Term
Which ion mediates phase 0 of the purkinje cells?
Phase 1
Phase 2
Phase 3
Phase 4 |
|
Definition
[image]
Phase 0: Na+ in
Phase 1: K+ out
Phase 2: Ca++ in
Phase 3: K+ out (Ca in)
Phase 4: Na and Ca in, K goes out |
|
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Term
What does Class I do as a whole? |
|
Definition
Blocks Fast Na+ channels
Local anesthetic effects
Binds open or inactive state |
|
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Term
What is dose dependent and which class is this referring to? |
|
Definition
Dose dependence: if HR increases, Class I can bind easily since more Na channels are in the open or inactivated state (which it binds best to). |
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|
Term
How does class I affect Vmax and what does this in turn do to slope of phase 0 in AP of the PK cell? |
|
Definition
Decreases Vmax of depolarization
Decrease the slope of phase 0 of PK AP |
|
|
Term
What does Class 1a bind to and how does it dissociate? |
|
Definition
Binds to open channels and dissociates slowly |
|
|
Term
What is the effect of Class 1a on PK and PM cell APs? |
|
Definition
PK cells: Decreases slope of phase 3 (blocking K channels too). This prolongs repolarization
PM cells: Decreases slope phase 4, so threshold for depolarization also increases
[image] |
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Term
What are the Class 1a drugs? |
|
Definition
Quinidine
Procainamide
Disopyramide
(Pretty Darn Quick)
or
(Quit procrastinating in climing the pyramid) |
|
|
Term
What is Quinidine used for? |
|
Definition
Supraventricular and ventricular arrhythmias |
|
|
Term
Is it bad to use high doses of quinidine? If so, why? |
|
Definition
YES- can cause fatal arrhythmias, including Torsades de Pointes- prolonged QT interval |
|
|
Term
What can increase the risk of Torsades de Pointes? |
|
Definition
|
|
Term
What is Chinconism and which drug can cause this? |
|
Definition
Quinidine can cause this
blurred vision, tinnitus, HA, disorientation and psychosis (antimuscarinic activity)
All these Sx occur after getting wasted at a loud concert (except psychosis maybe..)
|
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Term
What is a SE of quinidine that is not cardiac related? What is the worry with this SE? |
|
Definition
Diarrhea
Worry is that by having so much diarrhea, you are crapping out all your K and can have hypokalemia and this may induce Torsades de Pointes. |
|
|
Term
How is procainamide administered? |
|
Definition
|
|
Term
What is procainamide used for? |
|
Definition
An alternative to quinidine for various ventricular and Supraventricular arrhythmias. |
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Term
Explain the metabolism of Procainamide and why fast vs slow acetylation is so important. |
|
Definition
Procainamide-> NAPA (class III K+ blocker)-> enhances procainamide's effect on phase 3 repolarization (prolonging it further). |
|
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Term
Explain what happens if a patient has renal failure and is taking procainamide. How can you correct this? |
|
Definition
With renal failure, NAPA can accumulate and increase risk of Torsades de Pointes.
Give lower dose of Procainamide then |
|
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Term
If someone comes into the ER and needs rapid IV administration of Procainamide, what is wrong with this? |
|
Definition
Rapid IV administration can cause hypotension from ganglionic block |
|
|
Term
What are the SE of procainamide? |
|
Definition
Depression
Hallucination
Psychoses
Arrhythmias
(PHAD- Procainamide was a "phad" until ppl realized that the crazy SE) |
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|
Term
What is disopyramide used for? |
|
Definition
Ventricular and supraventricular arrhtymias |
|
|
Term
What are the SE of Disopyramide drug? |
|
Definition
Anti-muscarinic activity:
Constipation
Urinary retention
Blurred vision
dry mouth
(Poop, pee, see, salivate) |
|
|
Term
What does disopyramide do the contractility? What should you be careful about? |
|
Definition
It decreases myocardial cotractility despite having anti-muscarinic activity. This can lead to Heart Failure so beware if pt has pre-existing LV dysfunction. |
|
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Term
What is a condition with the eye that patients taking disopyramide should beware of? |
|
Definition
Glaucoma
It narrows the __?__ angle and increases the pressure.
