Amyloidosis

Sarcoidosis

Systemic lupus erythematosus Scleroderma SFeep apnea Drugs: Adenosine Amiodarone

Blockers Buplvicaine Carbamazepine Chbroquine DigoKtn Dillia^em Drbnedarone Hecainide

AV, atrioventricular, from Refs. 12,13,15.

Clinical Presentation and Diagnosis of AV Nodal Blockade Symptoms

Hyd rox y c h tor o q uine Paclitaxel

P he ny Ipropa nola mine

Propafenone

Propofol

Sotalol

Thioridazine

Tricyclic antidepressants

Verapamil

• First-degree AV nodal blockade is rarely symptomatic, because it rarely results in bradycardia

• Second-degree AV nodal blockade may cause bradycardia, as not all impulses generated by the SA node are conducted through the AV node to the ventricles

• In third-degree AV nodal blockade, or complete heart block, the heart rate is usually 30 to 40 bpm, resulting in symptoms

• Symptoms of bradyarrhythmias such as second-or third-degree AV block consist of dizziness, fatigue, light-headedness, syncope, chest pain (in patients with underlying CAD), and shortness of breath and other symptoms of heart failure (in patients with underlying left ventricular dysfunction)

Diagnosis

• Made on the basis of patient presentation, including history of present illness and presenting symptoms, as well as a 12-lead ECG that reveals AV nodal blockade

• Assess potentially correctable etiologies, including myocardial ischemia, serum potassium concentration (for hyperkalemia), and thyroid function tests (for hypo-thyroidism)

• Determine whether the patient is taking any drugs known to cause AV block

• If the patient is currently taking digoxin, determine the serum digoxin concentration and ascertain whether it is supratherapeutic (less than 2 ng/mL [2.6 nmol/L])

Pharmacologic Therapy

Treatment of first-degree AV nodal blockade is rarely necessary, because symptoms rarely occur. However, the ECGs of patients with first-degree AV nodal blockade should be monitored to assess the possibility of progression of first-degree AV nodal blockade to second-or third-degree block. Second-or third-degree AV nodal blockade requires treatment, because bradycardia usually results in symptoms. If the patient is taking any medication(s) that may cause AV nodal blockade, the drug(s) should be discontinued whenever possible. If the patient's rhythm still exhibits AV nodal blockade after discontinuing the medication(s) and after five half-lives of the drug(s) have elapsed, then the drug(s) can usually be excluded as the etiology of the arrhythmia. However, in certain circumstances, discontinuation of a medication that is inducing AV nodal blockade may be undesirable. For example, if the patient has a history of myocardial infarction or heart failure, discontinuation of a P-blocker is undesirable because P-blockers have been shown to reduce mortality and prolong life in patients with those diseases, and the benefits of therapy with P-blockers outweigh the risks associated with AV nodal blockade. In these patients, clinicians and patients may elect to implant a permanent pacemaker in order to allow the patient to continue therapy with P-blockers.

Acute treatment of patients with second-or third-degree AV nodal blockade consists primarily of administration of atropine, which may be administered in the same doses as recommended for management of sinus bradycardia. In patients with hemo-dynamically unstable or severely symptomatic AV nodal blockade that is unresponsive to atropine and in whom temporary or transvenous pacing is not available or is ineffective, epinephrine (2-10 mcg/min, titrate to response) and/or dopamine (2-10 mcg/kg/min) may be administered.14

In patients with second-or third-degree AV block due to underlying correctable disorders (such as electrolyte abnormalities or hypothyroidism), management consists of correcting those disorders.

Nonpharmacologic Therapy

Long-term management of patients with second-or third-degree AV nodal blockade due to idiopathic degeneration of the AV node requires implantation of a permanent pacemaker.12

Outcome Evaluation

• Monitor the patient for termination of AV nodal blockade and restoration of normal sinus rhythm, heart rate, and alleviation of symptoms.

• If atropine is administered, monitor the patient for adverse effects including dry mouth, mydriasis, urinary retention, and tachycardia.

Atrial Fibrillation

AF is the most common arrhythmia encountered in clinical practice. It is important for clinicians to understand AF, because it is associated with substantial morbidity and mortality and because many strategies for drug therapy are available. Drugs used to treat AF often have a narrow therapeutic index and a broad adverse-effect profile.

