Atrial Fibrillation



Atrial Fibrillation


Anurag Gupta

Paul J. Wang



BACKGROUND

Atrial fibrillation (AF) is the most common chronic cardiac dysrhythmia. The estimated prevalence of atrial fibrillation and atrial flutter is greater than 2.2 million individuals in the United States, with estimated incidence of greater than 75,000 cases per year.1 The median age of individuals with AF is approximately 75 years. The estimated lifetime risk for the development of AF, when studied in all individuals age 40 years or older free of AF in the Framingham Heart Study, was estimated to be approximately 1 in 4.2 The morbidity and mortality attributable to AF is significant as its presence confers an increased risk for congestive heart failure (CHF), embolic events including stroke, and death.


ELECTROPHYSIOLOGIC FEATURES

AF is supraventricular arrhythmia characterized by seemingly disorganized atrial depolarizations consequently accompanied by ineffectual atrial contraction. The mechanisms contributing to AF are under investigation with proposed, possibly coexisting, models that include the following:



  • Multiple-wavelet reentry, in which AF is maintained via multiple coexisting wave fronts of electrical activity that propagate randomly throughout the atria


  • Focal activation at areas of enhanced automaticity, with rapid discharge leading to heterogeneous, fibrillatory conduction. Of note, numerous foci have been identified though the region of the pulmonary veins in the left atrium appears to be most common3


  • Small reentrant sources (rotors) that lead to a hierarchical distribution of frequencies throughout the atria that maintain AF



  • Heterogeneity of autonomic innervation likely plays a further role in the initiation and maintenance of AF

AF appears to be initiated by atrial premature beats (most commonly), as well as by atrial flutter and other supraventricular tachycardias.


ELECTROCARDIOGRAPHIC FEATURES4

The ECG appearance of AF is most immediately suggested by an irregular ventricular rhythm with no discrete P waves. More specifically,



  • Atrial activity: P waves are replaced by f waves, typically smaller waves characterized by variable morphology, amplitude, and intervals, with rapid rate generally between 350 and 600 beats per minute (bpm).


  • Ventricular response: The ventricular response (R-R interval) is generally irregular with rate of 90 to 170 bpm in an untreated individual. The ventricular rate is significantly less than the atrial rate due to block at the A-V node and possibly due to collision of fibrillatory wave fronts. However, the ventricular rate varies significantly depending upon multiple factors including



    • action of drugs


    • electrophysiological properties of the A-V node and conducting tissue


    • autonomic tone


  • Accessory pathways? Assess for the possible presence of an accessory pathway(s) capable of antegrade conduction, as ventricular rates can be greater than 300 bpm and deteriorate into lethal ventricular fibrillation. The presence of an accessory pathway may be suggested by typical appearance on an electrocardiogram during sinus rhythm (namely, short P-R interval with delta wave), by extremely rapid ventricular rates greater than 200 bpm during AF, and/or by wide-QRS complexes during AF (although aberrant conduction or pre-existing conduction abnormality can also lead to wide complexes).


INITIAL MANAGEMENT



  • Attempt to identify and address underlying etiologies, risk factors, and/or triggers for AF, including potentially reversible causes of AF


  • Initiate appropriate antithrombotic therapy, if indicated and safe, based on an individualized assessment of overall stroke risk


  • Control the ventricular rate, if needed


  • Assess the acute and/or chronic effects of AF including associated symptoms and its hemodynamic consequences. This will help guide decisions of whether or not to pursue a strategy of attempting to restore and maintain sinus rhythm.



CLINICAL CONSEQUENCES


Hemodynamic Compromise

The hemodynamic derangements in AF may or may not be accompanied with symptoms, most commonly palpitations, dyspnea, decreased exercise tolerance, lightheadedness, syncope, and chest discomfort. The factors leading to hemodynamic deterioration include the following:



  • Loss of effective atrial contraction and thus atrioventricular (A-V) synchrony; this may be especially detrimental in those dependent upon diastolic ventricular filling


  • Irregularity of ventricular response


  • Inappropriately elevated heart rate. Chronically elevated atrial rates may lead to adverse atrial remodeling (including atrial dilatation), and persistently elevated ventricular rates may lead to the development of a tachycardia-induced cardiomyopathy. Excessive ventricular rates may also compromise diastolic ventricular filling.


