Cardiac Arrhythmias

From Topics and Advances in Internal Medicine, presented by the University of California, San Diego, School of Medicine

Educational Objectives

The goal of this program is to improve the diagnosis and treatment of cardiac arrhythmias. After hearing and assimi­lating this program, the clinician will be better able to:

1.   Describe the challenges of choosing among antiarrhythmic agents for bradycardia and tachycardia, based on rate, mechanism, and location.

2.   Explain the differences between the 6 atrial fibrillation (AF) classifications and how most of them can progress to permanent status.

3.   Differentiate between warfarin, enoxaparin, and aspirin therapy to appropriately care for patients with AF.

4.   Discuss the pros and cons of implantable pacemaker usage for bradyarrhythmias.

5.   Illustrate when catheter ablation can be effectivelyimplemented in clinical settings.

Faculty Disclosure

In adherence to ACCME Standards for Commercial Support, Audio-Digest requires all faculty and members of the planning committee to disclose relevant financial relationships within the past 12 months that might create any personal conflicts of in­terest. Any identified conflicts were resolved to ensure that this educational activity promotes quality in health care and not a proprietary business or commercial interest. For this program, the faculty and planning committee reported nothing to disclose. In his lecture, Dr. Krummen presents information related to off-label or investigational use of a therapy, product, or device.

Acknowledgements

Drs. Krummen and Blanchard were recorded at Topics and Advances in Internal Medicine, sponsored by the University of California, San Diego, School of Medicine, and held March 9-11, 2009, in San Diego, CA. The Audio-Digest Foundation thanks the speakers and the University of California San Diego School of Medicine for their cooperation in the production of this program.

Cardiac Arrhythmias

David E. Krummen, MD, Assistant Professor of Medicine, Division of Electrophysiology, University of Califor­nia, San Diego, and Veterans Affairs San Diego Healthcare System

Bradyarrhythmias

Intrinsic electrical system of heart: specialized tissue with ability to depolarize spontaneously and serve as pace­maker; sinoatrial node (SA) node drives heart; atrioventricular (AV) node and His-Purkinje system serve as backup pacemakers if SA node fails; injury to conduction system results in bradyarrhythmias

Backup pacemakers: unreliable; may stop working spontaneously, leading to sudden death; slower than SA node; backup rate may not generate sufficient cardiac output to maintain normal activity

Sinus bradycardia: etiologies  —  include hypothyroidism, hypothermia, and idiopathic fibrosis; symptoms  —  include fatigue, dyspnea, and syncope or near syncope; diagnosis  —  in relative sinus bradycardia (heart rate does not in­crease enough during exercise) treadmill test, electrocardiography, or combination of these useful; treatment  —  medications, eg, atropine, used acutely for symptomatic treatment, but side effects preclude long-term use; pace­maker frequently required

AV blocks: first degree AV block (prolonged PR interval)  —delay >200 ms from onset of P wave to onset QRS com­plex; benign and usually does not require treatment; Mobitz I (second degree type 1 AV block)  —  progressive lengthening of PR interval before dropped QRS complex; block within compact AV node itself; does not rapidly progress to complete heart block, and not associated with higher risk for sudden death, so no treatment required; if symptoms present, pacemaker used (rarely needed); Mobitz II (type II AV block)  —  conduction block in His-Pur­kinje system; fixed PR interval followed by blocked QRS complex; can progress rapidly to sudden cardiac death; pacemaker recommended, even without symptoms; complete heart block  —  total AV node or His-Purkinje conduc­tion block; atria and ventricles at independent, fixed rates; third degree AV block; symptoms include shortness of breath; patients at risk for sudden death; pacemaker recommended

Tachyarrhythmias

Definition: rate >100 bpm; may be physiologic or nonphysiologic; located above ventricles (supraventricular tachy­cardia [SVT]) or in ventricles (ventricular tachycardia [VT])

Sinus tachycardia: most common; normal sinus tachycardia (NST)  —  physiologic response to catecholamines and should not be treated; resolves after cause found and treated; inappropriate sinus tachycardia (IST)  —  persistent tachycardia at rest, out of proportion to physiologic, pharmacologic, or pathologic stimuli; thought due to defective norepinephrine uptake in synaptic cleft; typically treated with b-blockers, but if treatment unsuccessful, ablation of SA node may correct problem

