Intensive Care Unit Arrhythmias S.M. Hollenberg

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S.M. Hollenberg

Introduction

Arrhythmias are common in the intensive care unit (ICU) and represent a major source of morbidity and increased length of stay. Arrhythmias are most likely to occur in patients with structural heart disease. The inciting factor for an arrhythmia in a given patient may be a transient imbalance, often related to hypoxia, infection, cardiac ischemia, catecholamine excess (endogenous or exogenous), or an electrolyte abnormality. Management includes correction of these imbalances as well as medical therapy directed at the arrhythmia itself.

The physiologic impact of arrhythmias depends on ventricular response rate and duration. Bradyarrhythmias may decrease cardiac output due to heart rate alone in patients with relatively fixed stroke volumes, and loss of an atrial kick may cause a dramatic increase in pulmonary pressures in patients with diastolic dysfunction. Similarly, tachyarrhythmias can decrease diastolic filling and reduce cardiac output, resulting in hypotension, in addition to producing myocardial ischemia. Clearly, the impact of a given arrhythmia in a given situation depends on the patient’s cardiac physiology and function. Similarly, urgency and type of treatment is determined by the physiologic impact of the arrhythmia as well as by underlying cardiac status.

The purpose of this chapter is to provide an update regarding current concepts of diagnosis and acute management of arrhythmias in the ICU. A systematic approach to diagnosis and evaluation will be presented, followed by consideration of specific arrhythmias.

Diagnosis of Arrhythmias

Basic Principles

The first principle in managing arrhythmias is to treat the patient, not the electrocardiogram (EKG). Accordingly, one must first decide whether the problem is an arrhythmia or an artifact and whether the cardiac rhythm is sufficient to account for the patient’s problem.

The next step is to establish the urgency of treatment. Clinical assessment includes evaluation of pulse, blood pressure, peripheral perfusion, and the presence of myocardial ischemia and/or congestive heart failure. If the patient is unconscious or hemodynamically unstable in the presence of a tachyarrhythmia other than sinus tachycardia, prompt cardioversion is indicated. If the patient is stable, there is time to establish the rhythm diagnosis and decide upon the most appropriate course of

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treatment. Bradyarrhythmias produce less diagnostic challenge and treatment options are relatively straightforward.

The goals of antiarrhythmic therapy depend on the type of rhythm disturbance.

The initial goal for the treatment of tachyarrhythmias in the critical care unit is to slow the ventricular response (or to increase it in the case of a bradyarrhythmia).

The next goal is to restore sinus rhythm, if possible. If sinus rhythm cannot be restored, prevention of complications becomes an issue.

Evaluation of Bradycardias

A comprehensive description of the diagnosis of arrhythmias is beyond the scope of this chapter. A 12-lead EKG with a long rhythm strip and a previously obtained 12- lead EKG for comparison are ideal; If a previous EKG is not available, a systematic approach using a current 12 lead EKG is essential.

For evaluation of bradycardias, the first step is to locate the P wave. P-waves are often best seen in leads II and V₁. Normal p-waves are upright in leads II, III, and aVF, and may be biphasic in leads II and V₁. Ectopic atrial and junctional rhythms often present with negative P-waves in leads II, III, and aVF. The next step is to establish the relationship between the P-wave and the QRS complex. If there are more P-waves than QRS complexes, then AV block is present. If there are more QRS complexes than P-waves, the rhythm is likely an accelerated junctional or ventricular rhythm. If the relationship of the P-wave and QRS is 1:1, then measurement of the PR interval can yield useful diagnostic clues.

Management of Bradycardias

Sinus Node Dysfunction

Bradycardias associated with sinus node dysfunction include sinus bradycardia, sinus pause, sinoatrial block, and sinus arrest. These disturbances often result from increased vagal tone [1]. If bradycardia is transient and not associated with hemodynamic compromise, no therapy is necessary. If bradycardia is sustained or compro- mises end-organ perfusion, therapy with antimuscarinic agents, such as atropine, or beta agonists, such as ephedrine, may be initiated. Transcutaneous or transvenous pacing may be necessary in some cases.

