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Pharm 2 > Antiarrhythmic meds > Flashcards

Antiarrhythmic meds Flashcards

1
Q

Medication or poison?

A

most antiarrhythmics are toxic-> depend on dose and duration

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2
Q

Rules of medication dosing

A

ALWAYS LOOK IT UP- can always give more cant take away

START LOW AND GO SLOW (GO UP IN DOSE TO GET DESIRED EFFECT= TITRATION)

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3
Q

Terminology

A
  1. Arrhythmia- abnormal heart rhythm (rate, rhythm or origin)
  2. Dysrhythmia- abnormal hear rhythm- bad or ill
  3. Arrhythmia=Dyshythmia
    Tachy arrhythmia- rate too fast
    Bradyarrhythmia- rate too slow
  4. Inotropic- modifying muscle contraction= + increase for and - decreases contractility
  5. Chronotropic- modifying heart rate- + increases and - decreases
  6. Dromotropic- modifying the speed or velocity of a conduction impulse thru AV node-> + will increase velocity (norepi or epi- symp), - will slow velocity (acethylcholine- parasym)
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4
Q

Cardiac electrophysiology

A

SA node, AV node, bundle of HIS, RBB, LBB, PF = Nodal cells
Myocardial contractive cells= Myocytes
Extrinsic stimuli= symp and parasymp nervous system
Intrinsic stimuli- AP from unique cells-> AUTOMATICITY
Redundancy is built in

SA node-> AV-> Ventricular pacing

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5
Q

Cardiac Action Potentials

A

Early After depolarizations (EAD) and Delayed After depolarizations (DADs)-> can lead to cardiac arrhythmias

EAD- usually are channels being opened to allow positive charge back in-> preventing normal repolarization

DAD- spontaneous calcium release during phase 4 of repolarization producing new AP too soon

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6
Q

Classes of Antiarrhythmic medications

A

Class 1: Sodium channel blockers
Class 2: anti-sympathetic nervous sys-> Beta Blockers
Class 3: Potassium channel blockers
Class 4: Calcium channel blockers
Class 5: Miscellaneous

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7
Q

management of arrhythmias

A
  1. All antiarrhythmic drugs= potentially PROARRHYTHMIC
  2. in acute setting= ANY UNSTABLE PT= IMMED SYNCH ELECTRICAL CARDIOVERSION OR DEFIB- drugs come after Joules for unstable arrhyth
  3. Know the goal? Shock within certain amount of time or else the stasis blood-> clots -> normal rhythm and stroke out
    RATE CONTROL VS RHYTHM CONTROL
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8
Q

Class 1 antiarrhythmics- Na+ channel blockers

A

depress Phase 0 rate of depolarization-> change effective refractory period ERP of an AP
1. 1a= Moderate Blocking NA channel
2. 1b= Mildly Blocking NA channels
3. 1c= Strong Blocking NA channel

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9
Q

Class 1 antirrhy Class 1A NA channel blocker? rare

A

Quinidine- from chinchona tree bark
*used to tx certain Ventricular arrhythmias
*Proarrhythmic
SE: Chinchonism- Headache, Dizziness, and Tinnitus
RARELY USED

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10
Q

Class 1 antirrhy Class 1A Na channel blockers

A
  1. Quinidine
  2. Procainamide
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11
Q

Class 1 antirrhy Class 1A NA channel blocker? regularly used

A

Procainamide- MOST USED CLASS 1A ANTIARRHY
*can b proarrh
USED TO MANAGE WOLF PARKINSON WHITE- ASSOCIATED TACHYCARDIA
- also for ventr arrhyth, not common

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12
Q

Class 1 antirrhy Class 1B NA channel blocker

A

Lidocaine (2nd line)
-anesthetic
used for Ventr Arrhy -> 2nd line to amiodarone
SE: tinnitus, sluured speech, Circumoral paresthesia, seizure

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13
Q

Class 1 antirrhy Class 1C NA channel blocker

A

Flecainide and Propafenone
- used for RHYTHM CONTROL -> pts w/ SVT and AFIB
- can be maintenance PO or PRN “Pill in Pocket” strategy
ONLY PTS W/PUT STRUCTURAL HEART DISEASE

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14
Q

Class 2 antiarrhy Beta Blockers

A

Block symp nervous sys of beta receptors by norepi/epi
BB-> Heart rate control in tachycardia and Suppression of vent arrh and ectopy (PVC)

BB WILL NOT CONVERT ARRH TO NORMAL SINUS RHYTHM- RATE ONLY
BB FOR STABLE HF BC decrease hr and increase filling time even tho inotropic

Metoprolol (Lopressor)- MC-> Rate control in tachy

SE: HYPOTENSION, BRADYCARDIA (AV BLOCKS), reduced exercise tolerance, sexual dysfunction

