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no longer used for rhythm control, modestly effective, very Increased TdP = hypotension syncope
toxic and sudden death within the 1st few
Moderate Na channel Blocker which supraventricular and ventricular arrhythmias like atrial days; Nausea, diarrhea, abdominal
also blocks K channelsprolongs fibrillation & atrial flutter (moderately effective), ventricular cramping; Cinchonism = vertigo, HA,
QRS&QTaction potential; reduce extrasystoles and VT(poorly effective) tinnitus, psychosis, blurred vision; rash, Do not use in pt with long QT Rarely used;has a vasodilator effect so can be used in reduced
Quinidine (Antiarrhythmic automaticity and conduction velocity Major clinical use: atrial fibrillation, atrial flutter, & thrombocytopenia, hemolytic anemia;lupoid syndrom, TdP history, or vent function or HF; also has a indirect anticholinergic effect that
Class IA) (Phase 0 and phase 3) ventricular tachcycardia hepatitis and 2X to 3X increase in mortality hypokalemia (increases TdP) Put Na in your tonic and call it quinidine will decrease vagal tone and may facilitate condion in the AV node
Class 1B
Reduce automaticity
CNS symptoms: seizures!! (mental Shorten APD (narrow QRS)
modest Na channel blockers (both acute rapid suppression of V arrhythmias, raises status changes), drowsiness, dyarthria, Slow conduction velocity
active and inactive Na channels) ventricular fibrillation threshold as well as suppresses dysesthesi, and coma; can depress cardiac Remember: class I be (B) ventin (works only on Have little or no effect on atrial tissue
Reduce automaticity arrhythmias caused by abnormal automaticity (observed pt function leading to decreased clearance, ventricle) with the short fuse temper (shortens all other classes work above ventricles
Lidocaine (Antiarrhythmic Shorten APD (narrow QRS) continuoulsy for SE), no atria effect; very effective membrane and produce greater SE; sinus node AP) Moderately effective for ventricular arrhythmia
Class IB) Slow conduction velocity stabilizer (numbing) dysfunction only used for V!!
CNS symptoms: seizures!! (mental
modest Na channel blockers (both status changes); dose related tremor, Remember: the Mexican (Mexiletine) injected
active and inactive Na channels) ventricular arrhythmias & refractory arrhythmias; useful in visual blurring, dizziness, dysphoria, and his toe (tocainamide) with lidocaine to numb Typically hepatic metabolism (CYP2D6), can be increased with
Reduce automaticity pts with torsades de pointes (TdP) or long QT syndrome (if nausea; thrombocytopenia and postivie the 1 Bee sting (class IB), but goes into a phenobarbital, phenytoin, or rifampicin; Pts with hepatic CYP2D6
Mexiletine (Antiarrhythmic Shorten APD (narrow QRS) other drugs contra), no effect in atrium; very effective ANA; worsen heart block with high seizure and wishes he'd injected dilantin deficiency are dependent on renal excretion. (notice, quinidine
Class IB) Slow conduction velocity membrane stabilizer (numbing) concentration instead inhibits the CYP2D6 Ez)
modest Na channel blockers (both
active and inactive Na channels)
Reduce automaticity
Tocainamide Shorten APD (narrow QRS)
(Antiarrhythmic Class IB) Slow conduction velocity similar to lidocaine
Effective for Atypical Ventricular Tachycardia;
Phenytoin [Dilantin] more typically used for seizures (also a membrane stabilizer,
(Antiarrhythmic Class IB ) Na channel blocker arrthymia in brain) Remember: die laughing so had a seizure
highly effective Na channel blocker; proarrhythmia!!; CHF; CNS=blurred drug interactions: cimetidine
Prolongs PR and QRS (prolongs AP), Potent inhibitor of ventricular arrhythmia; effective vision, headache, ataxia;decreases LV its clearance its half-life;
Flecainide (Antiarrhythmic reduces automaticity and conduction stabilization of atrial rhythm; supraventricular arrhythmias in function and depresses the SA node in pt digoxin, propranolol, & Remember: flick a cain in someones one eye eliminated by the liver (CYP2D6) and kidney(so not effected by
Class IC) velocity in A and V; negative inotrope pt with no structural heart dz with SA node dysfunction amiodarone its levels and they can't see (1C) CYP2D6 deficiency except in renal insufficiency)
Dofetilide (Antiarrhythmic
mixed Class IC & III) similar to Flecainide similar to Flecainide similar to Flecainide
facial flushing, dyspnea, or chest pressure dont use for AFib, sick sinus
DOC for acute Paroxysmal SVT caused by re-entry thru AV lasts <60 sec; sometimes nausea, syndrome, or 2 and 3 heart
Adenosine (antiarrhythmic Slows AV node conduction - causes node; lightheadedness, headache, sweating, block unless they have a Half life of 1.5 to 10 sec (shortest half life of any drug);
class V) transient heart block in the AV node diagnostic tool (see extra notes) palpitation, hypotension and blurred vision pacemaker metabolized in the plasma
Disopyramide:
Moderately effective for atrial arrhythmia and poorly effective for
Antiarrhythmics: limited usefulness because of toxicity and ventricular arrhythmia
lack of efficacy; may worsen mortality. Every agent has Antiarrhythmic Class I (A, B, & C): local anesthetic or Reduces automaticity and conduction velocity
Antiarrhythmic Class IA include quinidine, procainamide, potential for serious toxicity. Classified according to membrane-stabilizing activity; block fast inward Na Side effects include decreased contractility and urinary retention
and disopyramide - increase venticular refractoriness and electrophysiology (see Cecil 341) for Vaughan William s Class channel, decreasing maximum depolarization rate, Vmax, has anticholinergic effects - stops peeing, pooping, salivating
prolong the QT inverval (I, II, III, & IV) of the AP (phase 0); basically Na Channel Blockers
Antiarrhythmic Class Class IB include lidocain, mexiletine, Synergistic depression of myocardial function with combo of Lidocaine works on slightly depolarrized or ischemic tissue Note: Infiltration of inflammation mediators and necrotic materials
and tocainide - modest Na channel blockers that shorten other antiarrhythmic agents (especially propranolol). Pts with more so than normal tissue, due to its state-dependent lower tissue pH (eg abcess) and render lidocain anestheic less
the action potential duration (APD) and refractoriness with heart failure (HF) achieve lidocaine levels that are double blocking. Therefore, use lidocaine (IV) to suppress acute effective (lidocaine is a weak base, does not work when
little effect on PR, QRS, or QT intervals the levels of normal pts (reduce dose by half) MI-associated ventricular arrhythmias protonated)
Class 1C
Antiarrhythmic Class Class IC include flecainide and Reduce automaticity and conduction velocity in atria and Class IC do same thing as class1A, but more powerful
propalenone - potent Na channel blockers that slow ventricles very powerful side effects, the worst SE is accutally
conduction velocity, little effect on repolarization, and increase Prolong action potential duration worsening arrhythmia
PR and QRS intervals, little change on QT interval Major side effect is proarrhythmia Class IC kills people; thus, they are not used as first line agents
Amiodarone:
prolonged half-life of 30 days - makes difficult to use to
reach steady state (4-5 half lives) requires half a year (3
months for effect), and if make a mistake, takes 5 half lives to
get ride of , must follow pt closely (have foresight)
Rapid effect when given IV
Side Effects
Hepatotoxicity
Hypo and hyperthyroidism
Corneal deposits hypothyrodism SE either as a result of its high iodine content Dose dependent toxicity especially with long-term use
Irreversible pulmonary fibrosis (permanent) or by inducing thyroiditis (avoid use in young pts) Increased AP duration causes the increase in QT interval
When macula densa sense increase NaCl, they send signal (via extraglomerular mesanginum) to granular cells to secret
Used diagnostically to determine whether ventriclar drug interactions: carbamazepine and dipyridamole adenosine which vasoconstricts primarily the afferent a. (know that in most areas of the body adenosine is a vasodilator,
tachycardia was induced supraventricularly or pretreatment its potency; caffeine and theophylline not so in the kidneys), decreasing GFR (moderate constriction; if severe constriction then GFR decreases because blood
ventricularly antagonize it flow becomes so stagnant that proteins clog up on exam always assume moderate efferent a. constriction)
Procainamide:
Moderately effective for atrial or ventricular arrhythmia
Metabolized in liver to active component NAPA
this metabolite is more effective (acetly group)
must check prodrug and metabolite to prevent toxcity
Reduce automaticity and conduction velocity
effects phase 4 and 0
Antiarrhythmic Class III: prolong duration of cardiac action Universal adverse effect is lupus
potential (AP) and refractoriness