atrial fibrillation is the most popular arrhythmia and iagnosed by the finding of an irregularly irregular ventricular rhythm without discrete P waves atrial fibrillation is a supraventricular tachycardia in atrial fibrillation or AF for short the atria do not contract in a synchronous rhythm instead they quiver or fibrillate this means that they beat very rapidly and irregularly the most concerning thing about atrial fibrillation is clot formation and embolism due to stasis in the atrium the left atrium is commonly involved in clot formation resulting in embolization to the brain causing a stroke the sinoatrial node is a dominant pacemaker in the heart which sends impulses to the atrium causing atrial contraction in a synchronous pattern atrial contraction is represented by the P wave on the ECG from there the impulse arrives at the atrioventricular node the atrioventricular node conducts the impulse slower it is a gatekeeper to the ventricles from the atrioventricular node the impulse travels rapidly along the bundle of hiss under branches and Purkinje fibers where the impulse travels causing ventricular contraction ventricular contraction is represented by the QRS complex on the ECG a F is a result of an initial trigger thought to be from a local ectopic foci firing rapidly from the pulmonary veins or a single localized reentry circuit in the atrial myocardium let us take a look at these two mechanisms and how they lead to atrial fibrillation or AF ectopic foci are pacemaker cells which initiate an impulse from another location than the normal conduction system route the ectopic foci most often occurs from the left atrium in the muscular sleeves of the pulmonary veins less often in the right atrium near the superior vena cava or the inferior vena cava the ectopic foci will fire rapid impulses to the atrioventricular node and other parts of the atria canceling out the normal impulses that are generated thus the atrioventricular node will pick up impulses irregularly resulting in an unsecured nice rhythm and a rapid ventricular rate the initial trigger for AF could also be as a result of a re-entry circuit a re-entry circuit can form as a result of ischemic heart disease age hypertension which all changes atrial morphology it changes the atrial shape and anatomy in af the re-entry circuit originates in the atrial myocardium which have now varying conductivity and excitability an example of this morphology change could be an atrial myocardium which has slow conducting properties surrounded by normal conducting areas the slow conducting myocardium typically have a short refractory period meaning they are able to rest and be recited faster whereas the normal conducting myocardium have a longer refractory period they require a longer time to rest before being activated so when another impulse from the sign of a chill note arrives to the slow conducting area they can be recited again and thus the slow conducting area can then re excite other normal surrounding myocardial tissue as well which can trigger a re-entry circuit once the re-entry circuit is formed the impulse generated here will collide and cancel out other impulses around the atrioventricular node will thus capture the impulses irregularly resulting in an unsynchronized rhythm and a rapid ventricular rate an ectopic foci may fire impulses and encounter atrial myocardium with varying conductivity and excitability as well when the impulses from the ectopic foci encounter these areas they can then also trigger a reentry circuit early in atrial fibrillation the initial trigger is usually a few ectopic foci that will terminate within seven days now this is termed paroxysmal atrial fibrillation when atrial fibrillation lasts over seven days it is known as persistent AF in permanent AF restoration to sinus rhythm is impossible persistent and permanent atrial fibrillation is due to progressive conduction and anatomical remodeling in the atria continuous and recurrent atrial fibrillation itself will induce electrical conduction and anatomical changes in the atrium which will increase the number of ectopic foci and reentry circuits thus increase the risk for triggering and maintaining atrial fibrillation other causes of atrial remodeling include ischemic heart disease heart failure pulmonary hypertension obstructive sleep apnea obstructive pulmonary disease and so all of these are risk factors for atrial fibrillation the classic ECG findings in AF are absent P waves with irregularly irregular ventricular rate the ISO electric bass line is not straight and is characterized by F waves which are fibula Tory waves F waves can be very small or large but these must not be mistaken for atrial flutter the heart rate will vary between everyone and can range from a hundred two hundred eighty beats per minute if the heart rate is fast this is termed atrial fibrillation with rapid ventricular rate atrial fibrillation is a supraventricular tachycardia and thus the QRS complex is narrow diagnosis of paroxysmal atrial fibrillation is by halter monitor or implantable loop recorder if really necessary for persistent atrial fibrillation this can be diagnosed with an ECG of course when thinking of management of atrial fibrillation it's good to think about it as acute or long-term management let's talk about acute management of atrial fibrillation in an acute setting anyone who is tachycardic and his unstable requires electrical cardioversion synchronized cardioversion picks up the QRS complex and delivers a shock and it targets the are waves in the ECG electrical cardioversion is followed by an amiodarone infusion