Chapter 24. Cardiac Arrhythmias, Pacing, Cardioversion, and Defibrillation in the Critical Care Setting

• Correct diagnoses and understanding of arrhythmia mechanisms are crucial to successful arrhythmia management.
• The hemodynamic effects of an arrhythmia are important in developing an appropriate treatment strategy.
• Predisposing conditions and reversible causes should be recognized and corrected.
• Knowledge of antiarrhythmic drug therapy, cardiac pacing, electrical cardioversion, and defibrillation are essential to successful arrhythmia management.
• The proarrhythmic potential of antiarrhythmic drugs must be recognized and preventive measures taken whenever possible.
• Knowledge of antiarrhythmic drug pharmacokinetics and pharmacodynamics and the effect of multisystem organ disease on these parameters are important in preventing drug toxicity.
• The intensivist should be skilled in the implantation of temporary pacing systems, external cardioversion, and defibrillation.
• The intensivist should recognize when temporary and implantable pacemakers or cardioverter defibrillators are not functioning appropriately.
• Not all arrhythmias require long-term prophylactic treatment.

Cardiac arrhythmias are common in the critical care setting. Many arrhythmias detected are benign, may occur in healthy individuals, and require no investigation or treatment (e.g., sinus tachycardia, sinus bradycardia, Mobitz type I second-degree atrioventricular [AV] block, or premature atrial and ventricular beats). Correct diagnosis and understanding of arrhythmia mechanisms and knowledge of antiarrhythmic drug pharmacology and nonpharmacologic therapies of arrhythmias are crucial for successful arrhythmia management. This chapter focuses on the mechanisms, investigation, and management of the most common, clinically significant arrhythmias encountered.

Mechanisms

Tachycardia mechanisms have been classified as due to abnormalities of impulse formation or impulse conduction.1–3 Abnormalities of impulse formation may be due to normal automaticity, abnormal automaticity, or triggered activity occurring within atrial or ventricular muscle tissue or the specialized conduction system (Fig. 24-1A).1,2 Natural pacemaker cells are found in the sinus node, parts of the atria, the atrioventricular node, and the His-Purkinje system. These cells exhibit phasic spontaneous depolarization during diastole, resulting in an action potential when the threshold potential is reached.1 Although the sinus node is the dominant pacemaker in the normal heart, subsidiary pacemakers may become dominant under certain conditions, such as sympathetic stimulation or digitalis toxicity (see Fig. 24-1). Normal atrial and ventricular muscles maintain a high negative resting potential (−90 mV) and only depolarize when stimulated. Under certain pathophysiologic conditions, including electrolyte abnormalities and ischemia, the resting membrane potential may decrease (−60 mV) and cells may depolarize spontaneously.

Triggered activity is caused by after-depolarizations that occur early in repolarization (early after-depolarizations) or after repolarization is complete (delayed after-depolarizations; see Fig. 24-1B).1,2 Early after-depolarizations may reach threshold to activate the slow inward current generating a new action potential, and this cycle may repeat, generating a sustained tachycardia. Early after-depolarizations are believed to be the mechanism of torsade de pointes ventricular tachycardia (VT).2 Delayed after-depolarizations initiate a triggered response only when their amplitude reaches a critical threshold (see Fig. 24-1C). Increasing the heart rate or the prematurity of an extrastimulus increases the amplitude of a delayed after-depolarization, thus increasing the probability of inducing a tachycardia. Delayed after-depolarizations are thought to cause arrhythmias secondary to digitalis toxicity.

Abnormalities of impulse conduction are due primarily to reentry (see Fig. 24-1).3 Reentry requires an area of fixed or functional unidirectional block in one pathway, slow conduction in an alternate pathway, and return of the impulse along the original path after this tissue has recovered excitability (see Fig. 24-1D). Reentry is the mechanism of many types of supraventricular tachycardias (SVTs; atrioventricular node reentry or in the Wolff-Parkinson-White syndrome) and VT that occur after a myocardial infarction. Table 24-1 summarizes the mechanisms of common tachyarrhythmias.

