Anti-arrhythmia Therapy Flashcards

(34 cards)

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
What are SE of amiadarone
``` 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
What do you do prior to starting
U+E, LFT, TFT | CXR
27
What do you monitor every 6 months
TFT and LFT
28
What does adenosine do
Slows conduction through AV node causing transient heart block
29
When is it used
SVT to convert to sinus
30
How do you give
IV | Fast bolus as short bolus through large bore cannula followed by saline flash
31
What does it cause intially
Systole | Warn patients that may feel like death
32
When is it CI
Asthma / COPD due to bronchospasm | HF / Severe hypo / heart block
33
What are SE
Chest pain Spasm FLushing WPW
34
What do you do for all class 3 (amiadaraone and stall) and fliecanide (class 1)
Monitor ECG as risk of QT prolongation