Atherosclerosis and Coronary Atherosclerotic Heart Disease
Atherosclerosis is the most common and important type of arteriosclerosis. It is characterized by the lipid infiltration of the intima of the affected arteries, the accumulation of complex sugars followed by fibrous tissue hyperplasia and calcium deposition, as well as lesions in the middle layer of the artery.
The disease mainly affects large and medium-sized muscle-elastic arteries, which are more common in the aorta, coronary arteries and cerebral arteries, often leading to serious consequences such as occlusion of the lumen or rupture of the wall of the vessel.
Atherosclerosis is more common in men over 40 years of age and postmenopausal women. The disease is often accompanied by hypertension, hypercholesterolemia or diabetes. Mental workers are more common, and they are very harmful to people’s health, which is one of the main causes of illness and death in the elderly.
Cause of Atherosclerosis
Although the cause of atherosclerosis is not fully understood, it is known to be closely related to the following factors (susceptibility factors):
1. The clinical and autopsy data of hypertension showed that the incidence of atherosclerosis in patients with hypertension was significantly increased. This may be due to the particularly high pressure on the arterial wall during high blood pressure, damage to the intimal layer and endothelial cell layer, low density lipoprotein easily enters the arterial wall, and stimulates smooth muscle cell proliferation, causing atherosclerosis.
2. Hyperlipidemia: Clinical data show that atherosclerosis is common in hypercholesterolemia. High cholesterol diet in experimental animals can cause atherosclerosis.
Recent studies have found that the increase in low density lipoprotein and extreme density lipoprotein and the decrease in high density lipoprotein are related to atherosclerosis.
The increase of triglyceride in blood is also related to the occurrence of atherosclerosis. Recent studies have found that lipoprotein a [Lp (a)] is closely related to the occurrence of atherosclerosis.
3. Smoking: The concentration of carboxyhemoglobin in the blood of smokers can reach 10-20%, insufficient oxygenation in the arterial wall, increased fatty acid synthesis in the intimal layer, reduced release of prostacyclin, and platelets are easy to adhere to the arterial wall.
In addition, smoking can reduce the amount of high-density lipoprotein in the blood and increase the serum cholesterol content, which can lead to atherosclerosis.
Further, the nicotine contained in smoke during smoking can directly affect the heart and coronary arteries and cause arterial spasm and myocardial damage.
4. Diabetes: Diabetes is often accompanied by hypertriglyceridemia or hypercholesterolemia. If accompanied by hypertension, the incidence of atherosclerosis is significantly increased.
Diabetics also often have elevated blood factor IX and platelet activity. Factor IX is produced by cells in the arterial wall. An increase in this factor indicates endometrial disease.
Increase in platelet activity makes it easier to accumulate on the arterial wall, accelerates atherosclerotic thrombosis and causes occlusion of the arterial lumen.
Recent studies suggest that insulin resistance has close relation to the occurrence of atherosclerosis.
Patients with type 2 diabetes often have insulin resistance and hyperinsulinemia with coronary heart disease.
5. Obesity is also a risk factor for atherosclerosis. Obesity can lead to an increase in plasma triglyceride and cholesterol levels. Obese people are often accompanied by hypertension or diabetes.
In recent years, studies have shown that obese people often have insulin resistance, and the incidence of atherosclerosis has increased significantly.
Pathogenesis of Atherosclerosis
There are many theories of the pathogenesis of atherosclerosis, such as the theory of lipid infiltration, the theory of thrombosis, the theory of hemodynamics, the theory of hyperplasia of smooth muscle cells, the theory of endometrial injury and the theory of receptors.
The pathogenesis is complex and is a comprehensive long process. Endothelial injury of the arterial wall is the initiating factor of atherosclerosis.
Arterial wall endothelial cells have important physiological functions such as regulating vascular tone, vascular permeability, antithrombotic and secreting various active substances.
Endothelial cells can be stimulated by certain factors such as hypertension, hypercholesterolemia, angiotensin II, epinephrine, norepinephrine, bradykinin and reduced blood oxygen saturation in the blood.
Endothelial damage: Damaged endothelial cells undergo functional changes and increased permeability.
Monocytes in the blood adhere to endothelial cell lesions and enter the endothelium, phagocytosing lipids into foam cells, and forming fatty plaques.
Platelets aggregate and adhere to the lesions of the endothelium.
Phagocytic cells, endothelial cells, and platelets adhering to endothelial cell injury release growth factors to stimulate smooth muscle cells to enter the intima and proliferate, fatty plaques become fibrous plaques.
The permeability of injured endothelial cells changes, and the low density of plasma and very low-density lipoprotein enters the intima more, causing atherosclerosis.
Recent studies have shown that lipid peroxidation plays an important role in the occurrence of atherosclerosis.
Free radicals in the body are chemically modified by low-density lipoprotein (LDL).This produces peroxidized LDL, which has a damaging effect on endothelial cells, and can inhibit the synthesis of PGI2 (prostacyclin I2). The modified LDL can be taken up by monocytes-macrophages or smooth muscle cells through specific receptors, making cells Lactone esters increased significantly.
Clinical Manifestations of Atherosclerosis
This is mainly determined by the degree of ischemia of the vascular lesions and the affected organs. Aortic atherosclerosis is often asymptomatic.
Coronary atherosclerosis can cause angina pectoris, myocardial infarction, and arrhythmia if the diameter of the stenosis is more than 75% Sudden death.
Cerebral arteriosclerosis can cause cerebral ischemia, brain atrophy, or cause cerebral vascular rupture and bleeding. Renal atherosclerosis often causes nocturia, refractory hypertension, and severe renal dysfunction.
Mesenteric atherosclerosis can manifest as symptoms such as abdominal pain and blood in the stool after a full meal.
Lower limb atherosclerosis causes severe stenosis of the blood vessel lumen, intermittent claudication, dorsal foot artery pulsation disappears, and severe gangrene may even occur.
Laboratory and other inspections Atherosclerosis
Patients often have elevated blood cholesterol and triglycerides, reduced high-density lipoproteins, and abnormal lipoprotein electrophoretic patterns. Most patients present with type III or type IV hyperlipoproteinemia.
X-ray examination shows aortic elongation, dilation and distortion, and sometimes calcium deposits.
Arteriography can show stenosis, lesions and areas of the limb arteries, renal arteries, and coronary arteries due to atherosclerosis. Doppler ultrasound can help determine the smooth blood flow of the arteries of the limbs and the renal arteries.
Diagnosis of Atherosclerosis and Coronary Atherosclerotic Heart Disease
Patients over 40 years of age may have aortic atherosclerosis if the aorta is widened and distorted and other diseases can be ruled out.
If there is a sudden appearance of dizziness or unstable gait without signs of increased intracranial pressure, they should be suspected. Insufficient cerebral blood supply caused by basal atherosclerosis.
Short-term sternal or anterior cardiac pain or oppression after exercise may be suspected of insufficient coronary blood supply.
