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CHAPTER 132 Supraventricular Tachyarrhythmias

Elbert B. Chun, MD

Gerard M. McGorisk, MD, FACC, MRCPI

Key Clinical Questions

What electrocardiographic findings help differentiate between the common supraventricular tachyarrhythmias (SVTs)?

What acute and chronic management strategies are indicated for various SVTs? What comorbid conditions increase the risk of thromboembolic complications in patients with atrial fibrillation?

Which patients with atrial fibrillation deserve anticoagulation, and which of these patients need bridging anticoagulation until oral warfarin attains therapeutic international normalized ratio (INR)?

Which SVTs deserve electrophysiologic intervention over medical management?

EPIDEMIOLOGY

Supraventricular tachyarrhythmias (SVTs) comprise an array of narrow-complex arrhythmias that originate above the ventricles and include both the most commonly

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encountered arrhythmia, atrial fibrillation (AF), and the uncommon ones, such as Wolfe- Parkinson-White (WPW) syndrome. Based on Medicare and a sampling of national community hospital discharge database, AF occurs 10-fold more frequently than paroxysmal SVTs such as AVnRT. This chapter describes in detail the common atrial arrhythmias encountered by hospitalists, and explains the uncommon arrhythmias that hospitalists should recognize and manage with cardiologist or electrophysiologist consultation or referral. The chapter will briefly describe arrhythmia mechanisms while focusing on arrhythmia diagnosis, management options in the acute setting, and long- term management strategies—all essential for a seamless transition beyond the inpatient setting.

PRESENTATION Common presenting symptoms of SVTs include rapid palpitations, chest discomfort, dyspnea, presyncope, and syncope. Additionally, atrial fibrillation and atrial flutter may present with new stroke symptoms. Particularly in the elderly with atrial fibrillation, palpitations and chest discomfort are often absent and excessive fatigue is the predominant symptom.

RISK STRATIFICATION

As SVT is a heterogenous disorder describing different arrhythmias with vastly different clinical prognosis. As such, the crucial initial step is the proper recognition of the rhythm disorder to individualize treatment strategy and prevention of adverse events.

RHYTHM IDENTIFICATION

When evaluating patients with a narrow-complex arrhythmia, the QRS complex is by definition less than 120 ms. The regularity of the RR intervals then helps reduce the numerous possibilities, as indicated in the SVT recognition algorithm (Figure 132-1). Only four possibilities exist if the RR intervals are irregular: (1) atrial fibrillation, (2) atrial flutter with variable atrioventricular (AV) node blockade, (3) atrial tachycardia with variable AV node blockade, and (4) multifocal atrial tachycardia (MAT).

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Figure 132-1 Supraventricular tachyarrhythmia recognition algorithm. AF, atrial fibrillation; Aflutter, atrial flutter; AT, atrial tachycardia; AV block, atrioventricular block; AVnRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentry tachycardia; MAT, multifocal atrial tachycardia; PJRT, paroxysmal junctional reentrant tachycardia; SNRT, sinus node reentry tachycardia.

More challenging to diagnose is the SVT with a regular RR interval. If, however, no P- wave can be identified, this indicates the most common form of paroxysmal SVT: atrioventricular nodal reentrant tachycardia (AVnRT). The P-wave in typical AVnRT is buried within the QRS complex. If the P-wave is identified then determine if there is more than one P-wave for each conducted QRS. If so, then only atrial flutter or atrial tachycardia remains as possible diagnoses.

Finally, if only a one-to-one relationship between the P-waves and QRS complexes exists, measuring the RP interval will further narrow the likely rhythms (Figure 132-2). The response of the rhythm to bedside vagal maneuvers or intravenous adenosine can be used to better differentiate the regular narrow-complex arrhythmias by transiently slowing the

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AV conduction and revealing the P-waves, converting the rhythm to sinus, or gradually slowing and reaccelerating the tachycardia (Table 132-1).

Figure 132-2 ECG rhythm intervals demonstrating how to measure the PR and RP intervals.

TABLE 132-1 Effect of Transient Atrioventricular Node Blockade on Supraventricular Tachyarrhythmia Diagnosis

Rhythm Response to Transient AV Node Blockade (Vagal Maneuvers or IV Adenosine)

AVnRT Sudden termination AVRT Sudden termination Sinus reentry tachycardia Sudden termination Focal atrial tachycardia Sudden termination, or gradual slowing and

reacceleration Ventricular tachycardia (high septal or fascicular origin)

No response

Sinus tachycardia Gradual slowing, then reacceleration Nonparoxysmal junctional tachycardia

Gradual slowing, then reacceleration

Atrial flutter Persistent atrial tachycardia and transient high-grade AV blockade

Macro reentrant atrial tachycardia Persistent atrial tachycardia and transient high-grade AV blockade

AVnRT, atrioventricular nodal reentrant tachycardia; AVRT, atrioventricular reentry tachycardia; VTACH, ventricular tachycardia.