Antiarrhythmic drug therapy may be required for the termination of tachyarrhythmias and prevention of recurrence. Knowledge of the potential mechanisms of an arrhythmia and of the pharmacology of antiarrhythmic drugs are important in selecting appropriate drug therapy. Because the critical care patient often has multisystem disease, special attention to factors that influence drug absorption, protein binding, drug metabolism and excretion and knowledge of potential drug interactions are essential (see Chap. 103).4

The cardiac action potential varies strikingly in duration and morphology in specific regions of the heart, reflecting differences in ion channel expression or differences in modulators of ion channel function.4 Antiarrhythmic drugs may therefore exert different effects on these various cardiac cells. Moreover, the effects of antiarrhythmic drugs may be modified in diseased cardiac tissue. For example, the effects of sodium channel blockers may be exaggerated in ischemic myocardium, and the effects of potassium channel blockers may be exaggerated in the setting of left ventricular hypertrophy.4 Antiarrhythmic drugs are classified most commonly by their dominant mechanism of action.4–6 However, this drug classification scheme is imperfect because many of these drugs have effects on multiple ion channels or cell membrane receptors (Table 24-2). Efficacy of one drug does not predict the efficacy of another drug in the same class.

Class I drugs block the inward sodium current, resulting in slowing of conduction in atrial and ventricular muscles.6 Their subclassification is based on the rate of recovery from sodium channel block. Class Ia antiarrhythmic drugs have an intermediate rate of recovery of sodium channel block and may cause prolongation of the QRS duration at physiologic heart rates. Class Ib drugs have a rapid recovery from sodium channel block and thus slow ventricular conduction only at very rapid heart rates. Class Ic drugs have a slow rate of recovery from sodium channel block and may cause significant prolongation of the QRS duration at resting heart rates. Class Ia and Ic drugs also block different potassium channels that cause prolongation of the atrial and ventricular action potential durations. This may manifest as prolongation of the QT interval. Class II drugs are β-adrenergic receptor blocking drugs.7 Some of these agents are selective β1-receptor blockers (see Table 24-2). Class III drugs are predominantly potassium channel blockers and prolong repolarization in atrial and ventricular muscle.8 They can cause significant prolongation of the QT interval. Class IV drugs are calcium channel blocking drugs that decrease intracellular calcium concentrations.7

The mechanisms of action of commonly used antiarrhythmic drugs are listed in Table 24-2. Many of these agents are used to treat supraventricular and ventricular arrhythmias. Perhaps the most serious adverse response to antiarrhythmic drugs is the risk of proarrhythmia.9,10 Proarrhythmia is defined as provocation of a new arrhythmia or worsening of an existing arrhythmia during therapy with a drug at concentrations not considered to be toxic. Class Ia and Ic drugs may cause excessive slowing of conduction in diseased atrial or ventricular muscle tissue that may exacerbate the clinical arrhythmia (e.g., atrial flutter or VT). These drugs increase the risk of sudden cardiac death in patients after myocardial infarction. Thus, class I antiarrhythmic drugs are contraindicated in patients with ischemic heart disease and a prior myocardial infarction because of the risk of ventricular proarrhythmia. Drugs that cause excessive prolongation of the QT interval may cause torsade de pointes VT.4,9,10 Torsade de pointes VT may occur in 1% to 8% of patients exposed to QT interval prolonging antiarrhythmic drugs.4

The pharmacokinetic characteristics of commonly used antiarrhythmic drugs are summarized in Table 24-3.6,11–14 Drug dosing, adverse effects, and potential interactions are listed in Table 24-4.4,6–8,11,15,16 Adverse effects may develop from pharmacokinetic or pharmacodynamic drug interactions. Pharmacokinetic drug interactions develop when one drug modifies the absorption, distribution, metabolism, or elimination of a second drug, such as warfarin with amiodarone or digitalis with quinidine.4,11 Pharmacodynamic interactions occur when a drug or condition increases or decreases the pharmacologic effect of a drug without changing plasma drug concentrations, such as increased protein binding of propafenone, verapamil, or lidocaine secondary to elevated α1-acid glycoprotein after myocardial infarction.11 Several enzymes in the cytochrome P450 family are responsible for drug metabolism. Some drugs may inhibit or induce these enzymes, resulting in important drug interactions (see Table 24-4).4,11,12

Ventricular Tachyarrhythmia Classification and Mechanisms

Sustained ventricular arrhythmias including monomorphic VT, polymorphic VT, and ventricular fibrillation (VF) usually occur in the setting of structural heart disease, most frequently in the setting of coronary artery disease, previous myocardial infarction, and poor left ventricular function.17 However, any form of structural heart disease may be associated with ventricular arrhythmias. In addition, some individuals have primary electrical disease, usually associated with a mutation affecting one or more ion channels or proteins that regulate ion channels, as in the long QT syndrome and Brugada syndrome.18

The QRS complexes are uniform in monomorphic VT, whereas the QRS complexes change continuously in polymorphic VT. In VF, the surface electrocardiogram is disorganized without discernible QRS complexes. VT frequently precedes the development of VF, particularly in patients with a prior history of myocardial infarction. These arrhythmias are considered to be sustained if they last longer than 30 seconds or if they require acute intervention for termination.14,19

