请教ST段降低的问题

氟马西尼

今天看 麻醉学-问题为中心的病例讨论p148，上面的主题是st段降低提示心肌缺血，或者是氧耗增加，或是氧供减少，处理方法包括增加氧供和降低氧耗。我觉得讲得有点概念了，大家能否告诉我点具体措施以及实施中的注意事项，还有书上讲的大多是全麻和运用血管活性药物，我想知道在局部神经阻滞下（麻醉效果确切）不运用血管活性药物又该怎样实施，先谢了

心超

1# 氟马西尼

        感谢你提出一个很好的话题，我非常感兴趣，通过再次学习，我自己的收获很大，也有很多话要对你说，学和问是一对孪生兄弟，没有

问就没有学，但不能你问我学，要互学互问，这样才能激发更大的兴趣，提问也是一门学问，提出一个好问题比获得答案更重要，我们都需

要思考，什么样的问题才是好问题？什么样的问题能激发更大的学习热情？我体会，做为临床医生提问不能离开临床思维，需要考虑临床意

义，这也你的提问引起我的兴趣的原因。我还要建议你细化一下你的提问：如全麻患者ST段降低对术中决策的意义。


      让我们从基本概念入手，用 GOOGLE   图片搜索：ST段降低   （st segment depression）。搜索结果分析：第一张图的链接是NCBI

（美国国立医学图书馆）的，一般来说图片信息都是来源于其中的在线医学书架 NCBI BOOK SHELF ,用ST段压低搜到的书叫《临床方

法》 ，这本书给我们麻醉医生很好的启发，ST段降低是一个诊断学概念，内科医生使用这一概念时往往把胸痛、平板试验等概念纳入诊断和

治疗决策（Clinical Decision Making ）。而我们更关注诊断和治疗决策后的临床事件（clinical events that occur consequent to

diagnostic and therapeutic strategies ）。对麻醉医生而言我们除了需要在术前获取患者的病史资料，阅读心电图和超声心动图。也应该研究

术中的ST-T改变发生、发展、演变的规律。而且我也想去查“术中ST段压低”这个关键词，我想邀请读书版songhailong版主互动 查一下

这个概念在经典麻醉学教材中的叙述。



Figure 6.1

                               
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shows a picture of the normal ECG, and a change in the ST segment that would be associated with myocardial ischemia. This segment may become depressed to a variable degree; 0.5, 1.0, 1.5, or 2 mm or more. As the criterion (i.e., the "cutoff point") for an abnormal ST segment depression changes, the likelihood of making errors in interpretation also changes.

          我想邀请读书版的深秀版主互动 翻译一下图说


感谢  shenxiu2 版主翻译图说：


这儿显示了一个正常的EKG，和心肌缺血时引起的ST段压低EKG。这个ST段可以有不同程度的压低； 0.5, 1.0, 1.5,  2 毫米 或超过 2毫米。当我们把评定为非正常ST段压低的标准改变的时候，在EKG 意义解读上犯错误的可能性也会随着改变。




       这本中强调的一些科学的诊断学概念有些是麻醉医生知道的，比如敏感性、特异性、和预测值，还有我们不熟悉的，比如似然比

（Likelihood Ratios），这些概念一旦被广大青年麻醉医生掌握，其意义非常深远。掌握了科学的思维方法，就能够做去粗取精、去伪存真的

工作，就能让我们的学问得到真正的增长，也就掌握了自己的未来。

     掌握了正确的学习方法，我们还要勤奋，主动。 比如在一个病案讨论中，有人提出问题，量分子大于多少的分子不能通过胎盘屏障，当然

也有所谓的权威能拿出一些数字，但是我们真的要靠这些听来的数字去做临床决策么？现在资讯如此发达，个人自学的空间非常大，我希望

论坛的每一个人都能拿出热情，参与到互动的集体学习中来。

                               
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           让我们的兴趣继续前进，第2个值得思考的问题是，是不是所有的ST段压低都是心肌缺血? 下面这2个资料很好地回答了这个问题。

ST depression may occur in ischaemic heart disease: indicates myocardial ischaemia, and may be associated with the discomfort of angina rest leads to a reversal it is not a sign of infarction Other causes of ST depression include (1): biochemical causes hypokalaemia hypocalcaemia hypomagnesaemia digoxin glycosides can produce ST depression in the electrocardiogram, both in patients with cardiac disease and in healthy individuals.and in healthy individuals the ST depression that may secondary to cardiac glycoside use complicates the interpretation of rest and exercise electrocardiogram (ECG) left ventricular hypertrophy hypothermia stroke (especially subarachnoid haemorrhage) Reference: Hoffman I, Saltzman B. Is ATP-sensitive K+ channel (K+ATP) recruitment a common mechanism for ECG-ST segment depression and elevation? Medical Hypotheses 2003; 60(4): 593-597.

