recommended timing of administration is not specified. We suggest that antiarrhythmic drugs may be administered after a second unsuccessful defibrillation attempt in anticipation of a third shock, particularly among patients with witnessed arrest in whom time to administration may be shorter [47]. (See 'Refractory pulseless ventricular tachycardia or ventricular fibrillation' below.) When used, amiodarone (300 mg IV/IO bolus with a repeat dose of 150 mg IV as indicated) or lidocaine (1 to 1.5 mg/kg IV/IO bolus, then 0.5 to 0.75 mg/kg every 5 to 10 minutes) may be administered in VT/VF unresponsive to defibrillation, CPR, and epinephrine. Magnesium Magnesium sulfate (2 to 4 g IV/IO bolus followed by a maintenance infusion) is used to treat polymorphic VT consistent with torsade de pointes but is not recommended for routine use in adult cardiac arrest patients. (See 'Irregular wide complex' below and "Acquired long QT syndrome: Clinical manifestations, diagnosis, and management", section on 'Initial management'.) Other medications Vasopressin Outcomes of patients who receive vasopressin during CPR are not superior to those who receive epinephrine alone, so vasopressin administration is not recommended in the ACLS Guidelines [48]. Among patients who have suffered in-hospital https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 12/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate cardiac arrest, three randomized controlled trials support administration of vasopressin (20 IU IV with each dose of epinephrine) together with glucocorticoids (methylprednisolone 40 mg IV once) as an adjunct to standard CPR [49-51]. Across trials, addition of vasopressin and glucocorticoid to standard care increased the rate of ROSC but did not consistently result in improved survival or functionally favorable recovery. Vasopressin and glucocorticoid administration are not currently recommended by ACLS Guidelines but may be reasonable during resuscitation of in-hospital cardiac arrest. Calcium Calcium chloride has both vasopressor and inotropic effects but has not shown benefit when used to treat cardiac arrest. A randomized trial of calcium chloride versus placebo during resuscitation of out-of-hospital cardiac arrest was terminated early because of a trend towards reduced rates of ROSC in patients receiving calcium [52]. Calcium chloride (1g IV) should not be routinely administered during CPR but may be indicated in some special circumstances (eg, hyperkalemia, calcium-channel blocker toxicity). (See "Treatment and prevention of hyperkalemia in adults" and "Calcium channel blocker poisoning".) Sodium bicarbonate Sodium bicarbonate can mitigate acidosis and hyperkalemia that may incite or worsen during cardiac arrest. However, according to a meta-analysis of four randomized trials and 10 observational studies, routine sodium bicarbonate administration during CPR did not provide a benefit [53]. Selective use of sodium bicarbonate (50 to 100 mEq IV) may be reasonable when there is clinical suspicion or laboratory evidence of significant pre-existing metabolic acidosis or hyperkalemia. (See "Approach to the adult with metabolic acidosis", section on 'Overview of therapy' and "Bicarbonate therapy in lactic acidosis".) MANAGEMENT OF SPECIFIC ARRHYTHMIAS Immediate patient management is algorithmic and does not depend on cardiac rhythm, as detailed above. (See 'Initial management and ECG interpretation' above.) The potential sudden cardiac arrest victim is assessed for responsiveness, breathing, and presence of a pulse. For patients with effective respiration and a palpable pulse, treatment is determined by the ventricular rate (tachycardiac or bradycardia) and clinical assessment of overall stability. (See 'Arrhythmias with a pulse' below.) Pulseless patients are managed initially with cardiopulmonary resuscitation. Patients with pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF) are defibrillated as https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 13/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate rapidly as possible. Additional clinical considerations are discussed in greater detail below. (See 'Pulseless patient in sudden cardiac arrest' below.) Pulseless patient in sudden cardiac arrest Pulseless ventricular tachycardia and ventricular fibrillation Pulseless VT and VF are non-perfusing rhythms emanating from the ventricles for which early identification is critical. Successful resuscitation of patients with VT/VF requires excellent cardiopulmonary resuscitation (CPR) and rapid defibrillation. The American Heart Association (AHA) algorithm for the management of cardiac arrest can be accessed here ( algorithm 3). The most recent versions of the ACLS algorithms