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GPEP cardio > AF > Flashcards

AF Flashcards

1
Q

Why is AF important? What does it cause?

A

Irregular cardiac rhythm associated with AF decreases the heart’s ability to efficiently pump blood and promotes clot formation

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2
Q

People with AF have a higher risk of what?

A

Stroke
HF
MI
Dementia
Mortality

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3
Q

Does successful treatment reverse the risks associated with AF?

A

Successful treatment doesn’t completely reverse the increased risks associated with AF

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4
Q

Typical presentation (symptoms) of patients with AF

A

Often asymptomatic
If symptomatic symptoms can vary (palpitations, dizziness, SOB esp on exertion, angina, fatigue)

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5
Q

Who should you opportunistically screen for AF by feeling radial pulse?

A

≥ 65 yo (or younger if Maori/Pacific, previous TIA, HTN)

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6
Q

If AF is suspected on pulse what should you do?

A

Confirm with ECG

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7
Q

AF features on ECG

A

Irregularly irregular RR interval
No discernible distinct P waves

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8
Q

When might you request a Holter monitor for suspected AF?

A

If patient reports intermittent palpitations (i.e. paroxysmal AF suspected)

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9
Q

Role of smart watches in detecting AF

A

Positive predictive values for AF 84 – 98% → clinically significant but does not replace need for clinical assessment (pulse, ECG, holter if needed)

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10
Q

Underlying causes of AF include…

A

Infection
Dehydration
Surgery – cardiac or other major surgery
Cardiac (MI, hypertensive or valvular heart disease, cardiomyopathy, inherited conditions)
Respiratory, e.g. acute exacerbation of COPD, OSA, PE, pneumonia
Excessive alcohol intake
Thyrotoxicosis
Obesity

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11
Q

Bloods to order in work up for AF

A

CBC, UEC
LFTs and TFTs if not recently done
INR and APTT if starting oral anticoagulants

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12
Q

Investigations to request once AF confirmed on ECG

A

Echo

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13
Q

Classification of AF includes…

A

First diagnosed
Paroxysmal
Persistent
Long-standing persistent
Permanent

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14
Q

Definition of first diagnosed AF

A

AF not been diagnosed before, irrespective of sx presence/severity

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15
Q

Definition of paroxysmal AF

A

AF that resolves spontaneously or is cardioverted within 7 days

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16
Q

Definition of persistent AF

A

Continuous AF for >7 days that has not resolved spontaneously
Includes episodes that are cardioverted ≥7 days

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17
Q

Definition of long-standing persistent AF

A

AF has lasted continuously for ≥1 year and attempts to restore or maintain sinus rhythm are still being considered or attempted

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18
Q

Definition permanent AF

A

AF present for ≥1 year and cardioversion has been unsuccessful or not attempted

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19
Q

Who to refer to acutely to secondary care when presenting with AF

A

Onset AF definitely <12hrs
Haemodynamically unstable (hypotension, peripheral cyanosis, ongoing chest pain)

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20
Q

How do you determine decisions around anticoagulation with AF

A

Assess CHA2DS2-VASc score (stroke risk) and HAS-BLED score (bleeding risk)

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21
Q

Stroke risk between different types of AF

A

Stroke risk same regardless of underlying pattern & whether symptomatic or not

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22
Q

Consider anticoagulation if CHA2DS2-VASc is…

A

≥ 2 in females
≥ 1 in males

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23
Q

What CHA2DS2-VASc score indicates low risk of stroke (<1:100 per year) and therefore anticoagulation not generally considered

A

1 females
0 males

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24
Q

For patients with low stroke risk (low CHA2DS2-VASc scores) should you consider antiplatelets?

A

Antiplatelet not recommended as an alternative to anticoagulation

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25
Q

Need for anticoag primarily based on CHA2DS2-VASc or HAS-BLED?

A

CHA2DS2-VASc

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26
Q

What is HAS-BLED useful for?

A

Balance benefits and risks of anticoag e.g. high HAS-BLED, low CHA2DS2-VASC (≤ 2) risk may outweigh benefits
Identify factors to reduce bleeding risk (e.g. uncontrolled HTN, NSAID use, alcohol excess)
Identify pts at higher risk who could benefit from more frequent f/up

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27
Q

Are there specific cut offs with HAS-BLED score for not starting anticoag?

