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Anaesthetic FRCA Primary - eLFH Pharmacology > eLFH - Antiarrhythmic agents > Flashcards

eLFH - Antiarrhythmic agents Flashcards

1
Q

Definition of bradycardia

A

HR < 60

Treated only if signs of compromise

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2
Q

Interim treatment options for Bradycardia (whilst awaiting trans-venous pacemaker insertion

A

Glycopyrrolate
Atropine
Isoprenaline
Adrenaline
Aminophylline
Dopamine
Glucagon

Transcutaneous pacing

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3
Q

Indication for Atropine use

A

Bradycardia due to increased vagal tone or to counter muscarinic effects of anticholinergics

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4
Q

Chemical composition of Atropine

A

Racemic mixture of D- and L-hyoscyamine

Only L- is active

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5
Q

Dose of Atropine and route of administration

A

20 micrograms / kg IV or IM

200 - 600 micrograms PO

3 mg needed for complete vagal blockade in adults (hence repeat boluses of 0.5 mg up to 3 mg max)

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6
Q

Pharmacokinetics of Atropine

A

Low bioavailability (10 to 20%)

Crosses placenta and blood brain barrier

Elimination half life 2.5 hours

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7
Q

Atropine mechanism of action

A

Competitive antagonist of acetylcholine at muscarinic receptors

Minimal nicotinic receptor action

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8
Q

CVS effects of atropine

A

Bezold-Jarisch reflex - low dose can initially produce bradycardia

Slows AV node conduction time

Dilation of cutaneous blood vessels at high doses

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9
Q

Respiratory effects of atropine

A

Bronchodilation - increases physiological dead space

Increased RR

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10
Q

CNS effects of atropine

A

Can cause central anticholinergic syndrome

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11
Q

GI and GU effects of atropine

A

Reduces gut motility

Reduces urinary tract tone

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12
Q

Other effects of atropine

A

Mydriasis

Increased intraocular pressure

Reduced ADH secretion

Has local anaesthetic properties

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13
Q

Chemical structure of Glycopyrrolate

A

Charge quaternary amine

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14
Q

Glycopyrrolate dose and route of administration

A

200 - 400 micrograms IV or IM for adults

4 - 10 microgram/kg for paediatrics

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15
Q

Glycopyrrolate mechanism of action

A

Competitive antagonist at peripheral muscarinic receptors

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16
Q

Glycopyrrolate pharmacokinetics

A

Poor bioavailability (5%)

Can cross placenta but NOT blood brain barrier

80% excreted unchanged

Elimination half life 0.6 to 1.1 hours

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17
Q

CVS effects of glycopyrrolate

A

Vagolytic effects last 2 to 3 hours

Tachycardia at high doses

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18
Q

Respiratory effects of glycopyrrolate

A

Bronchodilation - increases physiological dead space

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19
Q

Other effects of glycopyrrolate

A

5x more potent than atropine at drying secretion

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20
Q

Isoprenaline features

A

Mixed Beta 1 and Beta 2 agonist

SVR can drop due to B2 agonism

Usually IV, but can be inhaled or PO

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21
Q

Adrenaline features

A

Low dose has chronotropic beta agonist effects
Increasing dose increases the alpha action

Diastolic BP can fall due to beta 2 vasodilation

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22
Q

Aminophylline features

A

Non specific phosphodiesterase inhibitor - increases intracellular cAMP

Mild chronotropic effects

23
Q

Dopamine features

A

Low dose infusion has beta 1 agonism
Higher doses increase alpha action

Increases atrio-ventricular conduction

24
Q

Glucagon features

A

Glucagon receptors Gs protein coupled
Increase intracellular cAMP

Limited to second or third line management of beta blocker overdose

25
Q

Classification of tachycardia

A

Supraventricular tachycardias

Ventricular tachycardias

26
Q

Supraventricular tachycardia examples

A

Sinus tachycardia
Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia (AVNRT)
AV re-entry tachycardia (AVRT) - e.g. Wolff-Parkinson-White syndrome

Note: An SVT with associated bundle branch block can mimic ventricular tachycardia

