pharmaco 4 arrhythmias

ability to initiate own activity via spontaneous depolarization

regularity of depolarization rates

ability to transmit impulses from cell to cell at appropriate rates

ability to resist partially or completely to stimulation during repolarization

P wave

QRS wave

T wave

SA node recovery

cardiac myocyte (working cell) resting potential

nodal cells (signal cells) resting potential

what is responsible for the depolarization in the nodal cells

"daughter impulses" or reentry circuits in the heart cause what

first degree heart block

second degree heart block

third degree heart block

caused by ectopic atrial focus
P waves are abnormal
QRST are normal

ventricular premature beat followed by comensatory pause
does not interrupt regular discharge of SA node

accelerated AV conduction
additional averrant connection between atria and ventricles (AV node is normal)
short PR interval
prolonged QRS deflection
together they have a normal interval between start of P wave and end of QRS complex

class IA ______  action potential duration

class IB ______  action potential duration

class IC ______  action potential duration

order of class I interaction with Na channels

action of IA agent on the conduction velocity

action of IA agent on repolarization

class IC effect of polarization

what is the atropine like toxicity of quinidine

ganglionic blocking properties - hypotension
lupus like syndrome with prolonged use
increase in immune response through increased antinuclear antibody titer
oral/ slow infusion only

first choice for sustained ventriicular arrythmias

second choice for sustainded ventricular arrythmias

class IA
useful for idiopathic hypertrophic subaortic stenosis
C/I in pt. with left ventricular dysfunction

which class is indicated for ventricular arrhythmias only

agent of choice for ventricular tachycardia and fibrillation after cardioversion

why is lidocaine a potent local anesthetic

least cardiotoxic of the Na blockers
problems with CNS toxicities

used for Digoxin induced ventricular arrhythmias
weak Na blocker
CNS toxicities

class I group that is the most potent
profound slow conduction velocity (QRS wideing) - avoid with heart insuficiency

class IC
potent blocker of Na & K channels
used for supraventricular arrhythmias
C/I in pt with heart failure
unique K channel not involved with repolarization

class IC
potent Na block
prodrug - metabolite has beta blocking effect
AE - metallic taste

class IC
used to treat ventricular arrhythmias
does not prolong action potential duraction

class II agents effects on QRS and QT intervals

class II effects of SA and AV conduction

class II slowing of the SA->AV conduction is what on the ECG

which class of drugs prevents the daughter currents - recurrent infarction

what two drugs are used together to improve conversion of atrial fibrillation to sinus rhythm

what two drugs are used together to control ventricular rate in a patient with atrial fibrillation or flutter

class III effects on effective refractory period

class III effect of action potential (repolarization)

class III effect on QT intervals

class III that is very effective at blocking inactivated Na channels
long half life - 103d
toxicity of yellow brown crystals on cornea
markedly prolongs AP duration

class III
short duration of effect
positive inotropic action
prolongs ventricular (not atrial) AP duration and effective refractory period
develop postural hypotensio
increased digoxin toxicity

class III
used in supraventricular and ventricular arrhythmias
toxicity of excess beta blockage

class III
indicated for conversion of atrial fibrillation and flutter
avoid in ventricular tachycardia

class IV effects of conduction (SA -> AV nodes)

class IV effects on effective refractory period

verapamil, diltiazem and bepridil effects on QT interval

class IV
blocks both activated and inactivated Ca channels
most marked effect in SA & AV nodes
used for reentrant suprventricular tachycardia (PSVT), atrial fibrillation & flutter
AE - increase digoxin