(I don't know name..) |
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|
Term
A diabetic pt comes into hospital also taking Disopyramide, what is your worry? |
|
Definition
Diabetics taking oral hypoglycemics should beware if on disopyramide bc can decrease blood glucose more because it increases insulin release (blocks sam Katp channels) |
|
|
Term
What are the main things to worry about if taking Dispyramide (summary)? |
|
Definition
Anti-muscarinic activity (poop, pee, see, salivate)
Heart failure
Glaucoma
Diabetes (hypoglycemia)
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|
Term
What do class 1b bind to and how do they recover? |
|
Definition
open and inactivated, but prefer inactivated.
Recover rapidly |
|
|
Term
How are PK cells and PM cells affected in class 1b drugs? |
|
Definition
PK cells: increases slope phase 3, thereby decreasing AP time and decreasing repolarization time
PM cells: Same as Class 1a
Decreases phase 4 slope and increases threshold |
|
|
Term
What is lidocaine used for? |
|
Definition
Ventricular arrhtymias
Also has local anesthetic effect |
|
|
Term
Why is lidocaine not used for atrial arrhythmias? |
|
Definition
Atrial APs are too short and channels aren't open long enough for lidocaine to penetrate
Atrial arrhythmias are usually not in ischemic tissues, which would be partly depolarized (more time spent in inactivated state)- ischemic tissue is ventricles and non-ischemic tissue is atrial |
|
|
Term
How should lidocaine be administered? |
|
Definition
Slow IV because of extensive 1st pass metabolism.
Fast IV causes arrhythmias or seizure** |
|
|
Term
What are the SE of lidocaine? |
|
Definition
nystagmus
tremors
slurred speech
dysarthria
altered consciousness |
|
|
Term
What is mexiletine used for?
How is it administered? |
|
Definition
Ventricular arrhythmias
Orally. |
|
|
Term
What is phenytoin used for? |
|
Definition
ventricular and digoxin-induced arrhythmias
seizures |
|
|
Term
What channels does phenytoin block? |
|
Definition
Blocks Na+ and some Ca++ influx. |
|
|
Term
What are the SE of phenytoin? |
|
Definition
Gingival hyperplasia
Enzyme induction- drug interactions
Hirsutism- give eflornithine (inhibits ornithine decarboxylase involved in hair growth) |
|
|
Term
What does class 1c bind to and how it its recovery? |
|
Definition
Open channels
Recover is very slow |
|
|
Term
What are some effects of class 1c having slow recovery?
What is this drug generally used for? |
|
Definition
Makes these Rx more dangerous. Class 1c are associated with excessive mortality or non-fatal cardiac arrest.
Used for life threatening situations |
|
|
Term
How does Class 1c affect PM and PK cells? |
|
Definition
PK cells: decreases slope of phase 0, increasing time for depolarization
PM cells: Same as for Class 1a/1b: decr slope phase 4 and incr threshold |
|
|
Term
What are the Class 1c drugs? |
|
Definition
Flecainide
Propafenone
(Probably Free ;p) |
|
|
Term
What are the class 1b drugs? |
|
Definition
Lidocaine
Mexiletine
Phenytoin
(Please Lick Me!) |
|
|
Term
What is flecainide used for?
How administered? |
|
Definition
Paroxysmal A-fib
Paroxysmal SVT
AV reentrant tachy
other SVTs
Oral |
|
|
Term
What does Flecainide block? |
|
Definition
Na+ channels
Ryanodine Ca channels in SR and prevents arrhthmogenic Ca rel from SR.
