Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
95 Cards in this Set
- Front
- Back
|
What were the first 2 antiarrhythmic drugs used?
|
digitalis first, then quinidine
|
|
|
What initiates cardiac rhythm under normal circumstances?
|
SA node
|
|
|
Where does electrical activity go once it leaves the SA node?
|
moves in a wave front through an atrial specialized conducting system and gains entrance to the ventricle via the AV node and bundle of His.
|
|
|
What happens after the bundle of His?
|
the cardiac conduction system bifurcates into 3 bundle branches: one right and 2 left bundles, conduction network of bundles is known as Purkinje system
|
|
|
What is the pathway the conduction system follows?
|
sa node - av node - bundle of his - purkinje system
|
|
|
What is the result of the conduction system?
|
contraction
|
|
|
What is the refractory period?
|
the brief time after a cell or group of cells is excited and can't be excited again
|
|
|
What happens when the wavefront encounters tissue refractory to stimulation?
|
it dies out and SA node begins the process again
|
|
|
When is the cell considered polarized?
|
when there is an electrical gradient between the inside and outside of the cell membrane
|
|
|
What is normal electrical gradient?
|
intracellular space is 80-90mV negative with respect to extracellular
|
|
|
What is the electrical gradient just prior to excitation?
|
resting membrane potential (difference in ion concentrations between inside and outside of cell)
|
|
|
How is the cell polarized at RMP?
|
by active membrane ion pumps, the most notable being NaK pump.
|
|
|
What does NaK pump want Na concentration in and out of the cell to be?
|
in: 10 meq/L
out: 140 meq/L |
|
|
What does NaK pump want K concentration in and out of the cell to be?
|
in: 135-140 meq/L
out: 3-5 meq/L |
|
|
What is depolarization?
|
electrical stimulation
|
|
|
What is phase 0 of action potential?
|
rapid depolarization of atrial and ventricular tissues by increased permeability of membrane to Na influx
|
|
|
What is phase 1 of action potential?
|
initial repolarization (notch) from Ca influx
|
|
|
What is phase 2 of action potential?
|
plateau phase, Ca influx and K efflux
|
|
|
What is phase 3 of action potential?
|
get repolarization, membrane remains permeable to K efflux
|
|
|
What is phase 4 of action potential?
|
gradual depoolarization, from Na leak into cell
|
|
|
Where are the Ca dependent tissues?
|
SA and AV nodes
|
|
|
What is differenct about the Ca dependent channels compared to the Na dependent channels?
|
Ca have less negative RMP and slower conduction velocity
|
|
|
Activation of SA and AV nodal tissue depends on what?
|
slow depolarizing current through Ca channels and gates
|
|
|
Activation of atrial and ventricular tissue is dependent on?
|
rapid depolarizing current through Na channels and gates
|
|
|
What are "automatic" tachycardias?
|
abnormality in impulse generation
|
|
|
What are "reentrant tachycardias"?
|
abnormality in impulse conduction
|
|
|
What are characteristics of automatic tachycardias?
|
onset is unrelated to an initiating event
initiating beat identical to subsequent beats can't be initiated by programmed cardiac stimulation onset preceded by gradual acceleration in rate and termination preceeded by gradual deceleration in rate |
|
|
What are examples of automatic tachycardias?
|
sinus tachycardia and junctional tachycardia
|
|
|
What is the underlying cause of TdP?
|
early after depolarizations
|
|
|
What are the type Ia antiarrhymic drugs?
|
quinidine, procainamide, and disopyramide
|
|
|
What do type 1a antiarrhythmic drugs do?
|
slow conduction velocity, prolong refractoriness, decrease automatic properties of Na dependent channels (Na channel blockers)
|
|
|
What type of arrhythmias are type Ia used for?
|
borad spectrum, supraventricular and ventricular arrhythmias
|
|
|
What are the type Ib antiarrhythmic drugs?
|
lidocaine and phenytoin and mexiletine
|
|
|
What action do type Ib antiarrhytmics have?
|
block Na channels
|
|
|
How does pH affect type Ib antiarrhythmics?
|
change in pH alters time that local anesthetics occupy Na channel receptor, intracellular acidosis in ischemia could cause lidocaine to become trapped in cell allowing increased access to receptor
|
|
|
What are the type Ic antiarrhythmics?
|
propafenone, flecainide, moricizine
|
|
|
What is MOA of type Ic?
|
extremely potent Na blockers, slowing conduction velocity and leaving refractoriness unaltered
|
|
|
What type of arrhythmias are 1c mainly used for?
|
supraventricular arrhythmias
|
|
|
What type I are slow on-off?
|
type 1c, why has potent effects on slowing ventricular conduction
|
|
|
What type I are fast on-off?
|
type Ib, binds and dissociates to channel receptor quickly
|
|
|
What type I are intermediate in binding kinetics?
|
type Ia
|
|
|
When is Na channel blockade (slowed conduction) evident for slow on-off drugs?
|
at normal rates
|
|
|
When is Na channel blockage (slowed conduction) evident for fast on-off drugs?
|
only apparent at rapid rates
|
|
|
What is the only Type I that isn't a weak base?
|
phenytoin
|
|
|
How does pH affect action of type I?
|
acidosis accentuates and alkalosis diminishes Na channel blockade
|
|
|
What type I also has K channel blocking activity?
