Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20

Supraventricular tachyarrhythmias in the intensive care unit David M. Salerno MD, PhD To cite this article: David M. Salerno MD, PhD (1992) Supraventricular tachyarrhythmias in the intensive care unit, Postgraduate Medicine, 91:6, 293-309, DOI: 10.1080/00325481.1992.11701330 To link to this article: http://dx.doi.org/10.1080/00325481.1992.11701330

Published online: 17 May 2016.

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Supraventricular tachyarrhythmias in the intensive care unit David M. Salerno, MD, PhD

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Preview What supraventricular tachyarrhythmias are common in the intensive care unit? What are the keys to their recognition? What drugs are effective in treating them? Or Salerno answers these important questions in this informative article.

Although supraventricular tachyarrhythmias are usually less dangerous than ventricular tachycardia, their precise diagnosis and acute management can be more complex. Successful therapy depends on correct identification of the type of tachyarrhythmia, adequate treatment of the underlying cardiac problem, and knowledgeable selection of antiarrhythmic drug therapy.

Causes of supraventricular

tachyarrhythmias Supraventricular tachyarrhythmias occur in a wide variety of illnesses in the intensive care unit. Any disorder that increases the pressure or volume in either the right or left side of the heart {atrium or ventricle) can lead to these arrhythmias. In the left side, these include myocardial infarction, hypertensive cardiomyopathy, aortic or mitral valvular disease, and dilated cardiomyopathy; in the right side, they include chronic obstructive lung disease, pulmonary embolism, congenital heart disease, and

tricuspid valvular disease. Other conditions that can cause supraventricular tachycardias include systemic conditions such as alcohol intoxication (holiday heart syndrome) and alcohol withdrawal, hyperthyroidism, the postoperative state, acute central nervous system disorders such as intracranial hemorrhage, and structural disorders of the conducting system such as Wolff-Parkinson-White syndrome. Finally, in some cases, these arrhythmias are idiopathic.

Diagnosis of supraventricular

tachyarrhythmias The answers to three key questions greatly aid in electrocardiographic (ECG) recognition of supraventricular tachyarrhythmias: I. Is the rhythm regular or irregular? Answering this simple question can reduce the differential diagnosis considerably, since the rhythms that produce regularity and irregularity differ (table 1).

2. Is the QRS complex narrow or wide? If it is wide, the diagnos-

tic possibilities include ventricular tachycardia, making the diagnostic challenge more difficult, since supraventricular tachyarrhythmias may produce raterelated aberrancy or the patient may have associated underlying bundle-branch block.

3. What are the atria doing? This question holds the key to the diagnosis but may be the most challenging to answer. One must be careful to avoid the traps involved in using monitored ECG leads (eg, recorded from a bedside monitor) for making decisions about atrial activity. Murphy's Law of Critical Care Monitoring states that "the least helpful lead will always be the one monitored." My corollary to this law is "get a 12-lead ECG for all new arrhythmias." A complete ECG will usually yield the right answer. For example, monitored leads often show what appears to be atrial fibrillation, whereas other leads may reveal atrial waves caused by other arrhythmias (figures 1 and 2). REGULAR SUPRAVENTRICULAR

TACHYCARDIAS-Regular supraventricular tachycardias are more challenging to diagnose but are typically easier to treat than irregular tachycardias (table 1). By far the most common type is atrioventricular (AV) nodal reentrant

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Regular supraventricular tachycardias are more challenging to diagnose but are typically easier to treat than irregular supraventricular tachycardias.

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Table 1. Causes of regular and irregular narrow-QRS-complex tachycardias

Regular (common) Atrioventricular (AV) nodal reentrant tachycardia Bypass tract tachycardia (AV reciprocating tachycardia) Atrial flutter Regular (uncommon) Atrial reentrant tachycardia Atrial automatic tachycardia Junctional tachycardia Sinus node reentrant tachycardia Irregular Atrial fibrillation Atrial flutter with variable block Multifocal atrial tachycardia (Very frequent premature atrial contractions may masquerade as tachycardia)

tachycardia. This paroxysmal tachycardia has been shown to cause most cases of what was formerly called paroxysmal atrial tachycardia or paroxysmal junctional tachycardia. It is caused by dual pathways through the AV node, which can create a small reentry circuit within the node. The P wave may be hidden within the QRS complex during tachycardia bur often occurs just

