ATRIAL FIBRILLATION ppt 1.pptx Definition, pathophysiolology

Atrial fibrillation

1. ATRIAL FIBRILLATION

2. INTRODUCTION It is characterised by disorganised, rapid, and irregularatrial activation with loss of atrial contraction and with an irregular ventricular rate that is determined by AV nodal conduction.

3. Epidemiology AF is the most common sustained arrhythmia and is a major public health problem. Prevalence increase with age, and >95% of AF patients are >60 years. of age. The lifetime risk of developing AF for men 40 years old is 25%. More common in men than women and whites than blacks. Associated with a risk of developing heart failure and vice versa. It increases the risk of stroke.

4. Etiopathogenesis Triggers Ectopic foci ↓ Electophysiologic remodelling fibrosis ↓ Chronic substrate fibrosis

5. The clinical pattern of AF suggests the underlying pathophysiology Paroxysmal AF ↓ Persistent AF ↓ Long standing persistent or permanent AF

6. Paroxysmal AF is defined by episodes that start spontaneously and stop within 7 days of onset. It is often initiated by small reentrant or rapidly firing foci in sleeves of atrial muscle that extend into the pulmonary veins. Some patients also have initiating foci in other locations which is more common in older patients and in patients with more severe underlying cardiac disease.

7. 2. Persistent AF has a longer duration exceedingly 7 days In many cases, will continue indefinitely unless cardioversion is performed. Persistence of AF is likely facilitated by structural and electrophysiologic atrial abnormalities like fibrosis that uncouples atrial fibres , promoting re entry and focal automaticity.

8. 3. Long standing persistent AF or permanent AF is when AF is persisting for >1 year Significant fibrosis is usually present and it is difficult to restore and maintain a sinus rhythm

9. Patients can progress from paroxysmal to persistent AF over the years Fibrosis developing with aging and atrial hypertrophy in response to hypertension and other cardiac disease appears to be important promoting factor. Electrophysiologic remodelling that affects conduction and refractoriness occur in response to chronic tachycardia Thus AF tends to promote AF.

10. AF is occasionally associated with an acute precipitating factor such as hyperthyroidism, acute alcohol intoxication, myocardial infarction or pulmonary embolism AF occurs in up to 30% of patients recovering from cardiac surgery, associated with inflammatory pericarditis.

11. Clinical features Clinical consequences of AF are related to rapid ventricular rates, loss of atrial contribution to ventricular filling, and predisposition to thrombus formation in the left atrial appendage with potential embolization. Exercise intolerance and easy fatiguability are common despite the absence of palpitations in many patients Dizziness or syncope Angina Tachycardia related cardiomyopathy can cause depressed ventricular function and is more common in patients who do not sense palpitations as they may not seek medical attention till heart failure symptoms develop.

12. Treatment It is primarily guided by -patient’s symptoms -hemodynamic effect of AF Duration of AF Risk of stroke Underlying heart disease

13. New onset AF that produces severe hypotension, pulmonary edema, or angina should be electrically cardioverted starting with a QRS synchronous shock of 200J, ideally after sedation or anaesthesia is achieved Greater shock energy and different electrode placements may be tried if shock fails to terminate AF Administraion of intravenous ibutilide lowers the energy requirement for atrial defibrillation and is avoided in patients with a prolonged QT interval or severe LV dysfunction because of a significant risk of torsedes de Pointes

14. If the patient is stable, immediate management involves rate control to alleviate or prevent symptoms, and consideration of whether anticoagulation is warranted to reduce stroke risk. Consideration is then given to whether therapy is warranted to restore sinus rhythm , or whether the patient will be allowed to continue in AF, and managed with rate control and measures for stroke prevention. It is critical to consider the risk of stroke when attempting to restore sinus rhythm.

15. If the duration of AF is unclear or is known to be > 48 hours, anticoagulation must be commenced before cardioversion In the absence of contraindications, it is usually appropriate to initiate systemic anticoagulation with heparin immediately or with an oral anticoagulant that has rapid onset of action

16. Cardioversion and anticoagulation Major source of thromboembolism and stroke in AF is the formation of thrombus in left atrial appendage where flow is relatively stagnant When AF has been present for >48 hour and patient is at high risk of thromboembolism, such as those with mitral stenosis or hypertrophic cardiomyopathy, cardioversion is associated with increased risk of thromboembolism

17. There are two approaches to mitigate the risk related to cardioversion To anticoagulation continuously for 3weeks before and a minimum of 4 weeks after cardioversion To start anticoagulation and perform a trabsesophageal echocardiogram to determine if thrombus is present in the left atrial appendage If thrombus is absent perform cardioversion can be performed and anticoagulation is continued for minimum of 4 weeks.

18. Long term maintainance of anticoagulation is considered based on patient’s individual risk for stroke, commonly assessed from the CHA2DS2-VASc score

19. Rate control Acute rate control -Beta blockers and or Calcium channel blockers verapamil and diltiazem either iv or orally as warranted Digoxin may be added particularly in heart failure patients Goal is to reduce the ventricular rate to less than 100 beats per minute

20. Chronic rate control -Beta adrenergic blockers and calcium channel blockers -Digoxin is added selectively if these are insufficient Exertion related symptoms are often an indication for inadequate control -lnitial goal is resting heart rate of <80 beats /minute that increases to <100 beats/minute with light exercise such as walking

21. If adequate rate control in AF is difficult to achieve, further consideration should be given to restoring sinus rhythm. -Catheter ablation of the AV junction to create heart block and implantation of permanent pace maker.

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