Treatment of Cardiac Arrhythmias

An organized approach to the treatment of cardiac arrhythmias is paramount. Initial steps include identification and verification of the arrhythmia type and an assessment of potential harm to the patient. Box 27-9 outlines various rhythms categorized by their cardiac chamber of origin. As previously described, inpatient evaluation is recommended in some patients. When pharmacologic therapy is recommended, the side-effects and proarrhythmia potential must be known. Table 27-16 outlines antiarrhythmic agents according to the Vaughan-Williams classification system. A newer classification based on channel effects and mechanisms of arrhythmogenesis, the Sicilian Gambit system, although helpful, is too complex for most individuals to use and has not gained favor in the current era of invasive arrhythmia therapy (Rosen and Schwartz, 1991).

Evaluation and treatment of patients with arrhythmias is a rewarding practice. Many arrhythmias can be symptomati-cally improved through use of medications, lifestyle changes, and reassurance. However, meta-analysis of antiarrhythmic drug trials and the Cardiac Arrhythmia Suppression Trial (CAST) demonstrated the potential dangers of drug therapy in the treatment of cardiac arrhythmias (Echt et al., 1991; Sodermark et al., 1975). In addition, invasive evaluation and treatment of common bothersome or malignant arrhythmias is carried out by cardiac specialists trained in electrophysiol-ogy. In addition to drug therapy, an electrophysiologist may offer invasive techniques to treat arrhythmias. Arrhythmia ablation, implantation of pacemakers and defibrillators, and cardiac resynchronization therapy are all techniques to help reduce morbidity and mortality.

Electrophysiology Study and Ablation

Patients recommended for invasive arrhythmia therapy are evaluated in special catheterization suites. During an electrophysiology study (EPS), several electrodes or wires are inserted through the femoral vein or jugular vein and advanced to the right atrium, right ventricle, coronary sinus, and in the region of the AV node/His-bundle complex. Special pacing sequences and premature beat delivery are used to initiate arrhythmias. The wires may then be moved to different sites within the heart. Application of radiofrequency current through the tip of the catheter electrode results in elimination of the arrhythmia focus. Variations in duration and power of the current are used to alter lesion size. Studies may last less than an hour to several hours depending on the nature of the arrhythmias treated. This essentially painless method replaced the traditional technique of direct-current lesion application, which was poorly controlled and quite painful and required general anesthesia. Radiofrequency ablation is now used as the standard technique is treatment of AV node-dependent arrhythmias, including AVNRT, AV reciprocating tachycardia, and junctional tachycardia. Atrial flutter is successfully cured in most cases (see Fig. 27-42), and even paroxysmal atrial fibrillation may be suppressed or cured by RF ablation. Future refinements of this technique may be used to cure many more patients with bothersome atrial fibrillation.

Alternate energy sources, including microwave, ultrasound, and cryotherapy, are being investigated and used. Radiofrequency, however, remains the energy source in almost all cases for the routine treatment of supraventricu-lar arrhythmias treated with ablation. Treatment of arrhythmias through open-chest procedures was once the only method to cure arrhythmias. Considered high risk in most patients and too invasive for nonlethal arrhythmias in the era of RF ablation, surgical ablation for AF has enjoyed a resurgence as adjunct therapy during valvular heart surgery with cryotherapy and RF therapy of pulmonary veins (Todd et al., 2003).

Pacemakers and Defibrillators

Significant development in the area of pacing has occurred since transvenous pacemakers were first produced and implanted. Once able to pace only in a single chamber at a preset rate and without the ability to detect underlying rhythms, current pacemakers are more sophisticated. A pacemaker in its simplest form is a battery, pulse generator, and a lead to deliver an impulse. The use of sensing and

Table 27-16 Common Antiarrhythmic Drugs

Type of Drug

Typical Indications

Route

Considerations, Contraindications, and Complications

Frequency of General Use

Class I

Class la

Disopyramide (Norpace)

PACs, AF, SVT, PVCs

PO

Useful in normal hearts without ischemia; prolongs QT; atropine effect

Atrial arrhythmias only

Procainamide (Procan, Procanbid)

AF, PAC, PVC, VT

PO, IV

Wider range of use in mild LV dysfunction; lupus side effect; prolongs QT and QRS; best used in normal hearts only

Renal excreted with active metabolite (class III)

Atrial arrhythmias

Acute suppression of VT post-

CABG

Quinidine (Quinidex, Quinaglute)

AF, PACs, PVC, VT

PO, IV

Marked QT prolongation, myasthenia, idiosyncratic blood defects; may enhance AV conduction

Limited use; mostly AF, AFL

Continued

Continued

Box 27-9 Classification of Rhythms

Atrial

Sinus rhythm Sinus bradycardia Sinus pause

Sinus node exit block (type I and type II)

