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CPTP > AF and anticoagulation > Flashcards

AF and anticoagulation Flashcards

1
Q

AF on ECG

A

irregulary irregular, no P waves, narrow QRS if tachycaridc

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2
Q

PC AF

A

Can be asymptomatic

SOB, palpitations, dizziness/collapse, oedema and fatigue

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3
Q

Causes of AF

A

Cardiac - MS,AS, pre excitation (WPW), HTN, IHD, Heart failure, cardiomyopathy

Non cardiac - thyrotoxicosis, infection, PE, alcohol, caffeine, cocaine, electrolyte abnormalites

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4
Q

Paroxysmal AF

A

Terminates spontaneously or with intervention within 7 days

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5
Q

Permenant AF

A

Refractory to cardioversion

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6
Q

Acute AF

A

<48hrs can present with haemodynamic instability needs immediate cardioversion

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7
Q

Persistant AF

A

Continuously lasting over 7 days

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8
Q

Pathogensis of AF

A

Disorganised atrial foci lead to rapid fibrillation of the atrial compromising filling time. Dilated atria due to HF, valve defects potentiates the problem. The turbulent inefficient blood flow can lead to thrombus formation and haemodynamic instability

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9
Q

Mx Acute AF haemodynamically unstable

A

LMWH to anticoagulate. DC cardioversion

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10
Q

Mx Acute AF haemodynamically stable

A

< 48hrs = rate vs rhythm control

>48hrs = anticoagulant and rate control

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11
Q

Rhythm control acute AF

A

Echo to determine structural heart disease

  • No structural problem = IV flecanide
  • Structural disease = IV amiodarone
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12
Q

Rhythm control for those

A

< 65 y/o
1st episode of AF due to reversible cause
Symptomatic HF

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13
Q

Complications of AF if untreated

A

Rate related cardiomyopathy
Acute HF - pul oedema/shock
Thromboembolic disease - stroke, acute limb ischemia

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14
Q

CHA2DS2VASc

A

Stratification of stroke risk

Congestive HF = 1
HTN = 1
Age > 75 = 2
Diabetes = 1
Stroke/TIA = 2
Vascular disease = 1
Age (64-74) = 1 
Sex (female) = 1
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15
Q

Mx according to CHA2DS2VASc

A

> 2 = DOAC

> 1 = DOAC above aspirin (only treat males)

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16
Q

HAS-BLED

A

Risk of bleeding

HTN = 1
Abnormal renal/liver =1-2
Stroke =1

Bleeding Hx= 1
Labile INR= 1
Elderly >75 = 1
Drugs (alcohol/anticoag) = 1-2

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17
Q

HAS-BLED vs CHA2DS2VASc

A

Crucial to weigh up risk of bleeding with risk of embolic event

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18
Q

Risk factors for recurrent AF

A

Hx of failed cardioversion
Structural heart disease
Previous AF recurrence

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19
Q

Cardioversion in those with AF >48hrs

A

Anticoagulation for 3 weeks prior and 4 weeks post procedure

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20
Q

Bradyarrthymias

A

Atropine 1st line antimuscarininc inhibitor of Ach @ SA/AV node leading to increased sympathetic effects

21
Q

SE of anticholingeric drugs

A

dry mouth, sweating, constipation, urinary retention, blurred vision

22
Q

MOA Flecanide

A

Class I antiarrthymic acts to block Na+ channels to increase the action potential duration at the purkenje fibres and overall slow the conduction velocity of the heart. Inhibits phase 0 depolarisation

23
Q

Flecanide uses

A

Used for rhythm control cardioversion in AF. CI in those with structural heart disease

24
Q

B-blockers in AF

A

Uses for rate control they increase the refractory period at the AVN slowing conduction, this reduces the rate in AF and may stop the self perpetuating circuit in the atria

Cardioselective - atenolol,

25
Q

SE of B-blockers

A

SE bronchospasm, hypotension, bradycardia, Raynauds

26
Q

MOA Amiodarone

A

Class III antiarrythmic acts to block K+, Ca2+ and Na+ channels all involved in cardiac repolarisation. This leads to reduced conduction velocity and AVN conduction resistance

