CVS drugs - Anti-arrhythmics, diuretics and anti-fat Flashcards
What four types of drugs are in the vaughn williams classification?
Na+ channel blockers
B-blockers
K+ channel blockers
Ca2+ channel blockers
What are the three mechanisms of action of Na+ channel blockers?
Decrease conduction velocity
Increase depolarisation threshold
Decrease automacity
Why would you use fleicanide?
Atrial Fib
Give two CIs for Flecainide
Heart failure (make it worse at beating) History of MI (can worsen arrhythmias)
What is the mechanism of action of felcainide?
Block fast, inward Na+ channels
Give three ADRs for flecanide
Dizziness, visual disturbances, arrhythmias
What could effect metabolism of flecainide?
GO-DEVICES
Grapefruit juice, omeprazole
When would you use lidocaine?
Ventricular arrhytmia following MI
What is the mech of action for lidocaine?
Blocks fast, inward Na+ channels
Give three adverse drug reactions for lidocaine
Hypotension, bradycardia (Negative inotrope)
Nystagmus (brain)
Seizures (Brain)
What do beta blockers do to ventricular action potential?
Shift to right
Give four indications for beta blockers
Angina
Post myocardial infarctioin
Hypertension
Arrhytmias
How do beta blockers work as anti-arrhytmics?
Antagonise β-adrenoreceptors. β1-receptors are found in the heart, when they are activated they cause increased Chronotropy and Inotropy.
Inhibit renin release
Give some of the 6 ADRs of beta blockers?
Bronchospasm Fatigue and insomnia Hypotension Bradycardia Decreased glucose tolerance - Don't feel adrenaline from hypoglycaemia due to B blockers
Give two significant DDIs of beta blockers
Prevents Salbutamol working (β2-adrenoagonist)
Verapamil – Both have –‘ve inotropic action
How do potassium channel blockers work?
Block potassium channels which -
Increases absolute refractory period
Increased AP duration
Suprress re-entry circuits by closing excitable gap
What is torsades de pointes
Ventricular tachycardia which can result in death
Why must you be careful using amiodarone in a patient on warfarin?
Amiodarione inhibits cyp450 which requires dose reduction of everything else which undergoes liver metabolism
How do calcium channel blockers work?
Decrease slop of pacemaker aciton potential at SA node and AV node - Dependent on Ca2+ influx and efflux!
This increaes refractory period, chronotrophy and inotropy
When should calcium channel blockers not be used?
Heart failure
Bradycardia
AV node block
What are four ADRs of calcium channel blockers?
Hypotension
Bradycardia
Heart failure
Heart block
What does adenosine effect?
AV node blocker
When is digoxin used?
Atrial fib
Heart failure
Give the mechanism of action and effects of digoxin
o Inhibits Na/K-ATPase o Direct Cardiac Effects Increased Inotrope – Used in heart failure, no mortality benefit o CNS Effects Decreased Sympathetic outflow Increased Parasympathetic outflow Sensitises baroreceptor reflex o Combined Effects Automaticity of SAN and AVN AVN refractory period Conduction velocity of AVN
Why is digoxin dangerous?
Narrow therapeutic index
What three things happen in digoxin toxicity?
bradycardia, AVN block, atrial tachycardia
What amplifies toxicity of digoxin?
Hypokalaemia
What increases digoxin levels in blood?
Quinidine, amiodarone, verapamil, spironolactone
What increases effect of digoxin in blood already?
Beta blockers (both decrease AV node conduction)
Verapamil (both decrease cardiac contractility)
Loop and thiazide diuretic (both cause hypokalaemia)
How must digoxin be given?
Two separate doses to minimise toxicity risk
