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  • 1. Official reprint from UpToDate ® Back | Print www.uptodate.comAdvanced cardiac life support (ACLS) inadultsAuthors Section Editors Deputy EditorCharles N Pozner, MD Ron M Walls, MD, FRCPC, Jonathan Grayzel, MD,Sayon Dutta, MD FAAEM FAAEM Richard L Page, MDLast literature review version 17.3: September 2009 | This topic last updated: August 24,2009 (More)INTRODUCTION — The field of resuscitation has been evolving for more than two centuries [ 1 ] . TheParis Academy of Science recommended mouth-to-mouth ventilation for drowning victims in 1740 [ 2]. In 1891, Dr. Friedrich Maass performed the first documented chest compressions on humans [ 3] .The American Heart Association (AHA) formally endorsed cardiopulmonary resuscitation (CPR) in1963 and by 1966 they had adopted standardized CPR guidelines for instruction to lay-rescuers [ 2] .Advanced cardiac life support (ACLS) guidelines have evolved over the past several decades basedon a combination of scientific evidence of variable strength and expert consensus. The AmericanHeart Association and European Resuscitation Council (ERC) developed the most recent ACLSguidelines in collaboration with the International Liaison Committee on Resuscitation (ILCOR) inNovember of 2005 [ 4 ] . Guidelines are reviewed continually but are formally released every fiveyears, and published in the journals Circulation and Resuscitation. The next iteration is expected in2010.This topic will discuss the management of cardiac arrhythmias in adults as described in theNovember 2005 ACLS guidelines. The evidence supporting these guidelines is presented elsewhere,as are issues related to controversial treatments for cardiac arrest patients, basic life support (BLS),and the emergency care of the critically ill adult. ( See "Supportive data for advanced cardiac lifesupport in adults with sudden cardiac arrest" and see "Therapies of uncertain benefit in basic andadvanced cardiac life support" and see "Basic life support (BLS) in adults" and see "Basic airwaymanagement in adults" and see "Rapid sequence intubation in adults" ).EVIDENCE BASED GUIDELINES —Because of the nature of resuscitation research, few randomizedcontrolled trials have been completed in humans. Many of the recommendations in the 2005 AHAACLS guidelines are made based on retrospective studies, animal studies, and expert consensus [ 4] .Guideline recommendations are classified according to the GRADE system [ 5 ] . The evidencesupporting the ACLS guidelines is reviewed in detail elsewhere. ( See "Supportive data for advancedcardiac life support in adults with sudden cardiac arrest" ).PRINCIPLES OF MANAGEMENTProper CPR and its importance —Although the 2005 American Heart Association (AHA) guidelinessuggest multiple treatment revisions, including medications, electrical therapy, and the timing ofvarious therapies, the key modification is the emphasis on well-performed cardiopulmonaryresuscitation (CPR) and its critical role in resuscitative efforts ( show algorithm 1 and show algorithm2 ) [4 ] . In the past, clinicians frequently interrupted CPR to perform pulse checks, intubate thepatient, or initiate venous access. The AHA now recommends that every effort be made not tointerrupt CPR.Other less vital interventions are performed either while CPR is performed or with the briefestpossible interruption [ 4 ] . Studies in both the in-hospital and prehospital settings demonstrate that
  • 2. chest compressions are often performed incorrectly, inconsistently, and with excessive interruption[6-10 ] . Patients are also often over-ventilated during resuscitations, leading to inadequatecardiocerebral resuscitation. ( See "Basic life support (BLS) in adults" ).A 30 to 2 compression to ventilation ratio (one cycle) is now recommended in patients withoutadvanced airway interventions. Asynchronous ventilations at 8 to 10 per minute are administered ifan endotracheal tube is in place, while continuous and simultaneous chest compressions are provided[11 ] .A single biphasic defibrillation is now recommended with immediate resumption of chestcompressions, as opposed to the long-established approach of three sequential defibrillations usingincreasing energy levels in refractory cases of ventricular fibrillation (VF) or pulseless ventriculartachycardia (VT) [ 4,12,13 ] . This new recommendation takes into account both the enhancedfirst-shock efficacy of biphasic defibrillators and recognition that the three shock method causes anunacceptably long interval without CPR, leading to cardiocerebral hypoperfusion [ 4,9,14,15 ] . Werecommend that all defibrillations be delivered at the highest available energy in adults (generally360 J for a monophasic defibrillator and 200 to 360 J for a biphasic defibrillator). Defibrillation isdiscussed in greater detail elsewhere. ( See "Basic life support (BLS) in adults" , section onDefibrillation, and see "Basic principles and technique of cardioversion and defibrillation" , section onOptimal biphasic defibrillation energies).The AHA now recommends that chest compressions continue until the defibrillator is ready to shockand should cease only when the defibrillator is ready for immediate discharge [ 12 ] . In addition, otherinterventions such as the administration of vasopressor agents, antiarrhythmics, and advancedairway management should be coordinated in order to minimize or avoid interruptions in CPR [ 4] .Necessary interruptions in CPR (eg, for repeat attempts at defibrillation) should occur no morefrequently than every two minutes, and for the shortest possible duration.Resuscitation team management — The resuscitation of a sudden cardiac arrest (SCA), by its naturea low frequency, high acuity event, is often chaotic. A growing body of literature demonstrates that byemploying the principles of Crisis Resource Management (CRM), adapted from the aviation industryand introduced into medical care by anesthesiologists, disorganization during resuscitationdecreases and patient care improves [ 16-18 ] .Two principles provide the foundation for CRM: leadership and communication [ 18 ] . Resuscitationsusually involve a number of healthcare providers from different