Sinus arrest

Sinus tachycardia

Premature atrial contraction

Wandering atrial pacemaker

Ectopic atrial rhythm

Ectopic atrial tachycardia

Multifocal atrial tachycardia

Atrial fibrillation

Atrial flutter

Junctional Rhythms

Premature junctional beat Junctional rhythm Accelerated junctional tachycardia Atrioventricular nodal reentrant tachycardia

Atrioventricular (AV) Conduction Block

First-degree AV block

Second-degree AV block (types I and II; 2:1; high grade) Third-degree AV block (complete AV block)

Ventricular Rhythms

Premature ventricular contractions Accelerated idioventricular rhythm Ventricular tachycardia (monomorphic and polymorphic) Ventricular fibrillation

Special Rhythms

Preexcitation

AV reciprocating tachycardia Long QT interval Paced rhythms

Table 27-16 Common Antiarrhythmic Drugs—Cont'd

Type of Drug

Typical Indications

Route

Considerations, Contraindications, and Complications

Frequency of General Use

Class Ib

Lidocaine

VT, torsade

IV

Rapid onset; may cause CNS changes and seizures

Acute VT termination and suppression

Being replaced by IV

amiodarone

Mexiletine (Mexitil)

PVCs, VT

PO

Significant GI upset, mild proarrhythmia, mild effect

Can be used carefully in setting of LV dysfunction

PVC suppression when other agents fail

Phenytoin (Dilantin)

VPB, VT

PO, IV

CNS effects, rash, blood dyscrasias

Rarely used; minimal effect

Tocainide (Tonocard)

VT

PO

CNS, blood dyscrasias, GI upset, pneumonitis

Rarely used

Class Ic

Flecainide (Tambocor)

AF, AFL, PACs, EAT, WPW

PO

Well tolerated; may increase conduction of slowed atrial flutter; contraindicated in CHF

Frequently used for AF, AFL

Propafenone (Rhythmol)

PACs, EAT, AF, AFL, PVC

PO

Contraindicated in CHF

Frequently used for AF, AFL

Class II

Beta Nonselective

Propranolol

ST, AT, IST, PVCs, VT, AF*

PO, IV

Excess bradycardia, hypotension, CNS effects Negative inotrope Pulmonary bronchospasm

Short acting, rapid onset; increased replacement by longer-acting cardiac selective agents

Beta Selective

Atenolol

ST, AT, IST, PVCs, VT, AF*

PO, IV

Excess bradycardia, hypotension, CNS effects Negative inotrope

Inexpensive, resulting in frequent use

Metoprolol (Lopressor, Toprol)

ST, AT, IST, PVCs, VT, AF*

PO, IV

Excess bradycardia, hypotension, CNS effects Negative inotrope

Frequently used, long-acting preparation with infrequent side effects

Pindolol

ST, AT, IST, PVCs, AF*

PO

Excess bradycardia, hypotension, CNS effects Negative inotrope

Intermediate-frequency use

Timolol

ST, AT, IST, PVCs, AF*

PO

Excess bradycardia, hypotension and CNS effects Negative inotrope

Low-frequency use

Esmolol (Brevibloc)

ST, AT, IST, PVCs, AF*

Excess bradycardia and nonselective at high doses

Low-frequency use caused by IV form only

Mixed Alpha/Beta

Carvedilol (Coreg)

CHF, PVCs, AF*

PO

Excess bradycardia, hypotension, exacerbation of CHF, fatigue

Infrequent as first choice for arrhythmias but primarily indicated for systolic heart failure

Class III

Ibutilide (Corvert)

AF, AFL

IV

Proarrhythmia frequent including PVCs, VT, and torsades; prolongs QT and slows heart rate; requires acute monitoring

Intermediate use; high efficacy in acute AF/AFL but with potential serious acute side effects

Dofetilide (Tikosyn)

PACs, AF, AFL

PO

High efficacy; prolongs QT and QRS; proarrhythmic including torsades; requires training to prescribe (Is mortality neutral in CHF and MI patients?)

Low-frequency use caused by inpatient initiation and potentially dangerous proarrhythmia

Table 27-16 Common Antiarrhythmic Drugs—Cont'd

Type of Drug

Typical Indications

Route

Considerations, Contraindications, and Complications

Frequency of General Use

Sotalol (Betapace)

ST, AT, IST, PVCs, VT, AF*

PO

Excess bradycardia; prolongs QT with potential torsades

Moderate-frequency use; reasonably safe in setting of mild LV dysfunction in absence of ischemia

Amiodarone (Pacerone, Cordarone)

ST, AT, AF, AFL, PVCs, VT, AF*

PO, IV

Class I, II, III, and IV effects Very well tolerated but may produce serious thyroid dysfunction and lethal pulmonary and liver dysfunction

