral blood flow directly.Ventilation may be started at 10 to 12 breaths per minute and titrated to achieve a PETCO2 of 35 to 40 mm Hg or a PaCO2 of 40 to 45 mm Hg. The clinician should assess vital signs and monitor for recurrent cardiac arrhythmias. Continuous electrocardio- graphic (ECG) monitoring should continue after ROSC, during transport, and throughout ICU care until stability has been achieved. Intravenous (IV) access should be obtained if not already established and the position and function of any intravenous catheter verified. IV lines should be promptly established to replace emergent intraosseous access achieved during resuscitation. If the patient is hypotensive (systolic blood pressure�90 mm Hg), fluid boluses can be considered. Cold fluid may be used if therapeutic hypothermia is elected. Vasoactive drug infusions such as dopamine, norepinephrine, or epinephrine may be initiated if necessary and titrated to achieve a minimum systolic blood pressure of�90 mm Hg or a mean arterial pressure of �65 mm Hg. Brain injury and cardiovascular instability are the major determinants of survival after cardiac arrest.13 Because ther- apeutic hypothermia is the only intervention demonstrated to improve neurological recovery, it should be considered for any patient who is unable to follow verbal commands after ROSC. The patient should be transported to a facility that reliably provides this therapy in addition to coronary reperfusion (eg, PCI) and other goal-directed postarrest care therapies. Overall the most common cause of cardiac arrest is cardiovascular disease and coronary ischemia.14,15 Therefore, a 12-lead ECG should be obtained as soon as possible to detect ST elevation or new or presumably new left bundle- branch block. When there is high suspicion of acute myocar- dial infarction (AMI), local protocols for treatment of AMI and coronary reperfusion should be activated. Even in the absence of ST elevation, medical or interventional treatments may be considered for treatment of ACS14,16,17 and should not be deferred in the presence of coma or in conjunction with Figure. Post–cardiac arrest care algorithm. Peberdy et al Part 9: Post–Cardiac Arrest Care S769 by on October 19, 2010 circ.ahajournals.orgDownloaded from hypothermia. Concurrent PCI and hypothermia are safe, with good outcomes reported for some comatose patients who undergo PCI. Patients who are unconscious or unresponsive after cardiac arrest should be directed to an inpatient critical-care facility with a comprehensive care plan that includes acute cardio- vascular interventions, use of therapeutic hypothermia, stan- dardized medical goal-directed therapies, and advanced neu- rological monitoring and care. Neurological prognosis may be difficult to determine during the first 72 hours, even for patients who are not undergoing therapeutic hypothermia. This time frame for prognostication is likely to be extended in patients being cooled.18 Many initially comatose survivors of cardiac arrest have the potential for full recovery such that they are able to lead normal lives.1,2,19 Between 20% and 50% or more of survivors of out-of-hospital cardiac arrest who are Table 1. Multiple System Approach to Post–Cardiac Arrest Care Ventilation Hemodynamics Cardiovascular Neurological Metabolic ● Capnography ● Frequent Blood Pressure Monitoring/Arterial-line ● Continuous Cardiac Monitoring ● Serial Neurological Exam ● Serial Lactate ● Rationale: Confirm secure airway and titrate ventilation ● Rationale: Maintain perfusion and prevent recurrent hypotension ● Rationale: Detect recurrent arrhythmia ● Rationale: Serial examinations define coma, brain injury, and prognosis ● Rationale: Confirm adequate perfusion ● Endotracheal tube when possible for comatose patients ● Mean arterial pressure �65 mm Hg or systolic blood pressure �90 mm Hg ● No prophylactic antiarrhythmics ● Response to verbal commands or physical stimulation ● PETCO2�35–40 mm Hg ● Treat arrhythmias as required ● Pupillary light and corneal reflex, spontaneous eye movement ● Paco2�40–45 mm Hg ● Remove reversible causes ● Gag, cough, spontaneous breaths ● Chest X-ray ● Treat Hypotension ● 12-lead ECG/Troponin ● EEG Monitoring If Comatose ● Serum Potassium ● Rationale: Confirm secure airway and detect causes or complications of arrest: pneumonitis, pneumonia, pulmonary edema ● Rationale: Maintain perfusion ● Rationale: Detect Acute Coronary Syndrome/ST-Elevation Myocardial Infarction; Assess QT interval ● Rationale: Exclude seizures ● Rationale: Avoid hypokalemia which promotes arrhythmias ● Fluid bolus if tolerated ● Anticonvulsants if seizing ● Replace to maintain K �3.5 mEq/L ● Dopamine 5–10 mcg/kg per min ● Norepinephrine 0.1–0.5 mcg/kg per min ● Epinephrine 0.1–0.5 mcg/kg per min ● Pulse Oximetry/ABG . . . ● Treat Acute Coronary Syndrome ● Core Temperature Measurement If Comatose ● Urine Output, Serum Creatinine ● Rationale: Maintain adequate oxygenation and minimize FIO2 . . . ● Aspirin/heparin ● Rationale: Minimize brain injury and improve outcome ● Rationale: Detect acute kidney injury ● SpO2 �94% . . . ● Transfer to acute coronary treatment center ● Prevent hyperpyrexia �37.7°C ● Maintain euvolemia ● PaO2�100 mm Hg . . . ● Consider emergent PCI or fibrinolysis ● Induce therapeutic hypothermia if no contraindications ● Renal replacement therapy if indicated ● Reduce FIO2 as tolerated . . . ● Cold IV fluid bolus 30 mL/kg if no contraindication ● Pao2/FIO2 ratio to follow acute lung injury . . . ● Surface or endovascular cooling for 32°C–34°C�24 hours . . . ● After 24 hours, slow rewarming 0.25°C/hr ● Mechanical Ventilation . . . ● Echocardiogram ● Consider Non-enhanced CT Scan ● Serum Glucose ● Rationale: Minimize acute lung injury, potential oxygen toxicity . . . ● Rationale: Detect global stunning, wall-motion abnormalities, structural problems or cardiomyopathy ● Rationale: Exclude primary intracranial process ● Rationale: Detect hyperglycemia and hypoglycemia ● Tidal Volume 6–8 mL/kg . . . ● Treat hypoglycemia (�80 mg/dL) with dextrose ● Titrate minute ventilation to PETCO2�35–40 mm Hg Paco2�40–45 mm Hg . . . ● Treat hyperglycemia to target glucose 144–180 mg/dL ● Reduce Fio2 as tolerated to keep Spo2 or Sao2 �94% . . . ● Local insulin protocols . . . ● Treat Myocardial Stunning ● Sedation/Muscle Relaxation ● Avoid Hypotonic Fluids . . . ● Fluids to optimize volume status (requires clinical judgment) ● Rationale: To control shivering, agitation, or ventilator desynchrony as needed ● Rationale: May increase edema, including cerebral edema . . . ● Dobutamine 5–10 mcg/kg per min . . . ● Mechanical augmentation (IABP) S770 Circulation November 2, 2010 by on October 19, 2010 circ.ahajournals.orgDownloaded from comatose on arrival at the hospital may have good one-year neurological outcome.1,2,11 Therefore, it is important to place patients in a hospital critical-care unit where expert care and neurological evaluation can be performed and where appro- priate testing to aid prognosis is available and performed in a timely manner. Attention should be directed to treating the precipitating cause of cardiac arrest after ROSC. The provider should initiate or request studies that will further aid in evaluation of the patient. It is important to identify and treat any cardiac, electrolyte, toxicological, pulmonary, and neurological pre- cipitants of arrest. The clinician may find it helpful to review the H’s and T’s mnemonic to recall factors that may contrib- ute to cardiac arrest or complicate resuscitation or postresus- citation care: hypovolemia, hypoxia, hydrogen ion (acidosis of any etiology), hyper-/hypokalemia, moderate to severe hypothermia, toxins, tamponade (cardiac), tension pneumo- thorax, and thrombosis of the coronary or pulmonary vascu- lature. For further information on treating other causes of cardiac arrest, see Part 12: “Special Resuscitation Situations.” Targeted Temperature Management Induced Hypothermia For protection of the brain and other organs, hypothermia is a helpful therapeutic approach in patients who remain coma- tose (usually defined as a lack of meaningful response to verbal commands) after ROSC. Questions remain about specific indications and populations, timing and duration of therapy, and methods for induction, maintenance, and subse- quent reversal of hypothermia. One good randomized trial1 and a pseudorandomized trial2 reported improved neurologi- cally intact survival to hospital discharge when comatose patients with out-of-hospital ventricular fibrillation (VF) cardiac arrest were cooled to 32°C to 34°C for 12 or 24 hours beginning minutes to hours after ROSC. Additional studies with historical control groups show improved neurological outcome after therapeutic hypothermia for comatose survi- vors of VF cardiac arrest.20,21 No randomized controlled trials have compared outcome between hypothermia and normothermia for non-VF arrest. However, 6 studies with historical control groups reported a beneficial effect on outcome from use of therapeutic hypo- thermia in comatose survivors of out-of-hospital cardiac arrest associated with any arrest rhythm.11,22–26 Only one study with historical controls reported better neurological outcome after VF cardiac arrest but no difference in outcome after cardiac arrest associated with other rhythms.27 Two nonrandomized studies with concurrent controls28,29 indicate a possible benefit of hypothermia after in- and out-of-hospital cardiac arrest associated with non-VF initial rhythms. Case series have reported the feasibility of using therapeu- tic hypothermia after ROSC in the setting of cardiogenic shock23,30,31 and therapeutic hypothermia in combination with emergent PCI.32–36 Case series also report successful use of fibrinolytic therapy for AMI after ROSC,37,38 but data are lacking about interactions between fibrinolytics and hypo- thermia in this population. The impact of the timing of initiating hypothermia after cardiac arrest is not completely understood. Studies of animal models of cardiac arrest showed that short-duration hypother- mia (�1 hour) achieved �10 to 20 minutes after ROSC had a beneficial effect that was lost when hypothermia was delayed.39–41 Beyond the initial minutes of ROSC and when hypothermia is prolonged (�12 hours), the relationship between the onset of hypothermia and the resulting neuro- protection is less clear.42,43 Two prospective clinical trials in which hypothermia was achieved within 2 hours2 or at a median of 8 hours (interquartile range [IQR] 4 to 16 hours)1 after ROSC both demonstrated better outcomes in the hypothermia-treated than the normothermia-treated subjects. Subsequent to these studies, one registry-based case series of 986 comatose post–cardiac arrest patients35 suggested that time to initiation of cooling (IQR 1 to 1.8 hours) and time to achieving target temperature (IQR 3 to 6.7 hours) were not associated with improved neurological outcome after dis- charge. A case series of 49 consecutive comatose post– cardiac arrest patients44 cooled intravascularly after out-of- hospital cardiac arrest also documented that time to target temperature (median 6.8 hours [IQR 4.5 to 9.2 hours]) was not an independent predictor of neurological outcome. The optimal duration of induce