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34 Cards in this Set

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What is the ionic basis of cardiac electrical conduction and action potential propagation? ie What ions and when?
SA and AV nodes: mostly Ca channels for depol, slow. myocardium: mostly Na channels, fast. K+ is inside and comes out for repolarization. Fewer channels or longer recovery time can generate arrhythmias.
What is the Vaughan WIlliams anti-arrhythmic classification system?
Class 1: Na+ channel blockers. 1A: intermediate. 1B: fast on-off. 1C: slow on-off. Class 2: beta-blockers. Class 3: K+ channel blockers. Class 4: Ca++ channel blockers. Extra: digoxin, adenosine, atropine.
Class 1A drugs
quinidine, procainamide, disopyramide. Na+ channel blockers.
--> slow phase 0 depol, longer AP, longer refractory period, slows conduction, decr reentry.
Used for: tachyarrhythmias (atrial, ventricular, A-V), maintain sinus rhythm after Afib/flutter cardioversion, prevent frequent V-tach.
Quinidine
Class 1A.
--> ACh block, incr AVN conduction, decr myocardium conduction.
works for arrhythmias caused by normal automaticity.
ADME: rapid abs, protein bound, placenta and breast milk, urine elim.
AE: exacerbates arrhythmias, N/V/D, cinchonism, etc.
INTAXN: CYP450, incr digoxin, phenytoin increases elim.
Procainamide
Class 1A. IV only. acts like quinidine.
Proc--> HV slowing. NAPA (metabolite) --> long QT & renal elim.
AE: exacerbates antiarrhythmias, flushing, N/V/D, etc.
Monitor: proc indicates metabolism (>10-12 is toxic), NAPA indicates renal clearance. Levels don't indicate function.
Class 1B
Lidocaine, Mexiletine, Phenytoin. shortens phase 3 depol, shorter AP. Bind open or inactivated Na+ channels, fast release, more effective in diseased myocardium. blocks depolarized or rapidly-driven tissues.
Lidocaine
Class 1B.
IV form, doesn't work for arrhythmias from normal automaticity. abolishes reentry. ONLY for ventricular arrhythmias.
ADME: big first-pass met (IV only), hep-elim.
AE: brady, hypoTN, dizziness, confusion, etc.
INTAXN:b-blockers, quinolones, phenytoin, propofol, St. John's Wort.
Monitor: >6 is toxic (seizures, agitation)
Mexiletine
Class 1B.
like lidocaine but po.
ADME: t1/2=12hrs. low first-pass met. CYP450 met.
AE: hypoTN, bad taste, N/V/D, liver enzymes, fatigue, etc.
INTAXN: chlorpromazine, quinolone, azoles, SSRIs, antacids, sodium barcabonate, acetazolamide incr mex, carbamezapine, phenobarbital decr mex.
Monitor: toxic >2mcg/mL. Liver enzymes, ANA, platelets.
Phenytoin
Class 1B-like anticonvulsant. like lidocaine. Not approved as an anti-arrhythmic and rarely used.
Class 1C
Flecainide, Propafenone.
most potent Na channel blocker, slow on-off. decrease rate of phase 0 upstroke.
Used for PVC, Paroxysmal SVT, Afib.
AE: depressing effects on heart-- use with caution., proarrhythmic, may incr mortality.
Flecainide
For refractory ventricular arrhythmias, negative inotrope, exacerbates CHF.
ADME: good abs, hep met, renal elim, t1/2= 7-22 hrs.
AE: rash, N/D, nervousness, tinnitus, etc.
INTAXN: protease inh, urinary alk agents incr flec, smoking and acidifying agents decr flec.
Monitor: vitals, renal and liver function.
Propafenone
broad-spectrum, some b-blocking activity.
ADME: high bioav, t1/2=8hrs, hep met, fast and slow metabolizers, first-pass met saturation.
AE: rash, N/V/D, blurred vision, etc.
INTAXN: enzyme inducer decrease blood levels, food may increase.
Class II
b-adrenergics. blocks symps, blocks pacemaker in SA node to decrease phase 4 depol (decr HR), inhibition in AV node decreases Ca++ and K+ levels (decr conduction)-- AV node is more sensitive.
Generations of b-blockers
1st gen: propanolol, nadolol, timolol-- nonselective, treats tachyarrhythmias caused by cats in exercise and emotions. doesn't prolong repol (used for long QT).
2nd gen: atenolol, metoprolol, acebutolol, bisoporlol, esmolol--pretty selective, only esmolol is antiarrhytmic.
3rd gen: labetolol, carvedilol-- also is a-ant, causes vasodilation
b-blocker uses
HTN (except esmolol and sotalol)
Post-MI prophylaxis: Decr sudden death due to arrhythmias, acute MI, angina, stable heart failure, arrhythmias
AE: bronchospasm, impotence, cold, neg inotropes, insomnia, depression
Class III
amiodarone, dofetilide, ibutilide, sotalol, dronedarone.
