Lecture 4-Antiarrhythmics Flashcards
What are the phases of the cardiac action potential?
- Phase 0
- Phase 1
- Phase 2
- Phase 3
- Phase 4
Phase 0 = ___
rapid depolarization
mostly d/t sodium entering the cell
Phase 1 = ___
early rapid repolarization
mostly d/t potassium leaving the cell; sodium channels inactivated
Phase 2 = ___
plateau
mostly d/t calcium slowly entering the cell and potassium slowly leaving the cell
Phase 3 = ___
rapid repolarization
mostly d/t potassium leaving the cell; no significant movement of sodium or calcium during this phase
Phase 4 = ___
spontaneous depolarization
d/t inward/outward movement of calcium and potassium; ATP-dependent pumps move ions to restore balance
Phase 0 rapid depolarization–increase in ___ (what electrolyte?) conductance through ion-specific fast channels; start out at ___ mV; ___ contraction; ___ channels change from “closed” to “open”; ends with ___ channels becoming “inactive” at ___ mV
Phase 0 rapid depolarization–increase in sodium conductance through ion-specific fast channels; start out at -70 mV; ventricular contraction; sodium channels change from “closed” to “open”; ends with sodium channels becoming “inactive” at +65 mV
What is the resting membrane potential? ___ mV
-70 mV
Phase 1 early rapid repolarization–___ permeability is rapidly inactivated; the cell starts to ___; ___ channels open, begin transient efflux, rapidly inactivated
Phase 1 early rapid repolarization–sodium permeability is rapidly inactivated; the cell starts to repolarize; potassium channels open, begin transient efflux, rapidly inactivated
Phase 2 plateau–repolarization is delayed by an increase in conductance of ___ (what electrolyte?) influx through slow channels; ___ channels open and maintain plateau through ___ efflux (delayed rectifier); maintains voltage at ___ to ___ mV
Phase 2 plateau–repolarization is delayed by an increase in conductance of calcium influx through slow channels; potassium channels open and maintain plateau through potassium efflux (delayed rectifier; maintains voltage at +10 to -20 mV
Phase 3 rapid repolarization–complete repolarization due to inactivation of ___ conductance and an increase in ___ permeability; no significant movement of ___ or ___
Phase 3 rapid repolarization–complete repolarization due to inactivation of calcium conductance and an increase in potassium permeability; no significant movement of calcium or sodium
Phase 4 spontaneous depolarization–slow depolarization characteristic of all pacemaker cells; results from a complex interaction between inward and outward currents of ___ and ___ during ___ (systole/diastole); ___-dependent pumps move ions to regain balance
Phase 4 spontaneous depolarization–slow depolarization characteristic of all pacemaker cells; results from a complex interaction between inward and outward currents of calcium and potassium during diastole; ATP-dependent pumps move ions to regain balance
Comparison of action potentials–in ventricular muscle cells, ___ (sodium/calcium) is responsible for initial depolarization
sodium
Muscle cells are more sodium dependent for initial depolarization; calcium accounts for the plateau phase in these cells
Comparison of action potentials–in SA/AV node cells, ___ (sodium/calcium) is responsible for initial depolarization
calcium
Automatic cells in the SA/AV node are calcium dependent
Slow, calcium mediated channels are responsible for phase ___ in SA/AV nodes and phase ___ in ventricular contractile cells
phase 0 in SA/AV nodes (slow conduction velocity) and phase 2 (prolongs refractory period) in ventricular contractile cells
What other phase do slow, calcium mediated channels affect?
Phase 4 spontaneous depolarization
Slow, calcium mediated channels are facilitated by ___
catecholamines–they can affect the movement of calcium through cyclic AMP
Calcium mediated channels are ___ (fast/slow)
slow
Sodium mediated channels are ___ (fast/slow)
fast
Sodium mediated channels are responsible for phase ___ and have a ___ (slow/rapid) conduction velocity
phase 0 and have a rapid conduction velocity
Mechanism of arrhythmias = impulse generation or ___
automaticity
Cells that undergo spontaneous phase 4 depolarization are automatic and capable of impulse generation–T/F?
