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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
What are the types of ventricular tachycardia?
* monomorphic VT * torsades de pointes
26
What should you to with a patient with a tachyarrhythmia with adverse features?
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
What should you do with a patient with a tachyarrhythmia with no adverse features and a broad QRS?
* 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
What should you do for a patient with a narrow QRS tachyarrhythmia?
* 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
What is amiodarone used for?
Management of Wolff-Parkinson-White syndrome and SVT or VTs resistant to or inappropriate for other drugs.
30
What is amiodarone? How does it work?
* 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
What is the dose of amiodarone?
**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
What is the bioavailibility of amiodaraone?
50-70%
33
How protein bound is amiodarone?
\>95% protein bound
34
What drugs can amiodarone potentiate the effects of?
* oral anticoagulants * digoxin * calcium antagonists * beta blockers as these are displaced from protein by the highly protein bound amiodarone
35
What is the elimination half life of amiodarone?
4hrs to 52 days
36
What are the potential SEs of amiodarone?
* 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
What is adenosine used for?
To differentiate between SVT and VT. SVT due to re-entry circuits can convert to SR with adenosine.
38
How does adenosine work?
* **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
What is the dose of adenosine?
* 3mg rapid IV, then 6mg and 12mg until effect seen * acts within 10s and lasts 10-20s
40
What CVS SEs does adenosine have?
* increases myocardial blood flow * can induce AF or flutter as it decreases atrial refractory period * decreases pulmonary vascular resistance in pulmonary HTN
41
What resp SEs does amiodarone have?
* bronchospasm * increased RR and depth
42
What other unwanted SEs can amiodarone have?
* can induce neuropathic pain * causes facial flushing and chest discomfort
43
What is digoxin used for?
SVTs, especially atrial fibrillation and flutter.
44
How does digoxin work?
* 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
What is the dose of digoxin?
10- 20 μg/kg as a loading dose 6hrly then maintenance Serum levels should be monitored initially (1-2 g/ml therapeutic)
46
How is digoxin excreted?
50-70% excreted unchanged in urine. Involves some active secretion. Dosing needs to be altered in renal failure.
47
What electrolyte abnormalities increase the risk of digoxin toxicity?
* hypokalaemia * hypomagnesaemia * hypernatraemia * hypercalcaemia * hypoxaemia * renal failure * other drugs incl. amiodarone, verapamil, diazepam
48
What SEs are caused by digoxin?
* GI disturbance incl. abdominal pain, nausea * muscle weakness * headache * drowsiness * arrhythmias incl. heart block and ventricular bigeminy * gynaecomastia (rare) * convulsions
49
What arrhythmias are beta-adrenoceptor antagonists indicated for?
SVTs For acute SVT use metoprolol/esmolol. Sotalol and bisoprolol are used for chronic management.
50
Which arrhythmias are calcium channel antagonists indicated for?
SVTs. Diltiazem orally (30 - 120mg 6-8hrly) Verapamil orally (240-480mg in 2-3 doses) or IV (5-10mg).
51
What is flecainide indicated for?
**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
What is bretylium?
Older agent used in refractory VT by inhibiting noradrenaline release
53
How does amiodarone affect myocardial potassium channels?
Blocks them
54
What effect does amiodarone have on the myocardial AP?
Slows the rate of repolarization and increases the refractory period.
55
What effects does amiodarone have on the Bundle of His?
No effect
56

Exam prep tutorials (Pharmacology) (8 decks)

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