Anti Aarhythmias Flashcards

1
Q

what is the problem in atrial arrhythmia ?

A

the artium (not SAN) produces random impulses leading to random heart beats

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2
Q

what does the P wave represent ?
QRS ?
T?

A
P = Atrial contraction 
QRS = Ventricle contaction
T = Ventricle repolarisation
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3
Q

what can cause arrhythmias ?

why are they dangerous ?

A

pacemaker impulse formation (SAN or AVN)- more likely bradycardia
Contraction impulse conduction
or combination

rate / timing of contraction not enough to maintain normal CO

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4
Q

what is happening phase 0 of Cardiac AP ?

A

Na + influx
lads to depolarisation
get graph out

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5
Q

what is happening phase 1 ?

A

K+ Efflux leading to transient repolarisation

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6
Q

what is happening phase 2 ?

A

Ca2+ influx leading to plateau due to K+ Efflux

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7
Q

what is happening phase 3 ?

A

VG calcium channels close and therefore only K+ Efflux leads to repolarisation

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8
Q

what is happening phase 4?

A

Na+/k+ ATPase is leading maintaining of RMP at -90mV

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9
Q

What do Class 1 drugs do ?

A

Block Na+ channels leading to mark slowing of conduction but little on APD

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10
Q

What do class 2 drugs do ?

A

Beta blockers

diminish phase 4 depolarisation and automaticity

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11
Q

Name 2 class 1 drug ?

A

Flecainide, Lidocaine

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12
Q

Name 2 class 2 drug ?

A

Labetalol, Propranolol, Bisoprolol

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13
Q

What do class 3 drugs do?

A

block K+ Channels leading to a longer plateau phase (3) which leads to longer APD

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14
Q

Name 2 class 3 drugs

A

Amiodarone, Sotalol

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15
Q

What do class 4 drugs do?

A

block calcium channels leading to decrease of plateau phase leading to decreased phase 4 depolarisation

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16
Q

what is happening in phase 0/2 of slow cardiac AP?

A

Look up graph

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17
Q

what do calcium channels blockers do to slow cardiac AP?

A

decreases slope of phase 0 = reduce conduction velocity

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18
Q

name 2 Class 4 drugs

A

Diltiazem, Verapamil

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19
Q

what do Beta agonist do on the slow cardiac AP?

A

increase slope of If = increased conduction velocity

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20
Q

What do musurarinic / Adenosine agents do to slow cardiac AP?

A

Decrease If slope

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21
Q

what is the pathophysiology of Wolf/ Parkinson white syndrome?

A

Excessive conductive tissue leading to re-entry circuit from retrograde backflow

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22
Q

how can the AVN cause re-entry loops?

A

fast pathway and slow pathway both present and different conduction times lead to repolarasiotn of fast pathway in node = Tachy

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23
Q

how can infracts causes Re-entry ?

A

functional re-entry =

= abnormal channels caused by scar tissue

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24
Q

Name 3 ways heart can cause abnormal impulse generation

A
Enhanced normal automaticity (AP increase from SAN)
Ectopi foci
Triggered rhythms -
Delayed After depolarisation 
Early after depolarisation
25
Q

Name 2 ways the heart can cause abnormal conduction

A

Conduction block - (1st , 2nd and 3rd)

Reentry loops

26
Q

What is the 2 main MOAs for treating abnormal generation of impulses?

A

Decrease slope of Phase 4 in pacemaker cells (CCBs or beta blockers)
Raise the threshold

27
Q

What is the 2 main MOAs for abnormal conduction of HBs?

A
Decrease conduction velocity (class 1)
Increase end refractory period
28
Q

what is Atropine ? what is it used for ?

A

Muscarinic antagnoists

used for Bradycardia as it competitively inhibits M2 Parasympathetics on the heart

29
Q

What are Class 1A drugs used for ?

A

wide use -
A fib/flutter and Brugada’s
acute SVTs and Ven arrhythmia’s

30
Q

What are Class 1A drugs side effects?

