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Pharmacology Flashcards

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1
Q

Na channel blockers - MOA

A

Bind to open and inactivated sodium channels. Dissociate during resting stage. More pronounced effect on rapidly firing cardiac tissue.

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2
Q

Use-dependent blockade: what does it mean?

A

Na channels in rapidly firing cardiac tissue spend more time open and inactivated. Since this is when the Na channel blockers bind to the channels, they suppress conduction more in e.g. tachycardia than in normal rhythm.

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3
Q

Na channel blockers - subdivisions (3) and their drugs (3, 2, 2)

A

Class IA: Quinidine, disopyramide, procainamide.
Class IB: Lidocaine, mexiletine.
Class IC: Flecainide, propafenone.

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4
Q

Main differences between the classes of Na channel blockers

A

Class IA: Open>inactivated Na channels. Slow dissociation.
Class IB: Inactivated>open Na channels. Rapid dissociation.
Class IC: Open>inactivated Na channels. Very slow dissociation.

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5
Q

Class IA - affinity for which channels and effects.

A

Fast Na channels and delayed K channels.
Decreased conduction velocity. Prolonged ventricular action potential and refractory period. (Prolonged QRS and QT intervals. Suppress ectopic automaticity without suppressing SA node automaticity.
Antimuscarinic activity - inhibit vagal effects on SA and AV nodes.

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6
Q

Degree of antimuscarinic activity of the class IA Na channel blockers

A

Disopyamidine - highest
Quinidine - intermediate
Procainamide - least

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7
Q

Quinidine - indications

A

Malaria and fever. Suppress supraventricular and ventricular arrhythmias.

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8
Q

Quinidine - adverse effects

A

Diarrhea.
Torsade de pointes. Reduced cardiac output causing syncope.
Thrombocytopenia.
High doses: tinnitus, dizziness, blurred vision

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9
Q

Procainamide - Adverse effects

A

Long-term: Reversible lupus like syndrome (arthralgia, butterfly rash)

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10
Q

Procainamide - indications

A

Acute ventricular arrhythmia

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11
Q

Disopyramide - indications

A

Life-threatening ventricular arrhythmias (sustained VT)

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12
Q

Disopyramide - contraindications

A

Asymptomatic ventricular premature contractions. Heart failure and elderly patients.

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13
Q

Lidocaine - effects

A

Has more pronounced suppression of conduction in ischemic tissue than normal tissue. (little effect on normal tissue)

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14
Q

Lidocaine - adverse effects

A

High serum level: nervousness, tremor, paresthesia.

Toxic doses: cardiac arrest.

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15
Q

Lidocaine - interactions

A

Metabolized by cytochrome P450 enzymes.

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16
Q

Lidocaine - indications

A

Local anesthesia. Refractory VT or ventricular arrhythmias associated with cardiac surgery.

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17
Q

Mexiletine - indications

A

Long-term suppression of life-threatening ventricular arrhythmias.

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18
Q

Class IC antiarrhythmic drugs - benefits

A

Do not prolong QT interval substantially.

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19
Q

Class IC Adverse Effects

A

Flecainide, Propafenone
No change to AP, Significantly increases QRS
- Use dependence (greater @ faster rates)
- Stop if QRS prolongs >25%
- Slows conduction and promotes reentry

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20
Q

Flecainide - indications

A

Supraventricular arrhythmias, documented life-threatening ventricular arrhythmias.

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21
Q

Flecainide - contraindications

A

MI / cardiac scar

Proarrhythmia — Flecainide was one of two class IC antiarrhythmic medications included in the CAST trial, which evaluated patients with asymptomatic, non-life-threatening ventricular arrhythmias who were six days to two years after an acute myocardial infarction (MI). Flecainide had an apparent proarrhythmic effect with a significantly increased incidence of mortality plus nonfatal cardiac arrest (6.1 percent versus 2.3 percent in the placebo group).

It has been proposed that the increase in malignant arrhythmias was due to the use of flecainide in the setting of ischemia and/or cardiac structural abnormalities (eg scar from the prior infarction).

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22
Q

Flecainide - adverse effects

A

Reentrant VT, bronchospasm, leukopenia, thrombocytopenia, seizures.