Patients with a combination of bradycardia with paroxysmal atrial tachycardias due to preexisting conduction system disease can be challenging to manage pharma- cologically. In these cases, insertion of a temporary pacemaker may allow the administration of rate-lowering agents.

Heart Block

The most common cause of acquired chronic atrioventricular (AV) heart block is fibrosis of the conducting system. Although pre-existing conduction system disease is a risk factor for the development of complete heart block, no single laboratory or clinical variable identifies patients at risk for progression to high degree AV block [2]. In first-degree AV block there is prolongation of conduction time of the atrial impulses to the ventricles, with a PR interval greater than 200 msec. In second- degree AV block, conducted atrial beats are interspersed with non-conducted beats.

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Second-degree AV block is divided into Mobitz type I (Wenckebach) and Mobitz Type II block. In Mobitz I block, the PR interval lengthens progressively until the P wave fails to conduct. In most cases the block occurs at the AV node. Mobitz I block can occur in healthy individuals, the elderly and in patients with underlying heart disease. In Mobitz type II AV block the PR interval remains constant until a P wave fails to conduct. Mobitz II block occurs below the AV node, and thus is more dan- gerous since it is much more likely to progress to complete heart block. In third- degree AV block none of the atrial impulses are conducted to the ventricles. The escape rhythm, whether junctional or ventricular, is generally regular.

Asymptomatic bradyarrhythmias do not carry a poor prognosis and in general no therapy is necessary [3]. If organ perfusion is compromised, or hemodynamic instability occurs, one or two doses of atropine (1.0 mg i.v.) may be tried, but pacing may be required. Pacing may also be useful in patients with bradycardia-tachycardia (“sick sinus”) syndrome, in whom treatment for tachycardia results in symptomatic bradycardia.

Conduction abnormalities, either transient or permanent, can complicate acute myocardial infarctions. Conduction abnormalities associated with an acute inferior myocardial infarction usually result from AV nodal ischemia, are transient, and carry a low mortality rate. Conduction abnormalities in association with an acute anterior myocardial infarction, however, represent extensive necrosis of the infra- nodal conduction system and the myocardium, and are associated with high in-hos- pital mortality [4]. The ACC/AHA/NASPE recommended guidelines for temporary pacing in patients with an acute myocardial infarction are shown in Table 1.

Table 1. Recommendations for temporary transvenous pacing after an acute myocardial infarction. Adapted from [49]

Class I 1. Asystole

2. Symptomatic bradycardia

3. Bilateral bundle branch block (alternating BBB or RBBB with alternating LAFB/LPFB, any age) 4. New or indeterminate-age bifascicular block (RBBB with LAFB or LPFB, or LBBB) with first-degree

AV block

5. Mobitz type II second-degree AV block Class IIa

1. RBBB and LAFB or LPFB (new or indeterminate).

2. RBBB with first-degree AV block 3. LBBB, new or indeterminate.

4. Incessant VT, for atrial or ventricular overdrive pacing.

5. Recurrent sinus pauses (greater than 3 seconds) not responsive to atropine.

Class IIb

1. Bifascicular block of indeterminate age.

2. New or age-indeterminate isolated RBBB.

Class III

1. First degree heart block.

2. Type I second-degree AV block with normal hemodynamics.

3. Accelerated idioventricular rhythm.

4. BBB or fascicular block known to exist before AMI

RBBB: right bundle branch block; LBBB: left bundle branch block; LAFB: left anterior fascicular block; LPFV:

left posterior fascicular block; AMI: acute myocardial infarction.

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Evaluation of Tachyarrhythmias

The first step in the evaluation of the critically ill patient with a tachyarrhythmia is to assess hemodynamic stability. If hemodynamics are compromised due to the arrhythmia, cardioversion should be performed unless pharmacologic treatment is immediately successful. However, before proceeding with cardioversion, one should consider whether the arrhythmia is in fact the basis for the deterioration in hemodynamics.

The next step in evaluation is to determine whether the arrhythmia is supraventricular or ventricular in origin. First, one examines QRS width. A narrow QRS complex (‹ 0.12 seconds) indicates a supraventricular tachycardia (SVT). One should try not to rely solely on a rhythm strip from one monitor lead for diagnosis, as there can be variability in QRS width depending on which lead is examined. A 12-lead EKG is more useful, and may also identify Q waves indicative of prior myocardial infarction or other abnormalities. Comparison with a previous EKG can be useful as well, to identify pre-existing bundle branch block, for example.