True
Factors that reduce automaticity at higher pacemaker sites will ___ (actively/passively) favor the movement of the pacemaker to ___ (higher/lower) sites
passively favor the movement of the pacemaker to lower sites
___ influences passively favor the movement of the pacemaker to lower sites–i.e.: ___ drugs; ___ drugs; ___ (what induction agent?)
Vagal influences–i.e.: digitalis drugs; parasympathomimetic drugs; halothane
___ result from enhanced automaticity at a site outside the SA node
Ectopic foci
What arrhythmia do we commonly see ectopic foci/ectopic pacemaker?
A-Fib
These factors increase the chance of ectopic foci–___ influences; ___carbia; ___oxia; ___ toxicity
sympathomimetic influences; hypercarbia; hypoxia; dig toxicity
Mechanism of arrhythmias–re-entry–for re-entry to occur, you must have unidirectional block of impulse conduction (area of injury) and slow conduction via an alternate pathway–T/F?
True
Re-entry can occur at many sites, including ___ node, ___, ___ node, ___
SA node, atrium, AV node, ventricle
Re-entry at atrium occurs in atrial ___ or ___
atrial tachycardia or flutter
Re-entry at ventricle occurs in ___
V-tach
Pharmacologic arrhythmia management relies upon the ___ responsible for impulse generation in the atria and ventricles versus the SA and AV nodes
different ion channels
Sodium channels are responsible for impulse management in the ___ and ___
atria and ventricles
Calcium channels are responsible for impulse management in the ___ and ___
SA node and AV node
This class of antiarrhythmics slows conduction and prolongs the QRS complexes in the atria and ventricles
Sodium channel blockers (Type I)
This class of antiarrhythmics slows the atrial rate (SA node effect) and slows conduction through the AV node (prolonging the PR interval)
Calcium channel blockers (Type IV)
This class of antiarrhythmics interrupts reentry by slowing conduction or increasing the refractory period; they prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT (Torsades de Pointes)
Potassium channel blockade (Type III)
Class I antiarrhythmics inhibit fast ___ channels
inhibit fast sodium channels
Class ___ = quinidine, procainamide, disopyramide, moricizine
Class IA
Class ___ = lidocaine, mexilitine
Class IB
Class ___ = flecainide, propafenone
Class IC
Class II antiarrhythmics decrease the rate of ___
depolarization
What medication class is considered a class II anti arrhythmic?
Beta blockers
Class III antiarrhythmics inhibit ___ ion channels
potassium ion channels
Amiodarone is a class ___ anti arrhythmic
class III
What beta blocker is considered a class III antiarrhythmic? Why?
Sotalol because it inhibits potassium channels
Class IV antiarrhythmics inhibit slow ___ channels
inhibit slow calcium channels
What two medications are considered class IV antiarrhythmics?
Diltiazem and verapamil (nondihydropyridine CCBs)
Effects of antiarrhythmics on the action potential–type IA slows phase ___, prolongs phase ___
slows phase 0, prolongs phase 3
Effects of antiarrhythmics on the action potential–type IB slows phase ___, shortens phase ___
slows phase 0, shortens phase 3
Effects of antiarrhythmics on the action potential–type IC very slow phase ___, no phase ___ effects
very slow phase 0, no phase 3 effects
Effects of antiarrhythmics on the action potential–type II reduces slope of phase ___
reduces slope of phase 4
Effects of antiarrhythmics on the action potential–type III prolongs phase ___
prolongs phase 3
Effects of antiarrhythmics on the action potential–type IV reduces slope of phase ___
reduces slope of phase 4
Which type of antiarrhythmic has the most significant effect on phase 0?
Type IC–very slow phase 0
Procainamide is type ___ antiarrhythmic; it is a ___ and ___ channel blocker; it depresses automaticity by decreasing the slope of phase ___, and increases ___
Procainamide is a type IA antiarrhythmic; it is a sodium and potassium channel blocker; it depresses automaticity by decreasing the slope of phase 0 depolarization, and increases refractoriness
Procainamide prevents reentry by converting ___ to ___ block
converting unidirectional to bidirectional block
Indications for procainamide include ventricular ___dysrhythmias and atrial ___ in the presence of accessory pathways
ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
What are 4 dysrhythmias that can be treated with procainamide?