Proceeding through the SVT recognition algorithm (see Figure 132-1) using a sample ECG (Figure 132-3), the clinician first recognizes that the rate is greater than 100 beats per minute (bpm). The QRS complexes are narrow, thus leading to a generic diagnosis of SVT. Following the SVT recognition algorithm, the regularity of the RR intervals is assessed, and

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the absence of P-waves leads to the conclusion that the SVT is attributable to typical AVnRT (see Figure 132-3).

Figure 132-3 Atrioventricular nodal tachycardia (AVnRT).

ATRIAL FIBRILLATION

EVALUATION

Before the age of 60, the prevalence of atrial fibrillation occurs uncommonly, in stark contrast to the prevalence estimate of 8% among those older than 80 years. As AF is the most common arrhythmia encountered by the inpatient clinician, this section will address the questions pertaining to the valvular and nonvalvular etiology of this arrhythmia, judicious utilization of cardioversion, thromboembolic and other complications, methods for estimating risk of stroke, and management strategies in the acute and chronic settings.

Patients with atrial fibrillation are classified in one of three categories: (1) paroxysmal AF, (2) persistent AF, or (3) permanent AF (Table 132-2).

TABLE 132-2 Atrial Fibrillation Nomenclature

Paroxysmal AF Episodes lasting <7 days and spontaneously converting to sinus rhythm

Persistent AF Episodes lasting >7 days unless chemical or electrically cardioverted to sinus rhythm

Permanent AF AF resistant to multiple attempts at cardioversion Lone AF AF in patients younger than 60 years old in the

absence of any predisposing factor

AF, atrial fibrillation.

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The atrium in patients with AF shows evidence of fibrosis and increased extracellular mass changes that are seen both in the myocardium of the elderly and in ischemia- induced hibernating myocardium. Within this scarred milieu, a focal-enhanced automaticity and variance in atrial tissue refractory and conduction times (known collectively as the multiple wavelet hypothesis) leads to this common arrhythmia. The enhanced automaticity often can be isolated to atrial tissue near the pulmonary veins. In addition to the aging process, any medical condition that leads to elevated left atrial pressure and dilated atrium—hypertension, mitral stenosis or regurgitation, and any cardiomyopathy—will predispose the patient to atrial fibrillation. Hyperadrenergic states— sepsis, alcohol ingestion or withdrawal, postoperative state, and thyrotoxicosis—also predispose to AF. Lone atrial fibrillation describes AF in patients younger than 60 years old in the absence of any predisposing factor.

INPATIENT MANAGEMENT

Hemodynamic compromise versus stable tachycardia

Common clinical scenarios for hospitalized patients with AF include those with stable tachycardia and those with hemodynamic compromise. For those with hypotension, a trial of short-acting rate-controlling agents (eg, esmolol) could be attempted to determine if slowing the tachycardia may improve the hemodynamics, keeping in mind that these very agents may exacerbate hypotension. Intravenous digoxin and amiodarone are options if hypotension prevents the use of β-blockers and calcium channel blockers. Synchronized direct cardioversion should be performed if the hypotension does not resolve (see Chapter 125). Currently there are two types of defibrillators: monophasic and biphasic. Biphasic defibrillators are now significantly more common and require less energy and reduced number of shocks delivered to achieve successful cardioversion. Biphasic defibrillators also have reduced skin injury. The monophasic device should be set at a minimum of 200 J and a maximum of 400 J. The biphasic device demonstrates effective cardioversion at 200 J and often times at just 100 J for AF.

Rate control

One or multiple rate-controlling agents may be needed to provide adequate control of the ventricular response (Table 132-3). After 24 hours on the intravenous infusion, switching to an oral regimen can be initiated. β-Blockers and nondihydropyridine calcium channel blockers are considered first-line agents. Intravenous digoxin and amiodarone are reasonable options, particularly in the setting of congestive heart failure. An important limitation of digoxin is that its vagally induced AV node blockade can be easily overcome in nonsedentary patients. Although very effective in rate control and even rhythm conversion, amiodarone has a long-term side effects profile which relegates its use as a distant second option. Clinicians should target a heart rate under 110 bpm at rest but consider patient symptoms in modification of rate control.