Epidemiology and Etiology

Approximately 2.3 million Americans have AF. The prevalence of AF increases with advancing age; roughly 9% of patients between the ages of 80 and 89 years have AF.16

Similarly, the incidence of AF increases with age, and it occurs more commonly in men than in women.16

Etiologies of AF are presented in Table 9-4. The common feature of the majority of etiologies of AF is the development of left atrial hypertrophy. Hypertension may be the most important risk factor for development of AF. However, AF occurs commonly in patients with CAD. In addition, heart failure is increasingly recognized as a cause of AF; approximately 25% to 30% of patients with New York Heart Association (NYHA) class III heart failure have AF, 7 and the arrhythmia is present in as many as 50% of patients with NYHA class IV heart failure.18

Clinical Presentation and Diagnosis of AF Symptoms

• Approximately 20% to 30% of patients with AF remain asymptomatic

• Symptoms typical of tachyarrhythmiassuch as AF include palpitations, dizziness, light-headedness, shortness of breath, chest pain (if underlying CAD is present), near-syncope, and syncope. Patients commonly complain of palpitations; often the complaint is "I can feel my heart beating fast" or "I can feel my heart fluttering" or "It feels like my heart is going to beat out of my chest."

• Other symptoms are dependent on the degree to which cardiac output is diminished, which is in turn dependent on the ventricular rate and the degree to which stroke volume is reduced by the rapidly beating heart

• In some patients, the first symptom of AF is stroke Diagnosis

• Because the symptoms of all tachyarrhythmias are dependent on heart rate and are therefore essentially the same, the diagnosis depends on the presence of AF on the ECG

• AF is characterized on ECG by an absence of P waves, an undulating baseline that represents roughly 350 to 600 attempted atrial depolarizations per minute, and an irregularly irregular rhythm, meaning that the intervals between the R waves are irregular and that there is no pattern to the irregularity

Table 9-4 Etiologies of AF

Hypertension

Coronary artery disease

Heart failure

Diabetes

Hyperthyroidism

Rheumatic heart disease

Diseases of the heart valves:

Mitral stenosis or regurgitation Mitral valve prolapse Chronic obstructive pulmonary disease Pulmonary embolism Idiopathic ("lone" AF) Thoracic surgery:

Coronary artery bypass graft surgery Pulmonary resection Thoracoabdominal esophagectomy Drugs:

Adenosine

Albuterol

Alcohol

Alendronate

Dobutamine

Enoximone

Ipratropium bromide

Methylprednisolone

Milrinone

Mitoxantrone

Paclitaxel

Propafenone

Theophylline

Verapamil

Zoledronic acid

AF, atrial fibrillation. FromRefs. 13,20,21.

Drug-induced AF is relatively uncommon, but has been reported (Table 9-4).

Acute ingestion oflarge amounts of alcohol may cause AF; this phenomenon has been referred to as the "holiday heart" syndrome.19 In addition, recent reports have associ-

20 21

ated use of the bisphosphonate drugs zoledronic acid and alendronate with new-onset serious AF. The potential relationship between bisphosphonate use and new-onset AF requires further study.

Pathophysiology

© AF may be caused by both abnormal impulse formation and abnormal impulse conduction. Traditionally, AF was believed to be initiated by premature impulses initiated in the atria. However, it is now understood that in many patients AF is triggered by electrical impulses generated within the pulmonary veins. 2 These impulses initiate the process of re-entry within the atria, and AF is believed to be sustained by multiple

re-entrant wavelets operating simultaneously within the atria. Some believe that, at least in some patients, the increased automaticity in the pulmonary veins maybe the sole mechanism of AF and that the multiple re-entrant wavelet hypothesis may be incorrect. However, the concept of multiple simultaneous re-entrant wavelets remains

the predominant hypothesis regarding the mechanism of AF.

AF leads to electrical remodeling of the atria. Episodes of AF that are of longer duration and episodes that occur with increasing frequency result in progressive shortening of atrial refractory periods, further potentiating the re-entrant circuits in the atria. Therefore, it is often said that "atrial fibrillation begets atrial fibrillation," that

23 24

is, AF causes atrial electrophysiologic alterations that promote further AF. ' AF is associated with 400 to 600 attempted atrial depolarizations per minute and chaotic, disorganized atrial electrical activity.

