458475
Beschreibung
Karteikarten von littlebluechair, aktualisiert more than 1 year ago
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Erstellt von littlebluechair
vor mehr als 10 Jahre
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| Frage | Antworten |
| Digoxin | Digoxin inhibits the Na+/K+-ATPase pump in myocardial cell membranes. |
| How does digoxin serve as an antiarrythmic? | It increases the refractory period and decreases the conduction time of the AV node. |
| How is digoxin used therapeutically? | For treating supraventricular arrhythmias and congestive heart failure. |
| What are the toxicities to watch for? | Atrial or ventricular dysrhythmias (most commonly atrial tachycardia) |
| What is the treatment for digoxin toxicity? | Digoxin antibodies. |
| Magnesium sulfate How does magnesium sulfate prevent arrhythmia? | The mechanism is not completely clear, but it is thought to stabilize cardiac cell membranes. |
| When do you use this drug? | For treating torsades de pointes |
| What are the adverse effects? | Bradycardia Respiratory paralysis Flushing Headache |
| How does adenosine work? | It activates acetylcholine-sensitive K+ channels, especially in the SA and AV nodes. This increases in K+ conductance results in shortening of action potential duration, hyperpolarization and decreased automaticity. |
| How is it administered? | IV only |
| Describe adenosine's clinical role | It is a beneficial drug for diagnosing and terminating paroxysmal supraventricular tachyarrhythmias because of its limited toxicites and rapid onset. |
| What are the adverse effects? | Flushing, Dyspnea, Chest pain, Headache. |
| Class IV antiarrhythmics-Calcium channel blockers What drugs belong to this group? | Verapamil, diltiazem, and nifedipine. |
| How do they work? | These drugs block L type calcium channels and decrease both SA node automaticity and AV nodal conduction. More specifically, they decrease the rate of phase 4 spontaneous depolarization and thus increase the effective refractory period. Verapamil has the greatest effect on cardiac tissue. |
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