Antipyretics for children are prescribed by a pediatrician. But there are emergency situations with fever when the child needs to be given medicine immediately. Then the parents take responsibility and use antipyretic drugs. What is allowed to be given to infants? How can you lower the temperature in older children? What medications are the safest?
Steffen wrote:
“A few weeks ago I was able to recognize a STEMI because I saw such a case on your blog.”“I recorded an ECG for a 50-year-old man who complained of chest pain. I was at my workplace (in Germany doctors work in ambulances). Surprisingly, the patient went on a long bike ride 2 days ago without any complaints.”
“Apart from hypertension, he had no other risk factors for atherosclerosis. However, right away I was not entirely sure that his problem was coronary.”
“But when I looked at his ECG, I smiled because I remembered your blog post.”
In Germany, ECGs are recorded at a speed of 50 mm/s:
What do you think?
In the image below, I've compressed them to make them look like they were recorded at 25mm/sec. I've also compiled them side by side:
The same, but at a speed of 25 mm/s.
What do you think?
“I remembered the ECG from your blog under the title: “ STEMI is better visible in extrasystoles, diagnosed by a paramedic, ignored by a doctor" 2013. The ECG looked similar (although recorded at a speed of 50 mm/s) and, not surprisingly, angiography revealed occlusion of the LAD.”
What is Steffen talking about?
Look at V2 and V3. The PVC has a right bundle branch block (qR or rSR) morphology because it originates in the left ventricle. The ST segment with the morphology of the blockade of the right leg should shift in the opposite direction from the terminal R wave." That is, there should be a slight depression of the ST segment. But there is its elevation, concordant with the R wave. This is a very specific sign of T1MI (acute anterior MI due to LAD occlusion).
We also note that in the PVC complex in V4-V6 there are giant coronary T wave waves, which are much more pronounced than the no more moderately acute T wave waves in the sinus complexes. In fact, of the normal complexes, only V4 has clearly hyperacute T.
Acute coronary T waves in the PVC complexes are also visible in the limb leads.
This is the case Steffen had in mind: STEMI Seen Best in PVC, Diagnosed by Medic, Ignored by Physician (text in English, sorry, didn’t get around to it).
Ken Grauer
Un grand merci Dr. Steffen for presenting this case which has a GEM that makes it easier to recognize acute STEMI in PVC morphology! His case perfectly demonstrates how sometimes acute coronary occlusion can only be recognized in complexes of PVCs!
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The ECG we are discussing (“compressed” version).
- Rhythm - ventricular bigeminy. According to Dr. Smith - evaluation of normal (sinus) beats on this recording is inconclusive regarding the presence of acute T1MI (occlusion-related myocardial infarction). In leads V1 and V2 there is slight ST elevation; and, perhaps, acute coronary T waves in V4(and probably V3); and subtle reciprocal changes in the inferior leads- but they are not enough to confirm the diagnosis.
- But as clearly captured by Dr. Steffen - based on the morphology of the PVC appears sufficient ECG evidence of acute T1IM!
- Most notable morphological anomaly PVC is observed in lead V2. To clarify the points made by Dr. Smith above, I conducted a vertical RED a line parallel to the vertical grid lines that indicates the end of the QRS complex of the PVCs in leads V1 and V2. The broken red line is extended downward to demonstrate the end of the QRS complex of the PVCs in leads V3-V6, as well as in the limb leads. Short horizontal YELLOW LINES indicate the position of the baseline.
- In V1 PVCs there is no ST segment elevation, which is usually observed in PVCs in the absence of MI. However, it should be obvious that in the PVC complex in V2 and V3 there is significant J-point elevation that simply should not be there. In addition, there is terminal T wave inversion in the PVC complexes in lead V2 ( RED arrow). Assess the entire QRST of the PVC in lead V2. Isn't the complex similar to the morphology of acute STEMI? (Look, I circled it BLUE rectangle).