Useful if genetic defect in Ryanodine Ca channels whcih causes CA polymorphic ventr tachy |
|
|
Term
What does propafenone block? |
|
Definition
Na channels
Produces significant Beta block (Class II activity) |
|
|
Term
What is propafenone used for and how is it administered? |
|
Definition
A-fib
A-flutter
paroxysmal SVT
other ventricular arrhythmias
Oral |
|
|
Term
How is propafenone metabolized? |
|
Definition
CYP2D6
This is absent in 7% pts, so can exaggerate effects and toxicity (mostly GI) if pt doesn't have this |
|
|
Term
|
Definition
|
|
Term
What are the effects of NE on heart? |
|
Definition
1) incr cAMP->activate PKA->phosph a1 subunit of Ca channels->incr Ca++ influx->incr myocardial contractility
2)Phosph Troponin-> incr sensitivity of contractile prots to Ca
3)Facilitates Ca capture by ryanodine-R on SR-> incr Ca available for release
4)Incr Ca entry increases automaticity-> delayed after-depolarizations. Via the Na/Ca exchanger, one Ca moves out for every 3 Na moving in->net influx of 1 charge per exhange.
*Beta blockers inhibit all this*
|
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|
Term
Beta blocker blocks which receptor that causes the therapeutic effects of antiarrhythmetics? |
|
Definition
B1- receptor that's on the heart
B2- on vasculature and bronchioles and no effect arrhythmias |
|
|
Term
How does Class II affect PK cells and PM cells? |
|
Definition
PK cells: NO EFFECT
PM cells: Phase 4 slope is decreased, so it takes longer to reach threshold (but threshold doesn't change)
Phase 3 slope is decreased, prolonging repolarization
-AP is wider
[image] |
|
|
Term
WHat is the main goal of beta blockers? |
|
Definition
Decrease 02 demand on th heart by preventing the effects of endogenous CAs. |
|
|
Term
What are the non-selective beta blockers?
Which are the B1 selective beta blockers? |
|
Definition
Acebutalol
Propranolol (non selective)
Esmolol
(APE- ooh ooh ahh ahh)
|
|
|
Term
What is propranolol used for? |
|
Definition
It blocks b1 and b2.
Supraventricular arrhythmias
ventricular arrhythmias indcued by CAs
digoxin-induced arrhtymias |
|
|
Term
|
Definition
Decreases HR and contractility
This decreases CO and leads to reflex vasoconstriction to maintain BP |
|
|
Term
What is an undesirable effect of propranolol |
|
Definition
Since it's non-selective, it also blocks B2 and leads to bronchoconstriction and causes resp crisis |
|
|
Term
What is acebutaolol used for? |
|
Definition
Premature ventricular contractions |
|
|
Term
Which Beta blocker has intrinsic sympathomimetic activity? |
|
Definition
Acebutalol- limits its use
(think Acebutalol is kinda like ASSbutalol and it has ISA which if say fast sounds like an english person saying ASS) |
|
|
Term
How is esmolol given? WHY? |
|
Definition
IV ONLY bc its rapidly metabolized by plasma esterases |
|
|
Term
What other beta blockers ares used for arrhythmias but are not FDA approved? |
|
Definition
Metoprolol
Atenolol
Pindolol
(MAP)
|
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|
Term
|
Definition
|
|
Term
What is the effect of blocking K channels? |
|
Definition
Inhibit K outward current and this prolongs the plateau and the AP.
This increases the refractory time and decreases risk of reentry, but increases risk of Torsades |
|
|
Term
How do Class III K blockers affect PK and PM cells? |
|
Definition
PK cells: decreases slope phase 3, prolongs repolarization (similar to class 1a)
PM cells: NO EFFECT |
|
|
Term
What are the Class III drugs? |
|
Definition
Bretylium
Amiodarone
Dronedarone
Dofetilide
Sotalol
Ibutilide
(BAD DIS- K)
|
|
|
Term
What is the affect of amiodarone? |
|
Definition
Has properties of all 4 classes:
Class I: decr rate firing of pacemaker
Class II: antagonism of beta receptors
Class IV: AV block and bradycardia |
|
|
Term
Which drug is linked with thyroid hormone? |
|
Definition
Amiodarone
It has I and is related to thyroid hormone.