The AV node is incapable of conducting 400 to 600 impulses per minute; however, it may conduct 100 to 200 impulses per minute, resulting in ventricular rates ranging from 100 to 200 bpm.

AF is classified as paroxysmal, persistent, or permanent (Fig. 9-4). Patients with paroxysmal AF have episodes that begin suddenly and spontaneously, last minutes to hours, or rarely as long as 7 days, and terminate suddenly and spontaneously. Some patients with paroxysmal AF have episodes that do not terminate spontaneously but require intervention, and this is known as persistent AF. Approximately 18% to 30% of patients with AF progress to the point of permanent AF; these patients are subsequently never in normal sinus rhythm but rather are always in AF.

AF is associated with substantial morbidity and mortality. This arrhythmia is associated with a risk of ischemic stroke of approximately 5% per year.2 The risk of stroke is increased two-to sevenfold in patients with AF compared to patients without this arrhythmia.25 AF is the cause of roughly one of every six strokes. During AF, atrial contraction is absent. Due to the fact that atrial contraction is responsible for approximately 30% of left ventricular filling, this blood that is not ejected from the left atrium to the left ventricle pools in the atrium, particularly in the left atrial appendage. Blood pooling facilitates the formation of a thrombus, which subsequently may travel through the mitral valve into the left ventricle and may be ejected during ventricular contraction. The thrombus then may travel through a carotid artery into the brain, resulting in an ischemic stroke.

Patient Encounter, Part 1

DA is a 58-year-old male who presents to the emergency department (ED) complaining that he can "feel my heart beating fast," which started when he was taking out the garbage. He also complains of feeling light-headed and short of breath. His pulse is irregularly irregular, with a rate of 135 bpm.

His physical exam is completely normal and no focal neurologic deficits were observed.

What information is suggestive ofAF?

What additional information do you need in order to develop a treatment plan?

FIGURE 9-4. Classification of atrial fibrillation. aEpisodes that generally last 7 days or less (most less than 24 hours). bEpisodes that usually last 7 days. cCardioversion failed or not attempted. dEither paroxysmal or persistent atrial fibrillation may be recurrent. AF, atrial fibrillation. (From Ref. 25.)

FIGURE 9-4. Classification of atrial fibrillation. aEpisodes that generally last 7 days or less (most less than 24 hours). bEpisodes that usually last 7 days. cCardioversion failed or not attempted. dEither paroxysmal or persistent atrial fibrillation may be recurrent. AF, atrial fibrillation. (From Ref. 25.)

AF may lead to the development of heart failure as a result of tachycardia-induced cardiomyopathy.26 AF increases the risk of mortality approximately twofold com-

pared to that in patients without AF; the causes of death are likely stroke or heart failure.

Treatment

Desired Outcomes

The goals of individualized therapy of AF are: (a) ventricular rate control, (b) termination ofAF and restoration of sinus rhythm (commonly referred to as "cardioversion" or "conversion to sinus rhythm"), (c) maintenance of sinus rhythm, or reduction in the frequency of episodes ofparoxysmal AF, and/or (d) prevention of stroke.

These goals of therapy do not necessarily apply to all patients; the specific goal(s) that apply depend on the patient's AF classification (Table 9-5).

Hemodynamically Unstable AF

For patients who present with an episode of AF that is hemodynamically unstable, emergent conversion to sinus rhythm is necessary using direct current cardioversion (DCC). Hemodynamic instability may be defined as the presence of any one of the following14: (a) patient has altered mental status, (b) hypotension (systolic blood pressure less than 90 mm Hg) or other signs of shock, (c) ventricular rate greater than 150 bpm, and/or (d) patient is experiencing squeezing, crushing chest pain suggestive of myocardial ischemia.

Patient Encounter, Part 2: Medical History, Physical Exam, and Diagnostic Tests

PMH: Hypertension x 15 years; coronary artery disease x 5 years; myocardial infarction 2005; heart failure x 5 years

Meds: Aspirin 81 mg once daily; metoprolol 50 mg twice daily; enalapril 5 mg twice daily; furosemide 40 mg daily

Ht 5'10" (178 cm), wt 80 kg (176 lb), BP 110/70 mm Hg, P 135 bpm, RR 20/min; remainder of PE noncontributory

Labs: All within normal limits

CXR: Mild pulmonary edema

Echo: Moderately reduced LV function, LVEF 35%

ECG: Atrial fibrillation

What is your assessment of DA's condition? What are your treatment goals?

