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42 Cards in this Set

  • Front
  • Back
procainamide
IA

mainly for acute tx of atrial arrhythmias, also ventric during arrest
lidocaine
IB

only useful for vent. arrhythmias by i.v. route
flecainide
IC

use: atrial arrhythmias in structurally normal hearts
metoprolol
II

beta blocker
used for rate control in A. fib
ibutilide
III

acute tx A fib and a. flutter
verapamil
IV

Ca+2 ch blk
NOt used for ventric arrhythmias
amiodarone
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)
what's the first choice drug in the elderly or abnl hearts as maintenance tx for atrial arrhythmias?
amiodarone
what's the problem with long term amiodarone tx?
considerable S/E's
what are the two different kinds of action potentials generated by parts of the heart's electrical system?
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
fast AP
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
what's the QT interval?
AP duration or time for complete membrane repol (phase 2 and 3)
what happens during the refractory period?
time which cell can not be depolarized again
slow AP
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
2 most common ways arryhthmias result?
1. abnl or enhanced automaticity (ectopic focus)

2. re-entry
cause of abnl automaticity
from inappropriately increased rate of AP generation: from abnl pacemaker or enhanced activity (Increased slope in phase 4) of abnl tissue
what would an increased slope in phase 4 mean?
enhanced activity ?
what's an ectopic focus?
abnl "pacemaker" site
how do drugs fix arrhythmias due to abnl automaticity?
suppress automaticity
what causes reentry?
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
how do antiarryhthmic drugs work (4 general ways)?
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
how do Class I agents work?
Na+ ch blk
affect phase 0
slow impulse conduction
prolong QRS and PR
what are the subclasses of class I antiarrhythmics?
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
weak Na channel blocker?
IB
lidocaine
potent Na ch blocker w/ marked QRS prolongation?
flecainide
IC
moderate Na ch blk that also blocks K+ ch (prolong phase 3 and QT interval)
procainamide
IA
what are IA most often used for?
procainamide:
atrial arrhyth, sometimes ventric after arrest
what's the problem with using procainamide?
causes severe hypotension during infusion; limited use in unstable pts
use of IB?
lidocaine:
not used for atrial arryth
commonly after cardiac arrest and malignant ventric arrhyth
i.v. only
use of IC
flecainide:
atrial arrhyth in pts w Normal hearts (no heart Dz)
dangerous in pts w/ MI or CAD
rarely used for ventr arrhy--toxicity
what are the side effects of class I drugs?
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)
how do class II drugs work?
beta adrenergic block (beta 1 R's)
metoprolol, atenolol
use of II?
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
some S/E's of class II drugs?
metoprolol:
fatigue and sex dysfxn in younger pts
bradycardia and hypotension at high D
mech of class III drugs?
ibutilide, amiodorone:
K+ ch blk
prolong phase 3 and QT interval
prolong repol

amiodarone has other II and IV effects
tX use of Class III?
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
S/E of class III?
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
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)
what are some side effects of amiodarone?
thyroid dysfxn
pulmonary fibrosis
blue skin
liver toxicity

(picture an alcoholic smurf with goiter struggling to breath)
mech of class IV?
verapamil/diltiazem:
Ca+2 ch blck
ONLY affect pacemaker tissue (slow AP) in sinus and AV
uses of IV?
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.
side effects of class IV?
1. dependent edema common
2. may cause heart blk w/ class II (beta blckers)
3. signif bradycardia at high D