Myocardial infarction

Introduction to myocardial infarction Myocardial infarction is also called myocardial infarction. Myocardial infarction is coronary occlusion and blood flow is interrupted, causing partial necrosis of some myocardium due to severe persistent ischemia. Clinically, there are severe and persistent post-sternal pain, fever, leukocytosis, accelerated erythrocyte sedimentation rate, increased serum myocardial enzyme activity and progressive electrocardiographic changes, which can occur arrhythmia, shock or heart failure. basic knowledge The proportion of sickness: 0.406% Susceptible people: no specific population Mode of infection: non-infectious Complications: arrhythmia, sudden death, shock, heart failure

Cause of myocardial infarction

The majority of patients occur on the basis of coronary atherosclerotic stenosis. Due to some incentives, the coronary atherosclerotic plaque ruptures, and the blood platelets accumulate on the surface of the ruptured plaque, forming a blood clot (thrombus) and suddenly blocking the coronary lumen. , leading to myocardial ischemia and necrosis, in addition, myocardial oxygen consumption increased significantly or coronary artery spasm can also induce acute myocardial infarction, the common incentives are as follows:

Overwork (30%):

Excessive physical labor, especially weight-bearing upstairs, excessive physical activity, continuous stress, etc., can increase the burden on the heart, sudden increase in myocardial oxygen demand, and the coronary artery of patients with coronary heart disease has hardened, narrowed, and cannot fully expand. And cause myocardial ischemia. Intense physical exertion can also induce plaque rupture, leading to acute myocardial infarction.

Overeating (15%):

Many cases of myocardial infarction occur after overeating. After eating a large amount of food containing high fat and high calorie, the blood lipid concentration suddenly rises, resulting in an increase in blood viscosity and an increase in platelet aggregation. A thrombus is formed on the basis of coronary artery stenosis, causing acute myocardial infarction.

Constipation (13%):

Constipation is very common among the elderly. Clinically, it is not uncommon for elderly people with myocardial infarction due to exertion of breath during constipation. It is necessary to give the elderly enough attention and keep the stool smooth.

Smoking, heavy drinking (10%):

Smoking and heavy drinking can induce acute myocardial infarction by inducing coronary artery spasm and increased myocardial oxygen consumption.

Excited (6%):

Induced by intense emotional changes such as excitement, nervousness, and anger.

Cold stimulation (5%):

Sudden cold stimuli may induce acute myocardial infarction. Therefore, patients with coronary heart disease should pay great attention to cold and warm, and the cold season in winter and spring is one of the reasons for the high incidence of acute myocardial infarction.

Myocardial infarction prevention

1. Avoid overwork: especially avoid lifting heavy items. Myocardial infarction may be induced in elderly patients with coronary heart disease.

2, relax the spirit: a happy life, you must be able to take care of anything.

3, pay special attention when taking a bath: Do not take a bath in a meal or hungry. The water temperature is preferably the same as the body temperature, and the bathing time should not be too long. When the patient with severe coronary heart disease is taking a bath, it should be carried out with the help of others.

Myocardial infarction complications Complications, arrhythmia, sudden death, heart failure

1. Papillary muscle dysfunction or rupture: papillary muscles (mainly mitral papillary muscles) contract or become weak due to ischemia, necrosis, etc., resulting in mitral regurgitation, and there is a loud systolic murmur in the apical region. And easy to cause heart failure.

2, heart rupture: for the early rare but serious complications, often appear within a week of onset, mostly ventricular free wall rupture, due to pericardial hemorrhage and acute pericardial occlusion and sudden death, occasionally ventricular septal rupture perforation, in the left sternum There is a loud systolic murmur between the fourth intercostal space, often accompanied by tremor, which can cause heart failure and quickly die.

3, wall swelling tumor: the incidence of domestic corpse data is 20%, the clinical data is 28%, under the influence of ventricular pressure, the ventricular wall of the infarction bulges outward, which is seen in the range of myocardial infarction The patient is often found only a few weeks after the onset of the disease. The physical examination shows that the right heart is enlarged, the heart beats more extensively, and there may be systolic murmur. When the wall thrombus occurs, the heart sound is weakened, and the ST segment of the ECG is continuously elevated. X-ray examination is visible. Local bulging in the heart, fluoroscopy or phonography can be seen that the beat is weak or abnormal, selective left ventricular angiography and portal radionuclide angiography can show swelling tumors, echocardiography can show the wall Abnormal pulsation of the expansion tumor, concurrent ventricular wall swelling tumor is prone to heart failure, arrhythmia or embolism, but there is no risk of rupture after myocardial infarction.

