4 Antiarrhythmic and Anti-Anginal Drugs

Question 1

antiarrhythmic drug MOA

Answer 1

• decrease ectopic pacemaker activity

- decrease conduction/excitability, increase refractory period

Question 2

4 classes of antiarrhythmic drugs

Answer 2

• Na* channel blockers
• b adrenoceptor blockers
• K+ channel blockers
• Ca2+ channel blockers

Question 3

class 1 Na+ channel blocker (eg. quinidine sulphate) MOA, use, toxicity

Answer 3

• blocks open Na+ channels, recovery slower in depolarized cells, decreases excitability and conduction in depolarized tissue
• for atrial and ventricular arrhythmias
• tox - arrhythmias because of SA/AV block

Question 4

class 1 Na+ channel blocker (eg. lidocaine) MOA, use, toxicity

Answer 4

• blocks Na+ channels in depolarize cells, little effect on SA/AV nodes so normal HR
• emergency IV use in ventricular arrhythmias, no oral bioavailability
• tox - CNS drowsiness, confusion, tremor, convulsions

Question 5

class 2 b adrenoceptor blocker (eg. non-selective prorpanolol, b1 selective metoprolol) MOA, use, toxicity

Answer 5

• decrease SNS inputs to heart –> decrease SA rate and AV conduction
• for atrial fib, supraventricular tachyarrhythias, decrease death do to arrhythmia following MI
• tox - not for px with slow AV conduction or decompensating heart disease, metoprolol decreases risk of bronchospasm

Question 6

class 3 K+ channel blockers/prolong AP (eg. amiodarone) MOA, use, toxicity

Answer 6

• blocks K+ channels –> slows repolarization –> increases refractory period/AP duration, decreases tachyarrhythmias/abnormal automaticity
• for supraventricular and ventricular tachyarrhythmias
• tox - pulmonary fibrosis, GI upset, tremor, ataxia

Question 7

class 4 Ca2+ channel blockers (eg. verpamil and diltiazem) MOA, use, toxicity

Answer 7

• binds to open depolarized Ca2+ channels –> decreases Ca2+ influx in cardiac cells –> decreases intracellular Ca2+ –> decreases contraction
• also decreases Sa node impulses/AV conduction
• for supraventricular tachyarrhythmias, decrease ventricular rate in atrial flutter/fibrillation
• tox - decrease rate/contractility (not for px with decreased cardiac function), hypotension

Question 8

organization of drugs used to treat angina

Answer 8

• vasodilators
• • nitrates
• • calcium channel blockers
• cardiac depressants
• • calcium channel blockers
• • b blockers

Question 9

nitrates pharmacokinetics, MOA, effects, tolerance, toxicity

Answer 9

• sublingual preferred, liver removes nitrate groups
• increase [NO] in smooth muscles –> relaxation and vasodilation
• decrease preload –> decrease cardiac size
• decrease afterload –> decrease PVR and BP
• overall, decrease O2 requirement
• tolerance - continuous exposure –> decreased effectiveness
• tox - due to vasodilation, reflex tachycardia, positional hypotension, throbbing headache

Question 10

sildenafil (Viagra) MOA, pharmacokinetics, toxicity, interactions

Answer 10

inhibits PDE-5 –> increase [cGMP] –> increase blood flow into corpus cavernosum

• oral, Tadalafil = weekend pill
• tox - mild, headache, flushing, nasal congestion
• potentiate nitrates for angina –> severe hypotension
• effects on colour vision (blue-green discrimination)