A

No
Consequences of stroke usually more severe than consequences of bleed

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28
Q

What is first line treatment for stroke prevention in patients with AF

A

Oral anticoagulants - warfarin, dabigatran or rivaroxaban

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29
Q

Absolute contraindications for oral anticoagulation

A

Active serious bleeding
Bleeding-associated co-morbidities, e.g. severe thrombocytopenia (< 50 platelets/microlitre) or severe anaemia
History of recent high-risk bleeding event, e.g. intracranial haemorrhage

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30
Q

Why are DOACs preferred over warfarin?

A

Superior for reducing stroke risk and all-cause mortality
Reduce risk of intracranial bleeding
Comparable risk of major bleeding
No INR monitoring required
Fewer medicine and food interactions
More rapid onset of action

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31
Q

Pros/cons of dabigatran and rivaroxaban

A

Dabigatran twice daily dosing, rivaroxaban once daily
Rivaroxaban can use to CrCl 15, dabigatran to CrCl 30

32
Q

Dosing of dabigatran

A

150mg BD if CrCl >50
110mg BD if ≥ 80yo, 75-80yo with low clot risk and high bleeding risk, CrCl 30-49

33
Q

Dosing of rivaroxaban

A

20mg once daily if CrCl >50
15mg once daily if CrCl 15-49

34
Q

When to consider warfarin?

A

DOACs C/I
Significant hx of GI disease
Comorbid antiphospholipid syndrome (rare)
Patients who develop thrombosis while taking a DOAC

35
Q

Contraindications for DOACs

A

Mechanical heart valve or insufficient evidence to support their use (e.g. mod-severe mitral stenosis, severe liver or renal dysfunction)

36
Q

Anticoagulation in pregnancy

A

Refer O&G
Enoxaparin usually safest (doesn’t cross placenta or cause fetal anticoagulation)

37
Q

Can you use antiplatelets for stroke prevention in AF

A

Long term antiplatelet use alone not recommended in patients with AF

38
Q

Anticoags + antiplatelets in AF

A

After ACS or coronary stent patients can be on clopidogrel as well
DAPT + anticoag not recommended

39
Q

Should you stop anticoags if concerns re age or falls risk in a patient with high stroke risk?

A

No - Benefits usually outweigh risk of complications

40
Q

Should you stop anticoag if a patient reverts to sinus rhythm or is asymptomatic?

41
Q

Stopping anticoag should be based on…

A

Stroke and bleeding risk (CHA2DS2-VASc and HAS-BLED scores)

42
Q

What is rate control

A

Aims to improve sx by reducing HR

43
Q

What is rhythm control

A

Attempts to restore sinus rhythm either by electrical cardioversion or pharmacological cardioversion with antiarrhythmic medicines

44
Q

What is more effective - rate or rhythm control?

A

RCT suggests both strategies have similar effect on QoL and clinical outcomes (incl mortality)

45
Q

Should you start rate or rhythm control in primary care?

A

Start with rate control (simpler regimes, fewer S/E)

46
Q

Rhythm control may be started first with cardio advice in certain patients including…

A

Younger, esp if very physically active and no co-morbidities
High initial symptom burden
Symptomatic paroxysmal attacks
Clear trigger or reversible cause for AF e.g. recent cardiac surgery, acute illness, binge drinking
HF primarily caused or exacerbated by AF

47
Q

What reduces probability of successful rhythm control

A

Longer duration of persistent AF

48
Q

1st line rate control

A

BB, rate limiting CCB (e.g. diltiazem, verapamil)

49
Q

Can you use sotalol as rate control?

A

Not recommended - potential to cause arrhythmias

50
Q

How do you choose between BB and CCB for rate control?

