MANAGEMENT OF ATRIAL FIBRILLATION.pptx

During atrial fibrillation, the heart's upper chambers — called the atria — beat chaotically and irregularly. They beat out of sync with the lower heart chambers, called the ventricles. For many people, AFib may have no symptoms. But AFib may cause a fast, pounding heartbeat, shortness of breath or light-headedness.

1. ATRIAL FIBRILLATION

2. PRESENTATION Most common clinically significant cardiac arrhythmia, and its prevalence increases with advancing age. Common presentations:  younger patients often feel palpitations and non-anginal chest discomfort, vs. older patients often present with vague symptoms such as fatigue, lightheadedness and dyspnea Uncommon presentations:  TIA, CHF or ACS AF rarely causes syncope in itself – look for another cause: cardiomyopathy, Brugada syndrome, PE, WPW or vasovagal syncope AF is rarely the sole cause of a patient’s hemodynamic instability, so look for another cause – sepsis, hemorrhagic (GI, AAA), dehydration, etc

3. Definitions of AF: A Simplified Scheme Term Definition Paroxysmal AF   AF that terminates spontaneously or with intervention within 7 d of onset. Episodes may recur with variable frequency. Persistent AF Continuous AF that is sustained >7 d. Long-standing persistent AF Continuous AF >12 mo in duration. Permanent AF The term “permanent AF” is used when the patient and clinician make a joint decision to stop further attempts to restore and/or maintain sinus rhythm. Acceptance of AF represents a therapeutic attitude on the part of the patient and clinician rather than an inherent pathophysiological attribute of AF. Acceptance of AF may change as symptoms, efficacy of therapeutic interventions, and patient and clinician preferences evolve. Nonvalvular AF AF in the absence of rheumatic mitral stenosis, a mechanical or bioprosthetic heart valve, or mitral valve repair. AF indicates atrial fibrillation .

4. ECG FINDINGS IN ATRIAL FIBRILLATION Irregularly irregular narrow-complex tachycardia can be  Atrial fibrillation, Atrial flutter with irregular conduction multifocal atrial tachycardia  (MAT) – rate of 100-150/min with 3 different P wave morphologies variable PR length and poor response to typical medications find and treat the underlying cause (often COPD) ST Depression common and often due to rate-related ischemia in atheroscletoric coronaries of older patients; should not be investigated further UNLESS patient has anginal chest pain or ACS is likely, or ST segments do not resolve once the patient is not in fast A.fib anymore (after rate control or cardioversion)

5. 10 Most Common Comorbid Chronic Conditions Among Medicare Beneficiaries With AF Beneficiaries ≥65 y of Age (N=2,426,865)   Beneficiaries <65 y of Age (N=105,878) (Mean Number of Conditions=5.8; Median=6)   (Mean Number of Conditions=5.8; Median=6)   N %     N % Hypertension 2,015,235 83.0   Hypertension 85,908 81.1 Ischemic heart disease 1,549,125 63.8   Ischemic heart disease 68,289 64.5 Hyperlipidemia 1,507,395 62.1   Hyperlipidemia 64,153 60.6 HF 1,247,748 51.4   HF 62,764 59.3 Anemia 1,027,135 42.3   Diabetes mellitus 56,246 53.1 Arthritis 965,472 39.8   Anemia 48,252 45.6 Diabetes mellitus 885,443 36.5   CKD 42,637 40.3 CKD 784,631 32.3   Arthritis 34,949 33.0 COPD 561,826 23.2   Depression 34,900 33.0 Cataracts 546,421 22.5   COPD 33,218 31.4 Reproduced with permission from the Centers for Medicare and Medicaid Services.

6. Risk Factors for Symptomatic Atrial Fibrillation-Analysis of an Outpatient Database. Annabelle et al. Journal of Atrial Fibrillation . Jun-Jul 2019| Volume 12| Issue 1

7. Mechanisms of AF

8. ETIOLOGY OR PRECIPITANTS OF ATRIAL FIBRILLATION Etiology of Slow AF: AV nodal blocking agents (digoxin, beta-blocker or calcium-channel blocker toxicity or at too high doses), sick sinus syndrome severe hyperkalemia 1/3 are ‘ lone AF ’ with no demonstrable cause In most cases, when the underlying cause is addressed, the AF resolves

