acls UPTODATE

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Author Charles N Pozner, MD Section Editors Ron M Walls, MD, FRCPC, FAAEM Richard L Page, MD Deputy Editor Jonathan Grayzel, MD, FAAEM Advanced cardiac life support (ACLS) in adults Last literature review version 19.2: May 2011|This topic last updated: April 7, 2011 INTRODUCTION — The field of resuscitation has been evolving for more than two centuries [1 ]. The Paris 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) in 1963 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 based on a combination of scientific evidence of variable strength and expert consensus. The American Heart Association (AHA) developed the most recent ACLS guidelines in 2010 using the comprehensive review of resuscitation literature performed by the International Liaison Committee on Resuscitation (ILCOR) [4,5 ]. Guidelines are reviewed continually, but are formally released every five years, and published in the journals Circulation and Resuscitation. This topic will discuss the management of cardiac arrhythmias in adults as described in the 2010 ACLS Guidelines. The evidence supporting these guidelines is presented separately, 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 life support in adults with sudden cardiac arrest" and "Therapies of uncertain benefit in basic and advanced cardiac life support" and "Basic life support (BLS) in adults" and "Basic airway management in adults" and "Advanced airway management in adults" .) EVIDENCE BASED GUIDELINES — Because of the nature of resuscitation research, few randomized controlled trials have been completed in humans. Many of the recommendations in the American Heart Association’s 2010 Guidelines for advanced cardiac life support (hereafter referred to as the 2010 ACLS Guidelines) are made based upon retrospective studies, animal studies, and expert consensus [5 ]. Guideline recommendations are classified according to the GRADE system [6 ]. The evidence supporting the 2010 ACLS Guidelines is reviewed in detail separately. (See "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest" .) PRINCIPLES OF MANAGEMENT Excellent basic life support and its importance — Excellent cardiopulmonary resuscitation (CPR) and early defibrillation for treatable arrhythmias remain the cornerstones of basic and advanced cardiac life support (ACLS). Although the 2010 American Heart Association (AHA) Guidelines for ACLS (2010 ACLS Guidelines) suggest several revisions, including medications, electrical therapy, and monitoring, the emphasis on excellent CPR and its critical role in resuscitative efforts remains unchanged (algorithm 1 and algorithm 2 ) [5 ]. We emphasize the term “excellent CPR” because anything short of this standard does not achieve adequate cerebral and coronary perfusion, thereby compromising a patient’s chances for neurologically intact survival. CPR is discussed in detail separately. (See "Basic life support (BLS) in adults" .) file:/// 1 of 23 01/10/11 19:38

Transcript of acls UPTODATE

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AuthorCharles N Pozner, MD

Section EditorsRon M Walls, MD, FRCPC,FAAEMRichard L Page, MD

Deputy EditorJonathan Grayzel, MD, FAAEM

Advanced cardiac life support (ACLS) in adults

Last literature review version 19.2: May 2011|This topic last updated: April 7, 2011

INTRODUCTION — The field of resuscitation has been evolving for more than twocenturies [1]. The Paris Academy of Science recommended mouth-to-mouth ventilation fordrowning victims in 1740 [2]. In 1891, Dr. Friedrich Maass performed the first documentedchest compressions on humans [3]. The American Heart Association (AHA) formallyendorsed cardiopulmonary resuscitation (CPR) in 1963 and by 1966 they had adoptedstandardized CPR guidelines for instruction to lay-rescuers [2].

Advanced cardiac life support (ACLS) guidelines have evolved over the past severaldecades based on a combination of scientific evidence of variable strength and expertconsensus. The American Heart Association (AHA) developed the most recent ACLSguidelines in 2010 using the comprehensive review of resuscitation literature performed bythe International Liaison Committee on Resuscitation (ILCOR) [4,5]. Guidelines arereviewed continually, but are formally released every five years, and published in thejournals Circulation and Resuscitation.

This topic will discuss the management of cardiac arrhythmias in adults as described in the2010 ACLS Guidelines. The evidence supporting these guidelines is presented separately,as are issues related to controversial treatments for cardiac arrest patients, basic lifesupport (BLS), and the emergency care of the critically ill adult. (See "Supportive data foradvanced cardiac life support in adults with sudden cardiac arrest" and "Therapies ofuncertain benefit in basic and advanced cardiac life support" and "Basic life support (BLS)in adults" and "Basic airway management in adults" and "Advanced airway management inadults".)

EVIDENCE BASED GUIDELINES — Because of the nature of resuscitation research, fewrandomized controlled trials have been completed in humans. Many of therecommendations in the American Heart Association’s 2010 Guidelines for advancedcardiac life support (hereafter referred to as the 2010 ACLS Guidelines) are made basedupon retrospective studies, animal studies, and expert consensus [5]. Guidelinerecommendations are classified according to the GRADE system [6]. The evidencesupporting the 2010 ACLS Guidelines is reviewed in detail separately. (See "Supportivedata for advanced cardiac life support in adults with sudden cardiac arrest".)

PRINCIPLES OF MANAGEMENT

Excellent basic life support and its importance — Excellent cardiopulmonaryresuscitation (CPR) and early defibrillation for treatable arrhythmias remain thecornerstones of basic and advanced cardiac life support (ACLS). Although the 2010American Heart Association (AHA) Guidelines for ACLS (2010 ACLS Guidelines) suggestseveral revisions, including medications, electrical therapy, and monitoring, the emphasison excellent CPR and its critical role in resuscitative efforts remains unchanged (algorithm1 and algorithm 2) [5]. We emphasize the term “excellent CPR” because anything short ofthis standard does not achieve adequate cerebral and coronary perfusion, therebycompromising a patient’s chances for neurologically intact survival. CPR is discussed indetail separately. (See "Basic life support (BLS) in adults".)

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In the past, clinicians frequently interrupted CPR to check for pulses, perform trachealintubation, or obtain venous access. The 2010 ACLS Guidelines strongly recommend thatevery effort be made NOT to interrupt CPR; other less vital interventions (eg, trachealintubation or administration of medications to treat arrhythmias) are made either whileCPR is performed or during the briefest possible interruption. Interventions that cannot beperformed while CPR is in progress (eg, defibrillation, pulse check) should be performedduring brief interruptions at two minute intervals (after the completion of a full cycle ofCPR).

Studies in both the in-hospital and prehospital settings demonstrate that chestcompressions are often performed incorrectly, inconsistently, and with excessiveinterruption [7-11]. Chest compressions must be of sufficient depth (at least 5 cm, or 2inches) and rate (at least 100 per minute), and allow for complete recoil of the chestbetween compressions, to be effective.

