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Exam prep tutorials (Pharmacology) > Antiarrhythmic Agents > Flashcards

Antiarrhythmic Agents Flashcards

1
Q

What is the 1st line response to bradycardia with adverse signs?

A

500 mcg of Atropine IV

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2
Q

What are the next measures in treating bradycardia if there is no response to atropine?

A
  • further atropine 500mcg IV
  • repeat to a max of 3mg
  • isoprenaline 5 mcg/min
  • adrenaline 2-10 mcg/min

OR

  • transcutaneous pacing
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3
Q

What are the less common agents you can use for bradycardias?

A
  • isoprenaline
  • adrenaline
  • aminophylline
  • dopamine
  • glucagon
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4
Q

What is atropine made of?

A

Racemic mix of D and L-hyoscyamine (only L is active)

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5
Q

What is the dose of atropine?

A
  1. 015 - 0.02 mg/kg IV or IM
  2. 2 - 0.6 mg PO

3mg needed for complete vagal blockade in adults

*No longer given in PEA arrest*

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6
Q

What are the pharmacokinetics of atropine?

A

Low bioavailability 10-20%

Crosses placenta and BBB

Elimination half life 2.5hrs

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7
Q

What are the pharmacodynamics of atropine?

A

Competitive antagonist of acetylcholine at muscarinic receptors with minimal action at nicotinic receptors.

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8
Q

What CVS effects does atropine produce?

A
  • low dose can initially produce bradycardia
    • Bezold Jarisch reflex
  • slows AV node conduction time
  • at high doses, dilation of cutaneous blood vessels
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9
Q

What resp effects does atropine cause?

A
  • causes bronchodilation, increasing physiological dead space
  • increases RR
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10
Q

What CNS effects does atropine cause?

A

Central anticholinergic syndrome

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11
Q

What GI effects does atropine cause?

A
  • reduces gut motility
  • reduces tone within urinary tract
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12
Q

What random effects does atropine cause?

A
  • pupil dilation (mydriasis)
  • increased intraocular pressure
  • reduces ADH secretion
  • local anaesthetic properties
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13
Q

What is glycopyrrolate?

A

Charged quaternary amine.

Competitive antagonist at peripheral muscarinic receptors.

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14
Q

What is the dose of glycopyrrolate?

A
  • 0.2 - 0.4 mg IV or IM adult
  • (4 - 10 micrograms/kg paeds)
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15
Q

What are the pharmacokinetics of glycopyrrolate?

A
  • poor oral absorption - 5% bioavailibility
  • can cross placenta but not BBB
  • 80% excreted unchanged
  • elimination half life 0.6 - 1.1 hrs
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16
Q

What are the CVS and resp effects of glycopyrrolate?

A

CVS

  • vagolytic effects last 2-3hrs
  • tachycardia with high doses

Resp

  • bronchodilator with increased physiological dead space

Other

  • 5 times as potent as atropine at drying secretions
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17
Q

What is isoprenaline?

A
  • β1 and β2 agonist
  • SVR can drop due to β2 action
  • can be used in management of complete heart block until pacing can be arranged
  • Given IV but can be inhaled/oral
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18
Q

What is adrenaline?

A
  • low dose infusion has chronotropic beta agonist effects
  • increasing dose increases alpha action
  • diastolic BP can fall due to β2 vasodilation
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19
Q

What is aminophylline?

A
  • non-specific phosphodiesterase inhibitor, increasing intracellular cAMP
  • mild chronotropic effects
  • arrhythmogenic - can precipitate arrhythmias including VF
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20
Q

What is dopamine?

A
  • low dose infusion has β1 action, higher doses create an alpha action
  • increases AV conduction
  • ineffective if given orally
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21
Q

What is glucagon?

A
  • glucagon receptors are G-protein linked and increase intracellular cAMP
  • limited to 2nd or 3rd line management of β blocker OD
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22
Q

Can atropine cause ataxia?

A

Yes - because it crosses the BBB and can cause central anticholinergic syndrome

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23
Q

What receptors does atropine antagonize?

A

It antagonises ACh at muscarinic receptors and only has a minimal effect on nicotinic at higher doses

24
Q

What supraventricular tachycardias are there?

A
  • Sinus tachycardia
  • AV nodal re-entry tachycardia (AVNRT)
  • AV re-entry tachycardia (AVRT), caused by Wolff-Parkinson-White syndrome
  • Atrial flutter, regular or variable block
  • Atrial fibrillation
  • SVT associated with bundle branch block, which can mimic a ventricular tachycardia
25
Q

What are the types of ventricular tachycardia?

A
  • monomorphic VT
  • torsades de pointes
26
Q

What should you to with a patient with a tachyarrhythmia with adverse features?

A

If the patient has shock/syncope/MI/heart failure:

  • synchronised DC shock (up to 3 attempts)
  • amiodarone 300mg IV over 10-20mins
  • repeat shock followed by
  • amiodarone 900mg over 24hrs
27
Q

What should you do with a patient with a tachyarrhythmia with no adverse features and a broad QRS?

A
  • if regular - this is VT
    • give amiodarone 300mg IV over 20-60mins
    • then 900mg over 24hrs
    • or if it’s (previously confirmed) SVT with bundle branch
      • give adenosine
  • if irregular - seek expert help
    • ?AF with BBB (treat as for narrow complex)
    • ?pre-excited AF (consider amiodarone)
    • ?polymorphic VT (give Mg 2g over 10mins)
28
Q

What should you do for a patient with a narrow QRS tachyarrhythmia?

