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34 Cards in this Set
- Front
- Back
What is the ionic basis of cardiac electrical conduction and action potential propagation? ie What ions and when?
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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.
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What is the Vaughan WIlliams anti-arrhythmic classification system?
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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.
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Class 1A drugs
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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. |
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Quinidine
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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. |
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Procainamide
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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. |
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Class 1B
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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.
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Lidocaine
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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) |
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Mexiletine
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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. |
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Phenytoin
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Class 1B-like anticonvulsant. like lidocaine. Not approved as an anti-arrhythmic and rarely used.
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Class 1C
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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. |
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Flecainide
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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. |
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Propafenone
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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. |
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Class II
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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.
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Generations of b-blockers
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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 |
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b-blocker uses
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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 |
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Class III
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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. |
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Amiodarone
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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. |
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Dofetilide
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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). |
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Ibutilide
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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. |
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Sotalol
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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. |
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Dronedarone
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Similar to amiodarone w/o thyroid or pulm toxicities.
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Class IV
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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. |
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Diltiazem
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Class IV
ADME: rapid abs, large first pass, IV loading dose. t1/2= 3-4hrs. AE: edema, flushing, pain, heart block, gout, etc. |
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Verapamil
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Class IV
ADME: extensive first-pass. AE: periph edema, givingival hyperplasia, constipation, bradycardia, CHF, hypotension, ... |
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Adenosine (ATP)
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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 |
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(Digoxin)
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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. |
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Use for Class IA drugs
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1. treat atrial, AV junctional and ventricular tachyarrhythmias.
2. maintain NSR after Afib/flutter cardioversion. 3. prevent frequent ventricular tachyarrhythmia. |
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Use for Class IB drugs
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More effective with diseased myocardium.
*Ventricular arrhythmias. |
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Use for Class IC drugs
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1. PVC
2. paroxysmal SVT 3. A-fib (may increase mortality) |
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Use for Class II anti-arrhytmics
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post-MI prophylaxis of sudden death due to arrhythmias, arrhythmias
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Use for Class III
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(approved for VT, but it's the most effective AF drug we have.)
Convert Afib to NSR and maintain NSR after conversion. V-tach. |
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Use for Class IV drugs
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1. Reentrant SVT
2. reduce HR in Afib/flutter 3. HTN |
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Use for Adenosine
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converting narrow complex paroxysmal SVT to NSR
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(Use for digoxin)
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AF in CHF
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