disciplines, and at times from differentareas of an institution. Under these circumstances, role clarity can be difficult to establish. In CRM, itis imperative that one person assumes the role of team leader [ 18 ] . This person is responsible forensuring that all required tasks are being carried out competently, and continuously developing andimplementing management strategies that will maximize patient outcome. The team leader shouldavoid performing technical procedures, as performance of a task inevitably shifts attention from theprimary leadership responsibilities. In circumstances where staffing is limited (eg, small communityhospital), the team leader may be required to perform some necessary procedures. In thesesituations, leadership may be temporarily transferred to another clinician or the team leader may beforced temporarily to perform both roles, although this compromises the ability to provide leadership.In CRM communication is organized to provide effective and efficient care. All pertinentcommunication goes through the team leader and the team leader shares important information withthe team. When the team leader determines the need to perform a task, the request is directed to aspecific team member. That team member verbally acknowledges the request and performs the taskor, if unable to do so, informs the team leader that another team member should be assigned. This"closed-loop" communication leads to a more orderly transfer of information and is the appropriatestandard for all communication during resuscitations. Though most decisions emanate from the teamleader, a good team leader enlists the collective wisdom and experience of the entire team as needed.Extraneous personnel not involved with patient care are asked to leave in order to reduce noise and toensure that orders from the leader and feedback from the resuscitation team can be heard clearly.Initial management and ECG interpretation — As with all medical emergencies, the primary focus is
  • 3. on the airway, breathing, and circulation. Assessment and treatment occur in parallel. Properlyperformed cardiopulmonary resuscitation (CPR) is begun immediately. Initial interventions for ACLSinclude administering oxygen , establishing intravenous access, placing the patient on a cardiac andoxygen saturation monitor, and obtaining an electrocardiogram (ECG) [ 4 ] . Unstable patients mustreceive immediate care, even when data are incomplete or presumptive ( show algorithm 1 and showalgorithm 2 ).Stable patients require an assessment of their electrocardiogram in order to provide appropriatetreatment consistent with ACLS guidelines. Although it is best to make a definitive interpretation ofthe ECG prior to making management decisions, the settings in which ACLS guidelines are commonlyemployed require a modified, empirical approach. Such an approach involves answering the followingquestions [ 4 ] : Is the rhythm fast or slow? Are the QRS complexes wide or narrow? Is the rhythm regular or irregular?The answers to these questions often enable the clinician to make a provisional diagnosis and initiateappropriate therapy.MANAGEMENT OF SPECIFIC ARRHYTHMIASVentricular fibrillation and pulseless ventricular tachycardia — Ventricular fibrillation (VF) andpulseless ventricular tachycardia (VT) are nonperfusing rhythms emanating from the ventricles, forwhich early rhythm identification, defibrillation, and cardiopulmonary resuscitation (CPR) are themainstays of treatment ( show algorithm 3 ). Early defibrillation is the most critical action in theresuscitation effort, followed by the performance of excellent CPR. Manage potentially treatableunderlying causes as appropriate ( show table 1 and show table 2 ).In the case of a witnessed arrest, perform defibrillation as quickly as possible. Decreased time todefibrillation improves the likelihood of successful conversion to a perfusing rhythm and of patientsurvival. In patients with a high probability that VF/VT has been present longer than four or fiveminutes (eg, prolonged rescuer response time without adequate CPR prior to arrival), a period of CPRprior to defibrillation increases the likelihood of return of spontaneous circulation (ROSC) and oneyear survival. The ACLS guidelines suggest the performance of two minutes of CPR (five cycles at 30to 2) before defibrillation. The supportive data are presented elsewhere. ( See "Supportive data foradvanced cardiac life support in adults with sudden cardiac arrest" , section on Timing).Use of biphasic defibrillators is recommended in the 2005 ACLS guidelines because of theirincreased efficacy at lower energy levels [ 13,19,20 ] . When compared with monophasic defibrillatorsset at higher energy levels, biphasic defibrillators do not increase the rate of ROSC [ 20-23 ] .The ACLS guidelines recommend that when using a biphasic defibrillator the initial dose of energy bethe minimum effective dose of the specific defibrillator device. Evidence supporting use of a minimaleffective dose is uncertain, however, and we suggest a first defibrillation using 200 J with a biphasicdefibrillator or 360 J with a monophasic defibrillator for VF or pulseless VT. It should be noted thatmany automated AEDs do not allow for adjustment of the shock output.A single initial defibrillatory shock is now recommended, replacing the three shock sequence withescalating energy that had been the standard. The 2005 ACLS guidelines recommend the resumptionof CPR immediately after defibrillation without rechecking for a pulse. ( See "Basic life support (BLS) inadults" , section on Phases of resuscitation and see "Basic life support (BLS) in adults" , section onDefibrillation).Give epinephrine (1 mg IV every three minutes) while CPR is ongoing. Although the 2005 ACLSguidelines state that vasopressin (40 units IV) may replace the first or second dose of epinephrine,several well-performed, randomized controlled trials (RCT) have failed to show an improvement ininitial ROSC or survival to hospital discharge in patients treated with vasopressin. These studies arediscussed elsewhere. ( See "Supportive data for advanced cardiac life support in adults with sudden