What pharmacologic or nonpharmacologic alternatives are available for each treatment goal?

Table 9-5 Treatment Goals According to AF Classification

First detected Episode

Paroxysmal AF

Persistent AF

Permanent AF

Writikjul.* Fiwoancii>i itnoto? prívídiisri Convuf sion to iinus "tylhm

VíífltritiAli i<jtt«Jfl(lOl Sir-üfce |VPveriti<sn Mjinbcrwna: oí rhythm if vteX'Zvbf tifie rtfirroí is mjr íu/fcífjrt to control symptom

Uwir tutor riie CtXHrtX Jtrobf puf^entkini Gonwiiio" tu yi*H rhythm

wsnrriLdbi ijKconciol Sircilip prevention

AF, airwl fibrillation.

AF, airwl fibrillation.

DCC is the process of administering a synchronized electrical shock to the chest. The purpose of DCC is to simultaneously depolarize all of the myocardial cells, resulting in interruption and termination of the multiple re-entrant circuits and restoration of normal sinus rhythm. The initial energy level of the shock is 100 joules (J); if the DCC attempt is unsuccessful, successive cardioversion attempts may be made at 200 J, 300 J, and 360 J.14 Delivery of the shock is synchronized to the ECG by the cardioverter machine, such that the electrical charge is not delivered during the latter portion of the T wave (i.e., the relative refractory period), to avoid delivering an electrical impulse that may be conducted abnormally, which may result in a life-threatening ventricular arrhythmia.

The remainder of this section will be devoted to management of hemodynamically stable AR. The specific goals of therapy that apply to patients in each AF classification are presented in Table 9-5.

Pharmacologic Therapy

Ventricular Rate Control. Ventricular rate control can be achieved by inhibiting the proportion of electrical impulses conducted from the atria to the ventricles through the AV node. Therefore, drugs that are effective for ventricular rate control are those that inhibit AV nodal impulse conduction: P-blockers, diltiazem, verapamil, digoxin, and amiodarone (Tables 9-6 and 9-7).

In patients who present with their first detected episode of AF, or for those who present with an episode of persistent AF, ventricular rate control is usually initially achieved using IV drugs. A decision algorithm for selecting a specific drug for acute ventricular rate control is presented in Figure 9-5. In general, an IV CCB or P-block-er is preferred for ventricular rate control in patients with normal LV function, as ventricular rate control can often be achieved within several minutes. In patients with heart failure due to LV dysfunction, IV digoxin or amiodarone is preferred, because diltiazem and verapamil are associated with negative inotropic effects and may ex-

acerbate heart failure. Similarly, although oral P-blockers are indicated in patients with heart failure due to LV dysfunction, IV P-blockers are generally avoided due to the potential for acutely exacerbating heart failure.

A decision strategy for long-term rate control in patients with paroxysmal or permanent AF is presented in Figure 9-6. In general, while digoxin is effective for ventricular rate control in patients at rest, digoxin is less effective than CCBs or P-blockers for ventricular rate control in patients undergoing physical activity including activities of daily living. This is likely because activation of the sympathetic nervous system during exercise and activity overwhelms the stimulating effect of digoxin on the parasympathetic nervous system. Therefore, in patients with normal LV function, CCBs or P-blockers are preferred for long-term ventricular rate control. Diltiazem may be preferable to verapamil in older patients due to a lower incidence of constipation. However, in patients with heart failure, oral diltiazem and verapamil are con-traindicated as a result of their negative inotropic activity and propensity to exacerbate heart failure. Therefore, the options in this population are P-blockers or digoxin. The majority of patients with heart failure should be receiving therapy with an oral P-blocker with the goal of achieving mortality risk reduction. In patients with heart failure who develop rapid AF while receiving therapy with P-blockers, digoxin should be administered for purposes of ventricular rate control. Fortunately, studies have found the combination of digoxin and P-blockers to be effective for ventricular rate control, likely as a result of P-blocker-induced attenuation of the inhibitory effects of the sympathetic nervous system on the efficacy of digoxin.