Block K+ channels.
--> longer plateau and longer repol, increased refractory period, decreased reentry, increased TdP and early afterdepolarization. reverse use-dependency (works best at slow rates), no effect on conduction.
Amiodarone
Class III.
Most frequently used.
-->has effects of all classes: longer refractory period, slows pacemaker (Na channels, blocks a- and b-adrenergics (hypoTN, neg inotrope), AV nodal block (but low TdP)
ADME: hep met, t1/2 = 50d. peak effects w/in 1 wk to 5 mo.
Use for: 1. unstable V-tach or V-fib. 2. recurrenent V-tach, esp with MI or CHF. 3. prevent recurrent paroxymal A-fib/flutter.
AE: everything. hypoTN, CNS effects, derm, endocrine, hyper/hypothyroid, GI, liver enzymes, ocular, pneumonia.
INTAXN: any drug that incr QT. also enhances digoxin and warfarin effects.
Monitor: LFTs, TFTs, PFTs (or CXR), eyes, ECG.
Dofetilide
Class III.
incr QT b/c incr refractory period, only for ppl in a certain program.
Use: convert Afib/flutter to NSR and maintain NSR. Can be for V-tach.
ADME: good bioav, renal elim, low CYP3A4.
Use if QTc < 440 msec, correct K+ and Mg+, no interacting meds, initial dose is based on creatinine clearance, pts monitored for first 72 hrs. Then if QT prolongs >15%, readjust. Stop if QT > 500 msec.
AE: CNS, CV (some TdP, esp MI/CHF), rash, back pain, dyspnea).
INTAXN: contraindications are some drugs, HR<50, hypoMg, hypoK, creatine cl < 20 ml/min.
Monitor: renal function, QT, electrolytes (want K>4, Mg>2).
Ibutilide
Class III.
IV only.
Use: new onset afib/flutter (<90 d) (to convert it). Monitor through administration (may prolong QTc and TdP). Correct electrolytes before administration.
Sotalol
Class III and non-selective b-blocking activity.
Use: life-threatening ventricular tachycardia, maintain NSR for symptomatic afib/flutter.
AE: of both class II and III.
Dronedarone
Similar to amiodarone w/o thyroid or pulm toxicities.
Class IV
Verapimil and Diltiazem.
Ca++ channel blockers. decrease phase 4 spontaneous depol, slows AVN conduction, more effective against voltage-sensitive, binds only to open channels, use-dependent (better with fast HR).
Use: reentrant SVT, to decr HR in Afib/flutter, HTN.
Diltiazem
Class IV
ADME: rapid abs, large first pass, IV loading dose. t1/2= 3-4hrs.
AE: edema, flushing, pain, heart block, gout, etc.
Verapamil
Class IV
ADME: extensive first-pass.
AE: periph edema, givingival hyperplasia, constipation, bradycardia, CHF, hypotension, ...
Adenosine (ATP)
decreases AV node automaticity
Use: first line to convert narrow complex paroxysmal SVT to NSR.
AE: transient, flushing, headache, excessive AV/SA suppression, chest pain.
Shortens atrial and ventricular refractory period. Purk: longer refractory period, slower conduction. increased contractility.
AE: heart block, blurred vision, ataxia, N/V, confusion.
ADME: caution w/ loading dose (wait for distribution), renal elmin, t1/2 > 24 hrs
(Digoxin)
for Afib with CHF. Narrow therapeutic window, renal elim.
AE: ECG abnormalities. Lots of drug interactions.
Monitor: check levels, look for AEs.
toxicity --> conduction disorder, impulse formation problems. Use atropine for bradycardia, transvenous temp pacemaker, lidocaine or phenytoin for ventricular arrhythmias.
Use for Class IA drugs
1. treat atrial, AV junctional and ventricular tachyarrhythmias.
2. maintain NSR after Afib/flutter cardioversion.
3. prevent frequent ventricular tachyarrhythmia.
Use for Class IB drugs
More effective with diseased myocardium.
*Ventricular arrhythmias.
Use for Class IC drugs
1. PVC
2. paroxysmal SVT
3. A-fib
(may increase mortality)
Use for Class II anti-arrhytmics
post-MI prophylaxis of sudden death due to arrhythmias, arrhythmias
Use for Class III
(approved for VT, but it's the most effective AF drug we have.)
Convert Afib to NSR and maintain NSR after conversion.
V-tach.
Use for Class IV drugs
1. Reentrant SVT
2. reduce HR in Afib/flutter
3. HTN
Use for Adenosine
converting narrow complex paroxysmal SVT to NSR
(Use for digoxin)
AF in CHF