- ST-T wave morphology of PVCs in many other leads demonstrates increased T wave amplitude, which in the context of diagnostic changes in PVC morphology in V2 and V3 is consistent with acute T in these PVCs. And in the context of the apparently abnormal ST J point position in the PVC complexes in V2 and V3 - the dashed red lines in leads V3-V6 suggest that there is also abnormal ST elevation in these leads for. The overall picture strongly suggests acute LAD occlusion!
- Actually PEARL: If you can without a doubt to say that in one or two leads the ST-T wave morphology in the ventricular beats is not normal (as in this case in V2 and V3), then it becomes much easier to assess ST-T abnormalities in the beats and in other leads.
I thought for a long time about how to write this section for non-cardiologists and came to the conclusion that the most important thing would be to learn not to miss the signs of a heart attack. I believe that this will be a greater achievement than bothering oneself with such concepts as: endocardial, epicardial ischemia and the mechanisms of their development, how the stages of infarction of various walls occur, which arteries are responsible for this or that part of the heart, and so on. Let's leave these “aerobatic maneuvers” to cardiologists; our goals are more earthly.
So let's start with the most important thing - Myocardial infarction with ST elevation. Such a heart attack is accompanied by a very high mortality rate and requires urgent treatment; it is advisable to open the artery within the first 60-90 minutes. Therefore, missing it is an unforgivable mistake. Any doctor at all costs must learn to find ST elevation on an ECG. You may not know how to determine rhythm and blocks, but you need to know ST-elevation infarction in person.
From now on, we will get acquainted with the “pink ECGs” that you are used to seeing every day. As always, I will try to use high quality ECGs, but during a heart attack and/or when the patient is tossing around in bed with chest pain, “exemplary ECGs” are rarely obtained.
ST elevation and ST elevation infarction
In order to correctly assess the degree of elevation, you need to know where to measure it.
Look at the picture, where will you measure the elevation here? If you take it to the left, it will be less, if you take it to the right, it will be more.
In order to standardize measurements, a technique was introduced into practice for determining the j-junction point, which is located at the place where the S wave ends (if there is no S, then R) and the ST segment begins. If you step back 0.04 s from point j (that is, 2 mm at a belt speed of 50 mm/sec), then you will find point i at which you need to measure the height of elevation or depression.
Normally, elevation does not exceed 1 mm, but in leads V2-V3 it can be up to 2 mm or even 2.5 mm in people under 40 years of age. There are various figures, including those for point i, but I recommend that you use these indicators, even if you are “over-excited” someday, but it’s better than missing it.
Let's see what it looks like in life.
This is what the measurements look like. You can see at least 2 mm of elevation in lead III and almost 1.5 mm in lead AVF
Hover your cursor to enlarge the picture Now, regarding ST elevation infarction
The most important criterion, along with elevation, is reciprocal changes - ST depression in leads opposite to the area of infarction. That is, if there is elevation somewhere, then somewhere nearby there must be depression. In rare cases, reciprocal changes occur in those areas that are not visible on regular ECGs, but let’s agree right away - you send all patients with ST elevation and related complaints to hospitalization immediately or present them to a cardiologist.
Situations in which you can solve the problem yourself are limited to cases when you have an ECG on hand for comparison. That is, you can say with 100% confidence that the ECG looked like this before, for example: cases with post-infarction changes or early repolarization syndrome - we’ll talk about this later.
Now let's go back to the previous ECG. This is a heart attack.
ECG No. 1
Elevation is highlighted in red, and depression, which is reciprocal, is green. Such an ECG in 99.9999% of cases indicates an acute infarction in the area of the lower wall (III, aVF). Remember, to talk about the presence of a heart attack, you need to have changes in the adjacent leads. For example (III, aVF or I, aVL or two adjacent chest leads).
ECG No. 2
Let's look at another ECG with an inferior infarction. Do not pay attention to the small tremor in leads V1-V2 - these are artifacts and they do not mean anything.
Area highlighted in red elevation, green - reciprocal depression . Yellow is also a reciprocal change, but due to the presence of a complete block of the right bundle branch (I hope you noticed it), this statement can be disputed.