A
  • if regular
    • use vagal manoeuvres
    • adenosine 6mg rapid IV bolus - if unsuccessful give 12mg, if unsuccessful again give further 12mg
    • monitor ECG continuously
      • if SR restored - probably re-entry paroxysmal SVT
        • record 12 lead ECG
        • if recurs give adenosine again + consider anti-arrhythmic prophylaxis
      • If SR not restored - seek expert help, could be atrial flutter (control rate (eg beta blocker))
  • if irregular - probably AF
    • control rate with beta blocker or diltiazem
    • consider digoxin or amiodarone if evidence of heart failure
29
Q

What is amiodarone used for?

A

Management of Wolff-Parkinson-White syndrome and SVT or VTs resistant to or inappropriate for other drugs.

30
Q

What is amiodarone? How does it work?

A
  • benzofuran derivative
  • class III action - blocks K+ channels
  • partial antagonist of α and β-agonists
  • Higher doses can depress Na+ and Ca 2+ channels
  • Slows rate of repolarization and increases refractory period, prolonging phase III
  • Slows AVN automaticity and conduction
  • No effect on conduction through bundle of His and ventricles
31
Q

What is the dose of amiodarone?

A

IV: 5mg/kg IV loading over 1 hr then 15mg/kg over 24hrs

Oral: 200mg TDS for 1 week orally then BD for 1 week, followed by OD

32
Q

What is the bioavailibility of amiodaraone?

A

50-70%

33
Q

How protein bound is amiodarone?

A

>95% protein bound

34
Q

What drugs can amiodarone potentiate the effects of?

A
  • oral anticoagulants
  • digoxin
  • calcium antagonists
  • beta blockers

as these are displaced from protein by the highly protein bound amiodarone

35
Q

What is the elimination half life of amiodarone?

A

4hrs to 52 days

36
Q

What are the potential SEs of amiodarone?

A
  • most patients develop corneal deposits
  • can cause bradycardia, hypotension and prolonged QT interval
  • can develop pneumonitis + fibrosis which can be reversible if treatment stopped early enough
  • peripheral neuropathy
  • abnormal liver function
  • photosensitivity
  • abnormal thyroid function (amiodarone resembles thyroid hormone)
37
Q

What is adenosine used for?

A

To differentiate between SVT and VT. SVT due to re-entry circuits can convert to SR with adenosine.

38
Q

How does adenosine work?

A
  • Naturally occurring purine nucleoside of adenine and D-ribose
  • Acts on adenosine (A1) receptors in SA and AV node (Gi-protein receptors) causing hyperpolarization and dramatic negative chronotropy
  • Transient heart block occurs
  • A2 receptors have anti-inflammatory actions
  • Adenosine has cytoprotective properties in ischaemia
  • Causes direct smooth muscle relaxation in normal coronary arteries
39
Q

What is the dose of adenosine?

A
  • 3mg rapid IV, then 6mg and 12mg until effect seen
  • acts within 10s and lasts 10-20s
40
Q

What CVS SEs does adenosine have?

A
  • increases myocardial blood flow
  • can induce AF or flutter as it decreases atrial refractory period
  • decreases pulmonary vascular resistance in pulmonary HTN
41
Q

What resp SEs does amiodarone have?

A
  • bronchospasm
  • increased RR and depth
42
Q

What other unwanted SEs can amiodarone have?

A
  • can induce neuropathic pain
  • causes facial flushing and chest discomfort
43
Q

What is digoxin used for?

A

SVTs, especially atrial fibrillation and flutter.

44
Q

How does digoxin work?

A
  • glycoside
  • directly blocks Na/K/ATPase pump which increases refractory period of AV node and reduces conductivity
  • indirectly acts by increasing ACh release which slows conduction and prolongs refractory period
  • given orally or IV
45
Q

What is the dose of digoxin?

A

10- 20 μg/kg as a loading dose 6hrly then maintenance

Serum levels should be monitored initially (1-2 g/ml therapeutic)

46
Q

How is digoxin excreted?

A

50-70% excreted unchanged in urine.

Involves some active secretion.

Dosing needs to be altered in renal failure.

47
Q

What electrolyte abnormalities increase the risk of digoxin toxicity?

A
  • hypokalaemia
  • hypomagnesaemia
  • hypernatraemia
  • hypercalcaemia
  • hypoxaemia
  • renal failure
  • other drugs incl. amiodarone, verapamil, diazepam
48
Q

What SEs are caused by digoxin?

A
  • GI disturbance incl. abdominal pain, nausea
  • muscle weakness
  • headache
  • drowsiness
  • arrhythmias incl. heart block and ventricular bigeminy
  • gynaecomastia (rare)
  • convulsions
49
Q

What arrhythmias are beta-adrenoceptor antagonists indicated for?

A

SVTs

For acute SVT use metoprolol/esmolol.

Sotalol and bisoprolol are used for chronic management.

50
Q

Which arrhythmias are calcium channel antagonists indicated for?

A

SVTs.

Diltiazem orally (30 - 120mg 6-8hrly)

Verapamil orally (240-480mg in 2-3 doses) or IV (5-10mg).

51
Q

What is flecainide indicated for?

A

SVTs and VTs. Suppresses ventricular ectopics.

It’s an amide local anaesthetic.

Blocks fast Na channels and slows depolarization especially in conducting pathways.

Given orally 100-200mg 12hrly.

IV 2mg/kg bolus and an infusion.

52
Q

What is bretylium?

A

Older agent used in refractory VT by inhibiting noradrenaline release

53
Q

How does amiodarone affect myocardial potassium channels?

A

Blocks them

54
Q

What effect does amiodarone have on the myocardial AP?

A

Slows the rate of repolarization and increases the refractory period.

55
Q

What effects does amiodarone have on the Bundle of His?

A

No effect

56
Q
A

Exam prep tutorials (Pharmacology) (8 decks)

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