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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?
- Potassium
- Magnesium
- Sodium (correct)
- Calcium
Which of the following correctly describes phase 2 of cardiac action potentials?
Which of the following correctly describes phase 2 of cardiac action potentials?
- Plateau via Ca2+ (correct)
- Na+ channel blocking
- Phase 0 upstroke
- Repolarization by K+
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?
What is the effect of 'use dependence' in class 1 antiarrhythmics?
What is the effect of 'use dependence' in class 1 antiarrhythmics?
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?
Class 1 antiarrhythmics affect the SA and AV nodes.
Class 1 antiarrhythmics affect the SA and AV nodes.
What effect do class 1 antiarrhythmics have on the QRS complex?
What effect do class 1 antiarrhythmics have on the QRS complex?
Which of the following is a Class 1A antiarrhythmic?
Which of the following is a Class 1A antiarrhythmic?
What syndrome can quinidine toxicity cause?
What syndrome can quinidine toxicity cause?
Class 1B antiarrhythmics are primarily used to treat __________ arrhythmias.
Class 1B antiarrhythmics are primarily used to treat __________ arrhythmias.
What adverse effects are associated with class 1B antiarrhythmics?
What adverse effects are associated with class 1B antiarrhythmics?
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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