TABLE 132-3 Intravenous Medications for Rate-Control in Atrial Fibrillation or Atrial Flutter

Medication Loading Dose Maintenance Dose Side Effects

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Esmolol 500 mcg/kg over 1 min 60-200 mcg/kg/min IV

Hypotension

Metoprolol 2.5-5 mg IV over 2 min Up to 3 doses

NA Hypotension

Diltiazem 0.25 mg/kg IV over 2 min 5-15 mg/h Hypotension Verapamil 0.075-0.15 mg/kg IV over

2 min NA Hypotension

Digoxin 0.25 mg IV every 2 h up to total dose 1.5 mg

0.125-0.375 mg/day IV or orally

Digoxin toxicity, heart block

Amiodarone 150 mg IV over 10 min 0.5-1 mg/min IV Pulmonary toxcity, hepatitis, skin discoloration, thyroid dysfunction, corneal deposits, optic neuropathy

The presence of an accessory pathway would be an absolute contraindication in the use of AV node-blocking agents. As electrical impulses are conducted nondecrementally via the accessory pathway, the ventricular response in AF will actually increase and may degenerate into ventricular fibrillation (VFIB).

Rhythm control and consultation

After assessing clinical stability and adequately controlling the rapid ventricular response, the clinician should determine if the rhythm event is new, recurrent, or an exacerbation of a permanent form of the arrhythmia. If the condition is a new event or a paroxysmal one with infrequent yet very symptomatic recurrences and has been present for less than 48 hours, cardioversion—chemical or electrical—followed by an attempt to maintain a sinus rhythm may offer symptom benefit and is recommended by the ACC-AHA AF guidelines from 2006 (Table 132-4). If the AF duration is longer than 48 hours, cardioversion remains an option after transesophageal echo (TEE) is negative for left atrial thrombus. Cardioverting those with new-onset AF provides the theoretical benefit of curtailing the risk of developing permanent AF.

TABLE 132-4 Indication for R-Wave Synchronized Cardioversion in Atrial Fibrillation

Rapid ventricular response not responding to pharmacologic measures in setting of ongoing angina, heart failure, myocardial ischemia, or symptomatic hypotension Pre-excitation with rapid ventricular response or hemodynamic instability Stable hemodynamics, but poorly tolerated symptoms Early relapse of atrial fibrillation after attempted cardioversion, proceed with administration of antiarrhythmic medications first, then repeat cardioversion Consider patient preferences in the setting of infrequent relapses

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Cardioversion can be achieved not only with electrical means, but also chemical means (Table 132-5). The antiarrhythmics used for cardioversion should be considered after consultation with cardiology service. A class III agent, ibutilide, can be used in select patients that have no evidence of systolic dysfunction, normal magnesium and potassium levels, and a normal corrected QT interval (QTc). Due to the risk of torsades de pointes, this should be performed in a setting equipped to handle this potential complication. Ibutilide has the advantage of increasing the success of electrical cardioversion following a failed chemical cardioversion. An oral class III agent, tikosyn, can be used to both convert to a sinus rhythm and also maintain a sinus rhythm. This medication should be reserved for cardiology consultants due to the need for close monitoring of the QT interval, renal dose adjustments, and limitations of use in patients with liver dysfunction. If the QT interval is greater than 500 ms, this medication should not be initiated or should be discontinued. The use of medications to maintain a sinus rhythm should remain under the care of a cardiologist due to the frequency of treatment failure and significant risk of malignant ventricular arrhythmias.

TABLE 132-5 Medications for Pharmacologic Cardioversion of Atrial Fibrillation

Medication Antiarrhythmic Class Dosing Route Comments

Amiodarone (codarone, pacerone)

III 400 mg orally twice a day for 2 wks (10 g load), then 200 mg orally every day 150 mg IV over 10 mins, then 1 mg/min for 6 h, then 0.5 mg/min for 18 h (1 g load)

Orally Outpatient option: oral load (gastrointestinal side effects common) Other side effects common and severe: pulmonary fibrosis, corneal deposits, thyroid dysfunction, hepatitis, skin deposition

Ibutilide (corvert)

III If weight >60 kg, 1 mg IV once; may repeat dose if no response in 10 mins If weight <60 kg, then 0.01 mg/kg IV; may repeat if no response after 10 mins

IV Inpatient only usually cardioverts within 1 h monitor for QT prolongation Torsades 4% (more common in women) Must monitor K+ and Mg+2

Dofetilide (tikosyn)

III 500 mcg orally twice a day (restricted distribution in the US to trained prescribers and facilities)

Orally Inpatient initiation only; adjust for renal function, age, body size QT prolongation

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Many drug interactions (CYP3A4) Contraindicated with Bactrim, HCTZ, verapamil

Flecainide Ic Start 50 mg orally twice a day, may increase 100 mg/d every 4 days; max dose 300 mg every day

Orally or IV

Contraindicated in structural heart disease Adjust dose for renal dysfunction

Propafenone Ia Start 150 mg orally three times a day, then may increase to 225 mg orally three times a day after 4 days, then, up to 300 mg orally three times a day