A single biphasic defibrillation remains the recommended treatment for ventricularfibrillation (VF) or pulseless ventricular tachycardia (VT). CPR should be performed until thedefibrillator is ready for immediate discharge and resumed immediately after the shock isgiven, without pausing to recheck a pulse at that moment. Interruptions in CPR (eg, forsubsequent attempts at defibrillation or pulse checks) should occur no more frequentlythan every two minutes, and for the shortest possible duration.

Patients are often over-ventilated during resuscitations, which can compromise venousreturn resulting in reduced cardiac output and inadequate cerebral and cardiac perfusion. A30 to 2 compression to ventilation ratio (one cycle) is recommended in patients withoutadvanced airways. According to the 2010 ACLS Guidelines, asynchronous ventilations at 8to 10 per minute are administered if an endotracheal tube or extraglottic airway is in place,while continuous chest compressions are performed simultaneously [12]. We believe that 6to 8 ventilations are sufficient in the low-flow state of cardiac resuscitation and help toprevent over-ventilation.

Resuscitation team management — The resuscitation of a sudden cardiac arrest (SCA),by its nature a low frequency, high acuity event, is often chaotic. A growing body ofliterature demonstrates that by employing the principles of Crisis Resource Management(CRM), adapted from the aviation industry and introduced into medical care byanesthesiologists, disorganization during resuscitation decreases and patient care improves[13-15]. Training in these principles to improve the quality of ACLS performed byhealthcare clinicians is feasible and recommended [16].

Two principles provide the foundation for CRM: leadership and communication [15].Resuscitations usually involve a number of healthcare providers from different disciplines,sometimes from different areas of an institution, who may not have worked togetherpreviously. Under these circumstances, role clarity can be difficult to establish. In CRM, it isimperative that one person assumes the role of team leader [15]. This person isresponsible for the global management of the resuscitation, including: ensuring that allrequired tasks are carried out competently; incorporating new information and coordinatingcommunication among all team members; developing and implementing managementstrategies that will maximize patient outcome; and reassessing performance throughoutthe resuscitation.

The team leader should avoid performing technical procedures, as performance of a taskinevitably shifts attention from the primary leadership responsibilities. In circumstanceswhere staffing is limited (eg, small community hospital), the team leader may be requiredto perform certain critical procedures. In these situations, leadership may be temporarily

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transferred to another clinician or the team leader may be forced temporarily to performboth 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 importantinformation with the team. When the team leader determines the need to perform a task,the request is directed to a specific team member, ideally by name. That team memberverbally acknowledges the request and performs the task or, if unable to do so, informs theteam leader that someone else should be assigned. Specific emphasis is placed on theassigned team member repeating back medication doses and defibrillator energy settingsto the team leader. This "closed-loop" communication leads to a more orderly transfer ofinformation and is the appropriate standard for all communication during resuscitations.

Though most decisions emanate from the team leader, a good team leader enlists thecollective wisdom and experience of the entire team as needed. Extraneous personnel notinvolved with patient care are asked to leave in order to reduce noise and to ensure thatorders from the leader and feedback from the resuscitation team can be heard clearly.

Initial management and ECG interpretation — In the 2010 ACLS Guidelines, circulationhas taken a more prominent role in the initial management of cardiac arrest. The new‘mantra’ is: circulation, airway, breathing (C-A-B). Once unresponsiveness is recognized,resuscitation begins by addressing circulation (chest compressions), followed by airwayopening, and then rescue breathing. The 2010 ACLS Guidelines emphasize the importanceof excellently performed, uninterrupted chest compressions and early defibrillation. Rescuebreathing is performed after the initiation of excellent chest compressions and definitiveairway management may be delayed if there is adequate rescue breathing without anadvanced airway in place. (See 'Excellent basic life support and its importance' above and"Basic life support (BLS) in adults", section on 'Recognition of cardiac arrest'.)

The other initial interventions for ACLS include administering oxygen, establishingintravenous access, placing the patient on a cardiac and oxygen saturation monitor, andobtaining an electrocardiogram (ECG) [5]. Unstable patients must receive immediate care,even when data are incomplete or presumptive (algorithm 1 and algorithm 2).

Stable patients require an assessment of their electrocardiogram in order to provideappropriate treatment consistent with ACLS guidelines. Although it is best to make adefinitive interpretation of the ECG prior to making management decisions, the settings inwhich ACLS guidelines are commonly employed require a modified, empirical approach.Such an approach is guided by the following questions:

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 diagnosisand initiate appropriate therapy.

AIRWAY MANAGEMENT DURING ACLS — Ventilation is performed during CPR tomaintain adequate oxygenation and eliminate carbon dioxide. Nevertheless, during the firstfew minutes following sudden cardiac arrest (SCA), oxygen delivery to the brain is limitedprimarily by reduced blood flow [17,18]. Therefore, in adults, the performance of excellentchest compressions takes priority over ventilation during the initial period of basic lifesupport. In settings with multiple rescuers or clinicians, ventilations and chest

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compressions are performed simultaneously. (See "Basic life support (BLS) in adults".)

Although research has yet to identify the preferred parameters for ventilation (eg,respiratory rate, tidal volume, inspired oxygen concentration), it is widely believed that alower minute ventilation is needed for patients in cardiac arrest. Therefore, lowerrespiratory rates are used (the 2010 ACLS Guidelines recommend 8 to 10 breaths perminute with an advanced airway in place; we believe 6 to 8 breaths are adequate). Inaddition, we know that hyperventilation is harmful, as it leads to increased intrathoracicpressure, which decreases venous return and compromises cardiac output. Tidal volumesof approximately 600 mL delivered in a controlled fashion such that chest rise occurs overno more than one second is recommended in the 2010 ACLS Guidelines. (See "Basic lifesupport (BLS) in adults", section on 'Ventilations'.)

Taking these principles into account, the 2010 ACLS Guidelines support the use of abag-mask device or a blindly placed supraglottic airway for ventilation during the initialmanagement of SCA, deferring placement of an endotracheal tube, unless intubation canbe performed without interrupting chest compressions. Bag-mask ventilation is describedseparately. (See "Basic airway management in adults".)

A blindly inserted supraglottic airway (eg, laryngeal mask airway, Combitube™, laryngealtube) can be placed without interrupting chest compressions, provides adequate ventilationin most cases, and reduces the risk of aspiration compared to bag-mask ventilation.Therefore, clinicians may prefer to ventilate with a supraglottic device while CPR isongoing, rather than performing tracheal intubation. Supraglottic airways and trachealintubation are discussed separately. (See "Devices for difficult airway management inadults", section on 'Extraglottic devices' and "Direct laryngoscopy and tracheal intubation inadults".)

If rescuers decide that tracheal intubation is necessary during CPR, an experiencedintubator should perform the procedure. Ideally, intubation is performed while excellentchest compressions continue uninterrupted. However, if the operator is unable to intubateduring the performance of chest compressions, further attempts should be deferred to thetwo minute interval (after a complete cycle of CPR) when defibrillation or patientreassessment is performed. This approach minimizes loss of perfusion. Attempts atintubation should last no longer than 10 seconds.

