Myocardial infarction is caused by blockage of the coronary arteries, so the myocardium supplied by the coronary arteries rapidly undergoes ischemia, injury and necrosis. The electrocardiogram shows a corresponding series of changes in the T-wave, ST-segment and QRS wave groups. Therefore, ECG has a particularly important role in the diagnosis of myocardial infarction. The vast majority of patients can show significant and specific changes, but a small number of patients may have temporary difficulties in diagnosis for various reasons.
I. Identification of anterior septal and anterior wall myocardial infarction
(A) Change in the order of ventricular depolarization
1. Complete left bundle branch block (CLBBB): ①In CLBBB, due to right-to-left septal depolarization, there may be no r wave in the right anterior leads, but only QS wave; at the same time, CLBBB may produce secondary ST-T changes, resulting in ST elevation and upright and elevated T wave in the leads with QS waveform, which are easily misdiagnosed as acute anterior septal myocardial infarction. If the above changes extend to leads V5 and V6, the diagnosis of acute extensive anterior wall myocardial infarction is easily misdiagnosed. The key point of differentiation is the widening of QRS waves in all leads in CLBBB and the appearance of a typical CLBBB picture without dynamic changes in ST-T (no evolution of acute myocardial infarction). The key point to differentiate CLBBB combined with anterior septal myocardial infarction is that only QS waves will appear in Vl and V2 in CLBBB, and QS waves will not appear in V3. If Q waves also appear in V3, then CLBBB combined with anterior septal myocardial infarction is indicated.
2. left anterior branch block (LAH): LAH can sometimes mask the manifestation of myocardial infarction, for example, in some cases, the precordial leads can show qrS waves or qRS waves, that is, qRS waves or qRS waves in leads V1 and V2. how to distinguish LAH from anterior septal myocardial infarction when it occurs in combination is also an important topic of research in the field of electrocardiology. The qRS wave or qS wave, the duration of the q wave should generally not exceed 0.02 seconds. If the tracing is raised by one intercostal interval (at the 3rd intercostal interval), the chance of q waves appearing increases; when the tracing is lowered by one intercostal interval (at the 5th intercostal interval), the q waves should not be shown. Therefore, the presence of q waves in the right precordial leads with a time >0.02 seconds and the presence of q waves when the intercostal tracing is lowered by one intercostal interval suggests anterior septal myocardial infarction, and in addition, QS waves should not appear in the right precordial leads (Vl-v3) during LAH, and the amplitude of r waves should also increase progressively; if QS waves or r waves do not increase progressively, it also suggests anterior septal myocardial infarction.
3, right bundle branch block (RBBB): In RBBB, QR (or Qr) waves can also appear in the right ventricular leads and III and aVF leads occasionally, instead of the original rsR’ waves, which can be misdiagnosed as anterior septal myocardial infarction, this change is common in acute right ventricular overload, and the mechanism of its generation is the same as the abnormal Q waves in acute pulmonary heart disease, the key points of differentiation are In RBBB alone, waves in the right precordial leads are rarely seen in V2 and leads to the left. If QR waves appear in the central precordial leads (V2 or even V3 or V4), this supports anterior interval or anterior wall myocardial infarction. Or the original RBBB, when combined with anterior interval wall or anterior wall myocardial infarction.
4. Pre-excitation syndrome (W-P-W): In W-P-W, due to the presence of abnormal conduction bundles in the atria, the ventricles can be excited prematurely. If the site of premature excitation is the right ventricle (type B W-P-W), the excitation vectors point to the left and posterior, and QS waves can appear in the right anterior leads, while resembling anterior interval wall myocardial infarction. If myocardial infarction occurs at the same time, the abnormal Q waves and ST-T changes can be masked by the image of W-P-W. In this case, the diagnosis of myocardial infarction can only be determined when the image of W-P-W disappears (for example, when W-P-W appears intermittently) or based on other clinical manifestations.