Orally or IV

Contraindicated in structural heart disease including significant LVH, CHF, severe obstructive lung disease

Anticoagulation

The unorganized atrial contractions during AF will lead to the formation of thrombus or spontaneous echo contrast (SEC) within the left atrium or the left atrial appendage posing a substantial risk of thromboembolic phenomena to the arterial circulation, which usually manifests as stroke and, less commonly, mesenteric ischemia or an acutely ischemic limb. The transthoracic echocardiogram is considered the diagnostic test of choice for initial evaluation. It is useful in assessing left atrial size and left ventricular function, but cannot exclude atrial thrombus. The transesophageal echocardiogram provides high resolution of the left atrium and left atrial appendage and to exclude thrombus and permit early cardioversion. Thrombus or dense SEC would preclude the option for early cardioversion and necessitate the need for full anticoagulation for 4 weeks prior to cardioversion. In the absence of thrombus or SEC on TEE, the patient may receive early cardioversion in the setting of anticoagulation. For AF recognized greater than 48 hours after onset in patients who do not undergo TEE, full anticoagulation for 4 weeks is recommended followed by cardioversion, if indicated.

In either strategy, anticoagulation for a minimum of 4 weeks postcardioversion is necessary to reduce the risk of thromboembolic complications. The risk of embolic stroke is approximately 1% with either approach. Stroke risk postcardioversion is due to a “stunning” effect on the left atrium after any form of cardioversion (electrical, chemical, or even spontaneous). This stunning refers to a delay in the resumption of mechanical contraction of the left atrium, providing an environment ripe for stasis and thrombus formation. Benefits from an early cardioversion approach include quicker conversion to a sinus rhythm, accelerated care for the patient, and potentially less bleeding complications associated without the preceding 4 weeks of anticoagulation.

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PRACTICE POINT

Transesophageal echocardiogram is a highly sensitive test to rule out thrombus within the left atrium and left atrial appendage to permit an early cardioversion strategy, if indicated.

Ablation strategies

Invasive management options for atrial fibrillation should be considered secondary options following failure of medical therapies and recurrent admissions due to symptomatic palpitations or heart failure exacerbations. The palpitations associated with atrial fibrillation can be distressing to some individuals, particularly younger patients, and have significant negative impacts on quality of life. If the use of antiarrhythmic regimens has failed, options for catheter-based interventions or even intraoperative left atrial ablation, also known as the Maze procedure can be offered. One catheter-based approach called ablate-and-pace, entails ablating the AV node and then pacing the ventricle. Another catheter-based approach involves isolating the focus of automaticity, usually near the pulmonary veins of the cavoatrial isthmus, ablating the foci, and initiating anticoagulation therapy thereafter. The latter approach is relatively new and long-term outcome research is still pending. The short-term safety of the procedure in centers with established experience has been proven with death rates or stroke rates under 1% and overall major complications about 6% based on international survey data. However, the mean age of the patients enrolled in these trials was 55 years old with intact systolic function and relatively nondilated atrial diameters. More long-term outcome data will be needed before catheter- based interventions can be considered a parallel option to medical treatment. A final option usually reserved for those who are undergoing open heart bypass or valve replacement is the Maze procedure, and even left atrial appendage resection, both of which may prevent the occurrence of postoperative atrial fibrillation.

Death or significant neurologic deficits occur in 71% of patients with their first episode of embolic complications associated with AF. Reducing this risk is a crucial component in the management of AF. The annual risk of strokes for AF is approximately 4.5% per year, which is reduced by two-thirds (to 1.5% per year) if patients are fully anticoagulated. However, not all patients with this condition carry the same risk of embolic events and, therefore, should be managed based on risk. Clinicians must diagnose the etiology of AF, as that will help determine risk and direct management. The vast majority of AF is nonvalvular, but valvular etiologies such as significant mitral stenosis must be considered. A severalfold increase in thromboembolic risk occurs with mitral valve stenosis-associated atrial fibrillation, and mandates full anticoagulation regardless of other stroke risk factors present. Patients with other risk factors leading to atrial fibrillation have variable levels of evidence supporting full anticoagulation, and some patients with few stroke or embolism risk factors may not attain benefit from anticoagulation that outweighs its risks (Table 132-6).