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behind the QRS complex (figure 3) or, less frequently, very slightly in front of it, with an invened P wave in the inferior leads. Treatment of this tachycardia involves blockade of the AV node, which is discussed later. Bypass tract tachycardia, or AV reciprocating tachycardia, is usually due to Wolff-ParkinsonWhite syndrome. In most cases, it cannot be distinguished from AV nodal reentrant tachycardia during the arrhythmia, at which time the QRS complex appears normal (figure 4). Unlike in AV nodal reentrant tachycardia, during bypass tract tachycardia the P wave is usually fanher from the QRS but is often within the T wave and therefore very difficult to locate. This rhythm can usually be readily identified by obtaining a 12-lead ECG after termination of the tachycardia. The ECG reveals a shon PR interval and delta wave in sinus rhythm, unless the bypass is concealed, whereas in AV nodal reentrant tachycardia, the PR interval and QRS complex are normal in sinus rhythm. The acute treatment of both these tachycardias, discussed later, is to block the AV node. Indeed, blockade of the AV node is a use-

ful diagnostic tool to distinguish AV nodal reentrant and bypass tract tachycardias from other types of regular supraventricular tachycardias that do not require the AV node to maintain the arrhythmia. If blockade of the AV node terminates the tachycardia, the patient almost cenainly has one of these two most common types of tachycardia. Atrial flutter with 2:1 AV block may masquerade as sinus tachycardia or other forms of supraventricular tachycardia, since in some leads it may be hard to find flutter waves. Occasionally, it may be difficult to see the flutter waves in any of the surface ECG leads. In these cases, a specialized recording of atrial activity, such as an intra-atrial or esophageallead recording, may be helpful. Treatment is discussed later. Other types of regular supraventricular tachycardias are uncommon. These include intraatrial reentrant tachycardia, atrial automatic tachycardia, and junctional tachycardias. These arrhythmias usually require class I drug therapy. Finally, sinus node reentrant tachycardia occurs rarely: It looks like sinus tachycardia bur is paroxysmal, starring and stopping suddenly.

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Atrial flutter with variable AV conduction may be confused with atrial fibrillation in monitored leads.

Figure 1. Lead I (a) appears to show atrial fibrillation, but simultaneously recorded lead 11 (b) reveals atrial flutter with variable block (flutter waves marked).

IRREGULAR SUPRAVENTRICULAR

TACHYCARDIAS--The most common type of irregular supraventricular tachycardia is atrial fibrillation. It is easily recognized, but a 12-lead ECG should be obtained to rule out atrial flutter or multifocal atrial tachycardia. Its treatment is discussed later. Atrial flutter with variable AV conduction also occurs commonly and may be confused with atrial fibrillation in monitored leads (figure 1). Its treatment is similar to that of atrial fibrillation.

Figure 2. Lead I (a) appears to show atrial fibrillation, but simultaneously recorded lead 11 (b) reveals multifocal atrial tachy-

cardia (P waves marked).

Multifocal atrial tachycardia is also commonly misdiagnosed as atrial fibrillation (figure 2); this error is significant because digoxin (Lanoxin) and cardioversion are ineffective in treating it. This type of tachycardia is most commonly seen in severe lung disease with acute exacerbation and in severe congestive heart failure. The primary treatment of multifocal atrial tachycardia is management of the underlying condition. Although rate can be controlled with beta-adrenergic blocking agents, these drugs are

often contraindicated because of the underlying condition. Verapamil hydrochloride (lsoptin), 15 to 25 mg intravenously at about 1 mg/min, is very effective at slowing the rate.' This high a dose will almost always result in a significant lowering of blood pressure, but pretreatment with 1 ampule of calcium chloride or calcium gluconate can minimize this effect. "2 WIDE-Q.RS-COMPLEX TACHYCARDIA-This arrhythmia may be a type of regular supraventricular tachycardia, but 90% to 95% of cases are ventricular.

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The key to diagnosis of

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wide-QRS-complex tachycardia is to identify the atrial activity.

Figure 3. During regular tachycardia, lead 11 (a) shows small wave (marked) at end of QRS complex that could be either S or P wave. When sinus rhythm returns (b), this wave disappears, proving that it was a P wave, most likely caused by atrioventricular nodal reentrant tachycardia.

