acute myocardial infarction
Introduction
Introduction to acute myocardial infarction Acute myocardial infarction (AMI) refers to acute myocardial infarction caused by persistent and severe myocardial ischemia. Clinical manifestations of chest pain, acute circulatory dysfunction and a series of characteristic electrocardiographic changes reflecting myocardial injury, ischemia and necrosis, clinical manifestations often have persistent severe retrosternal pain, acute circulatory dysfunction, arrhythmia, heart Functional failure, fever, white blood cell count and elevated serum myocardial injury marker enzymes and progressive changes of myocardial acute injury and necrosis of electrocardiogram, according to the infarct size, myocardial infarction can be divided into transmural myocardial infarction and subendocardial infarction class. According to the development of the disease, myocardial infarction can be divided into acute myocardial infarction and old myocardial infarction. basic knowledge The proportion of illness: 0.002% Susceptible population: middle-aged and elderly people over 40 years old Mode of infection: non-infectious Complications: arrhythmia heart failure cardiogenic shock elderly papillary muscle dysfunction and fracture
Cause
Cause of acute myocardial infarction
Coronary intraluminal thrombosis (30%):
1. There is no history of angina before myocardial infarction: Coronary atherosclerosis makes the stenosis generally less than 70%, the original lumen is relatively smooth, there is no effective collateral circulation in the artery supplying blood, and the thrombus makes the lumen suddenly complete. Blockage, acute necrosis of the myocardium by this blood vessel, such patients have a rapid onset, severe symptoms, myocardial necrosis often from the subendocardial to subepicardial through the ventricular wall, the infarct site often thin and outward expansion In the first week of onset, the heart is easily ruptured, and the thrombus is blocked at the proximal end of the large branch of the coronary artery. The penetrating infarction has a wide range, and acute left heart failure, cardiogenic shock and ventricular aneurysm often occur.
2, the history of angina or old myocardial infarction: acute thrombosis occlusion of another coronary artery, not only cause acute myocardial necrosis at the blood supply site, and block the collateral circulation to provide the original ischemic and old myocardial infarction To make the condition more serious than before.
3, multiple coronary atherosclerosis: in a coronary plaque has caused the acute thrombosis of the stenosis of the stenosis, generally have a history of angina, due to the presence of a certain number of collateral circulation to the epicardium The lower myocardium plays a protective role. The myocardial necrosis caused by acute blockage may be limited to the subendocardial myocardium, which is characterized by multiple focal necrosis and a small infarct size, so it is not easy to cause cardiac rupture and ventricular aneurysm formation.
4, in the coronary plaque thrombosis incomplete occlusion: patients often have unstable angina, can also lead to subendocardial acute myocardial infarction, ECG no abnormal Q wave, this time should be serum myocardial enzymology, to Help diagnosis.
Coronary artery spasm (20%):
Some authors performed coronary angiography within 12 hours after onset of a group of patients with acute myocardial infarction, showing 40% of patients with coronary artery vasospasm. Injecting nitroglycerin into the occluded coronary artery can open or partially open the occluded lumen, indicating that the group Acute myocardial infarction is caused by coronary spasm.
Bleeding in atherosclerotic plaque or under plaque (15%):
The surface of the lipid-rich soft plaque has a thin fiber-covered cap, and the shape of the plaque, in which the fat stove is in an eccentric position, is easily broken by the impact of blood flow, except for the structure of these vulnerable plaques, the coronary artery Acute changes in intraluminal pressure; changes in coronary artery tension; with external factors such as coronary artery bending and torsion of each heart beat, vulnerable plaque rupture or subendocardial hemorrhage, platelet aggregation thrombosis, coronary artery occlusion Causes myocardial infarction.
A sudden drop in cardiac output (10%):
Shock, dehydration, hemorrhage, surgery or severe arrhythmia, resulting in a sudden drop in cardiac output, a sharp decrease in coronary perfusion.
Myocardial oxygen demand soared (10%):
Heavy physical activity, elevated blood pressure or emotional agitation, resulting in a significant increase in left ventricular load, increased secretion of catecholamines, myocardial oxygen demand, coronary artery blood supply is significantly insufficient, leading to myocardial ischemia and necrosis.
Incidence factor
For the onset of myocardial infarction, as with all coronary heart disease, hypercholesterolemia (or low-density lipoprotein), hypertension and smoking are important risk factors.
1. Gender and age: Male patients are more than females. The ratio of male to female is 2:1 to 3:1. The vast majority of acute myocardial infarction occurs in middle-aged and elderly people over 40 years old. 95%, individual patients are less than 30 years old, and the incidence rate increases significantly with age.
2, the original disease before the onset: China reported that myocardial infarction combined with hypertension accounted for 50% to 90%, in Beijing from 1972 to 1983, 53.1% to 70.2%, generally higher than the foreign recorded merger rate The number of cases with diabetes is 3.9% to 7.5%, which is slightly lower than that reported by most foreign countries. Nearly half of the patients have a history of angina.