TABLE 132-6 Antithrombotic Recommendations for Atrial Fibrillation by Etiology

AF Risk Factor Therapy Recommendation Level of Evidence

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Thyrotoxicosis Full anticoagulation (eg, warfarin)

Level C: Expert opinion (ACC/AHA guidelines)

Mitral stenosis Full anticoagulation (eg, warfarin)

Level C: Expert opinion (ACC/AHA guidelines)

Mechanical valve Full anticoagulation (eg, warfarin)

Level 1A (ACCP guidelines 2008)

CHADS2 score ≥ 2 Full anticoagulation (eg, warfarin)

Level 1A (ACCP guidelines 2008)

CHADS2 score = 1 Full anticoagulation (eg, warfarin) or aspirin (75-325 mg daily)

Level 1A (anticoagulation) Level 1B (asprin) (ACCP guidelines 2008)

CHADS2 score = 0 Aspirin therapy (75-325 mg daily)

Level 1B (ACCP guidelines 2008)

ACC/AHA, American College of Cardiology/American Heart Association; ACCP, American College of Chest Physicians. Level 1A (ACCP): Consistent evidence from randomized controlled trials without important limitations or exceptionally strong evidence from observational studies. Level 1B (ACCP): Evidence from randomized controlled trials with important limitations (inconsistent results, methodologic flaws, indirect or imprecise), or very strong evidence from observational studies. Level C (ACC/AHA): Recommendation based on expert opinion, case studies, or standards of care.

When considering the more common scenario of nonvalvular atrial fibrillation, multiple risk stratification strategies have been published over the decades to estimate the risk of thromboembolic complications, and to date the one most widely used and derived from large cohort data is known as the CHADS2 score. Congestive heart failure, Hypertension, Age ≥ 75, and Diabetes each contributes one point in this risk stratification tool whereas Stroke contributes two points. The total number of points corresponds to a level of risk (incidence) of embolic stroke each year (Table 132-7).

TABLE 132-7 CHADS2 Score and Stroke Risk

Number of Factors Risk of Stroke (%/y) 0 (lower risk) 1.9 (1.2-3.0) 1 (intermediate risk) 2.8 (2.0-3.8) 2 (high risk) 4.0 (3.1-5.1) 3 5.9 (4.6-7.3) 4 8.5 (6.3-11.1) 5 12.5 (8.2-17.5) 6 18.2 (10.5-27.4)

CHADS2 score is calculated by adding 1 point for each of the following:

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Recent Congestive heart failure, Hypertension, Age ≥75 years, Diabetes mellitus; and 2 points for prior Stroke/transient ischemic attack.

By using this risk stratification tool clinicians can balance the benefits of therapeutic anticoagulation against the well-known complication, bleeding. With no risk factors for thromboembolic phenomena, as in the scenario of lone atrial fibrillation, the risk of bleeding complications with coumadin outweighs the benefit of stroke prevention. An acceptable alternative stroke risk-reduction strategy for patients who have low baseline risk (CHADS2 = 0) or who have contraindications to anticoagulation is antiplatelet therapy with aspirin (81-325 mg daily).

For patients with intermediate risk (CHADS2 score = 1), one should implement an additional risk stratification tool known as the CHA2DS2-VASc (Table 132-8) to better define the risk of thromboembolic stroke. As recommended by national cardiology organizations, anticoagulation should be strongly considered if the score is 2 or greater. If the score 1 point, then either aspirin or anticoagulation are viable options. Major bleeding complication risk with anticoagulation can be estimated using a risk stratification scheme with the acronym HAS-BLED (Table 132-9).

TABLE 132-8 CHA2DS2-VASc

Number of Factors Risk of stroke (%/y) 0 0 1 1.3 2 2.2 3 3.2 4 4.0 5 6.7 6 9.8 7 9.6 8 6.7 9 15.2

CHA2DS2-VASc score is calculated by adding 1 point for each of the following: Recent CHF, hypertension, Age 65-74, DM, female gender, Vascular disease (PVD, CAD, aortic plaque); and 2 points for Age ≥75 and prior Stroke/TIA.

TABLE 132-9 HAS-BLED Score

Letter Clinical Characteristic Points H Hypertension 1 A Abnormal renal or liver disease 1 for each S Stroke 1

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B Previous major bleeding 1 L Labile INR 1 E Elderly (age >65) 1 D Drugs or alcohol 1

Hypertension – SBP >160 mm Hg Abnormal renal function: dialysis or serum creatinine >2.26 mg/dL (200 umol/L) Abnormal liver function: cirrhosis, or elevated AST or ALT >3 X upper limit of normal Labile INR: unstable INR or TTR (time in therapeutic range) <60% Drugs: aspirin, other antiplatelet medications, NSAIDS, or alcohol abuse

The HAS-BLED score contains the variables hypertension, abnormal renal function, abnormal liver function, stroke, previous bleeding, labile INR’s, age >65 years old, concomitant use of aspirin or antiplatelet agent, and excessive alcohol consumption with each counting as a point. The final score then correlates with the risk of major bleeding per 100 patients per year (ie, % major bleeds per year with anticoagulation therapy).