Carotid sinus massage and other maneuvers that increase vagal tone, slows AV conduction time and increases refractoriness, and this can aid in the diagnosis through demonstration of P waves or interruption of a re-entrant supraventricular tachycardia. Intravenous adenosine (6 mg bolus, with a second dose of 12 mg 1 to 2 minutes later if there is no response) can also be used for this purpose. The effects are more pronounced when given through a central venous line, in which case the dosage is usually halved. Responses to vagal maneuvers or adenosine are listed in Table 2. Side effects include bronchospasm, proarrhythmia (a 2.7 % incidence of induction of atrial fibrillation has been reported) [5], and also ventricular tachycardia (VT) and fibrillation [6], as well as bradycardia including asystole; these effects are usually transient because the half-life of adenosine is only 6 to 10 seconds.

VT can be diagnosed using some clinical and EKG clues. VT is approximately four times more common than SVT with aberrancy [7]. VT is much more common in patients who have a history of myocardial infarction or heart failure. Circulatory collapse is more common with VT than SVT, but patients with VT may maintain a normal blood pressure. A careful review of medications is important to exclude iat- rogenic causes of VT.

A QRS width of more than 0.14 seconds with right bundle branch block (RBBB) or 0.16 seconds during left bundle branch (LBBB) block favors VT [8]. Comparison of QRS morphology during the tachycardia with the morphology of ventricular premature beats in sinus rhythm can be helpful. Marked left axis deviation (–60° to – 120°) may indicate a ventricular origin of the arrhythmia. Other diagnostic clues suggestive of VT are fusion and capture beats, but these are seen in only 20 – 30 % of

Table 2. Differentiation of tachycardias by response to vagal maneuvers Arrhythmia Response to vagal maneuvers/adenosine

Sinus tachycardia Gradual slowing with resumption of the tachycardia AVNRT Abrupt termination or only very transient slowing

Atrial fibrillation/flutter Increased AV block briefly with slowed ventricular response rate Multifocal atrial tachycardia Increased AV block briefly with slowed ventricular response rate Ventricular tachycardia Usually no response

AV: atrioventricular; AVNRT: AV nodal re-entrant tachycardia.

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cases of VT [9]. Fusion beats, a hybrid of the supraventricular and ventricular complexes, occur when two impulses, one supraventricular and one ventricular, simulta- neously activate the same territory of ventricular myocardium. The implication is that the wide complexes are ventricular. Capture beats are occasional beats conducted with a narrow complex, and such beats rule out fixed bundle branch block.

AV dissociation is diagnostic of VT, but is present in less than 50 % of cases of VT and is difficult to identify at faster heart rates.

It is better to err on the side of overdiagnosis of VT. In a study analyzing adverse events incurred by patients with VT misdiagnosed as SVT and given calcium channel blockers [10], many of the patients decompensated promptly and some required resuscitation, despite the fact that all study patients were hemodynamically stable when first seen in VT.

It is also noteworthy that ST segment depression during SVT lacks specificity in predicting ischemia. In one series of 100 patients with SVT, associated ST segment deviation was only 51 % specific (with a positive predictive value of only 6 %) for significant angiographic coronary artery disease or scintigraphic evidence of ischemia [11].

It is useful to divide SVTs into regular and irregular rhythms, as this narrows the differential diagnosis and therapeutic options. Regular narrow complex SVT include sinus tachycardia, atrioventricular node reentrant tachycardia (AVNRT), AV re- entrant tachycardia (AVRT), ectopic atrial tachycardia, and atrial flutter with fixed conduction.

Management of Regular Narrow Complex Tachycardias

Sinus Tachycardia

Sinus tachycardia often occurs as a response to a sympathetic stimulus, such as hypoxia, vasopressors, inotropes, pain, hypovolemia, or hyperthyroidism. Treatment focuses on identifying and trying to correct the underlying cause. If ischemia is the cause and treatment is warranted, beta-blockers are the first treatment option. How- ever, it is worth considering that the sinus tachycardia may be an appropriate hemodynamic response to hypotension, hypovolemia, or low cardiac output; if this is the case, overzealous use of beta-blockers can reduce cardiac output, with potentially disastrous consequences.