The 2010 ACLS Guidelines include the following additional recommendations about airwaymanagement during the performance of ACLS [17]:

Although evidence is lacking, it is reasonable to provide 100 percent oxygen duringCPR.

Routine use of cricoid pressure is NOT recommended. (See "Basic airwaymanagement in adults", section on 'Sellick's maneuver'.)

Oropharyngeal and nasopharyngeal airways can be useful adjuncts. We encouragetheir use when performing bag-mask ventilation. (See "Basic airway management inadults", section on 'Airway adjuncts'.)

Continuous waveform capnography (performed in addition to clinical assessment) isrecommended for confirming and monitoring correct endotracheal tube placement. Ifwaveform capnography is not available, a non-waveform CO2 detector or esophagealdetector device, in addition to clinical assessment, may be used. Capnography alsoprovides important feedback on the patient response to resuscitation, which is

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discussed separately. (See "Carbon dioxide monitoring (capnography)", section on'Clinical applications for intubated patients'.)

MANAGEMENT OF SPECIFIC ARRHYTHMIAS

Sudden cardiac arrest

Ventricular fibrillation and pulseless ventricular tachycardia — Ventricularfibrillation (VF) and pulseless ventricular tachycardia (VT) are nonperfusing rhythmsemanating from the ventricles, for which early rhythm identification, defibrillation, andcardiopulmonary resuscitation (CPR) are the mainstays of treatment (algorithm 2). Earlydefibrillation is the most critical action in the resuscitation effort, followed by theperformance of excellent CPR. Manage potentially treatable underlying causes asappropriate (table 1 and table 2) [17].

Begin performing excellent chest compressions as soon as sudden cardiac arrest (SCA) isrecognized and continue while the defibrillator is being attached. If a defibrillator is notimmediately available, continue CPR until one is obtained. As soon as a defibrillator isavailable, attach it to the patient, charge it, assess the rhythm, and treat appropriately (eg,defibrillate VF or pulseless VT; continue CPR if asystole or PEA). Resume CPR immediatelyafter any shock is given. (See "Supportive data for advanced cardiac life support in adultswith sudden cardiac arrest", section on 'VF and pulseless VT'.)

In the case of a witnessed cardiac arrest, perform defibrillation as quickly as possible.Decreased time to defibrillation improves the likelihood of successful conversion to aperfusing rhythm and of patient survival.

Biphasic defibrillators are recommended because of their increased efficacy at lower energylevels [19-21]. The 2010 ACLS Guidelines recommend that when employing a biphasicdefibrillator clinicians use the initial dose of energy recommended by the manufacturer(120 to 200 J). If this dose is not known, the maximal dose may be used. We suggest afirst defibrillation using 200 J with a biphasic defibrillator or 360 J with a monophasicdefibrillator for VF or pulseless VT. It should be noted that many automated externaldefibrillators (AEDs) do not allow for adjustment of the shock output.

The 2010 ACLS Guidelines recommend the resumption of CPR immediately afterdefibrillation without rechecking for a pulse. Interrupt CPR to assess the rhythm andadminister additional shocks no more frequently than every two minutes. (See "Basic lifesupport (BLS) in adults", section on 'Phases of resuscitation' and "Basic life support (BLS)in adults", section on 'Defibrillation'.)

If VF or pulseless VT persists after at least one attempt at defibrillation and two minutes ofCPR, give epinephrine (1 mg IV every 3 to 5 minutes) while CPR is performed continuously.Vasopressin (40 units IV) may replace the first or second dose of epinephrine.

Evidence suggests that antiarrhythmic drugs provide little survival benefit in refractory VFor pulseless VT. Nevertheless, the current ACLS Guidelines state that they may be used incertain situations. The timing of antiarrhythmic use is not specified. We suggest thatantiarrhythmic drugs be considered after a second unsuccessful defibrillation attempt inanticipation of a third shock.

Amiodarone (300 mg IV with a repeat dose of 150 mg IV as indicated) may beadministered in VF or pulseless VT unresponsive to defibrillation, CPR, andepinephrine.

Lidocaine (1 to 1.5 mg/kg IV, then 0.5 to 0.75 mg/kg every 5 to 10 minutes) may be

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used if amiodarone is unavailable.

Magnesium sulfate (2 g IV, followed by a maintenance infusion) may be used to treatpolymorphic ventricular tachycardia consistent with torsade de pointes. (See'Irregular wide complex' below.)

Refractory VF or pulseless VT may be caused by an acute coronary syndrome (ACS), inwhich case percutaneous coronary intervention can be performed if the patient issuccessfully resuscitated and the procedure is feasible. Note that following cardiac arrestthe ECG may be insensitive for ACS; cardiology consultation is needed for patients withreturn of spontaneous circulation (ROSC) [4]. Causes other than ACS can lead to SCA(table 1 and table 2).

In summary, the ROSC in VF and pulseless VT hinges on early defibrillation and excellentCPR. Although, the 2010 ACLS Guidelines advocate the appropriate use of advanced airwaymanagement and treatment with specific medications, these interventions have not beenshown to improve survival in SCA. Therefore, such interventions must never be made atthe expense of performing excellent CPR and early defibrillation.

Asystole and pulseless electrical activity — Asystole is defined as a completeabsence of demonstrable electrical and mechanical cardiac activity. Pulseless electricalactivity (PEA) is defined as any one of a heterogeneous group of organizedelectrocardiographic rhythms without sufficient mechanical contraction of the heart toproduce a palpable pulse or measurable blood pressure. By definition, asystole and PEA arenon-perfusing rhythms requiring the initiation of excellent CPR immediately when either ispresent (algorithm 2).

In the 2010 ACLS Guidelines, asystole and PEA are addressed together because successfulmanagement for both depends on excellent CPR, vasopressors, and reversal of underlyingcauses, such as hypoxia, hyperkalemia, poisoning, and hemorrhage [17]. Asystole may bethe result of a primary or secondary cardiac conduction abnormality, possibly fromend-stage tissue hypoxia and metabolic acidosis, or, rarely, the result of excessive vagalstimulation. It is crucial to identify and treat potential secondary causes of asystole or PEAas rapidly as possible. Do not hesitate to perform invasive procedures to treat suspectedsecondary causes; if the patient is receiving CPR, there is little chance the intervention willmake the situation worse. The accompanying tables describe important secondary causesof cardiac arrest (table 1 and table 2).

