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Drugs for Dysrhythmias 19. Learning Outcomes 1. Explain how rhythm abnormalities can affect cardiac function. 2. Illustrate the flow of electrical impulses.

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Presentation on theme: "Drugs for Dysrhythmias 19. Learning Outcomes 1. Explain how rhythm abnormalities can affect cardiac function. 2. Illustrate the flow of electrical impulses."— Presentation transcript:

1 Drugs for Dysrhythmias 19

2 Learning Outcomes 1. Explain how rhythm abnormalities can affect cardiac function. 2. Illustrate the flow of electrical impulses through the normal heart. 3. Classify dysrhythmias based on their location and type of conduction abnormality.

3 Learning Outcomes 4. Explain the importance of ion channels to cardiac function and the pharmacotherapy of dysrhythmias. 5. Identify the importance of nonpharmacologic therapies in the treatment of dysrhythmias. 6. Identify basic mechanisms by which antidysrhythmic drugs act.

4 Learning Outcomes 7. For each of the classes in the Drug Snapshot, identify representative drugs, explain their mechanisms of action, primary actions, and important adverse effects: 8. Categorize antidysrhythmic drugs based on their classifications and mechanisms of action.

5 Core Concept 19.1 Some types of dysrhythmias produce no patient symptoms, whereas others may be life threatening.

6 Symptoms  Dizziness  Weakness  Decreased exercise tolerance  Shortness of breath  Fainting.  Palpitations

7 Core Concept 19.2 Dysrhythmias are classified by their location and type of rhythm abnormality produced.

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9 Types of Dysrrhythmias

10 Types of Dysrrythmias

11 Atrial fibrillations

12 Diseases Commonly Associated With Dysrhythmias:  Hypertension (HTN)  Cardiac valve disease, such as mitral stenosis  Coronary artery disease  Medications such as digoxin  Low potassium levels in the blood  Myocardial infarction

13 Diseases Commonly Associated With Dysrhythmias:  Adverse effect from antidysrhythmic medication  Stroke  Diabetes mellitus  Congestive heart failure

14 Core Concept 19.3 The electrical conduction pathway in the myocardium keeps the heart beating in a synchronized manner.

15 Common Factor  A defect in the formation or conduction of electrical impulses across the myocardium

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17 Normal ECG tracing

18 Core Concept 19.4 Most antidysrhythmic drugs act by blocking ion channels in myocardial cells.

19 The flow of ions through ion channels in myocardial cells

20 Core Concept 19.5 Antidysrhythmic drugs are classified by their mechanisms of action.

21 Categories of Antidysrhythmics  Sodium channel blockers (Class I)  Beta-adrenergic blockers (Class II)  Potassium channel blockers (Class III)  Calcium channel blockers (Class IV)  Miscellaneous antidysrhythmic drugs

22 Core Concept 19.6 Sodium channel blockers slow the rate of impulse conduction through the heart.

23 Sodium Channel Blockers  Largest group of antidysrhythmics  Three subgroups  IA, IB, and IC  Based on subtle differences in their mechanisms of action

24 Sodium Channel Blockers  Because progression of the action potential depends on the opening of sodium ion channels, a blockade of these channels will slow the spread of impulse conduction across the myocardium

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26 Core Concept 19.7 Beta-adrenergic blockers reduce automaticity and slow conduction velocity in the heart.

27 Beta Blockers  Ability to slow the heart rate and conduction velocity can suppress several types of dysrhythmias.  Slow the heart rate  Decrease conduction velocity through the AV node.

28 Beta Blockers  Myocardial automaticity is reduced  Many types of dysrhythmias are stabilized  Main value is to treat atrial dysrhythmias associated with heart failure.

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30 Core Concept 19.8 Potassium channel blockers prolong the refractory period of the heart.

31 Potassium Channel Blockers  Blocks potassium ion channels in myocardial cells  Prolong the duration of the action potential by lengthening the refractory period (resting stage)  Stabilizes dysrhythmias.

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33 amiodarone (Pacerone, Cordarone)

34 Core Concept 19.9 Calcium channel blockers are available to treat supraventricular dysrhythmias.

35 Calcium Channel Blockers  Slowconduction velocity  Stabilize certain dysrhythmias  Effects include  Reduced automaticity in the SA node  Slowed impulse conduction through the AV node  Prolongs the refractory period  Stabilizes many types of dysrhythmias

36 Calcium Channel Blockers  Only effective against supraventricular dysrhythmias.

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38 Core Concept Digoxin and adenosine are used for specific dysrhythmias, but do not act by blocking ion channels.

39 Adenosine (Adenocard, Adenoscan)  Given as a 1- to 2-second bolus IV injection  Actions  Terminates serious atrial tachycardia  Slows conduction through the AV node decreases automaticity of the SA node

40 Adenosine (Adenocard, Adenoscan)  Primary indication  Paroxysmal supraventricular tachycardia (PSVT), for which it is a drug of choice  10-second half-life, adverse effects are generally self-limiting.

41 Digoxin (Lanoxin, others)  Primarily used to treat heart failure  Prescribed for certain types of atrial dysrhythmia  Decreases automaticity of the SA node  Slows conduction through the AV node


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