27
Q

Ventricular tachycardia examples

A

Monomorphic VT
Polymorphic VT (Torsades de pointes)
VF

28
Q

Vaughan-Williams classification of antiarrhythmics

(Less useful these days as doesn’t account for some more modern agents)

A

Don’t stress about side effects too much

29
Q

Amiodarone mechanism of action

A

Mainly class III action - blocks K+ channels

Partial antagonist of alpha and beta adrenoreceptors

Higher doses can depress Na+ and Ca2+ channels

Slows rate of repolarisation and increases refractory period and phase III

Slows AV node automaticity and conduction

No effect on conduction through bundle of His and ventricles

30
Q

Amiodarone IV dose

A

5 mg/kg IV loading over 1 hour (max 300 mg)
Then 15 mg/kg over 24 hours (usually max 900mg)

31
Q

Amiodarone PO dose

A

200 mg TDS for 1 week
Then 200mg BD for 1 week
Then 200 mg OD

32
Q

Amiodarone pharmacokinetics

A

Bioavailability 50 - 70%

Highly protein bound (>95%)

Elimination half life 4 hours to 52 days

33
Q

Drugs which are potentiated by amiodarone (and why)

A

Can potentiate action of DOACs, digoxin, calcium antagonists and beta blockers as they are displaced from proteins

34
Q

Side effects of chronic amiodarone use

A

Pneumonitis and fibrosis - reversible if stopped early enough

Corneal deposits

Peripheral neuropathy

Thyroid disease

35
Q

Side effects of acute amiodarone use

A

Bradycardia

Hypotension

Prolonged QT interval

36
Q

Adenosine mechanism of action

A

Acts of adenosine (A1) receptors in SA and AV node
Gi protein coupled receptors - cause hyperpolarisation and negative chronotropy

Transient heart block occurs

A2 receptors have anti-inflammatory actions

37
Q

Adenosine onset and offset times

A

Onset 10s

Offset 10 - 20s

38
Q

Contraindication to Adenosine use

A

Asthma - can cause bronchospasm

39
Q

Adenosine dose in adults

A

6 mg, then 12 mg, then 18 mg

IV

40
Q

Adenosine dose in paediatrics

A

0.0375 to 0.25 mg/kg

41
Q

CVS effects of adenosine

A

Increases myocardial blood flow

Can induce AF or flutter as it decreases atrial refractory period

Decreases pulmonary vascular resistance in pulmonary HTN

42
Q

Respiratory effects of adenosine

A

Causes bronchospasm in susceptible people

Increases RR and respiratory depth

43
Q

Other effects of adenosine

A

Can induce neuropathic pain

Chest discomfort

Facial flushing

44
Q

Digoxin mechanism of action

A

Directly blocks Na+/K+ ATPase - increases AV node refractory period

Indirectly increases ACh release - slows conduction and prolongs refractory period

45
Q

Digoxin dose and route of administration

A

10 - 20 microgram/kg loading dose 6 hourly, then maintenance

Usually IV acutely followed by PO maintenance

46
Q

Digoxin target serum levels

A

1 to 2 g/ml therapeutic range

47
Q

Digoxin pharmacokinetics

A

50 - 70% excreted unchanged in urine - some active secretion

Dosing adjustments needed in renal failure

48
Q

Side effects of digoxin

A

GI upset

Muscle weakness

Headache and convulsions

Arrhythmias - heart block, ventricular bigemini

49
Q

Factors which increase risk of digoxin toxicity

A

Low K+
Low Mg2+
High Na+
High Ca2+
Hypoxaemia
Renal failure

Other drug use - amiodarone, verapamil, diazepam

50
Q

Flecainide features

A

Amide local anaesthetic

51
Q

Flecainide mechanism of action

A

Blocks fast sodium channels
Slows depolarisation

52
Q

Flecainide indications

A

Supraventricular and ventricular tachycardias

Supresses ventricular ectopics

53
Q

Flecainide doses and routes of administration

A

2 mg/kg IV bolus followed by infusion

100 to 200 mg PO 12 hourly

Anaesthetic FRCA Primary - eLFH Pharmacology (10 decks)

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