Avoid the trap: "The patient is tolerating the arrhythmia so well, it must be supraventricular arrhythmia with aberrancy... let's try some verapamil." This approach of using therapeutic trials is fraught with hazard. Verapamil is not only usually ineffective, since most of these patients actually have ventricular tachycardia, but is associated with a very high incidence of complications, as in-

Figure 4. During regular tachycardia, lead 11 (a) shows

normal QRS complex and no visible P wave. When sinus rhythm returns (b), short PR interval and delta wave appear, confirming diagnosis of Wolff-Parkinson-White syndrome.

dicated by a recent article entitled "Dire consequences of verapamil administration for wide-QRS tachycardias." 3 The key to diagnosis of wideQRS tachycardia is to identify the atrial activity. This should be done using 12-lead ECGs and intraesophageal or intra-atrial ECGs before any therapeutic maneuvers if the patient is tolerating the arrhythmia.

Management of reversible causes The first step in therapy for supraventricular tachyarrhythmias is to consider reversible precipitating factors (table 2). A catheter in the right atrium is a common cause of premature atrial contractions that may lead to supraventricular tachycardia. If the chest film shows that the catheter tip is below the junction

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Verapamil and diltiazem are the only available calcium blockers with demonstrated antiarrhythmic effect.

of the superior vena cava and the right atrial border, then the catheter should be withdrawn slightly. Inotropic drugs, such as dopamine (Dopastat, lntropin) and dobutamine (Dobutrex), and aminophylline (Phyllocontin) are common precipitants of supraventricular tachyarrhythmias. If they are required, their dosage should be reviewed when arrhythmia occurs. Often, improvement in congestive heart failure or pulmonary function can control recurrent episodes of supraventricular tachyarrhythmias.

Drug therapy The second step in management of supraventricular tachycardia is drug therapy. Among various effective antiarrhythmic drugs, three newer intravenous agentsdiltiazem hydrochloride (Cardizem), esmolol hydrochloride (Brevibloc), and adenosine (Adenocard)-have markedly improved the ability to manage supraventricular tachyarrhythmias. Each has a specific role, which is delineated in the following discussion of individual drugs. CALCIUM CHANNEL Bl.OCKERS-These drugs exert the ma-

jority of their action on the AV node. Verapamil and dilciazem are the only available calcium blockers with demonstrated antiarrhythmic effect. Their effects on the sinus node are modest. They manifest a property called use-dependence. Their blocking effects on the AV node are proportional to the underlying rate of conduction through the AV node-the higher the rate, the more their effect. For example, although they have very little effect at normal heart rates, they quite effectively slow the ventricular rate in rapid atrial fibrillation. VERAPAMIL-This drug is effective for terminating regular supraventricular tachyarrhythmias, particularly of the AV nodal reentrant or bypass tract reentrant type. Generally, a dose of 5 to 10 mg, given intravenously, is needed. Verapamil can slow the rate of atrial fibrillation quite nicely. 2 Oral maintenance therapy is feasible. The drug can slow the rate of multifocal atrial tachycardia, as already mentioned, in higher doses of 10 to 25 mg, given intravenously. 1 Verapamil is contraindicated in congestive heart failure and hypotension. Significant symptomatic hypotension occurs in

Table 2. Reversible causes of supraventricular tachyarrhythm1a in the mtensive care unit

Catheter in right atrium Inotropic drugs, eg, dopamine (Dopastat, lntropin), dobutamine (Dobutrex) Aminophylline (Phyllocontin) Congestive heart failure Respiratory failure

approximately 10% of patients who receive the drug intravenously. Intravenous fluids or, uncommonly, inotropes may be required. Intravenous calcium has been reported to reduce the incidence of hypotension. 1•2 Verapamil is contraindicated for chronic therapy ofWolffParkinson-White syndrome, because it has the potential to increase the ventricular rate during atrial fibrillation in that disorder. However, it can be used for managing AV bypass tract tachycardia (ie, the regular narrow-QRScomplex tachycardia that occurs in Wolff-Parkinson-White syndrome). After terminating the

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Esmolol is useful to terminate supraventricular tachycardia, to control rate in atrial fibrillation, or as a maintenance infusion for beta blockade.