ECG No. 3
Well, another ECG with a lateral wall infarction (I, AVL, usually there is also V5-V6, but not always), I think explanations are unnecessary.
ECG No. 4
And the last ECG with anterolateral infarction. There is some isoline drift here, so I chose the most “clean” area for measurements.
Synonyms: ST-segment elevation myocardial infarction, acute myocardial infarction (MI), acute transmural infarction, Q-wave myocardial infarction (MI).
Among cardiovascular diseases with a possible fatal outcome, acute myocardial infarction (MI), which is currently called STEMI, occupies an important place. This is the most severe form of ACS, short of sudden cardiac death.
Pathophysiology. Due to hemorrhage into an atherosclerotic plaque and gradually increasing thrombosis coronary artery stenosis of its lumen occurs, resulting in occlusion. This leads to ischemia of the myocardium supplied by the affected coronary artery and its necrosis.
Careful perennial epidemiological studies patients with myocardial infarction (MI) showed that they have risk factors. The combination of these factors contributes to the acceleration of the atherosclerotic process and a manifold increase in the risk of myocardial infarction (MI). Currently known risk factors include smoking, increased level cholesterol in the blood, high blood pressure and diabetes.
In addition to the above four main risk factors, others are also known, in particular, excess body weight, stress, physical inactivity, and hereditary predisposition.
Symptoms of ST-segment elevation myocardial infarction (STEMI):
Severe anginal pain lasting more than 15 minutes
ST segment elevation on ECG
Positive results blood test for creatine kinase, its MB fraction, troponins (I or T)
Diagnosis of myocardial infarction with ST segment elevation (STEMI)
ECG, as a rule, is crucial for making a diagnosis. Already 1 hour after the onset of a typical pain attack, in most cases the ECG shows clear signs THEM. Therefore, the diagnosis of MI is the most important task of electrocardiography.
When analyzing ECG In patients with myocardial infarction (MI), attention should be paid to the following features.
The signs of MI must be clear. In most cases, ECG changes are so typical that a diagnosis can be made without further testing.
Other important diseases, especially in the acute stage, such as an attack of stable angina in a patient with coronary artery disease, pericarditis or myocarditis, should not be misinterpreted as MI. For example, with pericarditis there are no clear signs of MI on the ECG.
In the process of diagnosing MI, it is also necessary to establish the stage of MI, i.e. it should be indicated, at least, whether it is an acute phase or an old infarction. This is important, since the treatment of MI has its own characteristics depending on the stage of the disease.
The diagnosis should also reflect the location of the MI. In particular, it is necessary to differentiate an infarction of the anterior wall of the LV from an infarction of its posterior wall. Depending on the location of the MI, it is possible to approximately determine which coronary artery is affected.
Interpretation of individual ECG indicators in myocardial infarction (MI)
1. Large Q wave (necrosis zone). Due to myocardial necrosis in the infarction zone, EDS does not occur. The resulting EMF vector is directed from the necrosis zone. Therefore, the ECG shows a deep and widened Q wave (Purdy's Q wave) in leads that are located directly above the MI zone.
2. ST segment elevation. The zone of myocardial necrosis is surrounded by a zone of damage. Damaged tissue, compared to healthy tissue, at the end of ventricular depolarization carries a smaller negative charge and is therefore less excitable. Therefore, in the damage zone, a vector appears that corresponds to the ST segment and is directed from the electrically negative myocardium to the electrically less negative one, i.e. to the part of the myocardium that is relatively positively charged. Therefore, on the ECG corresponding to the damage zone, ST segment elevation is recorded.
3. Peaked negative T wave. The ECG of the ischemic zone detects changes in the repolarization phase. The repolarization vector is directed from the ischemic zone to the healthy myocardium. When the epicardial layers of the myocardium are damaged, the EMF vector is directed from the outside to the inside. Therefore, in leads that normally show positive T waves, symmetrical peaked negative T waves (coronary Pardee T waves) now appear.
