Atrial fibrillation (CVS) Flashcards

(S)

1
Q

Define atrial fibrillation

A

Most common sustained arrhythmia characterised by irregular, uncoordinated atrial contraction at a rate of 300-600 beats per minute

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2
Q

What does it mean when the atrial contractions in AF are irregular and uncoordinated?

A

Uncoordinated - the fibres are not contracting together and are not in sync due to disorganised impulses (instead of one big contraction, its just lots of mini contractions looking like the atria are quivering/twitching)
Irregular - the rhythm of the atria beats is irregular

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3
Q

What are the rates of AF?

A

Atrial rate is 300-600 bpm, ventricular rate/HR is 100-160bpm

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4
Q

How is AF classified in terms of time?

A

Acute = episode less than 48 hrs
Paroxysmal = episodes are less than 7 days and terminate spontaneous/come and go
Persistent = episode more than 7 days but can be treated with therapy (long standing is if more than 12 months)
Permanent = ‘‘/continuous but resistent to therapy (e.g. cardioversion)

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5
Q

What are the most common causes of AF?

A

SMITH
Sepsis
Mitral valve (rheumatic heart disease - most common in less developed countries)
IHD (most common cause in UK)
Thyroid (hyper)
Hypertension

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6
Q

Cardiac causes of Afib?

A

IHD, Hypertension, rheumatic heart disease affecting mitral valve, pericarditis, myocarditis

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7
Q

Non cardiac causes of Afib

A

Dehydration, endocrine - hyperthyroidism, infective - sepsis, pulm - pneumonia or PE, alcohol abuse, electrolyte imbalance (e.g. hypokalaemia, hypomagnesaemia)

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8
Q

What are the risk factors of Afib?

A

Causes + other RFs

Age, hypertension, alcohol abuse, family history, obesity, diabetes, all the causes

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9
Q

What is the pathophysiology of AF?

A

Exact mechanism not understood well
1. Usually SAN produces APs that travel through a coordinated pathway to the ventricles. However this organised conduction is disrupted.
2. Often the rapid irregular initial impulses originate from ectopic foci near the pulm veins
3. Then, due to structural abnormalities (e.g. fibrosis/atrial dilation) we see uncoordinated propagation and earlier/later depols - asynch mini contractions
2. Due to this, multiple groups of myocytes are depolarising and contracting independently of eachother in an asynchronous manner.
4. Multiple re-entry circuits also cause the chaotic and async

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10
Q

Why do the ventricles not go into fibrillation in Afib?

A

The chaotic and disorganised impulses come together and get regulated at the AVN so come as one regular AP. However, the AVN is being stimulated at randomly and frequently as the atrial impulses are irregular/rapid so the vent rate is irregular and still fast (not as much as atria tho)

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11
Q

Why is there an increased risk of stroke in Afib?

A

Loss of coordinated atrial contraction results in the pooling of blood incr risk of clots (specifically in left atrial appendage). These can enter vents and go into circulation where they can occlude vessels causing strokes or other ischemic lesions

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12
Q

What are the symptoms of Afib?

A

Usually asymptomatic - usually discovered after stroke
- Palpitations
- Chest pain
- Shortness of breath/dyspnoea
- Dizzy, syncope

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13
Q

What are the clinical signs of Afib?

A

Irregularly irregular pulse with variable volume pulse
Single waveform on JVP (due to absent a wave)
An apical to radial pulse deficit (diff between them)
Auscultation - variable intensity first heart sound

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14
Q

What are the differentials of Afib?

A

Atrial flutter - however ECGs are different (flutter has sawtooth baseline but AF has absent p wave and fibrillating baseline)
SVT e.g. Atrial tachycardia, AVNRT, WPW syndrome (distinguishing diff types of SVT requires ECG)
Ventricular tachycardia - ECG patterns very different

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15
Q

What are the investigations for Afib?

A

Definitive diagnosis is done using 12 lead ECG (to exclude other causes of irregularly irregular pulses) - shows p wave absence with an irregularly irregular vent rhythm (+ irregular baseline, irregular and narrow QRS)
Bloods - look for reversible causes incl infection (raised WCC, CRP), hyperthyroidism (raised T3/4) alcohol use (raised MCV/GGT)
Imaging - Echocardiogram to see if cardiac cause e.g. left atrial dilation secondary to mitral valve disease

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16
Q

What conditions can cause an irregularly irregular pulse?

A

Afib, ventricular ectopic beats, Atrial flutter with variable block, Other atrial tachyarrhythmias

17
Q

Main goals/key components of management of AF

A

Rate control, rhythm control, management of acute AF, prevention of thromboembolic events

18
Q

Situations where emergency hospital admission should be done for Pt with AF?

A

New-onset AF within the past 48 hours and is haemodynamically unstable.
Severe symptoms of AF due to rapid (bpm > 150 ) or very slow (bpm < 40) ventricular rate
Accompanied acute decompensated heart failure
Complications of AF, such as TIA/stroke

19
Q

What is emergency presentation of AF and what is the management?

A

Acute AF within 48 hrs and haemodynamically unstable is an emergency.

