Antiarrhythmics Flashcards

(37 cards)

1
Q

Phase 0 of action potential

A
  • rapid depolarization
  • Na channels open, increased Na+
  • ventricular contraction
  • inactive when +65 mV
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2
Q

Phase 1 action potential

A
  • early rapid repolarization
  • Na permeability is inactivated
  • K+ channels open (K efflux)
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3
Q

Phase 2 of action potential

A
  • plateau phase
  • repolarization, increase in Ca++ through slow channels
  • K channels open and maintain plateau
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4
Q

Phase 3 of action potential

A
  • rapid repolarization
  • inactivation of Ca and increase in K permeability
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5
Q

Phase 4 of action potential

A
  • spontaneous depolarization
  • ion balance restored by ATP pumps
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6
Q

what channels do antiarrhythmic drugs work on for atria and ventricles?

A
  • Na channels
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7
Q

what channels do antiarrhythmic drugs work on for SA and AV node?

A

Ca++ channels

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8
Q

what do Na channel blockers do and what type are they?

A
  • slow the conduction and prolong the QRS complexes in the atria and ventricles
  • type 1
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9
Q

what do Ca++ channel blockers do and what type are they

A
  • slow the atrial rate (SA node effect) and slow conduction through the AV node (prolong the PR interval)
  • type IV
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10
Q

what do K channel blockers do and what type are they?

A
  • interrupt reentry by slowing conduction or increasing the refractory period
  • prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT
  • type III
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11
Q

class 1 antiarrhythmics inhibit what channels and phase

A
  • inhibits fast Na channels
  • affect phase 0
  • decreases depolarization rate and conduction velocity
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12
Q

class 1A antiarrhythmic drugs

A
  • quinidine
  • procainamide
  • disopyramide
  • moricizone
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13
Q

class 1B antiarrhythmic drugs

A
  • lidocaine
  • mexilitine
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14
Q

class 1C antiarrhythmics drugs

A
  • flecainide
  • propafenone
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15
Q

class II antiarrhythmics and what they do

A
  • decrease the rate of depolarization
  • beta blockers
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16
Q

class III antiarrhythmics inhibit what channels

17
Q

class III antiarrhythmics (drugs)

A
  • amiodarone
  • sotalol
  • ibutilide
  • dofetilide
  • bretylium
18
Q

class IV antiarrhythmics affect what channels

A
  • inhibit slow Ca channels
19
Q

class IV antiarrhythmics (drugs)

A
  • diltiazem
  • verapamil
20
Q

action of class 1A drugs

A
  • lengthen the action potential duration and effective refractory period and lengthen repolarization
21
Q

action of class 1B drugs

A
  • less powerful Na channel blockers
  • shorten the action potential duration and refractory period in normal cardiac ventricular muscle
22
Q

class 1C action

A
  • Na channel blockers
  • decrease the rate of phase 0 and speeds cardiac conduction
  • shortens DOA of action potentials in purkinje fibers but ventricular myocardial cells
23
Q

class II beta blockers action

A
  • decrease rate of phase 4
  • slow HR
  • slows conduction if impulses through atria (prolong P-R)
24
Q

class III action

A
  • block K+
  • prolong repolarization
25
class IV
- calcium channel blockers - inhibit slow Ca++ currents - verapamil, diltiazem
26
procainamide
- Na and K blocker - depresses automaticity by decreasing phase 0 - for ventricular tachydysrhythmias and atrial tachycardia
27
procainamide toxicity signs and symptoms
- myocardial depression - hypotension - QRS and QT prolongation - heart block - SLE like symptoms with chronic admin
28
metabolite of procainamide
- N-acetyl procainamide (NAPA)
29
quinidine
- class 1A - increase threshold for excitability - for a-flutter, a-fib, v-tach, v-fib
30
quinidine toxicity
- QT prolongation - v-tach - loose stools - thrombocytopenia - cinchonism
31
disopyramide
- class 1A - for atrial tach and ventricular tachyarrhythmias - known to cause cardiac arrest
32
lidocaine
- Na channel blocker, decrease phase 0 - for ventricular arrythmias, particularly reentry - ineffective against SVT - almost no effect on QT
33
early signs of lidocaine toxicity
- nystagmus - speech changes (CNS depression to seizures)
34
phenytoin
- Na channel blocker, depress phase 0 - useful in suppression of ventricular associated with digitalis toxicity - useful in v-tach or torsades (prolonged QT)
35
phenytoin toxicity
- rapid admin associated with respiratory arrest, hypotension, ectopy, and death - CNS: drowsiness, nystagmus, nausea, vertigo
36
flecainide (1C)
- blocks Na, K, Ca - depresses phase 0 - prolongs QRS less than PR - indicated for suppressing PVCs and atrial tachydysrhythmias including WPW - moderate inotrope (no CAD, LV failure, v-tach)
37
beta blockers
- slow S-A node (phase 4) - control SVT - toxicity can cause bronchospasm