  • 4. cardiac arrest" ).Evidence suggests that antiarrhythmic drugs provide little benefit in refractory VF or pulseless VT.Nevertheless, the current ACLS guidelines state that they may be used in certain situations. Thetiming of antiarrhythmic use is not specified in the ACLS guidelines. We suggest that antiarrhythmicdrugs be considered after a second unsuccessful defibrillation attempt in anticipation of a third shock. Amiodarone (300 mg IV with a repeat dose of 150 mg IV as indicated) may be administered in VF or pulseless VT unresponsive to defibrillation. Lidocaine (1 to 1.5 mg/kg IV, then 0.5 to 0.75 mg/kg every 5 to 10 minutes) may be used if amiodarone is unavailable. Magnesium sulfate (2 g IV, followed by a maintenance infusion) is used to treat polymorphic ventricular tachycardia consistent with torsade de pointes.In summary, ROSC in VF and pulseless VT hinges on early defibrillation and coordinated CPR, alongwith the administration of vasopressor agents.Pulseless electrical activity — Pulseless electrical activity (PEA) is defined as any of aheterogeneous group of organized electrocardiographic rhythms without sufficient mechanicalcontraction of the heart to produce a palpable pulse or measurable blood pressure. By definition, PEAis a non-perfusing rhythm and CPR is initiated immediately ( show algorithm 4 ).PEA may be caused by reversible conditions including hyperkalemia, hypothermia, hypoxia, tensionpneumothorax, drug ingestion, hemorrhage, and cardiac tamponade ( show table 1 and show table 2 ).Treat these conditions as appropriate. PEA does not respond to defibrillation. Give epinephrine (1 mgIV every three to five minutes). The ACLS guidelines state that a single dose of vasopressin (40units IV) may also be given, but several trials raise questions concerning the drugs efficacy. ( See"Supportive data for advanced cardiac life support in adults with sudden cardiac arrest" ).Atropine (1 mg IV every three to five minutes for a total of three doses) may be given in bradycardicPEA [ 24 ] .In summary, treatment for PEA consists of early identification and treatment of reversible causes,and effective CPR with vasopressor administration until either ROSC or a shockable rhythm occurs.Asystole — Asystole is defined as a complete absence of demonstrable electrical and mechanicalcardiac activity ( show algorithm 5 ). In the most recent ACLS guidelines, asystole and pulselesselectrical activity (PEA) are addressed together because successful management for both dependson excellent CPR, vasopressors, and a search for and reversal of underlying causes. Asystole may bethe result of a primary or secondary cardiac conduction abnormality, possibly from end-stage tissuehypoxia and metabolic acidosis, or, rarely, the result of excessive vagal stimulation.Management begins with immediate CPR. Treat reversible conditions as appropriate ( show table 1and show table 2 ). Give epinephrine (1 mg IV every three to five minutes). The ACLS guidelines statethat vasopressin may be given (40 units for the first 10 minutes of resuscitation), but several trialsraise questions concerning the efficacy of this approach. ( See "Supportive data for advanced cardiaclife support in adults with sudden cardiac arrest" ).Atropine (1 mg IV every three to five minutes for a total of three doses) may be used to treatasystole, but the ACLS guidelines are equivocal. Although atropine has been part of ACLS treatmentprotocols for asystole for decades, data supporting its use are limited. Only one case series of 8patients suggests benefit, supposedly from vagolytic effects [ 24 ] . A larger case series showed nosurvival benefit [ 25 ] .Several studies have failed to show a survival benefit from transcutaneous pacing in asystole, and itis no longer recommended [ 26,27 ] .Bradycardia — Bradycardia is defined conservatively as a heart rate below 60 beats per minute. The
  • 5. ACLS guidelines recommend that clinicians not intervene unless the patient exhibits evidence ofinadequate tissue perfusion thought to result from the slow heart rate ( show algorithm 6 ) [4 ] . Signsand symptoms of inadequate perfusion include hypotension, altered mental status, evidence of acutepulmonary edema, or ongoing ischemic chest pain. If any such symptoms are present in the setting ofbradycardia, immediately prepare for transcutaneous pacing. Preparations for pacing are not delayedto administer medications. Before using transcutaneous pacing, assess whether the patient canperceive the pain associated with this procedure, and if so provide appropriate sedation and analgesia.While preparing for transcutaneous pacing, it is reasonable to administer atropine (0.5 mg IV, whichmay be repeated every five minutes to a total dose of 3 mg), unless there is evidence of high degree(second degree [Mobitz] type II or third degree) atrioventricular (AV) block [ 28 ] . Atropine exerts itsantibradycardic effects at the AV node and is unlikely to be effective if this block is at or below theBundle of His.If transcutaneous pacing fails to capture, prepare for transvenous pacing. While doing so, epinephrine(2 to 10 micrograms/minute) or dopamine (2 to 10 micrograms/kg/minute) infusions, titrated to thepatients response, may be started. Patients requiring transcutaneous or transvenous pacing alsorequire immediate cardiology consultation, and admission for evaluation for permanent pacemakerplacement.Glucagon may be given (3 mg IV followed by a 3 mg/hour drip as necessary) if symptomaticbradycardia is thought to result from supratherapeutic levels of beta-blockers or calcium channelblockers [ 29 ] . Additional treatments for beta blocker and calcium channel blocker overdose arediscussed elsewhere. ( See "Beta blocker poisoning" and see "Calcium channel blocker poisoning" ).Tachycardia Approach — Tachycardia is defined as a heart rate above 100 beats per minute. Management oftachydysrhythmias is governed by the presence of clinical symptoms and signs caused by the rapidheart rate ( show algorithm 7 ).First determine if the patient is unstable (eg, has ongoing ischemic chest pain, mental statuschanges, hypotension, or signs of acute pulmonary edema). If the instability appears related to thetachycardia, treat immediately with synchronized