Exam Prep Flashcards

(26 cards)

1
Q

Mechanism of Action and Risk of TDP

A
  • Lengthens action potential duration by prolonging repolarization which prolongs the QT interval.
  • QT prolongation with hypokalemia (↓ K+),
    hypomagnesemia (↓ Mg+), or bradycardia (↓ HR) may predispose to torsades de pointes.
  • Torsades de Pointes (TDP) – polymorphic ventricular tachycardia.
  • Polymorphic → poly – many, morphic – QRS shape.
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2
Q

Cardiac Cell Properties and the Action
Potential.

A
  • Contractility.
  • Automaticity.
  • Excitability.
  • Conductivity.
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3
Q

Class
III

A

Potassium channel blockers or antagonists:
* Sotalol
* Amiodarone
* Ibutilide
* Dofetilide
* Dronedarone

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4
Q

Amiodarone

A
  • Lengthens effective refractory period in all cardiac tissues, including accessory pathways
  • Class III
  • Class IA
    properties for lengthening action potential
    potent sodium channel blocker
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5
Q

Sotalol

A

Class II
beta-blocker properties, sinus and AV node depression

Class III
lengthens action potential in atrial and ventricular

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6
Q

Ibutilide

A

Prolongs repolarization by activation of a slow inward sodium current, as well as by inhibition of rapid component of delayed rectifier potassium current (Ikr), during repolarization.
* Administered intravenously.
* Conversion of atrial fibrillation or atrial flutter to sinus rhythm.

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7
Q

Dofetilide

A

Similar to Ibutilide and prolongs repolarization by inhibiting only rapid component of delayed rectifier potassium current (Ikr)
* Mild negative chronotropic (rate) effect
* Administered orally

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8
Q

Vernakalant

A

Blocks Ikr just like other class III agents, but is more selective for ultra-rapid current (Ikur), which is more predominant in the atria as well as blocking other ion currents selectively in the atria.
* Rate-dependent slowing (more potent at higher heart rate).
* Administered intravenously due to short half-life.
* Indicated for acute cardioversion of atrial fibrillation and atrial flutter to sinus
rhythm.

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9
Q

How do class III antiarrhythmics treat
re-entry rhythms?

A

A: Increase effective refractory period
prolonging the repolarization phase

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10
Q

Class IV agents

A

calcium channel blockers or antagonists

Non-Dihdropyridines
Diltiazem
Verapamil

Dihdropyridines
Nifedipine
Amlodipine
Felodipine

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11
Q

CCB group 1

A

L channel blockers
No action on SA or AV nodes
Dihydropyridines (DHP)
Nifedipine
Amlodipine
Felodipine

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12
Q

CCB group 2

A

L channel blockers, some T channel blockade Action on SA and AV nodes (Affects pacemaker action Non-dihydropyridines (Non-DHP)- Benzothiazepines
: Diltiazem- Phenylalkylamines
: Verapamil

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13
Q

CCB group 3

A

T type channel blocker
No current agents on the market

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14
Q

How does CCBs decrease oxygen demand and increase O2 supply.

A

Decreased Oxygen Demand
* +(DHP) or ↓ (non-DHP) heart rate
* ↓↓ (non-DHP) or ↓↓↓ (DHP) afterload
* ↓ BP
* + preload or ↓↓ contractility

Increased Oxygen Supply
* ↑ coronary dilation
* ↑ collateral coronary blood flow
* ↑↑↑ vasodilation

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15
Q

Indications for CCBs.

A

Indications
* Stable Angina – second line agents- ↓ BP, ↓ contractility, ↓ HR- ↑ coronary dilatation
* Coronary artery spasm- Coronary artery vasodilation
* Hypertension- Arterial vasodilation
* Supraventricular arrhythmias- Verapamil and Diltiazem- ↓ AV node conduction

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16
Q

Contraindications for CCBs

A

Contraindications
* Acute MI
* Unstable Angina – DHPs are contraindicated
* Bradycardias and AV blocks with Verapamil and Diltiazem

17
Q

Nifedipine

Indications
* Vasospastic angina
* Hypertension
* Raynaud’s syndrome

A
  • DHP calcium channel blocker
  • Powerful vasodilator
  • Mild negative inotropic
  • Grapefruit and grapefruit juice increase nifedipine levels
18
Q

Amlodipine

A

DHP calcium channel blocker

19
Q

Felodipine

Indications
* Hypertension
* Raynaud’s syndrome

A
  • DHPcalcium channel blocker
  • Hypertension
  • Decreases risk of stroke in hypertension
  • Reduce dosage in elderly and liver dysfunction
  • Grapefruit and grapefruit juice increase felodipine levels
20
Q

Diltiazem

Indications
* Angina - vasospastic
* Hypertension
* Supraventricular Arrhythmias

A
  • A benzothiazepine Non-DHP calcium channel blocker
  • Moderate dilation of arteries, < Nifedipine or other DHPs
  • Effect on SA node > Verapamil
  • Action on AV node < Verapamil
  • ↓ rate pressure product (RPP) at any given level of exercise
21
Q

Verapamil

Indications
* Angina - effort, vasospastic
* Hypertension
* Arrhythmias, supraventricular

A
  • A phenylalkylamine Non-DHP calcium channel blocker
  • Moderately potent vasodilator
  • Marked negative inotropic effect
  • Mild depression of sinus node function and AV nodal conduction
22
Q

Why are DHP calcium channel blockers
(CCB’s) preferred in the treatment of
hypertension over non-DHP CCB’s?

A

DHP CCB’s have greater vascular
selectivity, reducing afterload more than
non-DHP CCB’s.

23
Q

Adenosine

Indications: Terminating narrow-complex PSVTs,
pharmacological stress-testing, and diagnostic testing (e.g. for atrial flutter or wide-complex tachycardia)

A

Mechanism: Class V – Adenosine acts on adenosine receptor, especially the AV node.
-Interrupts re-entry rhythms.
-Can also dilate coronary arteries, increasing risk for coronary steal

24
Q

Ivabradine does not fit into a pre-defined class

A

Mechanism: selectively inhibits the funny current (If), which modulates slow depolarization phase of the action potential in the SA node.

Results in decreased heart rate by inhibiting phase 4 of the SA node action potential.

25
How does adenosine treat PSVT?
Slows conduction through the AV node, interrupting re-entry pathway and restoring normal sinus rhythm.
26
Why should patients with a heart rate below 70bpm avoid ivabradine?
Ivabradine slows depolarization phase 4 of the SA node action potential, resulting in reduced heart rate.