NUR 378 Chapter 49- Antidysrhythmic Drugs Test Questions and Correct Answers
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Course
NUR 378
Institution
NUR 378
How does the pro-dysrhythmic effect of antidysrhythmic drugs affect when they are used to treat dysrhythmias? They can also cause dysrhythmias or worsen existing ones. Only use it if benefits > risk
What is a common mechanism by which drugs cause dysrhythmias? Interferes with ventricular pumpin...
NUR 378 Chapter 49- Antidysrhythmic
Drugs Test Questions and Correct
Answers
How does the pro-dysrhythmic effect of antidysrhythmic drugs affect when they are
used to treat dysrhythmias? ✅They can also cause dysrhythmias or worsen existing
ones.
Only use it if benefits > risk
What is a common mechanism by which drugs cause dysrhythmias? ✅Interferes with
ventricular pumping
Describe how the following influences the use of antidysrhythmic drugs:
Sustained vs. non-sustained dysrhythmias ✅Non-sustained dysrhythmias: only use
when they are symptomatic
Sustained dysrhythmias: Can be dangerous, only use when benefits > risks
Describe how following influences the use of antidysrhythmic drugs:
Asymptomatic vs. Symptomatic dysrhythmias ✅Asymptomatic dysrhythmias: No
symptoms
Symptomatic dysrhythmias: Benefits
Describe how each of the following influences the use of antidysrhythmic drugs:
Supraventricular vs. ventricular dysrhythmias ✅Supraventricular dysrhythmias: benign,
but will harm if ventricles go too fast to fill
Goal: terminate dysrhythmia or prevent excessive atrial beats from reaching ventricles
(beta-blockers, CCB, digoxin)
Ventricular dysrhythmias: frequently interfere with pumping
Goal: terminate and prevent reoccurance
What are the expected pharmacological effects of sodium channel blockers?
IA Agents (Quinidine/Procainamide) ✅- Blocks sodium channels to slow impulse
conduction in atria, ventricles, and His-Purkinje system
- Blocks K+ channels to delay repolarization
- Both suppress dysrhythmias
Quinidine is anticholinergic (atropine-like): blocks vagal input of heart to increase SA
nodal automaticity and AV conduction, which can drive ventricles to an excessive rate
, Widens QRS complex
Prolongs QT interval
What are the therapeutic indications of sodium channel blockers?
IA Agents (Quinidine/Procainamide) ✅- Active against supraventricular and ventricular
dysrhythmias
- Long-term suppression of SVT, atrial flutter, atrial fibrillation, sustained ventricular
tachycardia
- Increase mortality of atrial flutter + atrial fillbration
- Also used for severe Malaria
What are the most potentially fatal adverse effects of sodium channel blockers?
IA Agents (Quinidine/Procainamide) ✅- Cardiotoxicity
- Arterial Embolism
Which clients are at increased risks of adverse effects from sodium channel blockers?
IA Agents (Quinidine/Procainamide) ✅- History of hypersensitivity to drug
- partial AV block, HF, hypotensive states, hepatic dysfunction
Procainamide:
- SLE, complete AV block, 2 or 3 degree AV block, procaine allergy
- Hepatic/renal dysfunction
Explain the most significant drug-drug interactions for sodium channel blockers.
IA Agents (Quinidine/Procainamide) ✅- Digoxin: doubles digoxin levels by displacing
digoxin from albumin
What assessments should the nurse perform before administering a sodium channel
blocker?
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