Cardio - antiarrythmics and endocarditis Flashcards

1
Q

What are the two mechanisms behind arrythmias?

A
  • disturbance in impuls formation
  • disturbance in impuls conduction

It could also be both

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2
Q

What are the mechanisms of the four classes of antiarrythmic drugs?

A

Class 1 - sodium channel blockade
Class 2 - blockade of sympathetic autonomic effects in
the heart,
Class 3 -prolongation of the effective refractory period
(k+ channel inhibition
Class 4 - calcium channel blockade

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3
Q

Name three unclassified antiarrythmic drugs

A
  • digoxin
  • adenosine
  • magnesium
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4
Q

What is the mechanism of Class IA anti arrythmics?

A
  • Blocks the open, active Na-channel
  • slows phase 0
  • prolong action potential (phase 3 - class III activity)
    (slow dissociation from sodium channel)
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5
Q

What is the classification and clinical indications for:

  1. Quinidine
  2. Disopyramide
  3. Procainamide
A

Class 1A

Use:

  1. Supraventricular arrythmias
  2. Ventricular arrythmias
  3. Both

rarely used due to possible Chinconism

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6
Q

What are the adverse effect of class 1A antiarrythmics?

A

Procainamide - lupus like, hematotoxicity
Disopyramide - antimuscarinic, heart failure
Quinidine - cinchonism, M and alpha block
All: arrythmias

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7
Q

What is the classification and clinical indications for:

  1. Lidocaine
  2. Mexiletine
  3. Phenytoin
A

Class 1B

Use:

  1. ventricular arrythmias(Amiodarone DOC)
  2. ventricular arrythmias (oral Lidocaine)
  3. Anticonvulsant, digitalis - dysrythmias
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8
Q

What is the mechanism of class 1B antiarrythmics?

A
  • Blocks the closed Na-channel
  • slows phase 0
  • shortens phase 3 repolarization
    (fast dissociation from sodium channel
    -> effect manifested at high firing rate)
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9
Q

What are the adverse effects of class 1B antiarrythmics?

A

CNS sedation or excitation

Mexeiletine - nausea, vomiting, dyspepsia

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10
Q

What is the classification and clinical indications for:
1. Flecainide
2. Propafenone
3 .Moricizine

A

Class 1C

Use:
1,2 - supraventricular arrythmias
3 - Ventricular arrythmias

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11
Q

What is the mechanism of class 1C antiarrythmics?

A
  • Blocks all three Na channels
  • slows phase 0
    (slowly dissociates from Na channels
    -> effects even at normal heart rate)
  • reduces automaticity by
    increasing threshold potential
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12
Q

What are the adverse effects of class 1C antiarrythmics?

A

Proarrythmic effect

Flecainide - B-blocking properties

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13
Q

What is the mechanism of class II antiarrythmics?

A

B - blocking:
-> Diminish phase 4 repolarization
-> depress automaticity, prolong AV conduction
decrease HR and contractillity

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14
Q

What are the clinical indications for type II antiarrythmics?

A
  • supraventricular arrythimas
  • ventricular arrythmias
  • thyrotoxicosis
  • reduce mortality after MI or CHF
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15
Q

What is the classification and clinical indications for:

  1. Amiodarone
  2. Dronedarone
  3. Vernakalant
  4. Dofetilide, Ibutilide
  5. Sotalol
A

Class 3 antiarrythimcs

Use:
1. supraventricular/ventricular arrythmias
   safe in CAD and HF
2. (Increases mortality in afib and HF)
3. Cardioversion of atrial fibrilation
4. atrial fibrilation
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16
Q

What are the adverse effects of class III antiarrythmics?

A
  • Amiodarone - thryoid abn., pulm. fibrosis
    photodermatitis,hepatitis, corneal deposits
  • Dronedarone - increases mortality
  • Vernakalant - altered taste, sneezing

All are potentially proarrythmic, but Amiodarone
ha a low proarrythmic affect

17
Q

What is the mechanism of class III antiarrythmics?

A

Blockage of K+ channels
-> prolong phase 3 repolarization

- Amiodarone - shows class 1,2,3,4, 
   and α block action
18
Q

What is the antiarrythmic classification and indications for:
Verapamil
Diltiazem

A

Class IV: antiarrythmic

Use:
- supraventricular arrhythmias
reduce the ventricular rate in atrial fibrillation and flutter

19
Q

What is the mechanism of class IV antiarrythmics?

A

Blockage of cardiac calcium channels
-> decrease phase 4 depolarization
-> slows conduction in SA and AV nodes
(blocks Ca-channels in phase 0)

20
Q

What is the mechanism of Adenosine?

What are the uses?

A

less cAMP (like M2) activation of an inward K+ current and inhibition of Ca2+ current -> conduction block

Use:
acute supraventricular tachycardias

T 1/2 < 10s

Causes bronchospasm!
Antagonised by methylxanthines
synergy with dipyridamole

21
Q

When is MgSO4 used in arrythmias?(I.V)

A

In digitalis arrythmia, Torsade de points
+ hypomagnesaemia, hypokalaemia

It is necessary for Na,Ca,K transport
across cell membranes
‘‘competes with Ca’’

22
Q

When is Ca2+ used in arrythmias?

A

PEA caused by: hyperkalaemia, hypocalcaemia, overdose of calcium channel-blocking drugs

23
Q

When is HCO3 used in arrythmias?

A

life-threatening hyperkalaemia,
cardiac arrest associated with hyperkalaemia,
tricyclic overdose.

24
Q

When is K+ used in arrythmias?

A
  • Digitalis toxicity

- arrythmia + low K+

25
Q

What are the typical causative organisms of endocarditis?

A
  • Streptococcus viridans (the most frequent)
  • Streptococcus bovis
  • Staphylococcus aureus (healthcare-associated )
  • enterococci
  • HACEK group
26
Q

Which drugs are recommended as prophylaxis for high risk patients against endocarditis?

A

Amoxicillin

Clindamycin (penicillin allergy)