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Atrial fibrillation Flashcards

1
Q

What is the prevalence of AF in the age groups 70-75 and 80-85?

A

70-75: 5%

80-85: 10%

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2
Q

What are 3 problems to tackle in AF, from most to least important?

A
  1. Reducing increased risk of stroke
  2. Inefficient cardiac function
  3. Symptomatic palpitations
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3
Q

What are 4 types of atrial fibrillation classification?

A
  1. First detected episode
  2. Paroxysmal
  3. Persistent
  4. Permanent
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4
Q

What is paroxysmal AF?

A

Recurrent AF i.e. 2 or more episodes, but episodes terminate spontaneously

Episodes last less than 7 days, typically <24 hours

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5
Q

What is persistent AF?

A

2 or more episodes of AF that are not self-terminating

Usually episodes last greater than 7 days

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6
Q

What is permanent AF?

A

Continuous AF which cannot be cardioverted or if attempts to do so are deemed inappropriate

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7
Q

What are the 2 treatment goals in permanent AF?

A

Rate control and anticoagulation if appropriate

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8
Q

What are 4 symptoms and signs of AF?

A
  1. Palpitations
  2. Dyspnoea
  3. Chest pain
  4. Irregularly irregular pulse
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9
Q

What is the key investigation to diagnose atrial fibrillation?

A

ECG - will help distinguish from ventricular ectopics or sinus arrhythmia

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10
Q

What are the 2 elements of management of patients with atrial fibrillation?

A
  1. Rate/ rhythm control
  2. Reducing stroke risk
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11
Q

What are the 2 main strategies that can be employed in dealing with the arrhythmia element of AF? What are the aims of each?

A
  1. Rate control: accept pace will be irregular but slow rate down to avoid negative effects on cardiac function
  2. Rhythm control: try to get patient back into, and maintain, normal sinus rhythm - this is termed cardioversion. Drugs (pharmacological cardioversion) and synchornised DC electrical shocks (electrical cardioversion) may be used
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12
Q

What are the 2 types of cardioversion (used for rhythm control of AF)?

A
  1. Drugs - pharmacological cardioversion
  2. DC electrical shocks - electrical cardioversion
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13
Q

What type of control are most patients with AF managed with?

A

Rate control - rather than trying to maintain sinus rhythm

(except in certain situations - coexistent heart failure, first onset AF or obvious reversible cause)

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14
Q

What is the RATE treatment approach for AF?

A

Beta blocker or rate limiting CCB e.g. diltiazem used first line. If one drug doesn’t control, combo therapy with any 2 of:

  1. Betablocker
  2. Rate limiting calcium channel blocker e.g diltazem
  3. Digoxin

If doesn’t work/ pt doesn’t want medication - CATHETER ABLATE

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15
Q

What is the key risk of rhythm control in AF?

A

The moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke

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16
Q

Of what 2 condtions must ONE be met prior to attempting cardioversion (i.e. rhythm control) in AF?

A
  1. Short duration of symptoms <48hrs
  2. Anticoagulated for a period of time prior
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17
Q

What stratifying tool can be used to determine the most appropriate anticoagulation strategy in AF?

A

CHA2DS2-VASc

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18
Q

What does the CHA2DS2VASc score comprise of?

A
  • C: congestive heart failure 1
  • H: hypertension (or treated hypertension) 1
  • A2: age >= 75: 2 65-74: 1
  • D: diabetes 1
  • S2: prior stroke or TIA 2
  • V: vascular disease (IHD and peripheral arterial disease) 1
  • S: sex category (female) 1
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19
Q

What is the suggested anticoagulation strategy in AF based on the CHADSVASc score?

A
  • 0: no treatment
  • 1: males: consider anticoagulation
    • females: no treatment (because this score is only due to gender)
  • 2 or more: offer anticoagulation
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20
Q

Why is digoxin usually not considered first line as rate control for AF any more and when IS digoxin the preferred choice?

