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Pharm exam 5 > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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1
Q

what channels/receptors do class III agents effect

A

K+, Ca2+, Na+ channels & autonomic receptors

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2
Q

main effect of class III agents

A

prolong phase 3 repolarization; increase QT

Effective in many types of arrhythmias

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3
Q

what are the class III agents

A

Amiodarone

Ibutilide

Dofetelide

Dronedarone

Sotalol

(AIDDS)

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4
Q

class III

Blocks K+ channels –> prolongs refractoriness and APD

Blocks Na+ channels that are in the inactivated state

Block Ca2+ channels –> slows SA node phase 4

Slows conduction through the AV node

Noncompetitive blockade of α-, β-, and M receptors

Explains diverse antiarrhythmic actions

A

Amiodarone

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5
Q

clinical applications of amiodarone

A

Conversion and slowing of Af, maintaining sinus rhythm in Af (rx of choice)

AV nodal reentrant tachycardia

IV for acute termination of VT or VF and is replacing lidocaineas first-line therapy for out-of-hospital cardiac arrest

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6
Q

explain pharmacology of amiodarone

A

highly lipophilic

metabolize to DEA: DEA has antiarrythmic potency >/= amiodarone

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7
Q

what may be responsible for early recurrence of arrhythmias after discontinuation or rapid dose reduction of amiodarone

A

Until all tissues are saturated, rapid redistribution out of the myocardium

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8
Q

most serious adverse rxn to amiodarone

other SE

A

most serious: lethal pulmonary fibrosis

Hyperthyroidism or hypothyroidism

elevated serum hepatic enzyme levels

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9
Q

what should be checked when someone is taking amiodarone

A

Check PFTs (CXR/3 months), LFTs, & TFTs when using amiodarone

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10
Q

MOA of Ibutilide

A

Blocks the rapid component of the delayed rectifier K+ current –> slows cardiac repolarization.

Activation of slow inward Na+ current --> prolong AP.
(other class III are not acting on Na+)
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11
Q

therapeutic use of ibutlide

A

IV: acute conversion of atrial flutter and atrial fibrillation to NSR (20 min

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12
Q

SE of ibutilide

A

Excessive QT-interval prolongation and Torsades de Pointes.

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13
Q

MOA of dofetilide

A

Dose-dependent blockade of delayed rectifier K+ current (IKr) (blockade IKrincreases in hypokalemia)

Does not block other K+ channels.

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14
Q

clinical use of dofetilide

A

Restore & maintenance of normal sinus rhythm in patients with Afib.

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15
Q

SE of dofetilide

A

Dose-dependent QT interval prolongation and ventricular proarrhythmia

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16
Q

MOA of sotalol

A

Has both β-blocking & AP-prolonging actions.

acting on K+ channe

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17
Q

clinical use of sotalol

A

Life-threatening ventricular arrhythmias

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18
Q

SE of sotalol

A

Dose-related torsades de pointes

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19
Q

class IV agents

A

Verapamil

Diltiazem

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20
Q

what channels do class IV agents blcok

A

Ca2+

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21
Q

action of class IV agents

A

depressed SA nodal automaticity,

AV nodal conduction,

decreased ventricular contractility

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22
Q

what interval is increased by class IV

A

PR interval

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23
Q

which Ca2+ subunit contains pores

A

alpha1

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24
Q

Ca2+ channel blockers (CCBs) interfere with the entry of Ca2+into cells through voltage-dependent _____ channels.

