Cadio Antiarrhythmic Flashcards
Cardiac fast fiber AP phase 0
Na+ channels open, sodium enters down concentration gradient. Speed of depolorization depends on number of channels open (Class I drugs slow or block phase 0 in fast response fibers) *the more negative the resting potential the more fast NA+ channels will be ready (M gate closed) to respond and the faster AP conduction response.
Cardiac fast fiber AP phase 1
‘Notch’ Na+ channels inactivated (h gate closed) (no antiarrythmics affect the notch)
Cardiac fast fiber AP phase 2
Plateau phase influx Ca+ L-type late open balanced with K+ efflux . (no antiarrythmics affect the plateau phase)
Cardiac fast fiber AP phase 3
repolarization delayed K+ efflux rapidly increseases L-type Ca+ influx dimminishes (Class III antiarrhythmics slow the repolorization)
Cardiac fast fiber AP phase 4
return to resting potential maintained by Na/Katpase pp *the more negative the resting potential the more fast NA+ channels will be ready (M gate closed) to respond and the faster AP conduction response.
Cardiac slow fiber AP phase 0
SA, AV, and specialized cells phase 0: No Na+ current (absent or innactive) Ca+ influx depolorizez cells (class IV antiarrythmics slow or block)
Cardiac slow fiber AP phase 3
Repolarization K+ rectifyin influx
Cardiac slow fiber AP phase 4
spontanious depolozrixation rising slope Pace maker potential inward Na+ and outward K+ (class II and IV antiarrythmics slow depolarizatio potential usually driven by the SA node)
Cardiac refractory periods
Effective RP: no stimulus can ellicit a response Relative RP: strong stimulus can elicit a response but out of synch with the rest of the heart leading to arrythmias
ANS regulation of the heart
B1 (Gs): slow fiber phase 4 slope increased by increasing cAMP increasing HR. Shortens AP duration by increasing K+ efflux, depolarization velocity increased by increasing Ca+ influx. M2 (Gi): decreases cAMP
Class IA antiarrhythmic
Fast NA+ channel blocker preferentially in the open state - increase AP duration and effective refractory period K+ channel blocker - prolongs repolarization (quinidine and procainamide)
Quinidine
Class IA antiarrythmic.
- Fast Na+ channel blocker preferentially in the open state (slow phase O)
- K+ channel blocker (prolong AP/refractory period phase 2)
- Muscarinic receptor blocker increasing HR and AV conduction (paradoxically remove partial AV block causing vent tachy)
- Alpha 1 blocker vasodilation and possible reflex tacchycardia
Oral. weak base (antacids greatly increase absorption to toxic levels)
TX. atrial fibrilation (with initial digitalization to slow AV)
ADV: [cinhona bark derivative] cinchonism (GI, tinnitis, ocular dysfunction, CNS excitation), hypotension, syncope/torsades (prolongation of QRS and increse QT interval)
Procainamide
Class IA antiarrythmic.
- Fast NA+ channel blocker preferentially in the open state
- K+ channel blocker.
oral/IV. metabolized N-acetyltx (genotypic variation) to active metabolite
ADV. SLE like syndrome, hematotoxicity (thrmobocytopenia, agranulocytosis), torsades, toxicity in hyperkalemia.
tox tx. sodium lactate (increase Na+ concentration and alkalinize tissue)
Class 1B antiarrhythmic
Fast Na+ channel blocker preferentially in the inactive state (h gate closed) partly depolarized tissue. Increase threshold for excitation and less excitability of hypoxic heart muscle. decreased AP duration increasing diastole and recovery time. (lidocaine and mexiletine)
Lidocaine
Class 1B antiarrhythmic. Block fast Na+ channel in depolarized (h gate closed)
IV (high first past metabolism)
TX. post-MI (reduce ventricular automaticity), open heart surgery, digoxin detox
ADV. CNS seizures, least cardio tox compared to other antiarrhythmic
Mexiletine
Class 1B antiarrhythmic. Block fast Na+ channels in depolorized state
Oral formula of lidocaine
TX. post-MI, open heart surgery, digoxin detox
ADV. CNS seizures, least cardio tox compared to other antiarrhythmic
Class 1C antiarrhythmic
Fast Na+ channel block preferential for His-Purkinje tissue. No AP duration effects No ANS effects flecainide
Flecainide
Class 1C antiarrhythmic. ADV. proarrhythmogenic effect (increase HR)sudden death post MI and prophylactic VT.
Class II antiarrhythmic
Beta blocker decrease SA, AV node activity decrease phase 4 slope (distolic current) (propanolol, acebutolol, esmolol)
Class III antiarrhythmic
K+ channel blocker slowing phase 3 repolarization increase AP duraion and effective refractory period (especially in purkinje and ventricuar diseases) Amiodarone, sotalol
Amiodarone
Class III antiarrhythmic K+ channel blocker (AND mimics class I, II, III, IV) t1/2 >80days. binds extensively to tissues. TX. any arrhythmias ADV. pulmonary fibrosis, blue pigmentation of the skin (smurf), phototoxicity, corneal deposits, hepatic necrosis, thyroid dysfunction.
Sotalol
Class III antiarrhythmic K+ channel blocker AND beta 1 blockade decreasig HR and AV conduction TX. life threatening ventricula arrhythmias
Class IV antiarrhythmics
Ca+ slow channel blockers decrease phase 0 and 4 decrease SA and AV node Verapamil, diltiazem
Verapamil
Class IV antiarrhythmics. Ca+ slow channel blockers TX. supraventricular tachycardia ADV. constipation, dissiness, flushing, hypotensive, AV block. Additive AV block with beta blockers (digoxin) byt displacing it from tissue binding sites
Diltiazem
Class IV antiarrhythmics.
Ca+ slow channel blockers
TX. supraventricular tachycardia
ADV. dissiness, flushing, hypotensive, AV block
Adenosine
unclassified antiarrhythmic Gi coupled adenosine receptors. decrease SA and AV node activity
T1/2<10seconds,
TX. paroxysmal supraventricular tachycardia and AV nodal arrhythmias
ADV. flushing, sedation, dyspnea. antagonised by methylxanthines (theophylline and caffeine)
Magnesium
unclassifiec antiarrhythmic TX. torsades caused by class Ia amd III k channel blockade, antipsychotics (thioridazine), and TCAs.
Long QT syndrome
mutation in cardiac K+ channels increased risk of ventricular arrhythmias Class 1a and III antyarruthmics increaes the risk of torsades.
Torsades
TX. correct hypoK+, correct hypoMg+, discontinue drugs prolonging QT interval, attempt to shorten AP duration (electrical pacing or isoproterenol)
