Read it and you will know how to read and handle common ECG I
I. Overview
(A) This article
1, this article is more rigorous, complex and much more difficult than the author’s “read it to understand most of the ECG in the ECG room” written a year ago, in order to facilitate understanding, even not rigorous, but basically correct; the clinical part is mostly personal experience and books, literature seen, if different from the textbook, the textbook shall prevail.
2, this article is suitable for internists or non-cardiology clinicians who have some basic ECG, if they do not know ECG at all.
3. The level that clinicians can achieve after reading this article: they can quickly diagnose most of the major problems of ECG in cardiology and make corresponding treatment; they can roughly judge the criticality of ECG by looking at the graphics on the ECG monitoring machine.
(B) Several basic issues that must be understood before reading.
1. The meaning of each waveform
(1) P wave: represents the atrial depolarization process: so the abnormal P wave often represents the atrial problem, for example, a COPD patient II lead P wave amplitude > 0.25mv, the diagnosis of right atrial hypertrophy.
(2) PR interval: not equal to PR segment, but = P wave + PR segment. It represents the beginning of atrial depolarization to the beginning of ventricular depolarization, so its prolongation is seen in atrioventricular block.
(3) QRS wave group: the whole process of ventricular depolarization. The normal QRS wave group is obvious to everyone, but if there is a wide and deformed QRS wave group, it often means that there is a problem in the ventricle. For example, ventricular premature manifestation as early appearance of wide distorted QRS waves, while as atrial premature, as long as not accompanied by intraventricular differential transmission, QRS pattern is normal. The heart pumps blood by the ventricle, and QRS waves are the manifestation of ventricular activity, atrial problems will not kill people immediately, but the ventricle will.
(4) ST-T: the whole process of ventricular repolarization: so its abnormalities are also mostly ventricular problems. Its clinical status is very high, but the specificity of its changes is poor.
(5) QT interval: the whole process of ventricular activity. Mainly look at the QTc interval, that is, the corrected QT interval, because the heart rate is slow QT interval must be long, in order to make the QT interval at various heart rates comparable, so the QTc interval [= QT interval / (root R-R)], where the R-R unit is S, generally only by looking at the computer to type or look up the table to obtain, or by feeling), QTc interval is the meaningful value.
2, as a non-ECG specialist, if you study the ECG from the principles of physiology, the result will be painful and useless. It is enough for clinicians to be able to understand what kind of chart it is and whether it is critical or not.
3. Two points of attention for ECG diagnosis.
(1) An ECG has several diagnoses when the order is somewhat elaborate, not found clear criteria, but certainly the rhythm must write the first, such as sinus rhythm, atrial rhythm, atrial fibrillation, while the electrical axis left and right bias to write the second, other criteria are not known.
(2) ECG diagnostic content is divided into three categories.
①Class A: mostly refers to anatomical and pathophysiological diagnosis: mainly each atrial hypertrophy, myocardial infarction, ischemia, coronary artery blood supply deficiency, each electrolyte disorder, etc., which must rely on clinical data. For example, for a typical infarct ECG with abnormal Q wave + ST segment arch-back elevation + T wave changes, the patient has no history of chest pain and chest tightness, which is generally not diagnostic of infarction, and the ECG report can be completely mean to write: abnormal Q wave, ST-T changes, please combine with clinical, but can the surgeon read this report? If you are responsible, you can write that you are considering the possibility of acute infarction, please combine with clinical; ECG alone is generally not enough to qualify for a direct diagnosis of infarction (pathophysiological diagnosis). For example, for an ECG with high left ventricular voltage, if there is a history of hypertension or other conditions that can cause a large left ventricle, the diagnosis of “left ventricular hypertrophy” (anatomic diagnosis) can be made directly, but if not, only “high left ventricular voltage” (no clinical significance) can be diagnosed. And so on.
②Class B: the ECG alone can be diagnosed directly without medical history, and all kinds of arrhythmias are the main force, such as atrial fibrillation, pre-excitation syndrome, third-degree AV block, which can be diagnosed only by looking at the diagram, without any medical history.
③ Other than the above two cases, such as ST-T changes, such as paraclonic transposition of the heart, such as left deviation of the electrical axis.
4. Methods of reading the chart.
For critical patients, it is certainly required to look at the main problem immediately, other minor problems first ignored; and in general, look at the chart from beginning to end, from P-wave to T-wave one by one, to see whether there are abnormalities in time, amplitude, morphology, from I-lead to V6-lead one by one. Therefore, we must memorize the normal values that are commonly used before we can talk about reading the chart.
