Introduction:
Arterial embolizationIt refers to a pathological process in which the embolus is detached from the heart or the proximal arterial wall or enters the artery from the outside, pushed to the distal side by the blood flow, and blocks the blood flow of the artery, resulting in ischemia or even necrosis of the limb or internal organs. Acute myocardial infarction (acutemyocardialinfarction) refers to sudden complete occlusion of the coronary artery, ischemia, injury and necrosis of the myocardium, and an acute ischemic heart disease characterized by severe chest pain, electrocardiogram and dynamic changes of myocardial enzymology. Most of the underlying lesions are coronary atherosclerosis, and a few are other lesions such as acute coronary embolism.
Cause:
Coronary atherosclerosis causes stenosis and myocardial insufficiency, and when the collateral circulation has not been established, myocardial infarction can occur due to aggravation of myocardial ischemia for the following reasons.
First, the coronary artery is completely occluded
Intravascular or subendocardial hemorrhage of the diseased atherosclerotic plaque, intraluminal thrombosis or persistent arterial spasm, complete occlusion of the lumen.
Second, the heart discharge volume plummeted
Shock, dehydration, hemorrhage, severe arrhythmia, or surgery cause a sudden drop in cardiac output, and coronary perfusion is severely inadequate.
Third, myocardial aerobic demand for blood surge
When severe physical labor, emotional agitation or blood pressure rises sharply, left ventricular load increases sharply, catecholamine secretion increases, and myocardial aerobic blood demand increases.
Acute myocardial infarction can also occur in coronary artery spasm without coronary atherosclerosis, and occasionally due to coronary embolism, inflammation, and congenital malformations.
Severe arrhythmia, shock or heart failure after myocardial infarction can further reduce coronary perfusion and expand myocardial necrosis.
an examination:
(1) Pain first appeared, mostly in the early morning, and the pain site and nature were the same as angina. However, the degree is heavy, the duration is long, rest or nitroglycerin is ineffective, can be accompanied by a sense of death, a few people from the beginning of shock or acute heart failure.
(2) systemic symptoms of fever, tachycardia, increased white blood cells and increased erythrocyte sedimentation rate. More fever occurs 24 to 48 hours after the onset of pain, and the body temperature is mostly around 38 °C.
(3) gastrointestinal symptoms, nausea, vomiting and upper abdominal pain, severe cases have hiccups.
(4) Arrhythmia often occurs within 1 to 2 weeks of onset, and is most common within 24 hours. Ventricular arrhythmias are most often ventricular premature contractions. There are also more compartmental and bundle branch block.
(5) hypotension and shock shock occur more than a few hours to one week after onset, mostly cardiogenic.
(6) Heart failure is mainly acute left heart failure. It is caused by weakened or contracted myocardial contractility after infarction.
diagnosis:
1 angina pectoris is light in nature, short in time, nitroglycerin is effective, blood pressure is elevated, systemic symptoms are less, and ST segment is temporarily depressed.
2 acute pericarditis pain and fever at the same time, breathing, coughing increased, early pericardial friction sound, ECG in addition to aVR, the rest of the lead is ST segment arch back up, no abnormal Q wave.
3 Acute pulmonary embolism was mainly due to right heart failure, electrocardiogram I guided S wave depth, and III guided Q wave was significant.
4 history of acute abdomen, physical examination, electrocardiogram and myocardial zymogram can be identified.
5 Aortic dissection separation The blood pressure and pulse of the two upper limbs are obviously different. The chest pain starts to reach the peak and is often radiated to the back, ribs and lower limbs. Aortic valve regurgitation can be identified, and two-dimensional echocardiography is helpful for diagnosis.
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