can be accessed online here. Excellent CPR is performed without interruption until the rescuer is ready to perform early defibrillation and is continued until return of spontaneous circulation (ROSC) is achieved. Treatable underlying causes should be identified and managed as quickly as possible ( table 3) [36,54,55]. Agonal breathing or transient convulsive activity may accompany these dysrhythmias, and responders should not delay initiating CPR by misinterpreting these signs. Begin performing excellent chest compressions as soon as cardiac arrest is recognized and continue while the defibrillator is being attached. If a defibrillator is not immediately available, continue CPR until one is obtained. As soon as a defibrillator is available, attach it to the patient ( figure 1) and charge it while continuing CPR, then stop compressions to assess the rhythm and defibrillate if appropriate (eg, VT/VF is present). If asystole or pulseless electrical activity is present, continue CPR. If defibrillation is performed, resume CPR immediately and continue compressions until the next pulse and rhythm check two minutes later. (See "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest", section on 'VF and pulseless VT'.) Decreased time to defibrillation improves the likelihood of successful conversion to a perfusing rhythm and patient survival. For the monitored patient who sustains a witnessed VT/VF arrest, if a defibrillator is immediately available and defibrillator pads are in place, immediately charge the defibrillator and deliver a shock. The 10 seconds or fewer of CPR that might have been applied prior to the shock are unlikely to have generated any meaningful perfusion. Biphasic defibrillators are recommended because of their increased efficacy at lower energy levels [56-58]. The ACLS Guidelines recommend that when employing a biphasic defibrillator 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 a first defibrillation at maximal energy for VT/VF. If a monophasic defibrillator is used, 360 J is the appropriate energy dose for initial and subsequent shocks. https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 14/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate ACLS Guidelines recommend the resumption of CPR immediately after defibrillation without checking for a pulse. This recommendation is made because effective cardiac contractility lags restoration of an organized electrical rhythm. Clinicians should stop compressions to perform a rhythm check only after two minutes of CPR, and not before the defibrillator is fully charged if the rhythm is VT/VF. (See "Adult basic life support (BLS) for health care providers", section on 'Phases of resuscitation' and "Adult basic life support (BLS) for health care providers", section on 'Defibrillation'.) If VT/VF persists after at least one attempt at defibrillation and two minutes of CPR, administer epinephrine (1 mg intravenous [IV] or intraosseous [IO] every three to five minutes) while CPR is performed [34,59]. Premature treatment with epinephrine (within two minutes of defibrillation) has been associated with decreased survival [60]. VT/VF that persists after defibrillation may be treated with amiodarone or lidocaine. (See 'Epinephrine' above and 'Amiodarone and lidocaine' above.) Refractory pulseless ventricular tachycardia or ventricular fibrillation Coronary artery disease and myocardial infarction are common causes of shock-refractory VT/VF. The likelihood of ROSC and favorable recovery decreases over time as whole-body ischemia causes progressive end-organ damage. Few patients with CPR ongoing after 40 to 50 minutes will recover [61-64]. Defibrillation strategies Defibrillation may be unsuccessful when insufficient energy transits the fibrillating ventricle. Modern biphasic defibrillators adapt to a range of patient characteristics that affect impedance to ensure adequate energy delivery. Nevertheless, if the vector of current between defibrillator pads does not fully capture the ventricles, VT/VF may persist. In such circumstances, changing the location of the defibrillator pads to the anterior- posterior (AP) position from the anterior-lateral position (termed "vector change") or adding a second set of AP pads may improve the chances of successful defibrillation. We prefer the former approach. Outside of a clinical trial, access to multiple defibrillators for a single patient may be limited, and their use adds complexity that might detract from high-quality CPR. In the absence of any proven benefit of double sequential defibrillation compared with vector change, and assuming a biphasic defibrillator is used, it is our opinion that vector change is preferable for the management of shock-refractory VF/VT