- SVT
- A-Fib
- PVCs
- VT
Procainamide toxicity–myocardial ___; profound ___tension; QRS complex/QT ___ leads to ___, complete ___, and ventricular ___
myocardial depression; profound hypotension; QRS complex/QT prolongation leads to Torsades, complete heart block, and ventricular ectopy
Chronic procaindamide administration can lead to a ___-like syndrome
systemic lupus erythematous-like syndrome
this can also occur with hydralazine; 50-80% of people had positive titers for SLE; lots of GI upset
Half-life of procainamide is ___-___ hours
3-4 hours
Does procainamide have an active metabolite?
Yes–N-acetyl procainamide (NAPA)
Half-life of N-acetyl procainamide is ___-___ hours; it is eliminated by the ___
6-10 hours; it is eliminated by the kidneys
Increased risk of ___ and ___ when procainamide is administered to patients with poor kidney function
Increased risk of side effects and QT prolongation/Torsades when procainamide is administered to patients with poor kidney function
Caution giving procainamide to patients with ___ dysfunction
renal dysfunction
Quinidine is a class ___ antiarrhythmic; it produces ___ and ___ blockade; ___ (increased/decreased) threshold for excitability, ___ (increased/decreased) automaticity; prolongs action potential, prolongs refractoriness
Quinidine is a class IA antiarrhythmic; it produces sodium and potassium blockade; increased threshold for excitability, decreased automaticity; prolongs action potential, prolongs refractoriness
There has been some evidence of ___ blockade and ___ inhibition with quinidine; this causes ___tension, ___cardia, atrial ___arrhythmias
some evidence of alpha 1 blockade and vagal inhibition with quinidine; this causes hypotension, tachycardia, atrial tachyarrhythmias
Quinidine can be used to treat what 4 arrhythmias? atrial ___, atrial ___, ventricular ___, and ventricular ___
atrial flutter, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation
Quinidine toxicity results in QT ___, which can lead to ___ and ___; loose ___; ___penia; and ___ism
QT prolongation, which can lead to torsades and VTach; loose stools; thrombocytopenia; and cinchonism (includes headache and tinnitus)
Quinidine pharmacokinetics–it is a potent CYP2D6 ___; PGP ___; half-life ___-___ hours
it is a potent CYP2D6 inhibitor; PGP inhibition; half-life 6-8 hours
Because it inhibits the metabolism of other medications, this can lead to toxicity
Disopyramide is a class ___ antiarrhythmic; it is similar to quinidine without the ___ effects; it has some ___ effects; used to treat atrial and ventricular ___arrhythmias
disopyramide is a class IA antiarrhythmic; it is similar to quinidine without the alpha effects; it has some anticholinergic effects (dries you out, agitation in children/elderly, delirium); used to treat atrial and ventricular tachyarrhythmias
Disopyramide toxicity results in ___ side effects; ___ exacerbation; ___ prolongation; ___penia
anticholinergic side effects; heart failure exacerbation; QT prolongation; thrombocytopenia
Procainamide, quinidine, and disopyramide (all class IA antiarrhythmics) can be used to treat any arrhythmia (atrial or ventricular), but they come with a lot of complications and thus have fallen out of favor–T/F?