A

Less effective at controlling heart rate during exercise

Preferred choice if coexistent heart failure

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21
Q

What are 3 drugs which are commonly used to maintain sinus rhythm with a history of atrial fibrillation?

A
  1. Sotalol
  2. Amiodarone
  3. Flecainide
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22
Q

What are 2 factors that favour rate control over rhythm control?

A
  1. Older than 65 years
  2. history of ischaemic heart disease
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23
Q

What are 5 factors that favour rhythm control over rate control in AF?

A
  1. Younger than 65 years
  2. Symptomatic
  3. First presentation
  4. Lone AF or AF secondary to a corrected precipitant e.g. alcohol
  5. Congestive heart failure
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24
Q

When is catheter ablation recommended in AF for rate control?

A

recommended for those who have not responded, or whish to avoid, antiarrhythmic medication for rate control

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25
Q

What is the aim of catheter ablation and how is it achieved?

A

Aim is to ablate the faulty electrical pathways that are resulting in AF - typically due to aberrant electrical activity between pulmonary veins and left atrium

Performed percutaneously, typically via groin

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26
Q

Where does the pathway causing AF usually exist in the heart?

A

Typically aberrant electrical activity between the pulmonary veins and left atrium

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27
Q

What are 2 things that can be used to ablate tissue in catheter ablation for AF?

A
  1. Radiofrequency - heat generated from medium frequency alternating current
  2. Cryotherapy
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28
Q

What must be performed prior to catheter ablation for AF and for how long?

A

Anticoagulation - 4 weeks

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29
Q

When should anticoagulation be used for catheter ablation in AF?

A

4 weeks prior AND during; ablation controls rhythm but not stroke risk, even if patients remain in sinus rhythm so still require anticoagulation as per CHADSVASc

30
Q

How long should anticoagulation be given following catheter ablation in AF?

A

CHADSVASc

If score 0: 2 months anticoagulation

If score >1: longterm anticoagulation recommended

31
Q

What are 3 notable complications of catheter ablation in AF?

A
  1. Cardiac tamponade
  2. Stroke
  3. Pulmonary valve stenosis
32
Q

What is the success rate of catheter ablation to treat AF?

A
  • around 50% of patients have early recurrence within 3 months, often resolves spontaneously
  • longer term, after 3 years, 55% who have had a single procedure remain in sinus rhythm.
  • of patients who’ve undergone multiple procedures, around 80% are in sinus rhythm
33
Q

What are the 2 broad scenarios when cardioversion may be used in atrial fibrillation?

A
  1. Electrical cardioversion as an emergency if patient is haemodynamically unstable
  2. Electrical or pharmacological cardioversion as an elective procedure where a rhythm control strategy is preferred
34
Q

How should TIME FRAME determine whether to offer a patient rate or rhythm control?

A
  • if onset definitely <48 hours: rate OR rhythm control
  • if onset >48 hours or uncertain: rate control
35
Q

What are the steps to take if a patient has AF that has definitely started within the past 48 hours?

A
  • Patient should be heparinised
  • Lifelong oral anticoagulation if risk factors for ischaemic stroke
  • Otherwise: electrical or pharmacological cardioversion
36
Q

What is the pharmacological form of cardioversion?

A

Amiodarone if structural heart disease, flecainide or amiodarone in those without structural heart disease

37
Q

If AF onset is <48h should you anticoagulate following electrical cardioversion?

A

No, further anticoagulation is unnecessary

38
Q

If you are going to cardiovert someone with AF onset >48h what must be done before? Give the 2 options

A

Give anticoagulation for at least 3 weeks prior

OR

perform transoeseophageal echo (TOE) to exclude a left atrial appendage (LAA) thrombus. If excluded, patients may be heparinised and cardioverted immediately

39
Q

If you decide to cardiovert in AF >48h onset, should you choose pharmacological or electrical cardioversion?

A

Electrical

40
Q

What are 2 factors that pose a high risk of cardioversion failure?