(II) Ventricular hypertrophy
1. QS waves can appear in leads V1 to V3 in left ventricular hypertrophy, but there should not be QS waves in leads V4 and I and aVL. If there are QS waves in v4, I and aVL, it indicates left ventricular hypertrophy combined with anterior wall infarction.
In right ventricular hypertrophy, Q waves may occasionally appear in leads V2 to V3, but QS waves usually do not appear in lead V4 in right ventricular hypertrophy, and right ventricular hypertrophy is often accompanied by rightward deviation of the electrical axis; therefore, right ventricular hypertrophy with leftward deviation of the electrical axis and QS waves in V4 also suggest right heart hypertrophy combined with anterior wall myocardial infarction.
3, the incidence of abnormal Q waves in hypertrophic cardiomyopathy is 41% to 56%, often in leads V1 to V4. Differentiation points ① Q wave morphology hypertrophic cardiomyopathy Q wave morphology is diverse, most deep and narrow, not more than O.04s, like a willow leaf, a few have cut or coarse stutter, or even a strange W-shaped. In hypertrophic cardiomyopathy, the T waves are often upright in the leads with QS, QR or W patterns, and the Q and T wave directions are separated, whereas in myocardial infarction-related leads, the T waves are generally deeply inverted and symmetrical in the descending and ascending limbs. (iii) The leads presenting Q waves in hypertrophic cardiomyopathy are often accompanied by upright T waves and rarely have ST-segment elevation, and in those with individual ST-segment elevation, the elevation amplitude is stable for a long time lacking the dynamic changes characteristic of myocardial infarction.
(C) Acute myocarditis
The ECG of transmural necrotizing myocarditis may show pathological Q waves, which may reflect temporary loss of myocardial function (myocardial electrostasis) or may be a manifestation of myocardial necrosis or myocardial fibrosis. Viral infections can also cause coronary artery occlusion due to coronary arteritis. Severe acute myocarditis may show a picture of extensive myocardial injury, with low R-wave amplitude and ST-T changes in most leads, and pathological Q waves and ST-segment elevation that are mostly transient. The key points of differentiation are ① abnormal Q waves in multiple leads in acute myocarditis and abnormal Q waves in the relevant leads in acute myocardial infarction. ②Q waves in myocardial infarction tend to be persistent, while in acute myocarditis they are mostly transient. (③The accompanying ST-T changes are often regular in acute myocardial infarction with time migration, while this pattern is not obvious in acute myocarditis, and ST-segment elevation even occurs when the Q waves have fully formed and stopped progressing.
(iv) Physiological or positional
1, misplaced electrodes in the thoracic leads, reversed connections in the limb leads, and normal variation in the aVL leads with a QS or Qr pattern.
2, left-sided pneumothorax, low voltage in leads V1 to V4, poor R-wave progression, QS type in right to mid-thoracic leads, occasionally no R-wave in V1 to V6, similar to extensive anterior wall infarction, and nonspecific low flattening or inversion of T-wave in precordial leads, and right deviation of the electrical axis. The key point of differentiation is that the above ECG changes in left-sided pneumothorax are obvious in the prone position, and when the patient is in sitting or standing position, the heart is close to the chest wall, the voltage increases, and R waves can appear, or the ECG returns to normal after exhausting the lungs to reopen.
3, chronic emphysema, can be in V1, V2 and even V3 to V6 leads appear QS waves, and T waves can be upright, but also inverted. Differentiation points ① Patients with emphysema often have low voltage, pulmonary P waves, inverted VavL, deep S waves in Vs-V6, and QRS waves with vertical or right deviation of the electrical axis, whereas in infarction, the electrical axis is left deviated, PavL is upright, and QRS waves in infarct-related leads are Qr or QS type. If the R-wave amplitude of precordial leads is reduced or V1 to V6 are QS-type, the ECG can be normalized if the precordial leads are shifted down by one intercostal tracing. (8) ST-T morphology, ST-segment elevation with T-wave inversion to its right is characteristic of myocardial infarction. In contrast, there is no characteristic ST-T wave evolution pattern in emphysema.