Can cause hyper-hypothyroidism |
|
|
Term
What is amiodarone's dominant effect? |
|
Definition
Prolongation of the Ap which decreases risk of reentry. |
|
|
Term
What is Amiodarone's T1/2 and why? |
|
Definition
T1/2=50 days
It's lipophilic and accumulates and is slowly eliminated
Increases risk of toxicity |
|
|
Term
What is amiodarone used for? |
|
Definition
Refractory supraventricular and ventri arrhythmias |
|
|
Term
What is the BBW with Amiodarone? |
|
Definition
Fatal acute pulmonary toxicity
-cough
-dyspnea
-bronchospasms
-infiltrates
-hemoptysis
-alveolar hemorrhage
-resp failure |
|
|
Term
What are the SE of amiodarone |
|
Definition
hypo/hyperthyroidism
Corneal deposits
Hepatotoxicity
peripheral neuropathies
photodermatitis (blus skin and ears-smurffs) |
|
|
Term
What does amiodarone inhibit? (enzyme?) |
|
Definition
Cyp3A4
Cyp2C9
P-glycoprotein |
|
|
Term
What is dronedarone used for? which drug is it similar to, except for what? |
|
Definition
Used for Afib/Aflutter
Analog of amiodarone but without the I. |
|
|
Term
Which channels does dronedarone block? |
|
Definition
Properties of all 4 classes |
|
|
Term
What are the CAUTION and SE of dronedarone |
|
Definition
CAUTION- increases risk of CV events including 2x incr risk of death in pts w/ Afib
SE: N,V,D, abdl pain, asthenia (weakness).
Rare, but severe liver injury could require liver transplant |
|
|
Term
What are the Rx interactions of Dronedarone? |
|
Definition
Cyp3A4 (same as amiodarone)
Cyp2D6
P-glycoprotein (same as amiodarone) |
|
|
Term
What is Bretylium used for and how is it administered? |
|
Definition
IV for life threatening V-tach, V-fib |
|
|
Term
What are the effects of bretylium? |
|
Definition
Prolongs AP thru ion channel effects
Displaces NE: initially increases NE release and contractility with a transient incr BP and potential ventr arrhythmias. This is followed by decr in BP as NE is depleted |
|
|
Term
What activity does Sotalol have? |
|
Definition
|
|
Term
What activity of sotalol is more apparent in lower doses? at higher doses? |
|
Definition
LOW: Class II- beta block
HIGH: effects on AP |
|
|
Term
What is sotalol used for? |
|
Definition
Supraventricular and ventr tachyarrhythmias |
|
|
Term
What is a dangerous cardiac risk with sotalol? |
|
Definition
|
|
Term
What is ibutilide and what is its main effect? |
|
Definition
Ikr blocker
Actiavtes slow inward Na channels |
|
|
Term
What is ibutilide used for? |
|
Definition
|
|
Term
What is a cardiac SE of ibutilide? |
|
Definition
Prolongs QT interval
monitor carefully |
|
|
Term
What is dofetilide and what is it used for? |
|
Definition
Pure Ikr blocker (no extracardiac effects)
Used to convert Afib/flutter |
|
|
Term
What should you not give dofetilide with? |
|
Definition
Thiazide Diuretic
it will increase dofetilide's level and cause significant prolongation of QT interval |
|
|
Term
What are Class IV antiarrhythmetics? what do they block? |
|
Definition
Ca channel blockers
specifically L-type slow Ca++ channels.
|
|
|
Term
what state of the channel do the class 4 bind to? what is this helpful in preventing then? |
|
Definition
open channels
Thus, are more effective against reentrant SVT |
|
|
Term
Where do these class IV drugs target best? What part of the heart? |
|
Definition
AV node because slow Ca channels predominate in the AV node causing depolarization?? |
|
|
Term
What is the overall effect of Class IV? |
|
Definition
Slow HR and terminates SVTs by causing partial AV block |
|
|
Term
What are the effects of Class IV drugs on PK and PM cellS? |
|
Definition
PK cells: NO EFFECT
PM cells: Decreases phase 4, 0 and 3 slope
Prolongs depolarization and repolarization and elongates the AP.