Links:

myocardial ischaemia
• ST segment depression in exercise ECG

MicroEKG Manual
ST and T Abnormalities

• ST Depresssion
• ST Elevation
• T Wave Abnormality
• Return to main MicroEKG manual index

ST segment depression
ST segment depression can be caused by ischemia, digitalis, rapid heart rate, and temperature or electrolyte abnormality. It can also be a “reflected” or reciprocal ST elevation (showing an inverted view of what’s happening at another place in the heart). The shape of the ST segment, and whether the abnormality is localized to leads looking at one area of the heart, often allows the cause of ST depression to be diagnosed.

ST segment depression is considered significant if the ST segment is at least one box below baseline, as measured two boxes after the end of the QRS. As with infarction, the location of the ischemia is reflected in the leads in which the ST depression occurs.

Causes of ST Depression Ischemia Hypothermia Hypokalemia Tachycardia Subendocardial infarct Reciprocal ST elevation Ventricular Hypertrophy Bundle branch block Digitalis Measure: 2 mm beyond QRS Significant: 1 mm

Ischemia:
When ST segment depression is transient, it’s almost always due to acute myocardial ischemia. The ECG signs of ischemia may come and go fairly quickly — over a matter of minutes.
ST segment depression is MOST specific for ischemia if the ST segment slopes down from the J point. Horizontal or flat STs are also quite suspicous for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.
“J point” depression at the beginning of the QRS complex is not significant if the location of measurement (two boxes past the QRS) finds the ST segment has risen back to the baseline.

Infarction:
ST depression can also be seen in infarction, typically in non Q-wave infarction, often called subendocardial infarction. This type of infarct does not extend through the ventricular wall (non-transmural). Subendocardial infarctions involve small areas of injured tissue, with larger areas of overlying ischemia. These infarctions may show ST segment depression (rather than elevation) because of the larger areas of ischemia.
ST depression can also be seen as a “mirror” of what’s happening on the other side of the heart. For example, the inferior leads may show ST depression as a reflection of what’s happening in the upper lateral side of the heart.

Ventricular hypertrophy:
Left ventricular hypertrophy or strain commonly causes ST segment depression, often with T wave inversions. These changes are seen in the “lateral” leads — those that record activity over the left ventricle. In LVH, ST and T wave abnormalities are commonly seen in leads I, L, and V4-V6.
Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.

Ventricular conduction block:
Left bundle branch block produces ST depression and inverted T waves in leads I, L, and V5-V6. In general, the ST will slope away from the direction of the QRS: a large wide R wave will have a down-sloping ST ending in an inverted T, while a deep wide S wave will have an upsloping ST segment ending in an upright T.

Other causes of ST segment abnormality:
Patients on digitalis often show mild ST depression. This depression is usually less than 1 mm, and produces a “scooped” appearance — the “Salvador Dali mustache” ST. These ST abnormalities are seen in multiple leads.
Hypothermia and severe hypokalemia routinely cause ST segment depression in multiple leads. Hypothermia will tend to lengthen all ECG intervals, including the PR and QT, while hypokalemia will often lengthen the PR while shortening the ST segment slightly.
ST segment depression is called “nonspecific ST abnormality” rather than “ST segment depression” if the ST segments are less than 1 mm depressed and are accompanied by a normally-oriented T wave.  [Chapter Menu]
ST segment elevation
ST segment elevation is usually attributed to impending infarction, but can also be due to pericarditis or vasospastic (variant) angina. In some healthy young adults, a form of ST elevation can be normal.

The height of the ST segment is measured at a point 2 boxes after the end of the QRS complex. ST segment elevation is considered significant if it exceeds 1 mm in a limb lead or 2 mm in a precordial lead.