in most situations. In a trial of patients with VF/VT out-of-hospital cardiac arrest refractory to three consecutive defibrillation attempts with anterior and lateral pad placement, patients were randomly assigned to vector change, the addition of AP pads followed by double sequential defibrillation from both anterior-lateral and AP pad locations, or continued usual care [65]. The study was https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 15/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate halted early because of low recruitment during the COVID-19 pandemic. The preliminary results were that both vector change and double sequential defibrillation improved the primary outcome of survival to hospital discharge compared with usual care (21.7 versus 30.4 versus 13.3 percent, respectively). Rates of VF termination and return of spontaneous circulation were also higher in both intervention arms. Extracorporeal cardiopulmonary resuscitation Patients with refractory VT/VF may achieve ROSC after coronary revascularization. Thus, there is substantial interest in use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) initiated as an adjunct to conventional CPR [66]. VA-ECMO results in substantially better systemic perfusion and oxygen delivery than CPR and may be a useful bridge to coronary revascularization and myocardial recovery. VA-ECMO initiated during CPR is considered extracorporeal CPR (ECPR). (See "Extracorporeal life support in adults: Management of venoarterial extracorporeal membrane oxygenation (V-A ECMO)" and "Extracorporeal life support in adults in the intensive care unit: Overview".) Programs for effective delivery of ECPR are complex and resource intensive, and they require expertise and substantial multidisciplinary coordination between pre-hospital and in-hospital providers [67]. Optimal patient selection and implementation strategies are uncertain. ECPR is most efficacious when initiated prior to development of severe global hypoxic-ischemic injury and as a bridge to intervention to reverse the inciting cause of arrest. Ideal patients have favorable arrest characteristics (eg, witnessed collapse, immediate CPR, and short duration from collapse to cannulation), evidence of adequate intra-arrest perfusion (eg, end-tidal carbon dioxide [EtCO ] less than 10 mmHg, low presenting arterial lactate), and a presumed reversable 2 etiology of arrest (eg, acute coronary syndrome, massive pulmonary embolism). ACLS Guidelines for ECPR were last updated in 2019 and state ECPR may be considered for selected patients when feasible [48]. Multiple observational studies show an association of ECPR with improved short- and long-term outcomes compared with conventional ACLS with both in- and out-of-hospital cardiac arrest [66]. In a single-center randomized trial, survival to hospital discharge occurred significantly more often among those treated with ECPR compared with standard ACLS (6 of 14 versus 1 of 15) [68]. A second single-center randomized trial of 256 participants demonstrated a non-significant improvement in 180-day functionally favorable survival with ECPR and immediate coronary angiography compared with standard ACLS (31.5 versus 22 percent) and superior 30-day functional recovery (30.6 versus 18.2 percent) [69]. Nevertheless, not all trials have found benefit from ECPR. This likely reflects uncertainty about optimal patient selection and the complexity of systems of care necessary to deliver the intervention. A pragmatic, multicenter randomized trial compared ECPR versus conventional CPR https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 16/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate in 160 adults with witnessed out-of-hospital cardiac arrest, an initial shockable rhythm, and failure to regain spontaneous circulation after 15 minutes [70]. At 30 days, there was no significant difference between groups in survival with good neurologic outcome (ECPR group 14 patients [20 percent] versus conventional CPR 10 patients [16 percent]; OR 1.4; 95% CI 0.5-3.5). In explaining the discrepancies in outcome from previous trials, the authors highlighted differences in team experience, logistics, and caseload. Asystole and pulseless electrical activity Asystole is defined as a complete absence of electrical and mechanical cardiac activity. Pulseless electrical activity (PEA) is defined as any one of a heterogeneous group of organized ECG rhythms without sufficient mechanical contraction of the heart to produce a palpable pulse or measurable blood pressure. By definition, asystole and PEA are non-perfusing rhythms requiring immediate initiation of excellent CPR. These rhythms do not respond to defibrillation. The AHA algorithm for the management