Atrial Tachyarrhythmias

Atrial tachycardia: atrial cells apart from SA or AV node fire abnormally fast and take over pacemaker function; symptoms include palpitations and lightheadedness; treatment  —  calcium channel blockers (CCBs) and b-blockers first-line; if ineffective, add antiarrhythmic drug, eg, flecainide; class IC agent); if drugs inadequate, find cells and ablate them

Atrial flutter: reentry around tricuspid valve annulus; sustained by cavotricuspid isthmus; electrocardiography (ECG) has sawtooth pattern; rate difficult to control medically; anticoagulation indicated; ablation first-line ther­apy, and has few complications because involved area known

Atrial fibrillation (AF): affects £10% of population over age 80 yr; involves abnormal automaticity, reentry, or com­bination of these; rapid and disorganized activation of atria with irregular fast activation of ventricles seen in elec­trophysiology laboratory; pulmonary veins often source of AF

Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial: rate control  —  slowing heart rate and anticoagulation; rhythm control  —  rate control plus antiarrhythmic agents or ablation; trial found no mortality difference between strategies, but higher quality of life (QOL) for AF patients on rhythm control

Types of AF: paroxysmal  —  starts and stops spontaneously; rate control recommended; class 1C antiarrhythmics used (eg, flecainide); ablation of symptomatic drug-refractory AF more effective than for persistent AF; repeat ab­lation plus antiarrhythmic drugs yield 90% to 92% success rate;  persistent  —  AF does not stop spontaneously; treat with rate control medications and anticoagulation; class III antiarrhythmics (eg, amiodarone, sotalol, dofetilide); 50%-70% success rate; repeat ablation and antiarrhythmic therapy can achieve control; ablation electrically isolates pulmonary veins so rapid firing not translated to rest of heart

AV nodal reentrant tachycardia (AVNRT): »40% of patients have slow and fast pathway in AV node; most of time, slow pathway does not function; in AVNRT, early beat wave front blocked in fast pathway, goes down slow path­way, activates His-Purkinje cells and ventricles, travels up fast pathway, and depolarizes atria; ECG shows irreg­ular narrow complex tachycardia with atrial activation immediately after QRS complex (pseudo R¢ wave)

Treatment: Class II b-blockers or Class IV CCBs can suppress reentry; >95% success rate with catheter ablation of slow pathway

Wolf-Parkinson-White (WPW) syndrome (atrioventricular reciprocating tachycardia [AVRT]): extra pathway outside of AV node that connects atria and ventricles (accessory pathway); early beat (not common), blocks path­ways and initiates reentrant loop, causing tachycardia

Treatment: acute  —  Valsalva maneuver, carotid sinus massage, or intravenous (IV) adenosine to terminate AVRT; long-term  —  antiarrhythmic drugs used to block conduction down accessory pathway (Class I or III) or slow AV node conduction (Class II or IV); catheter ablation treatment of choice (75%-95% success rate)

Ventricular Tachyarrhythmias

Premature ventricular contractions (PVCs): spontaneous ventricular depolarizations not preceded by P wave; not treated unless >15,000 per day (weakens heart; treat with b-blockers or ablation

Ventricular tachycardia (VT) and ventricular fibrillation (VF): responsible for most cases of sudden cardiac death (400,000 US deaths per year); £70% may survive if defibrillated early; <15% overall survival rate to hospi­tal discharge; drug therapy (eg, amiodarone) recommended for VT survivors; implantable cardioverter-defibrilla­tor (ICD) recommended for mortality benefits

Types of VT: monomorphic  —  one repeating pattern caused by reentry around myocardial infarction (MI) scar in ventricle; polymorphic  —  altering QRS complexes; normal QT interval at baseline; if long QT syndrome present, condition called torsades de pointes

VF: sinus rhythm  with PVC initiates VT, which then degenerates to VF; defibrillation only immediate option; ICD recommended for survivors of VF (sudden cardiac death) unless definite reversible cause of VT or VF identified and removed

Implantable cardioverter defibrillator: pulse generator placed under left clavicle; insertion of leads into axillary or subclavian vein under collarbone, then into heart; right atrial lead; right ventricular lead contains coils that de­liver high-energy shock to eliminate VT or VF

Indications for ICD: secondary  —  survivors of VT or VF who do not have reversible predisposing condition; pri­mary (2 groups)  —  1) left ventricular (LV) dysfunction due to ischemic cardiomyopathy (ejection fraction [EF] <30% or 2) any cause of cardiomyopathy with EF <35% and New York Heart Association (NYHA) Class II or III congestive heart failure (CHF) symptoms