AV Nodal Reentrant Tachycardia

AVNRT typically occurs with sudden onset at a heart rate of 140 – 180 beats per minute. It is more prevalent in females and is not usually associated with structural heart disease. AVNRT involves dual AV nodal pathways and re-entry. Typical AVNRT is initiated by a premature atrial contraction that conducts antegrade down a slow AV pathway with a short refractory period and then retrograde up a fast AV pathway with a long refractory period (which had been refractory to antegrade conduction when the premature beat occurred but has now recovered) (Fig. 1).

The key to treatment is to block AV conduction. Acute treatment may include Vagal maneuvers and intravenous adenosine may terminate the re-entrant cycle, or other AV nodal blockers, such as non-dihydropyridine calcium-channel blockers, beta-blockers, and digoxin may be used [12]. Preventive therapy usually entails medications that suppress the initiating premature atrial contractions, with beta-

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Fig. 1. a Atrioventricular (AV) node demonstrating dual pathways: a slow pathway with a short refractory period and a fast pathway with a long refractory period. b A premature impulse conducts down the slow pathway while the fast pathway is still refractory to conduction. c As the impulse conducts down slow pathway, the fast pathway recovers. d The impulse goes up fast pathway and also conducts to the ventri- cle. e The impulse cycles around the AV node, completing the re-entrant circuit.

blockers as the first choice. Catheter ablation of one of the pathways is another option for recurrences refractory to medications.

AV Re-entrant Tachycardia (Wolff-Parkinson White Syndrome)

AVRT using an accessory bypass tract occurs in 0.1 to 0.3 % of the general population. The accessory pathway bypasses the AV node and can activate the ventricles prematurely in sinus rhythm, producing the characteristic delta wave. The diagnosis of Wolff-Parkinson White syndrome (WPW) is reserved for patients with both preexcitation and tachyarrhythmias. In AVRT, conduction can go down the bypass tract and back up the AV node, producing a wide QRS complex (antidromic) or down the

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AV node and back up the bypass tract, producing a narrow QRS complex (orthodro- mic). AVRT should be suspected in any patient whose heart rate exceeds 200 bpm.

Atrial fibrillation (AF) is a potentially life-threatening arrhythmia in patients with WPW syndrome, as it can generate a rapid ventricular response with subsequent degeneration into ventricular fibrillation. This is important, as one third of patients with WPW syndrome have AF [13].

Adenosine should be used with caution in any young patient suspected of having WPW as it may precipitate AF with a rapid ventricular response rate down an antegrade accessory pathway. Procainamide, ibutilide, and flecainide are preferred agents, since they slow conduction through the bypass tract. The long-term treatment of choice for symptomatic patients is radiofrequency catheter ablation of the accessory pathway.

Management of Irregular Narrow Complex Tachycardias

Irregular narrow complex SVT includes atrial fibrillation, multifocal atrial tachycardia, atrial flutter with variable block, and sinus tachycardia with frequent premature atrial complexes.

Atrial Flutter and Fibrillation

Atrial flutter is a macro-re-entrant arrhythmia identified by flutter waves often best seen in the inferior leads, at 250 to 350 bpm. Patients often present with two-to-one AV conduction with a ventricular rate of 150 bpm, although the AV conduction ratio can change abruptly. Acute treatment consists of AV-nodal-blocking drugs for rate control. If the patient becomes clinically unstable, low energy DC-synchronized cardioversion (50 – 100 joules) has a success rate of 95 to 100 % [14]. Intravenous ibutilide converted about 75 % of patients to sinus rhythm in clinical trials, but prolongs the QT interval, and can provoke sustained polymorphic VT in 1 – 2 % of cases. Ibu- tilide should not be used in patients with a prolonged QT_cinterval (greater than 420 msec) [15, 16]. If a temporary or permanent pacemaker with an atrial lead is in place, atrial overdrive (burst) pacing can sometimes restore sinus rhythm via overdrive suppression.