Conversion to Sinus Rhythm. Termination of AF in hemodynamically stable patients may be performed using antiarrhythmic drug therapy or elective DCC. Drugs that may be used for conversion to sinus rhythm are presented in Table 9-8; these agents slow atrial conduction velocity and/or prolong refractoriness, facilitating interruption of reentrant circuits and restoration of sinus rhythm. DCC is generally more effective than drug therapy for conversion of AF to sinus rhythm. However, patients who undergo elective DCC must be sedated and/or anesthetized to avoid the discomfort associated with delivery of 100 to 360 J of electricity to the chest. Therefore, it is important that patients scheduled to undergo elective DCC do not eat within approximately 8 to 12 hours of the procedure to avoid aspiration of stomach contents during the period of sedation/anesthesia. This often factors into the decision as to whether to employ elective DCC or drug therapy for conversion of AF to sinus rhythm. If a patient presents with AF requiring nonemergent conversion to sinus rhythm, and the patient has eaten a meal that day, then pharmacologic methods must be used for cardioversion on that day, or DCC must be postponed to the following day to allow for a period of fasting prior to the procedure.

Table 9-6 Drugs for Ventricular Rate Control in AF

Drug

Mechani in of Action

Loading Dose

Pally Dose

Drug Interactions

lr,liilw AV nodjl vondut hon by sbiving AV nodal conduction ■inrh |:r:ili;ri-iim AV n:^l.il nefrac texmess

150 mg IVty.ii lOmift

Esmolol SOO mcg/kg

Wovcr i niinutu-PlQOrinfkjl O.IS- IV Melaprafol li-5 nig IV x 2-3 doses

(J.5-1 ii^/min W continuous infusion 3X? n^evirycjjy orally Esmolol SO-JOO nicgAg/tnln continuous IV infusion PiQpriflOkjl 513-^0 rtlriAJDy Mclopiobl 50-300 mgAtay

liJiiWiileiriiXi-ci digokin, warfattx JrKl Ollitf diugt

CHttiaaem

InhilHtii AVrvxJal conduction by -slowing AV nodal iJur'nt.;.. tiurt -Irtif-|lidCiriL|irKj to nodal refractoriness

D.Jb nig/lug IV lotdovfi 2 minutes. If necessity, 0.3S rYiij/lg IV inrti 2 mrnuies aflef first dose

Continuous intuslonof

5-15 mg/h 130-360 m^diyoially

Inhibits flhni nation of eye bspc« in?

Vteraeami

inhibit* av pyx^i condut tion

Isy slowing AV rod.il conviction and prolonging r\v nodal refractoriness

0JW5-O.15 iliQAg IV over 3 mJfiWie^ If neofssary, an additional dose of 0.0»[}.lii ring/Kg N may bfl administered 30 minutes lak'r

InlibitiClii] twill dnlnslfcn

ITjqonifi

Inhibits W nodal rondgc Hon by M) vjyJl Kirrnjljiio" Isy lfc>)dii«iiy-slowing av nodal conduction, anil (C) CtCtongino Hi nodal rifracTOiirifti

0.3J mg IVevay 1 hours up to 1J FTKf

0.1 ?5-0.}J5 mg orally once daily

Amiodarone, verapamil, qiA4dlne inhibit digokm elimination

Ah. .slri.U 11: II ill iritirr AV .iliiir.rtUrn ulii.: v (. 0, i:,.lk;iljm rhi.ifind ht>:. h.T

Ah. .slri.U 11: II ill iritirr AV .iliiir.rtUrn ulii.: v (. 0, i:,.lk;iljm rhi.ifind ht>:. h.T

wiiile owl &tiioctii s jie important «pirns lot mxirtsiiiy i«iuuk*ii in iMriew with ii«it toiluie. iv tf-Woi:^ s sroukl be ivtAfcd due to (h? potential for heart failure exaceihatlon.

