Cardiopulmonary Resuscitation (CPR)

6.1.1 Bradycardia
This section summarizes the management of bradyarrhythmias. Following the overview of bradyarrhythmias and summary of the initial evaluation and treatment of bradycardia, drugs used in the treatment of bradycardia are presented. See the Bradycardia Algorithm, Figure 3. Box numbers in the text refer to the numbered boxes in the algorithm.

6.1.1.1 Evaluation
Bradycardia is defined as a heart rate of <60 beats per minute. However, when bradycardia is the cause of symptoms, the rate is generally <50 beats per minute, which is the working definition of bradycardia used here ( Figure 3: Bradycardia Algorithm, Box 1). A slow heart rate may be physiologically normal for some patients, whereas a heart rate of >50 beats per minut1e may be inadequate for others. The Bradycardia Algorithm focuses on management of clinically significant bradycardia (ie, bradycardia that is inappropriate for the clinical condition).

Because hypoxemia is a common cause of bradycardia, initial evaluation of any patient with bradycardia should focus on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxyhemoglobin saturation as determined by pulse oximetry (Box 2 ). If oxygenation is inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen. Attach a monitor to the patient, evaluate blood pressure, and establish IV access. If possible, obtain a 12-lead ECG to better define the rhythm. While initiating treatment, evaluate the patient’s clinical status and identify potentially reversible causes.

The provider must identify signs and symptoms of poor perfusion and determine if those signs are likely to be caused by the bradycardia (Box 3). If the signs and symptoms are not due to bradycardia, the provider should reassess the underlying cause of the patient’s symptoms. Remember that signs and symptoms of bradycardia may be mild; asymptomatic or minimally symptomatic patients do not necessarily require treatment (Box 4 ) unless there is suspicion that the rhythm is likely to progress to symptoms or become life-threatening (eg, Mobitz type II second-degree AV block in the setting of acute myocardial infarction [AMI]). If the bradycardia is suspected to be the cause of acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock, the patient should receive immediate treatment.

Atrioventricular (AV) blocks are classified as first-, second-, and third-degree. Blocks may be caused by medications or electrolyte disturbances, as well as structural problems resulting from AMI or other myocardial diseases. A first-degree AV block is defined by a prolonged PR interval (>0.20 second) and is generally benign. Second-degree AV block is divided into Mobitz types I and II. In Mobitz type I block, the block is at the AV node; the block is often transient and asymptomatic. In Mobitz type II block, the block is usually below the AV node within the His-Purkinje system; this block is often symptomatic, with the potential to progress to complete (thirddegree) AV block. Third-degree AV block may occur at the AV node, bundle of His, or bundle branches. When third-degree AV block is present, no impulses pass between the atria and ventricles. Third-degree AV block can be permanent or transient, depending on the underlying cause.

6.1.1.2 Therapy (Figure 3 Box 5)

1 Atropine
* Atropine remains the first-line drug for acute symptomatic bradycardia. (Class IIa, LOE B)

Clinical trials in adults showed that IV atropine improved heart rate, symptoms, and signs associated with bradycardia. Atropine sulfate reverses cholinergic-mediated decreases in heart rate and should be considered a temporizing measure while awaiting a transcutaneous or transvenous pacemaker for patients with symptomatic sinus bradycardia, conduction block at the level of the AV node, or sinus arrest.

The recommended atropine dose for bradycardia is 0.5 mg IV every 3 to 5 minutes to a maximum total dose of 3 mg. Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate. Atropine administration should not delay implementation of external pacing for patients with poor perfusion. Use atropine cautiously in the presence of acute coronary ischemia or MI; increased heart rate may worsen ischemia or increase infarction size. Atropine will likely be ineffective in patients who have undergone cardiac transplantation because the transplanted heart lacks vagal innervation. One small uncontrolled study documented paradoxical slowing of the heart rate and high-degree AV block when atropine was administered to patients after cardiac transplantation.

Avoid relying on atropine in type II second-degree or third-degree AV block or in patients with third-degree AV block with a new wide-QRS complex where the location of block is likely to be in non-nodal tissue (such as in the bundle of His or more distal conduction system). These bradyarrhythmias are not likely to be responsive to reversal of cholinergic effects by atropine and are preferably treated with TCP or ß-adrenergic support as temporizing measures while the patient is prepared for transvenous pacing (Figure 3, Box 6).