A

Previous failure or AF recurrence

41
Q

What is recommended prior to electrical cardioversion if there’s a high risk of cardioversion failure, in AF >48h onset?

A

At least 4 weeks of amiodarone or sotalol prior to electrical cardioversion

42
Q

If AF onset is >48h should anticoagulation follow electrical cardioversion?

A

yes for at least 4 weeks; after this, further anticoagulation decisions should be on an individual basis depending on risk of recurrence

43
Q

When is the only time flecainide can be used for atrial fibrillation cardioversion?

A

if no structural heart disease

44
Q

What are 5 drugs that can also be used for pharmacological cardioversion in the UK that are less effective than amiodarone and flecainide?

A
  1. Beta blockers including sotalol
  2. Calcium channel blockers
  3. Digoxin
  4. Disopyramide
  5. Procainamide
45
Q

What are the 2 scoring systems used to guide anticoagulation in AF?

A
  1. CHADSVASc: score can be used to determine anticoagulation strategy
  2. HASBLED to determine risk of bleeds
46
Q

What does the HASBLED score comprise of?

A
  • H: Hypertension, uncontrolled, systolic BP>160) 1
  • A: Abnormal Liver function (cirrhosis, bilirubin>2x normal, ALT/AST/ALP >3x normal) and renal (dialysis or creatinine >200) 1 for liver 1 for renal
  • S: Stroke - hisory of 1
  • B: Bleeding - history of bleeding or tendency to bleed 1
  • L: Labile INR (unstable/high, time in therapeutic range <60%) 1
  • E: Ederly (>65) 1
  • D: Drugs predisposing to bleeding - antiplatelet agents, NSAIDs or Alcohol Use (>8 drinks/week) 1 for drugs 1 for alcohol
47
Q

What should be done if CHADSVASc suggests no need for anticoagulation? Why?

A

Important to ensure transthoracic echocardiogram to exclude valvular heart disease, which in combo with AF is an absolute indiction for anticoagulation

48
Q

What are the options for anticoagulants to reduce risk of stroke in AF?

A

Warfarin or DOACs (dabigatran, apixaban, rivaroxaban, edoxaban)

Discuss advantages and disadvantages of each with patient

49
Q

What are 4 things that might steer us away from using warfarin as an anticoagulant in AF?

A
  1. Falls
  2. Old age
  3. Alcohol excess
  4. History of previous bleeding
50
Q

How does HASBLED inform decisions in AF?

A

No formal rules but score of 3 ormore indicates high risk of bleeding, defined as intracranial haemorrhage, hospitalisation, haemoglobin decrease >2g/L, and/or transfusion

51
Q

What are 4 possible outcomes due to the high risk of bleeding indicated by a HASBLED score of 3 or more?

A
  1. intracranial haemorrhage
  2. hospitalisation
  3. haemoglobin decrease >2g/L
  4. transfusion
52
Q

What should be the management of stroke or TIA in a patient with AF? 3 options

A
  • Warfarin or a direct thrombin or factor Xa inhibitor should be given as the anticoagulant of choice
  • Antiplatelets should only be given if needed for the treatment of other comorbidities
  • In acute stroke patients, in absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks
    • if imaging shows very large cerebral infarction then initiation of anticoagulation should be delayed
53
Q

After how long should anticoagulation therapy be commenced in acute stroke patients (in absence of haemorrhage)?

A

after 2 weeks

54
Q

What should be done if a patient is on an anticoagulant for AF and an antiplatelet for established CVD?

A

Anticoagulant monotherapy should be given without addition of antiplatelets if secondary prevention of stable cardiovascular disease

55
Q

Should be done if a patient is on an anticoagulant for AF then develops acute coronary syndrome/ undergoes PCI?

A

Stronger indication for antiplatlet therapy than CVD; generally triple therapy for 4 weeks - 6 months (2 antiplatelets + 1 anticoagulant) and dual therapy (1 platelet + 1 anticoagulant) to complete 12 months. Variation from patient to patient

56
Q

What is the advice regarding antiplatelet and anticoagulant therapy in the case of VTE?