3, predisposing factors: According to domestic data, about 1/2 to 2/3 cases have incentives to find, which are overworked, emotional or mental stress is the most common, followed by full meals and upper respiratory tract or other infections, a few For the operation of hemorrhage or other causes of hypotension, shock and subarachnoid hemorrhage, etc., some patients have seizures during sleep or complete rest. The number of acute myocardial infarction cases in a group of hospitals in Beijing has obvious seasonal changes. Regularity, there are two peaks in the incidence from November to January and March to April, suggesting that the incidence is related to climate change.
Pathogenesis
On the basis of coronary atherosclerotic lesions, atherosclerotic plaque rupture, intravascular thrombosis, sub-arterial hemorrhage or persistent arterial spasm, resulting in persistent and complete occlusion of the lumen, leading to acute myocardial infarction .
1. Intracoronary thrombosis and myocardial infarction: The vast majority of acute myocardial infarction is caused by acute occlusion of the lumen on the basis of coronary atherosclerotic lesions, and the cause of this occlusion is mainly arteries. Thrombosis, recent studies have also confirmed that coronary artery acute thrombosis is the main cause of acute transmural myocardial infarction, when coronary atherosclerotic plaque rupture, its contents exposed, induce platelet aggregation, thrombosis and vasospasm Myocardial ischemia occurs when coronary blood flow is drastically reduced, and myocardial necrosis is caused by severe and long-lasting ischemia. In acute myocardial infarction, coronary thrombosis can be as high as 90%.
2. Coronary artery spasm and myocardial infarction: Coronary angiography was performed in 290 patients with myocardial infarction in Beijing Fuwai Hospital. It was found that 6.8% of patients showed normal coronary artery. Considering myocardial infarction caused by coronary artery spasm, the original coronary artery was not excluded. The thrombus is naturally dissolved, and persistent coronary artery spasm can cause acute myocardial infarction. Coronary artery spasm can also be caused by rupture of atheromatous plaque or subendocardial hemorrhage, induce platelet aggregation and release of thromboxane A2 and serotonin. Platelet aggregation and vasospasm can lead to thrombosis, resulting in acute myocardial infarction.
3, atherosclerotic plaque bleeding and ulcers and myocardial infarction: According to recent research, there are two ways of thrombosis after plaque rupture: one is the plaque surface erosion, the thrombus occurs at the rupture, which attaches to the surface of the plaque and blocks the blood vessels. Lead to myocardial ischemia and necrosis; and another type of thrombosis is the formation of thrombus in the deep rupture of the plaque, which gradually enlarges and blocks the blood vessels, causing acute myocardial infarction. In addition, atherosclerotic plaque can block the distal coronary artery branch and cause myocardial necrosis. .
4. Sympathetic excitation and myocardial infarction: stress, overwork, mental stress, etc. can stimulate sympathetic excitation, release catecholamines, induce myocardial infarction, and the possible mechanisms of catecholamine-induced myocardial infarction are as follows:
(1) Increased calcium influx in myocardial cells: increased myocardial contractility, increased myocardial oxygen consumption, and further damage to hypoxic myocardium.
(2) Catecholamine can damage myocardial cell mitochondria: reduce ATP production.
(3) Catecholamine excites alpha receptors: coronary vasoconstriction, beta receptor excitation, and increased heart rate, resulting in increased myocardial oxygen consumption and reduced oxygen supply.
(4) Increased plasma free fatty acid concentration: promote platelet aggregation, leading to vascular occlusion.
Pathophysiology
The pathophysiological changes of acute myocardial infarction are mainly manifested by some hemodynamic changes in ventricular involvement, electrophysiological instability and late ventricular remodeling.
1. Hemodynamic changes: The severity of hemodynamic changes in ventricular involvement depends primarily on the extent and location of the infarct.
(1) Left ventricular function: the coronary artery is interrupted by the forward blood flow, and the myocardial blood supply below the obstruction site loses the ability to contract, and the contraction cannot be completed. The myocardial in turn has four abnormal forms of contraction:
1 Motion synchronization imbalance, that is, the contraction time of adjacent myocardial segments is inconsistent.
2 contraction is weakened, that is, the range of myocardial contraction is reduced.
3 no contraction, that is, myocardial contraction is suspended.
4 abnormal, systolic bulging, and dysfunction at the infarction site, residual normal myocardial early hyperactivity, this is the result of acute compensation, including increased sympathetic nervous system activity and Frank-Starling mechanism, due to non-infarct segments Myocardial contraction causes abnormal movement in the infarcted area, so partial compensatory excessive exercise is ineffective. Excessive exercise in the non-infarcted area gradually disappears within 2 weeks of infarction, and some degree of contraction recovery occurs in the infarcted area, especially in the infarcted area. When there is reperfusion and the myocardial stagnation is relieved, the faster and more obvious these conditions appear.