cardioversion, unless the rhythm is sinustachycardia [ 30 ] . Some cases of supraventricular tachycardia may respond to immediate treatmentwith a bolus of adenosine (12 mg IV) without the need of cardioversion. Whenever possible, assesswhether the patient can perceive the pain associated with cardioversion, and if so provide appropriatesedation and analgesia.In the stable patient, use the electrocardiogram (ECG) to determine the nature of the arrhythmia. Inthe urgent settings in which ACLS algorithms are most often employed, specific rhythm identificationmay not be possible. Nevertheless, by performing an orderly review of the ECG, one can identify theappropriate ACLS management algorithm. Three questions provide the basis for assessing theelectrocardiogram in this setting: Is the patient in a sinus rhythm? Is the QRS complex wide or narrow? Is the rhythm regular or irregular?More detailed approaches to rhythm determination in tachycardia are discussed elsewhere. ( See"Approach to the diagnosis of narrow QRS complex tachycardias" and see "Approach to the diagnosisand treatment of wide QRS complex tachycardias" and see "Overview of the acute management oftachyarrhythmias" ). Regular narrow complex —Sinus tachycardia is a common response to fever, anemia, shock,sepsis, pain, heart failure, or any other physiologic stress. No medication is needed to treat sinustachycardia; care is focused on treating the underlying cause.Supraventricular tachycardia (SVT) is a regular tachycardia most often caused by a reentrant
  • 6. mechanism within the conduction system ( show algorithm 7 ). The QRS interval is usually narrow, butcan be longer than 120 ms if a bundle branch block (ie, SVT with aberrancy) is present. Vagalmaneuvers, which may block conduction through the AV node and result in interruption of thereentrant circuit, may be employed on appropriate patients while other therapies are prepared. Vagalmaneuvers alone, (eg, valsalva, carotid sinus massage) convert up to 25 percent of SVTs to sinusrhythm [ 31 ] . SVT refractory to vagal maneuvers may be treated with nucleoside adenosine [ 32 ] .Because of its extremely short half-life, adenosine (6 mg IV) is injected as rapidly as possible into alarge proximal vein, followed immediately by a 20 cc saline flush and elevation of the extremity toensure the drug enters the central circulation before its degradation. If the first dose of adenosinedoes not convert the rhythm, a second and third dose of 12 mg IV may be given.Prior to injection, warn the patient about transient side effects from adenosine, including chestdiscomfort, dyspnea, and flushing, and give reassurance that these effects are very brief. Performcontinuous ECG recording during administration. If adenosine fails to convert the SVT, consider otheretiologies for this rhythm, including atrial flutter, which may become apparent on the ECG when AVnodal conduction is slowed, or a nonreentrant SVT. If conversion fails, initiate rate control with eitherintravenous calcium-channel blockers or beta-blockers. Irregular narrow complex — Irregular narrow-complex tachycardias most often represent atrialfibrillation, atrial flutter with variable atrioventricular (AV) nodal conduction, or multifocal atrialtachycardia (MAT) ( show algorithm 7 ). The initial goal of treatment is to control the heart rate usingeither calcium channel blockers ( diltiazem 15 to 20 mg IV over two minutes, repeat at 20 to 25 mgIV after 15 minutes, or verapamil 2.5 to 5 mg IV over two minutes followed by 5 to 10 mg IV every15 to 30 minutes) or beta-blockers (eg, lopressor 5 mg IV for 3 doses every 2 to 5 minutes; then upto 200 mg PO every 12 hours). The management of atrial fibrillation and SVT is discussed in detailelsewhere. ( See "Overview of the evaluation and management of atrial fibrillation" and see "Rhythmcontrol versus rate control in atrial fibrillation" and see "Control of ventricular rate in atrial fibrillation:pharmacologic therapy" and see "Approach to the diagnosis of narrow QRS complex tachycardias"and see "Treatment of multifocal atrial tachycardia" ).Calcium channel blockers and beta-blockers may cause or worsen hypotension. Patients should beclosely monitored while the drug is given, and patients at risk of developing severe hypotension mayrequire loading doses that are below the usual range.Diltiazem is suggested in most instances for the management of acute atrial fibrillation with rapidventricular response (RVR). Beta-blockers may also be used and may be preferred in the setting of anacute coronary syndrome. Beta-blockers are more effective for chronic rate control [ 33 ] . For atrialfibrillation associated with hypotension, amiodarone may be used (150 mg IV over 10 minutes,followed by 1 mg/min drip for six hours, and then 0.5 mg/min) [ 34 ] . Treatment of MAT includescorrection of possible precipitants, such as hypokalemia and hypomagnesemia. The ACLS guidelinesrecommend consultation with a cardiologist. ( See "Control of ventricular rate in atrial fibrillation:pharmacologic therapy" ).Cardioversion of stable patients with irregular narrow complex tachycardias should NOT beundertaken without considering the risk of embolic stroke. If the duration of atrial fibrillation is knownto be less than 48 to 72 hours, the risk of embolic stroke is low, and the clinician may considerelectrical or chemical cardioversion [ 35 ] . Chemical cardioversion may be done with procainamide(50 mg/min IV, up to a dose of 18 to 20 mg/kg or until conversion), ibutilide (0.01 mg/kg IV over 15minutes), or amiodarone (5 mg/kg IV over 15 minutes). ( See "Rhythm control versus rate control inatrial fibrillation" ). Regular wide complex —A regular, wide-complex tachycardia is most often ventricular in etiology(show algorithm 7 ). Aberrantly conducted supraventricular tachycardias may also be seen. Becausedifferentiation between ventricular tachycardia (VT) and SVT with aberrancy can be difficult, assumeVT is present and treat clinically stable undifferentiated wide-complex tachycardia with amiodarone(150 mg IV given over 10 minutes, repeated as needed to a total of 2.2 g IV over the first 24 hours)or procainamide (20 mg/min IV up to a total of 17 mg/kg) [ 36,37 ] .
