Treatment of Arrhythmias

The diagnosis and treatment of arrhythmias can be simplified by using the following six questions as a checklist when looking at an electrocardiographic display and attempting to decide whether treatment is necessary:

1. What is the heart rate?
2. Is the rhythm regular?
3. Is there one P wave for each QRS complex?
4. Is the QRS complex normal?
5. Is the rhythm dangerous?
6. Does the rhythm require treatment?

Following are some common intraoperative arrhythmias to which the six questions should be applied.

Sinus Bradycardia

The pacemaker site is in the sinus node, but the rate is slower than normal. Etiologic factors include drug effects, acute inferior myocardial infarction, hypoxia, vagal stimulation, and high sympathetic blockade. Sinus bradycardia accounts for 11% of intraoperative arrhythmias:

1. Heart rate: The heart rate is slower than 60 beats/min. In patients on chronic β-blocker therapy, it is defined as a heart rate of less than 50 beats/min.
2. Rhythm: The rhythm is regular, except for occasional escape beats from other pacemaker sites.
3. P:QRS: There is a 1:1 relationship between the P waves and the QRS complexes.
4. QRS complex: Normal.
5. Significance: Heart rates lower than 40 beats/min are poorly tolerated even in healthy patients and should be evaluated on the basis of their effect on cardiac output. Treatment is recommended if hypotension, ventricular arrhythmias, or signs of poor peripheral perfusion are observed. Sinus bradycardia may be part of the sick sinus syndrome in which sinus node dysfunction can precipitate bradycardias, heart block, tachyarrhythmias, or alternating bradyarrhythmias and tachyarrhythmias ( Fig. 34-13 ). ^[38]
6. Treatment: Usually, none is necessary. A progression from atropine (0.5 to 1.0 mg by intravenous bolus, repeated every 3 to 5 minutes, up to 0.04 mg/kg or approximately a 3.0-mg total dose for the average 75-kg male patient), to ephedrine (5 to 25 mg by intravenous bolus), dopamine (5 to 20 µg/kg/min by intravenous infusion), epinephrine (2 to 10 µg/min by intravenous infusion), or isoproterenol (2 to 10 µg/min by intravenous infusion) to temporary transcutaneous pacing or transvenous pacemaker insertion may be necessary for severe or refractory sinus bradycardia. Immediate institution of transcutaneous pacing is especially important if the patient is symptomatic.

Sinus Tachycardia

The pacemaker site is in the sinus node, but the rate is faster than normal. Sinus tachycardia is the most commonly occurring arrhythmia in the perioperative period. It occurs with such frequency that it is not included in most incidence studies. Common causes include pain, inadequate anesthesia, hypovolemia, fever, hypoxia, hypercarbia, heart failure, and drug effects.^[4]

1. Heart rate: The rate is faster than 100 beats/min in the adult patient and can go up to 170 beats/min, which may be seen during a severe episode of hyperpyrexia.
2. Rhythm: Regular.
3. P:QRS: 1:1.
4. QRS complex: Normal. There may be associated ST-segment depression with severe increases in heart rate and resulting myocardial ischemia.
5. Significance: Prolonged tachycardias in patients with underlying heart disease can precipitate congestive heart failure because of the increased myocardial

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   work required. The tachycardia decreases coronary perfusion time, which can cause secondary ST-T wave changes and can precipitate angina pectoris in patients with coronary artery disease. A major diagnostic problem is encountered when the heart rate is 150 beats/min, because this is a common rate for sinus tachycardia, paroxysmal atrial tachycardia (PAT), or atrial flutter with a 2:1 block. These three arrhythmias can sometimes be separated by the use of carotid sinus massage, intravenous administration of edrophonium, or atrial or esophageal electrocardiographic leads to identify the P waves on the ECG more accurately.
6. Treatment: The underlying disorder should be treated. Hypovolemia and light anesthesia are most common causes. If necessary, in patients with ischemic heart disease who develop tachycardia and ST-segment changes, after excluding hypovolemia and while determining the cause, esmolol should be used to prevent further myocardial ischemia.