True
Disopyramide is ___ eliminated; half-life is ___ hours
renally eliminated; half-life is 6.7 hours
Lidocaine is a class ___ antiarrhythmic
class IB
Lidocaine is a ___ channel blocker–the channel is ___ and ___; it decreases the slope of phase ___, reduces ___
Lidocaine is a sodium channel blocker–the channel is open and inactivated; it decreases the slope of phase 4 depolarization, reduces automaticity
Lidocaine indications = ___ arrhythmias, particularly ___ dysrhythmias
ventricular arrhythmias, particularly reentry dysrhythmias
Lidocaine is ineffective against ___ arrhythmias
supraventricular arrhythmias (atrial beats)
Lidocaine toxicity–CNS changes range from ___ to ___
depression to seizure
Lidocaine toxicity CNS–early signs = ___, ___ changes
early signs = nystagmus, speech changes
Lidocaine toxicity CV–may depress ___ performance in pre-existing ___ dysfunction; rarely cause further slowing in patients with sinus ___cardia; almost no effect on ___ interval
May depress LV performance in pre-existing LV dysfunction; rarely cause further slowing in patients with sinus bradycardia; almost no effect on QT interval
Lidocaine does not prolong the QT interval, so the risk of Torsades is practically non-existent–T/F?
True
Lidocaine pharmacokinetics–significant ___ metabolism; half-life ~___ minutes (longer with ___)
significant first pass metabolism; half-life ~8 minutes (longer with continuous infusions)
Lidocaine dose should be reduced in patients with ___ or ___ disease; half-life could be up to ___ hours in these patient populations
dose should be reduced in patients with CHF or liver disease; half-life could be up to 8 hours in these patient populations
Lidocaine may accumulate with infusions > ___ hours
> 36 hours
Lidocaine can be used for atrial and ventricular arrhythmias–T/F?
FALSE–lidocaine can only be used to treat ventricular arrhythmias
Phenytoin is a class ___ antiarrhythmic
class IB
Phenytoin is a ___ channel blocker; depresses phase ___ diastolic ___
phenytoin is a sodium channel blocker; depresses phase 4 diastolic depolarization
Phenytoin indications–it is useful in the suppression of ___ dysrhythmias associated with ___ toxicity; it is also useful in paradoxical ___ or ___ that is associated with prolonged QTc interval
it is useful in the suppression of ventricular dysrhythmias associated with digitalis toxicity; it is also useful in paradoxical VTach or Torsades de pointes that is associated with prolonged QTc interval
Rapid phenytoin administration is associated with respiratory ___, severe ___tension, ventricular ___, and ___
respiratory arrest, severe hypotension, ventricular ectopy, and death
Phenytoin toxicity CNS effects–___ness, ___mus, ___ea, ___go
drowsiness, nystagmus, nausea, vertigo
Phenytoin ___ (is/is not) a first choice antiarrhythmic
is not–it is more commonly used as an antiseizure medication
Flecainide is a class ___ antiarrhythmic
class IC
Flecainide blocks ___, ___, and ___ channels; it depresses action potential phase ___; prolongs ___ and to a lesser extent ___ interval; may suppress ___ node like beta blockers and calcium channel blockers; delays conduction in ___ tracts
blocks sodium, potassium, and calcium channels; it depresses action potential phase 0; prolongs QRS and to a lesser extent PR interval; may suppress SA node like beta blockers and calcium channel blockers; delays conduction in bypass tracts
Flecainide is an ___ medication also known as ___
oral medication also known as tambocor
Flecainide is given to patients in a-fib who can’t tolerate ___
amiodarone
Flecainide is very pro-arrhythmic–T/F?
True
Flecainide indications–it is effective in suppressing ___; can be used to treat atrial ___dysrhythmias including ___ syndrome because it delays conduction in bypass tracts
it is effective in suppressing PVCs; can be used to treat atrial tachydysrhythmias including Wolff-Parkinson White syndrome because it delays conduction in bypass tracts
Flecainide side effects–moderate negative ___ effect; ___go; difficulty in visual ___
moderate negative inotropic effect (beta blocking effect); vertigo; difficulty in visual accommodation
Do not administer flecainide to patients with ___, ___ failure, ventricular ___ because of its ___ effects
CAD, LV failure, ventricular tachycardia because of its negative inotropic (beta blocking) effects
It will worsen ischemia!!!