typically following the electrical cardioversion hopefully the atrial fibrillation will revert back to sinus rhythm if the patient's stable electrical cardioversion can be done later or chemical cardioversion can be done instead using antiarrhythmics and there are a number of antiarrhythmic agents that can be used for chemical cardioversion and is based on the singh vagon williams classification which targets different parts of the cardiac action potential common medications for chemical cardioversion used include flecainide which is a class 1 antiarrhythmic inhibiting sodium influx in phase zero and thus inhibiting the action potential slowing the heart rate down so Dalal is a class 3 antiarrhythmic and inhibits potassium efflux this prolongs the action potential and increases the time before another electrical signal can be generated in the ventricle myocytes amiodarone is another class three antiarrhythmic agent and works the same way sotalol but with other mechanisms as well in summary chemical cardioversion will slow the conduction down and/or prolong the action potential patients who are cardioverted with chemical or electrical cardioversion means the heart will hopefully go back to normal sinus rhythm now it's very important to know that if the atrial fibrillation has been going on for over 48 hours or you are unsure a thrombus could have potentially formed from the stagnation and the station of blood in the atrium and so if AF has been going on for a while and is reverted back to sinus rhythm suddenly the thrombus that has been formed can actually lodge dislodge into the cerebral arteries causing a stroke or into the mesenteric arteries causing ischemia and so to prevent this before performing cardioversion a transesophageal echocardiogram is done to look for a thrombus in the left atrium or left atrial appendage prior to cardioversion alternatively anticoagulation for four weeks should be done to break any clots in the atrium prior to a cardioversion here's an example of a transesophageal echocardiogram note that sometimes patients with AF can have a thrombus form usually in the left atrium asides from cardioversion in a cute setting if the patient is stable it's important to rate control the atrial fibrillation because atrial fibrillation with a rapid ventricular response would cause uncomfortable symptoms such as palpitations dis Nia fatigue chest discomfort as well as dizziness or lightheadedness there are three main classes of heart rate medications used in atrial fibrillation these are beta blockers calcium channel blockers and digoxin all these drugs affects the atrial ventricular node it slows the conduction through the a chav in tricular node and this results in fewer atrial impulses being conducted to the ventricles slowing down the heart rate the outcome of acute management for AF will either be one the person has reverted back to normal sinus rhythm or two the person still has atrial fibrillation which will either be paroxysmal or persistent regardless there needs to be a long-term management plan for each of these outcomes so for long term management patients who have returned to sinus rhythm may develop atrial fibrillation again later it needs to be a decision whether long-term rhythm or rate control strategy is needed as well as stroke prevention using anticoagulation there is no difference in survival between using a rate or rhythm control management in the long term the choice really depends on a side-effect profile and contraindications of these medications so for rate control drugs used include beta blockers such as metoprolol calcium channel blockers and digoxin these drugs inhibit sympathetic activation as well as slowed down the a/o ventricular node conduction rhythm control drugs includes sotalol or amiodarone these drugs we've already talked about earlier and they target different parts of the cardiac action potential but essentially they will slow conduction and/or prolong the action potential long-term anticoagulation should be initiated if a person has significant or sufficient risk factors for a stroke the most common way of assessing this is by using the Chad's vas score which are a series of risk factors that get assigned a point and then they get either put into low medium or high risk of stroke low-to-medium Chad's Vasko do not support anticoagulation use as risk of bleeding tends to be higher a high Chas vas Kor supports anticoagulation there are different types of anticoagulants used for atrial fibrillation and they are really based on whether someone has valvular atrial fibrillation or non valvular atrial fibrillation it's very important to know the difference valvular atrial fibrillation is when someone has atrial fibrillation and also have mitral valve stenosis or they have a mechanical valve or they have rheumatic heart disease wolfram is the mainstay anticoagulant if patients have valvular atrial fibrillation it is also used in people who have atrial fibrillation and who have chronic kidney disease as well for non valvular atrial fibrillation doe acts also known as no acts are used these include factor 10a inhibitors such as rivaroxaban and apixaban or direct thrombin inhibitors such as the bigot Ram finally catheter ablation is a highly effective treatment for paroxysmal atrial fibrillation in paroxysmal AF there are few ectopic focus that can be localized in the pulmonary veins and eliminated with ablation therapy however as AF progresses these ectopic sites become more complicated and require more complex ablation procedures thank you for watching I hope you enjoyed this video on atrial fibrillation you