Figure 34-13 Sick sinus syndrome. (From Marriott HJL: Practical Electrocardiography, 7th ed. Baltimore, Williams & Wilkins, 1983.)

Sinus Arrhythmia

The pacemaker impulse arises from the sinoatrial node, but the arrhythmia is manifested by alternating periods of slower and faster heart rates. The PR interval is normal, as is the QRS complex. Most commonly, but not invariably, the rate increases with inspiration and decreases with expiration. This arrhythmia occurs more often in children than in adults.^[4]

1. Heart rate: 60 to 100 beats/min.
2. Rhythm: Irregular.
3. P:QRS: 1:1.
4. QRS complex: Normal.
5. Significance: Normal finding.
6. Treatment: None.

Atrial Premature Beats

An ectopic pacemaker site in the left or the right atrium initiates the atrial premature beat (APB). The shape of the P wave is different from the usual sinoatrial node P wave and may be inverted. The PR interval may be shorter or longer than normal, depending on the site of the ectopic focus and on the refractoriness of the atrioventricular nodal pathway. The APB spreads through the atrioventricular node and ventricular conduction system and, in retrograde fashion, reaches the sinoatrial node, resetting the sinus pacemaker. The interval from the APB to the next sinus beat is therefore a normal sinus cycle (i.e., no compensatory pause). The absence of a compensatory pause is an important distinguishing feature between APBs and VPBs. Occasionally, APBs may find part of the ventricular conduction system refractory. In that case, they travel down an aberrant pathway and create an abnormal QRS complex. They are then called APBs with aberrant ventricular conduction and can easily be confused with VPBs. Because the recovery period of the right ventricular conduction system outlasts that of the left, the most common form of aberration appears as a right bundle branch block (RBBB). Helpful points in separating APBs with aberrant ventricular conduction from VPBs include (1) the presence of a preceding P wave, usually abnormally shaped; (2) an RBBB configuration of the QRS complex; (3) the presence of an rsR' ventricular complex in V₁ ; and (4) the finding that the initial vector forces are identical to the preceding beat but are usually the opposite with a VPB. Other characteristics of APBs are as follows:

1. Heart rate: Variable, depending on the frequency of APBs.
2. Rhythm: Irregular.
3. P:QRS: Usually 1:1. The P waves have various shapes and may even be lost in the QRS or T waves. Occasionally, the P wave is so early as to find the ventricle refractory, and a nonconducted beat occurs.
4. QRS complex: Usually normal unless there is ventricular aberration.
5. Significance: In one study, APBs represented 10% of all intraoperative arrhythmias. They have little clinical significance, but frequent APBs may lead to other more serious supraventricular arrhythmias or may be a sign of digitalis intoxication.
6. Treatment: Rarely necessary, but digitalis, β-blockers, or verapamil may be considered if hemodynamic function is impaired.

Paroxysmal Supraventricular Tachycardia

Paroxysmal SVT (PSVT) is characterized by a rapid regular rhythm, usually with a narrow QRS complex and lacking

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Figure 34-14 Diagrammatic representation of various mechanisms of supraventricular tachycardia. A-VN, A-V node; BP, bypass tract; S-AN, sinus node. (Adapted from Marriott HJL: Practical Electrocardiography, 7th ed. Baltimore, Williams & Wilkins, 1983.)

1. Heart rate: 130 to 270 beats/min.
2. Rhythm: Usually regular unless the impulse originates from multiple atrial foci.
3. P:QRS: There is a 1:1 relationship, although the P wave may often be hidden in the QRS complex or T wave.
4. QRS complex: Generally normal, but ST-T changes indicative of ischemia may be observed. Aberration of ventricular conduction may occur, complicating the differential diagnosis with ventricular tachycardia. SVT may also be confused with sinus tachycardia, atrial flutter, and atrial fibrillation. In differentiating these rhythms, carotid sinus massage or edrophonium (5 to 10 mg given intravenously) traditionally was used. More recently, adenosine (6 to 12 mg by intravenous bolus) has been used to slow the rate by transiently enhancing the normal degree of atrioventricular block or terminate the arrhythmia.^[39] Esophageal electrocardiographic leads may also be helpful to better define atrial activity.^[40]
5. Significance: PSVT can be seen in 5% of normal young adults and in patients with Wolff-Parkinson-White syndrome or other preexcitation syndromes. During anesthesia, PSVT accounts for up to 2.5% of all arrhythmias, and the arrhythmia has been associated with intrinsic heart disease, systemic illness, thyrotoxicosis, digitalis toxicity, pulmonary embolism, and pregnancy. When a patient is under anesthesia, PSVT can be precipitated by changes in the autonomic nervous system tone, by drug effects, or by intravascular