Bi-Ventricular (Bi-V) ICD: LV lead  added; used in patients with any indication for ICD and NYHA Class III or IV symptoms with wide QRS (evidence of LV dyssynchrony)

Clinically Important Arrhythmia Situations

Digitalis toxicity: results in heart block  and VT; treatment  —correction of electrolytes; IV magnesium; digoxin-spe­cific antibodies; defibrillation; suspect if patient receiving digitalis has ECG evidence of toxicity (eg, downsloping ST segments after normal QRS) or frequent PVCs or VT

AF in WPW: rapid conduction through accessory pathway causes VT or VF; CCBs and b-blockers contraindicated (slow conduction through AV node and precipitate VT or VF); treat with procainamide to slow conduction through accessory pathway; ablation indicated once patient stabilized

Questions and Answers

Common complications during and after ablation: bleeding from groin site; cardiac perforation

Asymptomatic sinus bradycardia: does not require specific therapy (monitor patient); pacemaker recommended if pauses between QRS complex >3.5 sec in sinus rhythm or >5 sec if AF present

Pacemaker for asymptomatic patient with second-degree heart block: outpatient elective procedure; not urgent, but should not wait for months (risk for sudden cardiac death)

Evaluation for ICD in patient with low EF after MI: guidelines recommend ³30-day wait; speaker recommends waiting 3 mo while using b-blockers and angiotensin-converting enzyme inhibitors to speed LV recovery; trial showed no benefit from ICD implanted immediately after MI; evaluation before 90 days unhelpful

Role of magnesium: limited; useful in patients with ventricular tachyarrhythmias due to long QT interval

AV node ablation and pacemaker: used when other strategies for AF have failed

Syncope: work-up should include cardiac cause (eg, vasodepressor syncope, neurocardiogenic syncope, tachyar­rhythmias)

Alternating AF and atrial flutter: common combination; treat for AF (anticoagulation, rate control, and ablation)

Anticoagulation for atrial flutter: recommended in American College of Cardiology guidelines; same risk for stroke as AF

Atrial Fibrillation In The Office:Evaluation and Management

Daniel G. Blanchard, MD, Professor of Medicine, Chief of Clinical Cardiology, Division of Cardiology, Uni­versity of California, San Diego School of Medicine

Classification of AF: 1) first detected (duration unknown); 2) recurrent (³2 episodes); 3) paroxysmal (self-terminat­ing recurrences lasting <7 days); 4) persistent (events last >7 days and not self-terminating); 5) permanent (persis­tent; cardioversion unsuccessful); 6) secondary (occurring with acute MI, surgery, pericarditis, hyperthyroidism, pulmonary embolism [PE], myocarditis, and pneumonia)

Risks of persistent or permanent AF: increase in stroke, heart failure, and all-cause mortality (double that of pa­tients in NSR; risk higher in women); overall risk for stroke averages 5% per year for entire AF population and in­creases to »25% at age 80 yr; AF and CHF exacerbate one another

Initial evaluation: history and physical examination; electrocardiography; echocardiography; blood tests (eg, thy­roid, renal, hepatic function); refer to cardiologist

Cardiology work-up: stress test (exercise or chemical); event monitoring (to determine percentage of and time spent in AF and assess rate control); electrophysiologic evaluation (to determine whether ablation required)

Initial management: control ventricular rate; b-blockers for majority of patients; CCBs (eg, verapamil, diltiazem) for those with asthma; digoxin (increases vagal tone; does not work well for rate control); use in patients sensitive to CCBs or b-blockers

Risk for embolic events: high risk  —  previous cerebrovascular accident (CVA) or transient ischemic attack (TIA); mitral stenosis; valvular AF (higher risk for stroke than nonvalvular AF); prosthetic heart valve; moderate risk  —  age ³74 yr; hypertension; CHF (symptomatic or not); low EF (<35%); diabetes; lower risk  —  age 65 to 75 yr; fe­male sex; thyrotoxicosis; coronary artery disease (CAD)

Indications for warfarin: ³1 major risk factors; >1 moderate risk factor; 1 moderate risk factor (aspirin also accept­able); no risk factors (aspirin also accepted); CHADS₂ score  —  warfarin needed if score ³2 (no significant differ­ence with warfarin if CHADS score low, but if score high [eg, 4], incidence of stroke doubled if warfarin not taken); trials on preventing stroke  —  warfarin better than placebo; aspirin more effective than placebo; warfarin superior to aspirin; risk for ischemic stroke or intracranial hemorrhage  —  risk for stroke low with international normalized ra­tio (INR)  ³ 2; risk for major hemorrhage also low with INR 2 to 3