Causes of ST Elevation Infarction Vasospastic angina Pericarditis Early repolarization Measure: 2 mm beyond QRS Significant: 1 mm limb lead                      2 mm chest lead

Infarction:
In transmural infarction, ST segment elevation will be among the first manifestations. The ST segment elevation will be seen in those leads involved in impending infarction.
ST segment elevation decreases as T wave inversion begins. ST segments may remain elevated when ventricular aneurysm develops.
ST segment elevation that persists beyond three months following myocardial infarction suggests ventricular aneurysm. ST elevation will be present in about 1/3 of ventricular aneurysms. When the patient with ventricular aneurism presents with acute chest pain, a baseline ECG may help avoid misdiagnosis of impending infarction (and use of non-needed thrombolytic drugs).
Vasospastic angina:
ST segment elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetal’s angina. While exercise angina involves the subendocardium, vasospastic angina causes severe transmural loss of blood flow. ST elevation simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetal’s angina). At this point, the injury is reversible.
Pericarditis:
Pericarditis, an inflammation of the space between the pericardial sack and outer surface of the heart, causes widespread ST segment elevation. Physical damage and irritation of the heart’s surface produces a “current of injury” in virtually all ECG leads.
Generalized ST segment elevation, unrelated to the distribution of any coronary artery, implies pericarditis. One must be very cautious in diagnosing pericarditis from the ECG. For example, an inferolateral transmural infarction with pre-existing junctional ST elevation in the anterior leads, could produce widespread ST elevation that could be confused with pericarditis.
Later in the course of pericarditis, ST segment elevation resolves, without development of Q waves. After days to months, ST elevation is replaced by widespread T wave inversions.
Early repolarization:
“Early repolarization” is a cause of ST elevation. This innocent condition typically occurs in young healthy males. The T wave begins early, adding elevation to the ST segment.
Usually, early repolarization shows elevation of the J point (the junction between the end of the QRS and the ST segment) and a concave upward curve towards the T wave. (“Concave upward” means the hollow portion of the curve is on top.)
Early repolarization is usually seen in the anterior precordial leads of the ECG, but can be seen in limb leads to a lesser degree.
Early repolarization cannot always be differentiated from myocardial infarction. In the chest pain patient, it’s safest to assume ST elevation to be infarction until proven otherwise by reviewing a previous ECG or by obtaining serial ECGs.  [Chapter Menu]
T Wave Abnormalities
T wave abnormalities can provide added evidence to support clinical diagnosis. Except for hyperkalemia, T wave abnormality alone is not diagnostic of any particular condition. The T wave must be considered along with QRS and ST segment abnormalities. T waves will usually be abnormal in ventricular hypertrophy, left bundle branch block, chronic pericarditis, and in electrolyte abnormality.
Tall, peaked T waves occur due to hyperkalemia. If the tall T waves are seen throughout the ECG, general hyperkalemia is present. P waves will be small, PR interval short.
When typical tall, peaked T waves are seen only within a specific set of cardiac leads, it suggests impending infarction. The tall Ts are due to potassium leak through damaged membranes in the area of the infarct.

T Wave Categories Tall, peaked = hyperkalemia if generalized                        infarction if localized Inverted = evolving infarction                  chronic pericarditis                  conduction block                  ventricular hypertrophy                  acute cerebral disease                  other cardiac disease Flattened = nonspecific

In chronic pericarditis, T waves show wide-spread inversion, not corresponding to any coronary artery distribution. General inversion of T waves can also be due to an evolving global subendocardial infarct.
Inverted T waves are seen during the evolution of myocardial infarction. The T inversion appears in the leads “looking at” the infarcted area. Several hours after an infarct, T waves begin to invert. T wave inversion may persist for months.
Left ventricular hypertrophy or strain commonly causes T wave inversion. In “strain” pattern, the ST segment slopes down to an inverted T in the leads “looking at” the affected ventricle.
Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2. The T wave will be inverted over right heart leads showing evidence of hypertrophy and strain.
Left bundle branch block can cause ST depression and inverted T waves in leads I, L, and V5-V6. The ST depression is usually not great. The T wave tends to be oriented opposite the QRS in LBBB.
Flat T waves can be seen in many conditions, including ischemia, cardiac scar, evolving infarction, and electrolyte abnormality (such as hypokalemia).
In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T waves may be seen. These Ts are often biphasic or deeply and sharply inverted. The QT interval is often dramatically lengthened (0.5 to 0.7 seconds).  [Chapter Menu]
Go to Chapter 8, Myocardial Infarction

All material referenced through this menu is excerpted from copyrighted works by Bruce Argyle, MD. You are welcome to use selected portions, as long as appropriate credit is given. The credit for the text referenced through this menu is:

Argyle, B., MicroEKG Computer Program Manual.
Mad Scientist Software, Alpine, Utah

Back to Main Text Resource Index     Go to Mad Scientist Software's main index page