Close monitoring for side effects mandatory

High-frequency use caused by very low acute side effect profile and very high efficacy in variety of arrhythmias Indiscriminate use discouraged

Class IV

Diltiazem (Cardizem, Cartia)

AF*,PVCs, calcium dependent VT,

PO, IV

Bradycardia, hypotension, exacerbation of systolic heart failure Continuous infusion available

Used frequently for AVN slowing in setting of AF with or without LV dysfunction

Verapamil (Calan, Isoptin)

AF*,PVCs, calcium dependentVT

PO, IV

Bradycardia, hypotension, exacerbation of systolic heart failure

Used frequently for AVN slowing in setting of AF

Class V (Other)

Adenosine (Adenocard)

SVT

IV

Acute onset with very powerful AV node block and to less extent SA block, producing marked bradycardia and transient asystole; temporary pulmonary symptoms

Agent of choice for abrupt termination of most AV node-dependent arrhythmias

Digoxin

AF*

PO, IV

Proarrhythmic, including heart block and enhancing bypass tract conduction, GI side effects

Frequent adjuvant drug for slowing ventricular response in AF

Atropine

SB

IV

Avoid in patients with acute-angle glaucoma

Acute treatment for sinus bradycardia and heart block not caused by Purkinje failure

Magnesium sulfate

Torsades, PVC and VT suppression

PO, IV

Caution in renal failure

Frequent adjuvant drug for VT suppression

Drugs organized according to the Vaughan-Williams classification scheme. Indications represent both approved and nonapproved indications.

PO, Oral (per os); IV, intravenous; SA, sinoatrial; ST, sinus tachycardia; AT, atrial tachycardia; IST, inappropriate sinus tachycardia; AF, atrial fibrillation; AFL, atrial flutter; AF*, AV node blockade in atrial fibrillation; PACs, premature atrial contractions; PVCs, premature ventricular contractions; SB, sinus bradycardia; ]VT, ventricular tachycardia; torsades, torsades de pointes; LV, left ventricular; GI, gastrointestinal; CNS, central nervous system; CHF, systolic congestive heart failure; CABG, coronary artery bypass graft.

timing circuits coupled with motion detectors within the pacemaker allows inhibition of pacing when sensed events occur and an increase in paced rate with motion or activity. As technology advanced, pacemakers were able to pace effectively in the atrium and ventricle and AV node, or P-R intervals could be adjusted. Telemetry through the skin using proprietary programming devices allow adjustment in the physician's office. Miniaturization has now resulted in sophisticated pacemakers able to pace the heart when necessary, detect rapid rhythms, and attempt to pace terminate the arrhythmia in a package about the size of a halfdollar coin (Fig. 27-55) (Furman et al., 1993). Implantable defibrillators with endocardial leads were developed in the early 1990s, allowing for a safer and less invasive procedure. These devices are now able to identify and attempt to terminate ventricular arrhythmias through painless overdrive pacing or using an endocardial shock that can be uncomfortable if the patient is not syncopal (Figs. 27-56 and 27-57).

Figure 27-55 Dual-chamber pacemaker with endocardial passive and active fixation leads. (Courtesy Medtronic, Minneapolis).

Figure 27-56 Ventricular tachycardia is pace terminated by three rapid ventricular pulses from the implanted pacemaker-defibrillator. Atrioventricular sequential pacing resumes following termination of the ventricular tachycardia.

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Figure 27-57 Attempt at pace termination of ventricular tachycardia with acceleration of the ventricular tachycardia into ventricular fibrillation. The transient of the endocardial shock is noted, and pacing resumes with organized cardiac activity.

Figure 27-58 Radiographs from a dual-chamber biventricular defibrillator. Right and left anterior oblique views are shown in a patient treated for left ventricular systolic dysfunction and NYHA Class III heart failure. Standard leads terminate in the right atrium and the right ventricular septum. A third lead enters the coronary sinus from the right atrium and extends into a branching vein to provide synchronous left and right ventricular activation.

Figure 27-58 Radiographs from a dual-chamber biventricular defibrillator. Right and left anterior oblique views are shown in a patient treated for left ventricular systolic dysfunction and NYHA Class III heart failure. Standard leads terminate in the right atrium and the right ventricular septum. A third lead enters the coronary sinus from the right atrium and extends into a branching vein to provide synchronous left and right ventricular activation.

Figure 27-59 Left bundle branch block and right BBB are produced from contralateral ventricular pacing. Right ventricular pacing with left BBB morphology is noted on the left. Pacing activates one side of the ventricle earlier and therefore results in a BBB pattern of the opposite side of the chamber paced. On the right, inappropriate left ventricular endocardial lead placement delivered across a patent foramen ovale was detected before serious consequences of embolic stroke. Epicardial pacing of the left ventricle is also accomplished through lead placement through the coronary sinus.