Non-infarcted areas of AMI patients also often have a decline in systolic function, which may be related to the already existing non-infarcted coronary stenosis in the supply ventricle, and the newly occurring infarct-related arterial occlusion, resulting in loss of collateral blood supply in the non-infarcted area. The latter case is also called "distal ischemia". On the contrary, the presence of collateral circulation before MI can better prevent local systolic dysfunction in the occlusive arterial region, and early left ventricular ejection fraction after infarction. improve.
If myocardial ischemic injury is severe, left ventricular pump function declines; cardiac output, stroke output, blood pressure and dp/dt peak decrease; end-systolic volume increases, the latter is the most valuable predictor of mortality after AMI The index, the systolic period of a certain part of the ventricular muscle is abnormally expanded, further reducing the left ventricular stroke volume, but when the necrotic cardiomyocytes slide against each other, the infarct area is pulled and thinned and become longer, especially in patients with extensive anterior wall infarction. , leading to infarct extension, the first few hours to several days after infarction, local and whole ventricular muscle tension increased according to Laplace's law, in some patients, there is a vicious circle of further expansion of the left ventricle, degree of ventricular dilatation and infarct size, infarction The early and late opening of the relevant blood vessels is related to the activation of the local renin-angiotensin system in the non-infarcted area of the ventricle. The use of ACEI can effectively alleviate ventricular dilatation, even in the absence of symptoms of left ventricular dysfunction.
Over time, edema, cell infiltration and fibrosis occur in the ischemic necrosis site. This change can increase the hardness of the myocardium. The increase in the hardness of the infarct zone can prevent the contralateral movement of the wall during systole, thus helping to improve ventricular function.
Unless extremely severe myocardial infarction occurs, wall motion can be improved during the healing phase due to the gradual recovery of the stunned cell function, regardless of how long the infarction occurs, 20% to 25% of patients with left ventricular dysmotility It can show the hemodynamic signs of left ventricular failure.
Infarction and necrotic myocardium can change left ventricular diastolic function, increase left ventricular compliance first and then decrease, left ventricular end-diastolic pressure initially rises after a few weeks, end-diastolic volume increases, diastolic blood pressure begins to decline and tends to normal, just like myocardial necrosis As with systolic dysfunction, the extent of diastolic dysfunction is also related to the infarct size.
(2) Regulation of circulatory function: When the circulatory function of AMI is abnormal, and it occurs in the anatomical or functional stenosis of the coronary vascular bed, stenosis can lead to regional myocardial ischemia. If continuous development, MI can be formed. Infarct size reaches a certain level, will inhibit the entire left ventricular function, resulting in decreased left ventricular stroke volume and filling pressure, left ventricular stroke volume decreased significantly will eventually reduce aortic pressure and coronary perfusion pressure, which can aggravate the myocardium Ischemia causes a vicious circle, and the left ventricular emptying capacity is impaired to increase the preload, so that the part of the left ventricle with good perfusion function is expanded. This compensatory mechanism can restore the stroke volume to normal level, but make the ejection The score decreased, the left ventricle of the dilatation also increased the post-load, and the increase of the post-load not only inhibited the left ventricular stroke volume, but also aggravated myocardial ischemia. When the dysfunctional myocardial region was small and the rest of the left ventricle functioned normally, the compensatory mechanism It can maintain the function of the whole left ventricle. Once the left ventricle is mostly necrotic, although the remaining part of the ventricle is expanded, the whole left ventricular function is inhibited and cannot be maintained. Circulation pump failure occurred.
2, electrophysiological changes: infarcted myocardial cell edema, necrosis, inflammatory cell infiltration, etc. can cause ECG instability, atrial necrosis caused by ischemic necrosis, activation of ventricular intramuscular receptors, will increase sympathetic activity, increase The concentration of catecholamines in circulating blood and the amount of catecholamine released from the nerve endings in the heart, catecholamine release may also be directly caused by ischemic damage of sympathetic neurons, and the ischemic myocardial may cause arrhythmogenic effects on norepinephrine. Allergic reactions, and the effects of different concentrations of catecholamines in different parts of the ischemic myocardium are highly variable. Sympathetic stimulation of the heart can also increase the self-discipline of Purkinje fibers, and catecholamines accelerate calcium-mediated slow ions. Flow-reactive conduction, catecholamine stimulation of ischemic myocardium can induce arrhythmia by relying on these currents. In addition, transmural MI blocks the afferent and efferent branches of the distal sympathetic nerves that innervate the infarcted area, and, in addition to autonomic nerves In addition to coordinating changes in various cardiovascular reflexes, imbalances in regulation can contribute to arrhythmia This may explain why blockers also effective in treating ventricular arrhythmias, ventricular arrhythmias in effect when accompanied by other manifestations of hyperactivity increased adrenergic particularly evident.
