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Pharmacology > Drugs for Cardiac Dysrhythmia > Flashcards

Drugs for Cardiac Dysrhythmia Flashcards

1
Q

Sodium channel blockers - MoA

A

Slow phase 0 depolarization and cardiac conduction –> increases QRS duration.

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2
Q

Class I sodium channel blockers - MoA and subdivision

A

Bind to sodium channels when the channels are in the open and inactivated states, and dissociate from the channels during the resting state.

Subdivided into 3 gr based on whether they have greater affinity for the open state or the inactivated state and based on their rate of dissociation from sodium channels (rate of recovery).

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3
Q

Class IA drugs - MoA

A

Greater affinity for the open state and have slow recovery.

Block the fast sodium channel and delayed potassium channels –> they slow phase 0 depolarization and phase 3 repolarization in ventricular tissue. These actions decrease ventricular conduction velocity and prolong the ventricular action potential duration and refractory period –> increases QRS duration and prolong QT interval.
They suppress abnormal automaticity, but they usually do not affect SA node automaticity and HR.

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4
Q

Class IA drugs - Special consideration + Interactions

A

All of class IA drugs have some degree of antimuscarinic (atropine-like) activity and reduce vagal inh of SA depolarization and AV node. Conduction –> increased HR.

Alcohol
Serum level increased by: Carbonic anhydrase inhibitors, Erithromycin, Antacids, Cimetidine
Serum level decreases by Rifampin

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5
Q

Class IA drugs - Adverse effects

A

Prodysrhythmic effect

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6
Q

Class IA drugs + greatest to least antimuscarinic effect

A

Quinidine**
Procainamide*
Disopyramide***

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7
Q

Quinidine - Indication

A

Suppress supraventricular and ventricular arrhythmias

Combination with dextromethorphan for treatment of emotional lability (pseudobulbar affect) in patients with neurodegenerative disease

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8
Q

Quinidine - Adverse effects

A

Diarrhea
Excessive QT prolongation (torsade de pointes) –> syncope and decreased CO
Thrombocytopenia
Neurologic symptoms due to overdose- cinchonism; tinnitus, dizziness and blurred vision.

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9
Q

Procainamide - MoA

A

Converted to active metabolite N-acetylprocainamide –> Class III antidysrhythmic properties.

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10
Q

Procainamide - Indication

A

Terminate wide QRS complex form of acute ventricular tachycardia and convert atrial fibrillation to sinus rhythm.

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11
Q

Procainamide - Adverse effects + Special consideration

A

Reversible lupus erythematous like syndrome, with arthralgia and butterfly rash

Pt with slow-acetylator phenotype develop lupus-like syndrome more often and earlier during treatment than do rapid acetylators.

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12
Q

Disopyramide - Indication

A

Prevent life threatening ventricular dysrhythmias; sustained VT

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13
Q

Disopyramide - Contraindication/Caution

A

It should not be used to treat asymptomatic ventricular dysrhythmias because of its protentional prodysrhythmic effect. It has negative inotropic and antimuscarinic effects and should be used with caution in pat with HF and elderly persons.

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14
Q

Class IB drugs - MoA

A

Greater affinity for inactivated sodium channels and have rapid recovery.

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15
Q

Class IB drugs

A

Lidocaine

Mexiletine

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16
Q

Lidocaine - MoA

A

Local anesthetic. More pronounced effect on ischemic tissue then normal tissue. In ischemic tissue; cells are partly depolarized because they lack sufficient adenosine triphosphate to operate the sodium pump –> sodium channels in ischemic tissue spend more time in the inactivated state.

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17
Q

Lidocaine - Indication

A

Refractory ventricular tachycardia.

Ventricular arrhythmias during/after cardiac surgery

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18
Q

Lidocaine - Adverse effects and Interactions

A

CNS; nervousness, tremor, paresthesia.
Cardiac arrest

Toxic dose: slow cardiac conduction velocity –> cardiac arrest

Drugs that inhibit cyt P450; cimetidine, can increase levels and cause toxicity

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19
Q

Mexiletine - MoA

A

Greater effect on normal cardiac tissue. Slows conduction in the heart and makes it less sensitive.