Figure 27-59 Left bundle branch block and right BBB are produced from contralateral ventricular pacing. Right ventricular pacing with left BBB morphology is noted on the left. Pacing activates one side of the ventricle earlier and therefore results in a BBB pattern of the opposite side of the chamber paced. On the right, inappropriate left ventricular endocardial lead placement delivered across a patent foramen ovale was detected before serious consequences of embolic stroke. Epicardial pacing of the left ventricle is also accomplished through lead placement through the coronary sinus.

Cardiac Resynchronization and Defibrillator Therapy

Patients with refractory clinical congestive heart failure have a sixfold to ninefold increase in sudden cardiac death compared to the general population (AHA, 2002). Despite therapy with beta blockers, ACE inhibitors, angiotensin II receptor blockers, diuretics, spironolactone, digoxin, and invasive revascularization strategies, patients continue to have significant morbidity and mortality from systolic CHF.

Electrophysiologists have been impacting mortality and morbidity for over a decade through cardiac pacing resyn-chronization therapy and defibrillator placement.

The slowing of conduction through the left ventricle in the setting of BBB or significant scarring leads to asynchronous lateral and septal contraction. This dyssynchrony (asynchrony) results in excess energy expenditure and decreases cardiac performance. Placement of a pacing device capable of pacing in the right ventricle as well as at the lateral left ventricle has significantly reduced morbidity and mortality. The addition of a defibrillator further decreases mortality (Bristow et al., 2004; Cleland et al., 2005; Young et al., 2003). Figure 27-58 shows the radiographic appearance of a biventricular system. Pacing in both ventricles demonstrates a shortening of the QRS complex and is associated with improvements in cardiac contractility and over time, reduction in LV chamber size, reduction in mitral valve regurgitation, and improvements in 6-minute walk test, quality of life, and NYHA classification (Abraham et al., 2002). Changes in the QRS morphology depend on the site of electrical stimulation (Fig. 27-59). During right and left ventricular activation, the QRS morphology in lead V1 is shown.

Patients suffering from lethal tachycardia events such as ventricular tachycardia and ventricular fibrillation have been extensively studied. For much of modern electrophysiologic history, the EPS was used to induce VT in patients with syncope and structural heart disease, in patients with symptomatic stable VT, and in patients resuscitated from arrhythmic sudden cardiac death. Drugs were then initiated and repeat testing performed to test the success of the antiarrhythmic drug. More recent studies have challenged this approach. Drug versus implantable defibrillator therapy trials have demonstrated mortality benefit as secondary prevention of syncopal VT or resuscitated sudden cardiac death with

The complete reference list is available online at www.expertconsult.com.

www.diabetes.org/

American Diabetes Association site with information for patients and health professionals. www.americanheart.org/

American Heart Association site provides valuable range of Internet resources on a wide variety of cardiovascular diseases, including statistics on heart disease prevalence. www.legdisorders.org/

Comprehensive resource of peripheral arterial disease and other leg disorders; excellent resource for slides and current literature. www.cardiosource.com/

Journal of the American College of Cardiology site; outstanding functionality and features; requires subscription. www.clinicaltrialresults.org/

Outstanding resource on cardiovascular clinical trials with videos of principal investigators discussing results and slide decks. www.dashdiet.org/

Practical instructions on using diet to reduce blood pressure.

structural heart disease (AVID Investigators, 1997; Connolly et al., 2000; Kuck et al., 2000). Further studies have demonstrated mortality benefit from implantable defibrilla-tors compared to drug therapy in primary prevention trials. Specific groups demonstrating superiority of device therapy over drugs include patients with asymptomatic ventricular ectopy with inducible VT, those with prior MI and ejection fraction less than 30%, and those with LVEF less than 35% with NYHA II or III heart failure for longer than 3 months (Bardy et al., 2005; Buxton et al. 2000; Moss et al., 1996, 2002). Patients fulfilling these criteria should be referred to an electrophysiologist.

www.fammed.wisc.edu/integrative/modules/hypertension

Summary for clinicians and patients on how to lower blood pressure without medications. http://hypertensiononline.org/

Slide resource on hypertension management. www.lipidsonline.org/

Slide resource on dyslipidemia management. www.theheart.org/

Excellent resource with coverage of all areas of cardiology. www.nhlbi.nih.gov/guidelines/hypertension/index.htm

Joint National Commission guidelines on treating hypertension. http://hp2010.nhlbihin.net/atpiii/calculator.asp?usertype=prof

Calculator based on Framingham data to calculate 10-year cardiovascular risk. www.vbwg.org/

Slide resource for management of dyslipidemia, hypertension, insulin resistance, and diabetes mellitus; updated regularly.

References

Web Resources

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