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   volume shifts and can produce severe hemodynamic deterioration. Sometimes, the PSVT may be associated with atrioventricular block because of the fast atrial rate and slow atrioventricular conduction. PSVT with 2:1 block represents digitalis intoxication in many patients.
6. Treatment: This arrhythmia often must be treated because of its rapid rate and associated poor hemodynamic function. One or several of the following can be undertaken to treat this arrhythmia:
1. Vagal maneuvers such as carotid sinus massage should only be applied to one side.^{[41] [42] [43]}
2. Adenosine, which is the drug of choice, is given by 6-mg rapid intravenous bolus, preferably through an antecubital or more central vein. If no response is elicited, second and third doses of 12 to 18 mg of adenosine may be administered by rapid intravenous bolus.^[44]
3. Verapamil (2.5 to 10 mg given intravenously) terminates atrioventricular nodal reentry successfully in about 90% of cases. This was the drug of choice and is now the second choice.^[45]
4. Amiodarone (150 mg infusion over 10 minutes for the loading dose) is a recent addition.^[46]
5. Esmolol (1 mg/kg by bolus and 50 to 200 mg/kg/min by infusion) has been shown effective.^[47]
6. Edrophonium (5 to 10 mg by intravenous bolus) can be given.^[48]
7. Phenylephrine (100 µg by intravenous bolus) is administered if the patient is hypotensive.^[48]
8. Intravenous digitalization is performed with one of the short-acting digitalis preparations: ouabain (0.25 to 0.5 mg given intravenously) or digoxin (0.5 to 1.0 mg given intravenously).^[49]
9. Rapid overdrive pacing may be done in an effort to capture the ectopic focus.^[50]
10. Synchronized cardioversion may be performed with incremental doses of energy of 100, 200, 300, and 360 J, preferably after light sedative premedication with a benzodiazepine.^[51]
11. Procainamide is used in addition to cardioversion or antitachycardia pacing. Procainamide may be useful to treat SVT when antegrade conduction across an accessory atrioventricular path is the suspected mechanism.

Electrode catheter ablation using radiofrequency energy has evolved as the definitive, long-term treatment for most persistent atrioventricular reentrant or focal atrial SVT.^[52]

Atrial Flutter

Atrial flutter most commonly represents a macro-reentrant arrhythmia that circulates in a specific manner in the right atrium (i.e., counterclockwise rotation as viewed in the angiographic left anterior oblique view). Because it is associated with very fast heart rates, it is usually accompanied by atrioventricular block. Classic sawtooth flutter waves (F waves) are usually present. The characteristics of atrial flutter are as follows:

1. Heart rate: The atrial heart rate is 250 to 350 beats/min with a ventricular rate of about 150 beats/min (2:1 or 3:1 atrioventricular conduction block).
2. Rhythm: The atrial rhythm is regular. The ventricular rhythm may be regular if a fixed atrioventricular block is present or irregular if a variable block exists.
3. P:QRS: Usually, there is a 2:1 block with an atrial rate of 300 beats/min and a ventricular rate of 150 beats/min, but it may vary between 2:1 and 8:1. F waves are best seen in leads V₁ , II, and the esophageal lead.
4. QRS complex: Normal. T waves are lost in the f waves.
5. Significance: It usually indicates the presence of severe heart disease. It is seen with increased incidence in patients with coronary artery disease, mitral valve disease, pulmonary embolism, hyperthyroidism, cardiac trauma, cancers of the heart, and myocarditis.
6. Treatment: Pharmacologic or synchronized DC cardioversion, when indicated, should be performed only after careful consideration or evaluation of a possible thromboembolic event.