The results of the study become positive 2-6 hours after the development of ischemia.
Appearance serum troponins reflects the formation of a blood clot in the coronary artery. Therefore, a blood test for troponins, due to its high sensitivity (90% when performed after 6 hours) and specificity (approximately 95%), is a standard test in the emergency diagnosis of acute myocardial infarction (MI).
Definition serum markers of myocardial necrosis plays an important role not only in the diagnosis of acute myocardial infarction (MI), but also allows us to judge its dynamics. Their significance is especially great in cases where ECG data is erased or masked by PG branch block or WPW syndrome. Diagnosis of myocardial infarction (MI) is also difficult in cases where the infarction is localized in the circumflex branch of the left coronary artery.
Currently in diagnosis of myocardial infarction(MI) use both of these research methods: ECG and blood test for serum markers of myocardial necrosis. Moreover, they do not compete, but complement each other.
Despite this, as shown earlier completed In our research, the predictive value of the ECG is higher compared to a blood test for serum markers of myocardial necrosis, since in most cases of acute myocardial infarction, changes in the ECG, when carefully read, appear within 1 hour after the onset of ischemia and are reliable diagnostic signs, while increased levels of serum markers in many cases are not associated with ischemic myocardial damage.
In addition, a significant advantage ECG also lies in the fact that it can be performed as many times as necessary without causing any inconvenience to the patient.
If chest pain occurs, you should always register ECG. If MI is suspected, it is recommended to perform a monitoring ECG at least every 3 days in combination with a blood test for serum markers of myocardial necrosis.
On ECG in acute myocardial infarction(MI) the following changes appear: regardless of the location of the MI, i.e. both with an infarction of the anterior wall and with a infarction of the posterior wall in the acute phase, a significant change in the ST segment occurs. Normally, there is no ST segment elevation, although sometimes slight elevation or depression is possible even in practically healthy people.
At acute myocardial infarction(MI), the first sign on the ECG is a distinct rise in the ST segment. This rise merges with the following positive T wave, and, unlike the norm, the boundary between them disappears. In such cases, they speak of monophasic deformation of the ST segment. Such a monophasic deformity is pathognomonic for the acute phase, i.e. for “fresh” MI.
Differential diagnosis of myocardial infarction with ST segment elevation(STEMI) with a positive T wave is shown in the figure below.
Shortly before the appearance monophasic deformation of the ST segment upon careful analysis, extremely tall pointed T waves (so-called asphyxial T waves, or hyperacute T waves) can be noted, caused by acute subendocardial ischemia.
Sharp and wide Q wave can be registered already in the acute stage of MI, but this sign is not mandatory. A negative T wave may still be absent in the acute stage.
At "old" myocardial infarction(MI) the previously occurring ST segment elevation is no longer detected, but other changes appear affecting the Q and T waves.
IN normal Q wave not wide (0.04 s) and shallow, not exceeding in height the fourth part of the R wave in the corresponding lead. With “old” MI, the Q wave is wide and deep.
T wave is normally positive and is at least 1/7 of the height of the R wave in the corresponding lead, which distinguishes it from the T wave in MI after the acute stage (i.e. in the early phase of stage II), when it becomes deep, pointed and negative (coronary Purdy's T wave), in addition, ST segment depression is noted. However, sometimes the T wave is located on the isoline and is not reduced.
Usually for determining the ECG stage of myocardial infarction(IM) the classification presented in the figure below is sufficient. The classification presented in the figure above allows you to more accurately assess the dynamics of MI.
In general, it is believed that the more leads, which note pathological changes, the wider the zone of myocardial ischemia.
Changes ECG, namely a large Q wave (a sign of necrosis, Purdy's Q wave) and a negative T wave with or without ST segment depression are typical for a formed scar in “old” MI. These changes disappear as the patient's condition improves. However, it is known that, despite clinical improvement and healing, signs of old infarction, especially the large Q wave, persist.
