On the issue of ECG diagnosis of right ventricular myocardial infarction
The article draws attention to the importance of diagnosing right ventricular myocardial infarction. ECG diagnosis of right ventricular myocardial infarction is carried out by removing the so-called additional right chest leads V3R-V6R, which reveals pathological Q, ST segment elevation, negative T. The motivation for removing additional right chest leads are both the features of the clinical picture of the disease and mainly, the presence of ECG signs of inferior diaphragmatic or posterobasal myocardial infarction.
To question about ECG diagnosis of myocardial infarction of right ventricle.
The article pay attention to the importance of diagnostics of myocardial infarction of the right ventricle. ECG diagnosis of myocardial infarction of the right ventricle is carried out when removing the so-called additional right precordial leads V3R-V6R, in this case show pathological Q, rise segment ST, negative T. The motivation for the withdrawal of additional right precordial leads are both features of clinical disease and, mainly, the presence of ECG-signs inferior phrenic or posterobasal myocardial infarction.
Recognition of right ventricular myocardial infarction in widespread practice is casuistic. At the same time, its frequency is about 3%. A large number of patients have simultaneously myocardial infarction of the left and right ventricles, while right ventricular myocardial infarction is especially common in patients with damage to the lower wall of the left ventricle (up to 30% of patients). 13% of patients have a combination of myocardial infarction of the right ventricle and the anterior wall of the left ventricle. At autopsy, combined lesions of both ventricles are detected in 14-84% of the deceased (N.A. Mazur, 2009). Unfortunately (in terms of diagnosis), in patients with right ventricular myocardial infarction there are no clear specific differences in the clinical manifestations of the disease. ON THE. Mazur (2009) notes that some patients experience rapid development of right ventricular failure without stagnation of blood in the pulmonary circulation. At the same time, A.V. Shpector and E.Yu. Vasilyeva (2008) draw attention to the fact that in the acute stage of right ventricular infarction, right ventricular failure is usually manifested not by stagnation of blood in the systemic circulation, which develops later as fluid accumulates, but by hypotension. This is due to the fact that a feature of the mechanics of the right ventricle is its high dependence on preload. And therefore, if a patient with signs of right ventricular myocardial infarction has reduced blood pressure, he needs massive infusion therapy. At the same time, vasopressors are dangerous because, by increasing systemic pressure, they increase the pressure in the vessels of the pulmonary circulation, which sharply increases the load on the affected right ventricle. The volume of required infusion for hypotension associated with right ventricular myocardial infarction often reaches several liters. This is quite safe if there is an isolated lesion of the right ventricle, because with a healthy left ventricle, pulmonary edema does not develop. However, if there is combined damage to both ventricles, then the infusion must be carried out under the control of wedge pressure in the pulmonary artery to avoid overload of the pulmonary circulation. Due to the increased sensitivity of the right ventricle to preload, another feature of the treatment of right ventricular myocardial infarction is extreme caution in the use of nitrates and diuretics (as they reduce preload). Caution is also necessary in the use of morphine in such patients, because morphine has a moderate vasodilating effect.
Is it necessary to use thrombolytics for right ventricular myocardial infarction? No special studies have been conducted on this issue, but there is expert agreement on the advisability of their use, especially in the case of hypotension; Angioplasty is also indicated for patients with right ventricular myocardial infarction. It should be noted that the occurrence of atrial fibrillation in patients with right ventricular myocardial infarction leads to rapid deterioration of the condition; in such cases, urgent electrical cardioversion is necessary.
How is right ventricular myocardial infarction diagnosed in routine clinical practice using an ECG?
It is known that the right coronary artery is the common source of blood supply to both the posterior parts of the left ventricle and the right ventricle. Therefore, up to 1/3 of posterior left ventricular myocardial infarction is combined with right ventricular myocardial infarction. With the extreme right type of coronary circulation, the branches of the right coronary artery can extend to the lateral wall of the left ventricle and to the apex. A.V. Shpector and E.Yu. Vasilyeva (2009) note that 75% of patients with myocardial infarction have multiple lesions of the coronary arteries, which often leads to the development of collateral circulation. At this stage, the extent of myocardial infarction may not correspond to the classical anatomy of the coronary bed. Thus, if the patient had subtotal stenosis of the anterior interventricular artery and the blood supply to its zone was provided largely by collaterals from the right coronary artery, then thrombosis of the right coronary artery can lead to the development of a huge circular myocardial infarction.