[image] |
|
|
Term
What are the Class IV drugs? |
|
Definition
|
|
Term
Explain the worry about IV vs Oral administration for verapamil. |
|
Definition
The L racemate is more potent than the D, but L undergoes more 1st pass metabolism.
A certain amt given IV prolongs the PR interval more than the same amt given orally so be careful. (bc oral causes 1st pass and metabolism) |
|
|
Term
What is a major SE (non-cardiac) of verapamil |
|
Definition
CONSTIPATION
more notable with verapamil than other Ca channel blockers bc it has high affinity for GI sm.
*Treat this bc if strain to poop (valsalva), can increase o2 consumption of heart and since there is an increase in intrathoracic pressure the volume going back to heart decreases, so could cause an MI |
|
|
Term
Where does verapamil work?
What about diltiazem? |
|
Definition
More selective for heart
Acts on heart and vascular sm |
|
|
Term
What should you watch for with diltiazem? |
|
Definition
Decreased BP from vasodilitation
Decrease in contractility
|
|
|
Term
Why do the Ca channel blockers not affect Skeletal MM? |
|
Definition
Ca channels affect all ca channels, but skeletal mm gets most of its Ca from the Sarcoplasmic Reticulum, therefore blocking the extracellular Ca channels and decreasing influx of Ca into the skeletal mm cell will not affect its function bc it's getting its Ca from elsewhere. |
|
|
Term
What are the Miscellaneous antiarrhythmetics? |
|
Definition
Digoxin
Atropine
Aenosine
Magnesium
(DAAM- imagine a goat saying Dam..) |
|
|
Term
What is Digoxin used for? |
|
Definition
Afib
Aflutter
Also used for CHF (Rx increases contractility) |
|
|
Term
What is Digoxin's MOA to prevent arrhythmias? |
|
Definition
its vagomimetic (mimics parasympathetics)
a) inhibits stmpathetics
b)vagal stimulation->
incr ACh release->
incr K efflux->
hyperpolarized SAN->
closes Ca++ channels->
Decr Ca influx->
decreased slope 0 in AVN->
and this slows ventricular contraction |
|
|
Term
What is Digoxin better at?
Ventricular arrhythmias or Atrial arrhythmias? |
|
Definition
Atrial Arrhthmias=
There isn't much parasympathetic activity in ventricles.
BUT by controlling conduction thru the AV node, Digoxin controls the ventricular response to Afib and Aflutter |
|
|
Term
What can cause increased risk of Digoxin toxicity?
What can this toxicity lead to potentially? |
|
Definition
Hypokalemia (low K)
Can lead to Torsades de Pointes |
|
|
Term
How does low K lead to digoxin toxicity? |
|
Definition
In cardiac cells, digoxin binds to phosphorylated form of NA/K ATPase.
The problem is that K promotes dephosphorylation of this pump. If there is low K, then dephosphorylation doesn't happen and you get phosphorylaton of the channel.
Phosphorylated channel promotes digoxin binding and toxicity. |
|
|
Term
What should you not mix Digoxin with and why?
|
|
Definition
Diuretic
CAuses K+ loss and if low K, will have phosphorylated Na/K pumps and lead to toxicity of digoxin.. |
|
|
Term
How do you treat Digoxin toxicity? |
|
Definition
Digoxin immune Fab (digibind)- an antibody to digoxin that forms a 1:1 complex w/ digoxin and is then rapidly excreted.
Give IV over 15-30 minutes
IV K- this would work bc K causes dephosphorylation of the channel that digoxin binds to. Without this channel, Digoxin has not effects. |
|
|
Term
How with Ca affect Digoxin toxicity? |
|
Definition
Makes it worse
The more Ca you have, the more Na that is brought out of the cell...
