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Atrial Fibrillation Overview - ECG, types, pathophysiology, treatment, complications — Transcript

by Armando Hasudungan · 1,790 words · 317 segments · language en · Watch on YouTube

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0:10atrial fibrillation is the most popular
0:13arrhythmia and iagnosed by the finding
0:16of an irregularly irregular ventricular
0:19rhythm without discrete P waves
0:25atrial fibrillation is a
0:27supraventricular tachycardia
0:33in atrial fibrillation or AF for short
0:36the atria do not contract in a
0:39synchronous rhythm instead they quiver
0:41or fibrillate this means that they beat
0:45very rapidly and irregularly the most
0:48concerning thing about atrial
0:50fibrillation is clot formation and
0:52embolism due to stasis in the atrium the
0:56left atrium is commonly involved in clot
0:59formation resulting in embolization to
1:02the brain causing a stroke
1:09the sinoatrial node is a dominant
1:12pacemaker in the heart which sends
1:14impulses to the atrium causing atrial
1:17contraction in a synchronous pattern
1:20atrial contraction is represented by the
1:23P wave on the ECG from there the impulse
1:29arrives at the atrioventricular node the
1:33atrioventricular node conducts the
1:35impulse slower it is a gatekeeper to the
1:38ventricles from the atrioventricular
1:40node the impulse travels rapidly along
1:44the bundle of hiss under branches and
1:47Purkinje fibers where the impulse
1:50travels causing ventricular contraction
1:54ventricular contraction is represented
1:57by the QRS complex on the ECG
2:05a F is a result of an initial trigger
2:09thought to be from a local ectopic foci
2:12firing rapidly from the pulmonary veins
2:14or a single localized reentry circuit in
2:18the atrial myocardium let us take a look
2:22at these two mechanisms and how they
2:25lead to atrial fibrillation or AF
2:31ectopic foci are pacemaker cells which
2:35initiate an impulse from another
2:38location than the normal conduction
2:39system route the ectopic foci most often
2:44occurs from the left atrium in the
2:46muscular sleeves of the pulmonary veins
2:48less often in the right atrium near the
2:52superior vena cava or the inferior vena
2:55cava
3:00the ectopic foci will fire rapid
3:04impulses to the atrioventricular node
3:07and other parts of the atria canceling
3:10out the normal impulses that are
3:12generated
3:13thus the atrioventricular node will pick
3:17up impulses irregularly resulting in an
3:21unsecured nice rhythm and a rapid
3:24ventricular rate
3:30the initial trigger for AF could also be
3:33as a result of a re-entry circuit a
3:37re-entry circuit can form as a result of
3:40ischemic heart disease age hypertension
3:44which all changes atrial morphology it
3:49changes the atrial shape and anatomy
3:54in af the re-entry circuit originates in
3:59the atrial myocardium which have now
4:03varying conductivity and excitability an
4:07example of this
4:09morphology change could be an atrial
4:13myocardium which has slow conducting
4:16properties surrounded by normal
4:19conducting areas the slow conducting
4:23myocardium typically have a short
4:25refractory period meaning they are able
4:28to rest and be recited faster whereas
4:32the normal conducting myocardium have a
4:34longer refractory period they require a
4:37longer time to rest before being
4:39activated so when another impulse from
4:42the sign of a chill note arrives to the
4:44slow conducting area they can be recited
4:47again and thus the slow conducting area
4:50can then re excite other normal
4:53surrounding myocardial tissue as well
4:55which can trigger a re-entry circuit
4:58once the re-entry circuit is formed the
5:01impulse generated here will collide and
5:04cancel out other impulses around
5:07the atrioventricular node will thus
5:11capture the impulses irregularly
5:14resulting in an unsynchronized rhythm
5:16and a rapid ventricular rate
5:22an ectopic foci may fire impulses and
5:26encounter atrial myocardium with varying
5:29conductivity and excitability as well
5:31when the impulses from the ectopic foci
5:34encounter these areas they can then also
5:38trigger a reentry circuit
5:47early in atrial fibrillation the initial
5:49trigger is usually a few ectopic foci
5:53that will terminate within seven days
