Anti-arrhythmics

Question 1

Atropine Drug and doses

Answer 1

Racemic mixture of D + L hyoscyamine- only L is active
DOse is 0.015-0.02mg/kg IV or IM
0.2-0.6mg PO
3mg is needed for complete vagal blockade in adults

Question 2

Atropine pharmacokinetics

Answer 2

Low bioavailability
Crosses placenta and blood brain barrier
Elimiation half like 2.5hrs

Question 3

Atropine pharacodynamics

Answer 3

COmpetitics antagonist of Ach at muscarinic receptors with little action at nicotinic receptors
CV- initially can actually produce bradycardia, slows AV conduction time, dilates blood vessels at high doses
REsp- bronchodilation, increases physiological dead space, incr. rr
CNS- anticholinergic syndrome
GI- reduces gut motility and urinary tract tone
Other- mydriasis, increased IOP, reduces ADH secreiton

Question 4

What is the bezold jarisch reflex?

Answer 4

cardioinhibitory reflex- bradycardia, vasodilation and hypotension from stimulation of cardiac receptors
Originates from inhbitoy receptors in the LV. Stimulation increases PNS and inhibits sns

Question 5

Glycopyrollate drug and dosing

Answer 5

Charged quaternary amine
Competitice antagonist at peripheral muscarinic receptors
0.2-0.4mgIV or IM
4-10microg paeds

Question 6

Glycopyrrolate pharmacokinetics

Answer 6

Poor oral absorprion (5% bioavailability)
Can cross placenta but not bbb
80% is excreted unchanged
Elimiation half life half an hour to an hour

Question 7

Glycopyrrolate pharmacodynamics

Answer 7

CV- vagolytic effects last 2-3 hours
Resp- bronchodilator, increases dead space
5 x more potent than atropine at drying secretions

Question 8

Other agents used in bradycardia?

Answer 8

Isoprenaline
adrenaline
aminophylline
Dopamine
GLucagon

Question 9

Isoprenaline moa in bradycardia

Answer 9

B1 + B2 agonist
Can causea drop in svr due to b2 action
given IV

Question 10

Adrenaline moa in bradycardia

Answer 10

Low dose has B chronotropic effects, increasing doses increases alpha action

Question 11

Aminophylline bradycardia MOA

Answer 11

Non specific PDE inhibitor, increasing cAMP. Mild chronotropic effects

Question 12

Dopamine MOA in bradycardia

Answer 12

Low dose infusion has B1 action, higher doses increase a action
increases av conduction

Question 13

Glucagon moa in bradycardia ?

Answer 13

receptors are Gs linked and increase cAMP. 2nd/3rd line mx in B Blocker OD

Question 14

Amiodarone drug and doses

Answer 14

Benzofuran derivative
Class 3 action- blocks K+ channels
Partial antagonist of a and b
Higher doses can depress na and ca channels
Slows rate of repolarisation and increases refractory perid- prolonging phase 3
Slows AVN automaticity and conduction
5mg/kg iv over one hour then 15mg/kg over 24 hours
orally- tds for one week then bd then od

Question 15

Amiodarone pharmacokinetics

Answer 15

Bioavailability of 50-70%
Highly protein boud, can potentiate actions of anticoag, dioxin, calcium antagonists and B blockers as they are displaced from proteins
Elimination half life 4 hours to 52 days

Question 16

Amiodarone pharacodynamics

Answer 16

Can cause bradycardia, hypotension and prolonged QT
Can develop pneumonitis and fibrosis
Corneal deposits
PEripheral neuropathy, LFT changes, phtosensitivity
ABdnormal thyroid fx can occur as it resembles thyroid hormone- both hyper and hypo reported

Question 17

Adenosine drug and dosage

Answer 17

Naturally occuring purine nucleoside of adenine and d ribose
Acts on adenosine (a1) receptors in the sa and av node (Gi receptors) causing hyperpolarisation and dramatic negative chronotropy- transient heart block
A2 receptors have anti inflammatory actions
Cytoprotective properties in ischaemia
smooth muscle relaxation in coronary arteries
Dsoe: 3mg/6mg/12mg
Acts within 10s, lasts 10-20

Question 18

Atropine pharmacodynamics

Answer 18

CV- increases myocardial blood flow
Induces AF/flutter as it decreases atrial refractory period
Decreases PVR in pulm htn
Resp- bronchospasm, increases rr+ depth
Other- can induce neuropathic pain. facial flushin. chest discomfort

Question 19

DIgoxin drug and dosage

Answer 19

Glycoside
Directly blocks sodium/potassium/ATPase pump which increases refractory period of AV node and reduces conductivity
Indirectly acts by increasing acetylcholine release which slows conduction and prolongs refractory period
Given orally or IV
10-20 μg/kg as a loading dose 6 hourly then maintenance
Serum levels need monitoring initially (1-2 g/ml therapeutic)

Question 20

Digoxin pharmacokinetics

Answer 20

50-70% excreted unchanged in urine, involving some active secretion
Dosing needs to be altered in renal failure

Question 21

Digoxin pharmacodynamics

Answer 21

Digoxin side-effects are common due to the narrow therapeutic window
Gastrointestinal disturbance common including abdominal pain and nausea
Muscle weakens, headache and drowsiness can occur
Arrhythmias including heart block and ventricular bigemini
The risk of toxicity is increased in the presence of:

Hypokalaemia
Hypomagnesaemia
Hypernatraemia
Hypercalcaemia
Hypoxaemia
Renal failure
Other drugs including amiodarone, verapamil and diazepam

Question 22

Magnesium indications?

Answer 22

Torsades, AF

Question 23

MAgnesium drug and dose

Answer 23

2-5g IV depending on indication and levels

Question 24

B blockers indications in tachycardia ?

Answer 24

Supraventricular arrhythmias

Question 25

Calcium channel blockers indications in tachycardia

Answer 25

Supraventricular arrhythmias

Question 26

Common calcium channel blockers used in tachycardias?

Answer 26

DIltazemn (30-120mg 6-8hrly) and verapamil (240-480mg in 2-3 doses)

Question 27

Flecainide indication and doses

Answer 27

Used for all tachycardias, suppresses ventricular ectopics
Amide local anaesthetic- blocks fast na channels and slows depolarisation
100-200mg 12 hrly (can be given IV)