Beta blockers are class ___ antiarrhythmics
class II
Beta blockers lead to slowing of the ___ node, decreased slope of phase ___ depolarization; slow the rate of depolarization of ___ pacemakers; prolonged ___ nodal conduction; ___ (increased/decreased) refractoriness of AV node
beta blockers lead to slowing of the SA node, decreased slope of phase 4 depolarization; slow the rate of depolarization of ectopic pacemakers; prolonged AV nodal conduction; increased refractoriness of AV node
Indications for beta blockers–control of ___; convert atrial tachyarrhythmias to ___ rhythm; slow ventricular response to atrial ___ and ___
control of SVT; convert atrial tachyarrhythmias to sinus rhythm; slow ventricular response to atrial fib and flutter
Beta blockers are good for ___ (atrial/ventricular) arrhythmias only
ATRIAL arrhythmias only
Any arrhythmia originating distal to the AV node, beta blocker will not help
Beta blocker toxicity–profound ___cardia or ___; ___ failure; acute broncho___
profound bradycardia or asystole; LV failure; acute bronchospasm
Which (3) beta blockers can cause bronchospasm?
- propranolol
- carvedilol
- labetalol
^ because they are nonselective and block both beta 1 and beta 2 receptors (beta 2 activation usually causes bronchodilation)
Treatment of beta blocker toxicity = ___, ___, ___
atropine, glucagon, pacemaker
Amiodarone is a class ___ antiarrhythmic
class III
Amiodarone is a potent inhibitor of abnormal ___; it prolongs the effective ___ period and action potential duration in all cardiac tissues, including accessory bypass tracts
potent inhibitor of abnormal automaticity; it prolongs the effective refractory period and action potential duration in all cardiac tissues, including accessory bypass tracts
Amiodarone blocks inactivated ___ channels and ___ movement; has an anti___ effect–noncompetitive blockade of ___ and ___ receptors; prolongs ___, ___, and ___ intervals
amiodarone blocks inactivated sodium channels and potassium movement; has an antiadrenergic effect–noncompetitive blockade of alpha and beta receptors; prolongs PR, QRS, and QT intervals
Amiodarone may potentiate slowing of the SA node and AV conduction–T/F?
True
Amiodarone may potentiate what (2) medication classes?
beta blockers and calcium channel blockers
Amiodarone indications–IV for the acute termination of ___ and ___ arrhythmias
ventricular and supraventricular arrhythmias
Amiodarone indications–recurrent V ___ or recurrent unstable V ___ in patients unresponsive to or unable to tolerate other agents
recurrent V Fib or recurrent unstable V Tach in patients unresponsive to or unable to tolerate other agents
Amiodarone is effective in maintaining sinus rhythm in patients with ___
Amiodarone is effective in maintaining sinus rhythm in patients with a fib
Amiodarone can effectively suppress tachydysrhythmias associated with ___ syndrome
amiodarone can effectively suppress tachydysrhythmias associated with Wolff Parkinson White (WPW) syndrome
Half-life of amiodarone in patients on the oral agent for several years can be prolonged for ___ to ___
can be prolonged for weeks to months
Because the half-life can be prolonged in patients on amiodarone for several years, omission of 1 or 2 doses is unlikely to result in recurrence of arrhythmia–T/F?