Ventricular enlargement after AMI, remodeling is easy to cause ventricular depolarization inconsistency and reentry, leading to fatal arrhythmia, electrolyte imbalance such as hypokalemia, hypomagnesemia, acidosis will increase the concentration of free fatty acids in the blood, resulting oxygen free Base can also cause arrhythmia, the severity of these lesions, the size of the infarct size and the state of infarct-related arterial perfusion determine the risk of severe arrhythmia in patients - primary ventricular fibrillation (ie, ventricular fibrillation occurs in non-congestive heart) In the event of failure or cardiogenic shock).
3. Ventricular remodeling: After myocardial infarction, the left ventricular size, geometry and thickness of the infarcted and non-infarcted segments have changed. These changes are collectively referred to as ventricular remodeling. The remodeling process includes infarct expansion and ventricular enlargement. Can affect ventricular function and prognosis, ventricular load status and infarct-related arterial patency is an important factor affecting left ventricular dilatation, elevated ventricular pressure can lead to increased wall tension and risk of infarct expansion; and infarct-related artery patency can accelerate scarring Formation increases the filling of the infarcted tissue and reduces the risk of infarct expansion and ventricular dilatation.
(1) Infarct expansion: acute expansion of the infarct area, which cannot be explained by additional myocardial necrosis, and thinning makes the increase of the infarct area called infarct expansion. The reason is that the sliding between the muscle bundles reduces the room of the entire thickness. Number of parenchymal cells; rupture of normal cardiomyocytes; loss of tissue in the necrotic area, characterized by disproportionate thinning and dilatation of the infarcted area, and then the formation of a strong fibrotic scar, the extent of infarct expansion is related to the thickness of the wall before infarction, Previous cardiac hypertrophy prevents myocardial thinning, and the apical wall is the thinnest, which is the most vulnerable to infarct expansion.
The occurrence of infarct expansion not only increased the mortality rate, but also the incidence of non-fatal complications such as heart failure and ventricular aneurysm was significantly increased. More than 3/4 of patients who died of AMI had myocardial infarction expansion, 1/3 ~2/3 is the anterior ST-segment elevation infarction. Echocardiography is the best method for diagnosing infarct expansion. The ventricular free extension zone can be found. When the expansion is severe to a certain extent, the most typical clinical manifestation is There is a loud running horse, as well as pulmonary congestion or deterioration of the original pulmonary congestion, which is the most serious consequence of infarct expansion.
(2) Ventricular dilatation: In addition to infarct expansion, the expansion of the ventricular survival part is also associated with remodeling. Ventricular dilation begins immediately after the infarction, and may continue for several months or even years after the expansion of the non-infarcted area. Considered as a compensatory mechanism for maintaining stroke volume for a wide range of infarctions, the additional burden on residual functional myocardium may be responsible for cardiac hypertrophy. Hypertrophic myocardium may help to compensate for functional damage caused by infarction. Some patients are The hemodynamic improvement seen in the months after MI is due to this, the surviving myocardium is finally damaged, leading to further myocardial expansion, myocardial global dysfunction, and finally heart failure, although the spherical expansion of the non-infarcted area can be partially Compensatory maintenance of cardiac function, but also makes the myocardial depolarization tend to be inconsistent, making patients prone to fatal arrhythmias.
The basis of myocardial remodeling is the phenotypic change, which is mainly caused by the re-expression of embryonic genes caused by pathological stimulation, which leads to rapid myocardial growth to compensate for the increase of myocardial load after myocardial infarction and the increase of myocardial mass. Partly due to cardiomyocyte hypertrophy, however, the quality of these proteins does not meet the requirements of adult myocardium, eventually leading to myocardial dysfunction, another consequence of changes in gene expression is collagen deposition, causing diffuse interstitial fibrosis, perivascular fibers And focal repair fibrosis, which leads to decreased myocardial compliance and diastolic dysfunction. Perivascular fibrosis affects coronary compliance, reduces coronary reserve, and causes myocardial ischemia. In addition, Fibrosis may also contribute to ventricular arrhythmias, which are living tissues and contain living cells. Therefore, fibroblasts can continue to secrete collagen, and macrophages can continue to phagocytose these collagens, which consume large amounts of oxygen. , energy and nutrition, which leads to the lack of corresponding substances in the working myocardium, these Su resulted in cardiac disorder constantly death and ventricular systolic function.
There is a lack of blood vessels in the reconstructed myocardium, further reducing the supply of oxygen and nutrients to viable cardiomyocytes, and promoting progressive cell death and remodeling. Cardiomyocyte hypertrophy also leads to a relative decrease in mitochondrial density, resulting in energy production. Insufficient and myocardial dysfunction.
Remodeled myocardium also has Ca2 transport disorder, which is caused by the relative reduction of sarcoplasmic reticulum, Ca2 channel and Ca2 pump. The quality of Ca2 transporter has also decreased due to changes in gene expression, which also promotes myocardial dysfunction.