Thromboembolic Risk

Multiple factors contribute to increased thromboembolic events in individuals with AF, although static flow within the left atrial appendage (LAA) appears most significant. The rate of ischemic stroke varies significantly depending upon the presence of associated stroke risk factors, but on average is estimated to be approximately 5% per year in individuals with nonvalvular AF (that is, AF not associated with rheumatic mitral valve disease, valve replacement, or valve repair). This represents an approximately sixfold increase in the risk of thromboembolic events in individuals with nonvalvular AF as compared to individuals without AF. The attributable risk of stroke in individuals with AF increases significantly with advancing age.5


CLASSIFICATION6

The following definitions apply to episodes of AF lasting longer than 30 seconds without a reversible cause. It is useful to identify a first-detected episode of AF, acknowledging that the duration of that episode is generally unknown and prior undetected episodes may have been present. When AF has been detected at least 2 times, it is termed recurrent AF.

First-detected or recurrent AF can be further classified as the following:



  • Paroxysmal: AF episode(s) usually lasts 7 days or less (and most less than 24 hours) and terminates spontaneously


  • Persistent: AF episode(s) usually lasts greater than 7 days and does not terminate spontaneously


  • Permanent: Cardioversion has failed and/or attempts have been foregone



ETIOLOGIES

The delineation of the following risk factors for AF is somewhat arbitrary, overlap exists, and multiple etiologies are often present in one individual. Nonetheless, “secondary” AF is intended to draw attention to cases in which AF may not be the primary problem, and may be ameliorated or terminated by treatment of the underlying disorder.


“Primary” AF

Established risk factors for the development of AF include the following:



  • Advancing age


  • Hypertension (systemic and/or pulmonary), especially when accompanied by left ventricular hypertrophy


  • Coronary heart disease, especially when complicated by history of myocardial infarction (MI) or CHF


  • Valvular heart disease, especially mitral regurgitation, mitral stenosis, and tricuspid regurgitation. In developed nations, this etiology is decreasing in frequency due to the reduced incidence of rheumatic heart disease.


  • Heart failure


  • Other factors, possibly including hypertrophic cardiomyopathy, congenital heart disease, intracardiac (or adjacent) tumors or thrombi, obstructive sleep apnea, and obesity


  • Lone or “idiopathic” AF is said to be present in individuals younger than 60 years of age with no known cardiopulmonary disease (including hypertension) per clinical and echocardiographic assessment. The risk profile, including thromboembolic complications and death, is typically lower, though these individuals generally progress beyond the lone AF category with time. Multiple factors including genetic determinants, “sick sinus” syndrome, degenerative conduction disease, and other electrophysiologic abnormalities likely account for a significant proportion of incident AF but their role remains incompletely defined at present.


“Secondary” AF

Potentially reversible, “acute” causes and/or triggers for AF include the following:



  • Acute MI (usually as a complication of transmural ST segment elevation MI [STEMI])


  • Pericarditis


  • Myocarditis


  • Endocrine disorders including uncontrolled hyperthyroidism and pheochromocytoma


  • Infection


  • Postoperative state, especially with cardiac, pulmonary, or esophageal interventions



  • Acute pulmonary disease, such as pulmonary embolus, pneumonia, and exacerbation of obstructive lung disease


  • Neurogenic disease, such as major stroke and subarachnoid hemorrhage


  • Toxins, such as alcohol, cocaine, amphetamines, and caffeine, including withdrawal states


  • Medications, such as theophylline or positive inotropes


  • Electrolyte disturbance, such as hypokalemia and hypomagnesemia


  • Other supraventricular arrhythmias


  • Enhanced sympathetic or parasympathetic tone


EVALUATION

It is critical to carefully consider in every single patient potential etiologies and risk factors predisposing one to AF. This provides an opportunity to identify and modify significant concomitant medical disease. However, one must be cognizant that even despite correction of a suspected reversible cause of AF, a patient may have underlying paroxysmal AF necessitating long-term therapy.

To evaluate possible etiologies of AF and to guide management decisions, it is reasonable to obtain the following diagnostics, with further studies guided by the clinical scenario.


History and Physical Examination

Characterize the patient’s pattern of AF; define her symptoms; document her response to prior therapies; identify possible etiologies, risk factors, and triggers; and assess for clinical evidence of heart failure.