2 Pacing
* It is reasonable for healthcare providers to initiate transcutaneous pacing (TCP) in unstable patients who do not respond to atropine. (Class IIa, LOE B)
* Immediate pacing might be considered in unstable patients with high-degree AV block when IV access is not available. (Class IIb, LOE C)
* If the patient does not respond to drugs or TCP, transvenous pacing is probably indicated (Figure 3, Box 6). (Class IIa, LOE C)

3 Alternative Drugs to Consider
Although not first-line agents for treatment of symptomatic bradycardia, dopamine, epinephrine, and isoproterenol are alternatives when a bradyarrhythmia is unresponsive to or inappropriate for treatment with atropine, or as a temporizing measure while awaiting the availability of a pacemaker. Alternative drugs may also be appropriate in special circumstances such as the overdose of a ß-blocker or calcium channel blocker.

3.1 Dopamine
Dopamine hydrochloride is a catecholamine with both α- and ß-adrenergic actions. It can be titrated to more selectively target heart rate or vasoconstriction. At lower doses dopamine has a more selective effect on inotropy and heart rate; at higher doses (>10 mcg/kg per minute), it also has vasoconstrictive effects.

* Dopamine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, in whom atropine may be inappropriate or after atropine fails. (Class IIb, LOE B)

Begin dopamine infusion at 2 to 10 mcg/kg per minute and titrate to patient response. Use of vasoconstrictors requires that the recipient be assessed for adequate intravascular volume and volume status supported as needed.

3.2 Epinephrine
Epinephrine is a catecholamine with α- and ß-adrenergic actions.

* Epinephrine infusion may be used for patients with symptomatic bradycardia, particularly if associated with hypotension, for whom atropine may be inappropriate or after atropine fails. (Class IIb, LOE B)

Begin the infusion at 2 to 10 mcg/min and titrate to patient response. Use of vasoconstrictors requires that the recipient be assessed for adequate intravascular volume and volume status supported as needed.

3.3 Isoproterenol
Isoproterenol is a ß-adrenergic agent with ß-1 and ß-2 effects, resulting in an increase in heart rate and vasodilation. The recommended adult dose is 2 to 10 mcg/min by IV infusion, titrated according to heart rate and rhythm response.

6.2 Tachycardia
This section summarizes the management of a wide variety of tachyarrhythmias. Following the overview of tachyarrhythmias and summary of the initial evaluation and treatment of tachycardia, common antiarrhythmic drugs used in the treatment of tachycardia are presented. See the Tachycardia Algorithm, Figure 4. Box numbers in the text refer to the numbered boxes in the algorithm.

6.2.1 Classification of Tachyarrhythmias
Tachycardias can be classified in several ways, based on the appearance of the QRS complex, heart rate, and regularity. ACLS professionals should be able to recognize and differentiate between sinus tachycardia, narrowcomplex supraventricular tachycardia (SVT), and wide-complex tachycardia. Because ACLS providers may be unable to distinguish between supraventricular and ventricular rhythms, they should be aware that most widecomplex (broad-complex) tachycardias are ventricular in origin.

Narrow–QRS-complex (SVT) tachycardias (QRS <0.12 second), in order of frequency
Sinus tachycardia
Atrial fibrillation
Atrial flutter
AV nodal reentry
Accessory pathway–mediated tachycardia
Atrial tachycardia (including automatic and reentry forms)
Multifocal atrial tachycardia (MAT)
Junctional tachycardia (rare in adults)

Wide–QRS-complex tachycardias (QRS ≧0.12 second)
Ventricular tachycardia (VT) and ventricular fibrillation (VF)
SVT with aberrancy
Pre-excited tachycardias (Wolff-Parkinson-White [WPW] syndrome)
Ventricular paced rhythms

Irregular narrow-complex tachycardias are likely atrial fibrillation or MAT; occasionally atrial flutter is irregular. The management of atrial fibrillation and flutter is discussed in the section “Irregular Tachycardias” below.

6.2.2 Initial Evaluation and Treatment of Tachyarrhythmias
Tachycardia is defined as an arrhythmia with a rate of >100 beats per minute, although, as with defining bradycardia, the rate of a tachycardia takes on clinical significance at its greater extremes and is more likely attributable to an arrhythmia rate of ?150 beats per minute (Figure 4: Tachycardia Algorithm, Box 1). A rapid heart rate is an appropriate response to a physiologic stress (eg, fever, dehydration) or other underlying conditions. When encountering patients with tachycardia, efforts should be made to determine whether the tachycardia is the primary cause of the presenting symptoms or secondary to an underlying condition that is causing both the presenting symptoms and the faster heart rate. Many experts suggest that when a heart rate is <150 beats per minute, it is unlikely that symptoms of instability are caused primarily by the tachycardia unless there is impaired ventricular function.

