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CVS > Anti-arrhythmia Therapy > Flashcards

Anti-arrhythmia Therapy Flashcards

1
Q

What causes cardiac cells to excite and contract

A

Na enters = depolarisation
Ca enters = contraction
K leaves = depolarisation

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2
Q

What do class 1 drugs do

A

Block Na channels so slow rate of depolarisation
Block AV node
Stabilise membrane

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3
Q

Example of class 1

A

Fleicanide

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4
Q

When is it used and when is it CI and what should you do prior to prescribing

A

AF / flutter for chemical cardio version
SVT with accessory pathway e.g. WPW
Some ventricular arrhythmia’s

CI
Post MI
Structural heart
HF 
AV block
Flutter

Need to do ECHO to look for structural heart as -ve inotropic

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5
Q

What are class 2 drugs and what do they do

A

BB
Block sympathetic system
Depress depolarisation
Depress SVT and VT

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6
Q

When is it 1st line

A

AF

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7
Q

What are class 3 drugs

A

Amiodarone

Sotalol

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8
Q

How do they work

A

K blocker
Increase AP duration
Prolonged repolarisation

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9
Q

When are they used

A

Difficult to treat arrhythmia

Life threatening VT, VF, AF, flutter

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10
Q

What is class 4 drug

A

CCB

  • Verapamil
  • Dilitizem
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11
Q

How do they work

A

Depress depolarisation

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12
Q

When are they used

A

Paroxysmal SVT

Control AF and flutter

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13
Q

What is digoxin

A

Cardiac glycoside
Inhibits Na / K pump
Positive inotrope - allows Ca to improve contraction

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14
Q

When is digoxin used

A

Heart failure - improve Sx due to inotropic but not mortality
AF for rate control

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15
Q

What must you monitor

A

U+E - K level

Toxicity

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16
Q

When is it commonly used

A

Elderly for rate control in AF with poor heart

17
Q

Why should you use with caution

A

Renal excreted so increases in renal failure / AKI which elderly prone too

18
Q

What do you do if this happens

A

Monitor U+E

Reduce dose

19
Q

What other AA will increase level of digoxin / other factors which increase toxicity

A

Amiadarone

Other

  • Hypokalaemia / Mg
  • Hypernatraemia / Ca
  • Hypothermia
  • Hypothyroid
  • Age
  • Renal failure
  • Acidosis
  • MI
  • Spirnolactone
  • Thiazide
20
Q

What are SE of digoxin

A 
Hyperkalaemia - causing arrhythmia
Gout
Nausea
Anorexia
Confusion
Gynaecomastia
21
Q

What are signs of toxicity

A

Yellow glow (xanthopsia)
N+V
Confusion
Arrhythmia - AV block / Brady

ECG 
Reverse ST tick
Flattened T wave
Short QT 
Av block
VT / VF
22
Q

What do you do if toxicity

A 
Measure digoxin level 8-12 hours after last dose 
U+E= monitor 
ECG
Give digiband
Correct electrolyte
23
Q

When is amiodarone used

A

Atrial and ventricular tachycardia

24
Q

What may amiadarone interact with

A

Digoxin - increases level
p450 inhibitor
Warfarin increased

25
Q

What are SE of amiadarone

A 
Thrombophlebitis of central vein 
Bradycardia 
Long QT 
Thyroid dysfunction - hypo and hyper
Pulmonary fibrosis 
Hepatic toxicity 
- Discontinue if LFT spike >2/3x 
- Do not start if liver issue
- Cirrhosis is rare 
Pneumonitis
Grey / blue  pigmentation 
Optic neuritis 
Corneal opacification 
Peripheral neuropathy
Photosensitivity
26
Q

What do you do prior to starting

A

U+E, LFT, TFT

CXR

27
Q

What do you monitor every 6 months

A

TFT and LFT

28
Q

What does adenosine do

A

Slows conduction through AV node causing transient heart block

29
Q

When is it used

A

SVT to convert to sinus

30
Q

How do you give

A

IV

Fast bolus as short bolus through large bore cannula followed by saline flash

31
Q

What does it cause intially

A

Systole

Warn patients that may feel like death

32
Q

When is it CI

A

Asthma / COPD due to bronchospasm

HF / Severe hypo / heart block

33
Q

What are SE

A

Chest pain
Spasm
FLushing
WPW

34
Q

What do you do for all class 3 (amiadaraone and stall) and fliecanide (class 1)

A

Monitor ECG as risk of QT prolongation

CVS (30 decks)

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