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Questions and Answers
What is the phase 0 cardiac action potential upstroke caused by?
What is the phase 0 cardiac action potential upstroke caused by?
Which of the following correctly describes phase 2 of cardiac action potentials?
Which of the following correctly describes phase 2 of cardiac action potentials?
What do class 1 antiarrhythmics primarily block?
What do class 1 antiarrhythmics primarily block?
Sodium channels
How do class 1 antiarrhythmics affect the slope of the phase 0 upstroke?
How do class 1 antiarrhythmics affect the slope of the phase 0 upstroke?
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What is the effect of 'use dependence' in class 1 antiarrhythmics?
What is the effect of 'use dependence' in class 1 antiarrhythmics?
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What current is present in phase 2 and phase 3 of the action potential?
What current is present in phase 2 and phase 3 of the action potential?
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Class 1 antiarrhythmics affect the SA and AV nodes.
Class 1 antiarrhythmics affect the SA and AV nodes.
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What effect do class 1 antiarrhythmics have on the QRS complex?
What effect do class 1 antiarrhythmics have on the QRS complex?
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Which of the following is a Class 1A antiarrhythmic?
Which of the following is a Class 1A antiarrhythmic?
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What syndrome can quinidine toxicity cause?
What syndrome can quinidine toxicity cause?
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Class 1B antiarrhythmics are primarily used to treat __________ arrhythmias.
Class 1B antiarrhythmics are primarily used to treat __________ arrhythmias.
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What adverse effects are associated with class 1B antiarrhythmics?
What adverse effects are associated with class 1B antiarrhythmics?
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Match the following Class 1 antiarrhythmics with their respective subclasses:
Match the following Class 1 antiarrhythmics with their respective subclasses:
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Study Notes
Cardiac Action Potentials
- Phase 0: Upstroke of cardiac AP is driven by Na+ influx.
- Phase 2: Plateau phase maintained by Ca2+ currents.
- Phase 3: Repolarization occurs via K+ outflow.
Class 1 Antiarrhythmics
- Block sodium channels, impacting phase 0 upstroke and conduction velocity.
- Category 1A drugs (quinidine, procainamide, disopyramide) slow the conduction of cardiac action potentials.
- Class 1A drugs also block K+ channels, prolonging phases 2 and 3, which extends the refractory period.
Use-Dependence
- Class 1 antiarrhythmics have greater effects on rapidly depolarizing tissues; higher heart rates can lead to slower phase 0 upstrokes.
Pharmacological Classes
- Class 1A: Intermediate sodium channel binding strength; effective in atrial and ventricular arrhythmias.
- Class 1B: Low affinity for Na+ channels, effective primarily in ventricular arrhythmias, especially in ischemic tissue.
- Class 1C: Strongest sodium channel binding, used for atrial fibrillation and flutter.
Specific Drug Effects
- Quinidine: Potentially causes cinchonism (tinnitus, headache, dizziness) and thrombocytopenia.
- Procainamide: Long-term use can trigger lupus-like syndrome.
- Disopyramide: Negative inotropic effects may worsen heart failure.
- Lidocaine and Mexiletine (Class 1B) known for neurological side effects like paresthesias and tremors.
Cardiac Implications
- Class 1A agents increase QT interval, risk of torsades de pointes due to prolonged action potential duration.
- Class 1C drugs do not affect AP duration, but strongly inhibit Na+ channels, associated with widest QRS complex during dysrhythmias.
Contraindications
- Class 1C antiarrhythmics contraindicated in patients with structural or ischemic heart disease due to potential proarrhythmic effects.
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Description
Test your knowledge on antiarrhythmic drugs with these engaging flashcards designed for Class 1A, 1B, and 1C. Each card contains key concepts related to cardiac action potentials and the mechanisms of these medications. Perfect for quick revision and memorization!