A

Based on echo results (LVEF)

51
Q

If no echo then it is safest to start
___________ for rate control

A

Beta blocker
Verapamil and diltiazem not recommended if LVEF <40% or HFrEF due to negative inotropic effects

52
Q

Why is diltiazem not usually used as monotherapy

A

Potential for medicine interactions
Lack of effect on HR during physical activity
Narrow therapeutic index

53
Q

First line monotherapy for rate control if LVEF ≥ 40%

A

Beta blocker - bisoprolol, metoprolol succinate, carvedilol
Rate limiting CCB - verapamil, diltiazem
Digoxin

54
Q

Dose of bisoprolol for rate control

A

1.25 – 20 mg, once daily
(usual range 2.5 mg – 10 mg)

55
Q

Dose of metoprolol for rate control

A

23.75 – 190 mg, once daily

56
Q

Dose of carvedilol for rate control

A

3.125-50 mg BD

57
Q

Dose of diltiazem for rate control

A

60 mg TDS, increased to 360 mg max total daily dose in divided doses (IR form)

or

120 – 360 mg, once daily (MR form)

58
Q

Dose of verapamil for rate control

A

40-120 mg TDS (IR form)

or

120-240 mg, once daily, increased to 240 mg BD if necessary (MR form)

59
Q

Dose of digoxin for rate control

A

0.75-1.5 mg, over 24 hours in divided doses (loading dose) then 0.0625-0.25 mg, once daily (maintenance dose)

60
Q

Combination treatment for rate control with BB and CCB for LVEF ≥ 40%

A

Add digoxin to either the BB or rate-limiting CCB
Combine a BB with diltiazem (i.e. without digoxin)

61
Q

Do not use ___________ with a BB due to the risk of hypotension and systole as a result of the potentially additive negative inotropic effects.

62
Q

First line rate control if signs of CHF and LVEF < 40%

A

BB (1st line)
Digoxin

63
Q

Combination treatment for rate control with BB and digoxin when signs of CHF and LVEF < 40%

A

BB - add digoxin
Digoxin - add BB at lowest possible dose for acute HR control

64
Q

Treatment targets - HR

A

Most patients aim resting HR <110
More intensive if ongoing symptoms or LV dysfunction e.g. HR 80-90

65
Q

How to titrate medication for rate control

A

Start low dose and f/up 1-2 weeks for titration
Consider combination treatment if HR target not achieved with optimal monotherapy

66
Q

What should you do if sustained increase in HR despite previous adequate control

A

Assess for temporary/modifiable causes before increasing treatment e.g. post-op stress, changes in alcohol consumption.
Consider ECG ?atrial flutter (may require different Rx approach)

67
Q

Options for pharmacological cardioversion for rhythm

A

Amiodarone
Flecainide
Sotalol

68
Q

What should you do if pharmacological cardioversion fails

A

Refer for consideration of electrical cardioversion, catheter or surgical ablation

69
Q

Antiarrhythmic meds usually continued for _________ post ablation to limit recurrence

A

≥ 3 months

70
Q

Modifiable risk factors for AF

A

HTN
Obesity
Sedentary lifestyle
Diabetes
OSA
Alcohol
Smoking

71
Q

Is caffeine a risk factor for AF

A

No evidence that caffeine is a significant risk factor for AF (but can trial reduction if triggers/worsens sx)

72
Q

Is vigorous exercise a risk factor for AF

A

Increasing evidence of an association between prolonged vigorous exercise (e.g. endurance exercise) and increased AF risk. Risk highest in middle age

73
Q

F/up if patient is on a DOAC

A

UEC every 6 – 12 months if normal at baseline; more frequent if baseline CrCl is reduced.
Baseline liver dysfunction may also need regular LFTs (can influence DOAC clearance → increasing the degree and/or duration of anticoagulation

74
Q

When to refer to cardiology

A

Ongoing sx and poorly controlled HR e.g. >110 despite appropriate pharmacological Rx
Recurrence of AF after cardioversion
Paroxysmal AF with ongoing sx (for consideration of ablation or other advanced Rx)
An elevated stroke risk but long-term oral anticoagulation is contraindicated
Symptomatic bradycardia with no improvement after reducing or withdrawing rate control
Other signs of deteriorating cardiac health, e.g. HF, esp if reduced LVEF on echo

GPEP cardio (3 decks)

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