of cardiac arrest can be accessed here ( algorithm 3). The most recent versions of the ACLS algorithms can be accessed online here. In the ACLS Guidelines, asystole and PEA are addressed together because successful management for both depends on excellent CPR and rapid reversal of underlying causes, such as hypoxia, hyperkalemia, poisoning, and hemorrhage [36,54,55]. Epinephrine is administered as soon as is feasible after chest compressions are begun [4,11]. Asystole may be the result of a primary or secondary cardiac conduction abnormality, possibly from end-stage tissue hypoxia and metabolic acidosis, or, rarely, the result of excessive vagal stimulation. It is crucial to identify and treat all potential secondary causes of asystole or PEA as rapidly as possible. As tension pneumothorax and cardiac tamponade make CPR ineffective and are often rapidly reversible, the clinician should not hesitate to perform immediate needle thoracostomy or pericardiocentesis if thought necessary. Delay in performing either procedure can worsen outcomes, and there is little chance either intervention will make the situation worse. The accompanying tables describe important secondary causes of cardiac arrest ( table 3). After initiating CPR, immediately consider and treat reversible causes as appropriate and administer epinephrine (1 mg IV every three to five minutes) as soon as feasible [4,34,59]. As with VT/VF, studies of epinephrine in patients with asystole or PEA report mixed results, and further study is needed [34,43,71]. Neither asystole nor PEA responds to defibrillation. Atropine is no longer recommended for the treatment of asystole or PEA. Cardiac pacing is ineffective for cardiac arrest and not recommended. Evidence around the management of asystole and PEA, and cardiac arrest generally, is reviewed in detail separately. (See "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest".) https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 17/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate Intra-arrest monitoring ACLS Guidelines encourage the use of clinical and physiologic monitoring to optimize performance of CPR and to detect ROSC [15]. Assessment and immediate feedback about the rate and depth of chest compressions, adequacy of chest recoil between compressions, and rate and force of ventilations improve CPR. These parameters should be monitored continuously and any necessary adjustments made immediately. Accelerometers have been integrated into several brands of defibrillator pads or freestanding devices that can be placed on the patient's sternum during chest compressions to provide these metrics and real-time feedback. EtCO measured from continuous waveform capnography can provide a rough estimate of 2 cardiac output (and therefore the quality of CPR). EtCO less than 10mmHg suggests inadequate 2 cardiac output and the need to improve CPR quality or provide other interventions such as needle thoracostomy. Sudden, sustained increases in EtCO >10 mmHg during CPR likely 2 indicate ROSC. (See "Carbon dioxide monitoring (capnography)", section on 'Effectiveness of CPR' and "Carbon dioxide monitoring (capnography)", section on 'Return of spontaneous circulation'.) Data from other physiologic monitors are less likely to be available in patients with sudden cardiac arrest, but measurements obtained from arterial catheters already in place can provide useful feedback about the quality of CPR and ROSC [36]. CPR should not be interrupted to place arterial or central venous catheters. Arterial diastolic pressure is a reasonable proxy for coronary perfusion pressure. A reasonable goal is to maintain an arterial diastolic pressure above 20 mmHg. In the hands of skilled operators, point-of-care ultrasound may be useful during cardiac arrest for identifying underlying pathology, monitoring resuscitation, and determining the presence of cardiac activity and likelihood of recovery [72,73]. However, studies of point-of-care ultrasound in the setting of cardiac arrest are preliminary, and high-quality trials are needed. While such research is ongoing, it is crucial that ultrasound-related interventions not cause interruptions or otherwise interfere with the performance of excellent CPR. Arrhythmias with a pulse Bradycardia Definition and clinical findings Bradycardia is defined as a heart rate below 60 beats per minute, but symptomatic bradycardia generally entails rates below 40 beats per minute. The ACLS Guidelines recommend that clinicians not intervene unless the patient exhibits evidence of inadequate tissue perfusion thought to result from the slow heart rate [36,54,55]. Signs and symptoms of inadequate perfusion include hypotension, lightheadedness or a pre-syncopal