These risk estimation tools can be used to counsel patients regarding treatment choices, including benefits and risks, and help identify patients who might gain more overall benefit from antiplatelet aspirin therapy rather than anticoagulation. The HAS- BLED tool might also be used to help determine which patients deserve more intensive outpatient monitoring of their anticoagulation (eg, in an anticoagulation clinic). National organizations recommend using caution when the HAS-BLED score ≥ 3 and a detailed discussion of risk and benefits with the patient.

More data over the past several years have demonstrated a larger role of AF in patients with cryptogenic strokes. Insertable cardiac monitors in a study published in 2015 have been utilized in this cohort of patients and have detected up to 8.9% patients with AF at 6 months compared to just over 1% in the cohort following standard of care monitoring. The most recent national medical organizations do not provide strong guidance in the intensity and duration of monitoring for potential AF detection in cryptogenic, but this data suggests a 24-hour Holter monitor is vastly insufficient.

ATRIAL FIBRILLATION AND OLDER PEOPLE: WARFARIN CONTROVERSY

Often a difficult clinical management decision, the use of anticoagulation in older patients is controversial. Atrial fibrillation is the etiologic factor for 36% of strokes in individuals over the age of 80. The morbidity and mortality of a first stroke due to this disease is 71%. Meta-analysis data estimate the overall risk reduction with vitamin-K antagonists at 66% and with aspirin at 21%. Recent data have also demonstrated that patients over the age of 85 benefit more from anticoagulation than younger cohorts. Thus, the argument for anticoagulation with warfarin in this group is compelling. However, the risk of major bleeding complications is still relevant. The rate of intracranial hemorrhage (ICH) while taking warfarin is approximately 0.3% to 0.6% per year (RR ~ 2, compared to control). Aspirin also carries an increased risk of ICH (RR ~ 1.4 compared to control). Although the risk of ICH seems low, this estimate may be underestimated as older patients were underrepresented in the early randomized trials performed almost 20 years ago. More

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recent observational studies have estimated the risk of a major bleeding complication in individuals over the age of 80 to be 13% per year including a 2.4% per year risk of ICH.

Additional concerns for anticoagulation in older people are the increased risk for falls, likely drug interactions due to polypharmacy, complexity of coumadin regimens, need for close monitoring, and the large representation of nursing home patients. Even in research trials studying the efficacy of coumadin to prevent strokes, only two-thirds of the INRs were in the therapeutic range. Some of these concerns can be addressed with the novel oral anticoagulants that reduce the need for frequent laboratory monitoring and reduce the concerns for drug interactions associated with polypharmacy. The data comparing coumadin with the direct thrombin inhibitor, dabigatran, demonstrate better stroke prevention with the higher dose of dabigatran at 150 mg orally twice a day and even a trend toward an overall mortality benefit after a median follow-up period of 2 years. The downside is the increased propensity of gastrointestinal bleeding compared to warfarin. The lower dose, 110 mg orally twice a day, was found to have an equivalent reduction of stroke risk and a lower risk of major bleeding complications but is not available in the United States. There are also three factor Xa inhibitors that Food and Drug Administration (FDA) approved to prevent strokes in the setting of nonvalvular AFIB, rivaroxaban, apixaban, and edoxaban. Rivaroxaban has been shown to be noninferior in stroke prevention, major bleeding complications, and mortality with warfarin. Apixaban however has been shown to prevent slightly more strokes, reduce risk of major bleeding outcomes, and reduce risk for mortality compared to warfarin. The most recent FDA approval of edoxaban in January 2015 was based on randomized trial data demonstrating superior stroke prevention compared to warfarin, less major bleeding complications, but slightly higher gastrointestinal bleeding complications. All of the novel anticoagulants compared to Coumadin have half as many intracranial bleeds. As no head-to-head studies have been conducted among the novel agents, all are considered viable options for stroke prevention for nonvaluvular AFIB.

PRACTICE POINT

Novel anticoagulants reduce the need for frequent laboratory monitoring and reduce the concerns for drug interactions associated with warfarin and polypharmacy. These medications (dabigatran, rivaroxaban, apixiban, edoxaban) are approved for use in atrial fibrillation for stroke prevention. However, the cost may be prohibitive if not insured. Apixiban received FDA approval in 2015 for use in patients with ESRD on hemodialysis despite the absence of randomized control data but supported by pharmacokinetic data. Risk scores such as CHADS2, CHA2DS2-VASc apply only to nonvalvular AFIB. AFIB related to mechanical valves, mitral stenosis or rarely hyperthyroidism are at much higher risk for thromboembolic phenomena and require anticoagulation. The novel anticoagulants have not been FDA approved in patients with mechanical heart valves. In fact, dabigatran has been shown to have been inferior to coumadin in preventing embolic stokes with mechanical heart valves. The ACCP 2012 guideline on antithrombotics recommends the use of bridging anticoagulation in AF in high risk patients with a CHADS2 score of 5 and 6. This has

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been supported by 2015 randomized trial BRIDGE which demonstrated more bleeding complications and no change in stroke prevention in those undergoing a bridging strategy. Bridging anticoagulation for those with low or moderate risk AFIB increases the risk of major bleeding complications and has not been proven to prevent more thromboembolic events via recent observational data and large randomized control trial in 2015.

