心肌缺血的电生理改变-中英对照-Richard E. Klabunde, PhD

心超 · 发表于 2010-1-16 17:55:31

本帖最后由心超于 2010-1-16 18:34 编辑

            心肌缺血的电生理改变
                                                         -------------Richard E. Klabunde, PhD

   （正常心肌细胞内高K，细胞外高Na状态，形成细胞内外带电离子的极化状态，保持极化状态需要消耗能量）心肌缺血/缺氧导致细胞外 K+.  升高，其原因是缺氧导致心肌细胞内ATP水平下降，ATP 调控的K通道开放（K外流增加）同时 Na+/K+-ATP酶泵活性下降，(K内流减少)。

      细胞外 K+ 升高触发细胞膜出现去极化（membrane depolarization ）（激活快Na通道），与Nernst 公式相一致。(尽管细胞外K的轻微增加可使gK增加产生超极化)。去极化（发生后）可使快Na++ 通道失活，从而降低动作电位（action potential ）的激发速度（？）。这将引起传导速度（conduction velocity）下降。由此常导致心律失常（arrhythmias），需要抗心律失常药物（antiarrhythmic drugs.）。

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心血管生理

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      损伤电流是从除极化的缺血区流向正常区域，导致心电图ST段（ST segment ）升高或降低，如果缺血区域为非透壁、心内膜下缺血则

表现为ST段压低，多与需求增加性心肌缺血(demand ischemia )相关比如劳累型心绞痛（exertional angina）；如若为透壁性心肌缺血则

表现为ST段升高（注意和透壁性心梗相鉴别），与供给不足性心肌缺血（supply ischemia ）相关比如冠脉阻塞（coronary occlusion）。

      对于非透壁性心肌缺血（ non-transmural ischemia）, ST段压低的原因是：当心室处于静息和复极状态，已经发生去极化

的心肌缺血区由于存在点位差产生了可被置于其上的心电图电极记录的电流。当该除极电流（depolarizing currents）指向一个正电极，QRS

波群QRS complex 前的基线（正常状态下为等电位，如，0v）将会上升。心室除极完成后（depolarized）所有的心肌都已除极，通常电极记

录的电压应该为（0v）zero volts。这就是说，基线电压上升的净效应（net effect ）为ST段相对于基线降低。(由于心电图默认基线的电压为

0，所以基线电压上升后ST段看上去就比QRS波群前的基线低)。

      对于透壁性心肌缺血（transmural ischemia），ST段上抬是因为心室在静息和复极的状态下，完成去极化的缺

血区产生的电流背离正电极，QRS波群前的基线电压下降。当心室除极完成，所有心肌完成去极化电极记录的电压为0v，这意味着基线电压

降低的净效应（net effect ）为ST段相对于基线抬高。(由于心电图默认基线的电压为0，所以基线电压降低后ST段看上去就比QRS波群前的

基线高译者按)。

                                                                                                                                                            新青年麻醉心超编译

心血管生理 http://www.cvphysiology.com/CAD/CAD012.htm

Ischemia/hypoxia causes an elevation in extracellular K+.  This occurs because K+ leaks out through KATP channels (normally inhibited by ATP) and because of decreased activity of the Na+/K+-ATPase pump. These changes occur because ATP levels decline in hypoxic cells.
Increases in extracellular K+ cause membrane depolarization in accordance with the Nernst equation (although very small increases in extracellular K+ may cause hyperpolarization by increasing gK). Depolarization will inactivate fast Na++ channels and thereby decreased action potential upstroke velocity (fast Na+ channels inhibited). This will lead to decreased conduction velocity. These changes often lead to arrhythmias that may require the use of antiarrhythmic drugs.
Injury currents flowing from the depolarized ischemic regions to normal regions result in the appearance of ST segment elevation or depression, depending upon whether the ischemic region is non-transmural, subendocardial (ST depression) or transmural (ST elevation). The former is usually associated with demand ischemia (e.g., exertional angina), whereas the latter is associated with supply ischemia (e.g., coronary occlusion).

For non-transmural ischemia, the ST segment depression occurs because when the ventricle is at rest and repolarized states, the depolarized, ischemic region generates electrical currents that are recorded by an overlying electrode. If the depolarizing currents are traveling toward the positive electrode, the baseline voltage prior to the QRS complex (which is normally isoelectric - i.e., zero volts) will be elevated. In contrast, when the ventricle becomes depolarized, all the muscle is depolarized so that zero voltage is recorded by the electrode as usual. Therefore, the net effect of the elevated baseline voltage is that the ST segment appears to be depressed relative to the baseline.
For transmural ischemia, the ST segment elevation occurs because when the ventricle is at rest and repolarized, the depolarized, ischemic region generates electrical currents that are  traveling away from the positive electrode; therefore the baseline voltage prior to the QRS complex will be depressed. When the ventricle becomes depolarized, all the muscle is depolarized so that zero voltage is recorded by the electrode. Therefore, the net effect of the depressed baseline voltage is that the ST segment appears to be elevated relative to the baseline.
RK Revised 04/02/2007

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