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18 Cards in this Set
- Front
- Back
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What do cardiac arrhythmias result from?(2)
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1. Disturbances in impulse formation from pacemaker activity
2. Disturbances in impulse conduction due to reexcitation of tissue |
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What do antiarrhythmics do broadly?(2)
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1. Reduce pacemaker activity
2. Modify reentrant circuits |
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What are the 4 major mechanisms of antiarrhythmics?
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1. Block Na Channels
2. Block Beta 1 and 2 receptors 3. Block K Channels 4. Block Ca channels |
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Why is the SA node the pacemaker of the heart?
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1. Because it discharges the most rapidly, so its AP is the one that spreads to the rest of the heart
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Which groups of antiarrhythmics target the nodal fibers and which target the fast twitch muscle?
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1. Group 1 and 3 target the Fast twitch
2. Groups 2 and 4 target the nodal fibers |
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What do the group 1 antiarrhythmics do?2?3?4?
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1. Na channel blockers increase the slope of depolarization = slows it down
2. Group 2 are the beta blockers that decrease cAMP to shut down ion channels 3. Group 3 are the K blockers that prolong repolarization 4. Group 4 are the Ca channel blockers. They prolong nodal depolarization. |
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Which groups are preferential for which arrhythmias?(2)
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1. Groups 1 and 3 for ventricular
2. Groups 2 and 4 for supraventricular |
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In the fast twitch muscle fiber describe the depolarization/repolarization steps?(4)
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1. Huge Na efflux depolarizes it
2. K in, Ca out plateau 3. Rapid K influx repolarizes 4. 3Na out and 2K in keeps negative potential around -90mV |
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Describe the depolarization/repolarization in the nodal tissue?
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1. Slower Ca efflux depolarizes
2. Ca closes and K influx repolarizes 3. Na/Ca/K efflux/influx is a self depolarization that keeps the pace |
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Explain the M/H gate ion channels of the heart muscle?
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1. M gate starts closed with H gate open
2. AP opens M and Closes H with a complete open phase in between 3. H gate seals off the ion channel 4. Repolarization through the Na/K ATPase |
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Why does hypoxic tissue get arrhythmic?
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1. The Na/K ATPase that closes the M gate and opens the H gate does not work
2. APs can fall on top of one another |
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What are Quinidine, Procainamide, and Disopyramide? Describe their EKG potential?
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1. Three class 1a antiarrhythmics
2. Block the Na Channels 3. Good for both atrial and ventricular fibrillation 4. PR int = +; QRS = +++; QT = +++ |
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How is Quinidine taken? What are the main side effects of it?
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1. Orally
2. Cinchonism and Syncope 3. Cinchonism is headache, dizziness, tinnitus, and vision disturbances 4. Torsades de Pointes(syncope) |
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What is Procainamide? Adverse effects?
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1. Class 1a antiarrhythmic
2. Like Quinidine but more cardiodepressant 3. Causes Lupus like syndrome in slow acylators |
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What are Lidocaine, Mexilitine, Tocainide and Phenytoin?(3)
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1. Group 1b antiarrhythmics
2. No impact on the EKG 3. Act on purkinje and ventricular cells |
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Describe Lidocaine?(3)
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1. Common IV drug
2. Good following an MI or digitalis toxicity 3. Can cause CV depression, neurologic effects and Seizures |
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Describe Tocainide and Mexilitine?(4)
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1. Class 1b
2. Good oral 3. Ventricular arrhythmics 4. Termor, blurred vision, lethargy and nausea |
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What are Flecainide, Prophenone, and Encainide?
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1. Group 1c
2. very toxic = proarrhythmogenic 3. PR = +; QRS = +++; QT = +++ 4. LAST RESORT |
