Antidysrhythmics & Antihyperlipidemics Flashcards

1
Q

(Na)sty (B)oys (K)iss (Ca)ts

A

Class I - IV

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2
Q

principles of antidysrhythmic drug therapy

A
  • maintain normal sinus rhythm
  • choose based on: cause, side effects tolerable, other heart conditions
  • renal/hepatic function
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3
Q

How do you watch for toxicity levels with antidysrhythmics?

A

initiate therapy at low doses and titrate up

FOLLOW AND TRACK VERY CAREFULLY

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4
Q

Class I - Na Channel Blockers: how they work

A
  • suppress automaticity
  • decrease likelihood of ectopy
  • prolong QT interval (everything after Na sloooooooows doooowwwwwwwn)

BEWARE: increased refractory period means possible jolt into electrical chaos (Torsades or V Tach)

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5
Q

significant adverse effect of Class I (Na)

A

Increased QT therefore increased refractory period means possible random jolt into electrical chaos (Torsades or V Tach)

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6
Q

subclasses of Na channel blockers

A

IA: Quinidine, Procainamide
IB: Lidocaine, Mexiletine
IC: Flecainide, Propafenone

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7
Q

Class I indications

A

Atrial dysrhythmias: a fib, a flutter, SVT

Ventricular dysrhythmias: PVC, VT (IV ONLY), VF (URGENT)

– not used very much, but can be used in emergent situations or when patient is resistant to more conservative therapies –

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8
Q

supraventricular tachycardia

A

HR > 100, usually > 150

originates above the ventricular electrical conduction system

USE: Class I - Na channel blocker

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9
Q

Class I side effects

A
  • hypotension
  • bradycardia
  • arrhythmias
  • cardiac arrest
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10
Q

Class II - Beta Blockers: how they work

A

CARDIAC SPECIFIC BETA

decrease conduction velocity
decrease automaticity
prolongs refractory period

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11
Q

Class II - Beta Blockers: examples

A

Brevibloc (esmolol)
Inderal (propanolol) – anxiety too
Betapace (sotalol)

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12
Q

Class II indications

A

Atrial: a fib, a flutter, atrial tach

Ventricular: PVC (slow down automaticity), VT (NOT EMERGENT - only sustained VT is lethal)

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13
Q

Class II side effects

A

** bradycardia **
bronchospasms
hypotension

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14
Q

why are class II not used for emergent situations?

A

Snape’s guess: slow MOA

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15
Q

Class III - Potassium Channel Blockers: how they work

A
  • diminishes K movement during repolarization
  • prolongs refractory period
  • decrease automaticity
  • increases PR interval
  • widens QRS complex
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16
Q

Class III - K blockers: examples

A

Cordarone (amiodarone) —- USED MORE, huge side effect profile

Adenocard (adenosine) – specific, emergent situations

17
Q

Class III indications

A

atrial: a fib, a flutter, SVT
ventricular: VT, VF

18
Q

amiodarone half life

A

VERY LONG (50-70 days)

19
Q

amiodarone: use and adverse effects

A
  • use cautiously (toxicities!)
  • AE to: liver, thyroid, lungs, skin, eyes, bradycardia (THINK: half life is loooong so that is bad)

BELTTS

THE SMURF DRUG! (blue hints to the face)

20
Q

amiodarone: client education

A
  • take with food
  • photosensitivity, photophobia
  • regular eye exams (deposits!!!)
  • NOTIFY PROVIDER: dyspnea/cough
21
Q

Class IV - Ca channel blockers: how they work

A
  • blocks slow Ca influx (decreases myocardium excitability and contractility)
  • decrease contractility/HR
  • decrease conduction velocity
  • decrease aberrant pacemaker sites
  • prolong repolarization, esp AV node
22
Q

Class IV examples

A

cardizem (diltiazem) – negative inotrope

calan (verapamil) – non-dihydropyridine

23
Q

Class IV indications

A

atrial: a fib, a flutter – ONE OF THE FIRST DRUGS WE GO TO – and SVT

24
Q

Class IV is one of the drugs we go to for…

A

a fib or a flutter

25
Q

Class IV adverse effects

A

vasodilatory effects!!

  • flushed skin
  • headache
  • dizziness (orthostatic)
  • hypotension
26
Q

Class: “Other” example & what it’s used for

A

Digoxin (also HF, remember) - a fib, a flutter

paroxysmal a fib and atrial tachycardia