True
Amiodarone drug interactions–CYP3A4 substrate; CYP3A4, CYP2C9, and PGP ___ (inducer/inhibitor)
inhibitor
Amiodarone drug interactions–when given with anticoagulants (i.e.: rivaroxaban, warfarin, apixaban), ___ (increased/decreased) bleeding risk, ___ (increased/decreased) INR
increased bleeding risk, increased INR
Amiodarone drug interactions–when given with medications that prolong QT interval, can lead to ___
torsades de pointes
Amiodarone drug interactions–when given with digoxin, increases risk of ___
digoxin toxicity
Amiodarone drug interactions–when given with lidocaine, increases risk of ___
lidocaine toxicity
Amiodarone drug interactions–when given with statins (i.e.: simvastatin, lovastatin), increases risk of ___
myalgias
Amiodarone drug interactions–when given with versed, results in prolonged ___ effect, increased risk of respiratory ___
results in prolonged sedative effect, increased risk of respiratory depression
Amiodarone drug interactions–when given with suggamadex, increased risk of ___cardia (additive effects)
increased risk of bradycardia
Amiodarone drug interactions–when given with AV nodal blockers (i.e.: beta blockers), increased risk of ___cardia, sinus ___, and AV ___
increased risk of bradycardia, sinus arrest, AV block
Amiodarone toxicity–respiratory effects = ___, pulmonary ___
ARDS, pulmonary fibrosis
Amiodarone toxicity–CV effects = ___cardia, ___tension, dys___, heart ___, heart ___, sinus ___
bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
Amiodarone toxicity–hematologic effects = coagulation ___–prolongs ___, increased risk of ___
coagulation abnormalities–prolongs INR, increased risk of bleeding
Amiodarone toxicity–hepatic effects = increased ___, liver ___
increased LFTs, liver failure
Amiodarone toxicity–endocrine effects = ___ or ___thyroidism
hypo- or hyperthyroidism
Amiodarone molecule has an iodine component to it, which leads to hypothyroidism in most patients; most patients will be on Synthroid with amiodarone
Amiodarone toxicity–other effects = peripheral ___, muscle ___/___
peripheral neuropathy, muscle pain/weakness
Dronedarone (MULTAQ) indication is ONLY for ___
atrial fibrillation to maintain NSR
It only comes in 400 mg tablets, no injectable form
Dronedarone contraindications–increased risk of death, stroke, and heart failure for patients with decompensated ___ or permanent ___
decompensated heart failure or permanent a-fib
Dronedarone is also contraindicated in patients with ___/___ degree heart block, HR < ___ bpm; medications that ___ (induce/inhibit) CYP3A4, prolong ___; ___; significant ___ disease
Dronedarone is also contraindicated in patients with second/third degree heart block, HR < 50 bpm; medications that inhibit CYP3A4, prolong QTc interval; pregnancy; significant liver disease
One benefit of dronedarone over amiodarone is that is does not have effects on the ___
thyroid
Ibutilide = ___ formulation; dofetilide = ___ form
ibutilide = IV formulation; dofetilide = oral form
Ibutilide/dofetilide is a class ___ antiarrhythmic
class III
Ibutilide/dofetilide is used for conversion of ___ to ___
atrial fibrillation to NSR
Ibutilide/dofetilide has high incidence of ___ and ___
torsades and ventricular tachyarrhythmias
How is ibutilide/dofetilide typically given?
It has to be started in a hospital under direct observation
Verapamil is a class ___ antiarrhythmic
class IV antiarrhythmic
Verapamil selectively blocks slow channels by inhibiting the normal ___ influx into the cell
calcium influx
Verapamil’s effect on slow channel activity is most important in ___ and ___
SA and AV nodes
It prolongs AV nodal conduction/refractoriness and depresses the rate of SA node discharge
Verapamil indications–treat ___, slow ventricular rate in ___ and ___
treat SVT, slow ventricular rate in A-fib and flutter
Verapamil has no effect on ___
accessory tracts
Verapamil toxicity–___ is a major side effect, most common; it is a very potent ___ compared to ___ and ___
hypotension is a major side effect, most common; it is a very potent vasodilator compared to cardizem and beta blockers
Verapamil toxicity–___cardia, ___, and ___ block have been seen
bradycardia, asystole, and AV block have been seen
Myocardial depression with verapamil is common in patients with reasonable LV function–T/F?
False–is Uncommon in patients with reasonable LV function
Diltiazem is a class ___ antiarrhythmic
class IV
Diltiazem MOA–slow channel blocking prolongs ___ nodal conduction and refractoriness
prolongs AV nodal conduction and refractoriness
Diltiazem indications–ventricular rate control in ___ or ___
a fib or a flutter
Diltiazem is a potent CYP3A4 ___ (inducer/inhibitor)
inhibitor–many drug interactions
Diltiazem toxicity–___cardia, ___tension, lower extremity ___, ___ation
bradycardia, hypotension, lower extremity edema, constipation
Digoxin MOA–inhibits ___
Na+/K+ ATPase
Digoxin directly prolongs the effective refractory period in the ___ node
AV node
Digoxin slows the ventricular response rate in ___ but enhances conduction through ___
slows the ventricular response rate in a fib but enhances conduction through accessory pathways
Because digoxin enhances conduction through accessory pathways, it can increase the ventricular response in what condition?
