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CV > B2 Drugs > Flashcards

B2 Drugs Flashcards

1
Q

Quinidine - EP Effects

A

Class 1A Drugs

Direct Effects

  • Increase AP threshold
  • decrease Vmax
  • increase ERP

Indirect Effects

  • blocks K+ channels—> EADs
  • Vagolytic Effect

Use

  • Atrial flutter or fibrillation
  • Prevent ventricular tachycardia and fibrillation
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2
Q

Quinidine – Major Side Effects (and quick metabolism detail)

A

Class 1A Drugs

􏰀 -Severe GI effects - Diarrhea, cramps
􏰀 -Heart – vagolytic
􏰀 -Proarrhythmic – not necessarily related to the
arrhythmia being treated.

-Metabolized in liver; tolerated in patients with renal failure

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3
Q

Quinidine - Drug interactions

A

Class 1A Drugs

  • Inhibits the cytochrome P450 system (CYP2D6: metabolism of narcotics is reduced)
  • Reduces the renal clearance of digitalis; increases plasma levels of digitalis
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4
Q

Lidocaine

A

Class 1B Drugs

Direct effects
-Increase AP threshold
-increase Block of Na+ channels (􏰂 decrease Vmax)
at high HR (greater than 120 bpm; use-dependent) and in depolarized cells (can target diseased (ischemic) cells)
- decrease AP duration and ERP
-“cool” because it is dynamic

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5
Q

Lidocaine (side effects)

A

Class 1B Drugs

-dizziness, seizures, nausea

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6
Q

Lidocaine (use)

A

Class 1B Drugs

  • Ventricular tachycardia
  • Digitalis – induced arrhythmias
  • Safe for patients with Long QT Syndrome
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7
Q

Lidocaine (drug interactions)

A

Class 1B Drugs

Drugs that interfere with the cytochrome P450 system (CYP3A4), e.g. cimetidine

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8
Q

Flecainide

A

Class 1C Drug

-Increase AP threshold
- decrease Vmax (conduction velocity)
-Variable effects on ERP (net effect = 0)
-Dissociates from Na+ channel
slowly (POTENT)

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9
Q

Flecainide (SE)

A

Class 1C Drug

Pro-arrhythmic (CAST Trial)

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10
Q

Flecainide (use)

A

Class 1C Drug

Approved for used in life-threatening situations when supraventricular and ventricular arrhythmias are resistant to other drugs

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11
Q

Flecainide (Drug interactions)

A

Class 1C Drug

-Drugs that inhibit cytochrome P450: CYP2D6

For example:

  • Bupropion (antidepressant)
  • Ritonavir (antiretroviral)
  • Terbinafine (antifugal)
  • Cimetadine (H2-receptor antagonist)
  • Amiodarone (antiarrhythmic drug)
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12
Q

Class II: 􏰃beta-Adrenoceptor antagonists (beta􏰃-blockers)

A

-Propranolol – Long acting blocker (oral)
-Esmolol [Brevibloc] – Short acting blocker (IV)
􏰀
-Bind to 􏰃beta-adrenergic receptors on cardiac cell membranes to competitively inhibit epinephrine and norepinephrine binding.
􏰀-Antagonize effects of sympathetic stimulation.
􏰀
-In the presence of catecholamines, the main action of Class II agents is to slow the rate of diastolic (phase 4) depolarization.

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13
Q

Uses of 􏰃beta-Blockers

A

-Used for all atrial arrhythmias, ventricular tachycardia and
fibrillation - high levels of catecholamines present

  • The beta blockers are currently the most useful antiarrhythmic drugs available due to their safety record and wide clinical applications.
  • beta􏰃-blockers do not prolong repolarization in ventricular tissues. They are safe for use in patients with Long QT Syndrome.
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14
Q

􏰃beta-Blockers side effects

A

Major side effects of the 􏰃-blockers are negative inotropic effect, heart block, bradycardia and bronchospasm.

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15
Q

Class III: K+ channel blockers

A

Amiodarone
Sotalol
Dofetilide

􏰀-Main common property is K+ channel block;
prolongs action potential repolarization (action potential
duration increases); reverse use-dependence.
-slower the HR, the more potent….
-􏰀Among the many K+ channels, most common target is IKr (hERG channel).
-􏰀Main common effect is increased ERP.

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16
Q

Amiodarone – multiple actions

A

Class III: K+ channel blockers􏰀

  • Potent K+ channel blocker (blocks both IKr and IKs)
  • 􏰀Modest Na+ channel blocker
  • 􏰀Modest Ca++ channel blocker 􏰀
  • Modest 􏰃beta-adrenoreceptor blocker
  • cumulative targets make it effective
17
Q

Amiodarone (uses)

A

Class III: K+ channel blockers

-􏰀Effective against ventricular tachyarrhythmias and fibrillation.
􏰀-Also used in the prevention of recurrent paroxysmal atrial fibrillation or flutter.