ECG

Verify the presence of AF, assess for accessory pathways, determine ventricular rate, document concomitant cardiac disease (e.g., atrial size, left ventricular hypertrophy [LVH], prior MI), monitor intervals in response to pharmacologic therapy, and assess for other arrhythmias.


Transthoracic Echocardiogram (TTE)

Determine LV size and function, screen for valvular and pericardial disease, measure atrial size, assess for LVH, and estimate pulmonary pressure. The sensitivity for detection of LA thrombus is low for TTE as opposed to TEE.


Laboratory Tests

Tests include thyroid panel, serum electrolytes, complete blood count (CBC), renal and hepatic function, and coagulation tests in part to assess for possible risk factors for AF and to guide pharmacologic therapy.


Additional tests may be indicated. This notably may include but is not limited to the following:



  • Chest imaging


  • Holter monitoring or event recording (in part to assess rate control, confirm diagnosis of AF, assess concomitant arrhythmias, and correlate symptoms)


  • Exercise testing (in part to evaluate for ischemia prior to using Class 1C antiarrhythmic drugs, assess rate control, define exercise tolerance, and possibly reproduce exercise-induced AF)


MANAGEMENT—OVERALL STRATEGY

While the management of patients with AF is highly individualized, principal components include the following:



  • Carefully consider and address the potential etiologies, risk factors, and/or triggers for AF


  • Control the ventricular rate, if needed


  • Initiate appropriate antithrombotic therapy, if safe, based primarily on assessment of overall stroke risk


  • Consider employing measures to restore and maintain sinus rhythm, if indicated, generally via cardioversion and antiarrhythmic drugs. If the patient’s condition is unstable, urgent cardioversion should be performed.

Specific guidelines regarding each of these components are discussed in depth for the remainder of the chapter.

In all stable patients with atrial fibrillation of any clinical pattern, it is recommended that they be started on appropriate antithrombotic therapy (if safe) and rate control (if needed). However, the issue of whether or not attempts should also be made to maintain sinus rhythm is debatable. Despite the hypothesized benefits of maintaining sinus rhythm over rate control alone, randomized clinical trials comparing these two strategies have failed to show a statistically significant difference in mortality, stroke, or quality of life (see “Landmark Clinical Trials” section for further details).7, 8, 9, 10, and 11 Importantly, regardless of the strategy pursued, appropriate antithrombotic therapy is generally warranted.


MANAGEMENT—RATE CONTROL


Acute Setting



  • The goal for the ventricular rate will vary significantly depending upon the clinical scenario.


  • As outlined below, amiodarone may be an acceptable agent for rate control despite its multiple toxicities, if other measures are unsuccessful or contraindicated. The additional antiarrhythmic potential of amiodarone for facilitating conversion to sinus rhythm must be considered prior to use. (See Table 8-1.)









TABLE 8-1 Selected agents for rate control in the acute setting

































































Drug

Loading Dose

Maintenance Dose

Selected Side Effects and Comments


Patients without accessory pathways and no acute heart failure


βB

Esmolol

0.5 mg/kg IV over 1 min; may repeat q 4 min while titrating IVCI

50-200 µg/kg/min IVCI

↓BP, HB, ↓HR, bronchospasm, HF; exercise extreme caution if used despite HF or hypotension though very short half-life


Metoprolol

2.5 to 5 mg IV over 2 min; may repeat q 5 min up to 3 doses

No IVCI available

↓BP, HB, ↓HR, bronchospasm, HF; exercise extreme caution if used despite HF or hypotension


Propranolol

0.15 mg/kg (˜1 mg) IV q 2 min

No IVCI available

↓BP, HB, ↓HR, bronchospasm, HF; exercise extreme caution if used despite HF or hypotension


CCB

Diltiazem

0.25 mg/kg (˜20 mg) IV over 2 min; may repeat in 15 min at dose of 0.35 mg/kg (˜25 mg) IV over 2 min

5-15 mg/h IVCI

↓BP, HB, HF; exercise extreme caution if used despite HF or hypotension


Verapamil

0.075 to 0.15 mg/kg (˜5-10 mg) IV over 2 min; may repeat in 15-30 min

0.125 mg/min IVCI

↓BP, HB, HF; exercise extreme caution if used despite HF or hypotension


Patients with accessory pathway: Rate control may be appropriate though conversion to sinus rhythm and/or catheter ablation of the accessory pathway is generally recommended. Agents that slow conduction across the A-V node (including nondihydropyridine CCB, β-blockers, and digoxin) are not recommended as they may lead to rapid antegrade conduction across the accessory pathway during AF.