A feature of myocardial remodeling is the conversion of actin to slow-moving isomers, which causes myocardial contraction to slow down and cause myocardial dysfunction; another important feature is cardiomyocyte necrosis and apoptosis, which can lead to fibrosis. The remodeling is aggravated because the lost cells are replaced by collagen to avoid gaps in the myocardium.
In summary, ventricular remodeling is a complex process that begins after an acute onset and can continue for months or years, such as early recanalization of the occluded coronary artery, reduction of infarct size, nitrate and angiotensin transformation. The use of enzyme inhibitors can reduce the pressure of ventricular expansion in the early stage of infarction, and can play a beneficial role in ventricular dilatation.
Prevention
Acute myocardial infarction prevention
Because epidemiological data show that coronary heart disease is one of the most important diseases causing human death, and there is still no radical measures in clinical practice, it is of great significance for the active prevention of coronary heart disease. The prevention of coronary heart disease involves In the primary prevention and secondary prevention, primary prevention refers to taking measures to control or reduce the risk factors of coronary heart disease in people who have not suffered from coronary heart disease to prevent disease and reduce the incidence rate. Secondary prevention means Patients with coronary heart disease take medicinal or non-pharmacological measures to prevent recurrence or prevent exacerbations.
1. First-level preventive measures
Primary prevention measures for coronary heart disease include two situations:
(1) Health education: educate the whole population on health knowledge, improve citizens' self-care awareness, avoid or change bad habits, such as quitting smoking, paying attention to reasonable diet, exercising properly, maintaining psychological balance, etc., thereby reducing the incidence of coronary heart disease.
(2) Control high-risk factors: for high-risk groups of coronary heart disease, such as hypertension, diabetes, hyperlipidemia, obesity, smoking, and family history, etc., positive treatment, of course, some of these risk factors can be controlled Such as high blood pressure, hyperlipidemia, diabetes, obesity, smoking, less active lifestyle, etc.; and some can not be changed, such as family history of coronary heart disease, age, gender, etc., including the use of appropriate drugs for continuous control Blood pressure, correct abnormal blood lipid metabolism, limit smoking, limit physical activity, control physical activity, control weight, control diabetes, etc.
2, secondary prevention measures
The secondary prevention content of patients with coronary heart disease also includes two aspects. The first aspect includes the content of primary prevention, that is, the risk factors of various coronary heart diseases should be controlled. The second aspect is to use drugs that have been proven effective. To prevent the recurrence of coronary heart disease and the exacerbation of the disease, the drugs that have been confirmed to have preventive effects are:
(1) Antiplatelet drugs: A number of clinical trials have confirmed that aspirin can reduce the incidence of myocardial infarction and reinfarction rate. The use of aspirin after acute myocardial infarction can reduce the reinfarction rate by about 25%; if aspirin can not tolerate Or allergic, clopidogrel can be used.
(2) -blockers: as long as there are no contraindications (such as severe heart failure, severe bradycardia or respiratory diseases, etc.), patients with coronary heart disease should use beta blockers, especially in the occurrence of acute coronary After the arterial event; there are data showing that the use of beta blockers in patients with acute myocardial infarction can reduce the mortality and reinfarction rate by 20% to 25%. The drugs available are metoprolol, propranolol, Thiolol and so on.
(3) ACEI: used in patients with severe impairment of left ventricular function or heart failure, many clinical trials (such as SAVE, AIRE, SMILE and TRACE, etc.) have confirmed that ACEI reduces mortality after acute myocardial infarction; Therefore, after acute myocardial infarction, patients with ejection fraction <40% or wall motion index 1.2, and no contraindications should use ACEI, commonly used captopril, enalapril, benazepril and blessing Simplice and so on.
(4) statin lipid-lowering drugs: the results of studies from 4S, CARE and recent HPS show that long-term lipid-lowering therapy for patients with coronary heart disease not only reduces the overall mortality rate, but also improves the survival rate; and requires coronary intervention The number of patients with CABG is reduced, which is due to the improvement of endothelial function, anti-inflammatory effects, effects on smooth muscle cell proliferation and interference with platelet aggregation, blood coagulation, fibrinolysis and other functions, simvastatin, and deforestation. Statins, fluvastatin, and atorvastatin all have this effect.
In addition, coronary angiography has coronary atherosclerotic mild stenotic lesions and clinically no ischemic symptoms, although it is not clearly diagnosed as coronary heart disease, it should be regarded as a high-risk group of coronary heart disease, giving active prevention, Long-dose aspirin can also be given for a long time, and risk factors such as dyslipidemia and hypertension can be eliminated.
Complication
Acute myocardial infarction complications Complications, arrhythmia, heart failure, cardiogenic shock, papillary muscle dysfunction and fracture
Complications and treatment
Common complications of AMI include: arrhythmia, heart failure, cardiogenic shock, papillary muscle dysfunction and rupture, ventricular septal perforation and ventricular free wall rupture, ventricular aneurysm formation, thrombosis and embolism, and post-infarction syndrome. Timely diagnosis and treatment of complications is one of the important links to reduce hospital mortality and improve prognosis.
