Pharmacology - Arrhythmias Part 1 Flashcards by amanda kastel

Vaughan-Williams class I are also called…..

sodium channel blockers

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Vaughan-Williams Class III are also called….

postassium, or multi channel blockers

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name some things that can lead to the development of an arrhythmia

channel myopathies
CAD (insufficient blood supply)
QT prolongation
stress
too much caffeine

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arrhythmia increases the risk for what 2 things

stroke (esp atrial) and heart failure

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an arrhythmia is an abnormal heart _____ that affects ____

abnormal heart rhythm/rate that affects cardiac output

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can arrhythmias be drug-induced?

YES - digitalis (digoxin)

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can CHF cause arrhythmia

yes

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what is the term for a genetic cause of arrhythmia? what is the mutation?

WPW syndrome (Wolff-Parkinson-White syndrome)

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true or false

anesthetized patients are not at risk for getting arrhytmia

FALSE- they are

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name 4 NONPHARM therapies for arrhythmia

pacemakers
ablation
surgery
cardioversion

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what is the natural pacemaker of the heart

SA node

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define bradycardia and tachycardia (specifically)

bradycardia - under 60bpm

tachycardia - over 100 bpm

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true or false

electrolyte imbalances can affect the HR

YES

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name 3 atrial arrhythmias

PAC (premature atrial contraction)

PAR (paroxysmal atrial tachycardia)

AF - atrial fibrillation

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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

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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

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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

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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

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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

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torsades de pointes is a type of ____

V-tach (ventricular tachycardia)

often caused by drug adverse effects!

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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)

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name the flow of ions in the Na+/Ca2+ exchanger

3Na+ in and 1 Ca++ out

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name the flow of ions in the Na+ - K+ ATPase pump

2K in, 3 Na out

1 ATP used

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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

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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

Pharmacology - Arrhythmias Part 1 Flashcards

(75 cards)