tachycardia, it should not be used as chronic therapy. DILTIAZEM-Intravenous diltiazem is another extremely useful agent for treating supraventricular tachyarrhyrhmias. The usual dose is 20 to 25 mg given as a slow (2-minute) bolus injection. The agent has now had extensive clinical study and has recently been approved by the US Food and Drug Administration. It is very effective for converting supraventricular tachycardia, working within 1 to 2 minutes after injection. 4 Intravenous diltiazem effectively slows the ventricular rate in atrial fibrillation. Its peak effect occurs within 4 minutes of being administered intravenously as a slow bolus. 5 A second dose can be given in 15 minutes if the first dose has not achieved maximum therapeutic effect. Continuous intravenous maintenance dosing has been better defined with diltiazem than with verapamil; the recommended dosage is 5 to 15 mg/hr. 6 The duration of effect in atrial fibrillation averages about 3 hours. After the rate has been slowed by an intravenous bolus dose of diltiazem, a continuous intravenous infusion can be initiated. Both verapamil and diltiazem act

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more rapidly than digoxin to control the rate of atrial fibrillation and are better as oral maintenance therapy for atrial fibrillation, since digoxin does not effectively block the exerciseinduced excessive increase in heart rate that often occurs in atrial fibrillation. There appears to be less hypotension with intravenous diltiazem than with intravenous verapamil (occurring in about 2% of patients versus 10%, respectively).2· 5· 6 Diltiazem, like verapamil, has negative inotropic effects, bur small studies have shown that it can be given to patients with heart failure. 7 These studies require further confirmation. Diltiazem should be used cautiously in heart failure. The drug is also contraindicated in Wolff-Parkinson-White syndrome as chronic oral therapy, and in hypotensive patients. The role of calcium pretreatment before diltiazem is unknown. BETA-ADRENERGIC Bl.OCKERS-These

drugs block the sinus and AV nodes. They typically reduce the resting heart rate more than the calcium blockers. PROPRANOLOL AND METOPROLOL-for use in the intensive care unit, intravenous propranolol {lnderal) and metoprolol tar-

trate (Lopressor) are available. Their onset of action is approximately 10 to 30 minutes. Hypotension and bradycardia may occur. ESMOLOL-This is an ultrashort-acting beta blocker that has significantly facilitated the use of intravenous beta blockers. 8 It has a half-life of less than 10 minutes, being metabolized by red blood cells. This property makes it safer to use than propranolol and metoprolol in patients with asthma, since its action abates quite soon after the infusion is stopped. Esmolol is useful to terminate supraventricular tachycardia, to control rate in atrial fibrillation, or as a maintenance infusion for beta blockade. The drug is also useful in patients with alcohol withdrawal or beta-blocker withdrawal, as may be seen in patients who have been taking an oral beta blocker bur are unable to continue doing so in the intensive care unit. Although esmolol's onset of action is quite rapid, occurring within 5 minutes, the dose range is wide, so it often takes 30 to 60 minutes to find the optimal dose. The loading dose is 500 IJ.g/kg given over 1 minute. Maintenance therapy is then initiated at

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Adenosine is practical only for treatment of regular supraventricular tachycardia.

50 f.Lg/kg/min. If no effect is seen in 5 minutes, the maintenance infusion is increased to 100, 150, and then 200 f.Lg/kg/min. Additional loading doses may be given at each increase in maintenance. Hypotension severe enough to require discontinuation of therapy occurs in about 10% of patients. ADENOSINE-This compound has been recently approved for clinical use. It directly blocks the AV node, but its mechanism of action is unknown. It has an extremely shon half-life; its duration of effect is only 2 to 3 minutes.9 Thus, it is practical only for treatment of regular supraventricular tachycardia, effectively terminating the tachycardia approximately 80% of the time. Adenosine can also be useful diagnostically, since the underlying atrial activity will be revealed briefly while AV block is produced. The initial dose is 6 mg given intravenously as a very rapid bolus, preferably into a central vein. If it is ineffective within the first 1 to 2 minutes, 12 mg can be given. Administering the bolus slowly reduces its effectiveness because of the drug's rapid metabolism. Adenosine can cause a transient dyspnea or flushing,

Davld M. Salemo, MD, PhD Dr Salerno is associate professor of medicine at the University of Minnesota Medical Schooi-Minneapolis and director of the electrocardiography laboratory, Hennepin County Medical Canter, Minneapolis.

