anti arrhythmic Flashcards
two gradients that influence energy requiring pumps
130-140 Na (high outside)
3.5-5 K
gradient
also creates electrical differential
two types of gates in the sodium channel
activation M
and inactivation h
inactivation contributes to the early repolorization of phase 1
inactivation gate is closed at what resting potential
-75– -55
but the activation gates are opened
this is important because during the activation
which nodes are more Ca dependent
SA and AV
more Ca dependent because of funny channel
no the non-dihydropyridine work here
(CLASS IV)
CLASS I arrhythmicss are
Na channel blockers
characterized by their ability to block these entry potins into the cell during depolarization
and decrease the rise of phase 0
no phase 1 or 2 in what AP
OF the pacemaker cells
how do cardiac muscle cells differ
resting membrane potential is at -90 due to constant leak of K
Na rushese in causing rapid depolarization
then K channels open (voltage gated)
leading to small dip that is phase 1
positive K ions leave and Ca go in
cause plateau of phase 2
then rapid depolarization of phase 3 of K leaving
abnormal automaticity
increased permeability to Na in phase 4
triggered activity
normal leakage of Ca ions that causes after dopolorization
and
rentry
This class of drugs slow the rate of rise of phase 0 and prolong the effective refractory period of the ventricle
Class 1a
these drugs shorten action potential duration and refractory period of purkinje fibers
1B
IC drugs work by
having the greates effect on the early depolarization and have less of an effect on the refractory period of ventricle
Class 1A 1B and 1C drugs
Class IA = Disopyramide, Quinidine, and Procainamide
Class IB = Lidocaine and Mexiletine
Class IC = Flecainide and Propafenone
Double Quarter Pounder
Lettece Mayo
Fries Please
class II drugs
LOL
class III drugs
AIDS A = amiodarone I = ibutilide D = dofetilide S = Sotalol
Class IV
• Class IV Antiarrhythmics are the
calcium channel blockers verapamil and diltiazem.
hyperkalemia effects
increases in serum K can depolarize the resting membrane potential
can inactivate Na channels resulting in increased refractory period duration and slowed impulse propagation
elevated potassium
slows a pacemaker
euthanasia
high doses dead
hypokalemia
make a pacemaker worse
inactivation gates close
-75 and -55
-55
and stimulation will have less Na here
what exacerbates arrhythmia
ischemia hypoxia acidosis electrolyte abnormalities excessive catecholamine drug toxicity overstretching of cardiac tissue
MOA of procaniamide
blocks Na
prolongs QRS
increases refractory period
slow upstroke
procainamide can only be given ___ for
IV
WBW
VT
Afibb with others to slow HR
these drugs are used for rate control
digoxin
BB
CCB
when we talk about rhythm control
we are talking about turning quivering into normal depolarization
why can’t you use CCB with HFrEF
increase contractility
can only use BB or digoxin
anticholinergic effect of 1a is concerning
because it can increase the rate
has vagolytic effects
this is why they need to be used in conjunction with rate control
AE of procainamide
hypotension lupus like depression agranulocytosis PROLONGS QT
quinidine SE
tinnitius
HA
disopyramide ADE
very strong anticholinergic effects can cause sxs like urinary retention
can worsen HF
lidocaine is used for these three events
VENTRICULAR ARRHYTHMIAS ONLY:
PVC VT VF
or post MI
binds to both activated and inactivated
greater suppression in the tissues and long acting
need to reduce lidocaine in
liver failure and HF
lidocaine SE
seizures
CNS effects: drowsiness or aggitation
mexiletine is used
orally instead of topically or IV like lidocaine
more GI
propafenone SE
also has some BB effect so you need to be worried about bronchospasms
CAN’T USE IN HF
main effect of amiodarone
increasing APD (prolongs re-polorization through Na channel blockade)
BB and
Ca channel blockade so can be used for rate and rhythm
what do we need to monitor with amiodarone
TSH can cause hypo hyperthyriod
CXR: pulmonary fibrosis
hepatotox: LFTs
like procainamide (except no ganglion blockade
quinidine
SE of quinidine
•cinchonism: HA, vertigo, tinnitus (can decrease hearing) altered color >5mcg •hypotension •hypersensitivity, diarrhea, nausea •Prolongs QT (Torsades risk)
quinidine adjustments needed with
Liver (80%) and renal. Reduce dose renal failure, liver dysfunction, HF.
