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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