9. INVESTIGATIONS Serum electrolytes and TSH (for possible causes) Renal & hepatic function blood tests (to guide selection of drug Tx) Stool Hemoccult test (before starting anticoagulation) Transthoracic ECHO (to measure left atrial size and assess for valvular heart disease, pericardial disease, and LV hypertrophy) Transesophageal ECHO (excludes atrial clot and is indicated when transthoracic images are inadequate or cardioversion is planned in a pt therapeutically anticoagulated <3 wks ) Additional tests as necessary for possible PE, AMI, or HF

10. DIAGNOSIS Electrocardiogram recordings during episodes are the only way to confirm the diagnosis. If the diagnosis is suspected and the ECG is normal, longer monitoring with a loop recorder or a Holter monitor can be helpful. The initial assessment should include laboratory tests for electrolytes, thyroid-stimulating hormone, and renal and hepatic function to rule out underlying disorders or contraindications to therapies. An echocardiogram should be done to look for structural heart disease.

11. MANAGEMENT

12. CONSIDERATION OF IMMEDIATE CARDIVERSION When duration of arrhythmia is <48h (e.g., hospitalized pt on cardiac monitoring) May be appropriate in selected pts with Decompensated HF Severe angina or acute infarction Hypotension High risk for acute stroke In patients with extremely rapid AV conduction mediated by the accessory pathway in Wolff-Parkinson-White syndrome Most pts with AF don’t require immediate cardioversion

13. RATE CONTROL VS RHYTHM CONTROL Traditionally clinicians preferred rhythm control to rate control Recently high-quality clinical trials  AFFIRM trials have found that rhythm control doesn’t improve mortality, stroke, hospitalization, or QOL compared with rate control Rate control easier to accomplish, prevents exposure to the potential adverse effects of antiarrhythmic agents Rhythm control is useful in select pts with severe symptoms (before or after rate control failure) or younger pts without structural heart disease The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial 2002

14. RATE CONTROL VS. RHYTHM CONTROL Update 2014: Risk of stroke and death in paroxysmal vs persistent AF ROCKET-AF TRIAL In patients with AF at moderate-to-high risk of stroke receiving anticoagulation, those with persistent AF have a higher risk of thrombo-embolic events and worse survival compared with paroxysmal AF. Update 2014: Time to Cardioversion for Acute Atrial Fibrillation and Thromboembolic Complications paper from JAMA showing that significant stroke risk may occur with cardioversion as early as 12hrs after symptoms start delay to cardioversion of 12 hours or longer from symptom onset was associated with a greater risk of thromboembolic complications (1.1%). When the duration of AF was less than 12 hours, the risk of thromboembolism was low (0.3%) without anticoagulation. 

15. RATE CONTROL STRATEGY Consider drugs to control ventricular rate in all pts with AF even those being treated for rhythm control Traditional target heart rate has been 60-80 beats/min at rest and 90-115 beats/min during mod exercise (criteria varies by age) Recent data found no advantage of a target of ≤80 beats/min compared to a target of ≤110 beats/min (Van Gelder et al, 2009)

16. Convenient IV admin in NPO pts, rapid onset action, dependable AV nodal blockade Side effects: Bradycardia, hypotension, heart block, bronchospasm (less frequently than nonselective ß-blockers), worsening of CHF ß-Blockers : 1 st -line Tx to  AV nodal conduction (works in 70% of patients) Metoprolol Short-acting, titratable on or off w / very rapid half-life Side effects: Bradycardia , hypotension, heart block, bronchospasm (less frequent) Occasionally inconsistent effect in high-catecholamine states Less bradycardia , less bronchospasm ; less propensity for heart block than other ß -blockers Side effects: Bradycardia , hypotension, heart block Doesn’t cross blood-brain barrier, fewer CNS side effects Side effects: Bradycardia , hypotension, heart block Lower incidence of crossing blood–brain barrier, fewer CNS side effects Side effects: Bradycardia , hypotension, heart block Available in oral form only Propranolol Esmolol Pindolol Atenolol Nadolol Inexpensive, commonly avail Side effects: Bradycardia , hypotension, heart block, bronchospasm , worsening CHF RATE CONTROL STRATEGY

