Pharmacology (2) Flashcards

1
Q

What are the 4 antiarrhythmic drug classes?

A

Class 1 - Na+ Channel Blockers

Class 2 - Beta (receptor)-Blockers

Class 3 - K+ Channel Blockers

Class 4 - Nondihydropyridine Calcium channel blockers

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2
Q

What parts of the cardiac action potential do each drug class inhibit?

A

Class 1 - Phase 0 (Na+ Channel Block)

Class 2 - Phase 4 (Beta-Blocker; inhibit sympathetic stimulation)

Class 3 - Phases 0-3 (K+ Channel Block)

Class 4- Phase 2 (Ca2+ Channel Block)

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3
Q

Which drugs can block the AV node? (4)

A

Class 2
Class 4
Adenosine
Digoxin

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4
Q

Lidocaine and Flecainide are which drug class type? What are their mechanisms of action? Which is strong? Weak?

A

Class 1

Blocks Na+ channel to slow cardiac AP and HR

Flecainide (1c) – Strong
Lidocaine (1b) – Weak

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5
Q

Classify & describe the mechanism of action of amiodarone. What is unique about amiodarone?

A

Class 3
Blocks K+ channel to increase refractory period of AP –> Lower HR

Has both rhythm and rate control

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6
Q

Sotalol and Dofetilide are which drug class type? What are their mechanisms of action?

A

Class 3

Blocks K+ channel to increase refractory period of cardiac AP –> lower HR

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7
Q

Classify and describe the mechanism of action of Dilitazem and Verapamil.

A

Class 4

Blocks Ca2+ channels to slow conduction speed (& cardiac contractility) –> lower HR.

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8
Q

What’s the difference between a dihydropyridine and nondihydropyridine calcium channel blocker?

A

Dihydropyridine - Will block Ca2+ channels on vascular smooth muscle (for HTN)

Nondihydropyridine - Will block Ca2+ channels on the heart (pacemaker cells & myocytes)

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9
Q

What is the effective refractory period (ERP)?

A

The period of time in which the cell is not excitable.

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10
Q

What effect do class 4 drugs have on the ECG waveform? How is this achieved?

A

By slowing AV node conduction velocity, you will see a prolonged PR interval.

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11
Q

What effect do class 4 drugs have on heart muscle contraction? How is this achieved?

A

They weaken heart muscle contraction. This is because blocking Ca2+ channels shortens phase 2 of the cardiac action potential which means less myocyte contraction.

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12
Q

Classify and describe the mechanism of action of Beta-Blockers.

A

Class 2
Decrease HR by blocking cardiac beta (1>2) receptors that allow Ca2+ influx via GPCR.
This slows down pacemaker conduction (slower upstroke) and decreases myocyte contractility (Phase 2)

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13
Q

Classify and describe the mechanism of action of Adenosine.

A

Miscellaneous
Binds Adenosine Receptor 1 of pacemaker cell to inhibit Ca2+ influx and stimulate K+efflux. –> Slows conduction –> slows HR

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14
Q

Classify and describe the mechanism of action of Digoxin.

A

Miscellaneous

Mimics the vagal nerve to decrease HR (phase 4) and AV node conduction (phase 0).

Also blocks Na/K plus channel leading to more intracellular ca2+ –> increased contractility.

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15
Q

Contraindications/Toxicities of Class 1c Drugs?

A

Contraindicated in patients with coronary artery disease (CAD), history of myocardial infarct (MI), or signs of heart failure (HF)

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16
Q

What is a sign of coronary artery disease? Heart Failure?

A

CAD - positive stress test

HF - low Ejection Fraction (EF) (<55%)

17
Q

Contraindications/Toxicities Class 3 Drugs?

A

Prolong QT interval –> Torsades de Pointes

18
Q

Contraindications/Toxicities of Amiodarone (Class 3)?

A

Amiodarone has a lot of iodine which makes it lipophilic. It also has a long half-life.

This can lead to a variety of toxicities in which you must monitor and test for (PulmonaryFT, ThyroidFT, LiverFT)

Increases INR (contraindicated in warfarin patients)

Increases serum drug concentration of statins & Digoxin

19
Q

Contraindications/Toxicities of Class 2 Drugs?

A

Contraindicated in patients with bradycardia & hypotension.

20
Q

Describe the Van Gogh (“Xanthopsia”) Effect. What drug causes it?

A

Vision becomes tinted with a “yellow haze.”

Caused by Digoxin.

21
Q

What drugs are capable of rhythm control? What are their classifications? (6)

A
Flecainide (Class 1c)
Sotalol (Class 3)
Dofetilide (Class 3)
Amiodarone (Class 3)
Lidocaine (Class 1b)
Adenosine (Misc)
22
Q

What drugs are capable of rate control? What are their classifications? (3)

A

Digoxin (Misc)
Beta-Blockers (Class 2)
Calcium Channel Blockers (Class 4)

23
Q

AVRT & AVNRT are best terminated by what drug (or what maneuver)?

A

Adenosine (Misc)

Valsalva maneuver can also terminate this (not guaranteed)

24
Q

Scars/Infarcts of the left ventricle are substrates for ____.

A

Ventricular Tachycardia (Wide complex)

25
Q

What are some common criteria for long-term amiodarone use? (3)

A

Frequent Episodes of V-Tach
Frequent shocks from ICD
Need maintenance of sinus rhythm to prevent recurrence of a-fib/flutter

26
Q

Which should be used to treat ventricular tachycardia (narrow or wide complex)? (4) What can also be used to treat atrial fibrillation/flutter?

A

Amiodarone - Also treats a-fib/flutter
Adenosine - AVRT and AVNRT
Lidocaine
Valsava Maneuver

27
Q

What should be used to treat atrial flutter/fibrillation? (5)

A
Class 1 Drugs (Flecainide only)
Class 2 Drugs
Class 3 Drugs
Class 4 Drugs
Digoxin
28
Q

Nausea and vomiting are most indicative of what type of anti-arrhythmic drug toxicity?

A

Digoxin toxicity

29
Q

For a sudden (acute) onset of SVT should you use Adenosine or a Class 4 anti-arrhythmic?

A

Class 4 anti-arrhythmic: In an acute onset of SVT you will want to control the rate. Adenosine should be used in a more chronic state.

If patient is hemodynamically unstable you should electrically cardiovert!