Pharmacology - Arrhythmias Part 1 Flashcards
Vaughan-Williams class I are also called…..
sodium channel blockers
Vaughan-Williams Class III are also called….
postassium, or multi channel blockers
name some things that can lead to the development of an arrhythmia
channel myopathies
CAD (insufficient blood supply)
QT prolongation
stress
too much caffeine
arrhythmia increases the risk for what 2 things
stroke (esp atrial) and heart failure
an arrhythmia is an abnormal heart _____ that affects ____
abnormal heart rhythm/rate that affects cardiac output
can arrhythmias be drug-induced?
YES - digitalis (digoxin)
can CHF cause arrhythmia
yes
what is the term for a genetic cause of arrhythmia? what is the mutation?
WPW syndrome (Wolff-Parkinson-White syndrome)
true or false
anesthetized patients are not at risk for getting arrhytmia
FALSE- they are
name 4 NONPHARM therapies for arrhythmia
pacemakers
ablation
surgery
cardioversion
what is the natural pacemaker of the heart
SA node
define bradycardia and tachycardia (specifically)
bradycardia - under 60bpm
tachycardia - over 100 bpm
true or false
electrolyte imbalances can affect the HR
YES
name 3 atrial arrhythmias
PAC (premature atrial contraction)
PAR (paroxysmal atrial tachycardia)
AF - atrial fibrillation
explain what a PAC (premature atrial contraction) is
it can happen in healthy people
there’s a surprise early atrial contraction, and a normal ventricular contraction follows. returns to normal
can happen bc of stress, caffeine
explain what PAR (paroxysmal atrial tachycardia) is
an early atrial contraction triggers a flurry of atrial activity, but the ventricles ARE ABLE to keep up with the pace and contract after each p wave
HR can go up to 180 BPM! patients feel this
explain what afib is and how high the HR can go
up to 500bpm
atrial quivers instead of contracting. ventricles CANNOT KEEP UP and will contract based on when the atria SHOULD be contracting
on an ECG wont be able to tell where the p wave is
explain what PVC (premature ventricular contractions) are and if they’re dangerous
happens when a ventricular cardiac cell or a purkinje cell depolarizes to threshold and triggers a premature contraction
just 1 isn’t dangerous
term for the cell that’s responsible is called an ectopic pacemaker
which arrhythmia is responsible for cardiac arrest and is rapidly fatal
why is it rapidly fatal?
ventricular fibrillation
the ventricles are quivering and stop pumping blood
torsades de pointes is a type of ____
V-tach (ventricular tachycardia)
often caused by drug adverse effects!
what is the therapy for torsades de pointes? what is a common drug-inducer?
therapy - IV magnesium
common inducer - sodium channel blockers (bc of reverse use dependence)
name the flow of ions in the Na+/Ca2+ exchanger
3Na+ in and 1 Ca++ out
name the flow of ions in the Na+ - K+ ATPase pump
2K in, 3 Na out
1 ATP used
differentiate between absolute refractory period and relative refractory period
absolute - the ion channels are INACTIVATED. they MUST REST before they can open again
relative - if you put in sufficient input, the channel can be activated again
sodium channel blockers are frequency or voltage dependent blockers?
explain
frequency dependent
the channels that are ACTIVATED and overactive are blocked – used the most
channel blockers can be ___ dependent or ____ dependent
voltage (state) dependent or use (frequency) dependent
state (voltage)-dependent channel blockers block what states of the channel?
open and inactivated
explain a disturbance in impulse CONDUCTION that can cause an arrhythmia
there can be a blockage in the heart due to ischemia or smth else
this causes a re-entrance current where the electrical signal comes BACK and a premature impulse is fired
explain how early depolarization can cause an arrhythmia
this shortens the refractory period
during the refractory period is when the ventricles are filling
therefore, the drugs should aim to increase the ERP (effective refractory period)
name 2 antiarrhythmic classes that increase the threshold potential
sodium and calcium channel blockers
name a class of antiarrhythmic that increases action potential duration
class III
true or false
the ultimate goal of antiarrhytmics is to speed up the automatic rhythms
FALSE - slow
what is phase 4
do we want drugs that increase or decrease the slope of phase 4?