In fact, the most important thing to memorize is actually a few: P-wave time should = 0.04S (2) amplitude >= 1/4R wave in the same lead. In addition to aVR and III lead, later you just see one of them, you can say loudly in public: it is pathological Q! We will say that it is with a small r. For the time being, we do not consider it pathological Q. When it is difficult to distinguish, we mainly look at the ST segment, if there is no elevation, it is not critical ECG, at most old infarction. (3) Another criterion (not diagnostic) is that: time >= 0.03S, amplitude >= 1mm, and tangential traces on Q wave, meeting one of them is pathological Q.
The localization of infarction has important clinical significance: (1) the degree of criticality and healing of different sites and ranges of infarction are different; (2) we usually cannot just write “acute myocardial infarction” in the diagnosis of infarction, which seems to be very unlevel, the correct one should be “acute extensive anterior wall infarction The correct one should be “acute massive anterior wall infarction” and so on.
However, students may be disgusted to read about “anterior interstitial wall” and “high lateral wall”, and in fact, the Anatomy does not have these concepts. It does not matter, now you can understand.
If you look at the table in Internal Medicine, you’re dead, and you need to look at these two diagrams.
In fact, the most common clinical infarction sites are: (1) extensive anterior wall (anterior descending branch blood supply) (2) inferior wall (right coronary or gyrus branch blood supply) (3) anterior wall (anterior descending branch blood supply) (4) anterior interstitial wall (anterior descending branch blood supply). The other XX walls will be left alone for now.
The top left figure involves the six-axis system, the tenderwares do not need to know why this is drawn, just read it. The diagram shows that II, III, and aVF are the most inferior, so when the above three leads are present, it is an inferior wall infarct.
The lower left figure involves the site where we do the ECG. It can be determined simply by the position of each lead on the body surface. As shown in the figure: V1-V5 are all present in the front of the thorax, so when they have performance, it is an extensive anterior wall infarction; if only V3-V5 is the anterior wall; accordingly, if V7-V9 (the site behind when doing ECG), it is a positive posterior wall infarction; if V1 is further to the right, it is the right ventricle in the 18 leads, so V1, V2 and V3 are spaced between the left and right ventricles, and if they have performance, it is an anterior interventricular wall infarction. We call V7-V9 in 18 leads the posterior wall and V3R-V6R the right ventricle. Therefore, if V3R-V6R has manifestations (the right ventricle can have Q waves normally, mainly depending on whether the ST segment is significantly elevated), it is a right ventricular infarction.
Clinically, it is the extensive anterior wall infarction that is most likely to present with cardiogenic shock and death. It is also common to see inferior wall + extensive anterior wall infarction together, which often leads to cardiogenic shock (the most severe type of acute heart failure).
In addition, 18-lead should be routinely checked whenever there is an infarction. Related to vascular anatomy, pure right ventricular or posterior wall infarcts are rare, mostly right or posterior wall infarcts usually occur at the same time as infarcts of other walls, but of course there are also pure right ventricular and right wall infarcts. If a multiwall infarction is found, the outcome may be even worse.
When it comes to acute infarction, surgeons naturally ask for emergency cardiology consultation; and internists should also know that whether they want emergency PCI or thrombolysis or conservative, they should immediately give Bayer Aspirin 300mg + Bolivar 300mg orally. Many acute heart attacks that are not treated are bound to die of cardiogenic shock or malignant arrhythmia.
The upper figure shows the electrocardiogram of a typical acute extensive anterior wall infarction; the lower figure shows an old inferior wall infarction.
B: [Severe tachyarrhythmia]
Those with underlying cardiovascular and respiratory disease, regardless of any arrhythmia, as long as the calm state ventricular rate is very fast (160 ah 170 ah, 180 ah or more), should be considered critical ECG, if there are palpitations (obviously fast heart rate is usually there), chest pain, shortness of breath and other symptoms, it is more serious, must be treated urgently to control the ventricular rate. Cordarone (Amiodarone) is the ace of treating tachyarrhythmias, with broad-spectrum antiarrhythmic effects, but it is okay not to use it indiscriminately, its not very safe.
(A) Ventricular tachycardia
Before looking at ventricular tachycardia, we must first understand ventricular premature, and then talk about ventricular tachycardia after understanding ventricular premature, because ventricular tachycardia is the appearance of three or more ventricular premature in a row. To put it plainly, it is the presence of three or more broad and malformed QRS wave groups in a row.
The scary thing about ventricular tachycardia is its tendency to deteriorate into ventricular flutter and ventricular fibrillation. This is especially true for sustained ventricular tachycardia (lasting more than 30S).
If there is a P wave (or if it is elevated by fusion with the preceding T wave), atrial tachycardia with intraventricular differential transmission should be considered.