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20
Q

Mexiletine - Indication

A

Suppression of symptomatic ventricular tachycardia

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21
Q

Class IC drugs - MoA

A 
Have greater affinity for the open state and a very slow recovery.
Block both fast sodium channels and the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs --> slow conduction throughout the heart and especially in the His-Purkinje system.
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22
Q

Class IC drugs

A

Flecainide

Propafenone

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23
Q

Flecainide

Propafenone - MoA

A

Also inhibit the potassium rectifier current (IKr) in ventricular tissue –> increases QT interval, but rarely cause torsades de pointes.
Prolongation of PR interval and QRS duration.

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24
Q

Flecainide - Indication

A

Supraventricular dysrhythmias

Documented life threatening ventricular dysrhythmias.

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25
Q

Flecainide - Adverse effects

A

VT

Brochospasm, leukopenia, thrombocytopenia, seizure

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26
Q

Flecainide - Special consideration

A

Increases mortality in pt who had experienced a MI

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27
Q

Propafenone - Indication

A

Long term; suppress supraventricular tachycardia and atrial fibrillation.

Life threatening forms of ventricular dysrhythmias such as sustained ventricular tachycardia.

28
Q

Propafenone - Adverse effects

A

Ventricular dysrhythmias, hematological abnormalities: agranulocytosis, anemia and thrombocytopenia.

29
Q

Class II drugs - MoA

A

beta-adrenoceptor antagonists.
Antiarrhythmic effect because of their ability to inhibit sympathetic activation of cardiac automaticity and conduction. They slow the HR, decrease AV node conduction velocity and increase AV node refractory period.

30
Q

Class II drugs - Indication

A

Prevent and treat supraventricular dysrhythmias and to reduce ventricular ectopic depolarizations and sudden death in patients with MI

31
Q

Class II drugs

A

Esmolol
Metoprolol
Propranolol

32
Q

Esmolol - Indication

A

Acute supraventricular tachycardia &
Ventricular arrhythmia
Hypertension during or after surgery

33
Q

Metoprolol and Propranolol - Indication

A

Suppress supraventricular and ventricular dysrhythmias

+ In pat with MI; metoprolol is given IV during early phase of treatment

34
Q

Class III drugs - MoA

A

They cause prolongation of the ventricular action potential duration and refractory period. Act by blocking potassium rectifier currents that repolarize the heart during phase 3 of the action potential (except Amiodarone)

35
Q

Class III drugs

A 
Amiodarone
Dronedarone 
Dofetilide 
Ibutilide 
Sotalol
36
Q

Amiodarone - MoA

A

Blocks potassium, sodium and calcium channels + beta-adrenoceptors.
Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods.
Increases PR interval and QT interval and causes a slight prolongation of the QRS duration.
Powerful inhibitor of ectopic pacemaker automaticity, and prolongs repolarization and refractory periods throughout the heart.

37
Q

Amiodarone - Indication

A

Suppress supraventricular and ventricular dysrhythmias, incl atrial fibrillation, atrial flutter, supraventricular tachycardia and VT

Effective adjunct to implantable cardioverter-defibrillators to reduce nr of shocks required to maintain sinus rhythm.

38
Q

Amiodarone - Adverse effects

A

Bradycardia
Impaired AV conduction
QT interval prolongation –> torsades de pointes
Corneal microdeposits
Photosensitivity to UV light
Blue-gray skin discoloration
Hypothyroidism (managed w levothyroxine replacement therapy)
Hyperthyroidsm
Tremor, ataxia and optic or peripheral neuropathy
Pulmonary fibrosis –> may be fatal.

39
Q

Amiodarone - Interactions

A

Elevate plasma levels of: digoxin, Flecainide, phenytoin, procainamide, warfarin –> by inh P-glycoprotein mediated drug transport.

Interacts w inhalation anesthetics and CNS depressants –> increases incidence of adverse cardiovascular effects like bradycardia

contra: pregnancy

40
Q

Dronedarone - Indications

A

Prevention of dysrhythmia in persons w paroxysmal atrial fibrillation or flutter

41
Q

Dronedarone - Adverse effects and Contraindications

A

Liver injury
Increase mortality pt w HF

Contraindications: permanent atrial fibrillation, pt w HF must be monitored every 6 months. Pregnancy

42
Q

Dofetilide - MoA

A

Selectively block the rapidly activating delayed rectifier channel (IKr) responsible for repolarizing (rectifying) myocardial tissue during phase 3 of the action potential. By inh this outward potassium current –> prolongation of ventricular repolarization and increases refractory periods and QT interval of the ECG.