After initiating CPR, treat reversible causes as appropriate and administer epinephrine (1mg IV every three to five minutes). The 2010 ACLS Guidelines state that vasopressin maybe given (40 units for the first 10 minutes of resuscitation) in place of the first or secondepinephrine dose. Neither asystole nor PEA responds to defibrillation. Atropine is no longerrecommended for the treatment of asystole or PEA. Cardiac pacing is ineffective for cardiacarrest and not recommended in the 2010 ACLS Guidelines. (See "Supportive data foradvanced cardiac life support in adults with sudden cardiac arrest".)

In summary, treatment for asystole and PEA consists of early identification and treatmentof reversible causes and excellent CPR with vasopressor administration until either ROSC ora shockable rhythm occurs.

Monitoring — The 2010 ACLS Guidelines encourage the use of clinical and physiologicmonitoring to optimize the performance of CPR and to detect the return of spontaneouscirculation (ROSC) [5]. Assessment and immediate feedback about important clinicalparameters, such as the rate and depth of chest compressions, adequacy of chest recoil

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between compressions, and rate and force of ventilations, can improve CPR. End-tidalcarbon dioxide (EtCO2) measurements from continuous waveform capnography accuratelyreflect cardiac output and cerebral perfusion pressure, and therefore the quality of CPR,while sudden, sustained increases in EtCO2 during CPR indicate a ROSC. (See "Carbondioxide monitoring (capnography)", section on 'Effectiveness of CPR' and "Carbon dioxidemonitoring (capnography)", section on 'Return of spontaneous circulation'.)

Data from other physiologic monitors is less likely to be available in patients with SCA, butmeasurements obtained from arterial and central venous catheters provide useful feedbackabout the quality of CPR and ROSC [17]. Measurements of arterial relaxation provide areasonable approximation of coronary perfusion pressure. During CPR, a reasonable goal isto maintain the arterial relaxation (or “diastole”) pressure above 20 mmHg. Central venousoxygen saturation (SCVO2) provides information about oxygen delivery and cardiac output.During CPR, a reasonable goal is to maintain SCVO2 above 30 percent.

Bradycardia — Bradycardia is defined conservatively as a heart rate below 60 beats perminute, but symptomatic bradycardia generally entails rates below 50 beats per minute.The 2010 ACLS Guidelines recommend that clinicians not intervene unless the patientexhibits evidence of inadequate tissue perfusion thought to result from the slow heart rate(algorithm 3) [17]. Signs and symptoms of inadequate perfusion include hypotension,altered mental status, signs of shock, ongoing ischemic chest pain, and evidence of acutepulmonary edema. Hypoxemia is a common cause of bradycardia; look for signs of laboredbreathing (eg, increased respiratory rate, retractions, paradoxical abdominal breathing)and low oxygen saturation. Mild symptoms may not warrant treatment. (See "Shock inadults: Types, presentation, and diagnostic approach", section on 'Clinical presentation'.)

If any significant symptoms are present in the setting of bradycardia, give atropine (ifeasily done) and immediately prepare to treat the patient with transcutaneous pacing or aninfusion of a chronotropic agent (dopamine or epinephrine). Do not delay treatment withtranscutaneous pacing or a chronotropic agent in order to give atropine.

The initial dose of atropine is 0.5 mg IV. This dose may be repeated every three to fiveminutes to a total dose of 3 mg. Do not give atropine if there is evidence of a high degree(second degree [Mobitz] type II or third degree) atrioventricular (AV) block [22]. Atropineexerts its antibradycardic effects at the AV node and is unlikely to be effective if aconduction block exists at or below the Bundle of His, or in transplanted hearts, which lackvagal innervation. Atropine may be harmful in the setting of cardiac ischemia. (See"Second degree atrioventricular block: Mobitz type II" and "Third degree (complete)atrioventricular block".)

Before using transcutaneous pacing, assess whether the patient can perceive the painassociated with this procedure and if so provide appropriate sedation and analgesiawhenever possible. Infusions of dopamine are dosed at 2 to 10 micrograms/kg per minute,while epinephrine is given at 2 to 10 micrograms per minute. Each is titrated to thepatient's response. (See "Procedural sedation in adults".)

If neither transcutaneous pacing nor infusion of a chronotropic agent resolves the patient’ssymptoms, prepare for transvenous pacing and obtain expert consultation if available.Patients requiring transcutaneous or transvenous pacing also require cardiologyconsultation, and admission for evaluation for permanent pacemaker placement.

Common toxicologic causes of symptomatic bradycardia include supratherapeutic levels ofbeta-blockers, calcium channel blockers, and Digoxin. These poisonings are discussedseparately. (See "Beta blocker poisoning" and "Calcium channel blocker poisoning" and

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"Digitalis (cardiac glycoside) poisoning".)

Tachycardia

Approach — Tachycardia is defined as a heart rate above 100 beats per minute, butsymptomatic tachycardia generally involves rates over 150 beats per minute, unlessunderlying ventricular dysfunction exists [17]. Management of tachyarrhythmias isgoverned by the presence of clinical symptoms and signs caused by the rapid heart rate(algorithm 4).

The fundamental approach is as follows: First determine if the patient is unstable (eg,manifests ongoing ischemic chest pain, acute mental status changes, hypotension, signs ofshock, or evidence of acute pulmonary edema). Hypoxemia is a common cause oftachycardia; look for signs of labored breathing (eg, increased respiratory rate, retractions,paradoxical abdominal breathing) and low oxygen saturation.

If instability is present and appears related to the tachycardia, treat immediately withsynchronized cardioversion, unless the rhythm is sinus tachycardia [23]. Some cases ofsupraventricular tachycardia may respond to immediate treatment with a bolus ofadenosine (6 to 12 mg IV) without the need of cardioversion. Whenever possible, assesswhether the patient can perceive the pain associated with cardioversion, and if so provideappropriate sedation and analgesia. (See "Procedural sedation in adults" and "Shock inadults: Types, presentation, and diagnostic approach", section on 'Clinical presentation'.)

In the stable patient, use the electrocardiogram (ECG) to determine the nature of thearrhythmia. In the urgent settings in which ACLS algorithms are most often employed,specific rhythm identification may not be possible. Nevertheless, by performing an orderlyreview of the ECG, one can determine appropriate management. Three questions providethe basis for assessing the electrocardiogram 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 separately.(See "Approach to the diagnosis of narrow QRS complex tachycardias" and "Approach tothe diagnosis and treatment of wide QRS complex tachycardias" and "Overview of theacute management of tachyarrhythmias".)

Regular narrow complex — Sinus tachycardia and supraventricular tachycardia arethe major causes of a regular narrow complex arrhythmia [17]. Sinus tachycardia is acommon response to fever, anemia, shock, sepsis, pain, heart failure, or any otherphysiologic stress. No medication is needed to treat sinus tachycardia; care is focused ontreating the underlying cause. (See "Sinus tachycardia".)