  • 7. Amiodarone is more effective at terminating wide-complex tachycardia than lidocaine [38 ] . Althoughamiodarone has some immediate effects on AV nodal conduction, its effects on myocardialconduction can require up to a week [ 39,40 ] . Procainamide may be more effective at rapidlyterminating or slowing monomorphic ventricular tachycardia [ 41,42 ] .If the wide-complex tachycardia persists, in spite of pharmacologic therapy, elective cardioversionmay be needed. SVT with aberrancy, if DEFINITIVELY identified (eg, old ECG demonstrates bundlebranch block), may be treated in the same manner as narrow-complex SVT, with vagal maneuvers,adenosine, or rate control. ( See "Irregular narrow complex" above ). Irregular wide complex —A wide complex, irregular tachycardia may be atrial fibrillation withaberrancy (bundle branch block), atrial fibrillation with preexcitation (eg, Wolf Parkinson White), orpolymorphic ventricular tachycardia (VT) ( show algorithm 7 ). Use of atrioventricular (AV) nodalblockers in wide complex, irregular tachycardia of unclear etiology may precipitate ventricularfibrillation (VF) and patient death, and is contraindicated.If the patient has a history of preexcitation (eg, Wolf-Parkinson White), or there is evidence ofpreexcitation on the ECG (eg, delta wave), procainamide is the preferred treatment (20 mg/mincontinuous IV drip until arrhythmia is suppressed, the patient becomes hypotensive, the QRS widens50 percent beyond baseline, or a maximum dose of 17 mg/kg is administered). The ACLS guidelinesstate that amiodarone is an alternative treatment, but according to several case reports treatmentwith amiodarone of an irregular wide complex dysrhythmia due to preexcitation can result in unstableVT or VF [ 43 ] .A clinically stable patient with atrial fibrillation and a wide QRS interval KNOWN to stem from apreexisting bundle branch block (ie, old ECG demonstrates preexisting block) may be treated in thesame manner as a narrow-complex atrial fibrillation. Polymorphic ventricular tachycardia consistentwith Torsades de Pointes is treated with magnesium sulfate (2 g IV, followed by a maintenanceinfusion) [ 44 ] .POST-RESUSCITATION INDUCED HYPOTHERMIA —The induction of mild to moderate hypothermia(target temperature 32 to 34ºC for 24 hours) may be beneficial in patients successfully resuscitatedafter a cardiac arrest. Improved neurologic outcome and reduced mortality have been demonstratedin series of patients with VF arrest in whom spontaneous circulation was restored, even when thepatient remained comatose after resuscitation. ( See "Anoxic-ischemic brain injury: Assessment andtreatment" , section on Induced hypothermia).TERMINATION OF RESUSCITATIVE EFFORTS — Determining when to stop resuscitation efforts isdifficult, and little data exist to guide decision-making. ( See "Outcome of sudden cardiac arrest" ).Physician survey data and clinical practice guidelines suggest that factors influencing the decision tostop resuscitative efforts include [ 45-49 ] : Duration of resuscitative effort >30 minutes without a sustained perfusing rhythm Initial electrocardiographic rhythm of asystole Prolonged interval between estimated time of arrest and initiation of resuscitation Patient age and severity of comorbid disease Absent brainstem reflexes NormothermiaMore objective endpoints of resuscitation have been proposed. Of these, the best predictor ofoutcome may be the end tidal CO2 level following 20 minutes of resuscitation [ 50-52 ] . End tidalCO2 values are a function of CO2 production and venous return to the right heart and pulmonarycirculation. A very low end tidal CO2 (<10 mmHg) following prolonged resuscitation (>20 minutes) isa sign of absent circulation and an excellent predictor of acute mortality [ 50-52 ] . It is crucial to notethat low end tidal CO2 levels may also be caused by a misplaced (esophageal) endotracheal tube,and this possibility needs to be excluded before the decision is made to terminate resuscitativeefforts. ( See "Carbon dioxide monitoring (capnography)" ).