Indications for heparin: AF with  —  recent embolic event; mechanical heart valve and subtherapeutic INR; new PE or deep venous thrombosis (DVT); pregnant women (because warfarin teratogenic)

Refer to emergency department (ED): patients with AF and  —  CHF, (systolic or diastolic); uncontrolled rapid ven­tricular rate; hypertrophic cardiomyopathy; hypo- or hypertension; mitral or aortic stenosis (cardioversion indi­cated); CAD with angina; AF with wide QRS complex

Antiarrhythmic therapy for AF: Type 1A agents (eg, quinidine, procainamide, disopyramide) not commonly used; Type 1C agents (flecainide, propafenone; use in younger patients without other heart disease); ibutilide (ED only); sotalol; amiodarone (works well but many side effects); cardioversion; indications  —  symptomatic AF; as­ymptomatic AF (for better QOL)

Sotalol Amiodarone Atrial Fibrillation Efficacy Trial (SAFE-T): patients had persistent AF; those on amiodarone had less AF and higher QOL scores, compared to sotalol; AFFIRM Trial challenged (patients may not live lon­ger, but feel better)

Dronedarone: similar to amiodarone, but without iodine and safer to use; 24-hr half-life; no accumulation in thyroid, lung or liver (adverse effects); as effective as amiodarone for prevention of AF

Electrophysiologic ablation of AF: last resort; transseptal catheter enters left atrium (LA); multiple burn lines iso­late portions of LA and pulmonary veins; success rate 75% to 80%, especially without marked LA dilation and par­oxysmal AF; success unlikely for permanent AF; operator-dependent; small risk for stroke or LA rupture into pericardium or into esophagus

Factors for guiding therapy: chronicity of AF; symptomatic or asymptomatic AF; must tailor therapy based on pa­tient age, comorbidities, LV function, LA size, patient preferences, contraindications for anticoagulation

Questions and Answers: patients at high risk for falls  — use   aspirin, not warfarin; enoxaparin (Lovenox)  —  effective as “bridge” therapy, or with warfarin if INR not therapeutic; cardioversion  —  for acutely ill decompensated pa­tients; otherwise, anticoagulation indicated before and after for 1 mo; aspirin  —  use at 325 mg (not 81 mg) for AF; b-blockers for rate control  —  long-acting metoprolol well tolerated (avoid atenolol); possible to add verapamil or diltiazem; sotalol  — can prolong QT and increase risk for VT and torsades de pointes; ³3 day hospital stay required

Suggested Reading

Bonanno C et al: Efficacy and safety of catheter ablation versus antiarrhythmic drugs for atrial fibrillation: a meta-analysis of randomized trials. J Cardiovasc Med (Hagerstown) 2009. [Epub ahead of print]; Calkins H et al: Treatment of atrial fibrilla­tion with antiarrhythmic drugs or radiofrequency ablation: two systematic literature reviews and meta-analyses. Circ Arrhythm Electrophysiol 2:349, 2009; Carnlöf C et al: Health-related quality of life in patients with atrial fibrillation undergoing pulmo­nary vein isolation, before and after treatment. Eur J Cardiovasc Nurs Oct 12, 2009. [Epub ahead of print]; Ferro CR et al: Postoperative atrial fibrillation after cardiac surgery. Arq Bras Cardiol; 93:59, 2009; Fischer GW: Atrial fibrillation in the el­derly. Anesthesiol Clin 27:417, 2009; Li D et al: Antiarrhythmic drug therapy for atrial fibrillation: focus on atrial selectivity and safety. Cardiovasc Hematol Agents Med Chem 7:64, 2009; Mathew ST et al: Atrial fibrillation: mechanistic insights and treatment options. Eur J Intern Med 2009 20:672-681. Patel U, Pavri BB: Short QT syndrome: a review. Cardiol Rev; 17:300-303, 2009. Priester R et al: Role of transesophageal echocardiography among patients with atrial fibrillation undergoing elec­trophysiology testing. Am J Cardiol 104:125, 2009; Sood MM et al: The intersection of risk and benefit: is warfarin anticoag­ulation suitable for atrial fibrillation in patients on hemodialysis? Chest 136:1128, 2009.