Multiple mechanisms contribute to VT. Monomorphic VT that develops in patients with a prior myocardial infarction is due to reentry near the border of the scar. In patients with dilated cardiomyopathy and an underlying intraventricular conduction delay, monomorphic VT usually with a left bundle branch block pattern may develop due to bundle branch reentry. In patients without structural heart disease, catecholamine-sensitive VT may originate in the right ventricular outflow tract due to triggered activity initiated by cyclic adenosine monophosphate. A verapamil-sensitive monomorphic VT that originates in the region of the left posterior fascicle is thought to be due to triggered activity.18

Polymorphic VT in the setting of a normal QT interval usually occurs in the setting of acute ischemia or significant hemodynamic instability,20 although it may also occur in otherwise healthy individuals due to a mutation of the ryanodine receptor.21 Torsade de pointes VT is a polymorphic, pause-dependent VT that develops in association with drugs or pathophysiologic conditions that excessively prolong the QT interval (Fig. 24-2 and Table 24-5).7,8 Torsade de pointes VT is initiated by focal triggered activity and maintained by ventricular reentry. Risk factors for the development of torsade de pointes VT include female sex, baseline QT interval prolongation, excessive QT interval prolongation on drug therapy (>550 ms), bradycardia/pauses, hypokalemia, hypomagnesemia, congestive heart failure, cardiac hypertrophy, prior history of VT or VF, and renal impairment. The drugs and pathophysiologic conditions associated with torsade de pointes VT are listed in Table 24-5.9 In addition to QT interval prolongation, electrocardiographic features that are harbingers of torsade de pointes VT include QT prolongation and T-wave morphology changes after an extrasystolic pause, T-wave alternans, late-coupled polymorphic ventricular premature beats, and repetitive polymorphic beats.9

VF is frequently associated with acute myocardial ischemia, or sustained VT may degenerate into VF. VF may be initiated by a triggered focus or reentrant mechanism and is maintained by multiple reentrant wavelets in the ventricles.

Evaluation of the Patient with VT/VF

The initial evaluation of the patient with sustained VT or VF should be directed at detecting underlying reversible causes.22 This evaluation should include a thorough history (if the patient is able to communicate) and physical examination. A 12-lead electrogram of VT is extremely valuable, as is a review of rhythm strips documenting the onset of VT/VF. Laboratory tests should include cardiac enzymes (creatine kinase or troponin), creatinine, and serum electrolytes including K+ and Mg2+. An echocardiogram should be performed to determine the presence of structural heart disease and to assess ventricular function. Cardiac hemodynamic data should be reviewed. A drug screen may be required if drug toxicity is suspected (e.g., digitalis or tricyclic antidepressants). Some electrocardiographic features that allow discrimination of VT from SVT with aberrant conduction are summarized in Table 24-6.

Management of Ventricular Tachyarrhythmias

General Principles of Treatment

Sinus rhythm should be restored as soon as possible in sustained VT or cardiac arrest.22–24 Treatment of underlying cardiovascular disease should be initiated and any reversible causes should be identified and corrected (Table 24-7).22–24 Serum potassium should be maintained 4.0 mmol/L or higher, and serum magnesium should be maintained above 0.7 mmol/L. Beta blockers should be prescribed unless contraindicated (see Table 24-4). Management of ischemic heart disease, left ventricular dysfunction, and hypertension must be optimized. If ongoing ischemia is present despite medical therapy, the patient should be considered for urgent coronary artery revascularization.

Nonsustained VT

Beta blockers should be prescribed unless contraindicated, and doses should be titrated to suppress nonsustained VT (see Table 24-4).16,22,25–27 If frequent, hemodynamically significant nonsustained VT persists, amiodarone may be initiated for suppression.16,22,24,28 Patients with mild to moderate left ventricular dysfunction (left ventricular ejection fraction [LVEF] >0.30) may be considered for risk stratification electrophysiology study to determine the risk of sudden cardiac death.16,29 Patients with severe left ventricular dysfunction in the setting of ischemic heart disease (LVEF ≤0.30) should be considered for an implantable cardioverter defibrillator (ICD) for prophylaxis of sudden cardiac death.19,30

Monomorphic Ventricular Tachycardia

The acute management algorithm for sustained monomorphic VT is shown in Fig. 24-3. This algorithm is based on the recommendations of the American Heart Association in collaboration with the International Liaison Committee on Resuscitation.22–25 Synchronized cardioversion with 50 to 150 J of biphasic shock or 50 to 200 J of monophasic shock is the initial approach for the patient with hemodynamically unstable VT. The higher energy shocks should be used if the patient is unconscious. If the patient is hemodynamically stable and has normal or only mild left ventricular dysfunction, intravenous procainamide or sotalol may promote conversion. Beta-blocker therapy should be initiated to prevent recurrence. The patient with hemodynamically stable VT in the setting of significant left ventricular dysfunction should be treated with intravenous amiodarone (see Table 24-4 and Fig. 24-3).22–25,28 If VT does not convert with pharmacologic therapy, synchronized electrical cardioversion may be required.