A

L- and T-type Ca2+

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25
where are CCB major cardiovascular sites of action
vascular smooth muscle cells cardiac myocytes SA and AV nodal cells
26
By binding to specific sites in Ca2+ channel subunits, CCBs diminish the degree to which the Ca2+ channel pores _____
open in response to voltage depolarization
27
which CCBs mainly effect the vasculature
Dihydropyridine (DHP): Nifedipine
28
which CCBs mainly effect the heart?
Non-dihydropyridine (NDHP) Phenylalkylamine - Verapamil Benzothiazepine - Diltiazem --used as antiarrhythmics
29
for CCBs where is vasodilation more seen
more marked in arterial and arteriolar vessels than on veins
30
which CBCs have Negative chronotropic and dromotropic effects are seen on the SA and AV nodal conducting tissue
NDHP agents only (verapamil, diltiazem)`
31
ratio of vasodilation to negative inotropy for the protoype CCBs?
10 : 1 for nifedipine, 1 : 1 for diltiazem and verapamil. 
32
do CCBs have effect on non-cardiovascular smooth muscles will skeletal muscles respond to CCBs?
no no
33
non-cardiovascular effect of CCBs
CCBs may relax uterine smooth muscle and have been used in therapy for preterm contractions
34
what CCBs have IV formulations available
Verapamil, Diltiazem, Nicardipine, Clevidipine (only IV)
35
MOA of verapamil
↓SA automaticity  ↓HR ↓AV conduction velocity --> ↑PR interval Increased ERP Cardiac depression (decrease ventricular contractility and HR) No effect on ventricular Na+ conduction --> ineffective on ventricular arrhythmia
36
clinical application of verpamil
Prevention (PO) or conversion (IV) of nodal arrhythmias: PSVT Rate control in Afib
37
SE of verapamil
Constipation | Exacerbate CHF
38
contraindications of verapmil
WPW syndrome with Afib Ventricular tachycardia
39
MOA of adenosine
Activates A1 receptors in SA & AV nodes --> open K+ channels --> increase K+ efflux --> - SA node hyperpolarization and decrease firing rate - Shortening of AP duration of atrial cells - Depression of A-V conduction velocity Activates A2 receptor in vasculature --> K+ channels - increase endothelial Ca2+ --> increase NO - Smooth muscle hyperpolarization --> vasodilation - stimulates pulmonary stretch receptors
40
clinical use of adenosine
Very effective for acute conversion of paroxysmal supraventricular tachycardia caused by reentry involving accessory bypass pathways.
41
Adenosine pharmacology: how is adenosine administered? what blunts adenosines effects?
t½=10-15 sec Must use as IV bolus to a central vein (brachial, antecubital) Effects blunted by adenosine receptor antagonists: theophylline & caffeine
42
clinical use of magnesium
Torsades de pointes Digitalis-induced arrhythmias
43
what can be used to tx bradycardia
atropine (vagal block increases HR) isoproterenol (B1 stim.) pacemaker
44
what can be used to tx sinus tachycardia, PSVT
vagal stimulation through carotid sinus massage or Valsalva maneuver
45
what are the 4 ways of decreasing spontaneous activity
decrease phase 4 slope increased threshold increased maximum diastolic potential increased action potential duration
46
what are two ways to increase refractoriness
Na+ channel blockade - shifts voltage dependence of recovery and so delays the point at which sufficient Na+ channels have recovered prolonging refractoriness Drugs that prolong AP will also extend ERP point without interacting with Na+ channels
47
Na+ channel blockers bind and block the channels when they are in the _1_ and _2_ states, but not in the _3_ state.
1. open 2. inactivated 3. resting
48
State-dependent blockade - consequences: Slower _1_ rates increases Na+ channel block _2_ increases Na+ channel block
1. drug dissociation | 2. Tachycardia
49
what are class I agents useful for?
***MI induced arrhythmia - ventricular dysrhythmia - digitalis
50
MOA for class I agents
* *Block fast inward Na+ channels to varying degrees in conductive tissues of the heart** - Decrease maximum depolarization rate (Vmax of phase 0) - reduce automaticity, delay conduction - Prolong ERP --> **ERP/APD increased**
51
how can class I agents tx re-entry
block Na+ channels - decrease excitability block K+ channels - increase ERP
52
what do class Ia agents include
Quinidine, Procainamide, Disopyramide | The Queen Proclaims Disos Pyramid
53
Class Ia agents ‘Moderate’ binding to _1_ channels - moderate effects on phase 0 depolarization _2_ channel blockade - delayed phase 3 repolarization - prolonged QRS and *_3_*
1. Na+ 2. K+ 3. QT
54
primary MOA of quinidine (class Ia)
Primary: Block rapid inward Na+ channel: - Decreased Vmax of phase 0 - Slowed conduction (His-Purkinje > atria) - Effects greatest at fast HR (state-dependent block)
55
aside from quinidines primary MOA of blocking rapid inward Na+ channels, what else do they do? - multiple actions - dose dependent effect
Block K+ channels - increase APD Block α receptors - decrease BP Block M receptors - increase HR in intact subjects
56
clinical application of quinidine