The evaluation and management of tachyarrhythmias is depicted in the ACLS Tachycardia With Pulse Algorithm ( Figure 4: Tachycardia Algorithm). Box numbers in the text refer to numbered boxes in this algorithm. If cardiac arrest develops at any time, see the ACLS Cardiac Arrest Algorithms in this document above under 4.1: “Management of Cardiac Arrest.”

Because hypoxemia is a common cause of tachycardia, initial evaluation of any patient with tachycardia should focus on signs of increased work of breathing (tachypnea, intercostal retractions, suprasternal retractions, paradoxical abdominal breathing) and oxyhemoglobin saturation as determined by pulse oximetry (Box 2 ). If oxygenation is inadequate or the patient shows signs of increased work of breathing, provide supplementary oxygen. Attach a monitor to the patient, evaluate blood pressure, and establish IV access. If available, obtain a 12-lead ECG to better define the rhythm, but this should not delay immediate cardioversion if the patient is unstable. While initiating treatment, evaluate the patient’s clinical status and identify potential reversible causes of the tachycardia.

If signs and symptoms persist despite provision of supplementary oxygen and support of airway and ventilation, the provider should assess the patient’s degree of instability and determine if the instability is related to the tachycardia (Box 3). If the patient demonstrates rate-related cardiovascular compromise with signs and symptoms such as acute altered mental status, ischemic chest discomfort, acute heart failure, hypotension, or other signs of shock suspected to be due to a tachyarrhythmia, proceed to immediate synchronized cardioversion (Box 4). However, with ventricular rates <150 beats per minute in the absence of ventricular dysfunction, it is more likely that the tachycardia is secondary to the underlying condition rather than the cause of the instability.

* If not hypotensive, the patient with a regular narrow-complex SVT (likely due to suspected reentry, paroxysmal supraventricular tachycardia, as described below) may be treated with adenosine while preparations are made for synchronized cardioversion. (Class IIb, LOE C)

If the patient with tachycardia is stable (ie, no serious signs related to the tachycardia), the provider has time to obtain a 12-lead ECG, evaluate the rhythm, determine if the width of the QRS complex is ?0.12 second (Box 5 ), and determine treatment options. Stable patients may await expert consultation because treatment has the potential for harm.

6.2.3 Cardioversion
If possible, establish IV access before cardioversion and administer sedation if the patient is conscious. Do not delay cardioversion if the patient is extremely unstable.

 Synchronized Cardioversion and Unsynchronized Shocks
(Refer to Figure 4: Tachycardia Algorithm – Box 4.)

Synchronized cardioversion is shock delivery that is timed (synchronized) with the QRS complex. This synchronization avoids shock delivery during the relative refractory period of the cardiac cycle when a shock could produce VF. If cardioversion is needed and it is impossible to synchronize a shock, use high-energy unsynchronized shocks (defibrillation doses).

Synchronized cardioversion is recommended to treat (1) unstable SVT, (2) unstable atrial fibrillation, (3) unstable atrial flutter, and (4) unstable monomorphic (regular) VT. Shock can terminate these tachyarrhythmias by interrupting the underlying reentrant pathway that is responsible for them.

 Waveform and Energy
* The recommended initial biphasic energy dose for cardioversion of atrial fibrillation is 120 to 200 J. (Class IIa, LOE A)

If the initial shock fails, providers should increase the dose in a stepwise fashion.

Cardioversion of atrial flutter and other SVTs generally requires less energy; an initial energy of 50 J to 100 J is sufficient. If the initial 50-J shock fails, the provider should increase the dose in a stepwise fashion.

* Cardioversion of atrial fabrillation with monophasic waveforms should begin at 200 J and increase in stepwise fashion if not successful. (Class IIa, LOE B)

Monomorphic VT (regular form and rate) with a pulse responds well to monophasic or biphasic waveform cardioversion (synchronized) shocks at initial energies of 100 J.