Nocturia is often an early symptom of renal atherosclerosis one. In addition, patients are often accompanied by atherogenic risk factors such as hypertension, hypercholesterolemia, low HDL, diabetes and smoking.
Diagnosis tools such as selective electrocardiogram, radionuclide heart, brain, kidney and other organ scans, doppler ultrasound, and selective angiography, etc., help clear diagnosis.
Differential Diagnosis of Atherosclerosis
Clinically, it is often necessary to consider the distinction between inflammatory arterial disease (such as multiple arteritis, thrombotic occlusive vasculitis, etc.) and congenital arterial stenosis (such as aorta, renal artery stenosis, etc.).
Inflammatory arterial diseases usually have low fever, rapid erythrocyte sedimentation, and other inflammatory manifestations.
Congenital aortic constriction is at a younger age and is not associated with susceptible factors for atherosclerosis.
Treatment and Prevention of Atherosclerosis
A. General Treatment
(1) Reasonable diet: The total calories in the diet should not be too high to prevent overweight, and should avoid eating too much animal fat and cholesterol-rich foods, such as fatty meat, cream, liver, brain, kidney and other internal organs and bone marrow, roe, egg yolk , Coconut oil, etc.
Overweight people should reduce total daily calories and limit sugar foods.
The diet should be light, eat more vitamin-rich vegetables, fruits, and protein-rich foods, such as lean meat, beans and their products, and try to use soybean oil, vegetable oil, sesame oil or corn oil as edible oil.
(2) Persist in proper physical activity: The amount of physical activity should be determined according to the original physical condition. It should be done step by step. It should not be forced to do strenuous exercise. For the elderly, it is recommended to take a walk to do health gymnastics, Tai Chi and meditation.
(3) Reasonable arrangement of work and life: Pay attention to the combination of work and rest, the law of life, and maintain a happy mood.
(4) Others promote non-smokers and drink a small amount of alcohol.
B. Controlling susceptibility factors
I. Antidiabetic drugs
If you have diabetes, you should promptly control blood sugar, including diet control. Antidiabetic drugs for type II diabetes should be suitable such as Damekang, etc. If there is high blood pressure, antihypertensive drugs should be given to reduce blood pressure to an appropriate level. If blood cholesterol is increased, it should be controlled High cholesterol is appropriately given to lipid-lowering drugs.
II. Lipid-lowering drugs
(1) Cholestyramine is an anion exchange resin, which is combined with bile acid after taking it to increase the excretion of cholesterol and bile acid and reduce blood cholesterol.
Dosage: 4-5g, orally, 3 times a day, side effects, gastrointestinal response is more obvious.
(2) Atromide (clofibrate) lowers plasma triglyceride than cholesterol, and its main effect is to inhibit the synthesis of triglyceride.
Usage: 0.25-0.5g, orally, 3-4 times a day, side effects, in addition to nausea, diarrhea, and can cause liver damage, serum GPT increased, so liver function should be checked regularly when taking it. Antomin derivative fenofibrate 0.1g orally, 3 times a day.
Nuo Heng 300mg orally, 3 times a day can maintain the lipid-lowering effect, and the side effects are significantly reduced.
(3) Nicotinic acid can reduce cholesterol and triglycerides. It mainly reduces cholesterol by inhibiting the liver from producing very low-density lipoprotein and converting it into low-density lipoprotein into the blood circulation.
Dosage: 0.5-1g, orally, each 3 times a day. After taking it, there are often side effects such as skin flushing, itching, or gastrointestinal reactions, which can cause increased blood uric acid, increased blood sugar and liver damage. Therefore, it should be taken at meals, starting with small doses (0.1-0.2g), gradually gradually Increase, and regularly check liver function, blood sugar and blood uric acid.
After being absorbed, Inositol Hexanicotinate gradually hydrolyzes out niacin in the body and plays a role. Usage: 0.2-0.4g, taken orally, 3 times a day, with fewer side effects, but the blood lipid regulating effect is also lower than that of niacin.
(4) Unsaturated fatty acids are high in edible corn oil, soybean oil and safflower oil, which can inhibit the absorption of lipids in the small intestine and the reabsorption of bile acids, thereby reducing the synthesis of cholesterol. The clinically used compounds mainly based on ethyl linoleate are Yishouning, Xuezhiping and Xinmaile.
(5) Sodium alginate diester can significantly reduce triglyceride and cholesterol, can inhibit the deposition of arterial wall lipids and connective tissue proliferation, and can inhibit thrombin activity and platelet aggregation.
(6) Chinese herbal medicines such as diarrhea, tea tree roots, evening primrose and pollen all have the function of reducing cholesterol and triglycerides.
III. Antiplatelet Drugs
(1) Aspirin The combination of acetyl and cyclooxygenase can inhibit arachidonic acid into prostaglandin H2 and G2, so that platelets cannot produce TXA2, but it also inhibits arterial wall production. PGI2, if aspirin is used in a small dose (0.1g / day), it can reduce platelet aggregation and slightly affect the production of PGI2.
(2) Pansentin can inhibit adenosine from entering platelets, increase the adenosine monophosphate in platelets, and prolong platelet life. If used in combination with aspirin, it has a synergistic effect on inhibiting platelet aggregation.
Dosage: 25-50mg orally, daily 3 Times.
(3) Ticlid has an inhibitory effect on platelet aggregation, which is stronger than aspirin. Usage 250mg, orally, once a day, suitable for atherosclerosis and arterial circulation disorders caused. Should be taken short-term, those who have bleeding tendency do not need to.
IV. Other Treatment Drugs
Lovastatin is a competitive inhibitor of the rate-limiting enzyme methyl glutaryl coenzyme A (HMG, COA) reductase in the cholesterol synthase system. It is currently an effective and safe drug for lowering serum cholesterol.
Metoprolol can not only lower blood pressure, but also prevent the occurrence of atherosclerosis by inhibiting the combination of LDL and arterial wall proteoglycans. Probucol can not only reduce LDL cholesterol, but also can prevent the oxidative modification of LDL, reduce the uptake of monocyte macrophages, prevent the formation of foam cells, and have a better anti-atherosclerotic effect due to its antioxidant effect.
Coronary Atherosclerotic Heart Disease
The clinical manifestations are different due to the different coronary artery lesions, the degree of lumen stenosis, the number of involved blood vessels, and the formation of collateral circulation.
According to the characteristics of clinical manifestations, there are the following types:
1. Angina pectoris acute transient myocardial ischemia, hypoxia caused paroxysmal posterior or anterior cardiac pain. According to the cause of the onset of the disease, it can be divided into: labor and spontaneity; according to whether the disease is stable, it can be divided into stable and unstable angina.
2. Myocardial infarction, acute occlusion of coronary lumen, interrupted blood flow, ischemic necrosis of local myocardium, clinical manifestations may have severe long-term sternal or anterior cardiac pain, shock, heart failure, and arrhythmia, and there is myocardial infarction. ECG changes and serum enzymes can be divided into acute or old myocardial infarction according to the course of the disease.
