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Table 1: Risk Factors for AF Factor (Risk, Precipitating)

Why/How

Age

Structural heart disease.

Lifestyle: • Alcohol (holiday heart syndrome) • Substance abuse • Smoking • Intense physical exercise • Obesity

• Holiday heart syndrome is related to binge drinking on weekends or holidays, typically in people without heart disease. • Substance abuse, such as cocaine and even over-the-counter cough and cold medications, can cause a sympathomimetic effect on the heart. • Intense physical exercise, as related to dehydration and electrolyte imbalance, can precipitate AF. • Obesity increases the workload on the heart, resulting in structural heart disease. See the Evidence-Based Practice box below. The concept here is that structural heart disease changes the heart’s function and electrical activity.

Structural heart disease: • Sick sinus syndrome • Left atrial enlargement • Valvular heart disease/rheumatic heart disease • Cardiomyopathy • Atrial myxoma

• Atrial septic defects • Pericardial disease • Hypertension (HTN) Ischemic heart disease Non-cardiac causes: • Acute infections (sepsis) • Electrolyte depletion • Diabetes mellitus • Pulmonary embolism

The concept is ischemic tissue is irritable tissue, and irritable tissue is arrhythmic tissue. Metabolic stress (sepsis, acute infections, thyroid) activates the neurohumoral cascade. Electrolyte depletion affects the Na-K-ATPase pump (keep potassium >/equal to 4.0; magnesium >/equal to 2.0). Recall magnesium is the co-factor for the Na-K-ATPase pump, hence normal potassium can be obtained by a normal magnesium.

• Obstructive Sleep Apnea (OSA) • Hyperthyroidism/thyrotoxicosis • Anemia • Post-operative • Idiopathic (lone AF

Cardiothoracic surgery

High catecholamine release, including the perioperative period and critical illness. Volume overload during surgery increases preload; diuretics are given after surgery to reduce atrial inflammation.

European ancestry and family history Genetic variation. Family history Genetic variation. Note : Chung et al., 2020; Kotecha et al., 2016; Walsh & Caple, 2018

AF CLASSIFICATIONS

● Long-standing persistent : Continuous AF of greater than 12 months duration. ● Permanent AF : A diagnosis made when there has been a joint decision by the patient and clinician to cease further attempts to restore and/or maintain sinus rhythm. ● Nonvalvular AF : AF in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair. ● Lone AF : Typically seen in younger patients without symptoms and structural heart disease who have a normal ECG.

The clinical type of AF is documented according to the length of time in AF. The four categories used to describe AF are: paroxysmal; persistent; long-standing persistent; and permanent (Hindricks & Potpara, 2020; Morillo et al., 2017; Walsh & Caple, 2018) ● Paroxysmal AF : AF that terminates spontaneously or with intervention within 7 days of onset. Episodes may recur with variable frequency. ● Persistent AF : Continuous AF that is sustained greater than 7 days.

ATRIAL FIBRILLATION HISTORY AND PHYSICAL

The indications for taking a health history on a patient with AF are extensive. The clinical presentation could range from the patient being asymptomatic to a patient with hemodynamic instability and signs and symptoms of cardiogenic shock. This wide range can be related to acute loss of atrial kick, reduced ejection fraction, or stroke volume. Initial history should include the following: ● Assessment of the type of atrial fibrillation encountered, duration, onset, and frequency of symptoms (presence of palpitations [pounding or fluttering], lightheadedness, syncope, pre-syncope, fatigue, dyspnea, chest pressure/ heaviness/pain, decreased exercise tolerance). Patients will

vary along the spectrum of quantified symptoms versus vague reports of fatigue. ● Estimation of how often and how long the episodes last based on the preceding clinical report. ● Assessment of precipitating factors/triggers (i.e., exertion, reduced sleep, excess caffeine, alcohol use, and dehydration) have been self-reported by patients as potential triggers for the occurrence of AF. ● Assessment of modes of termination (e.g., vagal maneuvers, “pill in the pocket”). Vagal maneuvers, which increase vagal tone, can slow the ventricular rate in AF, but do not terminate AF. “Pill in the pocket” is the administration of a Class IC antiarrhythmic such as flecainide or propafenone, which can be used in selected patients to terminate AF.

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