https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 18/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate sensation, altered mental status (including syncope), signs of shock, ongoing ischemic chest pain, and evidence of acute pulmonary edema. Hypoxia is a common cause of bradycardia. If peripheral perfusion is adequate, pulse oximetry should be used to assess oxyhemoglobin saturation. If perfusion is inadequate or pulse oximetry is unavailable, assess the patient for signs of respiratory failure (eg, increased or decreased respiratory rate, diminished respiratory volume, retractions, or paradoxical abdominal breathing). Bradycardia in the intubated patient should be considered to represent a malpositioned or displaced endotracheal tube until proven otherwise. Approach to bradycardia The AHA algorithm for the management of bradycardia can be accessed here ( algorithm 4). The most recent versions of the ACLS algorithms can be accessed online here. We generally administer atropine while simultaneously preparing for prompt temporary cardiac pacing (transvenous, if immediately available, or transcutaneous) and/or infusion of a chronotropic agent for bradycardic patients with clinically significant symptoms thought to be due to one of the following etiologies: High vagal tone (eg, inferior myocardial ischemia due to acute coronary syndrome) Medication-induced (supratherapeutic levels of beta blockers, calcium channel blockers, digitalis) High-degree atrioventricular (AV) block with a narrow QRS complex (thought to emanate at or above the AV node) If the bradycardia is thought to be due to a conduction disturbance at or below the bundle of His (wide QRS complex in complete heart block, or Mobitz type II second-degree AV block), we avoid atropine and move directly to cardiac pacing and/or administration of a chronotropic agent. Atropine The initial dose of atropine is 1 mg IV. This dose may be repeated every three to five minutes to a total dose of 3 mg. (See "Second-degree atrioventricular block: Mobitz type II" and "Third-degree (complete) atrioventricular block".) Temporary pacing If temporary transvenous cardiac pacing can be initiated promptly, prepare for transvenous pacing, and obtain appropriate consultation as available. If transvenous pacing cannot be initiated promptly, initiate transcutaneous pacing, and prepare for chronotropic infusion. Before using transcutaneous pacing, assess whether the patient can perceive the pain associated with this procedure, and if so, provide appropriate sedation and analgesia whenever possible. (See "Procedural sedation in adults: General considerations, preparation, monitoring, and mitigating complications".) https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 19/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate Patients requiring transcutaneous or transvenous pacing generally require cardiology consultation and admission for evaluation for possible permanent pacemaker placement unless a reversible cause of bradycardia such as hyperkalemia or overmedication with a beta blocker or calcium channel blocker is identified and corrected. Chronotropic agents For patients who remain symptomatic following atropine administration and for whom temporary cardiac pacing is either not readily available or not successful in alleviating symptoms, continuous infusion of a chronotropic agent is indicated. Either dopamine or epinephrine, but not both, should be initiated. Because of its superior vasoconstrictive effects, we prefer epinephrine as a first-line chronotropic agent when there is concomitant hypotension. The starting dose for infusions of dopamine is from 5 to 20 mcg/kg per minute, while epinephrine is started at 0.025 to 0.125 mcg/kg per minute (2 to 10 mcg per minute). Each should be titrated to the patient's response. Tachycardia Tachycardia is defined as a heart rate above 100 beats per minute, but symptomatic tachycardia generally involves rates over 150 beats per minute unless underlying ventricular dysfunction exists [36,54,55]. Management of tachyarrhythmias is governed by the presence of clinical symptoms and signs caused by the rapid heart rate. The AHA algorithm for the management of tachycardia can be accessed here ( algorithm 5). The most recent versions of the ACLS algorithms can be accessed online here. Approach to tachycardia 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 of shock, or evidence of acute pulmonary edema). Hypoxemia is a common cause of unstable tachycardia; look for signs of labored breathing (eg, increased respiratory rate, retractions, paradoxical abdominal breathing) or low oxygen saturation. If instability is present and appears related to the tachycardia, treat