cardiac arrhythmia

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slide 1 cardiac arrhythmia catherine seger medicinal chemistry hi, i’m catherine, and for my presentation i am going to talk about cardiac arrhythmias and the drug treatments that are available to treat them. there are two broad classes of arrhythmias, those based in the atrium, and that includes things like atrial flutter, atrial fibrillation, and basically any kind of abnormality in the sinus rhythm, and those that are based in the ventricles, like ventricular tachycardia, which is actually what i’m going to focus on in this talk. * types of arrhythmias ventricular cardiac action potential ion channels of interest classification of anti-arrhythmic drugs drugs and re-entry class i drugs class iii drugs side effects alternative treatments and future drug development topics covered ok, to get us started, here’s just a broad list of the topics that i’m going to cover today. we are going to start with the three main …

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in two contexts, either before the cell has recovered or after the cell has recovered. click automatic rhythms are rhythms whereby the heart normally beats. this can happen abnormally if for whatever reason some cardiac tissue develops spontaneous depolarization. it can occur abnormally, for instance, because of ph imbalances in certain parts of the cell click reentry is going to be the main issue that we are going to be concerned with since it causes most of the types of ventricular arrhythmias. * ventricular re-entry abnormal pattern of depolarization through the heart functional anatomic the main types of ventricular arrhythmia that we are going to be concerned with are going to come from reentry. re-entry is a self-perpetuating pattern of depolarization involving any cardiac tissues and does not depend on altered automaticity. it just depends on differences in the areas of the heart that allows for conduction in one area …

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vation of na+ channels phase 2:influx of ca2+ coupled with the slow outflow of k+ causing plateau phase 3: repolarization (release of k+) phase 4:resting membrane potential * ion channels relevent to the cardiac action potential ok, now for each phase of the action potential there are ion channels that are coming into play. in phase 0, the fast sodium channels open. phase 1 corresponds with the inactivation of the fast sodium channels. now, in phase 2, there is an inward movement of calcium through l-type calcium channels that is coupled with an outward movement of potassium through slow-rectifier channels (iks)…this coupling is what causes the plateau that is absent in the action potential of a normal muscle. in phase 3, the l-type calcium channels close, but the slow-rectifier potassium channels stay open, so the membrane potential is slowly becoming more negative, which ultimately causes more potassium channels to open …

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$g to focus on classes i and iii because these are the ones affecting the action potential directly so they will be most useful in these re-entry circuits * how these drugs affect re-entry class i: retards conduction enough so that beat still gets through normal cardiac tissue but not through any weakened tissue class iii: prolongs refractoriness the class i drugs can completely block conduction through the weakened tissue. since the weakened tissue isn’t going to block an entire pathway through the hear, just enough of one to cause some mischief, the wavefront will still be able to propogate in the surrounding normal tissue the class iii drugs prolong repolarization so the re-entry circuit will still begin to develop, but since only one side will have the issue, when the wave has circled all the way back around the cells that are slowed down still will not have recovered, …$

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inide, and propafenone indicated for the treatment of life-threatening ventricular tachycardia or ventricular fibrillation, or symptomatic pvcs * class ia as you can see here, it blunts the upstroke and prolongs phase 2 * class ia-procainamide procainamide n-acetyl procainamide analog of the local anesthetic procaine long term oral treatment poorly tolerated (can cause lupus syndrome) blocker of open na+ channels only has an cardioactive metabolyte (can also work as produg), procainamide and n-acetyl procainamide napa only blocks potassium channels metabolized into napa in the liver * class ib the ib drugs blunt the upstroke slightly because it is a weak sodium channel blocker, but it also has action at potassium channels which is why it shortens the action potential duration * class ib-lidocaine local anesthetic also used in the acute intravenous therapy of ventricular arrhythmias blocks both open and inactivated cardiac na+ channels exerts greater effects in ischemic or rapidly …

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slide 1 cardiac arrhythmia catherine seger medicinal chemistry hi, i’m catherine, and for my presentation i am going to talk about cardiac arrhythmias and the drug treatments that are available to treat them. there are two broad classes of arrhythmias, those based in the atrium, and that includes things like atrial flutter, atrial fibrillation, and basically any kind of abnormality in the sinus rhythm, and those that are based in the ventricles, like ventricular tachycardia, which is actually what i’m going to focus on in this talk. * types of arrhythmias ventricular cardiac action potential ion channels of interest classification of anti-arrhythmic drugs drugs and re-entry class i drugs class iii drugs side effects alternative treatments and future drug development …

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