5:55now this is termed paroxysmal atrial
5:58fibrillation
6:01when atrial fibrillation lasts over
6:03seven days it is known as persistent AF
6:07in permanent AF restoration to sinus
6:12rhythm is impossible persistent and
6:14permanent atrial fibrillation is due to
6:17progressive conduction and anatomical
6:20remodeling in the atria continuous and
6:23recurrent atrial fibrillation itself
6:26will induce electrical conduction and
6:28anatomical changes in the atrium which
6:30will increase the number of ectopic foci
6:33and reentry circuits thus increase the
6:37risk for triggering and maintaining
6:39atrial fibrillation other causes of
6:43atrial remodeling include ischemic heart
6:46disease heart failure pulmonary
6:49hypertension obstructive sleep apnea
6:53obstructive pulmonary disease and so all
6:56of these are risk factors for atrial
6:57fibrillation
7:01the classic ECG findings in AF are
7:05absent P waves with irregularly
7:08irregular ventricular rate
7:12the ISO electric bass line is not
7:15straight and is characterized by F waves
7:19which are fibula Tory waves F waves can
7:24be very small or large but these must
7:27not be mistaken for atrial flutter the
7:31heart rate will vary between everyone
7:34and can range from a hundred two hundred
7:35eighty beats per minute if the heart
7:39rate is fast this is termed atrial
7:41fibrillation with rapid ventricular rate
7:45atrial fibrillation is a
7:47supraventricular tachycardia and thus
7:49the QRS complex is narrow
7:54diagnosis of paroxysmal atrial
7:56fibrillation is by halter monitor or
7:59implantable loop recorder if really
8:02necessary for persistent atrial
8:04fibrillation this can be diagnosed with
8:06an ECG of course
8:11when thinking of management of atrial
8:13fibrillation it's good to think about it
8:15as acute or long-term management let's
8:21talk about acute management of atrial
8:23fibrillation in an acute setting anyone
8:27who is tachycardic and his unstable
8:29requires electrical cardioversion
8:32synchronized cardioversion picks up the
8:35QRS complex and delivers a shock and it
8:37targets the are waves in the ECG
8:40electrical cardioversion is followed by
8:42an amiodarone infusion typically
8:46following the electrical cardioversion
8:48hopefully the atrial fibrillation will
8:51revert back to sinus rhythm
8:55if the patient's stable electrical
8:58cardioversion can be done later or
9:01chemical cardioversion can be done
9:04instead using antiarrhythmics and there
9:08are a number of antiarrhythmic agents
9:09that can be used for chemical
9:11cardioversion and is based on the singh
9:14vagon williams classification which
9:17targets different parts of the cardiac
9:20action potential common medications for
9:23chemical cardioversion used include
9:26flecainide
9:27which is a class 1 antiarrhythmic
9:30inhibiting sodium influx in phase zero
9:33and thus inhibiting the action potential
9:36slowing the heart rate down
9:38so Dalal is a class 3 antiarrhythmic and
9:42inhibits potassium efflux this prolongs
9:46the action potential and increases the
9:48time before another electrical signal
9:51can be generated in the ventricle
9:52myocytes
9:55amiodarone is another class three
9:58antiarrhythmic agent and works the same
10:01way sotalol but with other mechanisms as
10:04well
10:05in summary chemical cardioversion will
10:10slow the conduction down and/or prolong
10:13the action potential patients who are
10:17cardioverted with chemical or electrical
10:19cardioversion means the heart will
10:22hopefully go back to normal sinus rhythm
10:25now it's very important to know that if
10:28the atrial fibrillation has been going
10:30on for over 48 hours or you are unsure a
10:35thrombus could have potentially formed
10:37from the stagnation and the station of
10:40blood in the atrium
10:42and so if AF has been going on for a
10:45while and is reverted back to sinus
10:48rhythm suddenly the thrombus that has
10:51been formed can actually lodge dislodge
10:53into the cerebral arteries causing a
10:56stroke or into the mesenteric arteries
10:59causing ischemia and so to prevent this
11:02before performing cardioversion a
11:05transesophageal echocardiogram is done
11:08to look for a thrombus in the left
11:10atrium or left atrial appendage prior to
11:13cardioversion alternatively
