CV arrythmias Flashcards

1
Q

ectopic beats compared to AF are often spontanoeous and resolve on their own

if tx is needed what drug class used?

A

beta blocker

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2
Q

AF tx aims to do what 2?

A

reduce symptoms and prevent complications, especially stroke

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3
Q

what is a stroke

A

blood doesn’t fully eject –> clot

blood pools in valve/ chambers -> clot and stroke risk

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4
Q

af managed through what 2?

A

ventricular rate control or sinus rhythm control

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5
Q

2 types of pts who may have AF acute

A

pt with or without life-threatening haemodynamic instability

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6
Q

treatment for pt with life-threatening haemodynamic instability caused by AF?

A

Emergency electrical cardioversion without delay to achieve anticoagulation!

prevents clotting

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7
Q

treatment for patients without life-threatening haemodynamic instability
Onset of AF <48 hours?
Onset of AF >48 hours?

A

Onset of AF <48 hours? Rate or Rhythm control

Onset of AF >48 hours? Rate control

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8
Q

what is meant by
rate control
rhythm control

A

rate: via medication
rhythm: cardioversion

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9
Q

2 Types of (Cardioversion) Rhythm Control to restore sinus rhythm?

A

Pharmacological
Electrical

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10
Q

pharmacological rhythm control examples 2

A

flecainide or amiodarone

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11
Q

electrical rhythm control examples?

A

start IV anticoagulation (heparin) and rule out a left atrial thrombus

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12
Q

3 Types of (ventricular) Rate Control Monotherapy?
this is preferred first line for AF except in pts with new onset

A

beta-blocker (not sotalol)
Rate-limiting CCB- verapamil/diltiazem
Digoxin (mainly sedentary patients with non-paroxysmal AF)

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13
Q

Choice of drug should be based on what?

A

individual symptoms
HR
comorbidities
patient preference

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14
Q

if monotherapy to control ventricular rate fails, what to do?

A

dual therapy:
combine any 2: beta blocker/digoxin/diltiazem

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15
Q

if symptoms not controlled w dual therapy, consider rhythm control and if LVEF < 40%, combine what 2 drugs?

A

bb and digoxin

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16
Q

AF maintenance,

if AF present > 48hrs, pt must be fully anticoaged for min 3 weeks and continue oral anticoag at least X after cardioversion

A

4 weeks

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17
Q

drugs tx usign what may be required post cardioversion?

A

standard bb
if symptoms persist or bb not appropriate: SPAF: sotalol, propadenone, amiodarone, or flecainide

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18
Q

whats paroxysmal AF?

A

paroxysmal: sudden attack/ increase insymptoms of diease
AF: irregular heart rhythm sudden and goes on its own

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19
Q

pill in pocket approach used to restore sinus rhythm what is this

A

take a tablet: flecainide or propadenone on onset of AF episode

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20
Q

ALL pts with AF should be assessed for stroke risk and thromboprophylaxis need balanced with risk of bleeding

using what tools?

A

stroke: CHA2DS2-VASc
bleeding risk: ORBIT

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21
Q

what does CHA2DS2-VASc consider?

A

Congestive HF
Hypertension
Age 75+ (2)
Diabetic
Stroke/TIA (2)
Vascular disease- DVT, aneurysm, etc
Age 65-74
Sex- female

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22
Q

When is thromboprophylaxis NOT needed? chadsvasc

A

Men= 0
Women= 1

needed if men: 1 and women: 2

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23
Q

thromboprophylaxis done with what 2 drugs?

A

Warfarin (vit K antagonist)
OR DOACs in non-valvular AF

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24
Q

name of condition described:
abnormal heart rhythm occurring in upper chambers of heart (atria). rapid, regular heartbeat

A

atrial flutter

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25
Q

Atrial flutter tx options same as af but responds better to which: electrical cardioversion or drug tx?

A

electrical

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26
Q

rate control of atrial flutter is normally temporary until sinus rhythm restored

name 2 possible classes of rate control drugs used

A

bb or RL CCBs

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27
Q

t/f paroxysmal supraventricular tachycardia usually goes away on tis own without tx

A

true

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28
Q

if paroxysmal supraventricular tachycardia requires tx, reflex vagal stimulation may be needed which involves what procedures?

A

stimulate vagus nerve:
- Valsalva manoeuvre, immerse face in ice-cold water, or carotid sinus massage

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29
Q

vagus nerve stim procedures should be performed with what monitoring?