diastole (filling)
decrease slope
true or false
we want antiarrhythmics to increase the max diastolic potential
true
name 2 antiarrhythmics that increase the max diastolic potential
adenosine and acetylcholine
name an anytiarrhythmic class that works by increasing the duration of the action potential
potassium channel blockers (CLASS III)
what class of antiarrhythmics decreases phase 4 slope
beta blockers (CLASS II)
name the 2 classes of antiarrhythmics that increase the threshold
class I and IV (sodium channel blockers and non dihydropyridine calcium channel blockers)
what does it mean to increase the refractoriness
increase the refractory period – increases filling time and increases time it takes for another action potential
name the 2 ways to increase the refractory period
in early after depolarization and in delayed after depolarization
(EAD and DAD)
*name the class Ia drugs
quinidine
procainamide
disopyramide
*name the class Ib antiarrhythmics
lidocaine
mexiletine
name the class Ic antiarrhytmics
flecainide
propafenone
name 3 class III antiarrhytmics
amiodarone
dofetilide
sotalol
compare the kinetics of class Ia-Ic sodium channel blockers
Ia - intermediate kinetics
Ib - fast kinetics (weak binding)
Ic - slow kinetics (strong binding)
how is the MOA of class Ia sodium channel blockers different from classes Ib and Ic?
Ia also inhibits potassium channels
which class of sodium channel blockers has no efficacy in atrial arrhythmias
class Ib
which class of sodium channel blockers is CONTRAINDICATED in coronary artery disease and structural heart disease
class Ic (flecanide, propafenone_
name 2 classes of antiarrhythmics which have a risk of torsades de pointes
class Ia and class III
which specific antiarrhytmic is a multichannel blocker and thus has extra cardiac side effects
amiodarone
rank the following according to their binding affinity:
class Ia
class Ib
class Ic
weakest (fastest kinetics) - Ib
Ia is moderate
Ic is strongest (slowest kinetics)
explain the MOA of non-DHP calcium channel blockers as antiarrhytmics
block L-type calcium channels - reduce heart rate and conduction mainly at the SA and AV nodes
which class of antiarrhythmics “ reduces phase 0 slope and the peak of the action potential”
class I - sodium channel blockers
which specific subclass of the sodium channel blockers decreases the phase 0 slope the MOST?
what is its effect on the action potential duration?
class Ic
NO effect on the action potential duration
which subclass of class I increases the action potential duration and which reduces the action potential duration
increases - IA
decreases - Ib
which class of antiarrhythmics significantly delays repolarization? what is the result of this?
potassium channel blockers
the action potential duration and the effective refractory period are increased
true or false
flecainide has minimal effects on the action potential duration
TRUE - it is class Ic
propafenone also
true or false
class Ic dissociates from the channel with fast kinetics
FALSE - slow kinetics
class Ib is fast and class Ia is intermediate
true or false
fast kinetics = weak binding
true
true or false
procainamide shortens the action potential duration
FALSE - class 1A prolongs the action potential duration
class 1B shortens and class IC has minimal effects
true or false
group IA drugs significantly prolong the action potential duration and the ERP
true - bc they also reduce the phase 3 potassium current
true or false
ALL group 1 drugs prolong the ERP
TRUE
bc they slow down the recovery of sodium channels from being inactivated
true or false
all group 1 drugs reduce both phase 0 and phase 4 sodium currents
true
true or false
procainamide is effective against most atrial and ventricular arrhythmias
true
true or false
procainamide speeds up the upstroke of the action potential
FALSE - slows
true or false
procainamide slows SA/AV node conduction
true
true or false
procainamide has no effect on the action potential duration
FALSE - prolongs duration due to its minor class III action (potassium blocking)
concern with all IA blockers
reverse-use dependence
can cause QT prolongation
extracardiac effects of procainamide
has ganglion blocking properties so can cause hypotension!!!
must infuse SLOWLY and contraindicated in shock patients
watch for syncope!
explain the metabolism of procainamide
acetylated to NAPA
NAPA accumulation can cause torsades de pointes - more common in fast acetylators.
how is procainamide eliminated
renally - need dose adjustment in renal failure
name some DDI procainamide
potentiates the effects of beta blockers on the heart — too much decrease in inotropy, chronitropy
also enhances the hypotensive effect of thiziades
anticholinergic effects
name a common and concerning toxic effect of procainamide
lupus
more common in slow acetylators bc more procainamide is accumulating
