web drugs for dysrhythmias

8/3/2019 Web Drugs for Dysrhythmias

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Drugs for Dysrhythmias

Chapter 26


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Dysrhythmias

What is a dysrhythmia?

Why is dysrhythmia a better term than the previously usedarrhythmia?

Describe the range of symptoms associated withdysrhythmias.

Discuss the typical symptoms.

Identify the underlying cause of the symptoms.


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Dysrhythmias

Why is it essential to terminate/control

dysrhythmias?

What is the most common dysrhythmia?

Why are ventricular dysrhythmias generallymore serious?


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Dysrhythmias

Most often classified by type of rhythmabnormality and location where it is produced.

Mary has a regular heart beat of 54 beats perminute. Her telemetry monitor shows a normalcomplex configuration. How would thisdysrhythmia be classified?

Why is correct diagnosis important?


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Associated Disorders

Heart disease

Myocardial infarction

Hypertension

Cardiac valve disease

e.g., mitral stenosis

CAD

Medications

e.g., digoxin

Hypokalemia

Stroke

Diabetes mellitus

Heart Failure


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Impulse Conduction

What is the importance of the action potential?

What is the purpose of the conduction system?

How long does it take an impulse to travel ?

Discuss synchronization.


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Conduction Abnormalities

Mary tells the nurse she feels like her heartskips a beat ever so often. Two nursescheck the apical pulse against the radial pulse

and find a difference of 4 beats per minute.The telemetry monitor occasionally has acomplex that looks different from the rest.

What is this difference in pulses called?

What is the reason for the difference?


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Nonpharmacologic Interventions

Cardioversion

Difibrillation

Catheter ablation

Implanted pacemaker

Implanted cardioverter defibrillator


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Antidysrhythmic Pharmacotherapy

Goals

Terminate existing dysrhythmias

Prevention of abnormal rhythms

Guiding principle

Pharmacotherapy should generally be used for

patients with overt symptoms or conditions not

controlled by other means


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Action Potentials

AP is initiated when cell membrane Na++

channels open andN

a++ rushes into the cell

rapid depolarization. Ca++ enters the cell

through Ca++ channels and the influx of Ca++

triggers release of intracellular Ca++ a lot of

Ca++ available for myocardial musclecontraction.


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Action Potentials

During depolarization inside of plasmamembrane becomes positively charged. Na/Kpump is activated and Na++ is moved out ofcell and K+ is moved back in throughrespective channels.

How is this process important to cardiacpharmacology?


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Antidysrhythmics

Mechanism ofAction

Alter specific electrophysiologic properties of the

heart

Accomplished by:

Blocking flow through ion channels

Altering autonomic activity


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Antidysrhythmic Classifications

Class I: Na++ Channel Blockers

Class II: Beta-Adrenergic Blockers

Class III: K+ Channel Blockers

Class IV: Ca++ Channel Blockers

Class V: Miscellaneous


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Sodium Channel Blockers

Prototype: procainamide (Pronestyl) p. 368

3 subclasses based on differences in MOA

Prevents depolarization

slowed impulseconduction and suppresses ectopic foci

Similar to anesthetic agents

Side effects vary by drug

What side effects would you expect?


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Sodium Channel Blockers

Quinidine and procainamide effective formany dysrhythmias

Other drugs in class reserved for life-

threatening dysrhythmias

Lidocaine can cause CNS toxicity.

What signs would indicate this?

Some drugs in class also exert ananticholinergic effect.

What signs would indicate this?


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NCs: Sodium Channel Blockers

Complete health hx and physical exam

Baseline: ECG, VS, LFTs, RFTs, e-lytes

Contraindications: HF, BP, MG, Renal or

Hepatic impairment Drug-Drug interactions

Monitor ECG

Frequent BP

Monitor for change in LOC, respiratory status

Drug plasma levels

Quinidine assess for diarrhea


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Client Teaching: Sodium Channel

Blockers

Do not skip dose

Do not double up if a dose is missed

No alcohol, caffeine, tobacco

Keep all scheduled lab appts

Immediately report:

SOB, signs of bleeding, excessive bruising, fever,nausea, persistent headache, vision changes,hearing changes, diarrhea, dizziness


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Beta-Adrenergic Blockers

Widely used

Decrease HR and conduction velocity suppression of many dysrhythmias

Approved: acebutolol, esmolol, propranolol

Avoid-

heart block, asthma, severe bradycardia,

Side effects: Bradycardia, hypotension, dizziness, syncope

Non-selective beta blockers can cause bronchospasm


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Potassium Channel Blockers

Prolong duration of action potential and reduceautomaticity

Delay repolarization and lengthen refractory

period stabilization of dysrhythmia Prototype: amiodarone (Cordarone) p. 372

Limited use due to side effects

Serious bradycardia and hypotension

Can worsen dysrhythmias

Elderly with HF at increase risk of adverse cardiaceffects


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NCs: Potassium Channel Blockers

Use cautiously in heart block

Baseline ECG and VS

Amiodarone: baseline CXR, PFTs

IV RX: continuous VS and ECG monitoring Withhold if pulse < 60, SBP < 90

Watch for s/s of HF

Monitor serum levels

Pregnancy category C or D

Not recommended during lactation


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Client Teaching: Potassium Channel

Blockers

Regular eye exams

Avoid prolonged sun exposure

Use sunscreen

Take with food

Immediately report:

SOB, palpitations, cough, vision changes, yellowsclera, jaundice, RUQ pain, dizziness


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Calcium Channel Blockers

Widely prescribed for cardiovascular disorders

Decrease conduction velocity stabilization of

dysrhythmia

Prototype: verapamil (Calan) p. 373

Dilatizem (Cardizem) and verapamil block calcium

channels in both heart and arterioles

Only effective on supraventricular dysrhtymias

Safe and well tolerated

Common side effects: bradycardia and hypotension

Increase risk of bradycardia and HP when concurrent with

betablockers


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Miscellaneous Drugs

Digoxin indicated for atrial fibrillation

Monitor closely for toxicity

Adenosine (Adenocard)

Only used for Paroxysmal SupraventricularTachycardia

Naturally occurring nucleoside

Slows impulse conduction throughA

-V node anddecreases automaticity

Dyspnea common but self-limiting

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