4, embolization: for ventricular wall thrombus or lower extremity venous thrombosis caused by broken, the general incidence rate in foreign countries is about 10%, China is generally less than 2%, seen in the first 1-2 weeks after onset, such as embolus from the left ventricle, It can produce arterial embolisms such as brain, kidney, spleen or limbs. For example, the embolus can be from the deep vein of the lower extremity, which can produce pulmonary embolism.

5, post-myocardial infarction syndrome: within a few weeks to several months after myocardial infarction, can occur after a few days, can occur repeatedly, manifested as pericarditis, pleurisy or pneumonia, fever, chest pain, shortness of breath, cough and other symptoms, May be caused by the body's allergic reaction to necrotic substances.

6, other: there are still respiratory (especially the lungs) or other parts of the infection, shoulder-hand syndrome (shoulder wall rigidity).

Symptoms of myocardial infarction Common symptoms Chest pain with chest tightness, palpitations, palpitations, cardiogenic chest pain, arrhythmia, upper abdominal pain, left ventricular diastolic function, chest pain, chest tightness, shortness of breath, myocardial necrosis, extensive post-sternal pain

According to typical clinical manifestations, characteristic ECG changes and laboratory tests have found that it is not difficult to diagnose the disease. Patients with painlessness are more difficult to diagnose. All elderly patients have sudden shock, severe arrhythmia, heart failure, upper abdomen. If the cause of pain or vomiting is unknown, or the original high blood pressure and the blood pressure suddenly drops and there is no reason to find it, the shock after surgery but the bleeding is excluded, the possibility of myocardial infarction should be considered, and the elderly patient If there is a heavier and persistent chest tightness or chest pain, even if there is no characteristic change in the electrocardiogram, the possibility of the disease should be considered. It is appropriate to treat the acute myocardial infarction first, and repeat the electrocardiogram observation and serum myocardial enzyme measurement in a short period of time. To determine the diagnosis.

Myocardial infarction

One,

1, white blood cell count: white blood cells can increase to 10.000 ~ 20.000 / mm3 within 1 week of onset, neutrophils mostly in 75% ~ 90%, eosinophils decreased or disappeared.

2, erythrocyte sedimentation rate: erythrocyte sedimentation rate increased, can be maintained for 1 to 3 weeks.

3, serum enzyme assay: serum creatine phosphokinase (CK or CPK) appeared within 6 hours of onset, peaked at 24 hours, disappeared after 48-72 hours, the positive rate reached 92.7%, after the onset of aspartate aminotransferase (AST or GOT) 6 It rises in ~12 hours, peaks in 24-48 hours, and falls to normal after 3-6 days. Lactate dehydrogenase (LDH) rises 8 to 12 hours after onset, peaks in 2 to 3 days, and recovers in 1 to 2 weeks. Normal, in recent years, -hydroxybutyrate dehydrogenase (-HBDH), -glutamyl phosphotranspeptidase (-GTP), pyruvate kinase (PK), etc., three kinds of creatine phosphokinase are also used. The enzyme, in which CK-MB is derived from the myocardium, has extremely high diagnostic sensitivity and specificity, reaching 100% and 99%, respectively. The magnitude and duration of its increase are often used to determine the extent and severity of infarction. Hydrogenase has five isoenzymes, of which LDH1 is derived from the myocardium. It has appeared several hours after the acute myocardial infarction, and it can last for 10 days, and its positive rate is over 95%.

4, myoglobin measurement: urinary myoglobin excretion and serum myoglobin content determination, also help to diagnose acute myocardial infarction, urinary myoglobin began to excretion 5 to 40 hours after infarction, lasting an average of 83 hours, serum The rise time of myoglobin was slightly earlier than that of CK. At about 4 hours, the peak disappeared faster than CK, and most of the time returned to normal after 24 hours.

5, other: serum myosin light chain or heavy chain, serum free fatty acid, increased after acute myocardial infarction, serum free fatty acid is significantly increased, prone to severe ventricular arrhythmia, in addition, acute myocardial infarction, due to stress The reaction, blood sugar can be increased, the glucose tolerance can be temporarily reduced, and return to normal after about 2 to 3 weeks.