To assess for this:
1. Clinical assessment (e.g. ABCDE approach) to assess haemodynamic stability (Presentation = shock, syncope, acute pulm oedema, myocardial ischemia)
2. If unstable, carry out emergency electrical DC cardioversion +/- amiodarone

20
Q

What is presentation and basic management of non emergency acute AF?

A

Presentation = Acute AFib with haemodynamic stability.
Management determined by time of onset.
1. If acute AF onset less than 48 hours - rate or rhythm control
2. If onset more than 48 hrs or unclear - rate control (bc incr risk of emboli with more than 48 hrs)

21
Q

What is the management of acute AF onset less than 48 hours and is haemo stable?

A

Rate or rhythm control.
Rhythm control is done either via immediate DC (electrical) cardioversion or pharmacological cardioversion.
Chemical cardioversion is done by the anti arrhythmics: fleicanide if no structural heart disease or amiodarone if has disease.

If the DC cardioversion is delayed, heparin is needed to anti coagulate the pt.

22
Q

What is the management of acute AF onset more than 48 hours/unclear time and is haemo stable? Why?

A

Only rate control - this is bc they are at a higher risk of thromboembolism (tf stroke). This is bc the blood has been pooling for a while so clots are likely, and as soon as AF -> sinus rhythm there is a very high risk of embolism (clot being pushed out of atrium).
So cardioversion/rhythm control can be done but 3 weeks anticoagulation prior.

23
Q

What is rhythm control in chronic AF, what are the indications + treatments?

A

The aim is to bring back sinus rhythm.
It is done by either electrical cardioversion or pharmacological (amiodarone, fleicanide, sotalol)
Indications = AF secondary to reversible cause, HF thought to be caused by AF, Acute AF less than 48 hrs

If acute AF onset was more than 48 hours, elective/scheduled cardioversion can be done but requires prior 3 weeks anticoagulate and 4 weeks after.

24
Q

What is rate control in chronic AF + treatments?

A

The aim of rate control is to reduce a pt’s heart rate in order to reduce symptoms.
First line in most patients.
1st line med = beta blocker (bisoprolol) or rate limiting calcium channel blocker (diltiazem)
2nd line med = if one doesn’t work, dual therapy used of BB, diltiazem or digoxin
Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary.

25
Q

What is catheter ablation for AF?

A

This is done for pts who haven’t responded to or wish to avoid anti-arrhythmic meds
- Percutaneous access via groin
- the arrhythmogenic foci are identified and the tissue is ablated (scarred) arrhythmogenic focus (e.g. between pulm veins and left atrium)
- Can use radiofrequency & cryotherapy to ablate tissue
- !!! Anticoagulate 4wks before & during procedure as it does not reduce stroke risk

There is a high risk of recurrence (50% still have recurrent AF).

26
Q

How is stroke management done in AF?

A

Stroke risk needs to be reduced in AF due to their incr risk.
CHA2DS2-VASc Score is used to assess stroke risk in AF pts
If 1 = male is consider anticoagua and female is no treatment, 2 = offer anticoag

27
Q

How is bleeding management done in AF?

A

Pts with AF should undergo a risk assessment for major bleeding if given anticoagulation using the ORBIT score (as bleeding risk incr with anticoag). Due to this, we need to weigh up risk of stroke and risk of bleeding to make the decision of anticoag

0-2 = low risk, 3 = medium, 4-7 high risk

28
Q

What are the anticoag options for AF?

A

1st line = Direct oral anticoagulants (DOACs) - apixaban, rivaroxaban, edoxaban & dabigatran (doesn’t require monitoring)
2nd line = warfarin (it is initially pro-thrombotic, so LMWH given 5 days initially). Done for DOAC CI or if not tolerated. Requires INR monitoring

Aspirin is not recommended for reducing stroke risk in patients with AF.

29
Q

Describe medications used for rhythm control in AF?

A

Flecainide - preferred in young patients with structurally normal hearts bc can induce fatal arrhythmias if has structural heart disease.
Amiodarone - controls both rate and rhythm but lot of side-effects so normally only given to older, sedentary patients.
Sotalol - beta blocker with K channel blocker action. 3rd line if above not appropriate for pt

30
Q

What are the meds for rate control in AF?

A

Beta-blockers - commonest in AF is bisoprolol, CI in COPD/Asthma/hypotension. SOTALOL CANNOT be used for rate control bc it has rhythm control action
Non-dihydropyridine calcium channel blockers - diltiazem or verapamil, CI in heart failure
Digoxin - used if hypotension or heart failure, avoided in young pts bc incr risk of cardiac mortality.

31
Q

Meds given to asthmatic/COPD pts with AF?

A

non-hydropiridine calcium channel blocker e.g. diltiazem or verapamil for rate control
This is BB is CI in these pts

32
Q

Meds given to HF pts with AF?

A

1st line is Beta blocker
2nd line is BB and/or digoxin

33
Q

What are the complications of AF

A

HF
Systemic emboli -> ischemic stroke, mesenteric or acute limb ischemia
Bleeding - GI or intracranial (due to anti coag meds)