The initial treatment should be control of the ventricular response rate with agents that slow atrioventricular node conduction:

1. β-Blockers such as intravenous esmolol (1-mg/kg by intravenous bolus) or propranolol.
2. Calcium channel blockers such as verapamil (5 to 10 mg given intravenously) or diltiazem.^[53]
   If the ventricular response is excessively rapid or secondary hemodynamic instability is present, or both, use the following guidelines:
3. Synchronized direct current (DC) cardioversion starting with a relatively high energy of 100 J and gradually increasing to 360 J is indicated.^[54]
4. The class III antiarrhythmic agent ibutilide (Corvert, 1 mg in 10 mL saline, or D₅ W, infused intravenously slowly over 10 minutes) has been documented to convert atrial flutter to sinus rhythm in most patients with relatively new-onset atrial flutter.^[55] This may be repeated once, ^[56] and although it is highly effective, life-threatening torsade de pointes (discussed later) may occur hours after ibutilide administration, making 4- to 8-hour monitoring after treatment highly desirable.
5. Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no faster than 0.5 mg/kg/min) may rarely be used in an attempt to restore sinus rhythm after the ventricular response has been adequately controlled.^[57]
6. Treatment: Rapid atrial pacing from within the atrium enhanced by ibutilide or procainamide also effectively terminates atrial flutter.^[58]

Atrial Fibrillation

Atrial fibrillation is an excessively rapid and irregular atrial focus with no P waves appearing on the ECG; instead, a fine fibrillatory activity (f waves) is seen. This is the most irregular rhythm; it is called irregularly irregular and may be associated with a pulse deficit. The characteristics are as follows:

1. Heart rate: The atrial rate is 350 to 500 beats/min, and the ventricular rate is 60 to 170 beats/min.
2. Rhythm: Irregularly irregular.
3. P:QRS: The P wave is absent and is replaced by f waves or no obvious atrial activity at all.
4. QRS complex: Normal.
5. Significance: The causes of atrial fibrillation are similar to those of atrial flutter. This rhythm is often associated