immediately with synchronized cardioversion unless the rhythm is sinus tachycardia [74]. Some cases of supraventricular tachycardia (SVT) may respond to immediate treatment with a bolus of adenosine (6 or 12 mg IV) without the need of cardioversion. Whenever possible, assess whether the patient can perceive the pain associated with cardioversion, and if so, provide appropriate sedation and analgesia if time permits. (See "Procedural sedation in adults: General considerations, preparation, monitoring, and mitigating complications".) In the stable patient, use the ECG to determine the nature of the arrhythmia. In the urgent settings in which ACLS algorithms are most often employed, specific rhythm identification may not be possible. Nevertheless, by performing an orderly review of the ECG, one can determine https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 20/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate appropriate management. Three questions provide the basis for assessing the ECG 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 "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Wide QRS complex tachycardias: Approach to the diagnosis" and "Overview of the acute management of tachyarrhythmias".) Regular narrow complex A narrow QRS complex implies that a tachycardic rhythm originates at or above the AV node. SVT, including sinus tachycardia, is the major cause of a regular narrow complex arrhythmia [36,54,55]. 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 sinus tachycardia; care is focused on treating the underlying cause. (See "Sinus tachycardia: Evaluation and management".) Reentrant SVT is a regular tachycardia most often caused by a reentrant mechanism within the conduction system ( algorithm 5). The QRS interval is usually narrow but can be longer than 120 ms if a bundle branch block (ie, SVT with rate-related aberrancy or fixed bundle branch block) is present. Vagal maneuvers slow conduction through the AV node and may interrupt the reentrant circuit, and they may be employed on appropriate patients while other therapies are prepared. Vagal maneuvers alone (eg, Valsalva, carotid sinus massage) convert up to 25 percent of SVTs to sinus rhythm, while Valsalva followed immediately by supine repositioning with a passive leg raise has been shown to be even more effective. SVT refractory to vagal maneuvers is treated with adenosine [75-77]. (See "Overview of the acute management of tachyarrhythmias" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Reentry and the development of cardiac arrhythmias" and "Vagal maneuvers".) Because of its extremely short half-life, adenosine (6 or 12 mg IV) is injected as rapidly as possible into a proximal vein followed immediately by a 20 mL saline flush and elevation of the extremity to ensure the drug enters the central circulation before it is metabolized. If the first dose of adenosine does not convert the rhythm, a second and third dose of 12 mg IV may be given. Larger doses (eg, 18 mg IV) may be needed in patients taking theophylline or theobromine or those who consume large amounts of caffeine; smaller doses (eg, 3 mg IV) should be given to patients taking dipyridamole or carbamazepine and those with transplanted hearts, or when injecting via a central vein. https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 21/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate Prior to injection, warn the patient about transient side effects from adenosine, including dysphoria, chest discomfort, dyspnea, and flushing, and give reassurance that these effects are very brief. Perform continuous ECG recording during administration. If adenosine fails to convert the SVT, consider other etiologies for this rhythm, including atrial flutter or a non- reentrant SVT, which may become apparent on the ECG when AV nodal conduction is slowed. If conversion attempts fail and the patient remains stable, initiate rate control with either an IV nondihydropyridine calcium channel blocker or a beta blocker. Agents to choose from include diltiazem, verapamil, and a number of beta blockers (including metoprolol, atenolol, esmolol, and labetalol). (See "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy", section on 'Urgent therapy'.) Irregular narrow complex Irregular narrow-complex tachycardias may be caused by atrial fibrillation, atrial flutter with variable AV nodal conduction, multifocal atrial tachycardia (MAT), or sinus tachycardia with frequent premature atrial complexes (PACs; also referred to as premature atrial beats, premature supraventricular complexes, or premature supraventricular beats) ( algorithm 5). Of these, atrial fibrillation is most common [36,54,55]. The initial goal of treatment in stable