Long-term antiarrhythmic drug therapy in addition to longterm β-blocker therapy may be required to prevent VT recurrence. This decision is made after treatment of underlying causes has been achieved and coronary artery revascularization, if required, has been accomplished. Class I antiarrhythmic drugs are contraindicated in patients with coronary artery disease and prior myocardial infarction, and class I drugs and sotalol are relatively contraindicated in patients with left ventricular dysfunction because of the risk of ventricular proarrhythmia.9,10 Patients with sustained VT in the absence of a reversible, correctable cause and in the setting of moderate to severe left ventricular dysfunction (LVEF ≤0.35) should be considered for an ICD. In this setting, the ICD has been shown to decrease cardiovascular mortality rate as compared with amiodarone therapy.31–33 In patients with less severe left ventricular dysfunction, amiodarone appears to be as efficacious as the ICD, and long-term therapy with amiodarone or an ICD may be individualized.33

Polymorphic Ventricular Tachycardia in the Setting of a Normal QT Interval

The acute management algorithm for sustained polymorphic VT is shown in Fig. 24-4.22,24 This algorithm is based on the recommendations of the American Heart Association in collaboration with the International Liaison Committee on Resucitation.24 Synchronized cardioversion with 50 to 150 J of biphasic shock or 50 to 200 J of monophasic shock is the initial approach for a patient with hemodynamically unstable sustained VT. Polymorphic VT in the absence of QT interval prolongation often is associated with myocardial ischemia.20 Catecholaminergic polymorphic VT also has been described in patients without structural heart disease who have mutations of cardiac ryanodine receptors.21 A patient with ischemia should be considered for urgent coronary angiography and revascularization, if required. This arrhythmia is frequently recurrent and intravenous β blockers or amiodarone should be administered to prevent recurrence. If a reversible cause, such as acute ischemia, is identified, long-term prophylactic antiarrhythmic drug therapy may not be required. Patients with significant left ventricular dysfunction should be considered for an ICD in the absence of a reversible, correctable cause.29–33

Torsade de Pointes VT

This arrhythmia frequently terminates spontaneously. However, cardioversion/defibrillation may be required if the patient develops sustained VT or VF. Magnesium, 1 to 4 g intravenously, is the initial treatment followed by cardiac overdrive pacing at 80 to 100 beats/min, which shortens the QT interval and prevents long pauses after premature beats (see Fig. 24-4).22,34 Atrial overdrive pacing is preferred to ventricular overdrive pacing. An isoproterenol infusion may be started until a temporary pacemaker is inserted. Drugs causing QT interval prolongation should be stopped and any electrolyte imbalances corrected. Temporary pacing should be continued until the VT has subsided and the QT interval returns to normal. If the patient has congenital long QT syndrome, long-term prophylactic therapy with β blockers or permanent cardiac pacing will prevent torsade de pointes VT.18,35 An ICD is the treatment of choice in patients with congenital long QT syndrome who have sustained a cardiac arrest or who have a significant family history of sudden cardiac death.18

Ventricular Fibrillation

Advanced life support should be initiated for VF, followed by prompt defibrillation (Fig. 24-5).22–24 If defibrillation is unsuccessful at least three times, amiodarone and adrenaline should be administered before repeat defibrillation.36 Intravenous amiodarone has been shown to improve resuscitation rates and overall survival rate if initial defibrillation is unsuccessful. If acute myocardial ischemia is the cause of VF, coronary angiography and percutaneous coronary intervention should be considered in the patient with recurrent VF. In the absence of a reversible cause, long-term therapy for prevention of sudden cardiac death should be prescribed. Patients with VF should be considered for an ICD, although in patients with well-preserved left ventricular dysfunction, amiodarone may also be a reasonable treatment option.29–33

VT/VF Electrical Storm

This is defined as multiple recurrent episodes of sustained VT or VF within a 24-hour period. Reversible causes should be identified and treated (see Table 24-7). Beta blockers are effective in suppressing some episodes of VT/VF storm.22,26 Even in the setting of congestive heart failure (except cardiogenic shock), intravenous β blockers can be administered safely. Amiodarone is very effective in suppressing VT/VF, although multiple boluses may be required in some patients.28 Combination β-blocker and amiodarone therapy is likely synergistic in suppressing recurrent VT/VF.22 In the patient with an ICD and VT electrical storm who is receiving frequent, painful shock therapies, the VT cardioversion or defibrillation therapies may need to be temporarily programmed off until pharmacologic therapy suppresses the frequency of VT.