* If there is no response to the first shock, it may be reasonable to increase the dose in a stepwise fashion. No studies were identified that addressed this issue. Thus, this recommendation represents expert opinion. (Class IIb, LOE C)

Arrhythmias with a polymorphic QRS appearance (such as torsades de pointes) will usually not permit synchronization. Thus, if a patient has polymorphic VT, treat the rhythm as VF and deliver high-energy unsynchronized shocks (ie, defibrillation doses). If there is any doubt whether monomorphic or polymorphic VT is present in the unstable patient, do not delay shock delivery to perform detailed rhythm analysis: provide highenergy unsynchronized shocks (ie, defibrillation doses). Use the ACLS Cardiac Arrest Algorithms in this document above under 4.1: “Management of Cardiac Arrest.”

6.2.4 Regular Narrow-Complex Tachycardia

1. Sinus Tachycardia
Sinus tachycardia is common and usually results from a physiologic stimulus, such as fever, anemia, or hypotension/shock. Sinus tachycardia is defined as a heart rate >100 beats per minute. The upper rate of sinus tachycardia is age-related (calculated as approximately 220 beats per minute, minus the patient’s age in years) and may be useful in judging whether an apparent sinus tachycardia falls within the expected range for a patient’s age. If judged to be sinus tachycardia, no specific drug treatment is required. Instead, therapy is directed toward identification and treatment of the underlying cause. When cardiac function is poor, cardiac output can be dependent on a rapid heart rate. In such compensatory tachycardias, stroke volume is limited, so “normalizing” the heart rate can be detrimental.

2. Supraventricular Tachycardia (Reentry SVT)
Evaluation
The rhythm (tachycardia) is considered to be of supraventricular origin if the QRS complex is narrow (<120 milliseconds or <0.12 second) or if the QRS complex is wide (broad) and preexisting bundle branch block or rate-dependent aberrancy is known to be present.

Most SVTs are regular tachycardias that are caused by reentry, an abnormal rhythm circuit that allows a wave of depolarization to repeatedly travel in a circle in cardiac tissue.
Reentry circuits resulting in SVT can occur in atrial myocardium (resulting in atrial fibrillation, atrial flutter, and some forms of atrial tachycardia).
The reentry circuit may also reside in whole or in part in the AV node itself. This results in AV nodal reentry tachycardia (AVNRT) if both limbs of the reentry circuit involve AV nodal tissue. Alternatively, it may result in AV reentry tachycardia (AVRT) if one limb of the reentry circuit involves an accessory pathway and the other involves the AV node. The characteristic abrupt onset and termination of each of the latter groups of reentrant tachyarrhythmias (AVNRT and AVRT) led to the original name, paroxysmal supraventricular tachycardia (PSVT).
This subgroup of reentry arrhythmias, due to either AVNRT or AVRT, is characterized by abrupt onset and termination and a regular rate that exceeds the typical upper limits of sinus tachycardia at rest (usually >150 beats per minute) and, in the case of an AVNRT, often presents without readily identifiable P waves on the ECG.

Distinguishing the forms of reentrant SVTs that are based in atrial myocardium (such as atrial fibrillation) versus those with a reentry circuit partly or wholly based in the AV node itself (PSVT) is important because each will respond differently to therapies aimed at impeding conduction through the AV node. The ventricular rate of reentry arrhythmias based in atrial myocardium will be slowed but not terminated by drugs that slow conduction through the AV node. Conversely, reentry arrhythmias for which at least one limb of the circuit resides in the AV node (PSVT attributable to AVNRT or AVRT) can be terminated by such drugs.

Yet another group of SVTs is referred to as automatic tachycardias. These arrhythmias are not due to a circulating circuit but to an excited automatic focus. Unlike the abrupt pattern of reentry, the characteristic onset and termination of these tachyarrhythmias are more gradual and analogous to how the sinus node behaves in gradually accelerating and slowing heart rate. These automatic arrhythmias include ectopic atrial tachycardia, MAT, and junctional tachycardia. These arrhythmias can be difficult to treat, are not responsive to cardioversion, and are usually controlled acutely with drugs that slow conduction through the AV node and thereby slow ventricular rate.

Therapy for Regular Narrow-Complex Tachycardia
1. Vagal Maneuvers
Vagal maneuvers and adenosine are the preferred initial therapeutic choices for the termination of stable PSVT ( Figure 4: Tachycardia Algorithm, Box 7). Vagal maneuvers alone (Valsalva maneuver or carotid sinus massage) will terminate up to 25% of PSVTs. For other SVTs, vagal maneuvers and adenosine may transiently slow the ventricular rate and potentially assist rhythm diagnosis but will not usually terminate such arrhythmias.

