exam 2: lecture 4 Flashcards
Explain the cardiac AP .
phase 0 - NA channel open up, goes into and starts depolarizing the cell
phase 1 = K channels open up and goes out of the cell starts repolarizaing
phase 2: pleatue phase. L TYPE. Ca channels open and goes inside the cell
phase 3: Ca channels close and K remain open
phase 4 = goes back to resting potential and restarts at -65mV
what is the diff between enhanced automaticity and triggers automatciity?
enhanced auto = is when there is increased rate of spontaouse discharge starting at the SA node
triggered auto = electrocyte distubrances, early depolarization or delayed depolarization
what are the four classes Myles Von William made?
Class 1 - Na blocker
2- BB
3 - K blockers
4 - CCB
what are the drugs part to Na channel blockers?
Class 1A: (PQN) procainamide, quininide, disopyramide
Class 1B: lidocaine, mexliletide
Class 1C; flecanide
how did sodium channel blokcers come about?
it all started with cocaine. Cocaine blocks sodium channels in the neurons. cocaine were used as anestheics but was too strong.
it was changed to procaine then to lidociane which had better success
what is the MOA, indication and S/E for procainamide?
given PO IV IM
MOA: blocks NA channel in the cardiac myocyte = depressing effect of SA/AV node
- prolongs AP and RP
- blocks some K channels
- prolongs QRS and QT intervals
indication: 2-3rd agent for MI induced arrthymias
S/E: excesive slowing of Heart, prolong QT so torsade, fainting and lupus like syndrome if given PO
what are quinidine and disopyramide?
they are part of CLASS 1A drugs,
quinidine = similiar to procainamide but is anti malaria. it has anti muscarinic effect (dry mouth, consitpation, urinary retention)
dispyramide = similiar to procainamide but even way worse
what are the class 1B drugs ?
lidocaine
mexiletine
what is the MOA, indication, S/E for lidocaine?
MOA:
1. blocks NA channels in both active and inacttive channels
2. bascially just takes neruon out of commison
3. shorterns AP and shortens RP
4. WORKS BEST W ISCHEMIC HEART AND FAST HR
indication: MI with induced arrthymias, Vtach/Vfib, CV
S/E - THE LEAST CARDIOTOXICITY
- AMS, parethesia, psychosis, euphoria , stupor
what is mexiletine?
part of the class 1B Na blocker drugs
it is similiar to lidocaine but given PO
good for long term tx and for chronic pain syndrome
what is flecainide? MOA/indication?
part of class 1C of NA blocker
it works w NORMAL tissue w NORMAL HR
MOA: blocks NA channels and some K channels, decreases slope of phase 0, NO CHANGES TO AP OR RP, prolong QRS
indication: supraventricualr arrhythmias, PVC
what is BB MOA?
B1 normally casues influx of CA and NA which leads to + chronotropic and inotropic effect
but BB will block this and decrease CA influx so decrease contract
BEST for ishemica heart bc it lowers demand for O2 and work
IT SLOWS AV CONDUCTION
what are the BB drugs in CLASS 2?
propranolol - 1st gen drug, if given in high dose can mimik class 1 drugs - block NA
sotalol - verstailie drug, to go BB
metoprolol - 2nd gen drug
esmolol - short half life 8 mins
what is the indication of BB?
sinus tachy
Afib/aflutter
ventricular tachy
long QT syndrome
re entry circut
what are the class 3 drugs?
K blocker drugs
- K-ADDI-
amiodarone
dronedarone
dofetilide
ibutilde
what is the MOA of amiodarone?
Amiodarone is liek a thyroid hormkone so it interacts w thyroid hormone receptor in the cardiac myocyte
it blocks EVERYTHING!!
it blocks K channel WHICH prolongs AP and RP
- andrenergic channels,
- NA channels
- Ca channels
what is the indication and pharmacokinetics for amiodarone?
indication: 1st in line for Vtachy/Vfib
- it also does rate control for Afib (slowing conduction through AV node)
- given IV or PO (long term)
- metabolzied by CYP3A4
- 3-6 months half life HAS A WIDE VOLUME OF DISTRUBUTION
what are the S/E for class 3 drugs?
- bradycardia
- skin and corneal discoloration but no visual impartment
- GI: N/V
- Hyper/hypothyroidism = since amiodarone is like a thyroid hormone, it will bind to the thyroid hormone receptor OR it can inhibit thyroid uptake of iodine
-
pulmonary fibrosis = the drug can accumulate O2 radically coupled
- “ground glass” w pul infiltrates = pneuomonittis
what are dronedarone, dofetilide, ibutitlide ?
they are class 3 K blocker drugs
dronedarone is an analog of amiodarone BUT NO IDOINE OR NO THYROID EFFECT, DECREASE PUL TOXICITY
dofetilide / ibutilide = same class but not often used
what is the MOA for class 4 CCB?
non dihydro (V and D) will block L type Ca channels on the SA and AV nodes
- OVERALL: slows AP, increases RP, prolong repolarization of AV node also increase PR interval
whats the indication and S/E for class 4 drugs?
indication: reentry rhythms, supraventricualr tachycarida, Afib, Aflutter
DONT GIVE IN VENTRICUALR ARRYHTMIAS due to poor CO
S/E = bradycarida SINCE were slowing heart
what is the class, MOA, and indication for adenosine?
adenosine is part of the CLASS 1E
MOA: it works on adenosine receptor GPCR linked to Gi protein, it OPENS K, increases hyperpolarization which SLOWS AP DURATION and decrease HR
= it also decreases CA in the heart
NET EFFECT: prolong RP, prolong PT interval, slow AV conduction, reduce Ca
indication: supraventircualr and reentry since we are SLOWING conduction throuhg AV NODEw
what is the MOA, class and pharmokinetics for ivabradine ?
ivabraidine is given PO
MOA = it blocks the Na funny channels in the SA node so it dramitcally decreases firing of SA NODE, which reduced HR
no change in ionotropic of the heart!!!
metabolized by CYP3A4
CLASS 0
what is the indication and s/e for ivabradine?
class 0 drug
indication: Heart failure (you are not affecting the contraction but slowing the heart down/less O2 needed which is good for HF)
S/E: bradycardia!, visual disturbances, aFIB, HTN