Atrial fibrillation is the most common narrow complex tachyarrhythmia in the ICU [17]. The prevalence of atrial fibrillation in the general population increases exponentially with age [18]. The most important risk factors for development of AF in the general population are structural heart disease (70 % in Framingham study over 22 year follow-up), hypertension (50 %) [19], valvular heart disease (34 %) [20], and left ventricular hypertrophy.

The three goals of therapy for atrial fibrillation are to control the rate, to restore and maintain normal sinus rhythm, and to prevent complications. Pharmacologic agents for acute rate control include beta-blockers, non-dihydropyridine calcium channel blockers, and digoxin.

Beta-blockers provide more effective rate control than calcium channel blockers at rest and during exercise [21]. The intravenous medication most often used is metoprolol given at 2.5 – 5 mg i.v. over 1 – 2 minutes every 5 – 10 minutes for a total of 15 mg as blood pressure tolerates. Esmolol, 0.5 mg/kg bolus, then 0.05 mg/kg/min infusion, is an alternative with a more rapid onset and offset, which can be useful in unstable patients.

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Non-dihydropyridine calcium channel blockers (diltiazem and verapamil) are also effective AV nodal blockers. Verapamil may have more negative inotropic prop- erties than diltiazem and thus may induce hypotension in patients with left ventricular dysfunction and borderline blood pressure [22]. Diltiazem is available in i.v.

form and is commonly used as a continuous infusion at a rate of 5 – 15 mg per hour.

Digoxin controls ventricular response through a centrally mediated vagal mecha- nism and by direct action on the AV node. It controls resting heart rates in patients who do not have increased catecholamine levels, but is less effective in the ICU.

Intravenous digoxin begins to slow the heart rate in 30 minutes [23].

Hemodynamically unstable patients with atrial fibrillation require emergent cardioversion without waiting for prior anticoagulation, and those with acute heart failure or ischemia should be considered for urgent cardioversion. Electrical cardioversion may be more effective when the defibrillator pads are placed in an anterior/posterior orientation to direct the current through the atria.

For other patients, cardioversion carries a stroke risk, even if the duration of atrial fibrillation is less than one week [24]. Due to delay between resumption of organized atrial electrical activity and of organized mechanical contraction, there can be delay between cardioversion and embolic events ranging from 6 hours to 7 days [25]. Anti- coagulation with i.v. heparin should be considered if atrial fibrillation persists for greater than 48 hours. The stroke risk in non-anticoagulated patients taken as a whole is about 2 % per year (0.05 % per day), but individual factors modulate that risk. The risk factors for stroke are heart failure, hypertension, age 8 75 years, diabe- tes, prior history of transient ischemic attack or stroke, and female gender [26].

Post-operative atrial fibrillation is common, especially after cardiac surgery, when the incidence is 25 to 40 % of patients, with peak onset on day two [27, 28]. There are numerous risk factors for postoperative atrial fibrillation, with advanced age being the most important. Rate control should be initiated, but atrial fibrillation often runs a self-correcting course in this setting, with resumption of sinus rhythm in more than 90 % of patients by 6 – 8 weeks after surgery, and so cardioversion is not always necessary [29]. Immediate cardioversion should be performed in patients with recent onset atrial fibrillation accompanied by symptoms or signs of hemodynamic instability resulting in angina, myocardial ischemia, shock, or pulmonary edema without waiting for prior anticoagulation.

Antiarrhythmic agents may be chosen to reduce the risk of recurrence of atrial fibrillation. The choice of an antiarrhythmic agent depends on the clinical setting.

Propafenone may be used in patients without structural heart disease, although other agents may be more effective. Sotalol can be used for adrenergically mediated atrial fibrillation. Amiodarone is recommended as the first line drug in patients with structural heart disease, with dofetilide as an alternative. Class IC antiarrhythmic agents (flecainide, encainide, moricizine) should be avoided in patients with coronary heart disease due to the increased mortality shown in the Cardiac Arrhythmia Suppression Trial (CAST) [30, 31].

Multifocal Atrial Tachycardia

Multifocal atrial tachycardia is an irregular atrial tachycardia diagnosed by identifi- cation of three or more P wave morphologies and PR intervals. Multifocal atrial tachycardia is most often associated with hypoxia in the setting of pulmonary disease, but may occasionally be due to use of theophylline, metabolic derangements, and end-stage cardiomyopathy. Treatment consists of correcting hypoxia by treating

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underlying pulmonary disease and/or correcting electrolyte abnormalities [32]. AV nodal blockers are sometimes useful to control the ventricular response in the interim.