2. Adenosine
If PSVT does not respond to vagal maneuvers, give 6 mg of IV adenosine as a rapid IV push through a large (eg, antecubital) vein followed by a 20 mL saline flush. (Class I, LOE B) If the rhythm does not convert within 1 to 2 minutes, give a 12 mg rapid IV push using the method above. Because of the possibility of initiating atrial fibrillation with rapid ventricular rates in a patient with WPW, a defibrillator should be available when adenosine is administered to any patient in whom WPW is a consideration. As with vagal maneuvers, the effect of adenosine on other SVTs (such as atrial fibrillation or flutter) is to transiently slow ventricular rate (which may be useful diagnostically) but not afford their termination or meaningful lasting rate control.

A number of studies support the use of adenosine in the treatment of stable PSVT. Although 2 randomized clinical trials documented a similar PSVT conversion rate between adenosine and calcium channel blockers, adenosine was more rapid and had fewer severe side effects than verapamil. Amiodarone as well as other antiarrhythmic agents can be useful in the termination of PSVT, but the onset of action of amiodarone is slower than that of adenosine, and the potential proarrhythmic risks of these agents favor the use of safer treatment alternatives.

Adenosine is safe and effective in pregnancy. However, adenosine does have several important drug interactions. Larger doses may be required for patients with a significant blood level of theophylline, caffeine, or theobromine. The initial dose should be reduced to 3 mg in patients taking dipyridamole or carbamazepine, those with transplanted hearts, or if given by central venous access. Side effects with adenosine are common but transient; flushing, dyspnea, and chest discomfort are the most frequently observed. Adenosine should not be given to patients with asthma.

After conversion, monitor the patient for recurrence and treat any recurrence of PSVT with adenosine or a longer-acting AV nodal blocking agent (eg, diltiazem or ß-blocker). If adenosine or vagal maneuvers disclose another form of SVT (such as atrial fibrillation or flutter), treatment with a longer-acting AV nodal blocking agent should be considered to afford more lasting control of ventricular rate.

3. Calcium Channel Blockers and ß-Blockers
* If adenosine or vagal maneuvers fail to convert PSVT, PSVT recurs after such treatment, or these treatments disclose a different form of SVT (such as atrial fibrillation or flutter), it is reasonable to use longer-acting AV nodal blocking agents, such as the nondihydropyridine calcium channel blockers (verapamil and diltiazem)(Class IIa, LOE B) or ß-blockers. (Class IIa, LOE C)

These drugs act primarily on nodal tissue either to terminate the reentry PSVTs that depend on conduction through the AV node or to slow the ventricular response to other SVTs by blocking conduction through the AV node. The alternate mechanism of action and longer duration of these drugs may result in more sustained termination of PSVT or afford more sustained rate control of atrial arrhythmias (such as atrial fibrillation or flutter). A number of studies have established the effectiveness of verapamil, and diltiazem, in converting PSVT to normal sinus rhythm.

For verapamil, give a 2.5 mg to 5 mg IV bolus over 2 minutes (over 3 minutes in older patients). If there is no therapeutic response and no drug-induced adverse event, repeated doses of 5 mg to 10 mg may be administered every 15 to 30 minutes to a total dose of 20 mg. An alternative dosing regimen is to give a 5 mg bolus every 15 minutes to a total dose of 30 mg. Verapamil should be given only to patients with narrow-complex reentry SVT or arrhythmias known with certainty to be of supraventricular origin. Verapamil should not be given to patients with wide-complex tachycardias. It should not be given to patients with impaired ventricular function or heart failure.

For diltiazem, give a dose of 15 mg to 20 mg (0.25 mg/kg) IV over 2 minutes; if needed, in 15 minutes give an additional IV dose of 20 mg to 25 mg (0.35 mg/kg). The maintenance infusion dose is 5 mg/hour to 15 mg/hour, titrated to heart rate.

A wide variety of IV ß-blockers are available for treatment of supraventricular tachyarrhythmias. These include metoprolol, atenolol, propranolol, esmolol, and labetolol (the latter more commonly used for acute management of hypertension than for arrhythmias). In principle these agents exert their effect by antagonizing sympathetic tone in nodal tissue, resulting in slowing of conduction. Like calcium channel blockers, they also have negative inotropic effects and further reduce cardiac output in patients with heart failure. More detailed information is provided below. Side effects of ß-blockers can include bradycardias, AV conduction delays, and hypotension. ß-blockers should be used with caution in patients with obstructive pulmonary disease or congestive heart failure.

