Drugs for Dysrhythmias

Chapter 26

Dysrhythmias
What is a dysrhythmia? Why is dysrhythmia a better term than the previously used arrhythmia? Describe the range of symptoms associated with dysrhythmias. Discuss the typical symptoms. Identify the underlying cause of the symptoms.

Dysrhythmias
Why is it essential to terminate/control dysrhythmias? What is the most common dysrhythmia? Why are ventricular dysrhythmias generally more serious?

Dysrhythmias
Most often classified by type of rhythm abnormality and location where it is produced. Mary has a regular heart beat of 54 beats per minute. Her telemetry monitor shows a normal complex configuration. How would this dysrhythmia be classified? Why is correct diagnosis important?

Associated Disorders
Heart disease Myocardial infarction Hypertension Cardiac valve disease
e.g., mitral stenosis

Medications
e.g., digoxin

CAD

Hypokalemia Stroke Diabetes mellitus Heart Failure

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.

Conduction Abnormalities
Mary tells the nurse she feels like her heart skips a beat ever so often. Two nurses check the apical pulse against the radial pulse and find a difference of 4 beats per minute. The telemetry monitor occasionally has a complex that looks different from the rest. What is this difference in pulses called? What is the reason for the difference?

Nonpharmacologic Interventions
Cardioversion Difibrillation Catheter ablation Implanted pacemaker Implanted cardioverter defibrillator

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

Action Potentials
AP is initiated when cell membrane Na++ channels open and Na++ 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 muscle contraction.

Action Potentials
During depolarization inside of plasma membrane becomes positively charged. Na/K pump is activated and Na++ is moved out of cell and K+ is moved back in through respective channels. How is this process important to cardiac pharmacology?

Antidysrhythmics
Mechanism of Action
Alter specific electrophysiologic properties of the heart Accomplished by:
Blocking flow through ion channels Altering autonomic activity

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

Sodium Channel Blockers

Prototype: procainamide (Pronestyl) p. 368 3 subclasses based on differences in MOA Prevents depolarization slowed impulse conduction and suppresses ectopic foci Similar to anesthetic agents Side effects vary by drug What side effects would you expect?

Sodium Channel Blockers

Quinidine and procainamide effective for many dysrhythmias Other drugs in class reserved for lifethreatening dysrhythmias Lidocaine can cause CNS toxicity.
What signs would indicate this?

Some drugs in class also exert an anticholinergic effect.

What signs would indicate this?

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

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

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

Potassium Channel Blockers

Prolong duration of action potential and reduce automaticity 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 cardiac effects

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

Client Teaching: Potassium Channel Blockers

Regular eye exams Avoid prolonged sun exposure Use sunscreen Take with food Immediately report:
SOB, palpitations, cough, vision changes, yellow sclera, jaundice, RUQ pain, dizziness

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

Miscellaneous Drugs
Digoxin indicated for atrial fibrillation
Monitor closely for toxicity

Adenosine (Adenocard)
Only used for Paroxysmal Supraventricular Tachycardia Naturally occurring nucleoside Slows impulse conduction through A-V node and decreases automaticity Dyspnea common but self-limiting