Symptom
Symptoms of acute myocardial infarction Common symptoms Chest tightness Myocardial necrosis Extensive chest pain Chest tightness Hemorrhoids Cardiopulmonary embolism Atrial ventricular contraction... Myoglobin high tachycardia surgery is no longer bleeding Myocardial cell turbidity
Clinical manifestation
1, aura symptoms
About 2/3 of patients with acute myocardial infarction have aura symptoms a few days before onset, most commonly angina pectoris, followed by upper abdominal pain, chest tightness, numbness, upper limb numbness, dizziness, palpitation, shortness of breath, irritability, etc., half of which is central angina pectoris. The other half of the original angina, sudden onset or increased pain, prolonged duration, incentives are not obvious, nitroglycerin efficacy is poor, angina pectoris accompanied by nausea, vomiting, sweating, tachycardia, acute cardiac insufficiency, severe heart rhythm Abnormalities or blood pressure have large fluctuations, while ECG shows that the ST segment is obviously elevated or depressed for a while, and the T wave is inverted or increased. It should be alert to the possibility of myocardial infarction in the near future, and find aura, timely and active treatment, which may cause some patients to avoid A myocardial infarction has occurred
2, the symptoms of the attack
(1) Pain: It is the first and most prominent symptom in acute myocardial infarction. The typical site is the back of the sternum until the pharynx or in the anterior region. It is radiated to the left shoulder and the left arm. The pain is sometimes in the upper abdomen or xiphoid. At the same time, the posterior part of the lower sternum is often discomfort, or accompanied by nausea and vomiting. It is common in the inferior myocardial infarction. The atypical part has a right chest, mandible, neck, teeth, rare head, lower extremity thigh and even toe pain. The pain is Squeezing or pressure pain, or a feeling of tightness, burning pain, often accompanied by irritability, sweating, fear, or sudden death, often lasting more than 30 minutes, even up to 10 hours, rest and Nitroglycerin is generally not relieved.
A small number of patients with acute myocardial infarction have no pain, but with cardiac dysfunction, shock, sudden death and arrhythmia as the first symptoms. No pain symptoms can be seen in the following cases:
1 patient with diabetes.
2 elderly people.
3 patients with acute myocardial infarction after surgical anesthesia recovery.
4 patients with cerebrovascular disease.
5 dehydration, acidosis of patients.
(2) systemic symptoms: mainly fever, accompanied by tachycardia, increased white blood cells and increased erythrocyte sedimentation rate, due to the absorption of necrotic substances, usually occurs 24 to 48 hours after the occurrence of pain, the degree is often positively correlated with the infarct size The body temperature is generally above and below 38 ° C, rarely exceeding 39 ° C for about 1 week.
(3) Gastrointestinal symptoms: Frequent pain is accompanied by frequent nausea, vomiting and upper abdominal pain, and vagus nerve is affected by necrotic myocardial stimulation and decreased cardiac output, tissue perfusion, etc. Intestinal flatulence is not uncommon, severe A hiccup can occur.
(4) arrhythmia: seen in 75% to 95% of patients, mostly occurred within 1 to 2 weeks of onset, and most commonly within 24 hours, may be associated with fatigue, dizziness, fainting and other symptoms, ventricular arrhythmia is most common , especially ventricular premature beats, if ventricular premature beats frequently (5 times / min or more), pairs appear or short ventricular tachycardia, multi-source or fall in the previous heart beat During the period (RonT), it is often indicated that ventricular tachycardia or ventricular fibrillation is about to occur. Some patients have ventricular fibrillation, which can cause sudden cardiac death. Accelerated ventricular autonomic rhythm also occurs from time to time. Ventricular block and bundle branch block are also more common, severe cases may be complete atrioventricular block, supraventricular arrhythmia is less common, mostly in heart failure, anterior wall myocardial infarction is prone to occur Ventricular arrhythmia; inferior myocardial infarction prone to atrioventricular block; ventricular anterior wall myocardial infarction if atrioventricular block, indicating a wide range of infarction, and often accompanied by shock or heart failure, so the situation is serious, the prognosis is more difference.
(5) hypotension and shock: blood pressure is common in the pain period, if the performance of no microcirculatory failure can only be called hypotension, such as pain relief and systolic blood pressure is still less than 80mmHg, the patient is restless, pale, cold skin The pulse is fine and fast, sweating is dripping, the amount of urine is reduced (<20ml/h), the consciousness is slow, and even the fainting is the performance of shock. The shock occurs within a few hours to one week after the onset, and is seen in 20%. The patient, mainly cardiogenic, is caused by extensive myocardial necrosis (40% or more) and a sharp decrease in cardiac output. Peripheral vasodilation caused by nerve reflex is a secondary factor. Some patients still have factors of insufficient blood volume. Severe shock can die within a few hours, usually lasting hours to days, and can occur repeatedly.