2. Identification of inferior wall myocardial infarction
1. In normal subjects, QS, QR or Qr waves can be seen in leads III and aVF, and similar to inferior wall myocardial infarction, their generation is related to the position of the heart. When the apex of the heart is rotated forward, the potential on the posterior basal surface of the heart (in the form of Qs or QR waveforms) can be transmitted to the left leg, resulting in such waveform changes in the aforementioned leads. This waveform change is reduced or even disappears completely, especially when the subject exhales or when the diaphragm is lowered in the prone position. However, in inferior wall myocardial infarction, the abnormal Q waveform in leads III and aVF may also change with breathing or position change. Key points of differentiation: ① the q wave on lead II in normal subjects is still normal, if abnormal Q wave appears, it is inferior wall myocardial infarction. ②If ST-T dynamic changes are present in II, III and aVF, the diagnosis of inferior wall myocardial infarction can be confirmed. ③In normal people, because the initial vector is unchanged, the aVR leads often do not show rS waveforms, but QS, QR, or Qr waves; in inferior wall myocardial infarction, because the initial vector often points upward, the aVR leads can show rS waves, but usually no QR or Qr waves, unless there is also anterior wall myocardial damage.
2. Type A and B W-P-W, if the vectors of ventricular preexcitation point upward, can all present ECG waveforms similar to those of inferior wall myocardial infarction in leads II, III, and aVF. Differentiation point: when W-P-W is QS or QR on II, III, and aVF leads, its T wave is always upright or isotonic; an inverted T wave is suggestive of concomitant inferior wall myocardial ischemia.
3, LAH is distinguished from inferior wall myocardial infarction; in LAH, the QRS vector on the frontal plane points to the left, while the T vector points down, so that the T wave is upright in the II, III and aVF leads, which can conceal the T wave inversion that should occur in inferior wall ischemia. Differentiation point: LAH alone and LAH combined with inferior wall myocardial infarction are more difficult to differentiate from the ECG. If the qRS waveform and T wave inversion are present in the leads reflecting the inferior wall, the diagnosis of LAH combined with inferior wall myocardial infarction is supported.
4, RBBB and inferior wall myocardial infarction, QR (or Qr) wave may appear in III and aVF during RBBB, instead of the original rSR’ wave. Mechanism: This is the same mechanism as the abnormal Q waves seen in acute pulmonary heart disease (associated with increased right ventricular load and cis-clockwise transposition of the heart). Differentiation point: Although simple RBBB may occasionally present QR waves in leads III and aVF due to acute right heart overload, QR waves should not be present in lead II in inferior wall myocardial infarction. Therefore, if QR waves are present in leads II, III and aVF, the inferior wall myocardial infarction is supported.
5. A few patients with chronic emphysema may present QS waves in leads II, III, and aVF. Differentiation point: If there is left deviation of the electrical axis, it is mostly suggestive of concomitant coronary artery disease or myocardial infarction.
6. Asymmetric hypertrophic cardiomyopathy (IHSS) is differentiated from inferior wall myocardial infarction: IHSS can resemble inferior wall myocardial infarction by the presence of QS, QR or Qr waves in any one or more of the inferior wall leads. Mechanism: The likely cause of the above myocardial infarction-like pattern is septal thickening with increased depolarization vector and prolonged depolarization time, a change that can result in deep Q waves in the inferior wall leads. Differentiation points: If the Q wave is wide or appears tangential, or if the T wave is inverted on the lead where the Q wave appears, it mostly supports inferior wall myocardial infarction.