17. Nondihydropyridine calcium-channel antagonists (1 st -line Tx to  AV nodal conduction) Verapamil Consistent AV nodal blockade Side effects: Hypotension, heart block, direct myocardial depression Do not use in Wolff-Parkinson-White syndrome Useful for rate control only with  LV systolic function Side effects: Heart block and arrhythmias; dosage adjustment required in renal impairment Not useful for rate control during exercise or conversion of AF/aflutter to NSR Diltiazem Cardiac glycoside digoxin RATE CONTROL STRATEGY

18. Dronedarone Recently approved, modestly effective, fewer side effects than amiodarone Amiodarone Blocks AV node, not recommended as 1 st -line monotherapy for rate control because of associated toxicities Occasionally used to  ventricular response if other agents fail Update 2018: Magnesium Sulfate –  A double-blind, randomized controlled trial (The LOMAGHI study) demonstrated IV MgSO4 dosed at either 4.5g or 9g, when combined with other AV nodal blockers, had a synergistic effect on improving rate control of rapid atrial fibrillation in the emergency department.  RATE CONTROL STRATEGY

19. RHYTHM CONTROL STRATEGY Consider rhythm control in younger patients and patients with highly symptomatic AF because trials did not include these groups Experienced clinicians may prefer rhythm control with cardioversion for 1 st episode symptomatic AF in younger patients because many such patients maintain sinus rhythm without drugs Rhythm control is no longer the preferred strategy based on trials comparing rate vs. rhythm control

20. RHYTHM CONTROL STRATEGY Direct electrical current to convert to NSR indicated if hemodynamically unstable Antiarrhythmic drugs: - conversion rate < direct electrical current in hemodynamically stable pts + deep sedation or general anesthesia not required

21. RHYTHM CONTROL STRATEGY Either direct electrical or antiarrhythmic drug cardioversion: AF >48h or undetermined duration: establish rate control & anticoagulation before elective cardioversion INR 2.0 – 3.0 for > 3 weeks prior and > 4 weeks after cardioversion Alternative- Transesophageal Echo:  No clot: heparin for 48 hr prior to cardioversion & warfarin for 4 wks after  Clot present: anticoagulation for 4 weeks; most confirm thrombus resolution with repeat TEE before cardioversion Serum K level should be >4.0 mmol /L, serum Mg level >1.0 mmol /L, and ionized Ca levels >0.5 mmol /L Conduct cardioversion in monitored hospital setting Because antiarrhythmic drugs generally have equal efficacy, except for amiodarone , c hoose a drug by side effects

22. RHYTHM CONTROL STRATEGY Class Ia antiarrhythmic drugs prolong conduction & slow repolarization by blocking inward Na+ flux Procainamide not recommended because of frequent side effects (hypotension, nausea, vomiting, lupus-like syndrome, QT prolongation, arrhythmia) Quinidine gluconate not recommended because of frequent side effects ( proarrhythmia , nausea, vomiting, diarrhea, QT prolongation) Disopyramide : Use in pts with hypertension & normal LV function Adverse effects include QT prolongation, torsades de pointes, and heart block Rarely used in current era

23. RHYTHM CONTROL STRATEGY Class Ic antiarrhythmic d rugs block Na+ channels Flecainide is effective in paroxysmal AF with structurally normal hearts Adverse effects include atrial flutter and atrial tachycardia with rapid ventricular response; also VT, and VF in diseased hearts Do not use in pts with structurally abnormal hearts Propafenone is effective in paroxysmal and sustained AF Adverse effects include atrial flutter or atrial tachycardia with rapid ventricular response Do not use in pts with structurally abnormal hearts

24. RHYTHM CONTROL STRATEGY Antiarrhythmic drugs (class III) Ibutilide prolongs action potential duration (and atrial and ventricular refractoriness) Effective in acute & rapid conversion of AF to NSR Adverse effects include torsades de pointes and QT prolongation

25. RHYTHM CONTROL STRATEGY Amiodarone blocks Na+ channels Safest agent for use in pts with structural heart disease, good efficacy maintaining NSR chronically; can be used in Wolff–Parkinson-White syndrome Adverse effects include bradycardia, QT prolongation, hyperthyroidism, lung toxicity, blue discoloration of skin Sotalol is a n onselective ß - and 1ß -blocking agent that prolongs action potential duration Similar in efficacy to quinidine but with fewer adverse effects and better rate control. Initiate on telemetry Adverse effects include fatigue, depression, bradycardia, torsades de pointes, and CHF ß-blocking properties, but some inotropic activity; lethal arrhythmias possible; adjust dose in pts with renal insufficiency