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15
Q

Class 3 K channel blocker

A

Amiodarone- MC
-Block efflux of K+ in phase 3 + blocks NA/CA channels, and Beta/alpha receptors
-extends refractory period -> prolongs QTc
USED TO CONVERT AFIB TO NSR OR MAINTAIN NSR IN PTS IN ADN OUT OF AFIB/AFLUTTER

GREAT FOR NEW EARLY ONSET AFIB/FLUTTER LESS THAN 48-72 hrs

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16
Q

Darkside of Amiodarone- class 3 K+

A
  1. Liver, thyroid, and lung toxicity possible
  2. long term use-> monitoring, LFT, Thyroid function, PFT, CXR
  3. drug d/c necessary if toxic
  4. 57-day LONG HALF LIFE
  5. Photosensitivity
  6. SMURFISM- stop drug and return to normal after months
17
Q

Class 4 Calcium Channel blocker

A

Pure vasodilators (dihydropyridines)-> SM relaxation
Others-> slow conduction thru AV node (decrease HR)

CARE ABOUT VERAPAMIL/DILTIAZEM FOR ARRHY- slow conduction

18
Q

Diltiazem (Cardizem)- ccb

A

MC USED CCB FOR ARRHYTH MANAGEMENT
HR control in pts with AFIB/FLUTTER W/ RVR-> SLOWS SA AND AV NODAL CONDUCTION
NOT GOOD FOR HF PTS-> reduce myocardial squeeze-> worsen pumping fxn
SE: hypotension, brady, dizziness, edema, HA, WORSENED CHF

19
Q

Verapamil (Calan)- ccb

A

Not commonly used for antiarrh
Primary- slows HR-> reduce SA/AV node conduction
SE: like diltiazem

20
Q

Class 5 misc antiarr- mc

A

Digoxin-> MC used for Afib, flutter, CHF
from foxglove
AV nodal + Inotropic
1. Competitively blocks NA/K pump-> increased NA in cell= increased CA in cell (inotropy)
2. produces vagal response= reduces AV conduction= Lower heart rate

21
Q

Digoxin toxicity

A

Narrow therapeutic index
SE: NVD, headache, dizziness
Toxicity: confusion, heart blocks, ventricular arrhyth
PT W/ ACUTE ILLNESS-> CHECK SERUM DIGOXIN LEVEL
-WORSEN HYPERKALEMIA BC PUMP BLOCKED

Antidote: Digibind

22
Q

Class 5 misc antiarr- for SVT

A

Adenosine (1ST LINE FOR STABLE)- electricity= 2st line for unstable
Treats Paroxysmal Supra Ventricular Tachy, mc with AV nodal re-entry Tachycardia
MOA: transient AV nodal block to allow the conduction system to reset
.6-10 sec short life
1. rapid IVP followed by push flush via three-way stopcock
MAY GET A PAUSE OF SEVERAL SECONDS AFTER PUSHING DOSE

23
Q

Class 5 misc- brady

A

Atropine
FOR SIGNIFICANT BRADYARRHYTHMIA- LESS THAN 40
ANTICHOLINERGIC=ANTIPARASYMP- blocks acetylcholine
MOA: blocks binding of acetylcholine-> blocks parasymp nervous sys-> speeds up heart rate
SE: dry mouth, dry eyes, constipation, urinary retention, mydriasis

24
Q

REVIEW CASES

A

REVIEW CASES

25
Q

KEY PT SUMMARY

A
  1. all antiarrh drugs can be proarrhythmic
  2. always eval stability, if unstable-> electricity over drugs
  3. drugs are titratable-> dose based pt response-> cant take back can give more
  4. think of goals-> Rate Control vs Rhythm control, suppression/prevention
  5. think of underlying problems that triggered arrhyth-> CHECK AND CORRECT ELECTROLYTES
26
Q

KEY PT SUMMARY

A
  1. all antiarrh drugs can be proarrhythmic
  2. always eval stability, if unstable-> electricity over drugs
  3. drugs are titratable-> dose based pt response-> cant take back can give more
  4. think of goals-> Rate Control vs Rhythm control, suppression/prevention
  5. think of underlying problems that triggered arrhyth-> CHECK AND CORRECT ELECTROLYTES
27
Q

Important antiarrhyth

A
  1. Amiodarone= Vtach/Vfib, AFIB/Flutter
  2. Adenosine (PSVT)
  3. Atropine (Bradycardia)
  4. Lidocaine (2nd line Vtach)
  5. Procainamide (1st line tachy arrh w/ WPW syndrome)
  6. Metoprolol (rate control in AFIB, suppress PVCs/ Suppression of Vent arrhythmia)
  7. Diltiazem ( Rate control AFIB)
  8. Digoxin (rate control in AFIB- improves pump fxn and good in CHF)

Pharm 2 (15 decks)

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