Second, ECG and heart vector chart check

Electrocardiogram has progressive and characteristic changes, which are helpful for diagnosing and estimating the location, extent and progression of the lesion. The ECG waveform changes include three types:

1. Waveform of the necrotic area: a deep and wide Q wave appears in the lead to the necrotic myocardium.

2. Waveform of the damaged area: the lead around the necrotic area, showing the elevated ST segment.

3. Waveform of the ischemic area: a lead directed to the periphery of the damaged area, showing T wave inversion.

The typical electrocardiogram evolution process is: abnormal Q-wave and ST-segment elevation in the lead-oriented area of the onset (acute phase), the latter has a one-way curve connecting the T wave and the T wave, and the R wave is reduced or disappears. The lead to the infarct area shows an increase in R wave and a ST-segment depression. From a few days to about 2 weeks after the onset (subacute phase), the lead to the infarct area, the ST segment gradually returns to the baseline level, T wave It becomes flat or significantly inverted; the T wave is increased in the lead to the infarct area, and several weeks to several months after the onset (chronic period), the T wave can be V-shaped inverted, the two limbs are symmetrical, the trough is sharp, and the abnormal Q wave is later. It is often permanent and T waves are likely to recover within months to years.

Electrocardiogram of acute anterior myocardial infarction:

The QRS complex of the V4 lead is qR type, the ST segment is obviously elevated, the V2 lead is qRS type, the ST segment is obviously elevated, and the ST segment of the V1 lead is also elevated.

Electrocardiogram of acute inferior myocardial infarction:

The aVF lead QRS complex is Qr-type ST-segment elevation, the II lead is qRsr'-type ST-segment elevation, and the I, aVL leads ST-segment depression.

In the earliest stage before the abnormal Q wave and ST segment elevation have not appeared, the ECG may be abnormal, or there may be asymmetrical changes in the T wave abnormally high limbs, multiple focal myocardial infarction, no typical ECG performance; In the case of bundle branch block, especially in the left bundle branch block, the electrocardiogram does not necessarily reflect the performance of acute myocardial infarction; when the acute myocardial infarction occurs again in the original site, the electrocardiogram performance is also atypical.

Diagnosis and diagnosis of myocardial infarction

Clinically, the disease should be identified with the following diseases:

1. Angina pectoris: The painful nature of angina pectoris is the same as that of myocardial infarction, but the episode is more frequent. Each episode has a short duration, generally no more than 15 minutes. There are often predisposing factors before the onset, without fever, white blood cells increase, and erythrocyte sedimentation rate increases. Or increased serum myocardial enzymes, no changes in ECG or temporary depression or elevation of ST segment, rarely arrhythmia, shock and heart failure, containing nitroglycerin tablets, etc., can be identified.

2, acute pericarditis: especially acute non-specific pericarditis, there may be more severe and persistent precordial pain, ECG has ST segment and T wave changes, but patients with pericarditis have fever and at the same time or before the pain The white blood cell count is increased, the pain is often aggravated by deep breathing and coughing. The physical examination can find the pericardial friction sound. The condition is generally not as serious as the myocardial infarction. In addition to the aVR, the ECG has a ST segment of the arch back up, no abnormal Q. Waves appear.

3, acute pulmonary embolism: pulmonary embolism can often cause chest pain, shortness of breath and shock, but there is a sharp increase in right heart load, such as a sharp increase in the right ventricle, pulmonary pulsation and the second heart sound hyperactivity, three There is systolic murmur in the cusp area, fever and leukocytosis appear earlier, the electrocardiogram shows the right axis of the electric axis, the S-wave or the original S-wave deepening in the I lead, and the Q-wave and T-wave inversion in the III lead. The high-R wave appears in the aVR lead, the chest lead transition zone shifts to the left, and the left chest lead T-wave is inverted. It is different from the myocardial infarction and can be identified.

4, acute abdomen: acute pancreatitis, peptic ulcer perforation, acute cholecystitis, gallstones, etc., patients may have upper abdominal pain and shock, may be confused with acute myocardial infarction patients with pain affecting the upper abdomen, but carefully ask the history and physique Examination, it is not difficult to make an identification, electrocardiogram and serum myocardial enzyme measurement help to confirm the diagnosis.

5, aortic dissection: separation with severe chest pain onset, quite similar to acute myocardial infarction, but the pain reached the peak at the beginning, often radiated to the back, ribs, abdomen, waist and lower limbs, the upper limbs blood pressure and pulse can be significantly different, A small number of aortic regurgitation, temporary paralysis or hemiplegia of the lower extremities, chest X-ray, CT, echocardiography to detect the fluid in the aortic wall sandwich, can be identified.

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