patients is to control the heart rate using either a nondihydropyridine calcium channel blocker (diltiazem 10 to 20 mg IV over two minutes, repeat at 20 to 25 mg IV after 15 minutes; or verapamil 2.5 to 5 mg IV over two minutes followed by 5 to 10 mg IV every 15 to 30 minutes) or a beta blocker (eg, metoprolol 5 mg IV for three doses every two to five minutes, then up to 200 mg by mouth every 12 hours). The management of atrial fibrillation and SVT is discussed in detail separately. (See "Atrial fibrillation: Overview and management of new-onset atrial fibrillation" and "Management of atrial fibrillation: Rhythm control versus rate control" and "Control of ventricular rate in patients with atrial fibrillation who do not have heart failure: Pharmacologic therapy" and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation" and "Multifocal atrial tachycardia".) Calcium channel blockers and beta blockers may cause or worsen hypotension. Patients should be closely monitored while the drug is given, and patients at greater risk of developing severe hypotension (eg, older adults) may require loading doses that are below the usual range. Adequate IV access should be established in case hypotension develops. Combination therapy with a beta blocker and calcium channel blocker increases the risk of severe heart block. Diltiazem is suggested in most instances for the management of acute atrial fibrillation with rapid ventricular response. Beta blockers may also be used and may be preferred in the setting of an acute coronary syndrome. Beta blockers are more effective for chronic rate control. For atrial fibrillation associated with hypotension, amiodarone may be used (150 mg IV over 10 https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 22/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate minutes followed by 1 mg/min drip for six hours, and then 0.5 mg/min) but may cause conversion to sinus rhythm, which may result in embolic injury if the atrial fibrillation was not short lived [78]. For atrial fibrillation associated with acute heart failure, amiodarone or digoxin may be used for rate control. Treatment of MAT includes correction of possible precipitants, such as hypokalemia and hypomagnesemia. The ACLS Guidelines recommend consultation with a cardiologist for these arrhythmias. Cardioversion of stable patients with irregular narrow complex tachycardias should not be undertaken without considering the risk of embolic stroke. If the duration of atrial fibrillation is known to be less than 48 hours or the patient has been receiving long-term therapeutic anticoagulation (eg warfarin with an international normalized ratio [INR] known to be therapeutic or a novel oral anticoagulant with good adherence), the risk of embolic stroke is low, and the clinician may consider electrical or chemical cardioversion [79]. A number of medications can be used for chemical cardioversion, and the best drug varies according to clinical circumstance. The questions of whether chemical cardioversion is appropriate and which agent to select are reviewed separately. Regular wide complex A regular wide-complex tachycardia is generally ventricular in etiology ( algorithm 5). Aberrantly conducted SVTs may also be seen. Because differentiation between VT and SVT with aberrancy can be difficult, assume VT is present. Treat clinically stable undifferentiated wide-complex tachycardia with antiarrhythmics or planned synchronized cardioversion [36,54,55]. In cases of regular wide-complex tachycardia with a monomorphic QRS complex, adenosine may be used for diagnosis and treatment. Do not give adenosine (or other AV nodal blocking medications) to patients who are unstable or manifest wide-complex tachycardia with an irregular rhythm or a polymorphic QRS complex. SVT with aberrancy, if definitively identified (eg, old ECG demonstrates bundle branch block), may be treated in the same manner as narrow- complex SVT, with vagal maneuvers, adenosine, or rate control (see 'Irregular narrow complex' above). Adenosine is likely to slow or convert SVT with aberrancy. Dosing is identical to that used for SVT. Adenosine also terminates some cases of VT, particularly those that originate in the left or right ventricular outflow tracts [80]. Thus, adenosine responsiveness cannot be used to confirm a diagnosis of SVT or to exclude VT. (See 'Regular narrow complex' above.) Other antiarrhythmic drugs that may be used to treat stable patients with regular wide-complex tachycardia include procainamide (20 to 50 mg/min IV), amiodarone (150 mg IV given over 10 minutes, repeated as needed to a total of 2.2 g IV over the first 24 hours), and sotalol (100 mg IV over five minutes). A procainamide infusion continues until the