27
Q

SE amiodarone

A

Acute - thrombophlebitis if not given through large vein, can prolong QTc leading to tornadoes de pointes and VF

Chronic - photosensitivity, hypo/hyperthyroidsm, lung fibrosis, blue/grey skin discolouration, corneal micro deposits, peripheral neuropathy

28
Q

CI to amiodarone

A

Pregnancy, increased QTc, hypotension and HB, active thyroid disease

29
Q

Interactions amiodarone

A

Inhibits the CYP450 enzymes - can increase drug concentration of warfarin, theophylline, statins

30
Q

Warfarin MOA

A

Anticoagulant used to treat venous clots. Inhibits the enzyme vit K epoxide reductase which prevents the recycling of vitamin K. Vit K is crucial to activate vit K dependent clotting factors - II, VII,IX,X

31
Q

Problems with warfarin

A

2-3 day lag period so LMWH must be used to rapidly reduce INR. Needs to be taken daily and have INR checked frequently. Concordance is crucial, pt must be independent and knowledgeable about their condition

32
Q

SE warfarin

A

haemorrhage
warfarin induced skin necrosis
osteoporosis and hepatic dysfunction

33
Q

Reversal of warfarin

A

If rapid reversal is needed beriplex can be given and IV vit K. Beriplex = PPC prothrombin complex concentrate and works in less than an hour. IV vit K in 12hrs, oral vit K in 24hrs

34
Q

Interactions with Warfarin

A

CYP450 inhibitors lead to reduced metabolism of warfarin and increased circulating levels = bleed risk
- SSRI’s,statins, PPI,NSAID’s,erythromycin

CYP450 inducers lead to increased metabolism, reduced free levels = stroke risk
- carbamazepine, COCP, fungal drugs, alcohol, phenytoin, st johns wort

35
Q

Reye syndrome

A

Encephalopathy and liver damage following infection with flu/chicken pox. Occurs when aspirin taken
Leads to mitochondrial damage in hepatocytes, increased NH3 products, cerebral oedema and swelling

36
Q

CI Warfarin

A

Pregnancy - teratogenic 1st trimester
high risk in liver disease due to reduced metabolism
elderly and recent surgery
PUD, bleeding history

37
Q

Cardiac glycosides - Digoxin

A

-ve chronotropes = reduce HR by slowing conduction at AV node via increasing vagal parasympathetic activity

+ve inotropes = increase contraction strength by inhibiting Na+/K+ atpase allowing more CA2+ to remain intracellularly

38
Q

Rate controlling drugs AF

A

B blockers, Calcium channel blocker, last resort = digoxin

39
Q

SE digoxin

A

Poor at controlling ventricular rate during exertion so only use in sedentary individuals. Narrow therapeutic window use with caution in renal impairment

40
Q

Calcium channel blockers - Non-dihydropyradine

A

Verapamil/dittiazem work on the heart to block calcium movement this slows conduction at the AVN

SE = constipation, red face, headache, tachycardia, and oedema

41
Q

CI CCB

A

Severe interaction with B-blockers leading to asystole, hypotension and HF

42
Q

SVT Mx

A

Adenosine

43
Q

Digoxin toxicity

A

arrthymias, dizziness, N/V, yellow vision

44
Q

LMWH heparin MOA

A

Enoxaparin, tinzaparin, dalteparin all act to activate antithrombin III which inhibits factor X preventing prothrombin being converted to thrombin

45
Q

SE heparin

A

haemorrhage, heparin induced thrombocytopenia, osteoporosis if long term, hyperkalemia

46
Q

DOAC

A

Factor Xa inhibitor = apixaban, rivoroxaban

Direct thrombin inhibitors = dabigatran

47
Q

+ve/-ves of DOACs

A

Given PO OD, no need for monitoring as predictable effects. Proven effectiveness

N/V, hepatic impairment, hard to reverse rapidly - agents very expensive!

48
Q

Fibrinolytics

A

Alteplase/streptokinas convert plasminogen to plasmin to breakdown fibrin rapidly. Used for ischemic stroke if within 4 1/2hrs. massive PE

CPTP (11 decks)

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