Atrial Fibrillation PDF

Atrial fibrillation Army and Hashini Definition + Epidemiology - Atrial Fibrillation: Uncoordinated electrical activity of the atria, ultimately leading to irregular activation of the AV node and irregular pulse. - AF affects approximately 2.2% of the general population – equiv...

Atrial fibrillation Army and Hashini Definition + Epidemiology - Atrial Fibrillation: Uncoordinated electrical activity of the atria, ultimately leading to irregular activation of the AV node and irregular pulse. - AF affects approximately 2.2% of the general population – equivalent to more than 500,000 people in 2021 - The proportion affected increases with age. An estimated 5.4% of the Australian population aged 55 and over have AF.  Pathophysiology + Risk Factors - Ischemia + Anything that expands the atria (which disrupts the electrical conduction) can cause AF Acute Causes (PIRATES) - Pulmonary disease - Can expand the atria and disrupt normal electrical activity → Hypoxia (from COPD,pneumonia, PE etc) causing aberrant electrical firing→ AF - Ischaemia (Myocardial) - previous MI, cardiac remodelling - Rheumatic heart disease - Anaemia, Atrial Myxoma - Thyrotoxicosis → High catecholamines, ectopic - Ethanol → Binge etoh- Holiday heart syndrome (K+, Mg2+ low and high catecholamines) - Sepsis → High catecholamine, ectopics develop Chronic Causes - Hypertension - Valvular diseases → Mitral Stenosis - Congestive heart failure → Particularly left sided HF (blood can't go anywhere) Clinical features - Often asymptomatic BUT: - Discoordinated atria → Ventricles not filled as much → LOWER CARDIAC OUTPUT → Syncope/Falls - Fatigue, weakness, SOB - Irregularly irregular pulse (ventricular contractions occur at random movements) - Mural embolism (As Atria are barely moving, blood is in stasis, clot forms → Stroke/TIA) - AFib can also cause a severe tachycardia → hemodynamic instability  Diagnosis - ECG to diagnosis→ erratic, low amplitude pre- QRS activity (No P waves → Atrial Depolarisation is abnormal) - Irregularly Irregular Differentials Other supraventricular tachycardias: Atrial flutter, atrial extrasystoles Multifocal atrial tachycardia Sinus tachycardia Ventricular ectopics Heart Failure: Especially when presenting with symptoms of congestion and shortness of breath. Thyrotoxicosis: Hyperthyroidism can cause palpitations and mimic AF. Pulmonary Embolism: Can cause rapid heart rate and chest discomfort. Electrolyte Imbalance: Such as hypokalemia or hyperkalemia, which can affect heart rhythm. Investigations Bedside: ECG If AF is paroxysmal → consider Holter monitoring Look for signs of heart failure/valvular disease → CVS examination Bloods: FBE, Electrolytes and urea, Thyroid-stimulating hormone (TSH), LFTs If oral anticoagulants are to be given, include INR and APTT. Imaging: Arrange echocardiography for all first episodes of AF, if Valvular or structural heart disease suspected or there is doubt about the risk or benefit for anticoagulation after calculating the CHA2DS2-VA score. Suitability for anticoagulation- stroke prevention: HAS-BLED score Assess stroke risk using the CHA₂DS₂-VA score Management The management of atrial fibrillation and atrial flutter consists of 3 major components: 1. Identification and treatment of comorbidities and factors precipitating atrial fibrillation 2. Prevention of thromboembolic events with anticoagulant therapy 3. Management of the arrhythmia itself, with rhythm control and/or rate control. Identification and treatment of comorbidities and factors precipitating atrial fibrillation long-term sustained weight loss Substantial reduction of alcohol intake Assessment for and aggressive treatment of these comorbidities and precipitating factors 1.Heart failure 2.Elevated blood pressure 3.Valvular heart disease 4.Myocardial ischemia 5.Obstructive sleep apnoea and other lung diseases 6.Diabetes mellitus Prevention of thromboembolic events with anticoagulant therapy As soon as atrial fibrillation is diagnosed, assess the patient’s stroke risk and start anticoagulant therapy if appropriate. Use HAS-BLED and CHADS-VASC scores to guide this. 1. A direct-acting oral anticoagulant (DOAC) (eg apixaban, rivaroxaban, dabigatran) 2. Warfarin: rheumatic mitral stenosis and/or a mechanical heart valve (also given for patients with kidney impairment, obesity) Adjust the warfarin dose to achieve an INR from 2 to 3 Management of the arrhythmia itself, with rhythm control and/or rate control. Atrial fibrillation is a dynamic condition, so treatment may vary over time and will require regular review. Rhythm control: 1. (DC) electrical cardioversion: restoration of sinus rhythm - Require anticoagulant therapy to reduce risk of stroke: start anticoagulant therapy in patients not already therapeutically anticoagulated. If atrial fibrillation has persisted for less than 48 hours, electrical cardioversion can be performed without delay. If atrial fibrillation has persisted for longer than 48 hours, or if the duration is unknown, cardioversion should be deferred until the patient has had a minimum of 3 weeks of anticoagulant therapy, unless transesophageal echocardiography (TOE) has ruled out atrial thrombus. - Unfractionated heparin (UFH), low molecular weight heparin (LMWH) or direct-acting oral anticoagulants (DOACs) - Anticoagulant therapy should be used for at least 4 weeks following electrical cardioversion; 2. Pharmacological - Anticoagulant therapy to reduce risk of stroke (same as DC cardioversion) - IF: LVEF > 40% and no significant coronary artery disease: flecainide 2 mg/kg (up to 150 mg) by intravenous infusion over at least 10 minutes - IF: LVEF < 40% or coronary artery disease: amiodarone 300 mg by intravenous infusion, over 30 to 60 minutes Rate control: The choice of drug is influenced by the patient’s comorbidities and possible adverse effects Beta blockers (atenolol, metaprolol) — FIRST LINE Nondihydropyridine calcium channel blockers - diltiazem or verapamil (avoid these in patients with LVEF of 40% or less) Digoxin Amiodarone. Long term management: Catheter ablation or antiarrhythmic drugs can be used for long-term rhythm control for atrial fibrillation. The aim of treatment is to reduce the patient’s symptoms. The long-term efficacy of antiarrhythmic drugs is modest. Catheter ablation is equivalent to pharmacological therapy in terms of hard outcome measures (eg mortality, thromboembolism, bleeding); however, catheter ablation has better quality of life outcomes.