|
quinidine and procainamide
|
|
|
What is metabolite of procainamide?
|
N-acetylprocainamide
|
|
|
What type I also has BB actions?
|
propafenone
|
|
|
What is antidote for excess Na channel blockade?
|
sodium bicarbonate and propranolol
|
|
|
What are type II antiarrhythmic drugs?
|
BB
|
|
|
What do BB decrease the likelihood of after MI?
|
sudden cardiac death
|
|
|
What can be used in HF pts to prevent AF?
|
BB, ACEI, ARBs
|
|
|
What agent is used to slow response in atrial tachycardias (AF)? and why do they work?
|
BB, work because of effect on AV node
|
|
|
What are the type III antiarrhytmics?
|
amiodarone, dofetilide, sotalol, ibutilide, bretylium
|
|
|
What is action of type III>
|
prolong refractoriness by glocking K channels
|
|
|
What is different about bretylium?
|
it first releases then depletes catecholamines. Effective in ventricullar fibrillation but ineffective in V. tach.
|
|
|
Which antiarrhythmic has characteristics of all the classes of antiarrhythmics?
|
amiodarone
|
|
|
What antiarrhythmic blocks K and is a BB?
|
sotalol
|
|
|
Which type III are only used for supraventricular arrhythmias?
|
ibutilide and dofetilide
|
|
|
What is the only dosage form for ibutilide?
|
IV
|
|
|
What is the only dosage form for dofetilide?
|
oral
|
|
|
Which antiarrhytmic drugs block the rapid component of the delayed K rectifer current (Ikr)?
|
N-acetylprocainamide, sotalol, ibutilide, dofetilide
|
|
|
Which antiarrhythmic drug blocks the slow component and rapid component of the delayed K rectifer current (Ikr) and (Iks)?
|
amiodarone
|
|
|
Why are type III better than type I for people with ICDs?
|
decrease defibrillation threshold
|
|
|
What is the main problem with type III?
|
can be proarrhythmic and form TdP
|
|
|
What are the type IV?
|
nondihydropyridine CCB (verapamil and diltiazem)
|
|
|
What type of calcium channels are operative in SA and AV nodal tissue?
|
L type and T type
|
|
|
What type of calcium channels do type IV block?
|
L channel blockers
|
|
|
Why do type IV work?
|
slow conduction and prolong refractoriness and decrease automaticity
|
|
|
What type of tachycardia are type IV effective in?
|
automatic and reentrant
|
|
|
What effect do type IV have on AF?
|
slow ventricular response by slowing AV nodal conduction
|
|
|
Do the dihydropyridine CCBs have antiarrhythmic activity?
|
no
|
|
|
What antiarrhythmic has lupus like syndrome SE?
|
procainamide
|
|
|
What antiarrhythmic has anticholinergic SE?
|
disopyramide
|
|
|
What antiarrhythmics can precipitate congestive HF in pt with LV systolic dysfunction?
|
flecainide, propafenone, disopyramide
|
|
|
What SE do type Ib cause?
|
neurologic and GI toxicity
|
|
|
What is the most frightening SE of antiarrhythmic drugs?
|
aggravation of underlying ventricular arrhythmias or precipitation of new ventricular arrhythmias
|
|
|
What is the most commonly prescribed antiarrhythmic drug?
|
amiodarone
|
|
|
What kind of t1/2 and vd does amiodarone have?
|
long, 100days, 150L
|
|
|
What is result of amiodarones long t1/2 and vd?
|
delayed onset of action from oral form, effects persist months after d/c
|
|
|
What kind of DI does amiodarone have?
|
many, inhibits P-glycoprotein and CYP450s.
doubles digoxin levels reduce warfarin dose by 1/3 or 1/2 |
|
|
What AE from amiodarone?
|
organ toxicities, bradycardia, hyper/hypothyroidism, photosensitivity, blue gray skin, fulminant hepatitis (uncommon), pulmonary fibrosis, corneal microdeposits (everyone, doesn't affect vision), optic neuropathy/neuritis (can lead to blindness)
|
|
|
Which antiarrhythmic has no change in conduction velocity?
|
amiodarone
|
|
|
Which antiarrhythmic has no change in refractory period?
|
flecainide
|
|
|
Which antiarrhythmic has no automaticity?
|
amiodarone
|
|
|
Which antiarrhythmic has the most decrease in conduction velocity?
|
flecainide
|
|
|
Which antiarrhythmic has the most increase in refractory period?
|
amiodarone
|
|
|
Which antiarrhythmic causes taste disturbances?
|
propafenone
|
|
|
Which antiarrhythmic causes cinchonism?
|
quinidine
|
|
|
What kind of tachycardia is AF?
|
supraventricular
|
|
|
What antiarrhytmic is adjusted if >60 years old?
|
quinidine
|
|
|
Who has more severe symptoms of AF?
|
pt with heart disease
|
|
|
What are the symptoms of AF?
|
rapid heart rate/palpitations, worsening of HF symptoms (shortness of breath, fatigue)
|
|
|
How is AF described?
|
irregularly irregular supraventricular rhythm with P wave
ventricular response 120-180bpm and pulse is irregular |
|
|
What is atrial flutter?
|
regular supraventricular rhythm with characteristic flutter waves (sawtooth pattern)
|