Actually I don't Know :/ |
|
|
Term
What is the effect of Mg?
What if have low Mg? |
|
Definition
It competes with Ca and decreases risk of arrhythmia because basically blocking Ca channels so depolarization doesn't happen like normal.
Low Mg causes increased risk for arrhthmia because there will be no competition w/ Ca and so depolarization happens.
|
|
|
Term
What is Atropine used for?
How is it administered?
Why? |
|
Definition
Bradyarrhythmias
IV
Atropine is a competitive antagonist of the muscarinic ACh-R, meaning that it blocks the effects of parasympathetics. It makes sense that if it's blocking Parasympathetics, which normally decr HR, it'd lead to an increased HR. |
|
|
Term
What is Adenosine used for and how is it administered? |
|
Definition
|
|
Term
What is the T1/2 of Adenosine?
Why is it good? |
|
Definition
T1/2= 15 seconds!!!!!
Easy to control and so decreases risk of significant SE. Yeay! |
|
|
Term
What is the MOA of adenosine? |
|
Definition
Stimulates P1 purine-R->
activates Ach-sensitive K channels->
K efflux in atria and SA/AV node->
Hyperpolarization->
decreases automaticity and causes a transient AV block |
|
|
Term
What other channel does Adenosine block?
What is the result? |
|
Definition
Blocks Ca currents and increases the AV node's refractoriness |
|
|
Term
What are the SE of adenosine |
|
Definition
Transient asystole (lasts less than 5 sec) Scares the shit out of new doctors who have to administer it
Facial flushing, chest pain, dyspnea, N, vfib, vtach or bradycardia. Short lived SE bc T1/2 is so short |
|
|
Term
What does Adenosine interact with? |
|
Definition
Methylxanthine is an antagonizer of adenosine
a purine base found in most human body tissues and fluids and in other organisms
Methylxanthines affect not only the airways but stimulate heart rate, force of contraction, cardiac arrhythmias at high concentrations. |
|
|
Term
|
Definition
Sotalol
Adenosine
Disopyramide
Propranolol
Amiodarone (for refractory)
Procainamide
Quinidine
Flecainide
(SAD PAP- Quit Fucking)
|
|
|
Term
Which drugs are for V-tach? |
|
Definition
Quinidine
Procainamide
Diopyramide
Lidocaine
Mexilitine
Phenytoin (digoxin induced)
Propafenone
Propranolol (Ca and digoxin induced)
Amiodarone
Bretylium
Sotalol
(All the drugs that Tx SVT are here except for Flecainide and Adenosine (Ademir flees). The extra ones are bolded and make
Lick My Butt Pretty Please! |
|
|
Term
Which drugs are used to treat Afib/Aflutter? |
|
Definition
Flecainide (fib)
Ibutilide
Bretylium (fib-life threatening)
Propafenone
Dronedarone
Dofetilide (converts them)
Digoxin
(FIB P-DDD)
Sounds like P-diddy and he "FIB"-ed us with all his name changes)- also Fib for A-fib.. DUH! |
|
|
Term
What drugs are used to treat reentry? |
|
Definition
Flecainide (AV)
Adenosine
(Ademir Flees.. and then reenters) |
|
|
Term
What drug treats Premature ventricular contractions? |
|
Definition
|
|
Term
Which drug is used for Bradyarrhythmias? |
|
Definition
Atropine
Makes sense because Atropine is a blocks ACh-R basically blocking parasympathetics, causing incr in HR. |
|
|
Term
Which class of anti-arrhythmetics prolongs repolarization in Purkinje cells? |
|
Definition
Class Ia
Class III
(Na and K blockers) |
|
|
Term
Which class of antiarrhythmetics shortens repolarization in Purkinje cells? |
|
Definition
Class 1b
(Na blocker- rapid recovery) |
|
|
Term
Which class of antiarrhythmetics has no effects on Purkinje cells? |
|
Definition
Class II
Class IV
(Beta blocker and Ca blockers- affect nodes) |
|
|
Term
Which Anti-arrhythmetic decreases phase 4 slope of the Pacemaker cells? |
|
Definition
All of them, except for Class III (which has NO EFFECT on PM cells) |
|
|
Term
Which antiarrhythmetics increase the threshold for firing in Pacemaker cells?