ST segment elevation with positive T wave, i.e. A monophasic ST segment deformity with a large Q wave that persists for more than 1 week and a transition of the ST segment into a slowly rising curve should raise suspicion of a cardiac aneurysm.
Further tactics after diagnosis of myocardial infarction with ST elevation (STEMI) are the same as for myocardial infarction without ST elevation (NSTEMI).
Most common cause ST elevation on the resting ECG in healthy individuals is called early ventricular repolarization syndrome (EVRS).
ST segment elevation must be differentiated depending on whether it is recorded against the background of a Q wave after myocardial infarction, or whether it appears in the absence of a Q wave. The mechanisms of its elevation in these cases are different. More often, ST elevation in the presence of a Q wave is observed in the anterior chest leads (V1 and V2).
ST segment elevation in leads with Q due to myocardial infarction. Previous myocardial infarction is the most common cause of ST elevation during exercise testing and is directly related to the existence of areas of left ventricular dyskinesia or aneurysm. Exercise-induced ST segment elevation is observed in approximately 50% of patients with anterior myocardial infarction when tested in the first 2 weeks after the onset of myocardial infarction and in 15% of those with inferior myocardial infarction, and by week 6 the incidence of ST segment elevation in these patients decreases. Individuals with documented ST elevation in such cases have more low fraction ejection than patients with Q waves, but without exercise-induced ST elevation. In most cases, exercise-induced ST segment elevation in leads with a pathological Q wave is not a sign of more severe CAD and rarely reflects myocardial ischemia.
It is believed that ST segment elevation in leads with Q in the case of ischemia is predominantly T-dominant in nature, while ST-dominant in the absence of ischemia, being a consequence of dyskinesia.
Initial myocardial damage (Q depth) has a greater influence on the degree of ST elevation than reflects the severity of myocardial dysfunction.
These changes may be the result of reciprocal ST depression, which reflects ischemia in the opposite leads and may indicate the emergence of new areas of ischemia. A simultaneous decrease and increase in ST in the opposite leads during the test suggests the presence of multivessel lesions of the coronary vessels, and in patients with a Q-myocardial infarction caused by a single-vessel lesion (confirmed by coronary angiography) 6-8 weeks ago - a probable residual stenosis of the infarct-related artery .
ST segment elevation in the absence of a Q wave. In patients without a history of myocardial infarction (absence of a Q wave on the resting ECG), ST segment elevation (except for leads V1 and AVR) during exercise indicates severe transient ischemia due to significant proximal stenosis or spasm of the coronary artery. This phenomenon is rare - 1 in 1000 tests, and in patients with obstructive coronary artery disease - in 1% of cases. It localizes the site of ischemia: for example, ST segment elevation in leads V2–V4 indicates damage to the anterior interventricular artery; in the lateral leads - about damage to the circumflex artery or diagonal branches; in leads II, III, AVF - about damage to the right coronary artery.
Key moment: Severe transmural ischemia causes ST-segment elevation during exercise in individuals without previous myocardial infarction (or without a Q wave on the resting ECG). ST segment elevation in this case localizes the ischemic zone, in contrast to ST depression, which is a consequence of general subendocardial ischemia and does not specify the location of the coronary artery lesion.
In patients with variant (spastic) angina, ST segment elevation is recorded simultaneously with the onset of angina, often occurring at rest. During exercise, ST segment elevation in such patients is observed only in 30% of cases. Many patients with ST segment elevation have reciprocal ST depression in opposite leads. ST segment elevation during exercise is arrhythmogenic - with it, ventricular arrhythmias are more often recorded.
The most common important changes in the ST segment and T wave include those that are characteristic of myocardial ischemia and infarction. Since ventricular repolarization depends on myocardial perfusion, patients with coronary disease often exhibit reversible changes in the ST segment and T wave during transient myocardial ischemia.