3. Primary cardiac arrest: Acute myocardial ischemia leads to ECG instability, sudden ventricular fibrillation or sinus arrest leading to sudden death. Primary cardiac arrest is more common in acute myocardial infarction or unstable angina pectoris. Occasionally, the disease is the first symptom.
4. Patients with unstable angina pectoris or acute myocardial infarction with congestive heart failure, weakened myocardial ischemia or infarct site, loss of contraction or abnormal bulging during systole, or papillary muscle ischemia, mitral regurgitation caused by infarction. There is diffuse atrophy of myocardial interstitial fibrosis, left ventricular contractility is weakened, left heart failure can occur, and sometimes acute pulmonary edema occurs.
5. Arrhythmia: Angina pectoris or acute myocardial infarction can cause various arrhythmias in the ischemic myocardium. If the conduction system is involved, it can lead to various types of conduction block.
6. Asymptomatic myocardial ischemia: In patients diagnosed with coronary heart disease, myocardial ischemia can be found during dynamic electrocardiogram monitoring, exercise tests, or radionuclide myocardial imaging, but the patient had no conscious symptoms at the time.
At present, it is thought that this type can cause myocardial infarction or sudden death as well as symptomatic myocardial ischemia, so it should be paid attention to.
Clinical patients may have one or more types of clinical manifestations, and may also progress from one type to another. This section mainly introduces two types of angina pectoris and myocardial infarction.
Angina Pectoris (AnginaPactoris)
Angina pectoris is a symptom caused by acute transient myocardial ischemia and hypoxia. It is clinically characterized by paroxysmal pain in the back of the sternum or in the front of the heart.
Cause of Angina Pectoris (AnginaPactoris)
The common cause is coronary artery atherosclerosis caused by stenosis of the large branch arteries, partly due to coronary spasm, other causes of coronary artery disease such as congenital malformations are extremely rare, and coronary artery embolism is rare, the latter mainly causes myocardium infarction.
In addition to the above, angina pectoris may also occur in severe aortic stenosis or insufficiency and hypertrophic cardiomyopathy. However, it does not fall into the category of coronary heart disease angina pectoris.
Pathology and pathophysiology for Angina Pectoris (AnginaPactoris)
The coronary arteries have left and right branches, which open in the left and right aortic sinuses, respectively.
The left coronary artery is only 1-3 cm long and is divided into anterior descending branch and trochanteric branch.
The anterior descending branch supplies blood to the middle, lower part of the left ventricular anterior wall and the first two thirds of the ventricular space. The upper wall, the left half or all of the palatal surface of the heart, and the left atrium.
The right coronary artery supplies blood to the right ventricle, the posterior third of the ventricular septum, and the right half or all of the patellar plane of the heart.
The sinoatrial node of the heart is accounted for by 60% of the right coronary blood donors, and the atrioventricular node and atrioventricular bundle of the heart are accounted for by 90% of the right coronary blood donors.
There are many small branches between the three coronary arteries that coincide with each other.
The left coronary artery is also used as a branch of the coronary arteries, collectively referred to as four coronary arteries.
Atherosclerosis of the artery can involve one, two, or three of the coronary arteries, or even four branches at the same time.
The left anterior descending branch is the most common and the lesion is the most severe. Then the right coronary artery, the left circumflex branch, and the left Coronary arterial trunk, the proximal lesion of the blood vessel is heavier than the distal end. Atheromatous plaques are mostly at the opening of the branch of the blood vessel, which is often biased to one side of the blood vessel, which gradually increases and causes the lumen to narrow or occlude.
Coronary atherosclerosis affects the blood supply to the heart muscle. Under normal circumstances, the blood supply of the myocardium and the blood supply of the coronary arteries are adjusted by nerves and body fluids to maintain a dynamic balance.
When the lumen is slightly narrowed, the myocardial blood supply is not affected and the patient is asymptomatic.
When the vascular stenosis is severe, the load on the heart increases to a certain extent, the coronary blood supply cannot meet the needs of the myocardium, and myocardial ischemia and hypoxia induce angina pectoris.
However, some angina pectoris occurs at rest, and there is no increase in myocardial oxygen demand index (product of heart rate and blood pressure systolic blood pressure) before the attack, and angina does not occur during labor.
Angina pectoris at rest is often the result of coronary arterial spasm. Common angina pectoris, such as variant angina pectoris, can occur in normal coronary arteries and more commonly in arteries with atherosclerotic lesions of varying degrees.
The mechanism of coronary artery spasm is complicated. Autonomic dysfunction and sympathetic nerve excitement cause the coronary artery alpha receptor to excite.
Arterial walls with atherosclerotic plaques are overly sensitive to the effects of neurohumoral fluids. They directly affect the metabolism of vascular wall smooth musclesthe increase in platelet release of vasoactive substance TXA2 and the decrease in the production of – prostaglandin PGI2, etc., which have a certain effect on changes in coronary artery tension. Impact.
The mechanism of pain in angina pectoris may be caused by certain products (such as peptides) in myocardial anaerobic metabolism that stimulate afferent nerve endings in the heart and often spread to superficial nerves of the spinal cord and cause pain, radiation.
Clinical manifestations of Angina Pectoris (AnginaPactoris)
I. Symptoms: Pain is an important symptom of angina pectoris. Typical angina pectoris attacks often have the following characteristics:
(A) incentives are often induced by physical labor, emotional excitement, satiety and cold. Angina pectoris induced by labor, rest can relieve it. Typical angina pectoris often occurs under similar working conditions. Severe conditions can occur during meals, dressing, defecation, or rest, and some can occur at night.
(B) The typical pain site is behind the upper or middle part of the sternum, or in the anterior region of the heart. The pain range is like the palm of the hand, and the boundaries are not very clear. The pain often radiates to the left shoulder along the front of the left shoulder to the ring finger of the little finger. Sometimes it is also possible. Radiation to the neck, lower jaw, and pharynx, but also to the left scapular region or upper abdomen with gastrointestinal symptoms. Occasionally, the pain in the radiation area is more obvious than the sternal area. This phenomenon is more common in the elderly.
(C) Nature: The nature of pain varies from person to person, most of which are oppression, stuffiness and austerity, and sometimes there is a sense of dying. The pain can be mild or severe. In severe cases, the expression of anxiety, paleness, and even sweating force the patient to stop moving until the symptoms are relieved.
(D) Duration and Relief: Pain usually relieves itself for 1 to 5 minutes, and occasionally for 15 minutes. The pain can be relieved within minutes after rest or immediately after nitroglycerin under the tongue. Seizures can occur once every few days or weeks, or multiple times a day.
Variant angina pectoris often occurs during rest at night and has nothing to do with labor. The pain is more severe and lasts longer.