Supraventricular Arrhythmia Classification and Mechanisms

Atrial fibrillation (AF) is the most common sustained arrhythmia observed, and its frequency increases with advancing age.37 AF is believed to be triggered by spontaneous depolarizations that originate most commonly in the pulmonary veins. These often fire repetitively, initiating an atrial tachycardia that degenerates into AF through the development of multiple wavelets of reentry in the atria. AF is characterized by the absence of distinct P waves on the electrogram and an irregular ventricular response. The ventricular response during AF is usually very rapid (120 to 170 beats/min) unless the patient is on AV node blocking drugs or the patient has coexisting AV conduction system disease. Atrial flutter is characterized by atrial rates of approximately 300 beats/min and is usually due to reentry in the atrium, most commonly in the right atrium involving the isthmus between the inferior vena cava and tricuspid annulus. AF and atrial flutter often occur in the same patient. In atrial flutter, distinct P waves are observed on the electrogram; these are often inverted in leads II, III, and aVF. In the absence of AV node blocking drugs or coexisting AV conduction disease, 2:1 AV conduction with ventricular rates of 150 beats/min is the most common pattern observed. Class I antiarrhythmic drugs in the absence of adequate AV node blocking drugs may slow the atrial rate during atrial flutter such that 1:1 AV conduction occurs. This may be misdiagnosed as VT because an intraventricular conduction delay may develop at rapid ventricular rates.9

The most common type of SVT is due to AV node reentry.38 This is characterized by swiftly and slowly conducting pathways in the AV node.3 The electrogram is characterized by a regular narrow complex tachycardia with a short RP interval; usually P waves, if visible, are observed in the early part of the ST segment. Reciprocating tachycardia is secondary to macro reentry involving an accessory atrioventricular connection, characterized by a narrow complex tachycardia with a longer RP interval. Most patients have overt ventricular preexcitation (Wolff Parkinson White syndrome); however, in some patients, ventricular preexcitation is not manifest on the electrogram and retrograde conduction through the accessory connection is concealed. True atrial tachycardia is most commonly due to enhanced or abnormal atrial automaticity or triggered activity. P waves usually precede each QRS complex unless there is AV conduction block. Multifocal atrial tachycardia is characterized by variation in P-wave morphology on a beat-to-beat basis.

Evaluation of the Patient with Supraventricular Tachyarrhythmia

The initial evaluation of a patient with a sustained supraventricular tachyarrhythmia should include a thorough history (if the patient is able to communicate) and physical examination with special attention to detecting structural heart disease.15 A 12-lead electrogram of the arrhythmia and during sinus rhythm should be obtained. Rhythm strips documenting onset and termination of the arrhythmia should be reviewed. Laboratory tests should include cardiac enzymes (creatine kinase or troponin), complete blood count, international normalized ratio, and thyroid-stimulating hormone. An echocardiogram should be made to determine the presence of structural heart disease and to assess ventricular function. In some instances, a transesophageal echocardiogram may be required to assess valve function or to determine whether intracardiac thrombus is present. Cardiac hemodynamic data during the arrhythmia, if available, should be reviewed.

Management of Supraventricular Tachyarrhythmias

General Principles of Treatment

Sinus rhythm should be restored as soon as possible if the patient is symptomatic. In the case of AF, therapy aimed at controlling the ventricular rate may be the initial approach. Any reversible causes should be identified and corrected. Underlying structural heart disease should be treated, in particular ischemic heart disease, left ventricular dysfunction, or hypertension. The probability of recurrence and the need for chronic prophylactic therapy should be determined.

Atrial Fibrillation or Flutter

The therapeutic approach for the management of sustained AF or atrial flutter is illustrated in Fig. 24-6.15,37 Synchronized electrical cardioversion may be required if the patient is hemodynamically unstable. Atrial flutter is frequently terminated with low-energy cardioversion (50 J), whereas higher energies may be required for AF (≥100 J). Since the incorporation of biphasic waveforms into external defibrillators, it is rare for cardioversion to fail to convert recent onset AF. Atrial flutter may be terminated by rapid atrial overdrive pacing. Some dual-chamber pacemakers and implantable defibrillators have atrial antitachycardia pacing therapies for pace termination of atrial flutter.

