Pharmacology - Chapter 48 - Antidysrhythmic Drugs Flashcards

1
Q

Dysrhythmia - def

A

abnormality in rhythm of the heartbeat.

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2
Q

In mildest forms of dysrhythmia, there are only ___ effects on cardiac output.
In severe forms, they can ___ the heart so that ___ cardiac output occurs.

A

Mild effects.
Disable.
No.

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3
Q

What are the 2 types of dysrhythmias?

A

Tachydysrhythmias and Bradydysrhythmias.

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4
Q

Drugs that treat dysthythmias can cause them. T/F?

A

True!

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5
Q

In healthy heart - impulse originates at ___ node, spreads rapidly through ____, passes slowly through __ node, spreads rapidly through the ___ via the ____ ___ ___.

A

SA Node
Atria.
AV node.
ventricle via the His-Purkinje System.

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6
Q

EKG - P wave =

A

depolarization in atria (atrial contraction.)

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7
Q

QRS Wave =

A

depolarization of ventricles (ventricular contraction.)

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8
Q

T-wave =

A

repolarization of ventricles (not associated with physical activity of heart.)

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9
Q

PR wave - represents the time between…

A

onset of the P wave and onset of the QRS complex.

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10
Q

Prolongation of the PR wave indicates….

A

delayed AV conduction.

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11
Q

QT Wave - the time between onset of the ….. and the completion of the….

A

QRS complex and completion of the T Wave.

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12
Q

QT prolongation indicates….

A

delayed ventricular repolarization.

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13
Q

What are the two types of disturbances that can generate dysrhythmias?

A

Disturbances of impulse formation (automaticity)(Sa or AV nodes) and Disturbances of conduction (like an AV block.)

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14
Q

What are the two major groups of Dysrhythmias?

A

Supraventricular and Ventricular!

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15
Q

Supraventricular Dysrhythmias - where do they come from? And what are some?

A

Impulses arise above the ventricule, like SVT (Supraventricular Tachycardia), Atrial flutter, A Fib, etc.

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16
Q

Ventricular Dysrhythmias - they are less dangerous than Supraventricular Dysrhytmia - T/F?

A

False! They are more dangerous!

17
Q

What are some ventricular Dysrhythmias?

A

Ventricular Tachycardia, Ventricular Fibrilation, and Ventricular Premature Beats (VPB)

18
Q

What are the Vaughan Williams Classifications?

A

Class 1-4.
Class 1 - blocks sodium channels and delays ventricular repolarization (Quinidine.)
Class 2 - beta blockers (Propanalol.)
Class 3 - potassium channel blockers, delay repolarization (Bretylium.)
Class 4- calcium channel blockers; reduces SA node activity (Cardizem.)
Others - Digoxin.

19
Q

Class 1A Agents - What is the drug?

A

Quinidine - Cinchona alkaloid, blocks sodium channels,delays repolarization.

20
Q

What are the adverse effects of Quinidine?

A

Diarrhea, Cinchonism, Cardiotoxicity.

21
Q

Class 1 B Agents - Drug

A

Lidocaine (Xylocaine) - Blocks sodium channels, reduces automaticity in ventricles, accelerates repolarization.

22
Q

What are the adverse effects of Lidocaine?

A

CNS effects, confusion, paresthesias (Paresthesia is a sensation of tingling, tickling, prickling, pricking, or burning of a person’s skin with no apparent long-term physical effect.)

23
Q

Class 2 Beta Blockers - What is the drug?

A

Propanalol - a nonselective beta adrenergic. It is used for tachydysrhythmias.

24
Q

What are the adverse effects of propranolol?

A

Bronchospasm, heart failure, av block, and sinus arrest.

25
Q

Class 3 Potassium Channel Blockers - what is the drug?

A

Bretylium. It delays repolarization of fast potentials. The QT interval is prolonged. It is used for Ventricular Tachycardia and V Fib.

26
Q

What is the adverse effect of Bretylium?

A

Profound hypertension.

27
Q

Class 4 Calcium Channel Blockers - Drug/what does it do, etc.

A

Verapamil - Reduces SA nodal automaticity, delays av nodal conduction, reduces myocardial contractility…it is used for SVT Atrial flutter, atrial fibrilation…

28
Q

What are the adverse effects of Verapamil -

A

Bradycardia, AV block, Heart failure.