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CPTP 4.24-26 > CPTP 4.24-26 > Flashcards

CPTP 4.24-26 Flashcards

1
Q

usual cause of AF in young

A

structural problem - valvular, heart muscle abnormality, cardiomyopathy, pericarditis

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2
Q

non cardiac causes of AF

A

acute infections (pneumonia), electrolyte depletion, lung cancer, intrathoracic pathology (e.g. pleural effusion), PE, thyrotoxicosis

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3
Q

Valvular abnormality that predisposes to AF

A

mitral stenosis - get left atrial dilation which predisposes to AF

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4
Q

4 types of AF

A

acute, paroxysmal, persistent, permanent

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5
Q

what is paroxysmal AF

A

2 or more episodes less than 48h duration.

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6
Q

what is persistent AF

A

longer than 7 days - but can be terminated with tx

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7
Q

mx of patient in AF who’s CV status is unstable

A

electrical cardioversion - synchronised DC shock.

remember heparin for thromboprophylaxis

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8
Q

is an alcoholic with cardiomyopathy and AF likely to be successfully treated with cardioversion?

A

no

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9
Q

is patient with mitral stenosis and dilated LA likely to be successfully treated with cardioversion?

A

no

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10
Q

if electrocardioversion is planned what must happen prior to this

A

anticoagulated 6w before cardioversion

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11
Q

who is suitable for rhythm control

A

AF with reversible cause
heart failure caused by AF
new onset AF
atrial flutter (suitable for ablation strategy)

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12
Q

initial monotherapy to AF patients who need rate control

A

beta blocker or rate limiting CCB

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13
Q

when is digoxin monotherapy considered

A

non paroxysmal AF patients that are sedentary

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14
Q

what should not be offered for LT rate control

A

amiodarone

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15
Q

if rate control monotherapy does not control sx?

A

consider rhythm control if eligible. if not but sx not controlled combination therapy with 2 of: a beta blocker, diltiazem, digoxin

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16
Q

what is diltiazem

A

rate limiting CCB

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17
Q

beta blockers is first line for rate control, but who is prescribed CCBs instead

A

asthmatics, COPD, PVD, tachy-brady syndrome

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18
Q

which beta blockers used

A

any except sotolol. cardioselective preferable

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19
Q

why not sotolol

A

increased risk of sudden death in IHD patients (QT prolongation)

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20
Q

chronic adverse effect of beta blockers

A

fatigue

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21
Q

are amlodipine and nifedipine good drugs in AF

A

no. CCBs must be non-dihydropyridine. diltiazem or verapamil (l type calcium channel inhibition)

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22
Q

verapamil side effect

A

constipation

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23
Q

what can precipitate digoxin toxicity

A

AKI

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24
Q

for which other patients would you also consider rhythm control

A

symptomatic patients (sob, lethargic, palpitations) or if have idea of LT anticoagulation

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25
Q

Tx of persistent AF >48h and already on anticoagulants

A

electrical cardioversion (consider amiodarone pre and post)

26
Q

tx of persistent AF >48h and not on anticoagulants

A

consider TOE guided cardioversion or anticoag for 3w before cardioversion

27
Q

common tx for paroxysmal AF

A

pill in the pocket

28
Q

in addition to beta blocker what drugs considered in paroxysmal AF patients with heart failure or left ventricular impairment

A

amiodarone

29
Q

what should you not offer patients with known ischaemic or structural heart disease (paroxysmal AF)

A

1c antiarrthythmic drugs such as flecanide or propafenone

30
Q

amiodarone administration

A

long line or central line as toxic to veins

31
Q

do you attempt to correct rhythm in new AF patient

A

yes

32
Q

name a class III agent

A

amiodarone

33
Q

name class Ic agent

A

flecanide, propafenone

34
Q

efficacy of class III vs class Ic agents

A

Ic more effective than amiodarone if given early (within 12h onset). by 24h no difference

35
Q

acute adverse effects of class III and Ic agents

A

heart failure and hypotension

36
Q

adverse effects of Ics in structural HD

A

increase risk of fatal (ventricular) arrhythmias

37
Q

when is amiodarone given in patient who has been electo-cardioverted

A

6w before and up to a year after

38
Q

chronic adverse effects of amiodarone

A

photosensitivity (solar urticarial rash), thyroid dysfunction, pulmonary fibrosis

39
Q

AF complications

A

rate related cardiomyopathy, pulmonary oedema, shock, stroke

40
Q

who are low risk CHADVASC patients

A

men with score of 0 women with score of 1

41
Q

recommended antithrombotic therapy if chadvasc 0

A

either aspirin or none. none preferred

42
Q

recommended antithrombotic therapy if chadvasc 1

A

OAC or aspirin. OAC preferred

43
Q

recommended antithrombotic therapy if chadvasc 2 or more

A

OAC

44
Q

which antithrombin therapies have lower risk IC haemorrhage

A

NOACs

45
Q

what induces warfarin metabolism

A

st johns wort, sulphonylureas, carbamazepine, rifampicin, chronic alcohol, phenytoin

46
Q

catastrophic scenario of warfarin patient who comes into hospital with pneumonia

A

given erythromycin, catastrophic bleed as inhibits metabolism

47
Q

what inhibits warfarin metabolism

A

sodium valproate/SSRIs, isoniazid, cimetidine, ketoconazole, fluconazole, amiodarone/acute alcohol, chloramphenicol, erythromycin, ciprofloxacin, omeprazole, metronidazole

48
Q

what drugs used in AF thrombosis prophylaxis

A

warfarin or NOACs

49
Q

what used in patients who cant take anticoag med

A

considered for left atrial appendage occlusion

50
Q

what anticoag drugs cant be taken in renal failure

A

NOACs

51
Q

what are NOACs

A

factor X inhibitors (apixaban etc), or DTIs (dabigatran)

52
Q

problem with apixaban

A

no reversing agent

53
Q

why is pharmacology of NOACs more reliable than warfarin

A

act further down clotting cascade

54
Q

AF mx <48h

A

rate or rhythm control

55
Q

AF mx >48h

A

rate control

56
Q

LT side effects of amiodarone (EXAM Q)

A

Photosensitivity, hepatotoxicity, pulmonary fibrosis, thyroid dysfunction

57
Q

acute side effects of amiodarone worried about

A

hypotension

58
Q

are patients with structural heart defects suitable for electrical cardioversion

A

no

59
Q

INR target in AF

A

between 2-3

60
Q

tx for INR >6, stable, minor bleeding

A

vitamin k

CPTP 4.24-26 (1 decks)

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