If AF or flutter has persisted for at least 48 hours in the absence of effective anticoagulation, therapy should be aimed at achieving ventricular rate control (heart rate <90 beats/min). Pharmacologic cardioversion to sinus rhythm can be considered if the patient has been in AF no longer than 48 hours. Anticoagulant therapy with heparin or low-molecular-weight heparin must be initiated. If cardioversion is performed, anticoagulant therapy should be continued for at least 3–6 weeks after cardioversion.15,37 Ibutilide or procainamide can be administered intravenously to promote pharmacologic conversion for recent onset AF or flutter or in patients who have been on effective long-term anticoagulation (Table 24-8).15 The electrogram must be monitored for significant QT interval prolongation because both drugs may cause torsade de pointes VT.9,15 Intravenous amiodarone is less effective in promoting conversion to sinus rhythm, although it may facilitate improved rate control.39 One important principle in the management of AF is that each patient deserves at least one attempt at restoration of sinus rhythm.37

The decision to initiate class I or III antiarrhythmic drug therapy to maintain sinus rhythm should be based the patient's symptoms and the hemodynamic significance of the arrhythmia. In the relatively asymptomatic patient, rate control is a reasonable first approach.40,41 Beta blockers, verapamil, or diltiazem should be prescribed in doses to achieve a ventricular rate at rest or with minimal activity at rates slower than 90 beats/min (see Table 24-4).15,37 Digoxin alone is frequently ineffective in achieving rate control of AF or atrial flutter, although it may be synergistic with class II or IV antiarrhythmic drugs. Rhythm control with class I or III antiarrhythmic drugs may be desirable in the very symptomatic patient or when these arrhythmias cause adverse hemodynamic effects.40–42 AV node blocking drugs are required in conjunction with class I or III antiarrhythmic drugs because AF or atrial flutter is usually paroxysmal in nature and these drugs are rarely 100% effective at suppression. The dosages, potential side effects, and drug interactions of these drugs are summarized in Table 24-4. Class I drugs are contraindicated for chronic prophylaxis in patients with a prior myocardial infarction, and class I drugs and sotalol are relatively contraindicated in those with significant left ventricular dysfunction because of the risk of ventricular proarrhythmia.9,10,37,43,44 Long-term antiarrhythmic drug therapy for prevention of AF or atrial flutter may not be required if the episode is thought to be due to a reversible cause, such as pneumonia or perioperative stress.

Catheter ablation for cure of atrial flutter is an effective therapy.45 Pulmonary vein isolation can be considered for long-term cure of AF in selected patients.46 AV junction ablation and ventricular pacing is an effective option in patients in whom effective ventricular rate control of AF cannot be achieved pharmacologically.47

The patient with AF or atrial flutter is at risk of thromboembolism, particularly if the patient is older or has structural heart disease.37 Aspirin is indicated for prevention of thromboembolism in low-risk patients, whereas anticoagulation with heparin and then warfarin is required in high-risk patients (see Table 24-8).37,48 If the patient has not been on anticoagulant therapy, electrical or pharmacologic cardioversion should be deferred for at least 3 weeks if the patient has been in AF or atrial flutter for at least 48 hours or if the duration is unknown. Alternatively, a transesophageal echocardiogram can be performed to demonstrate the absence of intracardiac thrombus if restoration of sinus rhythm is desired urgently. Patients should be maintained on oral anticoagulation for at least 6 weeks after electrical cardioversion.

Supraventricular Tachycardia

The therapeutic approach to the management of SVT is illustrated in Fig. 24-7.15,24 Vagal maneuvers (carotid sinus massage or Valsalva maneuver) may terminate AV node reentry or reciprocating tachycardia involving a bypass tract. Adenosine is the initial drug of choice for regular narrow complex SVT, although β blockers, verapamil, and diltiazem are also effective. Oral antiarrhythmic drug therapy may be required to prevent recurrent SVT (see Table 24-4). Infrequently, synchronized electrical cardioversion may be required; 25 to 50 J is usually sufficient. Catheter ablation is an effective cure for AV node reentrant tachycardias secondary to accessory pathways or atrial tachycardias.49 Multifocal atrial tachycardias may be difficult to suppress or to achieve rate control pharmacologically. In this case, implantation of a ventricular pacemaker followed by a total AV junction ablation is an effective treatment option.47

Disorders of impulse formation or conduction may cause bradyarrhythmias. Sinus node dysfunction characterized by sinus bradycardia, sinoatrial exit block, or sinus arrest causing symptomatic bradycardia is the most common indication for permanent cardiac pacing.50 AV block, permanent or intermittent, is the second most common cause for permanent cardiac pacing.

