Antidysrhythmic Drugs Flashcards
Response of cells to excitatory electrical stimuli is a function of what?
Available Na channels
What is the normal sinus rhythm?
60-90bpm
How do flutter and fibrillation differ?
Flutter: very rapid but regular contractions Fibrillation: disorganized contractile activity
How many phases are in a heart contraction and what generally happens in each?
Phase 0: Fast upstroke (Na channels open) Phase 1: Partial repolarization Phase 2: Plateau Phase 3: Repolarization Phase 4: Forward current
Two general mechanisms of arrhythmias? Which is more common?
- Abnormal impulse generation 2. Abnormal impulse conduction (more common)
Two ways to get abnormal impulse generation?
- Abnormal automaticity of normally automatic cells (SA, AV, His) 2. Generation of impulses in normally non-automatic cells
Two ways to get abnormal impulse conduction? More common?
- AV block: ventricle free to start own pacemaker rhythm 2. Re-entry: re-excitation around a conducting loop, producing tachycardia (more common)
What type of drug and how do quinines work (3)?
Class IA: 1. Moderate block of Na+ channels 2. Decrease automaticity of pacemaker cells 3. Increase effective refractory period/AP duration
In what state is abnormal heart tissue typically found and what three things does this cause?
Usually depolarized, reducing Na current, decrease dV/Dt and and decreases conduction velocity
How do antiarrhythmic drugs generally function?
Decrease # of functional Na channels, and recovery time of Na channels determines refractory period (thus RP is increased)
How do specific ion channels open/close in each phase? Which class affects which phase?
Phase 0: Na+ channels Open (I) Phase 1: Na+ closed, K+ open Phase 2: Ca2+ open, K+ open (leaky) (IV) Phase 3: Ca2+ close, K+ open, Na/K ATPase (III) Phase 4: Inc in Na+ permeability (IV)
What part of the heart has the steepest Phase 4? What does this infer?
SA then AV node; spontaneous repolarization
What are three general strategies of antidysrhythmic drugs?
- Decrease automaticity 2. Decrease conduction velocity 3. Increase refractory period
Which two drugs increase the QT?
Classes IA and III
T/F. All drug classes discussed will slow conduction.
T.
How do the subtypes of Class I differ with regards to the Action Potential Duration (APD)?
IA: Inc APD, IB: Dec APD, IC: No change in APD
How are quinidine and procainamide similar?
Class IA, Dec CV and Inc Qt/APD; S: blocks M- and alpha-adrenocreceptors (dec TPR), diarrhea, nausea, cardiac dep.
How do quinidine and procainamide differ (including side effects)?
Tx: Q=Atrial arrhythmias, SVT (chronic) and P=Ventric arrhyth and NAPA (acute) S: Q=tinnitus w/ CG and P=Lupus
What is NAPA?
N-acetylprocainamide and is procainamide’s metabolite with Class III Activity
What are the classes of drugs and what do they each generally do?
I: Na-Channel blocker II: Beta blockers (suppress phase 4 depol) III: K+ channel blocker (prolong repolar/RP) IV: CCB: slow conduction and inc RP and Ca-dependent slow responses
What does lidocaine do, where effect, how administered?
Class IB, VT/VF, IV/IM
What drug is an arrhythmia and oral anticonvulsant? What is its main side effect? CI?
Phenytoin; gingival hyperplasia; pregnancy