26. RHYTHM CONTROL STRATEGY Dofetilide prolongs refractoriness without slowing conduction More effective than quinidine in conversion to and maintenance of NSR; initiate on telemetry Adverse effetcs include QT prolongation and, torsades de pointes Dose strictly according to renal function, body size, & age; contraindicated in pts with creatinine clearance <20 mL/min Dronedarone is similar to amiodarone—blocks sodium, potassium, and calcium channels—but without iodine Adverse effects include GI intolerance Contraindicated for decompensated CHD; less efficacious but better tolerated than amiodarone

27. ELECTRICAL CARDIOVERSION More effective  than chemical cardioversion (90%), but patient may prefer not to use given fear or pain Do NOT attempt in patients at high risk of thrombo-embolic events (valvular heart disease, severe mitral disease, caridomyopathy , prosthetic valve or prior TIA/CVA), or when procedural sedation is contra-indicated Consider using initial  energy level of 150-200J  biphasic to increase the success rate and decrease the number of total shocks given

28. RECURRENCE OF AF Have only modest effects prolonging time to recurrence The Canadian Trial of Atrial Fibrillation randomly assigned 403 patients to amiodarone, sotalol, or propafenone and found that after mean follow-up of 16 months, recurrence of AF was 35% for amiodarone Tx compared w/ 63% for sotalol or propafenone Tx (NEJM, 2000) Some nonantiarrhythmic drugs (ACE-inhibitors, statins ) reduce the incidence of AF in pts with HF presumably because of antifibrotic effects

29. ANTICOAGULATION Consider long-term anticoagulation in pts with High risk for recurrent AF Asymptomatic AF Intracardiac thrombus Known risk factors for thromboembolism (age ≥75y, recent HF, LV dysfunction, diabetes mellitus, hypertension, previous thromboembolism) Many clinicians use cutoff of 65 rather than 75 yrs to initiate warfarin Tx when pt also has CAD Genetic tests can identify pts who require different warfarin dosing, but the tests are not recommended because they have not been shown to improve pt outcomes Update 2015 :  Study in Annals of Emergency Medicine suggests that patients given a prescription for warfarin in the ED may have better rates of long-term anticoagulation

30. Canadian Cardiovascular Society  recommends using  CHADS 2   score  to predict risk of CVA CHF, HTN, Age≥75, Diabetes, TIA/CVA (2 points) score ≥1 = dabigatran or warfarin; consider ASA if score of 1 and patient reluctant to anticoagulate , but urge follow up with GP or cardiologist also consider ASA if score is 0 and patient is not young European guidelines  recommend using  CHA 2 DS 2 VASc  score given that CHADS 2  does not include other risk factors CHF, HTN, Age ≥75 (2 points), Diabetes, TIA/CVA (2 points), Vascular diseases (CAD, MI, PVD), Age 65-74, Sex category (female 1 point, male 0 point) No anticoagulation in younger patients with presumably no structural heart disease and CHA 2 DS 2 VASc = 0

31. ANTICOAGULATION REGIMENS Warfarin is the preferred drug. Adjust the dose to an INR of 2.0-3.0 (2.5-3.5 for patients with prosthetic valves) Aspirin is an alternative to warfarin when there are contraindications to warfarin; no previous stroke or transient ischemic attack; no hypertension, diabetes, or HF, and the patient is < 75 Aspirin + clopidogrel together prevent more strokes than aspirin alone but are not as effective as warfarin and have a bleeding risk that is equivalent to warfarin Dabigatran recently has been approved by the FDA to prevent stroke and systemic embolism in pts with AF & creatinine clearance ≥30 mL/min

32. NON DRUG THERAPIES AV nodal catheter ablation inactivates parts of the atrium where AF begins Use when drug Tx doesn’t achieve rate control (usually because of drug intolerance in the elderly or in pts with advanced HF or COPD, which limits β-blocker use) Highly effective but requires pacemaker insertion, can lead to progressive LV dysfunction Pacing therapy without AV nodal ablation has little effect on burden of AF (but may help with paroxysmal AF and symptomatic bradycardia, a side effect drug Tx) Prevents recurrent symptomatic AF in highly selected patients, ideally young, otherwise healthy person without structural heart disease & with paroxysmal AF May be reasonable when antiarrhythmic drug Tx fails in highly symptomatic pts with paroxysmal AF Selected high-risk pts not candidates for oral anticoagulation therapy Additional studies needed to verify the safety & effectiveness of these devices Occlusion of the left atrial appendage to prevent strokes