Amiodarone

150 mg IV over 10 min

0.5-1 mg/min IVCI

↓BP (though less significant than CCB and βB), HB, ↓HR, ventricular arrhythmia (attention to QTc), pulmonary toxicity, hepatotoxicity, hyper- or hypothyroidism, ocular toxicity, skin discoloration, warfarin and digoxin interaction


Patients with heart failure and without accessory pathway

Digoxin

0.25 mg IV; may repeat cautiously q 2 h up to 1.5 mg (reduce dosage if used in renal insufficiency)

0.125-0.375 mg IV or PO daily (reduce dosage if used in renal insufficiency)

Digitalis toxicity, HB, ↓HR, amiodarone interaction; the onset of digoxin is slow (over 60 min or greater)

Amiodarone

150 mg IV over 10 min

0.5-1 mg/min IVCI

(see above)


Consult pharmacopoeia/manufacturer recommendations for most accurate and complete listings, and for additional appropriate drugs.


↓BP, hypotension; IVCI, intravenous continuous infusion; HB, heart block; HF, heart failure; ↓HR, bradycardia; NA, not applicable; and QTc, corrected QT interval


Modified from Fuster et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. Circulation. 2006;114:700-752.6




Chronic Setting



  • It is reasonable to pursue a goal ventricular rate of 60 to 80 bpm at rest and 90 to 115 bpm during moderate exercise.


  • It is reasonable to consider using a 24-hour Holter monitor (with a goal overall average rate of approximately ≤100 bpm) and/or exercise testing as an adjunct in assessing the adequacy of rate control therapy.


  • In selected patients with symptomatic, medically refractory atrial fibrillation, nonpharmacologic attainment of rate control via catheter ablation of the A-V node in conjunction with permanent ventricular pacing has been demonstrated to be effective and is associated with improvement in symptoms.12

See Table 8-2.









TABLE 8-2 Selected agents for rate control in the nonacute and/or chronic setting












































Drug

Dosing Regimen

Onset

Major Side Effects and Comments


Metoprolol

25-100 mg PO twice a day

4-6 h

↓BP, HB, ↓HR, bronchospasm, HF


Propranolol

80-240 mg PO total daily, divided in 2-4 doses per day

60-90 min

↓BP, HB, ↓HR, bronchospasm, HF


Diltiazem

120-360 mg PO total daily, in divided doses depending upon formulation

2-4 h

↓BP, HB, HF


Verapamil

120-360 mg PO total daily, in divided doses depending upon formulation

1-2 h

↓BP, HB, HF, digoxin interaction


Amiodarone

Multiple dosing regimens are possible. One example is to load (in divided doses) with 800 mg PO daily for 1 wk, then 600 mg PO daily for 1 wk, then 400 mg PO daily for 4-6 wk, then 200 mg PO daily as maintenance dose

Days

↓BP (though less significant than CCB and βB), HB, ↓HR, ventricular arrhythmia (attention to QTc), pulmonary toxicity, hepatotoxicity, hyper-or hypothyroidism, ocular toxicity, skin discoloration, warfarin and digoxin interaction


Digoxin

May load with 0.5 mg PO daily up to 1.5 mg, then 0.125-0.375 mg daily as maintenance dose (reduce dosage if used in renal insufficiency)

2 days

Digitalis toxicity, HB, ↓HR, amiodarone interaction; consider monitoring digoxin serum levels. Not recommended as sole agent for rate control in paroxysmal AF.


Consult pharmacopoeia/manufacturer recommendations for most accurate and complete listings, and for additional appropriate drugs.


↓BP, hypotension; IVCI, intravenous continuous infusion; HB, heart block; HF, heart failure; ↓HR, bradycardia; NA, not applicable; and QTc, corrected QT interval


Modified from Fuster et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation. Circulation. 2006;114:700-752.6

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Jul 16, 2016 | Posted by in CARDIOLOGY | Comments Off on Atrial Fibrillation

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