Wolff-Parkinson-White syndrome
Digoxin indirectly ___ (increases/decreases) vagal activity and ___ (increases/decreases) sympathetic activity
indirectly increases vagal activity and decreases sympathetic activity
Digoxin is indicated for ventricular rate control in ___, ___, and ___
a fib, a flutter, and SVT
Ventricular rates are easier to control in a fib than a flutter
Digoxin’s alterations in cardiac rate and rhythm may stimulate almost every known rhythm disturbance–T/F?
True
What is the most common arrhythmia caused by digoxin?
PVCs
What is the most fatal arrhythmia caused by digoxin?
VFib
Cardiac toxicity from digoxin is enhanced by what electrolyte disturbance?
Hypokalemia
Adenosine MOA–activates ___ channels that hyperpolarize nodal tissue, causing a transient ___
activates potassium channels that hyperpolarize nodal tissue, causing a transient third degree AV block
Adenosine has less effect in he atrium because it is already hyperpolarized–T/F?
True
Adenosine causes depression of the action potential in the SA and AV nodes–T/F?
True
Adenosine inhibits the effects of increased ___, reduces ___ currents to increase AV node refractoriness
inhibits the effects of increased cAMP, reduces calcium currents
Bolus dose of adenosine may induce transient ___ (sympathetic/parasympathetic) activation via ___
may induce transient sympathetic activation via carotid baroreceptors
Continuous adenosine infusion causes ___tension
hypotension
Review–adenosine works through ___ channel activation
potassium channel activation–opens up the channels and lets them leak
Review–adenosine makes it more difficult for the heart to initiate the next beat; it’s so severe, the heart goes down to a ___, EKG ___, heart ___
heart goes down to a third degree heart block, EKG stops, heart resets
Review–adenosine is effective for treatment of ___
PSVTs–paroxysmal SVTs
Adenosine affects the atria–T/F?
False–does not affect anything in the atria
There are several subtypes of adenosine receptors, two particular ones = ___ and ___
A1 and A3 receptors
A1 receptor is a negative ___ (Inotrope, chronotrope, dromotrope), beta ___ (sympatholytic/sympathomimetic) activity
A1 receptor is a negative dromotrope [slows down conduction through cardiac pathway], beta sympatholytic [beta blocking] activity
A3 receptor is a negative ___, negative ___
negative Inotrope [weakens strength of contraction], negative dromotrope [slows down conduction through cardiac pathway]
Adenosine indications–treatment of ___, including those that involve accessory pathways
treatment of PSVTs–paroxysmal SVTs, including those that involve accessory pathways
Adenosine is effective in treating arrhythmias originating distal to the AV node–T/F?
False–NOT effective in treating arrhythmias distal to the AV node
Adenosine ___ (is/is not) effective in the treatment of a. fib or a. flutter
is not effective in the treatment of a. fib or a. flutter
Adenosine is contraindicated in patients who had a ___ transplant; patients who already have ___ or ___ degree AV block; ___ syndrome; ___cardia
Adenosine is contraindicated in patients who had a heart transplant; patients who already have second or third degree AV block; sick sinus syndrome; bradycardia
Adenosine is administered by rapid bolus followed by a saline flush–T/F?