33. FOLLOW UP Regular follow-up to Determine effectiveness of Tx Monitor warfarin anticoagulation Check if symptoms adequately controlled (ask about palpitations, easy fatigability, dyspnea on exertion) If on amiodarone , check liver and thyroid function every 6 months and order chest x-ray annually (otherwise routine tests for drug side effects unnecessary)

34. HOSPITALISATION Uncertain or unstable underlying arrhythmia Acute MI, altered mental status, decompensated HF, or hypotension Intolerable symptoms despite hemodynamic stability Elective cardioversion (if monitored outpatient setting unavailable) Acute anticoagulation for very high stroke risk high Telemetry monitoring when initiating some drugs For procedures such as cardiac catheterization, electrophysiologic studies, pacemakers, implantable defibrillators, or catheter or surgical ablation

35. COMPLICATIONS Symptoms (sometimes disabling) Usually caused by rapid ventricular rates or irregular ventricular response Loss of atrial contribution to ventricular filling (atrial kick) is well tolerated except by pts with ventricular hypertrophy Thromboembolism (stroke most common) In nonvalvular AF, the annual risk of arterial thromboembolism is 5% (higher in pts >75y) Atrial thrombi cause 75% strokes in AF Cardiomyopathy (prevent by treating tachycardia of AF)

36. ATRIAL FLUTTER Look in leads II, III, aVF to see saw-tooth waves  (or turn ECG upside down to see them better), especially if the narrow-complex tachycardia is around 150/min Pharmacological cardioversion and rate control are both MUCH less effective than with AF Unclear if it really takes less energy to cardiovert (50J), so consider using 150-200J initially

37. WOLFF-PARKINSON-WHITE SYNDROME (WPW) Differential of AF with wide QRS:  AF with aberrancy  (RBBB or LBBB – QRS usually has typical morphology) AF with pre-excitation  – eg , WPW: esp. when QRS morphology is bizarre, polymorphic and much faster than usual AF (sometimes approaching 300) NEVER give AV nodal blocking agent  (beta-blocker, calcium-channel blocker, adenosine, digoxin and even amiodarone) as the AV node will be blocked and impulses sent preferentially down the bypass tract – which doesn’t have any slowing mechanism – and trigger VF Treatment : electrical cardioversion, or procainamide is the safest medication

38. CONCLUSION Atrial fibrillation treatment goals include reducing the frequency and severity of symptoms, preventing stroke, and preventing tachycardia-related cardiomyopathy. Selection of patients for anticoagulation with aspirin or warfarin should be based on the CHADS2 score. Focus treatment first on rate control by using beta-blockers or calcium-channel antagonists aiming for a resting rate between 60 and 110 beats per minute. Rhythm control may be reasonable in patients who do not respond to rate control. Atrial ablation and atrioventricular nodal ablation therapy may be appropriate for selected patients with highly symptomatic AF despite drug therapy.

39. REFERENCES Wyse DG, Waldo AL, Dimarco JP, et al. A comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med. 2002;347(23):1825-33. Camm AJ, Lip GY, De caterina R, et al. 2012 focused update of the ESC Guidelines for the management of atrial fibrillation: an update of the 2010 ESC Guidelines for the management of atrial fibrillation–developed with the special contribution of the European Heart Rhythm Association. Europace . 2012;14(10):1385-413. Pisters R, Lane DA, Nieuwlaat R, et al. A Novel User-Friendly Score (Has-Bled) To Assess 1-Year Risk Of Major Bleeding In Patients With Atrial Fibrillation: The Euro Heart Survey. Chest. 2010;138(5):1093-1100. Cairns JA, Connolly S, Mcmurtry S, Stephenson M, Talajic M. Canadian Cardiovascular Society atrial fibrillation guidelines 2010: prevention of stroke and systemic thromboembolism in atrial fibrillation and flutter. Can J Cardiol . 2011;27(1):74-90. Stiell IG, Clement CM, Perry JJ, et al. Association of the Ottawa Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM. 2010;12(3):181-91.