antiarrythmic drugs Flashcards
What is the ion responsible for Phase 0 upstroke in cardiac muscle cells?
Na+ influx via fast voltage-gated sodium channels.
What is the ion responsible for Phase 0 upstroke in nodal cells?
Ca2+ influx via L-type calcium channels.
Why are calcium channel blockers more effective on nodal cells?
Because nodal cells rely on Ca2+ for depolarization and lack fast Na+ channels.
What ion contributes to repolarization (Phase 3) in both cardiac and nodal cells?
K+ efflux.
Why is Phase 3 repolarization important in antiarrhythmic therapy?
It is targeted by Class III drugs like amiodarone to prolong the action potential and refractory period.
What shape differences exist between cardiac muscle and nodal cell action potentials?
Cardiac muscle has a plateau phase, nodal cells have a gradual depolarization or pacemaker potential.
What are the main drug classes in the Vaughan-Williams classification?
Class 1: Na+ channel blockers, Class 2: Beta blockers, Class 3: K+ channel blockers, Class 4: Ca2+ channel blockers, Unclassified: Adenosine, Magnesium, Digoxin.
How do Class 1 antiarrhythmics affect the action potential?
They delay Phase 0, leading to a slower effective refractory period and a shift in the ERP profile.
What is a key representative drug in Class 1A antiarrhythmics?
Quinidine.
What are some of the pharmacologic effects of Quinidine?
It is antimuscarinic, increases heart rate, causes alpha blockade, and may cause reflex tachycardia.
Why is Quinidine often taken with digoxin?
To counteract Quinidine’s potential to increase heart rate.
What are some side effects of Quinidine?
Constipation, diarrhea, ocular disturbances, CNS excitation (tinnitus), and torsades de pointes.
What ECG changes are associated with Quinidine toxicity?
Prolonged QRS complex, loss of P and T waves, appearance of massive peaks.
How do Class 1A drugs affect sodium channels?
They block fast Na+ channels in the active state, preventing return to resting/closed state, reducing action potentials.