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   with significant cardiac disease; however, idiopathic, lone paroxysmal atrial fibrillation has become increasingly recognized. The clinical significance and treatment of atrial fibrillation are also similar to those of atrial flutter, except for two important considerations. The loss of an atrial "kick" from inefficient contraction of the atria may reduce ventricular filling and may significantly compromise cardiac output. After 24 hours, atrial fibrillation may be associated with the development of atrial thrombi, with resultant pulmonary and systemic embolization.
6. Treatment:
1. Acute atrial fibrillation: The treatment of acute atrial fibrillation is very similar to that for atrial flutter. More attention should be focused on ventricular response, especially with the administration of intravenous diltiazem or esmolol. Ibutilide may restore sinus rhythm, but it is less effective than in the treatment of flutter.^{[55] [56]} Synchronized DC cardioversion should be relied on in patients with pronounced hemodynamic instability. However, if fibrillation is present for longer than 48 hours, attempts to restore sinus rhythm may be associated with a heightened risk of thromboembolism. In this setting for a patient with normal coagulation function, adequate anticoagulation for 3 to 4 weeks should be considered before attempting to restore sinus rhythm. New developments in electrophysiologic techniques for ventricular defibrillation with biphasic current shocks have shown superiority to the conventional monophasic current techniques (discussed later). However, data regarding biphasic shocks for conversion of AF are still emerging. A randomized, double-blind, multicenter trial by the BiCard Investigators^[59] demonstrated that for the cardioversion of atrial fibrillation, a biphasic shock waveform has greater efficacy, requires fewer shocks and lower delivered energy, and results in less dermal injury than a monophasic shock waveform. These results mirror those seen in the ventricular fibrillation trials.
2. Long-term therapy: Long-term therapy of atrial fibrillation varies and depends on factors such as whether the arrhythmia is constant or paroxysmal, the nature of the underlying heart disease, and the state of ventricular function or hemodynamic stability or reserve. In the older individual or in the setting of specific risk factors (e.g., hypertension, diabetes mellitus, severe left ventricular systolic dysfunction), anticoagulation with warfarin should be strongly considered. When control of ventricular response is difficult with standard agents (e.g., β-blockers, calcium channel blockers, digitalis), electrode catheter ablation of the atrioventricular junction and permanent pacemaker insertion have seen increased use. This is definitive, curative, and not merely a rate-control procedure. For patients who are in and out of atrial fibrillation, implanted atrial defibrillators have been introduced (see Chapter 35 ). They function automatically, much like the implanted ventricular defibrillators. A detailed discussion is beyond the scope here, but a review of their indications is available elsewhere.^[60] These devices bypass the limitations and eliminate the side effects of current drug therapies, which may be life threatening. In the absence of coronary artery disease or significant left ventricular systolic dysfunction, class Ic antiarrhythmic agents (i.e., flecainide or propafenone) have become the agents of choice.^[61] Use of class Ia drugs (i.e., quinidine, procainamide, and disopyramide) has sharply diminished because of concerns about their significant proarrhythmic function and their systemic and organ side effects. The use of antiarrhythmic drugs that block repolarizing potassium currents (i.e., sotalol^[62] and amiodarone^{[63] [64]} ) has gained popularity for the suppression of atrial fibrillation in individuals with significant structural heart disease. Sotalol, however, has a much lower efficiency of converting atrial fibrillation than class Ic agents.^[65] New class III agents show good efficacy in converting atrial fibrillation. Ibutilide converts rapidly, can be effective in up to 50% of cases,^[66] and is more effective than sotalol or procainamide.^{[67] [68]} Dofetilide, another class III agent, exhibits a 32% conversion rate over 72 hours.^[69] All these drugs exhibit significant proarrhythmic properties, which are summarized in Table 34-5 .^[70] Their efficacy in maintaining sinus rhythm in patients with atrial fibrillation is summarized in Table 34-6 .

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Junctional Rhythms

The atrioventricular node itself shows no intrinsic phase 4 depolarization. Cells in the node cannot act as pacemakers. Ectopic activity, however, may be initiated from sites just above and below the atrioventricular node. It makes sense to consider these arrhythmias as atrioventricular junctional in nature. The resultant P wave is abnormal and, depending on the position of the ectopic pacemaker, may be very close to, buried in, or after the QRS complex. Depending on the rate of fire of the ectopic pacemaker, the resultant rhythm is nodal premature, nodal quadrigeminy, trigeminy, or bigeminy, nodal rhythm, or nodal tachycardia.

1. Heart rate: Variable, 40 to 180 beats/min (i.e., nodal bradycardia to junctional tachycardia).
2. Rhythm: Regular.
3. P:QRS: 1:1 but, there are three varieties:
1. High-nodal rhythm: The impulse reaches the atrium before the ventricle; the P wave therefore precedes the QRS but has a shortened PR interval (0.1 second).
2. Mid-nodal rhythm: The impulse reaches the atrium and the ventricle at the same time. The P wave is lost in the QRS.
3. Low-nodal rhythm: The impulse reaches the ventricle first and then the atrium, so that the P wave follows the QRS complex.
4. QRS complex: Normal, unless altered by the P wave.
5. Significance: Junctional rhythms are common in patients under anesthesia (about 20%) especially with halogenated anesthetic agents. The junctional rhythms frequently decrease blood pressure and cardiac output by about 15%, but they can decrease it up to 30% in patients with heart disease.^[71]
6. Treatment: Usually, no treatment is required, and the rhythm reverts spontaneously. If hypotension and poor perfusion are associated with the rhythm, treatment is indicated. Atropine, ephedrine, or isoproterenol can be used in an effort to increase the activity of the sinoatrial node so it will take over as the pacemaker. Amiodarone is again the drug of choice in pharmacologic therapy. A small dose of succinylcholine (10 mg given intravenously) may revert a nodal rhythm to a sinus rhythm during anesthesia with halothane or enflurane. This probably works as a result of the effect of succinylcholine as a sympathetic ganglionic stimulator. In some cases, propranolol may correct the rhythm disturbance if it is caused by sympathetic stimulation. Dual-chamber electrical pacing at a rate faster than a slow nodal rhythm is another option.