Caution is advised when encountering pre-excited atrial fibrillation or flutter that conducts to the ventricles via both the AV node and an accessory pathway. Treatment with an AV nodal blocking agent (including adenosine, calcium blockers, ß-blockers, or digoxin) is unlikely to slow the ventricular rate and in some instances may accelerate the ventricular response.

* Therefore, AV nodal blocking drugs should not be used for pre-excited atrial fibrillation or flutter. (Class III, LOE C)

Caution is also advised to avoid the combination of AV nodal blocking agents that have a longer duration of action. For example, the short elimination half-life of adenosine affords follow-up treatment, if required, with a calcium channel blocker or ß-blocker. Conversely the longer half-life of a calcium channel or ß-blocker means their effects will overlap; profound bradycardia can develop if they are given serially.

Although antiarrhythmic medications (eg, amiodarone, procainamide, or sotalol) can also be used to treat SVTs, the higher toxicity and risk for proarrhythmia make these medications less desirable alternatives to the described AV nodal blocking agents. A possible exception is in patients with pre-excited atrial arrhythmias; the typical AV nodal blocking drugs are contraindicated in these patients and rate control may be achieved with antiarrhythmic medications. Importantly, use of these agents for atrial-based SVTs, such as atrial fibrillation and flutter can result in their termination, which may be undesirable in the absence of precautions to prevent the thromboembolic complications that may result from such conversion.

6.2.5 Wide-Complex Tachycardia

Evaluation
The first step in the management of any tachycardia is to determine if the patient’s condition is stable or unstable (Figure 4: Tachycardia Algorithm, Box 3). An unstable patient with a wide-complex tachycardia should be presumed to have VT and immediate cardioversion should be performed (Box 4 and see above).

* Precordial thump may be considered for patients with witnessed, monitored, unstable ventricular tachycardia if a defibrillator is not immediately ready for use. (Class IIb, LOE C)

If the patient is stable, the second step in management is to obtain a 12-lead ECG (Boxes 6 and 7 ) to evaluate the rhythm. At this point the provider should consider the need to obtain expert consultation. If the patient becomes unstable at any time, proceed with synchronized cardioversion or unsynchronized defibrillation should the arrhythmia deteriorate to VF or be due to a polymorphic VT.

Wide-complex tachycardias are defined as those with a QRS ≧0.12 second. The most common forms of widecomplex tachycardia are
VT or VF
SVT with aberrancy
Pre-excited tachycardias (associated with or mediated by an accessory pathway)
Ventricular paced rhythms

The third step in management of a tachycardia is to determine if the rhythm is regular or irregular. A regular wide-complex tachycardia is likely to be VT or SVT with aberrancy. An irregular wide-complex tachycardia may be atrial fibrillation with aberrancy, pre-excited atrial fibrillation (ie, atrial fibrillation using an accessory pathway for antegrade conduction), or polymorphic VT/torsades de pointes. Providers should consider the need for expert consultation when treating wide-complex tachycardias.

Therapy for Regular Wide-Complex Tachycardias
In patients with stable undifferentiated wide-QRS complex tachycardia, a reasonable approach is to try to identify the wide-complex tachycardia as SVT or VT and treat based on the algorithm for that rhythm.

* If the etiology of the rhythm cannot be determined, the rate is regular, and the QRS is monomorphic, recent evidence suggests that IV adenosine is relatively safe for both treatment and diagnosis. (Class IIb, LOE B)

* However, adenosine should not be given for unstable or for irregular or polymorphic wide-complex tachycardias, as it may cause degeneration of the arrhythmia to VF. (Class III, LOE C)

If the wide-complex tachycardia proves to be SVT with aberrancy, it will likely be transiently slowed or converted by adenosine to sinus rhythm; if due to VT there will be no effect on rhythm (except in rare cases of idiopathic VT), and the brevity of the transient adenosine effect should be reasonably tolerated hemodynamically. Because close attention to these varying responses may help to diagnose the underlying rhythm, whenever possible, continuous ECG recording is strongly encouraged to provide such written documentation. This documentation can be invaluable in helping to establish a firm rhythm diagnosis even if after the fact. Typically, adenosine is administered in a manner similar to treatment of PSVT: as a 6 mg rapid IV push; providers may follow the first dose with a 12 mg bolus and a second 12 mg bolus if the rate fails to convert. When adenosine is given for undifferentiated wide-complex tachycardia, a defibrillator should be available.