Supraventricular tachycardia (SVT) is a regular tachycardia most often caused by areentrant mechanism within the conduction system (algorithm 4). The QRS interval isusually narrow, but can be longer than 120 ms if a bundle branch block (ie, SVT withaberrancy or fixed bundle branch block) is present. Vagal maneuvers, which may blockconduction through the AV node and result in interruption of the reentrant circuit, may beemployed on appropriate patients while other therapies are prepared. Vagal maneuversalone, (eg, Valsalva, carotid sinus massage) convert up to 25 percent of SVTs to sinusrhythm [24,25]. SVT refractory to vagal maneuvers is treated with adenosine [26,27]. (See

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"Reentry and the development of cardiac arrhythmias".)

Because of its extremely short half-life, adenosine (6 to 12 mg IV) is injected as rapidly aspossible into a large proximal vein, followed immediately by a 20 mL saline flush andelevation of the extremity to ensure the drug enters the central circulation before it ismetabolized. If the first dose of adenosine does not convert the rhythm, a second and thirddose of 12 mg IV may be given. Larger doses (eg, 18 mg IV) may be needed in patientstaking theophylline or theobromine, or who consume large amounts of caffeine; smallerdoses (eg, 3 mg IV) should be given to patients taking dipyridamole or carbamazepine,those with transplanted hearts, or when injecting via a central vein.

Prior to injection, warn the patient about transient side effects from adenosine, includingchest discomfort, dyspnea, and flushing, and give reassurance that these effects are verybrief. Perform continuous ECG recording during administration. If adenosine fails to convertthe SVT, consider other etiologies for this rhythm, including atrial flutter or a nonreentrantSVT, which may become apparent on the ECG when AV nodal conduction is slowed.

If conversion attempts fail, initiate rate control with either an intravenousnondihydropyridine calcium channel blocker or a beta blocker. Agents to choose frominclude: diltiazem, verapamil, and a number of beta blockers, including metoprolol,atenolol, esmolol, and labetalol. (See "Control of ventricular rate in atrial fibrillation:Pharmacologic therapy", section on 'Pharmacologic treatment'.)

Irregular narrow complex — Irregular narrow-complex tachycardias may be causedby atrial fibrillation, atrial flutter with variable atrioventricular (AV) nodal conduction,multifocal atrial tachycardia (MAT), or sinus tachycardia with frequent premature atrialbeats (algorithm 4). Of these, atrial fibrillation is most common [17].

The initial goal of treatment in stable patients is to control the heart rate using either anondihydropyridine calcium channel blocker (diltiazem 15 to 20 mg IV over 2 minutes,repeat at 20 to 25 mg IV after 15 minutes, or verapamil 2.5 to 5 mg IV over two minutesfollowed by 5 to 10 mg IV every 15 to 30 minutes) or a beta blocker (eg, metoprolol 5 mgIV for 3 doses every 2 to 5 minutes; then up to 200 mg PO every 12 hours). Themanagement of atrial fibrillation and SVT is discussed in detail separately. (See "Overviewof atrial fibrillation" and "Rhythm control versus rate control in atrial fibrillation" and"Control of ventricular rate in atrial fibrillation: Pharmacologic therapy" and "Approach tothe diagnosis of narrow QRS complex tachycardias" and "Treatment of multifocal atrialtachycardia".)

Calcium channel blockers and beta-blockers may cause or worsen hypotension. Patientsshould be closely monitored while the drug is given, and patients at greater risk ofdeveloping severe hypotension (eg, elders) often require loading doses that are below theusual range. Combination therapy with a beta blocker and calcium channel blockerincreases the risk of severe heart block.

Diltiazem is suggested in most instances for the management of acute atrial fibrillation withrapid ventricular response. Beta-blockers may also be used and may be preferred in thesetting of an acute coronary syndrome. Beta-blockers are more effective for chronic ratecontrol. For atrial fibrillation associated with hypotension, amiodarone may be used (150mg IV over 10 minutes, followed by 1 mg/min drip for six hours, and then 0.5 mg/min),but the possibility of conversion to sinus rhythm must be considered [28]. For atrialfibrillation associated with acute heart failure, amiodarone or digoxin may be used for ratecontrol. Treatment of MAT includes correction of possible precipitants, such as hypokalemiaand hypomagnesemia. The 2010 ACLS Guidelines recommend consultation with a

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cardiologist for these arrhythmias.

Cardioversion of stable patients with irregular narrow complex tachycardias should NOT beundertaken without considering the risk of embolic stroke. If the duration of atrialfibrillation is known to be less than 48 hours, the risk of embolic stroke is low, and theclinician may consider electrical or chemical cardioversion [29]. A number of medicationscan be used for chemical cardioversion and the best drug varies according to clinicalcircumstance. The questions of whether chemical cardioversion is appropriate and whichagent to select are reviewed separately.

Regular wide complex — A regular, wide-complex tachycardia is generally ventricularin etiology (algorithm 4). Aberrantly conducted supraventricular tachycardias may also beseen. Because differentiation between ventricular tachycardia (VT) and SVT with aberrancycan be difficult, assume VT is present. Treat clinically stable undifferentiated wide-complextachycardia with antiarrhythmics or elective synchronized cardioversion [17].

In cases of regular, wide-complex tachycardia with a monomorphic QRS complex,adenosine may be used for diagnosis and treatment. Do NOT give adenosine to patientswho are unstable or manifest wide-complex tachycardia with an irregular rhythm or apolymorphic QRS complex. Adenosine is unlikely to affect ventricular tachycardia but islikely to slow or convert SVT with aberrancy. Dosing is identical to that used for SVT. (See'Regular narrow complex' above.)

Other antiarrhythmics that may be used to treat stable patients with regular, wide-complextachycardia include procainamide (20 mg/min IV), amiodarone (150 mg IV given over 10minutes, repeated as needed to a total of 2.2 g IV over the first 24 hours), andsotalol (100 mg IV over 5 minutes). A procainamide infusion continues until the arrhythmiais suppressed, the patient becomes hypotensive, the QRS widens 50 percent beyondbaseline, or a maximum dose of 17 mg/kg is administered. Procainamide and sotalolshould be avoided in patients with a prolonged QT interval. If the wide-complex tachycardiapersists, in spite of pharmacologic therapy, elective cardioversion may be needed. The2010 ACLS Guidelines recommend expert consultation for all patients with wide complextachycardia.

SVT with aberrancy, if DEFINITIVELY identified (eg, old ECG demonstrates bundle branchblock), 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 atrialfibrillation with preexcitation (eg, Wolf Parkinson White syndrome), atrial fibrillation withaberrancy (bundle branch block), or polymorphic ventricular tachycardia (VT)/torsades depointes (algorithm 4) [17]. Use of atrioventricular (AV) nodal blockers in wide complex,irregular tachycardia of unclear etiology may precipitate ventricular fibrillation (VF) andpatient death, and is contraindicated. Such medications include beta blockers, calciumchannel blockers, digoxin, and adenosine. To avoid inappropriate and possibly dangeroustreatment, the 2010 ACLS Guidelines suggest assuming that any wide complex, irregulartachycardia is caused by preexcited atrial fibrillation.