Randomized trial data for the use of other antiplatelet agents (clopidogrel) in addition to aspirin for stroke prevention has been equivocal with respect to outcomes, with modest risk reduction of stroke but similar risk increase for major bleeding complications. Dual antiplatelet agents for stroke prevention are, therefore, not currently recommended.

POSTOPERATIVE ATRIAL FIBRILLATION

Postoperative atrial fibrillation (POAF) is the most common arrhythmia after surgery and observational data suggest an increased risk of short- and long-term mortality, increased length of stay, hospital costs, ICU length of stay, and stroke risk with this arrhythmia. Recent observational data in 2014 strongly suggest a twofold increase in stroke risk in patients with POAF compared to those with who didn’t develop AF after noncardiac surgery at 1 year. This was also true in those who underwent cardiac surgery but to a lesser degree (hazard ratio 1.3, CI 1.1, 1.6). POAF is also the most common reason for hospital readmission after open heart surgery. The risk of developing this arrhythmia varies based on the type of surgical intervention, with open heart procedures bearing the highest risk (Table 132-10). Some of the risk factors associated with POAF include age, atrial enlargement, procedures related to the heart such as valvular repair, and β-blocker discontinuation.

TABLE 132-10 Risk of Postoperative Atrial Fibrillation (POAF) Based on Type of Surgery

Surgery Type POAF/SVT % Thoracic (noncardiac) 9-29% Cardiothoracic 20-40% Orthopedics 4%

The peak incidence of POAF occurs on the second postoperative day, and the majority occurs within 5 days postoperative. The majority of recurrent episodes of POAF occurred within several days of the first episode. The majority of POAF rhythms will spontaneously revert to sinus rhythm by the sixth postoperative week. However, if POAF is poorly tolerated due to hemodynamic compromise, anticoagulation and cardioversion would be recommended. Preoperative β-blockade leads to significant reduction in POAF incidence, but conflicting data mire the actual effect on hospital length of stay, postoperative strokes, and mortality. The ACC/AHA 2006 guidelines for AF offer a class I recommendation of perioperative β-blockers for prevention of POAF in patients undergoing coronary revascularization surgery (CABG).

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POSTACUTE CARE: ATRIAL FIBRILLATION

If a patient is discharged on warfarin, rapid follow-up within 3 to 5 days is warranted as the risk of major bleeding complications is known to occur with initiation of anticoagulation. If an anticoagulation clinic is available, it would be strongly recommended to be monitored there. Within a week or two, the heart rate response can be reassessed as most patients will require AV nodal blocking agents to prevent a rapid ventricular response. The patient’s symptoms can be periodically reassessed to determine whether the treatment strategy, either rate-control or rhythm control, needs to be changed. It should be noted that the latter approach has not been proven to reduce mortality, but only to improve symptoms and quality of life for a select group a patients with intolerable palpations and fatigue associated with AFIB.

DISCHARGE CHECKLIST: AFIB

Transthoracic echocardiogram should have been performed recently to differentiate between valvular and nonvalvular AFIB and assess ventricular function and left atrial size. Thyroid function tests should have been completed to evaluate for hyperthyroidism. For new onset AFIB, early consultation with cardiology should be considered to evaluate the potential benefits of a rhythm control strategy. Ensure stroke risk stratification with CHADS2 or CHA2DS2-VASc has been discussed with the nonvalvular AFIB patient and documented. Ensure risk stratification for major bleeding complications via HAS-BLED has been discussed with patients on anticoagulation.

For those on vitamin-K antagonists, rapid follow-up within 3 to 5 days should occur to avoid the perils of major bleeding complications. For those on novel anticoagulants, ensure dosing has been based on level of renal function as FDA-approved antidotes are not available for the factor Xa inhibitors. For those with cryptogenic stroke, strongly consider longer-term monitoring via an event monitor or insertable cardiac monitor to sufficiently evaluate for potential unrecognized AF.

