Heart failure (positive Inotropic Drugs) and antidysrhythmics Flashcards

1
Q

What class is amiodarone? What does it do? What is it resistant to?

A

It is a class 3 potassium channel blocker
extends refractory period of cells
resistant to other drugs

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2
Q

Adverse effects of digoxin?

A

1.)Narrow theraputic window for digosin
-Drug levels must be monitored

2.) Low potassium levels increase toxicity

3.) GI (early adverse effects sign of dig toxicity)
-Anorexia, nausea, vomiting, diarrhea

4.) Colored vision (classic sign) (seeing yellow, green, purple, halo vision, flickering lights

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3
Q

Movement of ions across the cardiac cell membrane results in? What does it lead to?

A

Movement of ions across the cardiac cell membrane results in AP generation
AP leads to contraction of the myocardial muscle

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4
Q

Dysthrithmia Vs Arrhythmia?

A

Dysthrithmia: Any deviation from the normal rate/rhythm of the heart

Arrhythmia “no rhythm”

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5
Q

Example of a class 1b anti-dysthymic drug that is used for ventricular dysrhythmias only?

A

Lidocaine (blocks Na+ channels)

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6
Q

Example of Class II: b-adrenoceptor antagonists (beta blockers) ? What does it do?

A

-Metoprolol, esmolol (IV), propranolol, sotalol (also Class III)

Reduce or block sympathetic nervous system stimulation
AV Block

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7
Q

What is Ventricular Tachycardia (VT) ?

A

problem with ventricular muscle
eg non-sustained (<30 sec) and sustained (>30 sec)

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8
Q

Client care implications of digoxin?

A

Assess clinical parameters, including:
-Apical pulse (NOT radial) for 1 full minute
-Serum labs: potassium, sodium, magnesium, calcium, renal and liver function studies

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9
Q

What is flecainide, encainide, propafenone? What do they block?

A

It is a class 1c CCB that blocks Na+ channels

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10
Q

WHat does AP depend on?

A

AP depends on Ca2+ influx

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11
Q

What does digoxin do?

A

AV block
Slows HR

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12
Q

(Potassium Channel Blocker) -amiodarone, What is it used for?

A

-amiodarone

Used for Ventricular tachycardia or fibrillation, atrial fibrillation or flutter

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13
Q

What factors increase the risk of digoxin toxicity?

A

-Low K+ (loop diuretics)
-Lead to hypokalemia then to toxicity
amphotericin B, furosemide, thiazides, laxatives, steroids

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14
Q

What are Antidysrhythmics? What do most of them do?

A

-drugs used for the treatment and prevention of disturbances in cardiac rate and/or rhythm

-most suppress abnormal electrical impulse formation or conduction

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15
Q

Antidysrhythmic Drugs - Vaughan Williams Classification

A

Class I – Na channel blockers
Class Ia
Class Ib
Class Ic
Class II – b blockers
Class III – K channel blockers (+ others)
Class IV - Calcium channel blockers
Other (adenosine, digoxin)

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16
Q

What does diltiazem, verapamil act on? What do they do? What are they used for

A

Act on AV node – reduce conduction velocity
AV Block
Used for paroxysmal (“periodic attack”) SVT

17
Q

What does Digoxin and adenosine do?

A

Both decrease AV conduction and SA automaticity

18
Q

Antidote to Digoxin toxicity?

A

Digoxin immune fab
-This is employed during life threating cardiac dythrmthmina issues

19
Q

What is diltiazem, verapamil? What class is it apart of? What do they do? WhatWhat are they not used for?

A

Class IV: Calcium Channel Blockers
Inhibits Ca cell entry
Not for ventricular dysrhythmias

20
Q

Adverse effects of digoxin on the cardiovascular system?
What must we take? minium BPM?

A

-Dysrhythmias - including bradycardia
-Must take apical pulse

-Min 60 BPM
-If lower hold back dose

21
Q

WHat do class 2 B-adrenergic recepters increase? What do they reduce?

A

increase Ca influx
B-blockers reduce cell activity

22
Q

What is quinidine, procainamide, disopyramide? What are they used for?

A

It is a class 1a CCB that Block sodium channels
Slows atrial and ventricular rates

Used for ACUTE onset atrial fibrillation

23
Q

What are the 3 Ss of Digoxin?

A

1.) Strengthens
-Positive inotropic effect-
-Increase in force of myocardial contraction

2.) Slows
-Negative chronotropic effect-
-Reduce heart rate at SA node

3.) Slows
-Negative dromotropic effect
-Decreases AV nodal conduction and other effects

24
Q

What factors increase the risk of digoxin toxicity?

A

-Low K+ (loop diuretics)
-Lead to hypokalemia then to toxicity
amphotericin B, furosemide, thiazides, laxatives, steroids

25
Q

What is Supraventricular tachycardia?

A

Supraventricular tachycardia (SVT 120-250 beats/min)

26
Q

When is Digoxin used? Indications of use?

A

-Heart failure

*Supraventricular dysrhythmias – problem is above the ventricle
Atrial fibrillation and atrial flutter

27
Q

What can ALL antidysrhythmics can cause?

A

dysrhythmias!

28
Q

Digoxin Effects?

A

1.) Increases stroke volume (therefore cardiac output)
2.) Decrease in venous BP and vein engorgement
3.) Increase coronary circulation
*4.) Promotion of diuresis due to improved kidney perfusion
5.) Palliation of external, paroxysmal and nocturnal dyspnea, cough and cyanosis

29
Q

Example of Cardiac glycosides?

A

Digoxin

30
Q

Class I: Na Channel Blockers? What do they do?

A

block Na channels
slow depolarization

31
Q

What does Adenosine do? What kind of half-life does it have? How is it administered? What might it cause for a moment?

A

Slows conduction through the AV node
AV block

-Only administered as a FAST iv push

May cause asystole for a few seconds