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CV II Exam III > Pharmacology of Antiarrhythmics (kinder) > Flashcards

Pharmacology of Antiarrhythmics (kinder) Flashcards

1
Q

class Ia Na channel blockers

A

“Double quarter pounder”

a) Disopyramide (Norpace)
b) Quinidine
c) Procainamide ***

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2
Q

class I b Na channel blockers

A

“lettuce tomato mayo”

a) Lidocaine (Xylocaine)***
b) Mexiletine
c) Tocainide

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3
Q

class I c Na channel blockers

A

“more fries please”

moricizine,

flecainide ***

propafenone

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4
Q

Class II

A

beta adrenergic receptor blockers

esmolol
metoprolol
propranolol

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5
Q

class III

A

K+ channel blockers

“a big dog is scary”

a) Amiodarone (Cordarone) **
b) Bretylium
c) Dofetilide (Tikosyn)
d) Ibutilide
e) Sotalol (Betapace) **

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6
Q

Class IV

A

Ca channel blockers

Verapamil
Diltiazem

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7
Q

what is the major determinant of membrane potential in the resting cardiac cell

A

extracellular potassium concentration and inward rectifier channels

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8
Q

phase O of cell depolarization

A

rapid depolarization due to influx of Na

positive into the cell

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9
Q

phase 1

A

brief repolarization

(1) Transient and active K+ efflux, Ca2+ begins to move into intracellular space at about -60 mV causing slower depolarization

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10
Q

phase 2

A

plateau

ca 2+ influx continues (L channels in the myocardium)

balanced somewhat by K+ efflux

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11
Q

phase 3

A

cellular repolarization

membrane remains permeable to K+ efflux

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12
Q

phase 4

A

gradual depolarization

constant Na leak into intracellular space balanced by decreased K efflux overtime

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13
Q

diastolic interval (duration of diastole ) is determined by what

A

slope of phase 4 of action depolarization

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14
Q

what is early after depolarization (EAD)

when is this exacerbated

A

(3) Early afterdepolarization: transient depolarization that interrupts phase 3
(a) Exacerbated at slow heart rates, contributes to long QT

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15
Q

what is delayed after depolarization (DAD)

A

interrupts phase 4 - and typically occurs after a cell has repolarized

(a) Often occurs when intracellular calcium is increased, exacerbated by fast heart rates
(b) Responsible for some arrhythmias related to excess digitalis, catecholamines, and myocardial ischemia

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16
Q

what is reentry and what 3 conditions MUST be met for reentry to occur ?

A

impulse reenters and excites areas of the heart more than once

(1) 3 conditions must be met for reentry to occur
(a) Must be an obstacle, thus establishing a circuit
(b) Must be a unidirectional block
(c) Conduction time must be long enough that retrograde impulse does not encounter refractory tissues

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17
Q

what is the goal of pharm agents that depress autonomic properties of abnormal pacemaker cell

A

i) Action: decrease slope of phase 4 depolarization and/or elevate threshold potential
(1) If rate of spontaneous impulse < SA node → restoration of normal cardiac rhythm

NOTE anti-arrhythmics CAN induce arrhythmias

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18
Q

Type I a (sodium channel blockers) mechansim….
what is the effect on conduction velocity? refractory period?

clinical uses?

A

(1) Decrease conduction velocity, increase refractoriness, decrease autonomic properties of Na+ dependent conduction tissue

(2) unidirectional block transformed to bidirectional
(3) Has some potassium blocking properties

(4) Clinically effective in supraventricular and ventricular arrhythmias

intermediate kinetics

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19
Q

what is the mechanism of type Ib sodium channel blockers?

effect on refractoriness
effect on conduction velocity
effect on AP
clinical use?

A

shorten the action potential duration in some tissues in the heart and dissociate rapidly

(1) Decrease refractoriness with no effect on conduction velocity
(a) Improves antegrade conduction, eliminating area of unidirectional block
(2) However, in diseased tissue, refractoriness prolonged leading to bidirectional block

(3) Clinically effective in ventricular arrhythmias more than supraventricular arrhythmias

rapid kinetics

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20
Q

Type Ic sodium channel blockers

effects on AP
effect on conduction velocity
effect on refractoriness

A

minimal effects on action potential duration and dissociate slowly (slow kinetics)

(1) Profoundly decreases conduction velocity while leaving refractoriness
(a) Theoretically eliminate reentry by slowing conduction to the point where impulse extinguished
(2) Clinically effective for ventricular and supraventricular arrhythmias but use in ventricular arrhythmias limited due to risk of proarrhythmias

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21
Q

Type II sympatholytic b blockers

A

i) Decrease conduction velocity, increase refractoriness, decrease automacity in nodal tissues
ii) Anti-adrenergic actions

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22
Q

Type III potassium channel blockers….