Ventricular Tachycardia

VT can be monomorphic or polymorphic, sustained or non-sustained. Sustained VT is defined as persisting for longer than 30 seconds; non-sustained VT has at least 3 or more ventricular beats but lasts less than 30 seconds. Differentiation of VT into monomorphic and polymorphic varieties is useful because they occur in different settings and respond differently to treatment. Polymorphic VT, in turn, can be divided into that with a long QT interval (torsades de pointes) and that without QT prolongation, which is an ischemic rhythm. Three or more distinct episodes of ventricular tachycardia or fibrillation within a 24 hour period is termed ventricular storm.

Non-sustained VT is fairly common following a myocardial infarction. Prognosis is dependent upon the timing of onset of VT in relation to the incident myocardial infarction. Non-sustained VT occurring during the first 48 hours of myocardial infarction is most likely related to myocardial reperfusion and has no prognostic significance. However, non-sustained VT occurring more than 1 week after myocardial infarction doubles the risk of sudden cardiac death in patients with preserved left ventricular (LV) function [33]. Evaluation for recurrence of ischemia is appropriate, as is assessment of LV performance. The risk of sudden cardiac death is increased more than five-fold in patients with LV dysfunction (ejection fraction less than 40 %) [34].

Monomorphic Ventricular Tachycardia

Sustained monomorphic VT is a re-entrant rhythm that usually occurs from a fixed substrate rather than acute ischemia; it most commonly occurs more than 48 hours after a myocardial infarction, or in the setting of cardiomyopathy. Initial management of sustained monomorphic VT with a history of structural heart disease depends on its rate, duration, and the patient’s hemodynamic status. Unstable VT is an indication for prompt defibrillation. Hemodynamically stable patients with a risk of imminent circulatory collapse may be treated with an antiarrhythmic such as i.v.

amiodarone. Amiodarone can be given as a 150 mg i.v. bolus over 10 minutes followed by an infusion of 360 mg (1 mg/min) over six hours, and then 540 mg (0.5 mg/min) over the remaining 18 hours. Bradycardia and hypotension can result from i.v. amiodarone, in which case the rate of the infusion should be decreased. Current ACLS guidelines consider lidocaine and i.v. procainamide alternative choices, although lidocaine is more effective in VT due to ischemia than that due to post- infarction scar. Lidocaine is administered by i.v. bolus of 0.5 to 0.75 mg/kg, followed by continuous infusion at 1 to 4 mg/min. Procainamide is administered at 20 mg/

min i.v. for a loading dose of 17 mg/kg, then continued as an infusion at 1 to 4 mg/

min. The infusion should be stopped if the patient becomes hypotensive or the QRS widens by 50 % above baseline. The most serious side effects of procainamide are hypotension and proarrhythmia (most commonly torsades de pointes), both of which increase in frequency in patients with renal insufficiency because of decreased excretion.

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Recurrent monomorphic VT is an indication for i.v. antiarrhythmic drug therapy, with either amiodarone, lidocaine, or procainamide. Enthusiasm for the use of chronic antiarrhythmic agents to prevent ventricular arrhythmias was considerably dampened after CAST, which showed an increase in mortality in patients receiving flecainide or encainide in patients with coronary artery disease [30]. There has been concern that other antiarrhythmic agents could have the same proarrhythmic effects. Available data suggest that amiodarone and sotalol are the most effective antiarrhythmic drugs for preventing sustained VT.