A

If patient on antiplatelets (e.g. for CVD) develops VTE they’re likely to be prescribed anticoagulants for 3-6 months. HASBLED should be calculated, if low risk may continue antiplatelets. If intermediate-high, consider stopping antiplatelets to give the anticoagulants for VTE

57
Q

What class of drug is digoxin?

A

Cardiac glycoside with positive inotropic properties

58
Q

What is the mechanism of action of digoxin to treat AF with concurrent heart failure (not great for active patients)?

A
  • decreases conduction through the AV node which slows ventricular rate in AF and flutter
  • Increases force of cardiac muscle contraction due to inhibition of Na+/K+/ATPase pump. Also stimulates vagus nerve
59
Q

Is digoxin monitored routinely?

A

No - except in suspected toxicity (has narrow therapeutic index)

60
Q

How should digoxin be measured in suspected toxicity?

A

Measure concentration within 8-12 hours of the last dose

61
Q

What determines whether a patient has developed digoxin toxicity?

A

Plasma concentration alone doesn’t determine whether patient has it; may occur even when concentration is within therapeutic range.

BNF advises likelihood of toxicity increases progresively from 1.5 to 3 mcg/l

62
Q

What are 8 features of digoxin toxicity?

A
  1. Generally unwell
  2. Lethargy
  3. Nausea and vomiting
  4. Anorexia
  5. Confusion
  6. Yellow-green vision
  7. Arrhythmias e.g. aV block, bradycardia
  8. Gynaecomastia
63
Q

What is the classical precipitating factor of digoxin toxicity? What is the mechanism of this?

A

hypokalaemia: digoxin normally binds to ATPase pump on same site as potassium. Digoxin therefore binds more easily if low potassium, increases inhibitory effects on heart etc.

64
Q

What are 9 factors that can precipitate digoxin toxicity?

A
  1. hypokalaemia
  2. increasing age
  3. renal failure
  4. myocardial ischaemia
  5. hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
  6. hypoalbuminaemia
  7. hypothermia
  8. hypothyroidism
  9. drugs: amioarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduced excretion), ciclosporin. also drugs which cause hypokalaemia e.g. thiazides and loop diuretics
65
Q

What are 3 elements of the management of digoxin toxicity?

A
  1. Digibind
  2. Correct arrhythmias
  3. Monitor potassium
66
Q

What are 8 indications for the use of beta blockers?

A
  1. Angina
  2. Post-myocardial infarction
  3. Heart failure: for symptoms and mortality
  4. Arrhythmias: AF
  5. HTN - role diminished in recent years
  6. Thyrotoxicosis
  7. Migraine prophylaxis
  8. Anxiety
67
Q

What are 5 side effects of beta blockers?

A
  1. Bronchospasm
  2. Cold peripheries
  3. Fatigue
  4. Sleep disturbances, including nightmares
  5. Erectile dysfunction
68
Q

What are 4 contraindications for beta blockers?

A
  1. Uncontrolled heart failure
  2. Asthma
  3. Sick sinus syndrome
  4. Concurrent verapamil use: may precipitate severe bradycardia
69
Q

What is the mechanism of action of flecainide?

A

Vaughan Wiliams class 1c antiarrhythmic; slows conduction of action potential by acting as potent sodium channel blocker; widens QRS complex and prolongs PR interval

70
Q

What are 2 indications of flecainide?

A
  1. Atrial fibrillation
  2. SVT associated with accessory apthway e.g. Wolff-Parkinson-White syndrome
71
Q

What are 4 contraindications for flecainide?

A
  1. Post myocardial infarction
  2. Structural heart disease e.g. heart failure
  3. Sinus node dysfunction; second degree or greater AV block
  4. Atrial flutter
72
Q

What are 5 adverse effects of flecainide?

A
  1. Negatively inotropic
  2. Bradycardia
  3. Proarrhythmic
  4. Oral paraesthesia
  5. Visual disturbaneces

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