Atrial fibrillation Flashcards

1
Q

Atrial fibrillation

definition

range of bpm

what rhythm of heatrtbeat and why

A

Uncoordinated atrial contraction, typically at approx. 300-600 bpm

Delay at the AVN means that only some of the atrial pulses are conducted to the ventricles, resulting in an irregularly irregular heartbeat

Multiple wavelets with a chaotic reentry within the atria causes bombardment of the ventricles.

The most common sustained cardiac arrhythmia.

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2
Q

pathophysiology of atrial fibrillation

A
  • Atrial dilatation, volume overload or fibrosis
  • Discrepancies in refractory periods (Creation of long conductive and slow conductive pathways)
  • Uncoordinated relaxation/ contraction
  • Partial contraction
  • Numerous depolarisation waves spread out in all directions electrically neutralising what is picked up on ECG- therefore no P waves
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3
Q

Causes of AF:

cardiac

non-cardiac

A

Cardiac

  1. Ischaemic heart disease (most common cause in the uk)
  2. Hypertension
  3. Rheumatic heart disease
  4. Peri/myocarditis

Non-cardiac

  1. Dehydration
  2. Endocrine (hyperthyroidism)
  3. Infective (sepsis
  4. Pulmonary causes (pneumonia or PE)
  5. Environmental toxins (e.g., alcohol abuse)
  6. Electrolyte disturbances (e.g., hypokalaemia)
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4
Q

classifications of AF

A
  1. Acute (<48 hours)
  2. Paroxysmal (<7 days and intermittent)
  3. Persistent (> 7 days but is amenable to cardioversion)
  4. Permanent (>7 days but not amenable to cardioversion)

+ if HR is > 100 this is considered to be fast AF

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5
Q

symptoms of AF

A
  1. Palpitations
  2. Angina
  3. SOB
  4. Dizziness
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6
Q

Signs of AF

A
  1. Irregularly irregular pulse with variable volume pulse
  2. Single waveform on JVP
  3. Apical to radial pulse deficit
  4. On auscultation there may be variable intensity of first heart sound
  5. Features of underlying cause (e.g., hyperthyroidism)
  6. Features of AF complications (e.g., HF)
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7
Q

complications

A
  • Causes turbulent blood flow so increases thrombus formation >>> stroke or MI
  • Incomplete filling of ventricles leads to a decreased cardiac output and can lead to heart failure
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8
Q

diagnosis of AF (3)

A

ECG

Echocardiography

TFTs

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9
Q

diagnosis of AF via ECG

A
  1. Absent P waves
  2. Fibrillatory F waves between QRS complexes (irregular in timing and morphology)
  3. Baseline undulations
  4. Irregularly irregular R-R intervals
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10
Q

basic ECG physiology

  • standard Pr interval
  • QRS duration
  • standard ST interval
  • QT interval
A

Standard PR interval_;_ 0.12 0.20 seconds // 3-5 small squares

QRS duration; 0.08 0.12 secs // 2-3 small squares

Standard ST interval; 0.08 0.12 secs // 2-3 small squares

Q-T interval; 0.35 0.43 secs

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11
Q

principles of investigation and. management- SSSS

A
  1. Stroke risk
  2. Symptom severity
  3. Severity of AF burden
  4. Substrate severity
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12
Q

methods to detect AF

A
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13
Q

History for AF

A
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14
Q

management of AF

A

ABCDE- if unstable then initiate immediate DC cardioversion

Consider reversible causes:

Infection- give antibiotics and fluids

Dehydration- give fluids

Replace abnormal electrolytes

Start to think of rate control, rhythm control or electrical cardioversion

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15
Q

When to offer rate control in AF

A

First line in everyone unless patient:

  • Has a reversible cause to AF
  • Has heart failure thought to be caused primarily by AF
  • Has new-onset AF
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16
Q

how do you manage someone in acute AF who has syncope, shock, heart failure or angina?

A

DC cardiovert them

if this fails use amiodarone

do not delay this to start anticoagulation

17
Q

how do you treat someone who has been in AF <48 hours and is stable?

A

rate or rhythm control (rate go to)

for rhythm, DC cardiovert or give flecainaide (unless ACS). start LMWHeparin

18
Q

how would you treat someone in who has been in AF for >48 hours or unclear time of onset ?

A

rate control (e.g., bisprolol or diltiazem)

if you choose rhythm control they must have been anticoagulated for at least 3 weeks prior

19
Q

What is rate control

A
  1. A rate limiting calcium channel blocker (e.g., dilitiazem or verapamil) as initial monotherapy (better than beta blocker if asymptomatic)
  2. A B-blocker (e.g., bisprolol) (they can’t be used in people with hypotension) OR
  3. Consider digoxin (cardiac glycoside which increases the force of contraction and slows rate) monotherapy for people with paroxysmal AF or heart failure, only if they live a sedentary lifestyle
20
Q

What is rhythm control

A
  1. Chemical cardioversion
    1. Flecainide (preferrable in younger patients// “pill in the pocket”), dofetilide, propafenone, amiodarone (controls both rate and rhythm)
    2. Adenosine for SVT
  2. Electrical DC cardioversion (+sedation)
    1. When patient haemodynamically unstable

Lower rate to at least 120 first and try to anticoagulate (heparinised) them first if they have been in AF for 48 hours+

Shouldn’t be cardioverted if they’ve been in AF for 48hrs+ unless anticoagulated for 3 weeks min

atrial ablation possible in those that have an identifiable cause.

21
Q

What is HAS-BLED

A

Score for assessing risk- balance to anticoagulation

22
Q

what is CHA2DS2-VASc

A
23
Q

management for preventing stroke risk

A

long-term anti-coagulation therapy

  1. NOAC- Novel Oral Anti-Coagulant
    1. -direct thrombin inhibitor (e.g., Dabigatran)
    2. -factor Xa inhibitors (e.g., Rivaroxaban, apixaban, edoxaban)
  2. Vitamin K antagonist
    1. -warfarin (especially valvular AF)
  3. Low molecular weight heparin
24
Q

ECG for Afib

A
25
Q

atrial flutter

A
  • Circus movement also, travelling in a single large wave
  • Rapid rate of atrial contraction at 200 350 bpm
  • Signals reaching the atria are too fast for all of them to be conducted
  • Therefore 2;1/ 3;1 ratio of Pwaves to QRS
  • Sawtooth baseline