Patients with a wide complex, irregular tachycardia caused by preexcited atrial fibrillationusually manifest extremely fast heart rates (generally over 200 beats per minute) andrequire immediate electric cardioversion. In cases where electric cardioversion is ineffectiveor unfeasible, or atrial fibrillation recurs, antiarrhythmic therapy with procainamide,amiodarone, or sotalol may be given. The 2010 ACLS Guidelines recommend expertconsultation for all patients with wide complex tachycardia. Dosing for antiarrhythmic

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medications is described above. (See 'Regular wide complex' above.)

Treat polymorphic VT with emergent defibrillation. Interventions to prevent recurrentpolymorphic VT include correcting underlying electrolyte abnormalities (eg, hypokalemia,hypomagnesemia) and, if a prolonged QT interval is observed or thought to exist, stoppingall medications that increase the QT interval. Magnesium sulfate (2 g IV, followed by amaintenance infusion) can be given to prevent polymorphic VT associated with familial oracquired prolonged QT syndrome [30].

A clinically stable patient with atrial fibrillation and a wide QRS interval KNOWN to stemfrom a preexisting bundle branch block (ie, old ECG demonstrates preexisting block) maybe treated in the same manner as a narrow-complex atrial fibrillation.

Alternative methods for medication administration — Whenever possible, ACLSmedications should be given intravenously. When IV access cannot be established,intraosseous (IO) lines are safe, effective, and can be placed efficiently [17]. Medicationdoses for IO administration are identical to those for IV therapy. If neither IV nor IO accesscan be established, some medications may be given via the tracheal tube. (See"Intraosseous infusion".)

Multiple studies have demonstrated that lidocaine, epinephrine, atropine, vasopressin, andnaloxone are absorbed via the trachea [17]; however, the serum drug concentrationsachieved using this route are unpredictable. If the patient already has peripheral,intraosseous, or central venous access, these are always the preferred routes for drugadministration. When unable to obtain such access expeditiously, one may use theendotracheal tube while attempting to establish vascular or intraosseous access. At nopoint should excellent CPR be interrupted to obtain vascular access.

Doses for tracheal administration are 2 to 2.5 times the standard IV doses and medicationsshould be diluted in 5 to 10 mL of sterile water or normal saline before injection down thetracheal tube.

POST-RESUSCITATION CARE — The 2010 ACLS Guidelines recommend a combination ofgoal-oriented interventions provided by an experienced multidisciplinary team for allcardiac arrest patients with return of spontaneous circulation [17]. Important objectives forsuch care include:

Optimizing cardiopulmonary function and perfusion of vital organs

Managing acute coronary syndromes

Implementing therapeutic hypothermia

Implementing strategies to prevent and manage organ system dysfunction

The induction of mild to moderate hypothermia (target temperature 32 to 34ºC for 24hours) may be beneficial in patients successfully resuscitated after a cardiac arrest.Improved neurologic outcome and reduced mortality have been demonstrated in series ofpatients with VF arrest in whom spontaneous circulation was restored, even when thepatient remained comatose after resuscitation. (See "Hypoxic-ischemic brain injury",section on 'Induced hypothermia'.)

TERMINATION OF RESUSCITATIVE EFFORTS — Determining when to stopresuscitation efforts is difficult, and little data exist to guide decision-making. (See"Outcome of sudden cardiac arrest".) Physician survey data and clinical practice guidelinessuggest that factors influencing the decision to stop resuscitative efforts include [31-35]:

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Duration of resuscitative effort >30 minutes without a sustained perfusing rhythmInitial electrocardiographic rhythm of asystoleProlonged interval between estimated time of arrest and initiation of resuscitationPatient age and severity of comorbid diseaseAbsent brainstem reflexesNormothermia

More objective endpoints of resuscitation have been proposed. Of these, the best predictorof outcome may be the end tidal CO2 level following 20 minutes of resuscitation [36-38].End tidal CO2 values are a function of CO2 production and venous return to the right heartand pulmonary circulation. A very low end tidal CO2 (<10 mmHg) following prolongedresuscitation (>20 minutes) is a sign of absent circulation and a strong predictor of acutemortality [36-38]. It is crucial to note that low end tidal CO2 levels may also be caused bya misplaced (esophageal) endotracheal tube, and this possibility needs to be excludedbefore the decision is made to terminate resuscitative efforts. (See "Carbon dioxidemonitoring (capnography)".)

Resuscitation in the emergency department does not appear to be superior to fieldresuscitation by emergency medical services (EMS) personnel. Therefore, EMS personnelshould not be required to transport all victims of sudden cardiac arrest to the hospital, iffurther resuscitation is deemed futile [39,40].

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[41,42]. Both BLS and ALS criteria demonstrated high specificity for identifying out-of-hospital cardiac arrest patients with little or no chance of survival. Studies of anotherclinical decision rule suggest that it too accurately predicts survival and would reduceunnecessary transports substantially if implemented [39,43].

Preliminary evidence suggests that bedside echocardiography may be useful during cardiacarrest to assess cardiac activity and to help determine prognosis [44,45]. Ultrasoundassessment must never interfere with resuscitation efforts.

SUMMARY AND RECOMMENDATIONS

Cardiopulmonary resuscitation (CPR) and early defibrillation for treatable arrhythmiasremain the cornerstones of basic and advanced cardiac life support (ACLS). Excellentchest compressions without interruption are the key to successful CPR. (See'Excellent basic life support and its importance' above.)

The performance of teams providing ACLS improves when there is a singledesignated leader and the team practices clear, closed-loop communication. (See'Resuscitation team management' above.)

Begin properly performed cardiopulmonary resuscitation (CPR) immediately for anypatient with suspected cardiac arrest. Other initial interventions for ACLS includeadministering oxygen, establishing intravenous access, placing the patient on acardiac and oxygen saturation monitor, and obtaining an electrocardiogram (ECG).(See 'Initial management and ECG interpretation' above.)

In adults, properly performed chest compressions take priority over ventilation duringthe initial period of basic life support. When ventilating the patient in cardiac arrest,give 100 percent oxygen, use low respiratory rates (approximately 8 breaths perminute), and avoid hyperventilation, which is harmful. (See 'Airway management

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during ACLS' above.)

For the purposes of ACLS, ECG interpretation is guided by three questions:

Is the rhythm fast or slow?

Are the QRS complexes wide or narrow?