A

prolong the action potential duration

i) Prolong refractoriness in atrial and ventricular tissues
ii) Delay repolarization by blocking K+ channels

23
Q

type IV calcium channel blockers

A

slows conduction where action potential dependent on calcium (SA and AV nodes)
i) Decreases conduction, increases refractoriness, decreases automacity in calcium dependent tissues

non DHP’s

24
Q

procainamide

effect on upstroke
effect on conduction
effect on QRS
effect on SA and AV nodes

A

Type I a

slows upstroke of action potential, slows conduction, prolongs QRS, prolong APD (a class III action due to nonspecific blockage of K+ channels), direct depressant effects on SA and AV nodes

1/2 life 3-4 hours

25
what occurs in toxicity with procainamide
excessive action potential prolongation QT prolongation induction of TdP new arrhythmias. Reversible lupus erythematosus like syndrome (~33%) consisting of arthralgia and arthritis (some patients experience pleuritis, pericarditis, or parenchymal pulmonary disease, rarely renal lupus). Increased ANA titer without symptoms not an indication to stop therapy. Nausea and diarrhea (10%), rash, fever, hepatitis (< 5%), agranulocytosis (< 0.2%).
26
what is the metabolite of procainamide and what action does it have>
(a) Metabolite N-acetylprocainamide (NAPA) has class III activity → accumulation implicated in TdP (especially in renal failure)
27
what is the therapeutic use of procainamide
atrial and ventricular arrhythmias. Long-term therapy avoided due to frequent dosing and lupus-like adverse effects. Used second or third line for sustained ventricular arrhythmias after MI
28
quinidine MOA? toxicity?
type Ia MOA is like procainamide--> slows upstroke of AP, slows conduction, prolongs QRS, prolong ADP, depressant on SA and AV nodes (1)Toxicity: GI [diarrhea, nausea, vomiting (33-50%)], headache, dizziness, tinnitus, rarely immunologic reactions (thrombocytopenia, hepatitis, angioneurotic edema)
29
Disopyramide | toxicity?
type Ia very similar action to quinidine and procainamide (1)Toxicity: much more pronounced antimuscarinic effects (should also administer a drug that slows AV conduction), precipitates heart failure (with preexisting depression of LV function or de novo), urinary retention, dry mouth, blurred vision, constipation.
30
Lidocaine MOA
type I b blocks activated and inactivated sodium channels with rapid kinetics
31
toxicity of lidocaine
least cardiotoxic of Na channel blockers large doses may cause hypotension (especially if pre-existing heart failure) *** most common adverse effects are neurologic (paresthesias, tremor, nausea of central origin, lightheaded, hearing disturbance, slurred speech, convulsions)
32
how do you administer lidocaine?
IV b/c of extensive first pass metabolism t 1/2 is 1-2 hrs
33
how does lidocaine interact with alpha 1 acid glycoprotein (acute phase reactant)
(c) Occasional patients with MI or other acute illness require higher doses due to increased plasma α1-acid glycoprotein (an acute phase reactant) binding lidocaine making less free drug available
34
what is the therapeutic use of lidocaine?
DOC for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, prophylactic use of lidocaine may increase total mortality by increasing incidence of asystole. Most administer lidocaine to those with arrhythmias
35
what is mexiletine
orally active congener of lidocaine (1) PK and dosage: half-life 8-20 hrs, dosed two to three times daily (2) Toxicity: neurologic (tremor, blurred vision, lethargy), nausea (3) Therapeutic use: ventricular arrhythmias, off-label use for chronic pain
36
flecainide therapeutic use half life? MOA
type Ic potent blocker of sodium and potassium channels but does not prolong action potential or the QT interval t1/2 is 20 hrs therapeutic use? supraventricular arrhythmias
37
toxicity of flecainide
severe exacerbation of arrhythmia even when normal doses are administered to patients with preexisting ventricular tachyarrhythmias and those with previous MI
38
propafenone MOA toxicity uses?