True
Adenosine starting dose is ___ mg; adenosine second dose is ___ mg if first dose is ineffective
starting dose is 6 mg; second dose is 12 mg if first dose is ineffective
Adenosine pediatric dosing–incremental doses starting at ___ mcg/kg
50 mcg/kg
Adenosine half-life is ___ seconds
1.5 seconds
Adenosine is inactivated by ___
cellular uptake
Adenosine toxicity–facial ___, ___nea, and ___ pressure are most common side effects, but usually subside in < ___ seconds
facial flushing, dyspnea, and chest pressure are most common side effects, but usually subside in < 60 seconds
Adenosine may exacerbate broncho___ in asthmatic patients
bronchoconstriction
pro___ effects of antiarrhythmic medications = Brady or tachydysrhythmias that represent new cardiac dysrhythmias associated with chronic antidysrhythmic drug treatment
prodysrhythmic effects of antiarrhythmic medications
What are (3) common dysrhythmias associated with chronic antidysrhythmic drug treatment? ___, increased ventricular ___, ___ ventricular rhythm
- Torsades de pointes
- Increased ventricular tachycardias
- Wide complex ventricular rhythm
Torsades de Pointes may result from ___ channel blockade and prolonged ___ interval
potassium channel blockade and prolonged QT interval
Class ___ and class ___ antiarrhythmic drugs block potassium channels and prolong the QTc interval (and thus can lead to torsades)
Class IA and III antiarrhythmic drugs
Torsades occurs in 1-8% of patients who receive QT prolonging drugs–T/F?
True
What (2) antipsychotics prolong the QT interval?
Haldol, risperidone (risperdal)
Diuretics can prolong the QT interval d/t ___ abnormalities
electrolyte abnormalities
What antifungals can prolong the QT interval?
-azole antifungals (i.e.: fluconazole)
What (2) classes of antibiotics can cause QT prolongation?
- Macrolides (i.e.: azithromycin, clarithromycin, erythromycin, roxithromycin)
- Fluoroquinolones (i.e.: ciprofloxacin, levofloxacin)
What (2) classes of antidepressants prolong the QT interval?
- Celexa/Lexapro (SSRIs)
- TCAs (i.e.: amitriptyline)
What (3) antiemetics cause QT prolongation?
- 5HT3A inhibitors (i.e.: zofran)
- chlorpomazine (thorazine)–this is also an antipsychotic medication
- cisapride
(2) other medications that can prolong QT interval
- methadone
- aricept (donepezil–used to treat dementia in Alzheimer’s disease)
Volatile anesthetics ___ (do/do not) prolong QT interval
do prolong QT interval
Other QT prolongation risk factors–older than ___ years of age; ___cardia; congenital ___; electrolyte abnormalities–i.e.: ___kalemia, ___magnesemia, ___calcemia; ___ (male/female gender); ___ disease; ___ drug metabolism impairment
older than 65 years of age; bradycardia; congenital long QT syndrome; electrolyte abnormalities–i.e.: hypokalemia, hypomagnesemia, hypocalcemia; female gender; heart disease–MI, CHF, LV failure, HF with reduced EF; hepatic drug metabolism impairment
QT prolongation risk factors–increased QTc interval > ___ ms compared to the pretreatment value
> 60 ms compared to the pretreatment value
QT prolongation risk factors–QTc > ___ ms
QTc > 500 ms
QT prolongation risk factors–recent cardio___
recent cardioversion
QT prolongation risk factors–___etes, ___thyroidism, ___thermia
diabetes, hypothyroidism, hypothermia
Incessant ventricular tachycardia is precipitated by class ___ and class ___ drugs that slow conduction of cardiac impulses sufficiently to create a continuous ventricular tachycardia circuit (reentry)
class IA and class IC drugs
Incessant ventricular tachycardia is rarely associated with class ___ with a weaker blocking effect on sodium channels
class IB
Incessant ventricular tachycardia is more likely to occur with ___ (low/high) doses and in patients with a prior history of sustained ___ and poor ___ function
more likely to occur with high doses and in patients with a prior history of sustained V. tach and poor LV function
Incessant ventricular tachycardia is generally ___ (faster/slower) due to drug effect, but may be resistant to ___ or ___
generally slower d/t drug effect, but may be resistant to drugs or countershocks
Wide complex ventricular rhythm is usually associated with class ___ drugs in the setting of ___
usually associated with class IC drugs in the setting of structural heart disease
Excessive ___ concentrations of drug or an abrupt change in the ___ may result in wide complex ventricular rhythm
excessive plasma concentrations of drug or an abrupt change in the dose may result in wide complex ventricular rhythm
Wide complex ventricular rhythm is thought to reflect a ___ tachycardia and easily degenerates to ___
thought to reflect a reentrant tachycardia and easily degenerates to V. Fib
