Atrial Fibrillation1

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Atrial Fibrillation:

Atrial Fibrillation DR.TAMILMANI V

Atrial Fibrillation:

Atrial Fibrillation AF is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function.

Slide 3:

A rapid, irregular, sustained, wide-QRS-complex tachycardia strongly suggests AF with conduction over an accessorypathway or AF with underlying bundle-branch block. Extremely rapid rates (over 200 beats per minute) suggest the presence of an accessory pathway or ventricular tachycardia.

Electrocardiogram showing atrial fibrillation with a controlled rate of ventricular response :

Electrocardiogram showing atrial fibrillation with a controlled rate of ventricular response

Slide 5:

Atrial flutter in the typical form is characterized by a saw-tooth pattern of regular atrial activation called flutter () waves on the ECG, particularly visible in leads II, III, aVF , and V 1 . Atrial flutter commonly occurs with 2:1 AV block, resulting in a regular or irregular ventricular rate of 120 to 160 beats per minute (most characteristically about 150 beats per minute). Atrial flutter may degenerate into AF and AF may convert to atrial flutter

Electrocardiogram showing typical atrial flutter with variable atrioventricular conduction :

Electrocardiogram showing typical atrial flutter with variable atrioventricular conduction

Classification:

Classification R ecurrent AF When a patient has had 2 or more episodes . Paroxysmal- If the arrhythmia terminates spontaneously . persistent AF - sustained beyond 7 d . persistent AF - cases of long-standing AF (e.g., greater than 1 y), usually leading to permanent AF, in which cardioversion has failed or has not been attempted.

Slide 8:

Patterns of atrial fibrillation (AF). 1, Episodes that generally last 7 d or less (most less than 24 h); 2, episodes that usually last longer than 7 d; 3, cardioversion failed or not attempted; and 4, both paroxysmal and persistent AF may be recurrent.

Slide 9:

"lone AF" has been variously defined but generally applies to young individuals (under 60 y of age) without clinical or echocardiographic evidence of cardiopulmonary disease, including hypertension

Slide 10:

nonvalvular AF" is restricted to cases in which the rhythm disturbance occurs in the absence of rheumatic mitral valve disease, a prosthetic heart valve, or mitral valve repair.

Estimated age-specific prevalence of atrial fibrillation (AF):

Estimated age-specific prevalence of atrial fibrillation (AF)

Prevalence of AF in Patients With Heart Failure:

Prevalence of AF in Patients With Heart Failure

Slide 13:

Pathophysiological Mechanisms

Atrial Pathology as a Cause of Atrial Fibrillation:

Atrial Pathology as a Cause of Atrial Fibrillation The most frequent patho anatomic changes in AF are atrial fibrosis and loss of atrial muscle mass. Patients with mild or moderate fibrosis responded more successfully to cardioversion than did those with severe fibrosis, which was thought to contribute to persistent AF in cases of valvular heart disease

Slide 15:

Atrial fibrosis may be caused by genetic defects like lamin AC gene mutations . Other triggers of fibrosis include inflammation as seen in cardiac sarcoidosis and autoimmune disorders. Autoimmune activity is suggested by high serum levels of antibodies against myosin heavy chains in patients with paroxysmal AF who have no identified heart disease

Slide 16:

Fibrosis is also triggered by atrial dilation in any type of heart disease associated with AF, including valvular disease, hypertension, HF, or coronary atherosclerosis.

Slide 17:

Stretch RAAS TGF-beta1 connective tissue growth factor Fibrosis

Slide 18:

Transition of AV reentry into AF in patients with the Wolff-Parkinson-White (WPW) syndrome can produce a rapid ventricular response that degenerates into ventricular fibrillation, leading to death . Intravenous administration of drugs such as digitalis, verapamil , or diltiazem , which lengthen refractoriness and slow conduction across the AV node, does not block conduction over the accessory pathway and may accelerate the ventricular rate.

Slide 20:

A, Focal activation. The initiating focus (indicated by the star) often lies within the region of the pulmonary veins. The resulting wavelets represent fibrillatory conduction, as in multiple-wavelet reentry. B, Multiple-wavelet reentry. Wavelets (indicated by arrows) randomly reenter tissue previously activated by the same or another wavelet.

Etiologies and Factors Predisposing Patients to AF:

Etiologies and Factors Predisposing Patients to AF

Slide 26:

Management of patients with AF involves 3 objectives—rate control, prevention of thromboembolism , and correction of the rhythm disturbance,

Slide 27:

In patients with persistent AF and normal LV function, the combination of enalapril or irbesartan plus amiodarone resulted in lower rates of recurrent AF after electrical conversion than amiodarone alone

Slide 28:

statin -type cholesterol-lowering agents in maintaining sinus rhythm in patients with persistent lone AF. an inhibitory effect on the progression of CAD, pleiotropic (anti-inflammatory and antioxidant) effects , and direct antiarrhythmic effects involving alterations in transmembrane ion channels

Antithrombotic Therapy for Patients With Atrial Fibrillation:

Antithrombotic Therapy for Patients With Atrial Fibrillation

Slide 32:

Administration of flecainide , dofetilide , propafenone , or ibutilide is recommended for pharmacologicalcardioversion of AF. Administration of amiodarone is a reasonable option for pharmacological cardioversion of AF. Digoxin and sotalol may be harmful when used for pharmacological cardioversion of AF and are not recommended.