Second, when the signs are not seizures, there is no special performance. When they are seizures, they often show anxiety, blood pressure increases, and heart rate increases. The first heart sound of the apex weakened, and the fourth heart sound (atrial) galloping rhythm appeared.
This was due to decreased left ventricular function, increased end-diastolic pressure, and increased atrial contractility.
When the papillary muscles are ischemic, temporary mitral regurgitation may occur, and mid- and late-stage systolic murmurs may be heard.
Due to the weakened left ventricular systolic function, its contraction time is prolonged, and the closing of the aortic valve lags behind the closing of the pulmonary valve, resulting in a second heart sound split, which is more pronounced during exhalation. This is called second heart sound reverse split. The above signs are only seen in some patients during the angina pectoris. It can be helpful to diagnose if they can be found in time.
Clinical types of Angina Pectoris
The following types can be seen clinically:
(a) Labor Angina Pectoris
This refers to the common angina pectoris induced by increased myocardial oxygen demand due to physical labor or emotional agitation. The main cause is an increase in blood flow that cannot be met by organic coronary stenosis.
Clinically, it can be divided into the following types:
1. First-onset, angina pectoris occurred within the last month, and the seizures are frequent and worse.
2. Stable type, the condition is stable for more than one month, that is, the frequency of angina pectoris, the inducement and the time of onset are about the same.
3. Deteriorating type, originally stable angina pectoris, and the frequency of recent angina pectoris increases, the degree becomes worse, and the duration increases. It can be caused by lighter and lighter activities, and even occurs at rest. It is not easy to relieve with nitroglycerin.
4. Intermediate type, which occurs in one or more chest pains that last for more than 15 minutes, but there is no evidence of acute myocardial infarction. It is an intermediate myocardial ischemia between unstable angina pectoris and myocardial infarction.
5. Angina pectoris after myocardial infarction refers to recurrent angina pectoris after acute myocardial infarction.
(b) Spontaneous angina pectoris
Spontaneous angina pectoris or angina pectoris occurs at rest without significant increase in myocardial oxygen demand. The onset of angina pectoris is mainly caused by the larger branch spasm of the coronary artery. There are the following clinical types:
1. Variant angina pectoris
This was first proposed by Prinzmetal in 1959. Its characteristics are as follows:
i. Angina pectoris tends to occur at regular intervals, often in the middle of the night or in the early morning, without a clear cause.
ii. Angina pectoris is severe and lasts for a long time, which can reach 15-20 minutes.
iii. ST-segment elevation in some leads during the onset of ECG accompanied by ST-segment depression in the corresponding non-ischemic area, often with ventricular premature beats or ventricular tachycardia.
2. Severe exertional angina pectoris
This may cause angina pectoris at rest due to very slight activity or emotional agitation. This may also be accompanied by coronary artery spasm. The electrocardiogram showed depression in the ST segment.
3. Decubitus angina pectoris
This refers to angina pectoris that occurs when lying supine. Due to increased cardiac venous return and increased cardiac volume and muscle oxygen demand in the supine position, angina pectoris can occur if there is cardiac insufficiency and decreased cardiac output.
Except for labor-stable angina, all other types of angina are unstable angina.
Laboratory and other inspections of Angina Pectoris (AnginaPactoris)
(1) In some patients with conventional ECG, the ECG is normal when angina pectoris is not on, but there can also be abnormalities in ST segment and T wave and old myocardial infarction.
In the case of labor angina pectoris, the P wave is the main lead. There may be subendocardial ischemic changes such as ST-segment depression and T-wave depression or inversion. This is because the left ventricular subendocardial myocardium is provided with blood from the end of the coronary artery branch.
When the coronary artery has insufficient disease, Myocardial ischemic injury is more likely to occur under the endocardium. During the onset of variant angina pectoris, the main branch of the coronary artery is spasm, which causes acute myocardial ischemic injury of the whole ventricular wall thickness, which is manifested as ST segment elevation.
(2) Continuous ECG monitoring: Let the patient wear a slow-moving tape cassette. Take 1-2 bipolar chest leads to record the 24-hour ECG continuously, then quickly play it on the fluorescent screen and select a segment to record. You can find the changes in the ST-T wave of the ECG and various arrhythmias. The appearance time can be related to the patient\’s activity and the symptoms are contrasted.
(3) Electrocardiogram exercise test: Exercise increases the heart load and induces myocardial ischemia to cause ischemic symptoms and ECG changes. Commonly used are pedal and pedal tests. The subject performs step-by-step exercise on an active pedal or pedal exercise on a specially made vehicle. Exercise intensity is gradually upgraded in stages, and the amount of exercise reaches the end of the patient\’s angina pectoris or significant fatigue is called extreme exercise.
If you reach the exercise amount of 85-90% of the estimated maximum heart rate according to age, it is called sub-maximal exercise. Observe and record the ECG of 2, 4, 6, and 8 minutes before, during, and immediately after the exercise.
The ST segment appears in the ECG. Or down-slope depression of ≥0.1mv for 0.08 seconds is positive. Monitor blood pressure and heart rate before, during, and after exercise. Blood pressure or heart rate continues to decrease, suggesting severe multivessel coronary artery disease and cardiac insufficiency.
Those with gait instability, early ventricular, ventricular tachycardia, and decreased blood pressure during exercise should Immediately stop exercise, the contraindications of exercise test are: acute phase of myocardial infarction, unstable angina, heart failure or severe arrhythmia.
2. Echocardiography In patients with coronary heart disease, echocardiography may show abnormal ventricular septum or / and abnormal ventricular wall motion in the posterior part of the ventricle. Segmental motion may be weakened or dysfunctional in the ischemic area. The thickness of the ventricular wall during systole is normal. It is thin and can obtain the data of ventricular and atrial cavity size.
Inspection of Radionuclides
(1) 201 -Myocardial imaging Normal myocardium can absorb 201 in the coronary blood flow and show it, ischemic myocardium does not show, and ischemia area perfusion defect. The 201 exercise test can be used for crowns without abnormal performance at rest.
Cardiac patients, their exercise induces myocardial ischemia and presents a non-visual ischemic area.
(2) Radionuclide angiography: Intravenous injection of stannous pyrophosphate is adsorbed by red blood cells, and then injection of 99m, the red blood cells are labeled with radionuclides and the blood pool in the heart cavity is developed. The left ventricular ejection fraction can be measured and local wall motion abnormalities can be displayed.
4. Coronary angiography: Selective coronary angiography is one of the main methods for the diagnosis of coronary artery disease.
Methods Two left and right coronary arteriography were performed using two specially made catheters with different curvatures.
Percutaneous puncture is inserted from the femoral artery into the catheter and pushed to the root of the aorta and placed in the coronary artery mouth. Then a small amount of contrast agent is injected for movie photography or rapid continuous filming.
Repeated radiographs at different locations several times can more satisfactorily find the stenotic lesions caused by aortic atherosclerosis and its exact location, extent and extent, and can estimate the condition of the lumen at the distal end of the stenosis. It is generally believed that a reduction in lumen area of more than 75% is of some significance.
Indications for coronary angiography
i. For those who still have severe angina pectoris under medical treatment, the condition of coronary artery disease needs to be clarified to consider interventional therapy or bypass surgery.
ii. Chest pain is suspected of angina and cannot be diagnosed.
Diagnosis of Angina Pectoris (AnginaPactoris)
According to the typical onset of pain, nitroglycerin can be used to alleviate it, and patients over 40 years of age who have susceptibility to coronary heart disease can rule out angina pectoris caused by other reasons, that is, diagnosis should be considered.
In the ECG examination during the onset, the P wave-based lead showed that the ST segment was depressed, and the T wave was flat or inverted, and recovered quickly after the onset. Seizures are not typical, and those with no change in resting electrocardiogram should review the electrocardiogram at the time of the episode based on the condition. If necessary, an ECG stress test can induce a diagnosis of angina pectoris.
Electrocardiographic monitoring or exercise tests without angina pectoris and ischemic ST segment changes should be performed with radionuclide myocardial perfusion imaging, if necessary, coronary angiography can be used to confirm the diagnosis.
Differential diagnosis of Angina Pectoris (AnginaPactoris)
Angina pectoris must be distinguished from acute myocardial infarction and cardiac neurosis. Cardiac neurosis is more common in young women. It can occur during fatigue and rest. Most of the pain is located in the precardiac area or near the apex of the heart, and is usually limited to one point. Most of them are persistent hidden pain, suffocation, or throbbing tingling that lasts for hours or even days. Nitrate formulations have no significant effect.
Patients with atypical angina and above with abdominal pain as the main cause should be distinguished from ulcer disease, biliary tract disease, and diaphragmatic hernia. Angina pectoris radiation to the chest or shoulders and backs must be distinguished from pleurisy, intercostal neuralgia, spinal or shoulder arthritis.
Treatment of Angina Pectoris (AnginaPactoris)
In addition to the basic treatment of coronary heart disease, treatment focuses on improving coronary blood supply and reducing myocardial oxygen consumption, preventing the onset of angina pectoris and preventing its recurrence.
a. Stop the activity of angina pectoris. Immediately stop the activity. Sublingual nitroglycerin 0.3-0.6mg can be relieved for 1-2 minutes; 5-10mg isosorbide dinitrate is effective for 5 minutes; isosorbide nitrate can also be used (Yi Shunmai) Oral spray works in seconds. Side effects include dizziness, flushing, palpitations, and occasionally decreased blood pressure. Therefore, for the first time, you should lie down for a while, inhale oxygen if necessary, and avoid glaucoma.
b. To prevent seizures, commonly used drugs are nitrate, beta blockers and calcium blockers.
(1) The main effect of nitrate preparations is to dilate the veins to reduce the amount of blood returned to the heart, reduce the preload of the heart, and reduce myocardial oxygen consumption. Expand the coronary arteries and improve the myocardial blood supply in the ischemic area.
Commonly used are: 5-20 mg of isosorbide dinitrate (xiaoxintong), taken orally 3 times a day. 10-20 mg of pentaerythritol nitrate, orally, 3-4 times a day.
Half an hour before the activity that is expected to induce angina pectoris, 0.3-0.6 mg of nitroglycerin under the tongue can prevent angina pectoris.
1-2% nitroglycerin ointment is applied to the skin and gradually absorbed. It is suitable for angina pectoris at night. Applying medicine before going to bed can prevent seizures.
(2) The effect of β-blockers on angina pectoris is mainly through weakening the contractility of the myocardium, slowing down the heart rate, and thereby reducing myocardial oxygen consumption. It is suitable for labor angina pectoris, but should not be used in patients with variant angina pectoris, because Spontaneous angina.
1. Propranolol 10-40mg orally 3 times a day, it is advisable to start with a small dose and gradually increase according to the response. This drug is a non-selective beta blocker. The side effects are in addition to bradycardia and reduced heart function. Can cause bronchospasm, therefore, those with slow heart rate are not suitable, those with heart dysfunction should be used with caution, and digitalis preparations should be given in advance, and those with original bronchial asthma are banned.
2. The experience has a mild intrinsic sympathomimetic effect and less affects cardiac function. It can be taken orally 20-40 mg each time, 3 times a day.
3． Aminoacid is a β1-receptor selective blocker, which is not easy to cause bronchospasm or other side effects of β2-receptor block. The daily dose is 50-200mg. Due to the long time of action, it can be taken orally twice. Not suitable for patients with low blood pressure and cardiac insufficiency.
4． Metoprolol is a cardiac selective, β1 receptor blocker with no endogenous sympathetic activity, and has fewer side effects. It has recently been suggested that the drug can not only lower blood pressure, but also inhibit the binding of LDL to arterial wall proteoglycans to prevent atherosclerosis.
Myocardial infarction often occurs after a full meal (especially after eating a lot of fat), during quiet sleep, or after hard stools. This is because postprandial blood lipids increase, blood viscosity is high, platelet adhesion is enhanced, local blood flow is slow, and platelets It is easy to aggregate and cause thrombosis.
During sleep, the vagus nerve increases in tension, easily causes coronary artery spasm, and forced stool increases the heart load. These factors are conducive to the occurrence of acute myocardial infarction.
Acute myocardial infarction can also occur in coronary spasms without coronary atherosclerosis, and occasionally due to coronary embolism, inflammation, and congenital malformations.
Severe arrhythmias, shock or heart failure that occur after myocardial infarction can further reduce coronary perfusion flow and expand the scope of myocardial necrosis.
Pathophysiology and Pathology for Myocardial infarction
The location of myocardial infarction depends on the affected vessels. The left anterior descending coronary artery was occluded, and the infarcts were in the anterior wall of the left ventricle, the apex, the inferior wall, the anterior ventricular septum, and the anterior papillary muscle of the mitral valve.
Right coronary artery occlusion, the infarcted area is on the left ventricular plane (when the right coronary artery is dominant), the back of the interventricular septum, and the right ventricle, and can affect the sinoatrial node and the atrioventricular node. The left coronary artery is occluded.
The infarcted area is on the high side wall of the left ventricle, the diaphragm (when the left coronary artery is dominant), and the left atrium, which may involve the atrioventricular node. Occlusion of the left main coronary artery can cause extensive left ventricular infarction. Right ventricular and left and right atrium infarctions are rare.
The extent of myocardial necrosis depends on the location, velocity, and collateral circulation establishment of coronary artery occlusion. 20-30 minutes after lumen occlusion, there is a small amount of necrosis in the myocardium.
From 1 to 12 hours, most of the myocardium is coagulative necrosis, myocardial interstitial congestion, edema, and a large number of inflammatory cell infiltration. After 4 days, the boundary of necrosis is obvious.
Myocardium dissolves and granulation tissue is formed. Necrotic tissue begins to be absorbed after about 1-2 weeks, and gradually fibrosis. Scars are formed in 6-8 weeks to heal.
Myocardial infarction affects the whole layer of ventricular wall thickness or most are called transmural myocardial infarction. If the pericardium is involved in pericarditis, the endocardium will cause thrombosis in the ventricular cavity.
Myocardial infarction is focally distributed and involves only the inner layer of the ventricular wall, less than half the thickness of the ventricular wall, and is called subendocardial myocardial infarction.
The occurrence of myocardial infarction results in hemodynamic disorders and electrophysiological changes. The necrotic myocardial contractility of the infarcted area is weakened. The myocardial contractility is not coordinated. Maximum rate of left ventricular pressure curve dp / dt is reduced. The left ventricular compliance is reduced, and end-diastolic pressure increases. There is increase in end-diastolic and systolic volume, decrease in ejection fraction, decrease in cardiac output, reduced heart rate, or decreased blood pressure, and heart failure or cardiogenic shock.
The ventricular wall in the infarct area is weak enough to withstand ventricular pressure. Heart rupture can occur in the early stage, and ventricular dilatation tumors can occur in the later stage.
The electrophysiological changes include the specific changes of the electrocardiogram in the infarct area and the occurrence of various arrhythmias.
Clinical manifestations of Myocardial infarction
i. Infarction of infarction
Most patients may have prodromal symptoms a few days before the onset of illness. For example, the original angina pectoris frequently attacks in recent days, the degree is aggravated, the duration is longer, rest or nitroglycerin can not be relieved, and even attacks during rest or sleep. With or without history of angina pectoris, sudden abdominal pain, nausea, vomiting, acute heart failure, or severe arrhythmia, timely ECG examination can show temporary elevation or decrease of ST segment, T wave height or obvious inversion, At this time, patients should be alert to the possibility of myocardial infarction in the near future, such as timely treatment, or it can be avoided.
(1) Pain: The most prominent symptom of this disease. The seizures are usually without obvious causes, and often occur when they are quiet. The pain site and nature are the same as those of angina pectoris, but the pain is severe and lasts for a long time. Patients are often upset, sweating, fearful, or dying. A small number of patients may be pain-free and present with shock or acute pulmonary edema. Some patients have pain in the upper abdomen with nausea, vomiting, and are easily confused with acute abdomen such as gastric perforation and acute pancreatitis. More common in elderly patients. Patient pain can be radiated to the lower jaw, pharynx, neck and back.
(2) Shock: 20% of patients may be accompanied by shock, which usually occurs within hours to 1 week after the onset of illness. The patient was pale, irritable, skin was damp and cold, his pulse was weak, his blood pressure dropped <10.7Kpa (80mmHg), and he was even fainted. If the patient has only reduced blood pressure and no other manifestations are called hypotension. The main causes of shock are: due to severe damage to the myocardium, the left ventricular output decreases sharply (cardiogenic shock); second, severe chest pain causes dilated peripheral reflex vessels; There are factors that cause hypovolemia.
(3) About 75-95% of patients with arrhythmia are associated with arrhythmia, which is more common within 1-2 weeks of onset, and most common within 24 hours. Ventricular arrhythmias are the most common in arrhythmias, such as premature ventricular beats. Patients may experience sudden death from ventricular tachycardia or ventricular fibrillation.
Atrioventricular block and bundle branch block are not uncommon, and supraventricular arrhythmia is rare.
Anterior wall myocardial infarction is prone to bundle branch block, inferior wall myocardial infarction is prone to atrioventricular block, and supraventricular arrhythmia is more common in atrial infarction.
(4) Heart failure: The contractility of the heart is significantly weakened and uncoordinated after the infarction. Therefore, acute left heart failure is prone to occur in the first few days of onset, and symptoms such as dyspnea, cough, irritability, and inability to lie supine.
Severe cases of acute pulmonary edema may occur with cyanosis and a large amount of pink foam-like sputum, and later may have right heart failure.
Right ventricular myocardial infarction can start right heart failure at the beginning.
(5) Systemic symptoms: fever, tachycardia, increased white blood cells, and increased red blood cell sedimentation. This is mainly caused by the absorption of tissue necrosis, which usually occurs within 1-2 days after infarction, and the body temperature is generally about 38 ° C, rarely exceeding 39 ° C, and lasts for about a week.
Heart dullness can increase slightly to moderately, heart rate increases more quickly, and a few can slow down. The first heart sound weakens, the second heart sound splits inversely, the fourth heart sound and diastolic rhythm. If systolic murmur occurs in the apical region, it is mostly caused by papillary muscle insufficiency. A few cases of pericardial friction due to myocardial infarction involving the epicardium, more common in the 1-2 days after the onset, can last for several days, heart failure in both lungs can be heard and wet rales, blood pressure often decreases, before the onset of In patients with hypertension, blood pressure can drop to normal.
Laboratory and other Inspections for Myocardial infarction
(A) Characteristic Changes
1. Wide and deep Q waves appear on the leads facing the myocardial necrosis zone.
2. ST-segment elevation on the lead facing the myocardial injury area around the necrosis area was arched back.
3. A T wave inversion occurred on the leads facing the myocardial ischemic area around the injury area. There is no pathological Q wave in subendocardial myocardial infarction.
(B) Dynamic Changes
1. Within a few hours of the onset of the superacute crest, abnormally large T waves of asymmetric limbs may appear.
2. A few hours after the acute phase, the ST segment was significantly elevated, the back of the arch was upward, and connected with the upright T wave to form a one-way curve. Pathological Q waves appeared within 1-2 days, while R waves were reduced, and pathological Q waves or QS waves Often lasting.
3. The ST-segment elevation in the subacute phase lasted for about two weeks, gradually returned to the baseline level, and the T wave became flat or inverted.
4. After several weeks to months of recovery, the T wave is inverted in a V-shaped symmetry, which can be permanent or can be restored after months to years.
(C) Judgment site and scope
The site of myocardial infarction can be judged according to the leads with characteristic changes. For example, V1, V2, and V3 reflect the anterior wall and lateral wall of the left ventricle, and II, III, and aVF reflect the lower wall. I, avF reflects the left ventricular high sidewall lesions. Based on the above changes, we can preliminary determine which blood vessels are involved.
2. Echocardiography: Two-dimensional and M-mode echocardiography can detect thinning and abnormal movement of the infarcted wall, detect left ventricular function, and assist in the diagnosis of ventricular aneurysm.
(D) Radionuclide inspection
(a) Intravenous injection of 99m -pyrophosphate and 99m -pyrophosphate in blood combined with calcium ions in necrotic myocardial cells.
(b) Intravenous injection of 201 gadolinium, 131 cesium, and 43 potassium. Such radionuclides cannot enter the cells due to the necrosis of the blood supply to the myocardium. The necrotic area is not visualized, and the normal myocardium is visualized.
The above examinations are helpful to the location of myocardial infarction and to determine the extent of infarction. Gate circuit gamma scintigraphy for radionuclide cardiac blood pool imaging can detect abnormal wall motion and left ventricular function.
(E) Blood Test
(a) Leukocytes can increase to 10-20 × 109 / L (10,000-20, 000 / ul) neutrophils after 24-48 hours of onset of hemogram, eosinophils decrease or disappear, and red blood cell sedimentation rate The increase can last for 1-3 weeks.
(b) Serum enzymes: Myocardial cells contain a large amount of enzymes. Myocardial infarction myocardial cells are necrotic, and intracellular enzymes enter the blood, causing serum myocardial enzymes to increase.
Creatine phosphokinase (CPK) begins to increase at 6-8 hours and reaches its peak at 24 hours. 2-3 days to normal. This enzyme is not abundant in other tissues and cells, so its specificity is strong. Its isomerase CPK-MB is more specific and sensitive. The peak of CPK-MB often reflects the range of infarction.
Aspartate aminotransferase (SGOT) begins to increase within 6-12 hours of onset (normal value of 40 units), peaks at 20-48 hours, and returns to normal within 3-5 days. Because the enzyme is also present in liver cells, its specificity is poor. Lactate dehydrogenase starts to rise 8-10 hours after infarction, reaches its peak in 3-5 hours, and returns to normal after about 8-14 days. LDH1 is highly specific.
(c) Determination of serum myocardial specific protein blood and urine myoglobin increased. Myoglobin began to increase within 2-4 hours of myocardial infarction (normal value, 6-80ug / L of radioimmunotherapy), reached the highest peak within 4 hours, earlier than the appearance of serum enzymes, and returned to normal for 3-5 days.
Cardiac myosin and its light chain are specific contractile proteins of the myocardium. They begin to rise 4 hours after the onset of disease and last for 6-7 days.
The specificity and sensitivity are very strong, and it is a meaningful index reflecting acute myocardial infarction.
Diagnosis of Myocardial Infarction
Based on typical clinical manifestations and characteristic ECG changes and elevated serum enzymes, diagnosis is not difficult.
If elderly patients suddenly have unexplained shock, heart failure, severe arrhythmia or severe persistent chest tightness or epigastric pain, the possibility of this disease should be considered.
Diagnosis tools are Electrocardiogram, serum enzyme serial observation, serum myoglobin.
The determination of myosin light chain I and radionuclide myocardial scanning can help confirm the diagnosis.
Differential Diagnosis of Myocardial Infarction
This disease should be distinguished from the following:
1. Painfulness, heavy tightening, squeezing, more intense
2. Pain time, minutes, hours
3. Nitroglycerin effect, pain disappears quickly, ineffective
4. Predisposing factors Force, excitement, full meals, etc. Same as before, sometimes not obvious
5. Shock none often
6. Blood pressure can rise and often decrease
7. Shortness of breath or pulmonary edema
8. Necrotic tissue response
(1) Fever None Often
(2) Normal increase of white blood cell count
(3) ESR is fast
(4) Normal increase in serum aspartate aminotransferase, etc.
(5) Pericardial friction sound
9. ECG changes
(1) ST segment is reduced, recovery is fast, and elevated for more than a few hours
(2) T wave is temporarily flat or inverted, permanent change
(3) QRS complex does not change, often abnormal Q waves
2. Acute non-specific pericarditis: Acute non-specific pericarditis can also have more severe and persistent pain in the precardiac area. If the patient is older, it is easily confused with acute myocardial infarction.
Before the onset of this disease, there is often a history of upper respiratory infections, pain and fever appear at the same time, systemic symptoms are mild, and there are no signs of shock or heart failure.
Except for the AVR, most leads in the ECG had a slight ST segment elevation and the arch was down, and no abnormal Q wave appeared.
3. Acute pulmonary embolism: This disease often has chest pain, hemoptysis, dyspnea and shock. If it is embolized in the left pulmonary artery, left chest pain can be confused with myocardial infarction. Myocardial infarction is generally free of hemoptysis, and in addition to left heart failure, there is generally no significant dyspnea.
Pulmonary embolism is often manifested by acute overload of the right ventricle, such as second heart sounds in the pulmonary valve area, jugular vein filling, and liver enlargement.
The electrocardiogram has pulmonary P wave and the electrocardiogram in the precardiac area is obviously clockwise translocated. The chest radiograph can show the shadow of the pulmonary infarct area.
4. Acute abdomen: acute pancreatitis, peptic ulcer perforation, acute cholecystitis, cholelithiasis, etc. have upper abdominal pain, which may be accompanied by shock. A careful history, physical examination, electrocardiogram, and serum myocardial enzyme measurements can help identify.
Complication under Myocardial infarction
1. Papillary muscle dysfunction or rupture: The incidence of this disease is high, mainly due to papillary muscle ischemia and necrosis and inability to contract, causing mitral valve prolapse and insufficiency, and systolic karaoke sounds and loud blows systolic murmur occur.
If caused by ischemia or edema, the murmur can disappear as the condition improves. Rupture mostly occurs in the papillary muscles behind the mitral valve and is seen in the inferior myocardial infarction. Heart failure is severe, and pulmonary edema can quickly develop and die within a few days.
2. Rupture of the heart is rare. It usually occurs within one week after the onset of the disease. The free wall of the ventricle ruptures, which can cause acute pericardial tamponade and sudden death. When the ventricular septal infarction is perforated, a loud noise appears in the fourth intercostal space on the left margin of the sternum. Hairy systolic murmur, often accompanied by fine tremors, severe right heart failure and shock can occur, and death can occur within a few days.
If the heart rupture is subacute, the patient occasionally lives longer.
3. The incidence of embolism is 1 to 6%, which usually occurs 1 to 2 weeks after the onset. It is mainly the shedding of endocardial mural thrombus in the infarcted area, and corresponding embolism symptoms in the chest or other parts may occur.
4. The incidence of ventricular swelling tumors is 5-20%, mainly due to the infarct site under the action of the heart pressure, a significant bulge showed ventricular swelling tumors.
If the ventricular aneurysm occurs in the anterior wall or apical infarct area, the faint pulsations that occur at the 4th to 5th intercostal space in the anterior region of the heart and the apex may not have systolic murmur.
When mural thrombosis occurs in a tumour, the heart sounds weaken. The ECG showed persistent ST-segment elevation (more than half a year), and X-ray examination showed abnormal bulging and abnormal pulsation in the heart shadow.
5. The incidence of postoperative myocardial infarction syndrome is about 10%, which mostly occurs 2 to 4 weeks after myocardial infarction.
Manifestations include fever, chest pain, hemoptysis, pericarditis, pleurisy, pneumonia, or pericardial and pleural effusion. This sign can occur repeatedly.
Each episode lasts about a week. The cause may be the body\’s autoimmune response to the necrotic myocardium.