  • 8. Resuscitation in the emergency department does not appear to be superior to field resuscitation byemergency medical services (EMS) personnel. Therefore, EMS personnel should not be required totransport all victims of sudden cardiac arrest to the hospital, if further resuscitation is deemed futile[53,54 ] .Large, retrospective cohort studies have assessed criteria (BLS and ALS) for the prehospitaltermination of resuscitative efforts in cardiac arrest, initially described in the OPALS study [ 55,56 ] .Both BLS and ALS criteria demonstrated high specificity for identifying out-of-hospital cardiac arrestpatients with little or no chance of survival. Studies of another clinical decision rule suggest that ittoo accurately predicts survival and would reduce unnecessary transports substantially ifimplemented [ 53,57 ] . Use of UpToDate is subject to the Subscription and License Agreement . REFERENCES 1. DeBard, ML. The history of cardiopulmonary resuscitation. Ann Emerg Med 1980; 9:273. 2. Highlights of the History of Cardiopulmonary Resuscitation (CPR). American Heart Association 2006. Available online at: www.americanheart.org (Accesed on March 1, 2007). 3. Hermreck, AS. The history of cardiopulmonary resuscitation. Am J Surg 1988; 156:430. 4. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2005; 112:IV1. 5. Atkins, D, Best, D, Briss, PA, et al. Grading quality of evidence and strength of recommendations. BMJ 2004; 328:1490. 6. Valenzuela, TD, Kern, KB, Clark, LL, et al. Interruptions of chest compressions during emergency medical systems resuscitation. Circulation 2005; 112:1259. 7. Eilevstjonn, J, Kramer-Johansen, J, Eftestol, T, et al. Reducing no flow times during automated external defibrillation. Resuscitation 2005; 67:95. 8. Wik, L, Kramer-Johansen, J, Myklebust, H, et al. Quality of cardiopulmonary resuscitation during out-of-hospital cardiac arrest. JAMA 2005; 293:299. 9. Yu, T, Weil, MH, Tang, W, et al. Adverse outcomes of interrupted precordial compression during automated defibrillation. Circulation 2002; 106:368. 10. Abella, BS, Sandbo, N, Vassilatos, P, et al. Chest compression rates during cardiopulmonary resuscitation are suboptimal: a prospective study during in-hospital cardiac arrest. Circulation 2005; 111:428. 11. 2005 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Part 2: Adult basic life support. Resuscitation 2005; 67:187. 12. Deakin, CD, Nolan, JP, European Resuscitation, C. European Resuscitation Council guidelines for resuscitation 2005. Section 3. Electrical therapies: automated external defibrillators, defibrillation, cardioversion and pacing. Resuscitation 2005; 67 Suppl 1:S25. 13. Martens, PR, Russell, JK, Wolcke, B, et al. Optimal Response to Cardiac Arrest study: defibrillation waveform effects. Resuscitation 2001; 49:233. 14. Morrison, LJ, Dorian, P, Long, J, et al. Out-of-hospital cardiac arrest rectilinear biphasic to monophasic damped sine defibrillation waveforms with advanced life support intervention trial (ORBIT). Resuscitation 2005; 66:149. 15. White, RD, Blackwell, TH, Russell, JK, et al. Transthoracic impedance does not affect defibrillation, resuscitation or survival in patients with out-of-hospital cardiac arrest treated with a non-escalating biphasic waveform defibrillator. Resuscitation 2005; 64:63. 16. Blum, RH, Raemer, DB, Carroll, JS, et al. Crisis resource management training for an anaesthesia faculty: a new approach to continuing education. Med Educ 2004; 38:45.
  • 9. 17. Reznek, M, Smith-Coggins, R, Howard, S, et al. Emergency medicine crisis resource management (EMCRM): pilot study of a simulation-based crisis management course for emergency medicine. Acad Emerg Med 2003; 10:386.18. Murray, WB, Foster, PA. Crisis resource management among strangers: principles of organizing a multidisciplinary group for crisis resource management. J Clin Anesth 2000; 12:633.19. Schneider T, et al. Multicenter, randomized, controlled trialof 150-J biphasic shocks compared with 200-360-J monophasic shocks in the resuscitation of out-of-hospital cardiac arrest victims. Circulation 2000; 102:1780.20. Schwarz, B, Bowdle, TA, Jett, GK, et al. Biphasic shocks compared with monophasic damped sine wave shocks for direct ventricular defibrillation during open heart surgery. Anesthesiology 2003; 98:1063.21. Faddy, SC, Powell, J, Craig, JC. Biphasic and monophasic shocks for transthoracic defibrillation: a meta analysis of randomised controlled trials. Resuscitation 2003; 58:9.22. Higgins, SL, Herre, JM, Epstein, AE, et al. A comparison of biphasic and monophasic shocks for external defibrillation. Physio-Control Biphasic Investigators. Prehosp Emerg Care 2000; 4:305.23. Niemann, JT, Burian, D, Garner, D, Lewis, RJ. Monophasic versus biphasic transthoracic countershock after prolonged ventricular fibrillation in a swine model. J Am Coll Cardiol 2000; 36:932.24. Brown, DC, Lewis, AJ, Criley, JM. Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest. JACEP 1979; 8:448.25. Stueven, HA, Tonsfeldt, DJ, Thompson, BM, et al. Atropine in asystole: human studies. Ann Emerg Med 1984; 13:815.26. Cummins, RO, Graves, JR, Larsen, MP, et al. Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac arrest. N Engl J Med 1993; 328:1377.27. Barthell, E, Troiano, P, Olson, D, et al. Prehospital external cardiac pacing: a prospective, controlled clinical trial. Ann Emerg Med 1988; 17:1221.28. Brady, WJ, Swart, G, DeBehnke, DJ, et al. The efficacy of atropine in the treatment of hemodynamically unstable bradycardia and atrioventricular block: prehospital and emergency department considerations. Resuscitation 1999; 41:47.29. Love, JN, Sachdeva, DK, Bessman, ES, et al. A potential role for glucagon in the treatment of drug-induced symptomatic bradycardia. Chest 1998; 114:323.30. Lown, B. Electrical reversion of cardiac arrhythmias. Br Heart J 1967; 29:469.31. Lim, SH, Anantharaman, V, Teo, WS, et al. Comparison of treatment of supraventricular tachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med 1998; 31:30.32. DiMarco, JP, Miles, W, Akhtar, M, et al. Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. Ann Intern Med 1990; 113:104.33. Olshansky, B, Rosenfeld, LE, Warner, AL, et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: approaches to control rate in atrial fibrillation. J Am Coll Cardiol 2004; 43:1201.34. Cybulski, J, Kulakowski, P, Makowska, E, et al. Intravenous amiodarone is safe and seems to be effective in termination of paroxysmal supraventricular tachyarrhythmias. Clin Cardiol 1996; 19:563.35. Michael, JA, Stiell, IG, Agarwal, S, Mandavia, DP. Cardioversion of paroxysmal atrial fibrillation in the emergency department. Ann Emerg Med 1999; 33:379.36. Schutzenberger, W, Leisch, F, Kerschner, K, et al. Clinical efficacy of intravenous amiodarone in the short term treatment of recurrent sustained ventricular tachycardia and ventricular fibrillation. Br Heart J 1989; 62:367.37. Helmy, I, Herre, JM, Gee, G, et al. Use of intravenous amiodarone for emergency treatment of
  • 10. life-threatening ventricular arrhythmias. J Am Coll Cardiol 1988; 12:1015.38. Somberg, JC, Bailin, SJ, Haffajee, CI, et al. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol 2002; 90:853.39. Kowey, PR, Marinchak, RA, Rials, SJ, Filart, RA. Intravenous amiodarone. J Am Coll Cardiol 1997; 29:1190.40. Mitchell, LB, Wyse, DG, Gillis, AM, Duff, HJ. Electropharmacology of amiodarone therapy initiation. Time courses of onset of electrophysiologic and antiarrhythmic effects. Circulation 1989; 80:34.41. Callans, DJ, Marchlinski, FE. Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms. J Am Coll Cardiol 1992; 19:111.42. Gorgels, AP, van den Dool, A, Hofs, A, et al. Comparison of procainamide and lidocaine in terminating sustained monomorphic ventricular tachycardia. Am J Cardiol 1996; 78:43.43. Tijunelis, MA, Herbert, ME. Myth: Intravenous amiodarone is safe in patients with atrial fibrillation and Wolff-Parkinson-White syndrome in the emergency department. CJEM 2005; 7:262.44. Tzivoni, D, Banai, S, Schuger, C, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation 1988; 77:392.45. Mohr, M, Bahr, J, Schmid, J, et al. The decision to terminate resuscitative efforts: results of a questionnaire. Resuscitation 1997; 34:51.46. Marco, CA, Bessman, ES, Schoenfeld, CN, Kelen, GD. Ethical issues of cardiopulmonary resuscitation: current practice among emergency physicians. Acad Emerg Med 1997; 4:898.47. de Vos, R, Oosterom, L, Koster, RW, de Haan, RJ. Decisions to terminate resuscitation. Resuscitation Committee. Resuscitation 1998; 39:7.48. Bailey, ED, Wydro, GC, Cone, DC. Termination of resuscitation in the prehospital setting for adult patients suffering nontraumatic cardiac arrest. National Association of EMS Physicians Standards and Clinical Practice Committee. Prehosp Emerg Care 2000; 4:190.49. Horsted, TI, Rasmussen, LS, Lippert, FK, Nielsen, SL. Outcome of out-of-hospital cardiac arrest-why do physicians withhold resuscitation attempts?. Resuscitation 2004; 63:287.50. Levine, RL, Wayne, MA, Miller, CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest. N Engl J Med 1997; 337:301.51. Grmec, S, Klemen, P. Does the end-tidal carbon dioxide (EtCO2) concentration have prognostic value during out-of-hospital cardiac arrest?. Eur J Emerg Med 2001; 8:263.52. Ahrens, T, Schallom, L, Bettorf, K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care 2001; 10:391.53. Morrison, LJ, Visentin, LM, Kiss, A, et al. Validation of a rule for termination of resuscitation in out-of-hospital cardiac arrest. N Engl J Med 2006; 355:478.54. Ong, ME, Jaffey, J, Stiell, I, Nesbitt, L. Comparison of termination-of-resuscitation guidelines for basic life support: defibrillator providers in out-of-hospital cardiac arrest. Ann Emerg Med 2006; 47:337.55. Stiell, IG, Nesbitt, LP, Pickett, W, et al. The OPALS Major Trauma Study: impact of advanced life-support on survival and morbidity. CMAJ 2008; 178:1141.56. Ruygrok, ML, Byyny, RL, Haukoos, JS. Validation of 3 termination of resuscitation criteria for good neurologic survival after out-of-hospital cardiac arrest. Ann Emerg Med 2009; 54:239.57. Morrison, LJ, Verbeek, PR, Zhan, C, et al. Validation of a universal prehospital termination of resuscitation clinical prediction rule for advanced and basic life support providers. Resuscitation 2009; 80:324. GRAPHICS
  • 11. BLS algorithmAED: automated external defibrillator.Data from: Guidelines 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.Part 4: Adult Basic Life Support. Circulation 2005; 112:IV19.
  • 12. Advanced cardiopulmonary life support in adultsData from: Guidelines 2005 for Cardiopulmonary Resuscitation and Emergency CardiovascularCare. Part 4: Advanced life support. Circulation 2005; 112:III-25.