Evaluation of the Patient with Bradyarrhythmias

The initial evaluation of the patient with a documented bradyarrhythmia should include a thorough history (if the patient is able to communicate) and physical examination with a focus on detecting structural heart disease. A 12-lead electrogram and rhythm strips documenting the bradyarrhythmia should be reviewed. Carotid sinus massage should be performed to look for carotid sinus hypersensitivity unless contraindicated (carotid bruits or prior stroke). Cardiac hemodynamic data during the arrhythmia should be reviewed. Any drugs likely to contribute to the bradyarrhythmia should be identified and drug levels should be determined, if appropriate. Laboratory tests should include cardiac enzymes (creatine kinase or troponin). Echocardiography should be performed to determine the presence of structural heart disease and to assess ventricular function.

General Principles of Treatment

In a patient in the intensive care unit (ICU) with hemodynamically significant persistent bradycardia, transcutaneous pacing should be commenced until a temporary pacemaker can be inserted. A transvenous electrode catheter usually can be placed at the bedside and inserted through the internal jugular or subclavian route by using a flotation pacing catheter. Fluoroscopy may be required for positioning the pacing electrode if adequate pacing thresholds cannot be achieved. If the bradyarrhythmia is transient, temporary pacing may not be required and the risk/benefit of this intervention needs to be considered. Any reversible causes should be identified and corrected. Drugs contributing to bradycardia should be discontinued. Second-degree AV block or complete heart block after an inferior myocardial infarction may not be persistent. If the bradyarrhythmia does not resolve, permanent cardiac pacing may be required. The indications for permanent cardiac pacing are summarized in Table 24-9.50

Temporary Pacing

Transcutaneous pacing may be achieved by delivering a high current (40 to 100 mA) through defibrillation pads on most external cardioverters. Because this is painful for the conscious patient, the current should be decreased to the lowest setting that achieves continuous pacing. The rate programmed should be 60 to 70 beats/min and may need to be adjusted based on the patient's hemodynamic status. A temporary transvenous pacing lead should be inserted as quickly as possible. The initial current should be 3 to 5 mA. The current should then be reduced every five beats until there is failure to capture. The selected current for pacing should be twice the lowest current that effectively captured the atrium or ventricle.

Pacing Modalities

The codes that are frequently used to describe the functions of a pacing system are summarized in Table 24-10.51 The first letter describes the chamber paced, the second describes the chamber sensed, and the third describes how the chamber responds to a paced or intrinsic event. AAI indicates that the pacemaker paces and senses in the atrium and inhibits when an intrinsic cardiac signal is sensed in the atrium. DDD indicates that the pacemaker paces and senses in the atrium and ventricle and that there are dual responses to sensed events (e.g., the system inhibits in response to sensed events in both chambers, but a sensed or paced event in the atrium triggers a paced event in the ventricle after a programmed delay). The code R denotes a rate adaptive feature. VVIR indicates that the pacemaker paces and senses in the ventricle, inhibits when an intrinsic cardiac signal is sensed in the ventricle, and has the ability to change the pacing rate within a programmed range, for example, 60 to 130 beats/min, based on the programmable rate sensor settings.

Choice of Pacing Modality

Atrially based pacing (AAI/R or DDD/R systems) has been shown to prevent the development of paroxysmal and permanent AF as compared with ventricular pacing systems.52–54 In patients with sinus node dysfunction, atrially based pacing has been reported to reduce symptomatic heart failure in comparison with ventricular pacing.54 Atrially based pacing optimizes cardiac hemodynamics by preserving the atrial contribution to cardiac output, which is particularly important in patients with heart failure and patients with diastolic dysfunction. However, atrially based pacing therapies have not been shown to be associated with substantial improvements in quality of life, exercise tolerance, or overall survival rate when compared with ventricular pacing in several large, prospective, randomized, clinical trials.52–54 Thus, the choice of pacing modality should be individualized based on the patient's long-term prognosis, associated comorbidities, and expected functional status.

Cardiac Pacing Issues in the ICU

The pacing system consists of an implantable pulse generator, which contains the battery and integrated circuits that control pacing function, and one or more leads. The programming of a pacemaker is determined by the patient's underlying intrinsic rhythm. If the patient has only transient episodes of bradycardia, the pacemaker may be programmed to VVI at a low backup rate of 40 beats/min. If the patient has complete heart block, the pacemaker is usually programmed to a lower physiologic rate of 60 to 70 beats/min and an upper rate of 120 to 150 beats/min depending on age, type of heart disease, and activity level.