- shortens AP, shortens refractory period
- blocks activated and inactivated Na channels w/ rapid kinetics (the inactivated Na channel block ensures greater effect on Purkinje cells)
lidocaine
Active ventric AR only. Can use in HF but high dose may cause hypotension.
lidocaine
need normal heart inorder to take these medications
1C
think baby needs normal heart
how to BB (propanolol, atenolol, metoprolol) Work to slow HR
decrease phase 4 and increase PR
why can BB cause AV block
prolonged PR
SE of BB
bronchospasm, masks hypoglycemia in DM
when would you use a BB
rate control afib
SVT ST OF VT
Post MI!!!!
post-op afib rate control
why can’t you use propafenone in HF
negative inotropic effect will increase mortality in pts who have HF or MI
propafenone DDI
DI ritonovir and digoxin
as well as other drugs that prolong QT
IV BB that is short acting
esmolol
amidarone PK
good oral absorption
binds to a lot of tissues absorption is anywhere from 22-86%
gigantic Vd
1/2life is 40-113 days
steady state 200 days
most troubling SE of amiodarone
pulmonary fibrosis and inflammation
will start with cough and shortness of breath
need CXR at baseline
other than pulmonary fibrosis what do we worry about SE wise with amiodarone
photosens, blue-grey skin (permanent)
- corneal microdeposits (halos around lights at night)
- hypo/er thyroid: monitor TSHq6mos. HAS IODINE
- hepatotoxic: monitor LFTs q6mos (dc or dec dose if LFTs 3x ULN or 2x baseline). Risk of fulminant liver failure.
- pulm inflamm and fibrosis: do CXR and PFTs d6mos. Inquire about any new cough/dyspnea. Mortality 10%. May need steroids
- Severe brady (CCB and BB effect)
- Exacerbation ventricular ar (not as common as Class I agents)
- Hypotension, phlebitis (IV >3mg/mL)
neurological: paresthesias, tremor, ataxia, HA
DDI withamiodarone
increase dig levels
warfarin: need to reduce dose
increased risk of torsades with other prolonged QT: phenothiazines, FQ
ritonavir: large increases in serum amiodarone concentrations
how often do you need to check LFTs for amiodarone
every 6 months
don’t forget to check TSH too
dronedarone used
limited nonpermanent afib and flutter as well as rhythm control in structural heart dz
does not help with permanent HF or afib
SE of dronedarone
similar to amiodarone but with less risls
still prolongs QTs brady arrhythmias
Betablocker with class III properties
sotolol
Sotolol compare anc contrast to regular BB as far as SE go
pro arrythmic effect but ortherwise same SE
will lower bP
ibutilide is different that the other class III
does not affect K
ibutilide would be seen
in hosp
dofetilide mOA
block k current
conversion and maintenance of NSR
dofetilide
HA main one can also be seen with dyspnea
can use this K blocking drug in HF
doetilide
You can not use these antiarrythmics in HF
disopyramide (1a)
properafone (Ia)
flecainaid (Ia)
dronedarone (III)
sotalol (III)
Verapamil (IV)
dilitiazem (IV)
which class III can you use in HF
amiodarone
dofetilide
maybe ibutilide but that is used in the hospital
adenosine receptors are in the
AV node
digoxin works by
inhibiting Na/k pump
positive inotrope
adenosine use
emergency rate controls
SVT reentry
not good for converting afibb or a flutter
SUPER SHORT HALF LIFE
adenosine AE
facial flushing
SOB
can mimic angina
Mg is used for
torssades and digoxin arrythmias
Vasopressin
potent vasoconstrictor
atropine
anticholinergic so it is used for bradycardia
dopamine
can increase HR and positive inotropic effect
isoproterenol
B1 and B2 agonist may cause tachycardia
POST MI these two drugs have been shown to reduce arrhythmic death and improve survival
amiodarone and BB
HF seen as sudden cardiac arrest or sustain VT is best treated with
ICD
amiodarone
sotalol or mexilitine
AFIBB Rate control tx
for most casses can use BB or CCB except in LV dysfunction or HF
then use BB or dig
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negative inotropic
1c AND SOTALOL
which classes are proarrythmis
1B
1c
III
which drugs are CI in ptrs w/ prolonged QT
phase 3
