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84 Cards in this Set
- Front
- Back
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Class I
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sodium channel blockers
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Class IA: action
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moderate phase 0 depression and slowed conduction
prolong repolarization |
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Class IA: drugs
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quinidine, procainamide, and disopyramide
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Class IB: action
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minimal phase 0 depression and slow conduction, shorten repolarization
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Class IB: drugs
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lidocaine, mexiletine, tocainide
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Class IC: action
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marked phase 0 depression and slow conduction
little effect on repolarization |
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Class IC: drugs
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flecainide, propafenone, moricizine
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Class II
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beta-adrenergic blockers
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Class II drugs
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metoprolol and esmolol
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Class III
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K+ blockers
(prolong repolarization) |
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Class III drugs
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amiodarone, sotalol, ibutilide, and dofetilide
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Class IV
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Calcium channel blockers
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Class IV drugs
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verapamil and diltiazem
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Class I: Na+ channel blockers
general aspects |
act of FAST reponse cells:
reduce membrane responsiveness depress conduction velocity reduces Phase 4 diastolic depolarization Prolong effective refractory period |
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Class I Na+ channel blockers are USE DEPENDENT
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implies that the more the cells are in the open or inactivated state, the more impact of class I drugs...the faster the heart is beating, the more this will work...
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Drugs of Class IA
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quinidine, procainamide, and disopyramide
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Direct effects of Class IA drugs
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decrease phase 4 depolarization
decrease conduction velocity increase end refractory period |
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Indirect effects of Class IA drugs
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blocks K+ channels
after depolarizations |
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Uses of Class IA drugs
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atrial flutter or fibrillation
NOT a 1st line therapy only for structurally normal hearts (proarrhthmia risk) |
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Class IA: quinidine
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some alpha-adrenergic blockade effect
severe GI effects (anticholingergic) inhibits p450 system increase in mortality...dont use much anymore |
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Class IB drugs
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lidocaine and mexilitene
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Class IB direct effects
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decrease of phase 4 depolarization
increase block of sodium channels (decrease conduction velocity) at high HR or in depolarized cells decreases action potential duration and effective refractory period dissociates rapidly at resting Em INEFFECTIVE AGAINST MOST SVTs (minimal phase 0 depression and slowing of conduction...shortens repolarization) |
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Class IC drugs
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flecainide and propafenone
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Direct effects of Class IC
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decrease in phase 4 depolarization
decrease in conduction velocity dissociates from Na channel slowly |
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First line drugs for treatment of atrial fibrillaion if NO STRUCTURAL heart disease
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Class IC: flecainide and propafenone
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Side effects of Class IC
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significant structural heart disease (hypertrophy) with the myocardium itself
highly proarrhythmic drugs |
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Class II drugs
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beta blockers!!!
beta adrenergic blockers effect on diastolic depolarization |
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Drugs of Class II
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propranolol and esmolol
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Action of Class II drugs
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bind to beta-adrenergic receptors on cardiac cell membranes to competitively inhibit norepinephrine binding
NO EFFECT in absence of catecholamines THESE BLOCK THE SLOW RESPONSE!!!! |
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Class III
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K+ channel blockers
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Class III drugs
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amiodarone
sotalol ibutilide dofetilde |
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Amiodarone
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Class III
BETA BLOCKING CALCIUM CHANNEL BLOCK K+ channel blockade also has Na+ channel blocking properties NOT first line...has a lot of organ toxicities Effect on AP: increases AP duration and increases effective refractory period |
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Sotalol
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Class III
K+ channel blockade has beta-adrenergic blocking properties BETA BLOCKING excreted in the kidneys |
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Ibutilide
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Class III drugs
K+ channel blockade has fast acting IV form |
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Dofetilde
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Class III drugs
K+ channel blockade NO BETA BLOCKING Has fast acting IV form |
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Reverse use dependence
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class III drugs
when you slow down the heart, you extend down the repolarization and have more opportunity to work...can extend the action potential further |
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Amiodarone stuff
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potentially affects every organ system, except the joints
remind patients frequently about the lungs (and the sun) surveillance monitoring: TSH, LFTs, CXR every 3-6 months; annual optic nerve exam |
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Class IV
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Calcium channel blockers
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Class IV drugs
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diltiazem and verapamil
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Action of Class IV drugs
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acts primarily on slow response cells (SA and AV node), which are dependent on Ca++ influx for phase 0 of the action potential
depresses conduction velocity |
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Class IV: Calcium channel blockers
Major electrophysiologic effects |
Impact on slow response cells:
depress phase 4 depolarization depress conduction velocity depress Vmax |
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Major side effects for Calcium channel blockers
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*negative chronotropic effect (decreases automaticity of SA node)
*negative inotropid effect (decreases Ca++ influx during plateau phase of ventricular action potential) *hypotension (decreases Ca++ influx into vascular smooth muscle cells) can cause peripheral edema and constipation |
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Adenosine
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only acts on atrium
has very rapid onset/metabolism quick action if youa re AV node dependent, you can give this hyperpolarizes SN and AVN cells by causing outward flow of potassium...shortens refractory period and also causes bradycardia has a very direct effect on potassium channels...significantly slows conduction...basically causes heart block |
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Mechanisms of atrial fibrillation
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*multiple reentrant wavelets
*focally triggered AF *SVT-induced AF *multiple unstable reentrant circuits *single stable reentrant circuits |
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Slows AV node conduction
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adenosine (acute, iv only)
Digoxin (acute and long term) Calcium channel blockers Diltiazem and verapamil (both acute and long term) Beta blockers esmolol (acute and iv only) propranolol (acute and long term) metoprolol (acute and long term) AADs: amiodarone and sotalol |
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Sinus node function...suppressing drugs
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Beta blockers
Calcium channel blockers Class Ia, Ic, and III AADs sympatholytic antihypertensive drugs lithium, cimetidine, amitriptyline, phenytoin, digoxin |
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Class I basic mechanism:
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Sodium channel blockade
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What does class I do??