arrhythmia is suppressed, the patient becomes hypotensive, the QRS widens 50 percent beyond baseline, or a maximum dose https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 23/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate of 17 mg/kg is administered. Procainamide and sotalol should be avoided in patients with a prolonged QT interval. If the wide-complex tachycardia persists despite pharmacologic therapy, cardioversion may be needed. The ACLS Guidelines recommend expert consultation for all patients with wide complex tachycardia. Irregular wide complex A wide-complex, irregular tachycardia may be atrial fibrillation with preexcitation (eg, Wolf Parkinson White syndrome), atrial fibrillation with aberrancy (bundle branch block), or polymorphic VT/torsades de pointes ( algorithm 5) [36,54,55]. Use of AV nodal blockers in wide-complex, irregular tachycardia of unclear etiology may precipitate VF and death and is contraindicated. Such medications include beta blockers, calcium channel blockers, digoxin, and adenosine. To avoid inappropriate and possibly dangerous treatment, the ACLS Guidelines suggest assuming that any wide-complex, irregular tachycardia is caused by preexcited atrial fibrillation. Patients with a wide-complex, irregular tachycardia caused by preexcited atrial fibrillation usually manifest extremely fast heart rates (generally over 200 beats per minute) and require immediate synchronized electric cardioversion. In cases where electric cardioversion is ineffective or unfeasible, or atrial fibrillation recurs, antiarrhythmic therapy with procainamide, amiodarone, or sotalol may be given. The ACLS Guidelines recommend expert consultation for all patients with wide-complex tachycardia. Dosing for antiarrhythmic medications is described above. (See 'Regular wide complex' above.) Treat polymorphic VT with emergency defibrillation. Interventions to prevent recurrent polymorphic VT include correcting underlying electrolyte abnormalities (eg, hypokalemia, hypomagnesemia) and, if a prolonged QT interval is observed or thought to exist, stopping all medications that increase the QT interval. Magnesium sulfate (2 to 4 g IV administered via rapid IV bolus followed by a maintenance infusion) can be given to prevent polymorphic VT associated with familial or acquired prolonged QT syndrome [81]. A clinically stable patient with atrial fibrillation and a wide QRS interval known to stem from a preexisting bundle branch block (ie, old ECG demonstrates preexisting block with the same QRS morphology) may be treated in the same manner as a narrow-complex atrial fibrillation. Alternative methods for medication administration Although vascular access via the IO route is safe and more easily initiated in the setting of cardiac arrest, administration of medication via the IV route produces more favorable outcomes. Nevertheless, when IV access cannot be established, or its theoretical benefit is mitigated by the time and resources necessary to initiate it, IO lines have been found to be safe and effective according to observational studies [36,54,55,82]. https://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults/print 24/52 7/6/23, 11:24 AM Advanced cardiac life support (ACLS) in adults - UpToDate One large observational study reported inferior outcomes among victims of out-of-hospital cardiac arrest receiving IO access, but this finding could have been related to other variables in these patients [83]. More investigation is needed to assess whether proximal humeral IO placement versus pretibial placement results in enhanced medication delivery and survival. Medication doses for IO administration are identical to those for IV therapy. If neither IV nor IO access can be established, some medications may be given via the tracheal tube. (See "Intraosseous infusion", section on 'Indications'.) Multiple studies have demonstrated that lidocaine, epinephrine, atropine, vasopressin, and naloxone are absorbed via the trachea [36]; however, the serum drug concentrations achieved using this route are unpredictable. If the patient already has peripheral, IO, or central venous access, these are always the preferred routes for drug administration. When unable to obtain such access expeditiously, one may use the endotracheal tube while attempting to establish vascular or IO access. At no point should excellent CPR be interrupted to obtain vascular access. Doses for tracheal administration are 2 to 2.5 times the standard IV doses, and medications should be diluted in 5 to 10 mL of sterile water or normal saline before injection down the tracheal tube. USE OF ULTRASOUND AND ECHOCARDIOGRAPHY Bedside echocardiography must never interfere with resuscitation efforts and should not