Conduction abnormalities — Due to its significant effect on sodium channels, flecainide prolongs depolarization and can slow conduction in the AV node, the His-Purkinje system, and below. These changes can lead to prolongation of the PR interval, increased QRS duration, and first- and second-degree heart block. In addition, profound sinus bradycardia can be induced in patients with preexisting sinus node disease. In contrast, flecainide does not affect repolarization and therefore has little effect on the QT interval.

  • Use dependence (greater @ faster rates)
  • Stop if QRS prolongs >25%
  • Slows conduction and promotes reentry
  • Can slow atrial fibrillation into atrial flutter allowing 1:1 conduction through the AV node
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23
Q

Propafenone - indications

A

Long-term suppression of supraventricular tachycardia and atrial fibrillation. Life-threatening ventricular arrhythmias (sustained ventricular tachycardia).

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24
Q

Propafenone - adverse effects

A

Ventricular arrhythmias, agranulocytosis, anemia, thrombocytopenia.

Has a selective sodium channel blocker with use-dependent properties and can increase the risk of proarrhythmic at higher heart rates.

  • Use dependence (greater @ faster rates)
  • Stop if QRS prolongs >25%
  • Slows conduction and promotes reentry
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25
Class III antiarrhythmic drugs - 5 drugs
Amiodarone and dronedarone Dofetilide Ibutilide Sotalol
26
Class III antiarrhythmic drugs - general MOA and effects
Block K rectifier currents during phase 3. This causes prolongation of the ventricular action potential and refractory period. Do not slow ventr conduction velocity or increase QRS duration significantly (except amiodarone).
27
Amiodarone - Classification
Organic iodine compound, class III antiarrhythmic drug
28
Amiodarone - onset and duration of action
Onset after 2 weeks (unless loading dose is given). Half-life is about 40 days (ranges between 26-107 days).
29
Dronedarone - Classification
Nonionated analogue of amiodarone.
30
Dronedarone - indications
Paroxysmal AF or AFL.
31
Dronedarone - adverse effects
Liver injury and acute liver failure. Increased mortality in pts with heart failure.
32
Dronedarone - contraindications
Permanent A-fib. Heart failure.
33
Amiodarone - MOA
Blocks K-channels, Ca channels, Na channels, β-adrenoceptors.
34
Amiodarone - effects
Decrease SA node automaticity. Decrease AV node conduction. Prolong AV node and ventricular refractory periods. Increase PR and QT intervals. Slight QRS prolongation. Powerful inhibition of ectopic pacemaker automaticity. - Effects IKs and IKr equally - Consistent across HR - Less pro-arrhythmic
35
Amiodarone - Adverse effects
Bradycardia, impaired AV conduction, QT prolongation, torsades de pointes. Corneal microdeposits (90% of pts, usually benign). Photosensitivity, blue-gray skin discoloration. Hypo- and hyperthyroidism. Tremor, ataxia, optic/peripheral neuropathy. Hepatic dysfunction. Pulmonary fibrosis.
36
Amiodarone - interactions
Inhibits metabolism of e.g. digoxin, flecainide, phenytoin, procainamide, warfarin. Increased incidence of bradycardia if given with inhalational anesthetics and CNS depressants.
37
Amiodarone - indications + adm
Long-term: suppress supraventricular and ventricular arrhythmias - AF, AFL, SVT, VT (given orally). Short-term: terminate VF and sustained VT, adjunct to cardioverter-defibrilators (given IV).
38
Ibutilide - MOA
In addition to blocking the delayed rectifier K channels, it prolongs the action potential by promoting Na influx through slow inward Na channels.
39
Ibutilide - indications and adm
AF or AFL. Adm IV infusion.
40
Ibutilide and dofetilide - adverse effects
Torsades de pointes Because of the risk of VT, particularly torsades de pointes, patients treated with ibutilide should be observed with continuous ECG monitoring for at least four hours after the infusion is finished, or until the QTc interval has returned to baseline.
41
Ibutilide - contraindications
Prolonged QT interval, history of polymorphic VT.
42
Dofetilide - indications and adm
