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42 Cards in this Set
- Front
- Back
procainamide
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IA
mainly for acute tx of atrial arrhythmias, also ventric during arrest |
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lidocaine
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IB
only useful for vent. arrhythmias by i.v. route |
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flecainide
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IC
use: atrial arrhythmias in structurally normal hearts |
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metoprolol
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II
beta blocker used for rate control in A. fib |
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ibutilide
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III
acute tx A fib and a. flutter |
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verapamil
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IV
Ca+2 ch blk NOt used for ventric arrhythmias |
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amiodarone
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Several classes (II, III, IV)
all arrhythmias, lowest incidence of vent proarrhythmias iv form to control A Fib w/ defibrillation during arrest oral form for maintenance of atrial arrhyth in old or abnl hearts (1st line) |
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what's the first choice drug in the elderly or abnl hearts as maintenance tx for atrial arrhythmias?
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amiodarone
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what's the problem with long term amiodarone tx?
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considerable S/E's
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what are the two different kinds of action potentials generated by parts of the heart's electrical system?
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1. fast AP: by atrial/ventric myocardium and His Purkinje system; mediated by Na+ influx for rate of impulse conduction
2. slow AP: by pacemaker tissue (Sinus, AV node) due to slow inward Ca+2 current; slow impulse conduction w/ long refractory period |
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fast AP
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generated by atrial/ventric myocardium and His Purkinje system
Na+ rapid influx (phase 0) when threshold pot of -60mV reache rate of Na+ influx-->rate of impulse conduction (conduction velocity) measured by ECG by QRS interval |
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what's the QT interval?
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AP duration or time for complete membrane repol (phase 2 and 3)
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what happens during the refractory period?
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time which cell can not be depolarized again
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slow AP
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generated by pacemaker tissue (SA/AV node)
result of slow Ca+2 influx upstroke of phase 0 slow, so conduction slow through pacemaker tissue slow repolarization means long refractory period |
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2 most common ways arryhthmias result?
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1. abnl or enhanced automaticity (ectopic focus)
2. re-entry |
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cause of abnl automaticity
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from inappropriately increased rate of AP generation: from abnl pacemaker or enhanced activity (Increased slope in phase 4) of abnl tissue
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what would an increased slope in phase 4 mean?
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enhanced activity ?
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what's an ectopic focus?
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abnl "pacemaker" site
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how do drugs fix arrhythmias due to abnl automaticity?
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suppress automaticity
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what causes reentry?
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must have circuit or loop of 2 distinct pathways anywhere in the heart w/ different electrophysiologic properties
generally: 1 limb rapid w/ long refract, other slower w/ shorter reftract period 2 limbs join prox and distally |
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how do antiarryhthmic drugs work (4 general ways)?
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1. block Na+ channel--slow impulse conduction (phase 0 of AP)
2. blk K+ ch and prolong repol and RP (phase 2-3 of AP) 3. blk Ca+2 ch and affect electrophys prop of pacemaker tiss 4. blk symp stim which alters ion channels |
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how do Class I agents work?
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Na+ ch blk
affect phase 0 slow impulse conduction prolong QRS and PR |
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what are the subclasses of class I antiarrhythmics?
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IA: moderate Na+ ch blk and K+
prolong repol phase III and QT procainamide IB: weak Na ch blk; lidocaine IC: potent Na blk, marked QRS prolongation; flecainide |
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weak Na channel blocker?
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IB
lidocaine |
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potent Na ch blocker w/ marked QRS prolongation?
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flecainide
IC |
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moderate Na ch blk that also blocks K+ ch (prolong phase 3 and QT interval)
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procainamide
IA |
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what are IA most often used for?
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procainamide:
atrial arrhyth, sometimes ventric after arrest |
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what's the problem with using procainamide?
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causes severe hypotension during infusion; limited use in unstable pts
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use of IB?
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lidocaine:
not used for atrial arryth commonly after cardiac arrest and malignant ventric arrhyth i.v. only |
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use of IC
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flecainide:
atrial arrhyth in pts w Normal hearts (no heart Dz) dangerous in pts w/ MI or CAD rarely used for ventr arrhy--toxicity |
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what are the side effects of class I drugs?
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all may be proarrhythmic (espec IC in those w/ heart dz)
may cause torsade de pointes procainamide: drug-ind lupus quinidine: syncope, hemolytic anemia lidocaine:CNS tox (seizure/confusion) |
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how do class II drugs work?
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beta adrenergic block (beta 1 R's)
metoprolol, atenolol |
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use of II?
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1. rate control (AV node slowing) for A fib--but don't prevent A fib
2. reduce vent ectopy--may prevent sudden death 3. HF and MI pts |
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some S/E's of class II drugs?
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metoprolol:
fatigue and sex dysfxn in younger pts bradycardia and hypotension at high D |
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mech of class III drugs?
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ibutilide, amiodorone:
K+ ch blk prolong phase 3 and QT interval prolong repol amiodarone has other II and IV effects |
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tX use of Class III?
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ibutilide/amiodarone:
1.A/V arrhyth in pts w/ significant cardiac dz 2. may help prevent arrhyth (A fib)(not ibutilide) 3. amiodorone: after arrest 4. ibutilide: rapid conversion of A fib |
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S/E of class III?
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amiodarone/ibutilide:
1. signif prolong QT--predisposed to torsade de pointes 2. amiodarone: thryoid dysfxn, pulm fibrosis, blue discoloration of skin, liver tox 3. dofetilide: torsade de pointes in renal insufficiency |
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what's torsade de pointes?
which drugs may predispose to this condition? |
malignant ventric tachycardia
class III (amiodarone) due to prolongation of QT interval and class I (a/b/c) |
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what are some side effects of amiodarone?
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thyroid dysfxn
pulmonary fibrosis blue skin liver toxicity (picture an alcoholic smurf with goiter struggling to breath) |
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mech of class IV?
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verapamil/diltiazem:
Ca+2 ch blck ONLY affect pacemaker tissue (slow AP) in sinus and AV |
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uses of IV?
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verapamil/diltiazem:
1. rate control of A fib and other Atrial arrhythmias 2. NOT for ventric arrhyth 3. acute/ rapid control of supraventric arrhyth 4. oral or i.v. |
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side effects of class IV?
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1. dependent edema common
2. may cause heart blk w/ class II (beta blckers) 3. signif bradycardia at high D |