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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
SE of B-blockers
SE bronchospasm, hypotension, bradycardia, Raynauds
26
MOA Amiodarone
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
SE amiodarone
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
CI to amiodarone
Pregnancy, increased QTc, hypotension and HB, active thyroid disease
29
Interactions amiodarone
Inhibits the CYP450 enzymes - can increase drug concentration of warfarin, theophylline, statins
30
Warfarin MOA
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
Problems with warfarin
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
SE warfarin
haemorrhage warfarin induced skin necrosis osteoporosis and hepatic dysfunction
33
Reversal of warfarin
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
Interactions with Warfarin
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
Reye syndrome
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
CI Warfarin
Pregnancy - teratogenic 1st trimester high risk in liver disease due to reduced metabolism elderly and recent surgery PUD, bleeding history
37
Cardiac glycosides - Digoxin
-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
Rate controlling drugs AF
B blockers, Calcium channel blocker, last resort = digoxin
39
SE digoxin
Poor at controlling ventricular rate during exertion so only use in sedentary individuals. Narrow therapeutic window use with caution in renal impairment
40
Calcium channel blockers - Non-dihydropyradine
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
CI CCB
Severe interaction with B-blockers leading to asystole, hypotension and HF
42
SVT Mx
Adenosine
43
Digoxin toxicity
arrthymias, dizziness, N/V, yellow vision
44
LMWH heparin MOA
Enoxaparin, tinzaparin, dalteparin all act to activate antithrombin III which inhibits factor X preventing prothrombin being converted to thrombin
45
SE heparin
haemorrhage, heparin induced thrombocytopenia, osteoporosis if long term, hyperkalemia
46
DOAC
Factor Xa inhibitor = apixaban, rivoroxaban | Direct thrombin inhibitors = dabigatran
47
+ve/-ves of DOACs
Given PO OD, no need for monitoring as predictable effects. Proven effectiveness N/V, hepatic impairment, hard to reverse rapidly - agents very expensive!
48
Fibrinolytics
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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