Now mainly used in refractory patients to: - Convert symptomatic AF or flutter - Prevent recurrences of AF - Treat documented, life-threatening ventricular arrhythmias
57
SE of quinidine
Diarrhea (most common) cinchonism (headache, tinnitus, hearing loss, blurred vision) hypotension due to α-adrenergic blocking effect proarrhythmic (torsades de pointes – increased QT interval)
58
MOA of procainamide (class Ia)
Block rapid inward Na+ channel --> slows conduction automaticity excitability Blocks K+ channels --> prolongs APD & refractoriness
59
which class I agent has very little vagolytic activity and does not prolong the QT interval to as great an extent
procainamide
60
what does procainamide treat
Ventricular: treat documented, **life-threatening ventricular arrhythmias** Supraventricular: **acute** tx of: - Reentrant SVT - Atrial fibrillation - Atrial flutter associated with Wolff-Parkinson-White syndrome
61
SE of procainamide
Cardiac: - arrhythmia aggravation - torsades de pointes Extracardiac: - SLE-like syndrome - GI nausea and vomiting
62
when is procainamide contraindicated
(contraindicated in long QT syndrome, history of TdP, hypokalemia)
63
what are the class Ib agents
Lidocaine, Mexiletine | First Aid’s mnemonic: I’d Buy Liddy’s Mexican Taco
64
MOA of class Ib
‘Weak’ binding to Na+ channels - weak effect on phase 0 Accelerated phase 3 repolarization - shortened APD and QT interval
65
what are class Ib agents good to use for
digitalis and MI-induced arrhythmia
66
MOA of lidocaine
Blocks **inactivated >> open** Na+ channels - reduces Vmax  Shorten cardiac action potential Lowers the slope of phase 4; altering threshold for excitability produces variable effects in abnormal conduction system - Slows ventricular rate - Potentiates infranodal block
67
Lidocain is more effective in what tissues?
ischemic
68
how is lidocaine more effective in ischemic tissues
Ischemia causes: - Prolonged depolarization - Slow-inactivated state of Na+ channel - depolarized resting potential (-60 mv) 1) Lidocaine (Ib) blocks I >> O --> blocks slow-inactivated Na+ channels that are important in ischemic tissue --> shortens AP 2) Slower dissociation rate --> increase rx effect
69
clinical applications for lidocaine
post-MI (best)
70
how should lidocaine be administered
Extensive first-pass hepatic metabolism --> IV use. | need multiple loading doses and a maintenance infusion
71
SE of lidocaine
rapid bolus: tinnitus, seizure
72
what the class Ic agents?
Propafenone, Flecainide
73
MOA of class Ic agents (Propafenone, Flecainide)
* **Strongest binding to Na+ channels (O state) a) **slow dissociation** – strong effects on phase 0 depolarization b) ***lengthened QRS**, less on APD c) Little effect on repolarization - QT unchanged d) lengthened PR (depressed AV nodal conduction)
74
MOA of propafenone
**Strong inhibitor of Na+ channel Can inhibits beta-adrenergic R: marked structural similarity to propranolol
75
Clinical application of propafenone
ventricular arrhythmias in patients with no or minimal heart disease and preserved ventricular function
76
MOA of flecainide
potent Na+ channel blockade --> prolongs phase 0 and widens QRS ***markedly slows intraventricular conduction
77
clinical application for Flecainide
use only in the treatment of refractory life-threatening ectopic ventricular arrhythmia **not considered a first-line agent due to propensity for fatal proarrhythmic effects
78
Class Ic SE
Proarrhythmic, especially post-MI
79
what are class Ic agents contraindicated in?
structural and ischemic heart disease
80
what are the class II agents
Beta adrenergic antagonists Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol
81
MOA of class II agents (Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol)
decrease cAMP, decrease Ca2+ currents --> - decrease SA nodal automaticity (phase 4); - decrease AV nodal conduction - decrease Ventricular contractility
82
what are class II agents effective for?
supraventricular arrhythmias due to excessive sympathetic activity
83
Are the only antiarrhythmic drugs found to be clearly effective in preventing sudden cardiac death in patients with prior MI
class II agents - beta adrenergic antagonists Metoprolol, Propranolol, Esmolol, Atenolol, Timolol, Carvedilol
84
what class II agent has a very short half life and is only used IV - useful when short termed beta blockade is desired (aortic dissection, critically ill pts, postop HTN)
esmolol
85
SE of class II agents
1. Impotence 2. Exacerbation of COPD & asthma 3. Bradycardia, AV block, heart failure; mask signs of hypoglycemia 4. CNS: sedation, sleep alterations 5. Dyslipidemia: Metoprolol 6. Exacerbation of Prinzmetal angina: Propranolol 7. Unopposed alpha1 agonism if given alone in pheochromocytoma or cocaine toxicity, except carvedilol & labetalol (blocking both alpha and beta)
86
main clinical applications of CCBs - both dihydropyridines and nondihydropyridines
systemic HTN angina pectoris coronary spasm
87
Main clinical applications of CCBs for only nondihydropyridines
SVT Post-infarct

Pharm exam 5 (9 decks)

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