Right ventricular myocardial infarction is diagnosed on the ECG using additional ECG leads - the so-called right chest leads: V3R-V4R-V5R-V6R. These leads must be removed in all cases of posterodiaphragmatic and posterobasal myocardial infarction, as well as when the localization of myocardial infarction according to standard ECG leads is unclear (Candell - Riera J. et al., 1981; Wenger N. et al., 1981; Goldberger A., 1984 ; Wagner G., 1994; Shevchenko N.M., 1994; Doshchitsin V.L., 1999; Mazur N.A., 2009). Registration of V3R-V6R or at least V4R in the first hours of the disease is very important for recognizing right ventricular myocardial infarction (N.A. Mazur, 2009).
In order to remove additional right chest leads, the active electrode is applied to the right half of the chest “mirror”, symmetrically with respect to the traditional chest leads (Fig. 1). In this case, electrodes V1-2 are left unchanged, and electrodes V3-6, transferred to the right half of the chest, form the right chest leads.
Figure 1. Additional right chest leads
a - diagram of the application of additional right chest leads
b — application of chest electrodes on the patient
c - ECG taken with left chest leads and additional right chest leads in a practically healthy person
In case of myocardial infarction of the right ventricle, the following changes are detected in the right precordial leads:
1) the presence of ST segment elevation of 0.5-1 mm in these leads is highly specific (however, ST segment elevation in half of the patients persists for no more than 10 hours from the onset of the disease);
2) pathological Q wave; the QRS complex has the form QR or QS (V.L. Doshchitsin, 1999). ON THE. Mazur (2009) notes that pathological Q in the right precordial leads has low specificity;
3) negative T wave;
4) in the case of necrosis of the lateral and anterior walls of the right ventricle, the same changes are recorded when electrodes V3R-V4R-V5R-V6R are applied two ribs above (Lyusov V.A. et al., 2008).
In addition, ST segment depression in leads V2 and aVF has a high predictive accuracy (about 80%); Right bundle branch block and atrioventricular block often occur.
We observed patient Sh., 70 years old, in the 11th city hospital of Kazan with extensive circular myocardial infarction, when an ECG during the first day of hospitalization initially revealed an elevation of the ST segment by 3 mm in leads V1-V4, depression of the ST segment in I, aVL, then a complete block of the right bundle branch developed, and then ST segment elevation occurred in III and aVF. ECG signs of inferior myocardial infarction (ST segment elevation in III and aVF) prompted us to take the right precordial ECG leads. When removing the right chest leads, pathological Q, ST segment elevation and negative T in V3R-V6R were detected, which indicates the development of myocardial infarction in the right ventricle as well.
We present an ECG of patient Sh., 70 years old (Fig. 2).
Figure 2. ECG of patient Sh., 70 years old.
Extensive circular myocardial infarction with a Q wave: myocardial infarction with a Q wave of the anteroseptal region of the left ventricle spreading to the apex and lateral wall of the left ventricle, myocardial infarction with a Q wave of the inferior wall of the left ventricle and right ventricle; complete right bundle branch block
Subsequent selective coronary angiography (at the Moscow Clinical Clinical Center) revealed a right coronary type of coronary circulation. The details of the angiographic study are as follows: left coronary artery - trunk without features, LAD - occlusion in the middle segment, distal LAD is not contrasted, subocclusion of the 1st arterial artery in the proximal section, OB - stenosis of the high-outgoing 1st arterial artery in the proximal segment up to 50%, stenosis of the left artery in the middle segment up to 75%. Right coronary artery - stenosis in the middle segment up to 50%, stenosis of the RV ostium up to 90%, WMA - stenosis in the middle segment up to 90% and 80%. ZMZhV - occlusion in the proximal part, the distal parts are contrasted by intrasystemic anastomoses.
So, with this message we want to draw attention to the issue of ECG diagnosis of right ventricular myocardial infarction. In routine clinical practice, with ECG signs of myocardial infarction of posterior localization, it is necessary to take an ECG in additional right chest leads V3R-V6R, which makes it possible to diagnose right ventricular myocardial infarction when a pathological Q wave, ST segment elevation and a negative T wave are detected in these leads. right ventricular myocardial infarction makes a significant correction in the management of patients with myocardial infarction.