Clinical trials comparing insertion of automated implantable cardioverter defibrillators (AICD) to antiarrhythmic drug therapy have generally shown a benefit for AICD placement, particularly in high-risk patients with decreased ejection fraction or inducible sustained VT [35, 36]. The MADIT-II (Multicenter Automatic Defibrilla- tor Implantation-II) trial demonstrated that prophylactic placement of an ICD in patients with LV ejection fraction (LVEF) e 30% after myocardial infarction improved survival [37]. The timing of ICD implantation however, is uncertain. In the recent DINAMIT (Defibrillator in Acute Myocardial Infarction Trial) study, placement of an ICD immediately after a myocardial infarction did not reduce all- cause mortality [38]. and analysis of MADIT-II demonstrated that patients with a remote myocardial infarction (at least 18 months previous) benefited greatly from the ICD, whereas those with a more recent myocardial infarction (less than 18 months) did not [39]. Data from the SCD-Heft (Sudden Cardiac Death-Heart Fail- ure) trial also showed a survival benefit in patients with either an ischemic or a non- ischemic cardiomyopathy and EF ‹ 35 % after implantation of an ICD compared to amiodarone [40]. Due to the outcomes of these trials, referral for ICD implantation is recommended for survivors of sudden cardiac death and patients with a previous myocardial infarction and LVEF of less than 35 %.

Polymorphic Ventricular Tachycardia

Polymorphic VT with a normal QT interval is considered to be an ischemic rhythm that typically degenerates into ventricular fibrillation (VF). It is almost never asymptomatic and thus direct current synchronized cardioversion is the initial recommended treatment. Polymorphic VT with a normal corrected QT (QTc) is a more ominous sign than monomorphic VT in patients with myocardial ischemia. Medica- tions that might predispose to ischemia, such as inotropes or vasopressors, should be stopped or tapered, if possible, and beta-blockers started if blood pressure per- mits. Intra-aortic balloon pumping may be useful as a supportive measure, but revascularization is usually required. If withdrawal of vasopressors is contraindi- cated on a clinical basis, intravenous infusion of lidocaine or amiodarone should be initiated.

Torsades de Pointes

Torsades de pointes (‘twisting of the points’) is a syndrome comprised of polymorphic VT and a prolonged QTc interval (by definition & 460 msec). This may be due to various medications, including procainamide, disopyramide, sotalol, phenothia- zines, quinidine, some antibiotics (erythromycin, pentamidine, ketoconazole), some antihistamines (terfenadine, astemizole), and tricyclic antidepressants. Other etiolo- gies include hypokalemia, hypocalcemia, subarachnoid hemorrhage, congenital prolongation of the QTc interval, and insecticide poisoning [41]. A key to treatment is

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correction of any exacerbating factors and normalization of electrolyte disturbances, particularly hypomagnesemia, hypocalcemia, and hypokalemia. Magnesium (1 – 2 grams i.v.) should be given to all patients, without the need to check a level before- hand. Other potential treatments may include overdrive pacing, isoproterenol, or atropine to increase heart rate and thus shorten QTc.

Electrical Storm

The definition of electrical storm is more than three distinct episodes of VT/VF within a 24-hour period [42]. In patients with ventricular arrhythmias requiring ICD placement, the incidence of ventricular storm ranges from 10 to 30 % with the first episode occurring at an average of 133 „ 135 days after implantation [43, 44].

An identifiable precipitating factor (hypokalemia, myocardial ischemia, or prior exacerbation of acute heart failure) was found in only 26 % of the patients.

Evaluation should include measurement of serum electrolytes, obtaining an EKG, and investigation for ischemic heart disease, which may include coronary angiogra- phy. Proarrhythmia due to antiarrhythmic drugs that slow conduction velocity prominently, such as flecainide, propafenone, and moricizine, should be excluded [45, 46]. Treatment for proarrhythmia consists of hemodynamic support until the drug is excreted.

While exacerbating factors (acute heart failure, electrolyte abnormalities, proarrhythmia, myocardial ischemia, and hypoxia) are corrected, repeated doses of intravenous amiodarone should be given, even if the patient is already on oral amiodarone [47]. Deep sedation can help reduce sympathetic activation. Mechanical venti- latory support and i.v. beta-blockers can be used in conjunction, but i.v. amiodarone is the pharmacologic treatment of choice for this condition. If pharmacologic therapy and antitachycardia pacing are unsuccessful, electrophysiology mapping guided catheter ablation can be considered, although this is often difficult in unstable patients [48]. The prognosis of patients with electrical storm after ICD implantation is poor, with a 2.4-fold increase in the risk of subsequent death, independent of ejection fraction. The risk of sudden cardiac death is greatest three months after an electrical storm.

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