Is the rhythm regular or irregular?

The basic approach and important aspects of management for each arrhythmiacovered by the 2010 ACLS Guidelines are discussed in the text. (See 'Management ofspecific arrhythmias' above.)

Use of UpToDate is subject to the Subscription and License Agreement

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Abella BS, Sandbo N, Vassilatos P, et al. Chest compression rates duringcardiopulmonary resuscitation are suboptimal: a prospective study during in-hospitalcardiac arrest. Circulation 2005; 111:428.

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Murray WB, Foster PA. Crisis resource management among strangers: principles oforganizing a multidisciplinary group for crisis resource management. J Clin Anesth2000; 12:633.

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DeVita MA, Schaefer J, Lutz J, et al. Improving medical emergency team (MET)performance using a novel curriculum and a computerized human patient simulator.Qual Saf Health Care 2005; 14:326.

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Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular lifesupport: 2010 American Heart Association Guidelines for CardiopulmonaryResuscitation and Emergency Cardiovascular Care. Circulation 2010; 122:S729.

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Berg RA, Hemphill R, Abella BS, et al. Part 5: adult basic life support: 2010 AmericanHeart Association Guidelines for Cardiopulmonary Resuscitation and EmergencyCardiovascular Care. Circulation 2010; 122:S685.

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Martens PR, Russell JK, Wolcke B, et al. Optimal Response to Cardiac Arrest study:defibrillation waveform effects. Resuscitation 2001; 49:233.

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Schneider T, Martens PR, Paschen H, et al. Multicenter, randomized, controlled trial of150-J biphasic shocks compared with 200- to 360-J monophasic shocks in theresuscitation of out-of-hospital cardiac arrest victims. Optimized Response to CardiacArrest (ORCA) Investigators. Circulation 2000; 102:1780.

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Schwarz B, Bowdle TA, Jett GK, et al. Biphasic shocks compared with monophasicdamped sine wave shocks for direct ventricular defibrillation during open heartsurgery. Anesthesiology 2003; 98:1063.

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Brady WJ, Swart G, DeBehnke DJ, et al. The efficacy of atropine in the treatment ofhemodynamically unstable bradycardia and atrioventricular block: prehospital andemergency department considerations. Resuscitation 1999; 41:47.

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Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J 1967; 29:469.23.

Lim SH, Anantharaman V, Teo WS, et al. Comparison of treatment of supraventriculartachycardia by Valsalva maneuver and carotid sinus massage. Ann Emerg Med 1998;31:30.

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Wen ZC, Chen SA, Tai CT, et al. Electrophysiological mechanisms and determinants ofvagal maneuvers for termination of paroxysmal supraventricular tachycardia.Circulation 1998; 98:2716.

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DiMarco JP, Miles W, Akhtar M, et al. Adenosine for paroxysmal supraventriculartachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials. The Adenosine for PSVT Study Group. Ann Intern Med1990; 113:104.

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Holdgate A, Foo A. Adenosine versus intravenous calcium channel antagonists for thetreatment of supraventricular tachycardia in adults. Cochrane Database Syst Rev2006; :CD005154.

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Cybulski J, Kułakowski P, Makowska E, et al. Intravenous amiodarone is safe andseems to be effective in termination of paroxysmal supraventricular tachyarrhythmias.Clin Cardiol 1996; 19:563.

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Michael JA, Stiell IG, Agarwal S, Mandavia DP. Cardioversion of paroxysmal atrialfibrillation in the emergency department. Ann Emerg Med 1999; 33:379.

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Tzivoni D, Banai S, Schuger C, et al. Treatment of torsade de pointes with magnesiumsulfate. Circulation 1988; 77:392.

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Mohr M, Bahr J, Schmid J, et al. The decision to terminate resuscitative efforts: resultsof a questionnaire. Resuscitation 1997; 34:51.

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Marco CA, Bessman ES, Schoenfeld CN, Kelen GD. Ethical issues of cardiopulmonaryresuscitation: current practice among emergency physicians. Acad Emerg Med 1997;4:898.

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de Vos R, Oosterom L, Koster RW, de Haan RJ. Decisions to terminate resuscitation.Resuscitation Committee. Resuscitation 1998; 39:7.

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Bailey ED, Wydro GC, Cone DC. Termination of resuscitation in the prehospital settingfor adult patients suffering nontraumatic cardiac arrest. National Association of EMSPhysicians Standards and Clinical Practice Committee. Prehosp Emerg Care 2000;4:190.

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Horsted TI, Rasmussen LS, Lippert FK, Nielsen SL. Outcome of out-of-hospital cardiacarrest--why do physicians withhold resuscitation attempts? Resuscitation 2004;63:287.

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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.

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Grmec S, Klemen P. Does the end-tidal carbon dioxide (EtCO2) concentration haveprognostic value during out-of-hospital cardiac arrest? Eur J Emerg Med 2001; 8:263.

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Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as aprognostic indicator of outcome in cardiac arrest. Am J Crit Care 2001; 10:391.

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Morrison LJ, Visentin LM, Kiss A, et al. Validation of a rule for termination ofresuscitation in out-of-hospital cardiac arrest. N Engl J Med 2006; 355:478.

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Ong ME, Jaffey J, Stiell I, et al. Comparison of termination-of-resuscitation guidelinesfor basic life support: defibrillator providers in out-of-hospital cardiac arrest. AnnEmerg Med 2006; 47:337.

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Stiell IG, Nesbitt LP, Pickett W, et al. The OPALS Major Trauma Study: impact ofadvanced life-support on survival and morbidity. CMAJ 2008; 178:1141.

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Ruygrok ML, Byyny RL, Haukoos JS, Colorado Cardiac Arrest & ResuscitationCollaborative Study Group and the Denver Metro EMS Medical Directors. Validation of3 termination of resuscitation criteria for good neurologic survival after out-of-hospitalcardiac arrest. Ann Emerg Med 2009; 54:239.

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Morrison LJ, Verbeek PR, Zhan C, et al. Validation of a universal prehospitaltermination of resuscitation clinical prediction rule for advanced and basic life supportproviders. Resuscitation 2009; 80:324.

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Salen P, Melniker L, Chooljian C, et al. Does the presence or absence ofsonographically identified cardiac activity predict resuscitation outcomes of cardiacarrest patients? Am J Emerg Med 2005; 23:459.

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Breitkreutz R, Price S, Steiger HV, et al. Focused echocardiographic evaluation in lifesupport and peri-resuscitation of emergency patients: a prospective trial.Resuscitation 2010; 81:1527.

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Adult BLS algorithm for healthcare providers: 2010 guidelines

AED: automated external defibrillator; ALS: advanced life support; BLS: basic life support.* The boxes bordered with dashed lines are performed by healthcare providers and not by lay rescuers.Reprinted with permission. Adult Basic Life Support: 2010. American Heart Association Guidelines forCardiopulmonary Resuscitation and Emergency Cardiovascular Care. © 2010 American HeartAssociation, Inc.