ATRIAL FLUTTER

EPIDEMIOLOGY

Atrial flutter is the next most common form of SVT after atrial fibrillation and can manifest into the typical and atypical pattern. The typical pattern, also known as counterclockwise flutter due to the pattern of the macro reentry electrophysiologic mechanism, manifests as a sawtooth pattern, typical for the P-wave negative deflections (Figure 132-4). The second form of atrial flutter has the opposite pattern with positive deflections in the P-wave sawtooth pattern (Figure 132-5). Even though the atrial rate ranges from 240 to 300 beats/min, the AV nodal block will prevent all the atrial impulses from reaching the ventricle. The block at the AV node is frequently 2:1 but can also manifest as 3:1 and 4:1 or even variable block. The individuals that develop atrial flutter usually have a disorder that directly or indirectly involves the right atrium. Tricuspid valvular disease, various

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pulmonary disorders, postsurgical repair of congenital heart disease, or any process leading to the enlargement of the right atrium increase the risk for atrial flutter.

Figure 132-4 Atrial flutter (2:1 block) with typical negative deflection P-waves revealing the classic “sawtooth” pattern.

Figure 132-5 Atrial flutter (2:1 block) with positive deflection P-waves revealing an upward “sawtooth” pattern.

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PRACTICE POINT

Any disease process leading to the enlargement of the right atrium increases the risk for atrial flutter.

EVALUATION

Practice guidelines from national and international organizations recommend to approach atrial flutter in the same manner as atrial fibrillation. A priority should be to ensure hemodynamic stability in the setting of a rapid ventricular rate and use of early anticoagulation barring contraindications. An echocardiogram will evaluate for any potential structural heart disease and clinical evaluation for any medical condition leading to increased right-sided heart disease.

MANAGEMENT

The management of atrial flutter is similar to the management of atrial fibrillation. Ventricular rate control is achieved by increasing the block at the level of the AV node to reduce ventricular response to the rapid atrial rate. Certainly if the patient is hemodynamically compromised, direct cardioversion should be performed (biphasic 100 J, monophasic 200 J). In contrast to AF, using calcium channel blockers or β-blockers alone are frequently insufficient in rate controlling the rhythm. It is often necessary to consider the addition of a class Ic antiarrhythmic, such as flecanide, to achieve satisfactory results. The class I agents are able to suppress the frequency of premature atrial beats, which trigger the development of this arrhythmia. Other agents to consider would be class III agents such as ibutilide for chemical cardioversion. Sotalol and amiodarone may also be used, but side effects need to be considered in chronic management.

PRACTICE POINT

In atrial flutter, avoid using flecainide as the sole treatment due to its ability to decrease the reentry circuit cycle length and potentially induce a fast, unstable 1:1 ventricular response and subsequent degeneration into ventricular fibrillation.

The risk of thromboembolic complications in atrial flutter is thought to be similar to that of atrial fibrillation, although there is a relative paucity of data compared with AF. For these patients, full anticoagulation should be strongly considered. Additionally, approximately 75% patients with atrial flutter also develop atrial fibrillation.

In contrast to atrial fibrillation, catheter-based intervention should be considered early in atrial flutter with rapid ventricular rate as medical therapy is frequently suboptimal. Success rates approaching 90% are reported with radiofrequency ablation (RFA) of the cavotricuspid isthmus, leading to a bidirectional block inhibiting the macro reentry mechanism of flutter. Due to the remaining anatomic or electrophysiologic conditions that remain after the RFA, the procedure is not considered curative. The recurrence rate is 10% to 20% over a period of 2 years but compares very favorably to the 60% recurrence rate of

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medical treatment alone. Less-frequent hospitalizations, lack of concern for medication side effects, and improved sense of quality of life are other factors weighing favorably toward a catheter-based ablative approach to atrial flutter management.

PRACTICE POINT

A strong consideration of catheter-ablation strategy should be considered in patients with atrial flutter and rapid ventricular rate as medical management of rapid ventricular rate is frequently suboptimal.

ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA EPIDEMIOLOGY

Atrioventricular nodal reentrant tachycardia (AVnRT) is the most common form of paroxysmal SVT, responsible for almost two-thirds of episodes; it is estimated that 10% of the general population has AVnRT. The palpitations characteristically start abruptly and may last for just a few minutes to as long as a few hours. They terminate as abruptly as they start. Additional symptoms include chest discomfort, dyspnea, lightheadedness, neck pulsations, and associated anxiety. These symptoms are often misdiagnosed as panic attacks if the arrhythmia is not caught while on a monitor. Signs of the arrhythmia include regular tachycardia with a heart rate between 120 and 200 bpm. Vagal maneuvers such as carotid sinus massage or the Valsalva maneuver can break the reentry circuit. This arrhythmia is usually not associated with structural heart disease and carries very little risk of death.

The mechanism of this tachyarrhythmia is a reentry circuit composed of the atrium, AV node or perinodal tissue, and the ventricle. The perinodal tissue or AV node exhibits a dual c