Ventricular Premature Beats

VPBs result from ectopic pacemaker activity arising below the atrioventricular junction. The VPB originates in and spreads through the myocardium or ventricular conducting system, resulting in a wide (>0.12-second), bizarre QRS complex. The ST segment usually slopes in the direction opposite to that of the main deflection of the QRS complex. There is no P wave associated with a VPB, but retrograde depolarization of the atria or blocked sinus beats may obscure the diagnosis.

The most important entity in the differential diagnosis is APB with aberrant ventricular conduction. The distinction should be made whenever possible.

Although an APB normally reaches the sinoatrial node and resets the sinus rhythm, such an occurrence is rare when the ectopic pacemaker is in the ventricle. A VPB often blocks the next depolarization from the sinoatrial node, but the following sinus beat occurs on time. The result is a compensatory pause, consisting of the interval from the VPB to the expected normal QRS, which is blocked at the atrioventricular node, plus a normal sinus interval.

VPBs are common during anesthesia, accounting for 15% of observed arrhythmias. They are much more common in anesthetized patients with preexisting cardiac disease. Other than heart disease, known etiologic factors include electrolyte and blood gas abnormalities, drug interactions, brainstem stimulation, and trauma to the heart.

1. Heart rate: Depends on the underlying sinus rate and frequency of the VPBs.
2. Rhythm: Irregular.
3. P:QRS: No P wave with the VPB.
4. QRS complex: Wide and bizarre, with a width of more than 0.12 second. If it is of an RBBB nature, prominent R forces are present in V₁ . If it is a left bundle branch block (LBBB) in appearance, notching of the S wave and less acute downslopes are common.
5. Significance: The new onset of VPBs must be considered a life-threatening event because, in certain clinical situations, the arrhythmia may progress to ventricular tachycardia or fibrillation. These situations include coronary artery insufficiency, myocardial infarction, digitalis toxicity with hypokalemia, and hypoxemia. VPBs are more likely to lead to fibrillation if they are multiple, multifocal, or bigeminal; occur near the vulnerable period of the preceding ventricular repolarization (i.e., R-on-T phenomenon)^[72] ; or appear in short-long-short coupling sequences.
6. Treatment: The first step in treatment is to correct any underlying abnormalities such as decreased serum potassium or low arterial oxygen tension. If the arrhythmia is of hemodynamic significance or if it is believed to be a harbinger of worse arrhythmias, lidocaine is usually the treatment of choice, with an initial bolus dose of 1.5 mg/kg. Recurrent VPBs can be treated with a lidocaine infusion of 1 to 4 mg/min; additional therapy can be supplied with esmolol, propranolol,

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   procainamide, quinidine, disopyramide, atropine, verapamil, or overdrive pacing.

Ventricular Tachycardia

The presence of three or more sequential VPBs defines ventricular tachycardia. Diagnostic criteria include the presence of fusion beats, capture beats, and atrioventricular dissociation. The specific morphologic appearance of the QRS complex may also be helpful in distinguishing ventricular tachycardia from other arrhythmias. The characteristics of ventricular tachycardia are as follows:

1. Heart rate: 100 to 200 beats/min.
2. Rhythm: Usually regular, but may be irregular if the ventricular tachycardia is paroxysmal.
3. P:QRS: No fixed relationship because ventricular tachycardia is a form of atrioventricular dissociation in which the P waves can be seen marching through the QRS complex.
4. QRS complex: Wide, more than 0.12 second in width, with similar morphologic criteria in lead V₁ as for VPB.
5. Significance: Acute onset is life threatening and requires immediate treatment.
6. Treatment: Amiodarone administered as one or more doses of 150 mg given intravenously in 100 mL saline or D₅ W over 10 minutes, followed by an intravenous infusion of 1 mg/min for 6 hours and 0.5 mg/min thereafter, is the recommended current treatment (maximum intravenous dose 2.2 g/24 hours). Intravenous amiodarone has been as effective as bretylium. ^[73] Although amiodarone is associated with substantially less hypotension compared with bretylium, hypotension and bradycardia are its main side effects. Amiodarone's pharmacologic effects persist for more than 45 days. Lidocaine and procainamide have been used in the past with various degrees of success to treat ventricular tachycardia. Synchronized cardioversion is the indicated nonpharmacologic intervention in any wide complex tachycardia, whether monomorphic ventricular tachycardia or a wide complex supraventricular tachycardia. Polymorphic ventricular tachycardia with a normal QT interval is treated with amiodarone and cardioversion. Metabolic abnormalities and drug toxicity must be considered and treated. Polymorphic ventricular tachycardia with prolonged QT interval is a more serious rhythm disturbance and the recommended current treatment is intravenous infusion of 1 g of magnesium over 2 to 3 minutes. Precipitating metabolic or toxic causes should be treated. Overdrive pacing may also be helpful in this setting.

Ventricular Fibrillation

Ventricular fibrillation is an irregular rhythm that results from a rapid discharge of impulses from one or more ventricular foci or from multiple wandering reentrant circuits in the ventricles. The ventricular contractions are erratic and are represented on the ECG by bizarre patterns of various sizes and configurations. P waves are not seen. Important causes of the arrhythmia include myocardial ischemia, hypoxia, hypothermia, electric shock, electrolyte imbalance, and drug effects. The characteristics are as follows:

1. Heart rate: Rapid and grossly disorganized.
2. Rhythm: Totally irregular.
3. P:QRS: None seen.
4. QRS complex: Not present.
5. Significance: There is no effective cardiac output, and life must be sustained by artificial means, such as external cardiac massage.
6. Treatment: Cardiopulmonary resuscitation must be initiated immediately, and then defibrillation must be performed as rapidly as possible. Asynchronous external defibrillation should be performed with a DC defibrillator, using incremental energies in the range of 200 to 360 J. In extreme situations, the use of two defibrillators in tandem across the chest, with one applied in the anteroposterior direction and the second applied in the left midaxillary to right midaxillary direction, has been suggested. The two devices are discharged simultaneously to increase the likelihood of successful defibrillation. Animal studies have failed to demonstrate the superiority of dual-pathway simultaneous shocks over single-pathway shock.^[74] In contrast, introduction of the biphasic (and rectilinear) transthoracic shocks has reduced the energy levels required and increased the efficacy of ventricular defibrillation. In a prospective, randomized, multicenter trial conducted by the ZOLL Investigators,^[75] 120 joules of biphasic current were superior to 200 joules of monophasic current, especially in patients with increased chest wall impedance.

Early administration of 1g of magnesium sulfate may facilitate defibrillation. In some instances, epinephrine has been used to coarsen the fibrillation just before and to facilitate defibrillation. Vasopressin has been added as a drug for the treatment of ventricular fibrillation. The vasopressin dose is a single 40-unit intravenous bolus. If elected, subsequent administration of epinephrine should be not earlier than 5 minutes after vasopressin. Supportive pharmacologic therapy may include lidocaine, amiodarone, bretylium, procainamide, phenytoin, or esmolol.

Torsade de pointes, which may mimic ventricular fibrillation or ventricular tachycardia, is a life-threatening arrhythmia that occurs in the presence of disturbed repolarization (hence its association with prolonged QT interval).^[76] Discontinuation of drugs that predispose to QT-interval prolongation and correction of electrolyte abnormalities are essential in the treatment of torsades de pointes. Acute therapy may include defibrillation, 1 to 2 g of intravenous magnesium sulfate, intravenous amiodarone, intravenous isoproterenol, and overdrive pacing.^[77]