Which ones don't affect threshold?
Which one has NO EFFECT on Pacemaker cells? |
|
Definition
Class Ia
Class Ib
Class Ic
Class II and Class IV
Class III
|
|
|
Term
Which antiarrhythmetic affects the slope of all parts of the depolarization graph in the Pacemaker cell? |
|
Definition
Class IV
Decr slope of 4, 0, 3 |
|
|
Term
Which antiarrhythmetic class prolongs repolarization in the Pacemaker cells? |
|
Definition
|
|
Term
Which antiarrhythmetic Rx can induce Torsades de Pointes? |
|
Definition
Quinidine (in high doses)
Sotalol
Procainamide (if increased NAPA like in renal failure or if pt is a fast acetylator)
Digoxin
Class III- K blockers |
|
|
Term
Which Antiarrhythmetics can cause psychosis |
|
Definition
|
|
Term
Which anti-arrhythmetic can be used to treat CHF? |
|
Definition
|
|
Term
Which antiarrythmetic can cause blurred vision? |
|
Definition
Quinidine
Disopyramide
Digoxin |
|
|
Term
Which antiarrythmetic can cause Hursitism? |
|
Definition
Phenytoin
(Penny is a hairy little girl) |
|
|
Term
Which antiarrythmetics have ISA? |
|
Definition
Acebutalol
amiodarone
(ASS-ISA) |
|
|
Term
Which antiarrythmetic can cause Constipation? |
|
Definition
Disopyramide
Class IV- Ca channel blockers- ESP verapamil
(climbing pyramides makes you veray constipated)
|
|
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Term
Which antiarrythmetic can cause GI problems like NVD, HA? |
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Definition
Dronedarone
Digoxin (NV, HA)
Adenosine (N)
Quinidine (HA)
(Dronedarone sounds like Dramamine which you take for sea sickness... so just think about those Sx)
(Ademir makes me nauseous sometimes) |
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Term
Which antiarrythmetic can cause heart problems? |
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Definition
Disopyramide (heart failure)
Class 1c (cardiac arrest)
Dronedarone (CV events)
Adenosine (asystole, vfib, vtach, bradycardia) |
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Term
Which antiarrythmetic can cause toxicity? |
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Definition
Amiodarone (highly lipophilic and accumulates)
Digoxin (if low K because of phosphorylation of the Na/K pump.. remember?) |
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Term
Which antiarrythmetic can cause liver problems? |
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Definition
Amiodarone (hepatotoxicity)
Dronedarone (liver damage) |
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Term
Which antiarrhythmetics can cause a decrease in BP? |
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Definition
Procainamide (if rapid IV- ganglionic block)
Digoxin |
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Term
Which antiarrythmetic can cause hypoglycemia? |
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Definition
Disopyramide
Beta blockers- right? Blocks the B2 mediated stimulation of glycogenolysis and decrease blood sugar. |
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Term
Which antiarrythmetic can causes nystagmus? |
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Definition
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Term
Which antiarrythmetic can causes corneal deposits (halo)? |
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Definition
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Term
Which antiarrythmetics can cause dyspnea? |
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Definition
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Term
Which antiarrythmetics have a BBW? What is it? |
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Definition
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Term
Which antiarrhythmetic can cause thyroid problems?
What can you give instead? |
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Definition
Amiodarone
Contains Iodine and can cause hyper-hypothyroidism (potentially fatal thyrotoxicosis)
Can give dronedarone because it's an analog of amiodarone but without the Iodine |
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