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CHAPTER 17

Drugs for Dysrhythmias


Introduction

ď‚— Dysrhythmias are

abnormalities of electrical conduction or rhythm in the heart. ď‚— Sometimes called arrhythmias, they encompass a number of different disorders that range from harmless to life threatening.


Introduction

ď‚— Proper diagnosis and

optimum pharmacologic treatment can significantly affect the frequency of dysrhythmias and their consequences. ď‚— Fast Facts pg. 296


Introduction ď‚— The frequency of

dysrhythmias in the population is difficult to ascertain because many clients experience no symptoms.


Introduction

 Dysrhythmias are abnormalities of

electrical conduction or rhythm in the heart 

Aka arrhythmias

 Can be harmless to life threatening  Electrocardiogram (ECG/EKG)

used to make diagnosis  Persistent dysrhythmias increase risk of stroke and heart failure  Severe dysrhythmias may cause sudden death


Classified by the Location & Type of Rhythm Produced  Originate in atria (aka    

supraventricular) Premature atrial contractions (PACs) Atrial tachycardia Atrial flutter Atrial fibrillation— most common

 Originate in ventricles

—more serious  Premature ventricular contractions (PVCs)— more serious than PACs  Ventricular tachycardia  Ventricular flutter or fibrillation—require immediate treatment


Classified by the Location & Type of Rhythm ď‚— Sinus bradycardia

and heart blocks may require pacemaker


Disease Commonly R/T Dysrhythmias  1. HTN

 6. Myocardial infarction

 2. Mitral stenosis  3. Coronary artery

disease (CAD)  4. Medications such as digitalis  5. Low serum potassium levels

   

(MI) 7. Adverse effects from antidysrhythmic drug 8. Stoke (CVA) 9. Diabetes Mellitus (DM) 10. Congested heart failure (CHF)


The Electrical Conduction Pathway

ď‚— The electrical

conductionpathway in the myocardium keeps the heart beating in a synchronized manner. ď‚— In all types of dysrhythmias there is a defect in the formation or conduction of electrical impulses across the myocardium.


The Electrical Conduction Pathway  Normal conduction

pathway in the heart: Sinoatrial (SA) node  Atrioventricular (AV) node  Atrioventricular bundle (Bundle of His)  Right and left bundle branches  Purkinje fibers 


The Electrical Conduction Pathway

 Electrocardiogram

(ECG)—measures this electrical activity.  Ectopic foci or ectopic pacemakers— 

Other areas of the heart start to initiate beats. Potential to cause dysrhythmias


The Electrical Conduction Pathway

ď‚— Goal of conduction

system is to keep heart beat in a regular synchronized manner to maintain cardiac output.


Non-Pharmacologic Therapy

ď‚— Non-pharmacologic

therapy of certain dysrhythmias is often the treatment of choice. ď‚— All antidysrhythmic agents have the ability to cause rhythm abnormalities or worsen existing ones.


Non-Pharmacologic Therapy

ď‚— Because of this, non-

pharmacologic treatment is sometimes preferred over drug therapy. ď‚— Dysrhythmias may be corrected using cardioversion or catheter ablation.


Non-Pharmacologic Therapy  Cardioversion or defibrillation  Electrical shock to heart  Used for more serious dysrhythmias  Catheter ablation  Identification and destruction of myocardial cells responsible for abnormal conduction  Cardiac pacemaker inserter  Dysrhthmias that cause heart to beat to slowly  Implantable cardioverter defibrillation  Pacing the heart or  Giving an electrical shock when dysrhthmia occurs.


Changes in Na & K Levels

 Changes in sodium and

potassium levels generate the action potential in myocardial cells.  Antidysrhthmic drugs affect the action potential in myocardial cells.  They act by blocking sodium, potassium, or calcium channels in the cell membranes.


Classified by Mechanism of Action  All antidysrhythmic drugs can

    

correct, worsen or create new dysrhythmias. Class I—sodium channel blockers Class II—beta-adrenergic blockers Class III—potassium channel blockers Class IV—calcium channel blockers Miscellaneous antidysrhythmic drugs.


Sodium Channel Blockers  Sodium channel

blockers slow the rate of impulse conduction through the heart.  Largest group of antidysrhythmics  Block opening of sodium ion channels in membrane  Drug profile quinidine sulfate (Quinidex) pg. 304.


Beta-Adrenergic Blockers  Beta-Adrenergic blockers

    

reduce automaticity as well as slow conduction velocity in the heart. Used to treat large number of CV diseases. Serious side effects few used to treat dysrhythmias Slow heart heart Main value—treat atrial dysrhthmias r/t heart failure DP—propranolol (Inderal) 305.


Potassium Channel Blockers  Potassium channel

blockers prolong the refractory period of the heart.  Prolong duration of action potential  Restricted use because of serious side effects  DP amiodarone (Cardarone) pg. 306.


Calcium Channel Blockers

 Two calcium channel blockers are

   

available as antidysrhythmics— table 17.5 pg. 307. Widely prescribed for various CV disorders Reduce automaticity in SA node and slow impulse through AV node. Only effective against supraventricular dysrhythmias. DP—verapamil (Calan) pg. 307


Misc. Drugs

ď‚— Digoxin and several

other drugs are used for specific dysrhythmias but do not act by blocking ion channels—table 17.6 pg. 308.


Misc. Drugs

 Digoxin  Decrease automaticity of SA node and slows conduction through AV node  Used for certain types of atrial dysrhthmias  Can produce serious dysrhythmias


Misc. Drugs

 Adenosine (Adenocard)  Slows conduction through AV node and decreases automaticity of SA node.  Used to terminate serious atrial tachycardia.  Side effects self-limiting due to short half-life


PHARM CHAPTER 17 2008