A

ECG monitoring

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30
Q

if reflex vagal stim doesnt work, how is paroxysmal supraventricular tachycardia treated

A

a. iv adenosine
b. ineffective, give iv verapamil

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31
Q

Recurrent episodes of paroxysmal supraventricular tachycardia can be treated by what

A

catheter ablation,
or prevented with BBs or RL CCBS: diltiazem, verapamil, sotalol, flecainide, propafenone

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32
Q

Arrhythmias after myocardial infarction: how is bradycardia treated?

A

particularly if complicated by hypotension, IV atropine

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33
Q

Pulseless ventricular tachycardia or ventricular fibrillation require what?

A

very bad arrhythmias… resuscitation

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34
Q

pts with UNSTABLE or STABLE ventricular tachyardia tx with:
direct current cardioversion
if fails, iv amiodarone
repeat current cardioversion

A

unstable

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35
Q

pts with UNSTABLE or STABLE ventricular tachyardia tx with:

iv amiodarone
direct current cardioversion

non-sustained ventricular tachycardia can be treated with bb

36
Q

pts at high risk of cardiac arrest need maintenance therapy through what

A
  • implantable cardioverter defibrillator
  • can add bb/ amiodarone (in combo with standard bb)
37
Q

what is Torsade de pointes

A

form of ventricular tachycardia associated with a long QT syndrome

38
Q

long QT syndrome/ torsade can be drug induced OR caused by what 3 factors

A

hypokalaemia, severe bradycardia, and genetic predisposition

39
Q

what drugs can cause hypOkalaemia

A

amiodarone
sotalol
macrolides
haloperidol
ssris
tcas
antifungals

40
Q

torsade usually self limiting but can be recurrent leading to what

A

impaired consciousness

if torsade not controlled -> ventricular fibrillation –> death

41
Q

torsade treated how

A

iv magnesium sulphate
bb NOT sotalol and atrial/ ventricular pacing may be considered

42
Q

why should Anti-arrhythmics NOT be used in torsade?

A

can prolong QT interval more -> worsen condition

43
Q

Anti-arrhythmic drugs can be classified clinically into those that act on
- supraventricular arrhythmias (e.g. A),
- ventricular arrhythmias (e.g. B)
- both supraventricular and ventricular arrhythmias (e.g. C)

A

A. verapamil
B. lidocaine
C. amiodarone

44
Q

Anti-arrhythmic drugs can also be classified by effects on electrical behaviour of myocardial cells during activity (the Vaughan Williams classification)
less important

A

Class I: membrane stabilising drugs (e.g. lidocaine, flecainide)
Class II: beta-blockers
Class III: amiodarone; sotalol (also Class II)
Class IV: calcium-channel blockers (includes verapamil but not dihydropyridines)

45
Q

hypokalaemia enhances the arrhythmogenic (X) effect of many drugs.

A

pro-arrhythmic

due caution

46
Q

amiodarone is a high risk drug with very long half life
should be avoided in what 2 circumstances

A

bradycardia and heart block
bc as a side effect it can slow down HR

47
Q

6 main SEs of amiodarone

TCP PHD

A

thyroid disorders
corneal microdeposits
photosensitivity reaction

pulmonary tox
hepatotoxicity
driving and skilled tasks

48
Q

what is meant by corneal microdeposits
as a SE of amiodarone

A

pt dazzled by headlights of oncoming traffic
reversible when tx ends
if vision impaired: STOP

49
Q

amiodarone contains iodine so affects what function?

A

thyroid
can cause hypo or hyeprthyroidism
treated w levothyroxine

50
Q

how to treat photosensitivity reaction as SE of amiodarone

A

avoid sunlight
use sunscreen for months after tx end

51
Q

what other drugs cause photosensitivity reaction? SAN LIGHT

A

sulfonamides
amiodarone
nsaids

loop diuretics
isotretinoin
griseofulvin
hydro–terzole
tetracycline

52
Q

amiodarone loading dose

A

200mg TDS 7 days
200mg BD 7 days
200mg OD maintenance

53
Q

how may SE pulmonary tox be observed w amiodarone use

A

report new/ progressive SOB or cough

54
Q

hepatotox SE of amiodarone. stop if pt develops liver disease, how may this be noticed?