(6) Heart failure: the incidence rate is 30% to 40%. At this time, the general left ventricular infarction range is >20%. The myocardial contractility is significantly weakened after infarction, the ventricular compliance is reduced and the myocardial contraction is not coordinated, mainly acute. Left heart failure can occur in the first few days of the onset or in the pain, shock improvement phase, or sudden pulmonary edema is the initial manifestation, the patient has chest tightness, asphyxiating dyspnea, sitting breathing, coughing, coughing white or Pink foam sputum, sweating, cyanosis, irritability, etc., severe cases can cause jugular vein engorgement, liver enlargement, edema and other manifestations of right heart failure, right ventricular myocardial infarction can appear right heart failure at the beginning, with blood pressure drop .
3, signs
According to the size of the infarction and the presence or absence of complications, the infarction range is small and there is often no abnormal signs, and the left ventricular cardiomyocytes irreversible damage >40% of patients often have severe left heart failure, acute pulmonary edema and Cardiogenic shock.
(1) Vital signs:
1 Sense: small-scale myocardial infarction patients, or painless myocardial infarction, conscious can be clear; severe painful irritability, fear, etc.; patients with shock can be slow, even fainting; patients with pulmonary infarction may appear confused, Drowsiness, paralysis; concurrent cerebrovascular accident or sudden cardiac arrest, can appear coma.
2 blood pressure: within half an hour after onset, the patient presented with autonomic dysfunction, anterior wall infarction showed sympathetic hyperactivity, heart rate increased to 100 times / min, blood pressure can be increased to <160/100mmHg (21.28/13.3 kPa); If the cardiac output is significantly reduced, the blood pressure is significantly reduced, and the inferior wall infarction is mostly parasympathetic hyperactivity, such as heart rate slowdown, <60 beats/min, lower blood pressure, systolic blood pressure <100mmHg (13.3 kPa), and later with the heart muscle The use of necrosis and/or vasodilators, blood pressure will be lower in almost all patients with reduced blood pressure, bradycardia, tachycardia, cardiogenic shock or right ventricular infarction, and concurrent cerebrovascular accidents. After this blood pressure is lowered, it can no longer return to the pre-infarction level.
3 body temperature: most patients after infarction have low fever (about 38 °C), this is the systemic reaction caused by myocardial necrosis absorption, more than 3 to 4 days, usually within 1 week, self-resolved, after 1 week, the body temperature is still high may for:
A. Reinfarction or infarction extension;
B. Concurrent infection.
4 Respiratory: Most patients with acute myocardial infarction breathe faster, mainly due to pain, anxiety and stress stimulating sympathetic hyperactivity, acute left heart failure with pulmonary edema, or acute myocardial infarction complicated with acute pulmonary embolism, shock, breathing Up to 40 ~ 50 times / min; concurrent cerebrovascular accident can be seen in tidal breathing, Chen Shi breathing or Biot breathing, morphine, pethidine can have respiratory depression.
5 pulse: the pulse of myocardial infarction can be normal, increase or slow down, the rhythm is neat, the alternating pulse can occur in severe left heart failure, there may be intermittent during the contraction, the pulse can not touch the shock, and the ventricular flutter occurs. When the movement, ventricular fibrillation or electromechanical separation, the pulse disappears.
(2) Cardiac signs: mainly depends on the scope of myocardial infarction and the presence or absence of complications, the infarct size is not large, no positive signs can be found without complications, and when the pre-cardiac area is full, it is suggested that there is a large amount of pericardial effusion, neck Intermittent large pulse wave of the vein suggests a one- or three-degree atrioventricular block, such as a large infarct size, enlarged wall, multiple infarction, and hypertension or heart failure, the heart expands to the left, the apex beats, often Touching the pre-systolic filling wave (A wave), consistent with the auscultation of the fourth heart sound (S4) time, early left ventricular diastolic rapid filling wave, consistent with the third heart sound (S3) time, not often able to touch, large Anterior wall transmural infarction often hits the early, middle or late systolic pulsation in the most prominent apical pulsation. This dysfunctional region persists until 8 weeks after the onset of infarction, indicating the presence of apical anterior ventricular aneurysm. The newly appearing systolic tremor on the left sternal border suggests ventricular septal perforation, which touches the sensation of friction in the anterior region, suggesting pericarditis, and the percussion heart can be normal or mild to moderately enlarged.