Depending on the underlying rhythm, the response to adenosine challenge can be variable. Some studies showed that adenosine converted an undifferentiated wide-complex tachycardia to sinus rhythm. Another study showed poor rates of conversion to sinus rhythm in patients known to have VT. The following adverse effects were reported in patients with pre-excited atrial fibrillation treated with adenosine: conversion to atrial fibrillation with a rapid ventricular response in one patient later found to have preexcitation, conversion to VF in one patient with known WPW,384 conversion to VF in 4 patients with pre-excited atrial fibrillation, conversion to VF in 2 patients with WPW,386 and a single case of VF in a patient with VT.

* Verapamil is contraindicated for wide-complex tachycardias unless known to be of supraventricular origin. (Class III, LOE B)

Adverse effects when the rhythm was due to VT were shown in 5 small case series. Profound hypotension was reported in 11 of 25 patients known to have VT treated with verapamil.

For patients who are stable with likely VT, IV antiarrhythmic drugs or elective cardioversion is the preferred treatment strategy.

* If IV antiarrhythmics are administered, procainamide,(Class IIa, LOE B) amiodarone, or sotalol can be considered. (Class IIb, LOE B)

* Procainamide and sotalol should be avoided in patients with prolonged QT. If one of these antiarrhythmic agents is given, a second agent should not be given without expert consultation. (Class III, LOE B)

* If antiarrhythmic therapy is unsuccessful, cardioversion or expert consultation should be considered. (Class IIa, LOE C)

One randomized comparison found procainamide (10 mg/kg) to be superior to lidocaine (1.5 mg/kg) for termination of hemodynamically stable monomorphic VT. Procainamide can be administered at a rate of 20 to 50 mg/min until the arrhythmia is suppressed, hypotension ensues, QRS duration increases >50%, or the maximum dose of 17 mg/kg is given. Maintenance infusion is 1 to 4 mg/min. Procainamide should be avoided in patients with prolonged QT and congestive heart failure.

IV sotalol (100 mg IV over 5 minutes) was found to be more effective than lidocaine (100 mg IV over 5 minutes) when administered to patients with spontaneous hemodynamically stable sustained monomorphic VT in a double-blind randomized trial within a hospital setting.

In a separate study of 109 patients with a history of spontaneous and inducible sustained ventricular tachyarrhythmias, infusing 1.5 mg/kg of sotalol over ?5 minutes was found to be relatively safe and effective, causing hypotension in only 2 patients, both of whom responded to IV fluid. Package insert recommends slow infusion, but the literature supports more rapid infusion of 1.5 mg/kg over 5 minutes or less. Sotalol should be avoided in patients with a prolonged QT interval.

Amiodarone is also effective in preventing recurrent monomorphic VT or treating refractory ventricular arrhythmias, in patients with coronary artery disease and poor ventricular function. It is given 150 mg IV over 10 minutes; dosing should be repeated as needed to a maximum dose of 2.2 g IV per 24 hours. Higher doses (300 mg) were associated with an increased frequency of hypotension, although some reports, attributed the hypotension to the vasoactive solvents that are not present in a new form of the drug recently approved for use in the US.

By comparison, lidocaine is less effective in terminating VT than procainamide, sotalol, and amiodarone, and when given to patients with or without a history of MI with spontaneous sustained stable VT in the hospital setting. Lidocaine has been reported to variably terminate VT when administered intramuscularly to patients with AMI and VT in the out-of-hospital setting. Thus, while occasionally effective, lidocaine should be considered second-line antiarrhythmic therapy for monomorphic VT. Lidocaine can be administered at a dose of 1 to 1.5 mg/kg IV bolus. Maintenance infusion is 1 to 4 mg/min (30 to 50 mcg/kg per minute).

6.3 Irregular Tachycardias

6.3.1 Atrial Fibrillation and Flutter
Evaluation
An irregular narrow-complex or wide-complex tachycardia is most likely atrial fibrillation (with or without aberrant conduction) with an uncontrolled ventricular response. Other diagnostic possibilities include MAT or sinus rhythm/tachycardia with frequent atrial premature beats. When there is doubt about the rhythm diagnosis and the patient is stable, a 12-lead ECG with expert consultation is recommended.

