class 1a antiarrythmics Flashcards

1
Q

function of class 1

A

block na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

class 1a intermediate dissociation, efffects, and drugs

A
  • moderate na ch. inhibition slows upstroke
  • inhibit k ch -> prolonging repol.
  • slowing conduction + widened QRS
  • prolongs effective refractory period + ADP
  • quinidine, procainamide, disopyramide,prajmaline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

quinidine use, examples, indication, adverse effects

A

action: M blocker -< increase HR + av conduction, alpha block -> vasodilation w/ reflex tachycardia
pk: miduim dissociation from na ch, interaction w/ digoxin + hyperkalemia
indication: supraventricular arrythmia, afib
ae: - ionotripic, proarrythmogenic, inhibits vagal effects, sycope, VT, Vfib, torsades,
extracardiac: nausea, vomiting, hepatits, CINCHONISM, thrombocytopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

procainamide use, examples, indication, adverse effects

A

action: M block -> increase HR + av conduction, hapten - > hypersen. rxn
indication: SV arrythmia -> afib, wpw syndrome
ae: hypotension, LUPUS LIKE SYPMTOMS, HYPERSENSISTIVTY RXN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

dysopyramide use, examples, indication, adverse effects

A

M block-> increase HR + av conduction

indication: SV arrythmia, life threatning atrial/ ventricular arrythmia, HCM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

prajmaline

A

class 1a na ch blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

1B fast dissociation, effects and drugs

A

effects: low inhibition of na ch -> slow depol upstroke, shorten repol -> decrease duration of AP
0 effects on conduction + QRS
block inactive na ch: slow conduction in hypoxic + ischemic states, block slow Na window curret - > decreasing ADP
drugs: lidocain, mexiletine + tocainide, phenytoin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

lidocaine use, examples, indication, adverse effects

A

PK: IV infusion, quickly metabolized in liver 1st pass, EZ inducer decrease half life, bb, cyp3q4 inhibitors, decreases metabolism
indications: Vent. arrythmia *before cardioversion, heart surgery, digitalis intoxification)
Ae: nuerological paresthesia, tremor, hearing problems, convulsions
CI: ATRIAL ARRYTHMIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

mexiletine + tocainide

A

pk: oral
i: vent. arrythmias = chronic
ae: proarrythmogenic, BM supression, neurological problems, convulsions, liver, kidney toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

phenytoin

A

admin: i.v
i: vent arrythmia induced by digitalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

1C slow dissociation effects and drugs

A

strong Na channel inhibition -> slow depol.
minimal inhibition of k ch (herg) -> minimal increase of repol
drugs: flecainide, propafenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

flecainide use, examples, indication, adverse effects

A

action: weak B receptor blockade
pk: medium dissociation of na ch
admin oral
i: afib, aflutter, SVT, refractory ventricular arrythmia
ae: - ionotropic effect, VERY PROARRYTHMOGENIC RARELY USED!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

propafenone

A

pk: slow dissociation of Na ch, admin oral Iv
i: SV arrythmia + ventricular arrythmia (not recommended)
ae: bradycardia, impulse conduction disturbance,neurological effects ,PROARRYTHMOGENIC, METALLIC TASE, BRONCHOSPASM (due to non selective beta blocking action)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly