Antiarrythmia drugs Flashcards
Quinidine indications
!! broad spectrum
!! Acute or chronic tx of supraventricular (atrial ) and ventricular arrhythmias !!
rarely used
oral
Quinidine 2 MOAs
1) main: block activated Na channels (“state dependent” blockage)
- slows the rate of rise (depolarization of AP)
2) block K ch’s:
- keeps AP in plateau phase and widens AP/ prolongs AP duration (APD) and Effecitve Refractory Period (ERP)
Quinidine SE
SE:
- LOW THERAPEUTIC INDEX (narrow range bf SE)
- CARDIAC TOXICITY: SA block, AV block, ventr arr
-BLOCKS RECEPTORS -> severe HYPOtension and reflex tachy (increase HR and increase SNS on hrt = increase arr’s)
-PARADOXICAL TACHY: “anticolinergic” effect; reflex tachy due to vasodilation (why?)
-TORSADE DE POINTES (increased PVCs back to back , killer of child athletes)
-QUINIDINE SYNCOPE (widening of QRS and qT intervals):
pts with long QT intervals are at greater risk (child athletes)
- DIARRHEA (top diarrhea drug)
- CINCHONISM (unique problems): loss of hearing, angioedema (?), vertigo, tinnitus, visual disturbances, thrombocytopenic, purpura, vascular collaps
Procainamide
Blocks activated Na ch’s
Similar to Quinidine but SE: lupus erythematosus (also by hydrolysine, isoniazid)
and hepatic metabolism (fast and slow chelators - does this lead to Lupus?)
Lidocaine
Class IB
-blocks inactivated Na ch’s, fast binding and dissociateion
-preferentially affects damaged tissue which has more inactivated ——-receptors
- shortens APd/decreases ERP (effective refractory period) ———(blocks “window current”)
DOC for ventricular arr
IV only, only use in ER (acute) - that’s how to DDx from amiodorone
Rapid onset, met by liver
SE:
least toxic, LEAST NEGATIVE INOTROPIC
CONVULSIONS
which is the least toxic drug with least inotropic effects?
Lidocaine
which drug can cause CONVULSIONS?
lidocaine
which is DOC for ventricular arr?
Lidocaine
Flecainide (Tambocor)
-blocks ALL Na ch’s, STRONG binding (dissociates slowly)
-NO effect on ERP
-mo PRO-arryth drug - causes arr
Used for (last ditch effort drug - bc binds too strongly and causes arr)
-supraventricular arr
-life threatenign vetnricular arr
(Oral, hepatic met, renal excretion)
SE:
STRONG PRO ARR DRUG
which drug is the most strong pro-arr? will cause arr?
Flecainide
Beta Blockers:
Propranolo, Acebutolol, Esmolo
Esmolol: B1 shortest 1/2 life, IV only, ER acute tx only for PSVTs Propranolol - non specific b blocker Acebutolol - B1 blocker
Esmolol is
B1 blocker,
short 1/2 life
IV and acute tx only
Propranolol
non selective BB
Acebutolol
B1 blocker
Amiodarone MOA
Jack of all anti arr Class III - blocks K chs: slows rate of repolarization: prolongs plateau/AP duration/ERP and will prolong QT but will NOT CAUSE TORSADE (bc of all the good things it does below) plus: -blocks Na chs (class 1) -Beta Blocker (Class II) -some Ca ch blocking (class IV) - alpha blocker (oral or IV, 13-103 day half life)
Amiodarone Indications
- AGAINST BOTH SUPRAVENT AND VENTRICULAR ARR
-DOC FOR VENTRICULAR ARR (acc’g to brds)
(DDx from lidocaine - lidocaine only used IV and in ER)
SE: - NO TORSADE <- slows sinus rate, conduction and prolongs QT (most drugs that increase QT cause Torsade)
-PULMONARY FIBROSIS - IRREVERSIBLE (unique)
-DEPOSITED IN TISSUES, CORNEA (YELLOW-BROWN), SKIN (GRAYISH-BLUE), - THYROID DYSFX (iode in the name - made of high iodine content)
Sotalol (Betapace)
-K blocker - > prolongs AP duration (APD)
-Non selective B BLocker (B1 and B2)
For:
VENTRICULAR AND SUPRAVENTRICULAR ARR
(oral, excreted by kid)
SE:
-TORSADE
-blocks B receptors bc its a non sel beta blocker
VERApamil and DilTIAZEM
-blocks slow L-type cardiac Ca chs (Only good for atria bc this is where Ca is most impt in depolarization and setting rate)
For: (where Ca is used for depolarization)
- REENTRANT SUPRAVENTRICULAR TACHY
-PSVT
SE:
- Hallmark: !! most negative inotropic action, constipation !!
-avoid combo with b-blockers !!
Adenosine
MOA: increases K conductance = opens K channels and inh cAMP-induced Ca influs into cell (so decreases contractions?)
-increased K chs hyperpolarizes everything, heart stops for 10 seconds and resets the hearth hopefully to normal rhythm
1/2 life: 10 seconds, IV only
DOC FOR ACUTE PSVT AND WPW (WOLV PARKINSONS) SYNDROME
-effective ONLY for REENTRY ARRYTHMIAS
SE (flushing, SOB, chest burning, hypotension, whatever)
Magnesium
MOA unknown IV -anti arr in pts with normal mg levels -DOC for digitalis induced arr - DOC FOR TORSADE - for seizures in pregs due to toxemia (eclampsia)
which drug is DOC for Torsade de pointes?
Magnesium
Potassium
Both high and low K cause arr
MOA:
increased serum K makes resting potential more + (depolarizes) (is it because normally [K] inside cell is higher than outside and when K chs open during AP, the gradient allows K to leave the cell and repolarize it but when the [K] outside is too high, K stays inside the cell and keeps it more positive?
-high serum K has membrane potential stabilizing action by increasing K permeability (opening chs), and this action predominates (hyperpolarizes) This sounds like the opposite of the above action
When increase permiability for K:
- decrease AP duration (bc repolarizes faster)
- decrease conduction
- decrease pacemaker rate
- decrease pacemaker arrhythmogenesis
Which drug is the DOC for digitalis induced arrythmia?
Magnesium (as well as DOC FOR TORSADE)
Which drug causes Lupus?
PROcainamide
which is contraindicated with Beta blockers
VERApamil, and dilTiazem