18
Q

Amiodarone – Major Side Effects

A

Class III: K+ channel blockers

􏰀 -Triggered arrhythmias (EADs); but rarely
associated with Torsades de Pointes
􏰀 -Altered thyroid function (inhibits conversion of T4 to T3) - hypothyroidism
􏰀 -Pulmonary fibrosis – often irreversible*****example in class
􏰀 -Liver disease – hepatotoxicity (uncommon but not rare)

19
Q

Amiodarone (Drug interactions)

A

Class III: K+ channel blockers

Amiodarone inhibits the cytochrome P450 isozyme family; this results in the clearance of a number of drugs that are metabolized by the P450 system:
• Warfarin (anticoagulant)
• Digoxin (cardiac glycoside)
• Quinidine (antiarrhythmic drug)
• Flecainide (antiarrhythmic drug) •
• Sildenafil (PDE5 inhibitor)
• Simvastatin (statin)
20
Q

Sotalol (actions)

A

Class III: K+ channel blockers􏰀

-Major action is block of K+ channel (IKr).
􏰀-Also has beta􏰃-adrenergic receptor blocking actions
(secondary effect).
􏰀

21
Q

Sotalol (side effects)

A

Class III: K+ channel blockers

-Most serious side effect: triggered arrhythmias with Torsades de Pointes.
􏰀- Other side effects: fatigue, bradycardia

22
Q

Sotalol (uses)

A

Class III: K+ channel blockers

􏰀-Effective against ventricular tachyarrhythmias and fibrillation.
􏰀 -Also used against supraventricular tachycardias, atrial fibrillation.

23
Q

Sotalol (drug interactions)

A

Class III: K+ channel blockers

Administer with caution in conjunction with drugs that prolong the QT interval, for example, Class 1A antiarrhythmics, tricyclic antidepressants, quinolone antiobiotics

24
Q

Dofetilide

A

Class III: K+ channel blockers

􏰀 -Major action is block of K+ channel (IKr).
􏰀 -Common side effects: headache, dizziness, chest pain 􏰀
-Most serious side effect: triggered arrhythmias,
with Torsades de Pointes.

notes:
CAUTION!
The most serious side effect of dofetilide (Tikosyn) is Torsades de pointes: maybe effective in treating atrial arrhythmias, but can also trigger (concentration- dependent) life threatening arrhythmias. Per FDA requirements, doctors who prescribe Tikosyn are required to obtain certification.

25
Q

Dofetilide (uses)

A

Class III: K+ channel blockers

-􏰀Effective against atrial fibrillation and atrial flutter. (Not hepatotoxic like amiodarone)
􏰀-Safe for patients with left ventricular dysfunction.

26
Q

Dofetilide (drug interactions)

A

Class III: K+ channel blockers

-Dofetilide is eliminated via the kidney. Drugs that interfere with the renal secretion (active transport) system are contraindicated:
• Cimetidine (Tagamet) [also inhibits CYP3A4 – interferes with dofetilide metabolism in liver (􏰄20%)]
• Verapamil (antiarrhythmic; Ca channel blocker)
• Hydrochlorothiazide (diuretic)
• Ketoconazole (antifungal) [also inhibits cytochrome P450 system] • Trimethoprim (antibiotic)

27
Q

Class IV: Ca2+ Channel Blockers

A

Diltiazem (benzothiazepines)
Verapamil (phenylalkylamines)

Acts primarily on slow response cells (SA & AV node), which are dependent on Ca++ influx for action potential depolarization.

-􏰀 1,4-Dihydropyridines are generally not used as antiarrhythmic agents since they primarily target the vascular rather than cardiac cells.
􏰀- 1,4-Dihydropyridines are sometimes prescribed for the treatment of chest pain (angina pectoris) to relieve arterial spasms.

Major EP Effects of Ca2+ Channel Blockers
􏰀 -Increase threshold for AP firing in nodal cells 􏰀
-Increase nodal cell refractory period
􏰀 -Depress conduction velocity in the SA and AV nodes.

28
Q

Ca2+ Channel Blockers (Uses)

A

-􏰀Paroxysmal supraventricular tachycardia…ATRIAL!!!

Note: Rarely used for treatment of ventricular tachycardia

29
Q

Major Side Effects of Ca2+ Channel Blockers

A

􏰀-Negative chronotropic effect – decreases automaticity of SA node (bradycardia)
􏰀-Negative inotropic effect – decreases Ca++ influx during plateau phase of ventricular action potential
􏰀-Hypotension – decreases Ca++ influx into vascular smooth muscle cells

30
Q

Major Side Effects of Ca2+ Channel Blockers

A

-􏰀Peripheral edema (Nifedipine-type mostly)
􏰀-Constipation – decreases Ca2+ influx into GI smooth
muscle cells (Verapamil especially)
􏰀-Interacts with digitalis to slow conduction velocity in
the AV node LEADING TO heart block (Verapamil and Diltiazem)
􏰀-Increase plasma digitalis levels by competing for renal excretion (Verapamil and Diltizaem)

31
Q

Ca2+ Channel Blockers (Drug interactions)

A

Diltiazem and Verapamil are moderate inhibitors cytochrome P450 system (CYP3A4); leads to reduced clearance of some drugs, for example:
Quinidine

Digoxin

Simvastatin

32
Q

Adenosine

A
  • Very rapidly activates K+ channels to slow phase 4 depolarization at AV node (T1/2=10 seconds)
  • Blocks cAMP-enhanced Ca2+ channel activity at the AV node
  • Indicated for supraventricular tachycardia-slows AV conduction and heart rate
33
Q

Digoxin

A

Digitalis Glycosides

  • Enhances vagal parasympathetic activity to slow conduction at the AV node
  • Indicated for atrial fibrillation and supraventricular tachycardia to control ventricular response rate
34
Q

Class I: Na+ Channel Blockers

A

-Act on fast response cells
􏰀 -Reduce membrane responsiveness
􏰀 -Increase threshold for AP firing
􏰀 -Reduce Vmax (depress conduction velocity)
􏰀 -Prolong effective refractory period (ERP)

CV (5 decks)

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