43
Q

Dofetilide - Indications

A

Convert atrial fibrillation, long term suppression of dysrhythmia

44
Q

Dofetilide - Adverse effects

A

QT-prolongation

torsades de pointes

45
Q

Ibutilide - MoA

A

Activates the slow (late), inward sodium current –> increases sodium influx and counteracts the outward potassium current so as to slow atrial and ventricular repolarization.

46
Q

Ibutilide - Indication

A

Rapid conversion of atrial fibrillation or flutter to normal sinus rhythm.
Before cardioversion in pt that do not respond to cardioversion alone

47
Q

Ibutilide - Adverse effect + Contraindication

A

Can induce torsades de pointes

Contra: in pat with prolonged QT interval (QTc>440 ms) and polymorphic VT.

48
Q

Sotalol - MoA

A

Nonselective B-antagonist, that prolong the cardiac action potential duration and QT interval by blocking the delayed potassium rectifier current during Phase 3 of ventricular action potential. Decreases HR, slows AV node conduction velocity and increase AV node refractory period without affecting the ventricular conduction and QRS duration
Modest (-) inotropic effect

49
Q

Sotalol - Indication

A

Supraventricular dysrhythmias
Rhythm control in persons w atrial fibrillation and flutter
Adjunctive therapy in pt w implantable cardioverter-debrillator (facilitates defibrillation by lowering the defibrillation threshold and decreases nr of shock required.
Ventricular dysrhythmia

50
Q

Sotalol - Lower dose VS higher dose

A

Lower dose: acts through beta-receptor blockade

Higher dose: Class III action and prolongation of ventricular repolarization

51
Q

Sotalol - Adverse effects

A 
Bradycardia
Bronchospasm 
Dyspnea 
Pulmonary edema and heart failure 
Dose dependent torsades de pointes
52
Q

Class IV drugs

A

Diltiazem

Verapamil

53
Q

Class IV drugs - MoA

A

Decrease AV node conduction velocity and increase AV node refractory period. Smaller effect on SA node and HR

54
Q

Class IV drugs - Indication

A

Controlling/converting supraventricular dysrhythmias

Control ventricular rate in pt w atrial fibrillation or flutter and a rapid ventricular response.

Verapamil (IV): Terminate paroxysmal supraventricular tachycardia

55
Q

Class IV drugs - Adverse effects

A

Exacerbate wide QRS complex VT- must be diagnosed before giving the drugs

56
Q

Miscellaneous drugs

A 
Adenosine
Digoxin 
Magnesium sulfate 
Ivabradine 
Ranolazine
57
Q

Adenosine - MoA

A

Derived from ATP and activates specific G protein-coupled adenosine receptors. Stimulation of these receptors leads to activation of acetylcholine sensitive potassium channels and blockade of calcium influx in the SA node, atrium and AV node. Causes cell hyperpolarization, slows AV node conduction velocity and increases AV node refractory period. Av node conduction can be completely blocked for few seconds –> brief period of asystole

58
Q

Adenosine - Indication

A

Terminate supraventricular tachycardia by preventing retrograde conduction of reentrant impulses through AV node.
Cardioversion

Terminate acute PSVT
including Wolff-Parkinson white syndrome

59
Q

Adenosine - Adverse effects and Interactions

A

Bronchospasm
Vasodilatory effects: facial flushing, rash, diaphoresis
Metallic taste

Dipyridamole inh cellular uptake and increases its cardiac effects.

60
Q

Digoxin - Indication

A

Slow ventricular rate in atrial fibrillation

61
Q

Magnesium sulfate - Indication and Adverse effect

A

Suppress drug induced torsades de pointes, treat digitalis induced ventricular dysrhythmias and supraventricular dysrhythmias associated with magnesium deficiency.

Low BP
Skin flushing
Low blood calcium

62
Q

Ivabradine - MoA

A

Blocks funny current in the SA node which is a mixed Na/K inward current that is activated by hyperpolarization, modulated by the autonomic nervous system and responsible for diastolic depolarization and cardiac impulse initiation.

63
Q

Ranolazine - MoA

A

Blocks late sodium current in ventricular tissue

64
Q

Ivabradine and Ranolazine - Indication

A

Angina pectoris
Heart failure
Inoperative sinus tachycardia

65
Q

Ivabradine and Ranolazine - Adverse effects

A

Excessive bradycardia

Slow AV conduction in some patients.

Pharmacology (55 decks)

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