Auscultation of the first heart sound (S1) of the apex is reduced. About one-fourth of the patients may have left ventricular dp/dt due to the presence of atrioventricular block or large infarction, and there are often aortic areas in patients with hypertension. 2 heart sound (S2) hyperthyroidism, aortic valve calcification is obvious, S2 can be metallic, S2 reverse division, suggesting complete left bundle branch block or left heart failure; S2 wide division, suggesting complete right bundle branch conduction resistance Stagnation, cannon sound, suggesting a third degree of atrioventricular block, atrial or systolic before the galloping in almost 24 hours of the onset of the majority of patients can be heard, due to acute myocardial ischemia and infarction, ventricular compliance Lower, left lateral position, bell-shaped stethoscope auscultation is the clearest, but patients who are too obese or patients with chronic obstructive emphysema are not easy to hear clearly, the ventricular gallbladder is more than atrial or systolic before the horse is Rarely, it is often a severely damaged myocardium, an indication of heart failure, indicating an increase in pulmonary diastolic blood pressure or left ventricular end-diastolic pressure, ventricular anterior infarction with ventricular gallbladder is less than this diastolic extra tone, increased mortality 1 times, the ventricular galloping mostly disappeared within a few days. Patients while S3 and S4 were four temperament.
Pericardial friction sounds appear in the onset of 2 to 5 days, due to fibrinous pericarditis outside the infarction, often without obvious pericardial effusion, seen in 10% to 15% of patients, mostly a wide transmural myocardial infarction, With a membrane-type stethoscope, the patient's seat is slightly pressed forward, and the patient's sitting position is most clearly heard. The friction sound is affected by the breathing, and some are strengthened during inhalation, while others are strengthened during exhalation, which is like leather scratching or squeaking. Confused with mitral regurgitation caused by papillary muscle dysfunction, frictional sounds are sometimes heard in a wide pre-cardiac region, sometimes only at the left sternal border, sometimes for a few days, or disappear for a short time, the appearance of frictional sounds Need to differentiate with pulmonary embolism, such as pericardial friction sound began to appear 10 days after the onset, should consider the possibility of post-infarction syndrome.
Rough systolic murmurs appearing in the apex of the apex, or accompanied by middle and late contraction of the apex, suggesting papillary muscle dysfunction or chordae rupture, mostly caused by dysfunction of the mitral valve caused by papillary muscle dysfunction, about 55% The patient is caused by ischemia or necrosis of the papillary muscles, and the miscellaneous sound is changeable. When the time is strong or weak, the murmur of the papillary muscle dysfunction is sprayed, often full systolic murmur, which is most obvious at the apex. The lobes are radiated to the left sternal border or aortic region, which is easily confused with ventricular septal perforation or aortic stenosis. For example, the anterior flap is significantly involved in the murmur, often radiating to the back, thoracic or cervical vertebrae, and the anterior papillary muscle has a double crown. Arterial blood supply, the posterior valve papillary muscle only a single coronary artery blood supply, so the latter is more affected than the former, papillary muscle dysfunction caused by mitral regurgitation, most of the no hemodynamic importance, papillary muscle rupture similar The murmur immediately occurred pulmonary edema, and the newly developed systolic rough murmur between the 3 to 4 ribs on the left sternal border suggested a septal perforation.
(3)
Examine
Q QS 24h
1
2T
3Q
4
1
1A.(creatine kinaseCK)(creatinephosphokinaseCPK)CK 360h 1224h 34 CK 92%85%CK CK
2
(lactic dehydrogenaseLDH)LDH 2048h 35 814 LDH 23 LDH
LDH LDH 5 LDH15LDH2>LDHl>LDH3>LDH4>LDH5LDH1LDH1 LDH2LDH1LDH 824h LDH1 LDH1/LDH21 LDHl/LDH>0.5LDHl LDH LDHl/LDH2l LDHl/LDH>0.5
3--(-hydroxy-butyric dehydrogenase-HBDH)-HBDH 1224h 23 1014 HBDH -LDH LDH LDH
4(aspartic transaminaseAST)AST 612h 1836h 35 AST
2
1(cardiac troponinCTn)CTnCTnCTnICTnT CTnC CTnT CTnICTn CK-MBLDH CTn CTn CTnTCTnI
2(myoglobinMb)Mb 14h 48h 24h Mb Mb CK-MB Mb CK-MB CK-MB CK-MB
3
1(Iight chain cardiacmyosinCM-LC)46h 1512 CM-LC CM-LC CK
2(fatty acid binbing pro-teinFABP)Mb FABP13h510h1224hFABPCK-MBMbCK-MBMb99%FABPFABP1hCK-MBCTnTFABP
3BB(glyc-ogen phosphorylase BBGPBB)14hCKCK-MB 12GPBB4h CKCK-MBMb CT-nTCK-MB
4(alpha-actin) 1h510
112(1020)×l09/L24 0.750.901 1
212 23
365%100%
48
51h 24h40h
Diagnosis
diagnosis
1
2QQS24hTQ
3(CPK-MBLDH)
(1)()QSTT
(2)24h
()TSTSTSTQST-T
Differential diagnosis
1MI;;AMI;;XAMI()MI5%10%
2AMI;;(T);STTSTTSTMISTTSTAMISTQT
3AMI24h;2;AMISQTSQaVFTQ;(LDH1)(cPK-MB)
4STAMI;AMI25;STQ;;AMI
5AMI()()
630%75%()HammanXXX