氟马西尼

看到心超斑主的回复让我受宠若惊，看到回复时间更让人感动，也许我的题目取错了，我的本意其实是想问如何降低心肌负荷以达到降低氧耗，让心肌用最少的能量满足机体的需求，ST段降低我觉得其实只是一种心肌的电生理表现还不是血液动力学的表现，我记得有个帖子里大家评价机器说机器就是机器，我觉得如何评价心肌缺氧还是要结合临床症状在自己的心里有个谱。全麻我没做过心脏的一般做的是普外的，全麻我觉得还是相对比较容易控制，只要液体量得当，血压和心率我都能控制在一个比较满意的范围内。但全麻我门开展的不是很多，主要椎管内麻醉和周围神经阻滞，对于一些老年病人我能保证麻醉效果，但是我不敢加过多的辅助药，我自己就碰到老年加一丁点药副作用就被无限放大的例子，所以我在充分镇静和镇静药的呼吸抑制，使用血管药物和掩盖患者早期循环不稳定之间很是拿捏不住，当然我说的有点笼统和极端，我觉得我还有什么着的话我的麻醉禁忌可以缩小了，呵呵

xyz-cn99

看到心超斑主的回复让我受宠若惊，看到回复时间更让人感动，也许我的题目取错了，我的本意其实是想问如何降低心肌负荷以达到降低氧耗，让心肌用最少的能量满足机体的需求，ST段降低我觉得其实只是一种心肌的电生理表 ...
氟马西尼 发表于 2010-1-18 09:44

                               
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　　就读书中的某些问题拿出来深入讨论我觉得很好，谈谈我对降低心肌氧耗的理解：
　　首先我们看看心脏冠脉是如何供氧的，在心室舒张期开始主动脉瓣膜关闭后，含氧血液分别从左右冠脉进入冠状动脉－心肌小动静脉－冠状静脉－冠状静脉窦到右心房，冠脉血流驱动压力＝主动脉舒张压－心室舒张末压力－中心静脉压。从这个公式我们可以分析一下影响心肌供血的几个因素，首先是舒张压，如果舒张压过低，那么冠脉压力肯定低，血流少；若心室舒张压力过高，即我们通常所说的心室过涨，那么同样严重影响血流通过；还有一个大家容易忽略的因素，中心静脉压，从理论上讲，冠状动脉，静脉是一个通路，冠状静脉窦通向右房，有一个末端压力即右房压（通常等于中心静脉压），所以在考虑冠脉供血时不应忽略这个因素，即中心静脉压过高同样影响冠脉血流；从压力的因素我们可以看出，要维持满意的冠脉供血，舒张压必须高度重视，对于合并主动脉关闭不全等因素导致舒张压过低的老年患者我们必须维持舒张压在一个较高的水平；另外后两个因素实际涉及两个方面的问题，一是容量的问题，容量负荷过重，则舒张末压，中心静脉压均增高，会严重影响冠脉血流；另一个是心功能的问题，心功能差则心室舒张末压和中心静脉压均增高；针对不同的原因进行对症处理，降低容量负荷，增强心功能。
　　上面从压力的因素分析，再从冠脉血流供应的时间因素分析，因为左室是高压腔，在收缩期压力远远超过主动脉舒张压，所以左心室只有在心室舒张期才能得到冠脉供血，这点和右心室不同，右心室在收缩期舒张期均有供血（右心室收缩期压力仍可能小于主动脉舒张压）。那么我们就可以知道将心率维持在一个较慢的水平（不影响心输出量的前提下）就可以大大降低氧耗，因为心率减慢主要延长的是舒张期，而且心率减慢也降低了心肌氧耗。这就是为何冠心病患者对心率严重依赖的原因。
　　再看看其他影响冠脉供血的因素，冠脉粥样硬化导致冠脉管腔狭窄，手术中的冠脉气栓、搭桥术中的冠脉痉挛也会导致冠脉血流严重减少，另外还有少数先天性冠脉畸形。其中管腔狭窄在代偿期，冠脉痉挛我们可应用硝酸甘油等扩张冠脉，同时适当增加舒张压，减慢心率综合处理；冠脉气栓的问题要求我们对一些心脏，血管暴露性手术要严格排气，万一进气可通过增加血压，扩张冠脉方法来排气。很多外科手术中突发的心跳骤停均为冠脉近痉挛或气栓造成的。
　　ＳＴ段的变化是心肌氧供氧耗改变较为敏感的指标，对于一些高危因素如高龄，冠心病，心衰等患者应高度警惕，通过对影响冠脉氧供的各种因素进行综合分析然后对症处理。

氟马西尼

没想到惊动了管理员,我以前就在书上看到了关于舒张压的重要性论述,一直不明白,经祥子这么一说明白多了,但我记得麻醉学这本书上还反复强调了压差这个问题,我也觉得如果压差不够器官灌注还是成问题,不知大家对压差的控制有什么心得或者各类降压药对压差有什么影响

小麻将123

一般的麻醉药也有扩血管作用。