A

dark urine
jaundice
abdominal pain
nausea vom
light colour stools
pruritis

55
Q

why should you HALVE dose of digoxin when using amiodarone alongside it?

A

amiodarone: enzyme inhibitor

56
Q

why could effects and interactions of amiodarone last for several weeks/ months

A

very long t1/2

57
Q

what 4 main types of drugs can amiodarone interact with

A
  • drugs causing hypokalaemia bc amiodarone does too
  • drugs causing QT prolongation
  • cyp450 enzyme substrates
  • drugs causing bradycardia
58
Q

what drugs may cause QT prolongation thus interact with amiodarone

A

macrolides
quinolones
ssris
antipsychotics
ondansetron

59
Q

emiodarone is cyp450 inhibitor so other enzyme inhibitors and inducers affect it too eg

A

inhib grapefruit
warfarin
contraceptives
statin
inducer phenytoin, phenobarb

60
Q

what drugs can cause bradycardia thus interact w amiodarone

A

bb
rl ccbs
digoxin

61
Q

what to monitor with amiodarone use?
TLP-XE

A

thyroid function
liver function
Potassium

chest XRay
annual Eye exam

62
Q

how often to do thyroid and liver func tests with amiodarone

A

before tx then every 6 months

63
Q

when to do serum potassium and chest x ray w amiodarone tx

A

once before tx

64
Q

why are potassium and chest x ray done on amiodarone tx

A

causes hypokalaemia

due to pulmonary effects, rule out existing lung conditions

65
Q

what to monitor with IV amiodarone?

A

ecg and liver transaminases

66
Q

MHRA warning
pts who have stopped amiodarone in last few months and need to start sofosbuvir and daclatasvir, simeprevir and sofosbuvir, or sofosbuvir and ledipasvir should be monitored why?

A

risk of severe heart blokc - fatal!

67
Q

digoxin therapeutic range?

A

0.7-2.0 ng/mL

68
Q

when is there a toxicity risk in dogoxin conc and how is this treated?

A

Increased from 1.5-3.0 ng/mL.
Treated with digoxin-specific antibody

69
Q

signs of digoxin tox?
SICK AND SLOW

A

D&V
SA/AV block+bradycardia
Dizziness/confusion/depression
Blurred/yellow vision

70
Q

when do you take blood samples with digoxin

A

6-12 hrs after a dose

71
Q

what 2 to monitor with digoxin

A

serum elecs and renal function

72
Q

digoxin interactions?
BTHC

A

bb
TCA
hypokalaemia drugs - risk of dig tox
cyp450 enz inducers/ inhibitors

73
Q

why do bb interact w digoxin

A

increase AV block risk and increases plasma concs

74
Q

why do TCAs interact w digoxin

A

can induce arrhythmias

if we’re treating arrythmias no point giving drug than induces them!

75
Q

how do cyp450 enz inducers and inhibitors each affect digoxin plasma conc?

A

inducer: reduces conc
inhibitor: increases conc

76
Q

which following SEs is least associated with amiodarone?
hyperthyroidism
renal failure
pulmonary tox
photosensitivity
blurred vision

A

renal failure

77
Q

adenosine used for terminating paroxysmal supraventricular arryhmias and SEs short lived why

A

short duration of action
t1/2 only 8-10 secs but prolonged in px taking dipyridamole

78
Q

unlike X, adenosine can be used after a bb but X may be better than adenosine in asthma

79
Q

digoxin belongs to class X and slows ventricular response in AF and flutter

A

cardiac glycoside

80
Q

what may occur with large doses of verapamil

A

hypotension

81
Q

iv verapamil may be followed by oral tx but whats a serious DDI with iv verapamil?

82
Q

iv bb eg X or Y can be used for rapid control of ventricular rate

A

emolol or propamolol

83
Q

Supraventricular arrhythmias 4 main drugs

A

adneosin
digoxin
verapamil
bbs

84
Q

Drugs for both supraventricular and ventricular arrhythmias include what?

A

amiodarone,
beta-blockers,
disopyramide,
flecainide acetate,
procainamide (available from ‘special-order’ manufacturers or specialist importing companies),
propafenone hydrochloride.

85
Q

how do bb act an anti-arrhythmic drugs?

A

attenuating the effects of the sympathetic system on automaticity and conductivity within the heart.

86
Q

what drug can be used for life threatening ventricular arrythmias?
and which is normally used?

A

normally: lidocaine IV but no longer first choice
serious: mexiletine