Therapy
General management of atrial fibrillation should focus on control of the rapid ventricular rate (rate control), conversion of hemodynamically unstable atrial fibrillation to sinus rhythm (rhythm control), or both. Patients with an atrial fibrillation duration of >48 hours are at increased risk for cardioembolic events, although shorter durations of atrial fibrillation do not exclude the possibility of such events. Electric or pharmacologic cardioversion (conversion to normal sinus rhythm) should not be attempted in these patients unless the patient is unstable. An alternative strategy is to perform cardioversion following anticoagulation with heparin and performance of transesophageal echocardiography to ensure the absence of a left atrial thrombus; see the ACC/AHA Guidelines for Management of Patients with Atrial Fibrillation.

Rate Control
Patients who are hemodynamically unstable should receive prompt electric cardioversion. More stable patients require ventricular rate control as directed by patient symptoms and hemodynamics.

IV ß-blockers and nondihydropyridine calcium channel blockers such as diltiazem are the drugs of choice for acute rate control in most individuals with atrial fibrillation and rapid ventricular response. (Class IIa, LOE A)

Digoxin and amiodarone may be used for rate control in patients with congestive heart failure; however, the potential risk of conversion to sinus rhythm with amiodarone should be considered before treating with this agent.

A wide-complex irregular rhythm should be considered pre-excited atrial fibrillation. Expert consultation is advised. Avoid AV nodal blocking agents such as adenosine, calcium channel blockers, digoxin, and possibly ß-blockers in patients with pre-excitation atrial fibrillation because these drugs may cause a paradoxical increase in the ventricular response. Typically, patients with pre-excited atrial fibrillation present with very rapid heart rates and require emergent electric cardioversion. When electric cardioversion is not feasible or effective, or atrial fibrillation is recurrent, use of rhythm control agents (discussed below) may be useful for both rate control and stabilization of the rhythm.

Rhythm Control
A variety of agents have been shown to be effective in terminating atrial fibrillation (pharmacologic or chemical cardioversion), although success between them varies and not all are available as parenteral formulations. Expert consultation is recommended.

6.3.2 Polymorphic (Irregular) VT
Polymorphic (irregular) VT requires immediate defibrillation with the same strategy used for VF. Pharmacologic treatment to prevent recurrent polymorphic VT should be directed by the underlying cause of VT and the presence or absence of a long QT interval during sinus rhythm.

If a long QT interval is observed during sinus rhythm (ie, the VT is torsades de pointes), the first step is to stop medications known to prolong the QT interval. Correct electrolyte imbalance and other acute precipitants (eg, drug overdose or poisoning: see Part 12.7: “Cardiac Arrest Associated With Toxic Ingestions”). Although magnesium is commonly used to treat torsades de pointes VT (polymorphic VT associated with long QT interval), it is supported by only 2 observational studies that showed effectiveness in patients with prolonged QT interval. One adult case series showed that isoproterenol or ventricular pacing can be effective in terminating torsades de pointes associated with bradycardia and drug-induced QT prolongation. Polymorphic VT associated with familial long QT syndrome may be treated with IV magnesium, pacing, and/or ß-blockers; isoproterenol should be avoided. Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. The addition of pacing or IV isoproterenol may be considered when polymorphic VT is accompanied by bradycardia or appears to be precipitated by pauses in rhythm.

* In the absence of a prolonged QT interval, the most common cause of polymorphic VT is myocardial ischemia. In this situation IV amiodarone and ß-blockers may reduce the frequency of arrhythmia recurrence. (Class IIb, LOE C)

Myocardial ischemia should be treated with ß-blockers and consideration be given to expeditious cardiac catheterization with revascularization.

* Magnesium is unlikely to be effective in preventing polymorphic VT in patients with a normal QT interval, but amiodarone may be effective. (Class IIb, LOE C)

Other causes of polymorphic VT apart from ischemia and long QT syndrome are catecholaminergic VT (which may be responsive to ß-blockers) and Brugada syndrome (which may be responsive to isoproterenol).

6.4 Summary
The goal of therapy for bradycardia or tachycardia is to rapidly identify and treat patients who are hemodynamically unstable or symptomatic due to the arrhythmia. Drugs or, when appropriate, pacing may be used to control unstable or symptomatic bradycardia. Cardioversion or drugs or both may be used to control unstable or symptomatic tachycardia. ACLS providers should closely monitor stable patients pending expert consultation and should be prepared to aggressively treat those with evidence of decompensation.