Antiarrhythmic meds Flashcards
Medication or poison?
most antiarrhythmics are toxic-> depend on dose and duration
Rules of medication dosing
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)
Terminology
- Arrhythmia- abnormal heart rhythm (rate, rhythm or origin)
- Dysrhythmia- abnormal hear rhythm- bad or ill
- Arrhythmia=Dyshythmia
Tachy arrhythmia- rate too fast
Bradyarrhythmia- rate too slow - Inotropic- modifying muscle contraction= + increase for and - decreases contractility
- Chronotropic- modifying heart rate- + increases and - decreases
- 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)
Cardiac electrophysiology
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
Cardiac Action Potentials
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
Classes of Antiarrhythmic medications
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
management of arrhythmias
- All antiarrhythmic drugs= potentially PROARRHYTHMIC
- in acute setting= ANY UNSTABLE PT= IMMED SYNCH ELECTRICAL CARDIOVERSION OR DEFIB- drugs come after Joules for unstable arrhyth
- 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
Class 1 antiarrhythmics- Na+ channel blockers
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
Class 1 antirrhy Class 1A NA channel blocker? rare
Quinidine- from chinchona tree bark
*used to tx certain Ventricular arrhythmias
*Proarrhythmic
SE: Chinchonism- Headache, Dizziness, and Tinnitus
RARELY USED
Class 1 antirrhy Class 1A Na channel blockers
- Quinidine
- Procainamide
Class 1 antirrhy Class 1A NA channel blocker? regularly used
Procainamide- MOST USED CLASS 1A ANTIARRHY
*can b proarrh
USED TO MANAGE WOLF PARKINSON WHITE- ASSOCIATED TACHYCARDIA
- also for ventr arrhyth, not common
Class 1 antirrhy Class 1B NA channel blocker
Lidocaine (2nd line)
-anesthetic
used for Ventr Arrhy -> 2nd line to amiodarone
SE: tinnitus, sluured speech, Circumoral paresthesia, seizure
Class 1 antirrhy Class 1C NA channel blocker
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
Class 2 antiarrhy Beta Blockers
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
Class 3 K channel blocker
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
Darkside of Amiodarone- class 3 K+
- Liver, thyroid, and lung toxicity possible
- long term use-> monitoring, LFT, Thyroid function, PFT, CXR
- drug d/c necessary if toxic
- 57-day LONG HALF LIFE
- Photosensitivity
- SMURFISM- stop drug and return to normal after months
Class 4 Calcium Channel blocker
Pure vasodilators (dihydropyridines)-> SM relaxation
Others-> slow conduction thru AV node (decrease HR)
CARE ABOUT VERAPAMIL/DILTIAZEM FOR ARRHY- slow conduction
Diltiazem (Cardizem)- ccb
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
Verapamil (Calan)- ccb
Not commonly used for antiarrh
Primary- slows HR-> reduce SA/AV node conduction
SE: like diltiazem
Class 5 misc antiarr- mc
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
Digoxin toxicity
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
Class 5 misc antiarr- for SVT
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
Class 5 misc- brady
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
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