bur these side effects dissipate quite rapidly. Because of its shon duration of action, it has no role in slowing atrial fibrillation. ~ I DRUGS-The class I antiarrhythmic drugs may be used for termination of atrial fibrillation or atrial flutter in the intensive care unit. Intravenous quinidine and intravenous procainamide hydrochloride (Pronestyl) are both available and are similar in effectiveness and safety. Dosages are 5 to 10 mglkg of quinidine given intravenously over 30 to 60 minutes or 10 to 15 mg/kg of procainamide given

intravenously over 30 to 60 minutes. Blood pressure, QRS complex, and QT intervals should be observed during the loading infusion. The infusion should be slowed or terminated if adverse effects are seen. A number of available oral agents are effective for terminating atrial fibrillation. These include quinidine, procainamide, flecainide acetate (Tambocor), and propafenone hydrochloride (Rythmol). At this time, the safety of all class I drugs is questionable because of fatal proarrhythmia during outpatient long-term therapy. 1a- 13 In my opinion, they

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Therapy for paroxysmal regular supraventricular tachycardia is initially directed at blockade of the AV node.

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Table 3. Therapy for paroxysmal regular supraventncular tachycardia

Step1 Vagal maneuvers

Step 2 (depends on urgency of situation) Emergent

Carotid massage Valsalva's maneuver

Electrical cardioversion

Urgent

Adenosine (Adenocard) Electrical cardioversion Consider intravenous diltiazem HCI (Cardizem) or verapamil HCI (lsoptin)*

Nonurgent or recurrent

Adenosine Intravenous diltiazem Intravenous verapamil Esmolol HCI (Brevibloc)

Refractory

Electrical cardioversion Class I or Ill drugs

*If systolic blood pressure above 90 mm Hg.

should be used to terminate atrial fibrillation in the hospital but should not be used as long-term outpatient therapy unless absolutely required, because of frequent recurrences of atrial fibrillation or severe hemodynamic compromise during atrial fibrillation. AMIODARONE-Amiodarone hydrochloride (Cordarone) is also effective for maintaining si-

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nus rhythm in atrial fibrillation but is reserved for extremely refractory cases because of its high incidence of severe side effects. The drug may be effective when all other drugs have failed. 14

Management of paroxysmal regular supraventricular tachycardia Therapy is initially directed at blockade of the AV node (table 3).

Vagal maneuvers should be tried first because of the ease and rapidity of such treatment. If these fail, therapy should be tailored to the urgency of the situation. If the patient's hemodynamics are seriously compromised and the situation is emergent, electrical cardioversion should be performed. However, it is unusual for paroxysmal regular supraventricular tachycardia to cause a severe reduction in hemodynamic performance. In urgent situations when the patient is moderately symptomatic and in nonurgent cases, adenosine therapy is the treatment of choice. If the arrhythmia recurs or if adenosine fails, the drug of second choice, in my opinion, is diltiazem, since the incidence of hypotension with this drug appears to be less than that with esmolol or intravenous verapamil. Esmolol or verapamil can be given if diltiazem fails or has not been tolerated in the past. Intravenous digoxin is effective for some cases, but its action is so slow that it is the drug oflast choice. Class I and class Ill antiarrhythmic drugs have a very limited role in the acute management of paroxysmal regular supraventricular tachycardia. A calcium channel blocker or beta blocker may be

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The treatment of choice for control of ventricular rate in most cases of atrial fibrillation or flutter is intravenous calcium blocker therapy.

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given orally to prevent recurrent episodes. ~~entofabdu

Table 4. Intravenous drugs of choice for control of ventricular rate in atnal fibnllation or flutter

Drug*

Peak effect

Diltiazem HCI (Cardizem)

5-10 min

Verapamil HCI (lsoptin)

5-10 min

Esmolol HCI (Brevibloc)

5-30 min

Metoprolol tartrate (Lopressor)

20-60 min

Propranolol (lnderal)

20-60 min

Digoxin (Lanoxin)