The most common problems related to a pacing system are capture failure, undersensing, oversensing, and triggered pacing. Capture failure may be due to pacing lead dislodgement, lead perforation, lead fracture, disconnection of the pacing lead from the power source, power source failure, or pacing thresholds higher than programmed. Pacing threshold may increase secondary to myocardial infarction, fibrosis, antiarrhythmic drug use, electrolyte abnormalities (hyperkalemia), and acidosis. Failure to sense may occur due to lead dislodgment or perforation, changes in intracardiac electrograms due to underlying disease state, electromagnetic interference causing reversion to asynchronous pacing, or spontaneous occurrence of a spontaneous ventricular event in the pacemaker blanking period. Oversensing may occur due to myopotential inhibition (more common with unipolar leads), sensing extraneous signals (usually due to lead insulation failure), or P- or T-wave oversensing. Triggered pacing may occur inappropriately when the patient with a dual-chamber pacemaker develops AF or atrial flutter or the pacemaker senses retrograde P waves causing pacemaker-mediated tachycardia. Most of these problems can be identified by interrogation and evaluation of the pacing system by using the pacemaker programmer. Many of these problems can be solved by reprogramming the pacemaker.55

Electrical shocks delivered transcutaneously, transvenously, or epicardially induce changes in the transmembrane potential of myocardial cells.56 These stimuli may interrupt reentrant circuits by prolonging tissue refractoriness or by producing new excitation waves. Synchronized cardioversion effectively terminates most supraventricular tachyarrhythmias and monomorphically sustained VT. Biphasic waveforms have been incorporated into ICDs and the most recent generations of external defibrillators. These biphasic waveforms have been demonstrated to reduce cardioversion and defibrillation energy requirements.57 If an electrical shock is not synchronized to the QRS complex, the shock may be delivered during the vulnerable repolarization phase and initiate VF. External pads rather than handheld paddles improve tissue contact, decrease overall system impedance, and reduce the energy required for cardioversion or defibrillation.

Three major secondary prevention trials have demonstrated the superiority of the ICD over pharmacologic therapy for the prevention of sudden cardiac death in patients presenting with a life-threatening episode of VT or VF in the absence of a reversible cause.31–33 In several clinical trials, the ICD also has been shown to prevent sudden cardiac death in patients with coronary heart disease and no history of spontaneous, sustained VT/VF.29,30,58 As a consequence, more and more patients will receive ICDs, and knowledge of their functioning is important to the critical care physician.

ICD Therapies

ICDs provide antitachycardia pacing therapies for termination of sustained VT, internal cardioversion therapies for VT if pacing therapies are ineffective, and defibrillation therapies for VF and very rapid VT.59 In addition, pacing therapy for bradycardia may be programmed. The ICD is usually programmed to back up VVI pacing at 40 beats/min unless the patient has significant bradycardia at baseline. VT detection is based on rate and sometimes on onset characteristics, regularity of rhythm, or duration of the intracardiac electrogram. An example of effective antitachycardia pacing therapy for sustained VT is shown in Fig. 24-8. Occasionally, the antitachycardia pacing therapy accelerates the VT to a more rapid VT or VF for which a shock is delivered (Fig. 24-9). One of the most frequent complications associated with the ICD is the delivery of an inappropriate shock for sinus tachycardia or a rapid atrial tachyarrhythmia. This can be minimized by programming a high tachycardia-detection interval (the rate that the device classifies as VT), programming a sudden rate onset feature to eliminate detection of sinus tachycardia that is rarely abrupt in onset, or programming a rate regularity feature to prevent AF being detected as VT. Newer ICDs may discriminate between VT and atrial tachyarrhythmias by using ventricular electrographic morphologic changes. Dual-chamber ICDs enhance discrimination of AF or SVT from VT by comparing atrial activity relations with ventricular activity.

ICD Issues in the ICU Setting

Device malfunctions similar to those described in the section on cardiac pacing may occur in the ICD patient. If the patient experiences AF or atrial flutter or other SVT, this may be classified by the ICD as VT resulting in inappropriate ICD therapies. Transthoracic cardioversion or defibrillation in the region of, or over, an ICD or pacemaker may damage the electronic circuits. If performed, the device should be interrogated after the procedure to ensure that the device is functioning appropriately. If a patient is experiencing frequent incessant VT, cardioversion and defibrillation therapies may need to be programmed “off” until pharmacologic therapy has been initiated to suppress the frequency of episodes. If surgery is urgently required, precautions must be implemented to minimize the likelihood that electrocautery signals will be detected by the ICD.60