11:16anticoagulation for four weeks should be
11:19done to break any clots in the atrium
11:22prior to a cardioversion
11:27here's an example of a transesophageal
11:30echocardiogram note that sometimes
11:32patients with AF can have a thrombus
11:35form usually in the left atrium
11:41asides from cardioversion in a cute
11:44setting if the patient is stable it's
11:47important to rate control the atrial
11:50fibrillation
11:51because atrial fibrillation with a rapid
11:53ventricular response would cause
11:56uncomfortable symptoms such as
11:58palpitations dis Nia fatigue chest
12:03discomfort as well as dizziness or
12:05lightheadedness there are three main
12:08classes of heart rate medications used
12:11in atrial fibrillation these are beta
12:14blockers calcium channel blockers and
12:17digoxin all these drugs affects the
12:20atrial ventricular node it slows the
12:23conduction through the a chav in
12:25tricular node and this results in fewer
12:28atrial impulses being conducted to the
12:30ventricles slowing down the heart rate
12:35the outcome of acute management for AF
12:39will either be one the person has
12:41reverted back to normal sinus rhythm or
12:44two the person still has atrial
12:47fibrillation which will either be
12:49paroxysmal or persistent regardless
12:53there needs to be a long-term management
12:55plan for each of these outcomes
12:59so for long term management patients who
13:02have returned to sinus rhythm may
13:05develop atrial fibrillation again later
13:07it needs to be a decision whether
13:09long-term rhythm or rate control
13:11strategy is needed as well as stroke
13:14prevention using anticoagulation there
13:18is no difference in survival between
13:20using a rate or rhythm control
13:23management in the long term the choice
13:25really depends on a side-effect profile
13:27and contraindications of these
13:29medications so for rate control drugs
13:32used include beta blockers such as
13:34metoprolol calcium channel blockers and
13:37digoxin these drugs inhibit sympathetic
13:41activation as well as slowed down the
13:43a/o ventricular node conduction rhythm
13:47control drugs includes sotalol or
13:50amiodarone
13:52these drugs we've already talked about
13:53earlier and they target different parts
13:56of the cardiac action potential but
13:58essentially they will slow conduction
14:00and/or prolong the action potential
14:08long-term anticoagulation should be
14:11initiated
14:12if a person has significant or
14:15sufficient risk factors for a stroke
14:18the most common way of assessing this is
14:20by using the Chad's vas score which are
14:23a series of risk factors that get
14:25assigned a point and then they get
14:27either put into low medium or high risk
14:30of stroke
14:33low-to-medium Chad's Vasko do not
14:36support anticoagulation use as risk of
14:39bleeding tends to be higher a high Chas
14:42vas Kor supports anticoagulation
14:47there are different types of
14:48anticoagulants used for atrial
14:50fibrillation and they are really based
14:53on whether someone has valvular atrial
14:56fibrillation or non valvular atrial
14:59fibrillation it's very important to know
15:01the difference valvular atrial
15:03fibrillation is when someone has atrial
15:05fibrillation and also have mitral valve
15:08stenosis or they have a mechanical valve
15:12or they have rheumatic heart disease
15:16wolfram is the mainstay anticoagulant if
15:19patients have valvular atrial
15:21fibrillation it is also used in people
15:24who have atrial fibrillation and who
15:26have chronic kidney disease as well
15:33for non valvular atrial fibrillation doe
15:36acts also known as no acts are used
15:38these include factor 10a inhibitors such
15:42as rivaroxaban and apixaban or direct
15:46thrombin inhibitors such as the bigot
15:49Ram
15:52finally catheter ablation is a highly
15:55effective treatment for paroxysmal
15:57atrial fibrillation in paroxysmal AF
16:00there are few ectopic focus that can be
16:04localized in the pulmonary veins and
16:06eliminated with ablation therapy however
16:09as AF progresses these ectopic sites
16:12become more complicated and require more
16:15complex ablation procedures thank you
16:18for watching I hope you enjoyed this
16:20video on atrial fibrillation
16:29you

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