AF (adm orally, for both short- and long-term treatment) - Reverse use dependance (greatest at slower heart rates, most effective for maintaining NSR) - Prolongs repolarization (triggered early after depolarizations)
43
Dofetilide - contraindications
Renal insufficiency (reduce doses) - Reverse use dependance (greatest at slower heart rates, most effective for maintaining NSR) - Prolongs repolarization (triggered early after depolarizations)
44
Sotalol - classifications
Nonselective β-blocker, Ca channel blocker. Class III antiarrhythmic drug with class II effects.
45
Sotalol - indications
Ventr arrhythmias. Atrial arrhythmias (AF)
46
Sotalol - adverse effects
Dose-dependent incidence of torsades de pointes. Bronchospasm - Reverse use dependance (greatest at slower heart rates, most effective for maintaining NSR) - Prolongs repolarization (triggered early after depolarizations)
47
Adenosine - MOA
Activates G protein-coupled adenosine receptors. This further activates ACh-sensitive K channels and block Ca influx in SA node, atrium and AV node.
48
Adenosine - effects
Cell hyperpolarization slows the AV node conduction velocity, and increases the AV node refractory period. AV node conduction can be completely blocked for a few seconds.
49
Adenosine - adm and duration of action
Rapid IV bolus. Half-life is 10 seconds.
50
Digoxin - MOA as antiarrhythmic
Indirect increment of vagal tone.
51
Digoxin - effects
Slow the AV node conduction velocity & increase its refractory period. Positive inotropic effect.
52
Digoxin - indicaitons
Heart failure. Slow ventricular rate in AF (not preferred)
53
Benefits of using digoxin for AF
Causes less bradycardia than β-blockers, and do not reduce cardiac contractility as much as Ca channel blockers.
54
Magnesium sulfate - Indications
Drug-induced torsades de pointes. Digitalis-induced ventricular arrhythmias. Supraventricular arrhythmias associated with Mg deficiency.
55
What diseases may be caused by magnesium deficiency?
Arrhythmias, congestive heart failure, GI and renal disorders.
56
Ivabradine - MOA
Heart rate-lowering drug that block the funny current (If, mixed Na, K inward current) in the SA node.
57
Ivabradine - indications
Angina, heart failure, inappropriate sinus tachycardia.
58
Ivabradine - interactions
Metabolized by CYP3A4. With inhibitors of this enzymes ivabradine may cause excessive bradycardia.
59
Ivabradine - contraindications
Concurrent use of strong CYP3A4 inhibitors
60
Ivabradine - adverse effects
Excessive bradycardia.
61
Adenosine - indications
Acute PSVT (Wolff-Parkinson-White syndrome). NOT indicated for A-fib/A-flut.
62
Adenosine - interactions
Dipyridamole increases the cardiac effect of adenosine
63
Adenosine - adverse effects
Bronchospasm
64
Adenosine - contraindications
Caution in obstructive lung disease.
65
Use dependent channel block
- IC Na channel blockers, Flecainide and propafenone - Drug binds to the open or inactivated state - Greater effect at faster rates
66
Reverse use dependence
- Class III, K channel blockers, Dofetilide and sotalol - Drug effect greater when the rested state predominates at slow heart rates - Most effective for maintenance of NSR - Assess QT prolongation at rest - Potential for pause-dependent polymorphic VT
67
Metabolized through the liver
Amiodarone Lidocaine/ Mexiletine Verapamil/ Diltiazem Propafenone
68
Metabolized through the kidney
Sotalol Dofetilide Digoxin
69
Mixed metabolism
Flecainide (20% Hepatic) Procainamide (50/50) NAPA really Quinidine (50-70% Hepatic) Ibutilide (90% hepatic)
70
CYP 2D6 Medicine
- 7% of the population is deficient Metabolizers: Propafenone, flecainide, mexiletine, Coreg, propranolol Inhibitors: Amiodarone, Fluoxetine, Haloperidol, Paroxetine, quinidine, sertraline
71
CYP 3A4
Metabolizers: Amiodarone, Dofetilide (20%), quinidine, dronedarone, verapamil, diltiazem, cyclosporine Inhibitors: Macrolide antibiotics, Azoles, Diltiazem, grapefruit juice Inducers: Phenytoin, Phenobarbital, Carbamazepine, ST. Johns wart, Rifampin
72
Amiodarone Drug Interactions
Warfarin = increases INR Digoxin = Increases dig effect Cyclosporine, Tacrolimus = increases levels

Electrophysiology (4 decks)

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