Rapid Review·Cardiovascular

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Cardiovascular Pharmacology

T1Must know

Antiarrhythmic Drugs

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Key takeaways

blocks sodium channels (phase 0, slows conduction).
blocks beta receptors (slows the nodes).
blocks potassium channels (prolongs repolarization and the QT).
blocks nodal calcium channels (slows atrioventricular (AV) conduction).
every one can also cause arrhythmias.
class I drugs bind open sodium channels, so they act more at fast rates (IC more than IA more than IB) and widen the QRS at fast rates.
class III drugs prolong the QT more at slow rates, so the torsades risk is at rest and with bradycardia.
classes IA and III prolong the QT; class IV prolongs the PR at fast rates.
sinus bradycardia, heart block, QT prolongation (torsades risk).
the most common serious effect; cough, fever, dyspnea, infiltrates; stop the drug.
hypothyroidism or hyperthyroidism.
raised transaminases, hepatitis.
corneal microdeposits, optic neuropathy.
blue-gray discoloration, photosensitivity.
peripheral neuropathy.
it raises digoxin (halve the dose) and warfarin levels; monitor thyroid and liver tests, a chest film and pulmonary function at baseline and periodically.
normal heart, flecainide or propafenone; coronary disease, sotalol or dofetilide; heart failure, amiodarone (Atrial Fibrillation).
amiodarone, procainamide or lidocaine.
magnesium, never IA or III.
procainamide or ibutilide, never AV-nodal blockers.
class I (especially IC), a wide QRS at fast rates; classes IA and III, a long QT; classes II and IV, a long PR and sinus slowing; digoxin, a scooped ST segment with a short QT and long PR.

How it's tested

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High-yield images3
Class IA effect on the ventricular action potential: moderate sodium blockade reduces the slope of phase 0, and accompanying potassium blockade prolongs the action potential duration, so repolarization is later than the untreated grey trace. This is what lengthens the QT and creates the torsades risk.
Class IB effect on the ventricular action potential: weak sodium blockade slightly reduces the slope of phase 0, and the action potential duration is shortened relative to the untreated grey trace, repolarizing earlier.
Class IC effect on the ventricular action potential: strong sodium blockade markedly reduces the slope of phase 0, while the action potential duration is essentially unchanged from the untreated grey trace.

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