Type I c sodium channel blocking kinetics similar to flecainide but with weak b-blocking activity does not prolong AP (1)Toxicity: metallic taste, constipation, arrhythmia exacerbation used for supraventricular arrhythmias
39
Amiodarone MOA? extracardiac effects?
type IIII potassium channel blocker markedly prolongs action potential duration (and QT interval) by blocking IKR, chronic administration results in IKS blockage blocks AP over a wide range of heart rates Also significantly blocks sodium channels, weak adrenergic and calcium channel blockade. Broad spectrum of activity may account for high efficacy and low incidence of TdP Extracardiac effects--> peripheral vasodilation
40
what are the toxicity signs of amiodarone
symptomatic bradycardia heart block in those with preexisting sinus of AV node disease. Accumulates in heart (10-50x more than plasma), lung, liver, skin, and concentrates in tears. ***Most important ADR: pulmonary toxicity, fatal pulmonary fibrosis (1%). Abnormal LFTs, skin deposits, photodermatitis, gray-blue skin discoloration in sun-exposed areas, corneal microdeposits. Blocks peripheral conversion of thyroxine (T4) to triiodothyronine (T3), may result in hypo- or hyperthyroidism
41
drug interactions of amiodarone?
MANY increase amiodarone levels with CYP3A4 blockers (climetidine) decreases amiodarone levels with CYP3A4 inducers (rifampin) increased drug levels of statins, digoxin, warfarin (reduce dose by 33-50%) ****
42
what are the therapeutic uses of amiodarone
atrial fibrillation prevention of recurrent ventricular tachycardia not associated with increased mortality in patients with CAD or heart failure used as adjunct with implanted cardioverter-defibrillator (ICD) to reduce the frequency of uncomfortable discharges
43
Dronedarone
type III potassium channel blocker structural analog of amiodarone with iodine atoms removed. Designed to eliminate action of parent drug on thyroxine metabolism and modify half-life of drug. Multi-channel actions: IKr, IKs, ICa, INa, and B-blocking actions
44
toxicity of dronedarone
no thyroid dysfunction or pulmonary toxicity but liver toxicity has been reported (with two cases requiring transplant). ***Black box warning against use in acute decompensated or advance (class IV) heart failure
45
PK and dosage of dronedarone? | t 1/2 life?
t 1/2 is 24 hrs (a) Food increases absorption two-threefold (b) Non-renal elimination, but inhibits tubular secretion of creatinine resulting in 10-20% increase in SCr (c) Both substrate and inhibitor of CYP3A4, should not be co-administered with potent inhibitors (azoles, protease inhibitors)
46
therapeutic use of dronedarone?
atrial fibrillation (restores sinus rhythm in < 15% of patients)
47
sotalol
type III potassium channel blocker both β-adrengergic blocking actions and action potential prolonging actions. Racemic mixture, L-isomer responsible for β-blocking activity, both L and D-isomers responsible for action potential prolongation. β-blocking effects not cardioselective.
48
what is the electrical gradient in normal cells
-90 mv inside 0 mv outside
49
conc of sodium intracellular and extracellular
intra--> 5-15 extra -> 135- 142 like to flow in
50
conc of Potassium intracellular and extracellular
intra - 135-140 extra 3-5 like to flow out
51
which gates of the sodium channels are open and closed during threshold, depolarization, and repolarization
threshold--> opens m gates (activation gates) If inactivation (h) gates have not already closed, the channels are open and activated and depolarization occurs Opening is brief . Open (m) gates very quickly followed by closure of (h) gates and channel inactivation (repolarization)
52
what are the ion movements during contraction ?
1) ca entry from outside the cell triggers the release of much larger quantity of Ca from the SR 2) increased Ca initiates contraction process 3) ca is removed by reuptake into the SR and by Ca/Na exchanger Sodium balance restored by Na/K atpase
53
how do you reduce the rate of spontaneous discharge 4 ways
decrease phase 4 slope increase threshold potential increase maximum diastolic potential increase AP duration

CV II Exam III (14 decks)

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