Let us remember that pathological Q waves serve as indicators of myocardial infarction, but do not allow us to distinguish an acute one from one that occurred a week or a year ago. But during acute myocardial infarction, a series of characteristic changes in the ST segment and T wave occur, allowing one to differentiate between acute and non-acute myocardium (Fig. 4.24). In acute Q wave myocardial infarction, ST segment elevation is the first to appear, often accompanied by a tall T wave. At this early stage, myocardial cells are still viable and Q waves are not yet recorded. However, after a few hours, the death of myocytes leads to a decrease in the amplitude of the R wave and the appearance of pathological Q waves in the ECG leads located above the infarction zone. In the first two days from the onset of a heart attack, the ST segment rises, the T wave becomes negative, and the Q wave deepens. After several days, the ST segment returns to the baseline, but the T waves remain negative.
Weeks and months after a heart attack, the ST segment and T waves become normal, but abnormal Q waves remain, which is an invariable sign of myocardial infarction. If the ST segment remains elevated after several weeks, then there is a possibility of formation of a bulging fibrous scar (ventricular aneurysm) at the site of the infarction. A similar evolution of changes in the QRS complex, ST segment and T waves is recorded using leads located above the infarction zone (Table 4.3). In this case, as a rule, reciprocal changes are observed in leads located on the opposite side. For example, in acute anterior septal MI, ST segment elevation in precordial leads x and V2 is accompanied by reciprocal changes (ST depression) in leads II, III and aVF, i.e., in leads lying above the opposite (lower) wall of the heart ventricle.
The mechanism of ST segment elevation during acute MI is not yet completely clear. However, there is an opinion that such changes occur from damaged myocardial cells located directly near the infarction zone; they excite abnormal systolic and diastolic currents. Objecting to this explanation, others believe that such cells are not capable of depolarization, but have an abnormal permeability that does not allow them to fully repolarize (Fig. 4.25). As a result, in a state of rest, partial depolarization of such cells causes the appearance of forces directed away from the damaged segment, causing a downward shift of the isoline. Due to the fact that the electrocardiograph records only the relative, and not the absolute, voltage value, the deviation of the isoline is not captured. As all myocardial cells, including those in the affected area, become completely depolarized, the resulting electrical potential of the heart actually becomes zero. However, due to a pathological downward displacement of the isoline, the ST segment appears to be located above the isoline. During the process of repolarization, the damaged cells return to an abnormal state of increased permeability in diastole, and the ECG again displays an abnormal shift in the basal line due to the presence of abnormal forces directed away from the electrode. Thus, the magnitude of ST segment elevation during MI is influenced to a certain extent by the relative displacement of the isoelectric line.
With non-transmural myocardial infarction, in the leads crossing the area of the infarction, there is a decrease in the ST segment, not its elevation. In this situation, the diastolic permeability of damaged cells adjacent to the infarct area causes the appearance of electrical forces directed from the endocardium to the epicardium and, therefore, towards the ECG electrodes. Thus, basal ECG line shifted upward (Fig. 4.25). After complete depolarization of the heart, its electrical potential returns to its true zero value, but relative to the abnormal basal line creates an apparent depression of the ST segment.
Rice. 4.25. Theoretical explanation for the occurrence of ST abnormalities during acute MI. Upstairs. Ion leakage causes partial depolarization of the cell of the damaged myocardium before the process of propagation of electrical excitation begins, which causes the appearance of forces directed away from the affected area and a decrease in the basal line of the ECG. But this process is not displayed on the ECG, since it records the relative, not the absolute, voltage value. While the heart is completely depolarized, the true voltage is zero, but there is an apparent ST segment elevation relative to the abnormally low baseline. At the bottom. In non-transmural MI, the process proceeds in a similar way, but ion leakage occurs from the subendocardial tissue, so that the partial depolarization preceding excitation is directed towards the recording electrode; therefore, the basal line is elevated. After depolarization ends, the voltage is indeed zero, but the ST segment appears slightly depressed relative to the upwardly shifted basal line
Other common causes of changes in the ST segment and T wave associated with disturbances in the process of cardiomyocyte repolarization are described in Fig. 4.26.