V.N. Oslopov, O.V. Bogoyavlenskaya, Yu.V. Oslopova, M.A. Makarov, R.T. Khabibullina, M.G. Tregubova
Kazan State Medical University
City Clinical Hospital No. 11 UZ Kazan
Bogoyavlenskaya Olga Vladimirovna - Candidate of Medical Sciences, Associate Professor of the Department of Propaedeutics of Internal Diseases
Literature:
1. Mazur N.A. Practical cardiology. - M.: Medpraktika-M, 2009. - 616 p.
2. Shpector A.V., Vasilyeva E.Yu. Cardiology: clinical lectures. - M.: AST: Astrel, 2008. - 765 p.
3. Candell-Riera J., Figueras J., Valie V. et al. Right ventricular infarction. Relationships between ST segment elevation in V4R and hemodynamic, scintigraphic and echocardiographic findings in patients with acute inferior myocardial infarction. - Am. Heart J., 1981. - V. 101. - P. 281.
4. Wenger NK, Mock MB, Ringqvist I. Ambulatory electrocardiographic recording. — Chicago: Year Book Med. Publ., 1981. - 456 p.
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9. Lyusov V.A., Volkov N.A., Gordeev I.G. Myocardial infarction. In the book: Guide to Cardiology: Textbook in 3 volumes / ed. G.I. Storozhakova, A.A. Gorbachenkova. - M.: GEOTAR-Media, 2008. - T. 1 - P. 514-515.
Treatment of acute heart failure during right ventricular myocardial infarction
December 11, 2010 0
To determine the optimal criteria for infusion therapy, the study included 42 patients with lower myocardial infarction and UTI complicated by ventricular dysfunction. All patients were prescribed dobutamine and intravenous administration of rheopolyglucin (300 ml/hour) under the control of pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP). To assess perfusion, the cardiac index (CI) was determined using the thermodelution method.
Echocardiographic examination was performed before treatment and at optimal PAWP values. It was found that in patients with OPHL, with initially low values of PAP and PAWP (16.2 ± 0.21 and 7.0 ± 0.18 mm Hg), CVP was increased (11.2 ± 0.25 mm Hg. ). With the administration of rheopolyglucin, CI increased from 1.82 ± 0.03 to 2.51 ± 0.04 l/min/m2 (p <0.001) with PAWP 18 mm Hg. Art. There was no pronounced rise in central venous pressure. Further administration of fluid with an increase in PAWP to 20 mm Hg. Art. did not lead to a further increase in CI and was accompanied by a significant increase in CVP (from 13.7 ± 0.23 to 16.2 ± 0.24 mm Hg; p < 0.001).
During treatment, the LV size increased (from 52.3 ± 0.57 to 54.4 ± 0.60 mm; p < 0.05) and its ejection fraction increased (from 37.5 ± 0.87 to 41.9 ± 0.99%; p < 0.05) in the absence of significant dynamics in the right chambers of the heart. The data obtained indicate the advisability of increasing the preload on the right ventricle for the treatment of ARVD. Fluids should be administered in parallel with treatment with inotropic support drugs.
The target PAWP in the treatment of acute respiratory failure is 18 mm Hg. Art., at which the volume and LVEF increase, indicating an improvement in its filling. Fluid infusion is not advisable if the increase in CVP is greater than the increase in PAWP. In this case, the increase in LV end-diastolic pressure is offset by a higher rate of increase in RV filling pressure, and no increase in LV filling occurs. Right ventricular myocardial infarction (RMI) complicates the course of lower myocardial infarctions (MI) in 30–50% of cases. With extensive damage to the right ventricle (RV), its contractility decreases and acute right ventricular failure (ARF) develops, a characteristic feature of which is hypovolemia of the pulmonary circulation [1–4]. Treatment of ARVN is aimed at increasing the return of blood to the left chambers of the heart. On the one hand, this is an increase in RV contractility, on the other, an increase in preload on the right ventricle.
An increase in contractility is achieved by using inotropic drugs, an increase in preload is achieved by infusion of plasma expanders to increase the return of blood to the pancreas and, as a consequence, increase the release of blood into the pulmonary artery [3, 5]. While the dosing regimens of inotropic drugs are well known, there are no clear recommendations in the literature on the volume of fluid infused during OP.
Purpose of the study. To develop optimal values of pulmonary artery wedge pressure, which must be achieved when conducting infusion therapy under the control of central hemodynamic parameters, and also to compare the volume of infusion with the optimal values of PAWP.
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