Differentiation of acute pulmonary heart disease (pulmonary embolism) and inferior wall myocardial infarction: after pulmonary embolism, SI, QⅡQⅢTⅢ may appear on the limb leads. That is, sudden appearance of S waves in lead I (as part of RS or rS waves), Q waves and ST-T changes in one or more leads in III and aVF, coolly resembling acute inferior wall myocardial infarction. Mechanism, pulmonary embolism causes cis-clockwise transposition, resulting in right atrial and right ventricular dilatation. Differentiation points: SI, QII, TIII and inferior wall myocardial infarction are more difficult to differentiate. Generally, abnormal Q waves do not appear on lead II in acute pulmonary heart disease; whereas they often appear in inferior wall myocardial infarction. In addition, an rS wave on aVR supports inferior wall myocardial infarction, and a qR or QR wave on aVR is more often seen in acute pulmonary heart disease. In inferior wall myocardial infarction, the initial vector of ventricular depolarization points upward. Thus, r waves appear on the aVR leads, forming rS or RS waveforms. In acute pulmonary heart disease, Q waves in III and aVF leads are due to changes in heart position, and the inferior wall depolarization vector is not lost. On the frontal plane, the initial vector of ventricular depolarization generally points to the right, and the terminal vector points up and to the right, thus showing qR or QR waves on the aVR leads, which do not manifest as rs waves.
3. Identification of high lateral wall myocardial infarction
1. Identification of QS or Qr waves on aVL leads in normal subjects and high lateral wall myocardial infarction; when the heart is positioned vertically, the aVL leads are oriented toward the base of the heart, thus tracing the waveform of the left ventricular cavity (QS wave); if apical transposition occurs, the aVL leads can be oriented toward the back of the heart and Qr waves appear. Differential points: If Q waves are present in aVL, I, and V5 at the same time, it supports high lateral wall myocardial infarction. In addition, P-wave inversion of aVL also supports high lateral wall myocardial infarction.
2. Differentiation of left ventricular hypertrophy from high lateral wall myocardial infarction: In left ventricular hypertrophy, most of the QS waves in the right precordial leads appear only in leads V1 and V2, and rarely occur in lead V3, much less extend to leads V4, V5 and aVL and I. If abnormal Q waves appear in I, aVL, V4 and V5, they represent high lateral wall myocardial infarction.
3. Differentiation of right ventricular hypertrophy from high lateral wall myocardial infarction. In right ventricular hypertrophy, QS (or rS wave) can appear in I and aVL leads and resemble high lateral wall myocardial infarction, which is due to the significant dominance of right ventricular depolarization vectors. Key points of differentiation; in right ventricular hypertrophy, the electrical axis is always right deviated and QR waves do not extend to V4 and V5.
IV. Identification of positive posterior wall myocardial infarction
1. Differentiation of right bundle branch block (RBBB) from orthoposterior wall myocardial infarction. RBBB can present tall and tangential R waves in the right precordial leads, similar to orthoposterior wall myocardial infarction. Differentiation point: orthoposterior wall myocardial infarction often coexists with inferior or high lateral wall myocardial infarction. Therefore, if there is an abnormal Q wave on leads II, III, aVF or those reflecting the lateral wall at the same time as a tall, tangential R wave in the right precordial leads, it is an orthoposterior wall myocardial infarction.
2, W-P-WA type, V1 can appear high and wide R waves, which can be confused with orthoposterior wall myocardial infarction. Differentiation point: In addition to W-P-W ECG features, orthoposterior wall often occurs simultaneously with inferior wall and high lateral wall myocardial infarction, with corresponding characteristic ECG to assist in differentiation.
The differentiation between right ventricular hypertrophy and orthoposterior wall myocardial infarction is often difficult by conventional ECG alone, but the following points may help to determine: right ventricular hypertrophy is often suggested when the frontal QRS electrical axis is right deviated. mathur et al. found that in right ventricular hypertrophy, 2/3 of patients with frontal QRS electrical axis 75-2200; while only 5% of patients with orthoposterior wall myocardial infarction had this change. Conversely, in patients with orthoposterior wall myocardial infarction, 80% had a frontal electrical axis of 740-1100; only 28% showed this change in right ventricular hypertrophy.