Table 9-7 Adverse Effects of Drugs Used to Treat Arrhythmias

Drug

Adverse Effects

Adenosine

Chest pain, flushing shortness of breath, sinus bradycardia/AV block

Amkxtofone

W: Hypotension sinus bradycardia

Oral Blue-gray skin díscolo atxx\ photosensitivity, corneal moodeposits, pulmonary fibrosis, hepatotoxicity, sinus

bradycardia, hypo- or hyperthyroidism, peripheral neuropathy, weakness. AV block

Atropine

Tachycardia, urinary retention, blurred visJor\ dry mouth, mydriasis

Digoxin

Nausea, vomiting. anorexj&green-ydlow halos around objects, ventricular arrhythmias

Diltiazem

Hypotension, sinus bradycardia. heart failure exacerbation. AV block

Dofetillde

Torsades de pointes

Dronedarone

Diarrhea, asthenia, nausea and vomiting, abdominal pain, bradycardia. 01 cfctress

Esmolol

Hypotensjoa sinus bradycardia. AV bkxk, heart failure exacerbation

HeCAtfWie

Dizziness, blurred vision, heart failure exacerbation

Ibutilide

Torsades de pointes

Lidocaine

Dizziness, confusion, seizures (rf dose too high)

Metoprolol

Hypotension, sinus bradycardia. AV block, fatigue, heart failure exacerbation*

Mexiletine

Nausea vomiting. Gl distress, tremor, dizziness, falKjue. seizures (if dose too high)

Procainamide

Hypotension, torsades de pointes

Propafenone

Dtainess, blurred vision

Propranolol

Hypotension, bradycardia, AV block, heart faiure exacerbation*

Sotalol

Sinus bradycaicfca, AV block fatigue, torsades de pointes

Verapamil

Hypotension, heart failure exacerbation, bradycardia^ AV block, constipation (oral)

AV. atrioventricular.

AV. atrioventricular.

'Associated with IV administrattoa irupproprlatily high oral doses at initiation of therapy, or overly aggressive and raprf dose titration.

FIGURE 9-5. Decision algorithm for ventricular rate control using IV drug therapy for patients presenting with the first detected episode or an episode of persistent atrial fibrillation that is hemody-namically stable. aDrugs administered IV. bDiltiazem is generally preferred over verapamil because

of a lower risk of severe hypotension. (P-blocker, esmolol, metoprolol, or propranolol; bpm, beats per minute; CCB, calcium channel blocker [diltiazem or verapamil]; HF, heart failure; LV, left ventricular; LVEF, left ventricular ejection fraction.)

FIGURE 9-6. Decision algorithm for long-term ventricular rate control with oral drug therapy for patients with paroxysmal or permanent atrial fibrillation. With each therapy/dose change, assess heart rate control. Goal less than 100 bpm or reduction of heart rate by more than 20% with symptom relief. If goal is not met, move to next step in algorithm. (bpm, beats per minute; CCB, calcium channel blocker [diltiazem or verapamil]; HF, heart failure; LV, left ventricular function; LVEF, left ventricular ejection fraction.)

Table 9-8 Drugs for Conversion of AF to Normal Sinus Rhythm

ton! Inuouf Infusion

Trwtmint

L gating On»

Rut*

Drug Interaction*

Arvnodsrone

W mg/trf IV over HJ-WmlrMiet

\.?-uityji h

luiil iiK efimlnrtsn rf digoian and warfarin

DcJetilde

See below1 po:ienh must be hospitalized tor 3 i l.jv1. du r | ■nilhilkvi or rlx'T jpy

Cimelitfme, hydroctibnolhiazide, Mlrxoiiii/uli uVf Itrttyi'irafjL'tWi-uih*, pforreihasine, irimethopfim.verapamt f.JJ inhibit -'^>l> ■! ill: li - r1 m "..si vi il

IbuviJe

1 mglYavflrlOmlnuleSi followed by a -5 eccmd t mq Wiley!-* neiysmy

Props IWvjns

fcOOmg single oral rioae

-

-

Ffecainide

200-300 rug single oral dose

"Doltlilidk: dusintf (akutated GeoflWit CfrarLmi'i Gisalw than 60 mUmin 40-60 ittl/rmi* 20-+0 mUfnm Lew than 25rnL/niii'

JAjfrr.VibV Adsi1 500 meg Ivice daily 2» rTiOJ (witt'Afily 12= meg twice daily ConlrairxJtiJlud