A

hypotension, reduced CO, Seizures, GI effects, Proarrhythmia

31
Q

Name a class 1B drug
what is it used for ?
Why is it used for this ?

A

Lidocaine - IV only
acute ischaemic VT
only works on fast beating or ischaemic tissue (decrease phase 0)

32
Q

what are the side effects of 1B drugs ?

A

dizziness, drowsiness and GI symptoms

33
Q
Name a class 1C drug
what is the major difference in these drugs ?
A

Flecainide

substantially decrease phase 0 in normal

34
Q

What must you use flecanide with ? why is this

A

AVN blockers

as the flutter in atrium can transfer to ventricles

35
Q

what is class 1C drugs used for ?

A

SVT
ectopic ventricular foci
WPW syndrome

36
Q
What are some side effects of class 1C drugs ?
what mustn't a patient have?
A

proarrhythmia and sudden death, GI and CNS effects due to anesthetics

cardiac myopathy , ischemia

37
Q

what are ECG effects of class 2 drugs ?

A

increase PR

decrease HR

38
Q
What are the side effects of class 2 drugs?
when should you not sue them ?
A

Bronchospasm
Hypotension
partial AVN block or acute HF

39
Q

What are the cardiac effects of Class 3 drugs?

A
increase Refractory period 
decrease phase 0 
increase threshold 
decrease phase 4
decrease speed of AV conduction
40
Q

what are the effects on the ECG?

A

Increase PR, QRS and QT

decrease HR

41
Q

What are the side effects of class 3 drugs ?

A
pulmonary fibrosis 
hepatic injury 
increased LDL 
thyroid disease 
photosensitivity 
optic neuritis - transient blindless
42
Q

what must you do with patients on Amidarone ?

A

CYP3A4 Inhibtor -

adjust dose of digoxin and monitor warfarin

43
Q

what are side effects of sotalol ?

A

Proarrthythmia

fatigue and insomnia

44
Q

what is the main difference in solatol and amiodarone ?

A

sotalol is a partial beta blocker

45
Q
what is the side effects of class 4 drugs ?
what must you look out for in patients ?
A

hypotneison , decreased CO or sick sinus , constipation

Asytole if beta blocker is present

46
Q

How does adenosine work and how is it given ?

A

Nucleoside binds to A1 receptors and activated K+ currents in AV and SAN decreasing APD = hyper
polarisation
IV bolus - t1/2 = seconds

47
Q

when is adenosine given ?

what is a major side effect of adenosine ?

A

convert reentry SVTs
diagnosis of coronary artery diseases - ischeamia

bronchopasm

48
Q

what is vernakalant used for ?

MOA?

A

AFib that has just started -
slows atrial conduction = potency at higher rates
Blocks atrial specific K+ channels

49
Q

what are the side effects of vernakalant ?

A

Hypotension, AV block

sneezing and taste disturbance

50
Q

how does ivabradine work ?

what is special about this drug ?

A

blocks Ifunny in SAN

slows sinus node without affecting BP

51
Q

What is the use of ivabradine ?

side effects ?

A

Reduce sinus tacy , HR in HF and angina- avoids BP drops

Flashing lights - tetragenic

52
Q

how does digoxin work ?

what is it used with ?

A

block Na/K+ ATPase , decreasing activty of Na/Ca2+ exchanger leading to more calcium in cells = slows down AV conduction and HR
beta blockers or CCBs

53
Q

What is digoxin used for ?

A

Reduce Ventricular rates in AFib

54
Q

what drugs are used in AF?

A
Rate = CCBs, bisoprolol and digoxin
rhythm= sotalol, flecainide with bisoporlol and amiodarone
55
Q

what drugs should you use for VT?

A

Depends what drugs
Lignocaine
amiodarone

56
Q

what should be used for WPW?

A

flecainide

amiodarone

57
Q

what drugs for acute reentry SVT?

A

adenosine , verapamil

flecainide , vagal manoeuvres

58
Q

what drugs for chronic reentry SVT?

A

Bisoprolol , verapamil

sotalol

59
Q

what drugs for ectopic beats ?

A

beat blocker first line

flecainide