Ventricular tachycardia is often differentiated from atrial tachycardia with differential intraventricular conduction (the latter is often not critical). Sometimes it is difficult to differentiate, so it is better to treat it as ventricular tachycardia.
Asymptomatic short bursts of ventricular tachycardia do not require urgent treatment and can be treated with oral cortisone 0.2 Tid, mainly to find the cause (often coronary artery disease).
Persistent ventricular tachycardia if asymptomatic, can be up to 300mg + 5% GS50ml micropump, if angina, edema, hypotension, should be 100J synchronous electrical resuscitation. Pulseless ventricular tachycardia is the same as ventricular fibrillation, direct 360J electric defibrillation.
(B) Supraventricular tachycardia
The ECG term “supraventricular” actually includes atrial and junctional, and because it is sometimes difficult to distinguish, it is directly called supraventricular, and the treatment is the same. Supraventricular, that is, the conduction impulse above the ventricle, does not include sinus tachycardia here. Thus, supraventricular tachycardia is one of the atrial or junctional tachycardia.
If the ventricular rate is absolutely neat, ventricular rate > 160 should be considered supraventricular tachycardia may, if you can not find obvious sinus P waves, the basic diagnosis; if you also find atrial P waves, then atrial tachycardia should be very clear. The ventricular rate of supraventricular tachycardia can sometimes reach 180 or even 200 or more, and the patient will mostly have palpitations.
It is often difficult to distinguish from 2:1 conduction (?) It is often difficult to distinguish atrial flutter from 2:1 conduction (?), but it does not matter, the emergency treatment is to control the ventricular rate with a micro-pump of Kotarolone, other etiological treatment ah, catheter ablation ah is an afterthought. Sometimes it has to be distinguished from sinus tachycardia, but sinus tachycardia rarely reaches more than 160 heart rate.
(C) Atrial fibrillation with rapid ventricular rate
The diagnosis of atrial fibrillation is too simple, without the need to do an electrocardiogram, the majority of atrial fibrillation can be diagnosed by pressing the pulse or heart auscultation. Specific diagnostic criteria and typical atrial fibrillation have been described in the primary section. Atrial fibrillation with varying forms of f waves is something that people will see.
However, it is common to see atrial fibrillation without obvious f waves, and the baseline is basically flat, so young birds may not know how to see it. (Figure below)
A simple way to teach, in fact, as long as you encounter the ventricular rate is never regular, and the RR interval difference is large, basically 80% to be considered atrial fibrillation, if you can not find the sinus P wave, the basic diagnosis of atrial fibrillation, regardless of whether there is the so-called different forms of f waves.
In addition, it is generally believed that the ventricular rate of atrial fibrillation is absolutely irregular; that is, generally: if the ventricular rate is regular, it is not atrial fibrillation. (However, for example, atrial fibrillation with third-degree atrioventricular block or some other arrhythmia may have a regular ventricular rate)
Atrial fibrillation is often associated with a rapid ventricular rate, and if it is >150, it should be considered critical, and the risks are: (1) asynchronous atrial contraction, reduced blood displacement and increased afterload, and even angina pectoris and congestive heart failure; (2) easy formation of thrombus leading to arterial embolism.
If there is heart failure and there is no contraindication, Cetiran 0.3mg + NS20ml slow push is preferred, if not enough, also add up to the dragon static drip or micro pump, satisfactory ventricular rate is below 80. There is no contraindication to the use of warfarin, but it does not affect the use of a day early or late, and is not an emergency treatment.
C: [Malignant ECG that can lead to rapid death]
(A) Ventricular fibrillation and ventricular flutter
I didn’t want to talk about it, but when asked a clinical trainee who didn’t even understand it, I felt the need to mention the most serious and easiest to see arrhythmias.
Ventricular fibrillation = sudden cardiac arrest. When ventricular fibrillation/ventricular flutter occurs, the patient is usually in respiratory and cardiac arrest.
When this is seen in the cardiac monitoring machine, 300J electric defibrillation is given directly; if not available or not understood, immediate cardiac compressions and resuscitation.
I think, in addition to the kind of general condition is still good, sudden onset of ventricular fibrillation may be able to save back (to cardiology patients, cardiology when there are saved), the other patients are generally not saved back.
(B) tip-twisting ventricular tachycardia
Note that the ventricular tachycardia must have a prolonged QTc interval, as in the above figure, to be considered tip-twisting ventricular tachycardia.
It is very easy to become ventricular fibrillation.
Magnesium sulfate 2g + 5% GS 40ml slow iv and then 8mg/min ivdrip.
(C) Pre-excitation syndrome combined with atrial fibrillation with rapid ventricular rate
Pre-excitation syndrome sounds far-fetched to tender birds, but it is not rare clinically, mainly to say that it is understood.
(1)During PR