VrdtlUl liljfilUliOO

"Doltlilidk: dusintf (akutated GeoflWit CfrarLmi'i Gisalw than 60 mUmin 40-60 ittl/rmi* 20-+0 mUfnm Lew than 25rnL/niii'

JAjfrr.VibV Adsi1 500 meg Ivice daily 2» rTiOJ (witt'Afily 12= meg twice daily ConlrairxJtiJlud

A decision strategy for conversion of AF to sinus rhythm is presented in Figure 9-7. The cardioversion decision strategy depends greatly on the duration of AF. If the AF episode began within 48 hours, conversion to sinus rhythm is safe and may be attempted with elective DCC or specific drug therapy (Fig. 9-7). However, if the duration of the AF episode is longer than 48 hours or if there is uncertainty regarding the duration of the episode, two strategies for conversion may be considered. Data indicate that a thrombus may form in the left atrium during AF episodes of 48 hours or longer; if an atrial thrombus is present, the process of conversion to sinus rhythm, whether with DCC or drugs, can dislodge the atrial thrombus and cause a stroke. Therefore, in patients experiencing an AF episode of 48 hours or longer, conversion to sinus rhythm should be deferred unless it is known that an atrial thrombus is not present. In the past, common practice in patients with AF of greater than 48 hours duration was to anticoagulate with warfarin, maintaining a therapeutic International Normalized Ratio (INR) for 3 weeks, after which cardioversion may be performed. Patients were subsequently anticoagulated for a minimum of 4 weeks following the restoration of sinus rhythm. Today, rather than se nd patients with ongoing AF home for 3 weeks of anticoagulation, it has become standard practice at many institutions to perform a transesophageal echocardiogram (TEE) to determine whether an atrial thrombus is present; if such a thrombus is not present, DCC or pharmacologic cardioversion may be performed within 24 hours. If this strategy is selected, hospitalized patients should undergo anticoagulation with IV unfractionated heparin, with the dose targeted to a partial thromboplastin time (PTT) of 60 seconds (range 50-70 seconds), or warfarin therapy (target INR 2.5; range 2-3) during the hospitalization period prior to the TEE and cardioversion procedure. If no thrombus is present during TEE and cardioversion is successful, patients should maintain anticoagulation with warfarin (target INR 2.5; range 2-3) for at least 4 weeks. If a thrombus is observed during TEE, then cardioversion should be postponed and anticoagulation should be continued indefinitely. Another TEE should be performed prior to a subsequent cardioversion attempt.

Afib Algorithm
FIGURE 9-7. Decision algorithm for conversion of hemodynamically stable atrial fibrillation to normal sinus rhythm. (DCC, direct current cardioversion; HF, heart failure; LVEF, left ventricular ejection fraction; TEE, transesophageal echocardiogram.) international Normalized Ratio 2-3.

Conversion of AF to sinus rhythm is usually performed in patients with the first detected episode of AF or in patients with an episode of persistent AF. In patients with permanent AF, conversion to sinus rhythm is usually not attempted because cardioversion is unlikely to be successful, and in those rare patients in whom sinus rhythm is restored successfully, AF usually recurs shortly thereafter.

Maintenance of Sinus Rhythm/Reduction in the Frequency of Episodes of Paroxysmal AF. In many patients, permanent maintenance of sinus rhythm following cardioversion is an unrealistic goal. Many, if not most, patients experience recurrence of AF after cardioversion. Therefore, a more realistic goal for many patients is not permanent maintenance of sinus rhythm, but rather reduction in the frequency of episodes of paroxysmal AF.

In recent years, numerous studies have been performed to determine whether drug therapy for maintenance of sinus rhythm is preferred to drug therapy for ventricular

29_32

rate control. In these studies, patients have been assigned randomly to receive therapy either with drugs for rate control or with drugs for rhythm control (Table 9_9).

Table 9-9 Drugs for Maintenance of Sinus Rhythm/Reduction in the Frequency of Episodes of AF

Drug

Dose

Amiodarons

100-400 mg oratiy once dally

Dofetiiide

As described in Table 9-8

Dronedarone

400 mg orally twice daily

Solabl

30-160 mg orally twice dally

Propafenone

150-300 mg prally thrice daily

flecainide

100-150 mg orally three times daily

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