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reduces phase 0 slope and peak of action potential
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Drugs for Phase IA??
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quinidine, procainamide, and disopyramide
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What does Class IA do??
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has a moderate reduction in phase 0 slope
increases APD increases effective refractory period |
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What does IB do??
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this is a weak one
has a small reduction in phase 0 slope reduces APD decreases ERP |
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drugs of class IB??
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lidocaine and mexilitine
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What does class IC do???
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STRONG!!!!
pronounced reduction in phase 0 slope no effect on APD or ERP |
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What do phase II drugs do??
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beta blockade!!!
block sympathetic activity to reduce the rate and conduction |
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What do Class III drugs do??
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these are potassium channel blockades
these delay repolarization (phase 3) and thereby increase action potential duration and effective refracotry period |
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Drugs of Class III
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sotalol, dofetilide, and amiodarone
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What are class IV drugs??
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calcium channel blockers
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What do class IV drugs do??
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block L-type calcium channels
most effective at SA and AV nodes reduce the rate and conduction |
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Which drug will NOT prolong repolarization??
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flecainide
Because class IC drugs are strong Na channel blockers and will not change the ERP at all (only class 1a prolongs conduction and repolarization) |
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you can decrease automaticity with...
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beta blockers
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beta blockers...
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prolong depolarization
class II |
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Some of these drugs are proarrhythmics...
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Usually torsade from EAD's
K+ blockers!!!! incessant monomorphic VT: type 1C almost never: amiodarone |
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Which drugs are superior to other antiarrhythmic drugs in the treatment of sustained VT??
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sotalol
amiodarone |
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The best treatment in the prevention of SCD in a patient with a low EF and sustained VT or cardiac arrest is:
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empiric ICD
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Role for antiarrhythmic drug therapy for VT
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acute treatment strategy
chronic treatment has been relegated to secondary role (after ICD) in cardiac disease...WITH THE EXCEPTION OF BETA BLOCKERS If the EF is preserved Sotalol and Amiodarone may still be used but rarely Ablation rapidly supplanting the limited role of antiarrythmics in the treatment of VT |
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What about beta blockers?
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Class II
lots of them, IV and po hepatic metabolism and renal excretion short to long half lives mild efficacy for arrhythmia suppression BUT IMPROVE SURVIVAL!!!! causes fatigue, bradycardia, and impotence NO PROARRHYTHMIAS!!!! |
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Lidocaine
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Class Ib
rapid first pass metabolism (IV/IM only) hepatic metabolism short half life (3 hours) modest efficacy NEURTOXICITY |
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acute treatment for VT
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IV lidocaine and amiodarone are used
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Amiodarone
(KNOW THIS CARD!!!) |
IV and PO
liver metabolism very long half life (1-3 months) EXCELLENT EFFICACY liver, lung, thyroid, neurotoxicity, ocular issues (cornea and retina), photosensitivity VIRTUALLY NO PROARRHYTHMIAS!!! |
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Amiodarone - very heterogenous
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potent K+ channel blocker
modest Na channel blocker modest Ca channel blocker modest alpha and beta adrenergic receptor blocker |
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Uses of amiodarone
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used for all arrhythmias (V tach)
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Common drug interactions with Amiodarone
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can double or triple INR values in patients on warfarin
can increase levels of sodium channel blockers can increase digoxin levels |
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Sotalol
(know this one) |
Class III drug
IV or po form (no first pass metabolism) RENAL excretion medium half life (10-20hrs) reasonable efficacy fatigue, bradycardia PROARRHYTHMIA!!!! |
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Which antiarrhythmics are safe in renal disease?
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amiodarone, quinidine, mexilitine, and propafenone
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Which antiarrythmics do NOT prolong refractory periods?!?
(Torsade) |
IC (Flecainide, Propafenone)
IB (lidocaine/mexilitine) |
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Which two antiarrythmics have major drug interactions?
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amiodarone and quinidine
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Take home point 1
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antiarrhythmics (with the exception of Flecainide and Propafenon (ICs) and Lidocaine and Mexilitine (IBs) can SIGNIFICANTLY PROLONG THE REPOLARIZATION and therefore can result in Torsade de Pointe as a form of Proarrhythmia
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Take home point 2
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BETA BLOCKERS!!!!
the only antiarrhythmic that has ever been shown to improve mortality in the postinfarct patient |
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Take home point 3
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EMPIRIC USE OF AN ICD:
preferable to any antiarrhythmic in the treatment of high risk arrhythmia patients (low EF <40% or with sustained VT) |
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Lanoxin
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Digoxin
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Drug class of Digoxin
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most common member from this class is called digitalis glycosides
this is considered both an antiarrhythmic agent and an inotropic agent |
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Pharmacodynamics of Digoxin
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therpeutic levels cause a vagotonic effect that is useful in slowing AV conduction in patients with atrial fibrilliation
toxic levels increase automaticity of all areas of the heart except the SA node increase Ca++ flux into sarcomere |
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Pharmacokinetics of Digoxin
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bioavailability 60-95% (best with capsule)
can be given slowly IV redistribution over about 8 hours clearance 80% renal half life: 30-40 hours (normal GFR) markedly high Vd (about 6-7 L/kg) |
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Toxicity of Dogoxin
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contraindicated in patients with VF, hypertrophic cardiomyopathy (IHSS), AV block, WPW syndrome, sinus node disease, hypoxia
common ADRs: nausea, vomiting, visual changes, agitation or nightmares, increased automaticity, AV block |