  • 13. Ventricular fibrillation/pulseless ventricular tachycardia algorithm Data from Guidelines 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Part 4 advanced life support. Circulation 2005; 112:III-25Potentially treatable conditions associated with cardiac arrestCondition Common clinical settings Corrective actions
  • 14. Reassess adequacy of cardiopulmonary resuscitation, oxygenation, and ventilation; reconfirm endotracheal-tube Preexisting acidosis, diabetes, placement diarrhea, drugs and toxins,Acidosis prolonged resuscitation, renal Hyperventilate disease, and shock Consider intravenous bicarbonate if pH <7.20 after above actions have been taken Administer fluids; obtain bedside echocardiogram, if available Hemorrhagic diathesis, cancer,Cardiac pericarditis, trauma, after Perform pericardiocentesis. Immediatetamponade cardiac surgery, and after surgical intervention is appropriate if myocardial infarction pericardiocentesis is unhelpful but cardiac tamponade is known or highly suspected If hypothermia is severe (temperature <30°C), limit initial shocks for ventricular fibrilation or pulseless Alcohol abuse, burns, central ventricular tachycardia to three; initiate nervous system disease, active internal rewarming and debilitated or elderly patient, cardiopulmonary support. Hold further drowning, drugs and toxins, resuscitation medications or shocksHypothermia endocrine disease, history of until core temperature is >30°C exposure, homelessness, extensive skin disease, spinal If hypothermia is moderate (temperature cord disease, and trauma 30-34°C), proceed with resuscitation (space medications at intervals greatear than usual), passively rewarm, and actively rewarm truncal body areas Administer fluids Transfuse packed red cells if hemorrhage or profound anemia is Major burns, diabetes, presentHypovolemia, gastrointestinal losses,hemorrhage, hemorrhage, hemorrhagic Thoracotomy is appropriate when aanemia diathesis, cancer, pregnancy, patient has cardiac arrest from shock and trauma penetrating trauma and a cardiac rhythm and the duration of cardiopulmonary resuscitation before thoracotomy is <10 min Reassess technical quality of Consider in all patients with cardiopulmonary resuscitation,Hypoxia cardiac arrest oxygenation, and ventilation; reconfirm endotracheal-tube placement
  • 15. Alcohol abuse, burns, diabetic ketoacidosis, severe diarrhea, Administer 1-2 g magnesium sulfate Hypomagnesemia diuretics, and drugs (eg, intravenously over 2 min cisplatin, cyclosporine, pentamidine)Reproduced with permission from: Eisenberg, MS, Mengert, TJ. N Engl J Med 2001; 344:1304. Copyright© 2001 Massachusetts Medical Society.Potentially treatable conditions associated with cardiac arrest, continued Condition Common clinical settings Corrective actions Consider in all patients with Consider definitive care (eg, thrombolytic cardiac arrest, especially Myocardial therapy, cardiac catheterization or coronary those with a history of coronary infarction artery reperfusion, circulatory assist device, artery disease or prearrest emergency cardiopulmonary bypass) acute coronary syndrome Alcohol abuse, bizarre or Consult toxicologist for emergency advice on puzzling behavioral or resuscitation and definitive care, including metabolic presentation, classic appropriate antidote Poisoning toxicologic syndrome, occupational or industrial Prolonged resuscitation efforts may be exposure, and psychiatric appropriate; immediate cardiopulmonary disease bypass should be considered, if available If hyperkalemia is identified or strongly suspected, treat with all of the following: 10 Metabolic acidosis, excessive percent calcium chloride (5-10 mL by slow administration of potassium, intravenous push; do not use if hyperkalemia drugs and toxins, vigorous is secondary to digitalis poisoning), glucose exercise, hemolysis, renal and insulin (50 mL of 50 percent dextrose in Hyperkalemia disease, rhabdomyolysis, water and 10 units of regular insulin tumor lysis syndrome, and intravenously), sodium bicarbonate (50 mmoL clinically significant tissue intravenously; most effective if concomitant injury metabolic acidosis is present), and albuterol (15-20 mg nebulized or 0.5 mg by intravenous infusion) If profond hypokalemia (<2-2.5 mmoL of Alcohol abuse, diabetes, use of potassium per liter) is accompanied by diuretics, drugs and toxins, Hypokalemia cardiac arrest, initiate urgent intravenous profound gastroinstestinal replacement (2 mmoL/min intravenously for losses, hypomagnesemia 10-15 mmoL), then reassess Administer fluids; augment with vasopressors Hospitalized patient, recent as necessary surgical procedure, peripartum, known risk factors for venous Confirm diagnosis, if possible; consider Pulmonary thromboembolism, history of immediate cardiopulmonary bypass to embolism venous thromboembolism, or maintain patients viability prearrest presentation
  • 16. prearrest presentation Consider definitive care (eg, thrombolytic consistent with diagnosis of therapy, embolectomy by interventional actue pulmonary embolism radiology or surgery) Placement of central catheter, mechanical ventilation, pulmonary disease (including Tension Needle decompression, followed by asthma, chronic obstructive pneumothorax chest-tube insertion pulmonary disease, and necrotizing pneumonia), thoracentesis, and traumaReproduced with permission from: Eisenberg, MS, Mengert, TJ. N Engl J Med 2001; 344:1304. Copyright© 2001 Massachusetts Medical Society.
  • 17. Pulseless electrical activity algorithmData from Guidelines 2005 for Cardiopulmonary Resuscitation and EmergencyCardiovascularCare. Part 4: Advanced life support. Circulation 2005; 112:III-25.
  • 18. Asystole treatment algorithmData from Guidelines 2005 for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care. Part 4: Advanced life support. Circulation 2005;112:III-25.
  • 19. ACLS bradycardia algorithmReprinted with permission from: 2005 American Heart Association Guidelines for CardiopulmonaryResuscitation and Emergency Cardiovascular Care, Part 7.3: Management of SymptomaticBradycardia and Tachycardia. Circulation 2005;112:IV-67 - IV-77. Copyright © 2005 American HeartAssociation, Inc.
  • 20. ACLS tachycardia algorithm* If patient becomes unstable, go to box 4.Reprinted with permission from: 2005 American Heart Association Guidelines for CardiopulmonaryResuscitation and Emergency Cardiovascular Care, Part 7.3: Management of Symptomatic Bradycardiaand Tachycardia. Circulation 2005;112:IV-67 - IV-77. Copyright © 2005 American Heart Association,
  • 21. Inc.© 2009 UpToDate, Inc. All rights reserved. | Subscription and License AgreementLicensed to: Jeisson Osorio Trujillo