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Adult cardiac arrest algorithm: 2010 ACLS guidelines

CPR: cardiopulmonary resuscitation; ET: endotracheal tube; EtCO2: end tidal carbon dioxide; IO:intraosseous; IV: intravenous; PEA: pulseless electrical activity; VF: ventricular fibrillation; VT: ventriculartachycardia.Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010. American Heart AssociationGuidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. © 2010 American HeartAssociation, Inc.

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Adult bradycardia algorithm (with pulse): 2010 ACLSguidelines

ECG: electrocardiogram; IV: intravenous; mcg: microgram.Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010.American Heart Association Guidelines for Cardiopulmonary Resuscitation andEmergency Cardiovascular Care. © 2010 American Heart Association, Inc.

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Adult tachycardia algorithm (with pulse): 2010 ACLS guidelines

CHF: congestive heart failure; ECG: electrocardiogram; IV: intravenous; J: joules; NS: normal(isotonic) saline; VT: ventricular tachycardia.Reprinted with permission. Adult Advanced Cardiovascular Life Support: 2010. American HeartAssociation Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. ©2010 American Heart Association, Inc.

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Potentially treatable conditions associated with cardiac arrest

Condition Common clinicalsettings Corrective actions

Acidosis Preexisting acidosis, diabetes,diarrhea, drugs and toxins,prolonged resuscitation, renaldisease, and shock

Reassess adequacy ofcardiopulmonary resuscitation,oxygenation, and ventilation;reconfirm endotracheal-tubeplacement

Hyperventilate

Consider intravenous bicarbonate if pH<7.20 after above actions have beentaken

Cardiactamponade

Hemorrhagic diathesis, cancer,pericarditis, trauma, aftercardiac surgery, and aftermyocardial infarction

Administer fluids; obtain bedsideechocardiogram, if available

Perform pericardiocentesis. Immediatesurgical intervention is appropriate ifpericardiocentesis is unhelpful butcardiac tamponade is known or highlysuspected.

Hypothermia Alcohol abuse, burns, centralnervous system disease,debilitated or elderly patient,drowning, drugs and toxins,endocrine disease, history ofexposure, homelessness,extensive skin disease, spinalcord disease, and trauma

If hypothermia is severe (temperature<30°C), limit initial shocks forventricular fibrillation or pulselessventricular tachycardia to three;initiate active internal rewarming andcardiopulmonary support. Hold furtherresuscitation medications or shocksuntil core temperature is >30°C.

If hypothermia is moderate(temperature 30-34°C), proceed withresuscitation (space medications atintervals greater than usual), passivelyrewarm, and actively rewarm truncalbody areas

Hypovolemia,hemorrhage,anemia

Major burns, diabetes,gastrointestinal losses,hemorrhage, hemorrhagicdiathesis, cancer, pregnancy,shock and trauma

Administer fluids

Transfuse packed red cells ifhemorrhage or profound anemia ispresent

Thoracotomy is appropriate when apatient has cardiac arrest frompenetrating trauma and a cardiacrhythm and the duration ofcardiopulmonary resuscitation beforethoracotomy is <10 min

Hypoxia Consider in all patients withcardiac arrest

Reassess technical quality ofcardiopulmonary resuscitation,oxygenation, and ventilation;reconfirm endotracheal-tubeplacement

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Hypomagnesemia Alcohol abuse, burns, diabeticketoacidosis, severe diarrhea,diuretics, and drugs (eg,cisplatin, cyclosporine,pentamidine)

Administer 1-2 g magnesium sulfateintravenously over 2 min

Reproduced with permission from: Eisenberg, MS, Mengert, TJ. Cardiac resuscitation. N Engl J Med2001; 344:1304. Copyright © 2001 Massachusetts Medical Society. All rights reserved.

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Potentially treatable conditions associated with cardiac arrest,continued

Condition Common clinicalsettings Corrective actions

Myocardialinfarction

Consider in all patients withcardiac arrest, especiallythose with a history ofcoronary artery disease orprearrest acute coronarysyndrome

Consider definitive care (eg, thrombolytictherapy, cardiac catheterization or coronaryartery reperfusion, circulatory assistdevice, emergency cardiopulmonarybypass)

Poisoning Alcohol abuse, bizarre orpuzzling behavioral ormetabolic presentation, classictoxicologic syndrome,occupational or industrialexposure, and psychiatricdisease

Consult toxicologist for emergency adviceon resuscitation and definitive care,including appropriate antidote

Prolonged resuscitation efforts may beappropriate; immediate cardiopulmonarybypass should be considered, if available

Hyperkalemia Metabolic acidosis, excessiveadministration of potassium,drugs and toxins, vigorousexercise, hemolysis, renaldisease, rhabdomyolysis,tumor lysis syndrome, andclinically significant tissueinjury

If hyperkalemia is identified or stronglysuspected, treat with all of the following:10 percent calcium chloride (5-10 mL byslow intravenous push; do not use ifhyperkalemia is secondary to digitalispoisoning), glucose and insulin (50 mL of50 percent dextrose in water and 10 unitsof regular insulin intravenously), sodiumbicarbonate (50 mmoL intravenously; mosteffective if concomitant metabolic acidosisis present), and albuterol (15-20 mgnebulized or 0.5 mg by intravenousinfusion)

Hypokalemia Alcohol abuse, diabetes, useof diuretics, drugs and toxins,profound gastroinstestinallosses, hypomagnesemia

If profond hypokalemia (<2-2.5 mmoL ofpotassium per liter) is accompanied bycardiac arrest, initiate urgent intravenousreplacement (2 mmoL/min intravenouslyfor 10-15 mmoL), then reassess

Pulmonaryembolism

Hospitalized patient, recentsurgical procedure,peripartum, known risk factorsfor venous thromboembolism,history of venousthromboembolism, orprearrest presentationconsistent with diagnosis ofacute pulmonary embolism

Administer fluids; augment withvasopressors as necessary

Confirm diagnosis, if possible; considerimmediate cardiopulmonary bypass tomaintain patient's viability

Consider definitive care (eg, thrombolytictherapy, embolectomy by interventionalradiology or surgery)

Tensionpneumothorax

Placement of central catheter,mechanical ventilation,pulmonary disease (includingasthma, chronic obstructivepulmonary disease, andnecrotizing pneumonia),thoracentesis, and trauma

Needle decompression, followed bychest-tube insertion

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Reproduced with permission from: Eisenberg, MS, Mengert, TJ.Cardiac resuscitation. N Engl J Med2001; 344:1304. Copyright © 2001 Massachusetts Medical Society. All rights reserved.

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