2-6 hr

fibrillation or abdu flutter Atrial fibrillation or flutter is managed in four steps: (1) control of ventricular rate, (2) evaluation of the cause and cardiac function, (3) assessment of the risk of embolism and need for anticoagulation, and (4) restoration of sinus rhythm. RATE CONIROL-The treatment of choice for control of ventricular rate in most cases is intravenous calcium blocker therapy (table 4). In my opinion, intravenous diltiazem is preferred to intravenous verapamil, since its side effect profile appears to be lower while effectiveness is the same. Also, maintenance intravenous therapy has been better defined for diltiazem than for verapamil. Peak effect occurs with both these drugs in 5 to 10 minutes. The initial intravenous dose is 20 mg for diltiazem and 5 mg for verapamil. A repeat intravenous dose of25 mg of diltiazem or 5 to 10 mg of verapamil can be given after 10 to 15 minutes. Esmolol is the drug of second choice and can be used when calcium blockers have failed, although calcium blocker failure

'For all except digoxin: As soon as rate is controlled, start either continuous intravenous infusion therapy or oral therapy (need not be same drug).

occurs in only about 5% of patients. The onset of action of esmolol is very rapid (50 mm in diameter by echocardiogram), significant mitral valve disease, and a dilated left ventricle. 15 These fearures increase the likelihood of embolization and therefore the need for anticoagulation before cardioversion. The transthoracic echocardiogram cannot exclude the presence of atrial clots, since these are difficult to visualize. Next, the hemodynamic status of the patient should be considered. If the patient is clinically stable in atrial fibrillation, even if mildly dyspneic on exenion or with a mild sense of fatigue, and

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is able to tolerate an outpatient period of atrial fibrillation, warfarin sodium (Coumadin, Panwarfin) should be given for at least 3 weeks before cardioversion is performed. Of course, if the patient is seriously compromised, electrical cardioversion must be performed immediately. In intermediate situations, where the patient can tolerate atrial fibrillation for a period of time but is too ill to return home on warfarin therapy, a few days of intravenous heparin therapy may be considered prior to cardioversion. In most cases, it appears that some form of anticoagulation, either aspirin or warfarin, should be continued indefinitely, unless a reversible cause is identified. RFSIORATION OF SINUS

RHYIHM-Finally, a plan should be established for restoring sinus rhythm (table 6). For most patients, I think at least one try at restoring sinus rhythm is worthwhile. Ordinarily, this will initially include an attempt at drug therapy. Quinidine and procainamide are the drugs of first choice. If drug therapy fails, electrical cardioversion should be performed. Initial shock energy should be at least 50 J for flutter and at least 100 J for atrial fibril-

lation. Lower shock energies are so commonly unsuccessful that they are not worth trying. If these shock energies fail, energies should be increased promptly in one or two steps to the maximum output of the device. If full energy is ineffective, an anteriorposterior paddle configuration with a large posterior paddle should be tried. This will often lead to successful cardioversion when two anterior paddles have failed. The most effective anesthetic for cardioversion is unquestionably methohexital sodium (Brevital). This drug provides excellent amnesia and analgesia. The benwdiazepines are a poor second choice because patients commonly have pain and remember the shock, even though they are fully asleep at the time the shock is given. All shocks for atrial fibrillation and flutter should be

synchronized to the QRS complex.

Summary Several types of supraventricular tachyarrhythmias occur commonly during intensive care. The specific type can usually be diagnosed using standard electrocardiographic techniques. Several new drugs have significantly improved the ability to successfully manage these arrhythmias. FOYI Earn credit on this article. ~ See CME Quiz.

Address for correspondence: David M. Salerno, MD, PhD, Division of Cardiology, Hennepin County Medical Center, 701 ParkAve S, Minneapolis,

MN 55415.

References

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107(5):623-8 2. Haft Jl, Habbab MA. Treatment of atrial arrhythmias: effectiveness of veraparnil when preceded by calcium infusion. Arch Intern Med

1986; 146(6): 1085-9

3. Switzer P, Henthom RW, Olsansky B, et al. Dire consequences of veraparnil administration for wide-QRS tachycardias. (Abstr) Circulation 1986;74(II):II105 4. Huycke EC, Sung RJ, Dias VC, et al. Intravenous diltiazem for termination of reentrant supraventricular tachycardia: a placebo-controlled, randomized, double-blind, multicenter study.] Am Col! Cardiol 1989; 13(3):538-44

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S. s.Icmo DM, Diu VC, Klciger RE, et al. Efficacy and safety of intravenous diltiazem for treaanent of atrial fibrillation and atrial flutter. Am] Cardiol1989;63(15):1046-51

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