Antiarrythmia drugs

Question 0

Quinidine indications

Answer 0

!! broad spectrum
!! Acute or chronic tx of supraventricular (atrial ) and ventricular arrhythmias !!
rarely used
oral

Question 1

Quinidine 2 MOAs

Answer 1

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)

Question 2

Quinidine SE

Answer 2

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

Question 3

Procainamide

Answer 3

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?)

Question 4

Lidocaine

Class IB

Answer 4

-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

Question 5

which is the least toxic drug with least inotropic effects?

Answer 5

Lidocaine

Question 6

which drug can cause CONVULSIONS?

Answer 6

lidocaine

Question 7

which is DOC for ventricular arr?

Answer 7

Lidocaine

Question 8

Flecainide (Tambocor)

Answer 8

-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

Question 9

which drug is the most strong pro-arr? will cause arr?

Answer 9

Flecainide

Question 10

Beta Blockers:

Propranolo, Acebutolol, Esmolo

Answer 10

Esmolol:
B1
shortest 1/2 life, IV only, ER acute tx only for PSVTs
Propranolol - non specific b blocker
Acebutolol - B1 blocker

Question 11

Esmolol is

Answer 11

B1 blocker,
short 1/2 life
IV and acute tx only

Question 12

Propranolol

Answer 12

non selective BB

Question 13

Acebutolol

Answer 13

B1 blocker

Question 14

Amiodarone MOA

Answer 14

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)

Question 15

Amiodarone Indications

Answer 15

• 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)

Question 16

Sotalol (Betapace)

Answer 16

-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

Question 17

VERApamil and DilTIAZEM

Answer 17

-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 !!

Question 18

Adenosine

Answer 18

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)

Question 19

Magnesium

Answer 19

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)

Question 20

which drug is DOC for Torsade de pointes?

Answer 20

Magnesium

Question 21

Potassium

Answer 21

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

Question 22

Which drug is the DOC for digitalis induced arrythmia?

Answer 22

Magnesium (as well as DOC FOR TORSADE)

Question 23

Which drug causes Lupus?

Answer 23

PROcainamide

Question 24

which is contraindicated with Beta blockers

Answer 24

VERApamil, and dilTiazem