Anti-arrhythmic Flashcards
Sodium channel open inward sodium depolarization class 1 drugs affect this phase
phase 0 - fast response
sodium channel inactivated
outward K+ & inward chloride current contribute to notch & overshoot
phase 1 - fast response
inward L type Calcium and outward K+ current from plateau
phase 2 - fast response
repolarization by outward K+ current, note that a slow inward Na+ current (window current) prolonging APD class 3 drugs affect this phase
phase 3 - fast response
returning to resting potential by Na+/K+ ATPase
phase 4 - fast response
absolute no response to any stimuli
effective refractory period
strong stimulus can elicit a response, but not sync with rest of heart
relative refractory period
1) bradycardia, occurs with AV block
2) tachycardia, occurs when a reentrant circuit develops
mechanisms for arrhythmia
V max decrease
decrease conduction velocity
rate of phase 0 depolarization
less negative
slower conduction velocity
threshold potential
more negative the RP
faster conduction velocity
resting potential
pacemaker phase
inward Na+ funny & Ca2+ (T type) and inward K+ current
phase 4 - slow response
inward Ca2+ (L type) class 4 affect this phase
phase 0 - slow response
outward K+ current
classes 2 & 3 affect this phase
phase 3 - slow response
is innervated by PANS & SANS activated by M2 & B1 receptors
SA Node
In what phase is slope increased by increase in cAMP resulting from B1 activation and slowed by decrease in cAMP resulting from M2 activation
phase 4 of slow response
1) Increase upstroke velocity in pacemakers by increase calcium L type
2) shorten APD by increase K+
3) Increase HR by increase of funny Na thus increase slope of phase 4
Results of Increase cAMP
1) does opposite of increase cAMP
2) also produces K+ current, which slows the rate of diastolic depolarization and decrease HR
3) B Blockers prevent cAMP formation, with primary effects on SA and AV node tissues
Results of decrease cAMP
treats sinus bradycardia
makes slope steeped
blocks M2 causing increase cAMP, PKA & HR
Atropine
causes bradycardia
treats sinus tachycardia
Ivabradine
decrease slope of phase 0 upstroke (slows conduction of cardiac AP) AP will almost look tipped over with decrease slope by blocking sodium channels
Class 1
bind to open or inactivated sodium channels
class 1
use dependence - have greater effect on rapidly depolarizing tissues (increase heart rate causes slower phase 0 upstroke)
class 1
affect the sodium dependent cardiac AP (no action at the SA and AV nodes)
class 1
widen QRS complex (decrease AP conduction velocity) this will happen when the HR increases b/c that will increase effect of the drug
class 1
1) intermediate binding to Na channel
2) increase APD (dec phase 0)
3) block K+ ch prolonging phase 2 & 3 of AP = prolonged refractory period
4) treat SVT and ventricular arrhythmias
class 1A
1) use to treat atrial, AV juntion and ventricular tachycardia
2) block M receptor - increase HR & AV cond
3) block alpha 1 - postural hypotension and reflex tachycardia
4) effect dec by P450 inducers and enhance by P450 inhibitors
quinidine
1) cinchonism
2) severe headache
3) hypotension
4) prolong QT interval
ADR of quinidine
no anti M and anti alpha effect
metabolized by acetyltransferase
procainamide
reversible lupus erythematous like synd.
prolong QT - torsades de point
procainamide ADR
used to treat ventricular arrhythmias
contraindicated in HF
Disopyramide
anticholinergic
negative inotropic effect (dec contractility)
Disopyramide ADR
have low binding affinity to Na ch (dec APD)
shorten phase 2 & 3 of AP - shorten refractory period = no chance of tornadoes de point
class 1B
treat ventricular arrhythmias (ischemic tissues) in Na ch. spending more time in open and resting state b/c of longer AP
class 1B
greater tendency to work with ischemic heart problems
class 1B
treats ventricular arrhythmias by IV
not useful in atrial arrhythmias
decreases APD
SE: CNS toxicity
lidocaine
similar to lidocaine in action but given orally
Mexiletine
other drugs in class 1B
phenytoin and tocainide
strong binding affinity for Na ch (drastic slowing go phase 0) effects QRS, prolongs ERP in Av node, no change in APD
class 1C
treats supraventricular (a fib) and ventricular arrhythmias; can restore and maintain normal sinus rhythm in a fib and flutter
class 1C
Class 1C drugs
Flecainide
Propafenone
Class 1B drugs
Lidocaine
Mexiletine
Phenytoin
Tocainide
Class 1A drugs
Quinidine
Procainamide
Disopyramide
decrease cAMP - leads to closure of membrane Ca2+ ch preventing upstroke of AV node AP
Class 2
prolong phase 4 of nodal AP
decrease pacemaker activity
prolong conduction time and refractory period
class 2
can cause heart block
class 2
treats arrhythmias blocking SANS inout to SA and AV node
supra ventricular arrhythmias (A fib/ flutter
class 2
prevents rapid ventricular response in atrial fib/ flutter “rate control” but does not fix the atrial fib
class 2
class 2 drugs
beta blockers
Class 3 drugs
Amiodarone
Sotalol
block K+ ch prolonging phase 2 and 3 of AP - prolong refractory period
widen QT interval
induce torsades
Class 3
treats both SVT and ventricular arrhythmias and A fib / flutter
Class 3
can restore and maintain normal sinus rhythm in a fib and flutter
Class 3 (class 1C can also)
neurological SE grey corneal deposits hyperthyroidism hypothyroidism pulmonary fibrosis - restrictive lung dz induces HF hyposensitivity hepatitis grey blue skin discoloration photodermatitis inhibits cytochrome P450 inhibition
ADR of Amiodarone
Class 4 drugs
Diltiazem
Verapamil
blocks L type calcium channels blocks phases 4 and 0 prolong conduction prolong PR interval prevents RVR in A fib and flutter
Class 4
exert a greater effect on tissues that fire more freq. that use calcium current
class 4
treats SVT
use as IV to treat PSVT
Class 4
can cause heart block if used with a drug like digoxin
class 4
constipation
AV block
HF
class 4 ADR
Class 5 drugs
digoxin
magnesium
adenosine
exerts direct PANS effect by stimulating vagus nerve - AV nodal inhibition; useful in A fib (not 1st line); prevents RVR in A fib “rate control”
digoxin
treats torsades
magnesium
causes peak T waves and shortens QT interval
hyperkalemia
induces U waves at end of T waves on EKG
severe muscle weakness
abnorm glucose
hypokalemia
inhibitory A1 receptor on myocardium @ SA & AV nodes (outward increase K+ current(hyper polarize) and suppresses Ca2+ inward current)
prolongs AV refractory period
Adenosine
causes transient high grade heart block (direct AV node inhibition for about 10s)
Adenosine
1st line agent for acute treatment for PVST
Adenosine
causes coronary dilation (mediated by A2 receptor)
Adenosine
cutaneous flushing
SOB, chest pain and impending sense of doom
fainting, headache and hypotension
Adenosine ADR
inhibited by caffeine and theophylline
Adenosine