Treatment of Myocardial infarction
Local rescue work before hospitalization should be strengthened. The principle of treatment is to protect and maintain cardiac function, improve myocardial blood supply, save dying myocardium, reduce the scope of myocardial infarction, and deal with complications to prevent sudden death.
I. Monitoring and general treatment
(1) Patients who are clinically coagulated as a sign of myocardial infarction or acute myocardial infarction should closely observe changes in their condition. In 24-48 hours after the onset of acute myocardial infarction, blood pressure, heart rhythm, breathing, consciousness, pain, and general conditions should be closely monitored, and electrocardiogram monitoring should be performed. If necessary, we need to monitor pulmonary capillary wedge pressure and central venous pressure.
(2) Rest: Stay in bed for 2 weeks, keep the environment quiet, reduce visits, prevent bad stimulation, and relieve the burden of thought. Those who are stable and without complications can sit up after 2-3 weeks, and gradually get out of bed after 4-6 weeks.
(3) Oxygen intake: Give oxygen intermittently or continuously through the nasal tube mask for the first few days.
(4) Strengthening life care: It is not advisable to overeat and eat small meals frequently. It is advisable to lightly digestible, low-sodium, low-fat non-flatulent foods, but the necessary calories and nutrients must be given. Keep the stool open and avoid exertion. Laxatives can be given to constipation.
II. Symptomatic Treatment
(1) Relieve pain: Pain should be relieved as soon as possible. Generally, 50-100mg of rodentine or 5-10mg of morphine can be injected.
To avoid nausea and vomiting, atropine 0.5mg can be given at the same time. Those with tachycardia do not add atropine.
If necessary, it can be repeated once every 4-6 hours. Those with respiratory depression should not use morphine. Poppy tincture also has analgesic effect, 0.03 – 0.06g each time, intramuscularly or orally.
You can also try nitroglycerin 0.3mg or Xiaotongtong 5-10mg sublingual, pay attention to increase in heart rate and lower blood pressure.
(2) Control of shock: Those with conditions should perform hemodynamic monitoring, determine the cause of shock according to central venous pressure and pulmonary capillary wedge pressure, and provide targeted treatment.
1. Blood volume supplementation: It is estimated that those with insufficient blood volume, or reduced central venous pressure and pulmonary capillary wedge pressure, can use intravenous infusion of 706 generation plasma or 5-10% glucose. If the central venous pressure rises> 1.77Kpa (18cmH2O) and the pulmonary capillary wedge pressure > 2 – 2.4Kpa (15 – 18mmHg) after infusion, it should be stopped. During right ventricular infarction, a large amount of fluid should be infused to maintain left ventricular filling.
2. The application of booster drugs can be given to dopamine 10-30mg, or (and) m-hydroxylamine 10-30mg, 5% glucose solution 100-250ml intravenous drip, or dobutamine 20-25mg solution In 100ml of 5% dextrose solution, intravenously infused at a rate of 2.5 to 10 ug / kg per minute.
For patients with increased capillary wedge pressure in the lungs, decreased cardiac output, and severe contraction of peripheral blood vessels in limbs with cold limbs, while using booster drugs, vasodilators such as sodium nitroprusside or phentolamine can be used to closely monitor blood pressure Variety.
3. Correction of acidosis and severe shock, which are often accompanied by acidosis when it lasts for a long time.
You can intravenously drip 5% sodium bicarbonate 100-200ml, and then adjust the dose by referring to blood pH or carbon dioxide binding force.
4. The adrenal corticosteroid hydrocortisone 100-200mg or dexamethasone 10-20mg intravenously.
It can reduce the inflammatory response in the infarcted area, protect the hypoxic myocardium, and is conducive to anti-shock.
5. Assisted circulation Intra-aortic balloon counterpulsation for auxiliary circulation can increase diastolic blood pressure in the aorta, increase coronary blood flow, improve left heart function, and earn time for coronary angiography and surgical treatment.
III. Elimination of arrhythmia
Arrhythmia is an important cause of exacerbation and death. Special attention should be paid to the possibility of ventricular premature beats developing into ventricular tachycardia or ventricular fibrillation.
The following occur:
i. More than 5 ventricular premature beats in one minute
ii. Three or more ventricles become short array ventricular tachycardia
iii. Multisource ventricular premature
iv. Occur in the early diastole before the peak of the T wave Those should be treated in a timely manner.
1. Immediately after the onset, 200-250 mg of lidocaine (5% solution) was injected intramuscularly every 8 hours for 3 days to prevent ventricular arrhythmias.
2. Ventricular premature beats or ventricular tachycardia should be immediately infused with lidocaine 50-100mg intravenously, repeated every 5-15 minutes, until the premature beat disappears or the total amount has reached 300mg, followed by an intravenous rate of 1-3mg per minute Instillation maintenance (100 mg lidocaine plus 100 ml of 5% glucose solution, 1-3 ml intravenously per minute). This can be changed to oral chronic heart rhythm, or amiodarone when the situation is stable.
Poor efficacy can be changed to intravenous infusion of procainamide. Ventricular tachycardia can use synchronous DC cardioversion.
When ventricular fibrillation occurs, synchronous DC defibrillation should be performed immediately.
3. Supraventricular tachyarrhythmias who have not used digitalis in the near future can take a slow intravenous injection of cedilan 0.2-0.4mg plus 5% dextrose solution 20ml, or treat with verapamil and arrhythmia, and use synchronous direct current electrocardiogram when ineffective. Or use an artificial cardiac pacemaker for rapid suppression.
4. Chronic arrhythmia, severe sinus bradycardia or atrioventricular block, ventricular rate is less than 50 times per minute.
Atropine 0.3-0.6mg or 654-210mg can be used orally 3 times a day, type II or type III patients with ventricular block with Alzheimer’s syndrome should be treated with temporary ventricular pacing of the right ventricle.
IV. In the treatment of heart failure
In addition to strict rest, analgesia or oxygen, diuretics can be used first, as they are often effective and safe.
For patients with acute pulmonary edema, the treatment method is described in the section of cardiac insufficiency.
The vasodilator sodium nitroprusside or phentolamine can be used to reduce the afterload of the heart, especially for those with hypertension.
Angiotensin-converting enzyme inhibitor meproproline (Kapton) combined with Xiaotongtong can effectively control the symptoms of heart failure and improve the prognosis.
Digitalis drugs can be applied to patients with significant heart failure, but due to acute myocardial infarction.
At times, because of hypoxemia, acidosis, and myocardial ischemia, ventricular arrhythmias are prone to occur, especially myocardial congestion in the early stages of onset, edema and compliance are reduced, and the effects of using digitalis are not satisfactory.
During the day, the use of digitalis should be delayed as much as possible. Patients with right ventricular infarction should use diuretics with caution.
3. Rescue dying myocardium, reduce infarct size, reduce myocardial oxygen demand, increase myocardial oxygen supply, reopen blocked blood vessels as soon as possible, and promote ischemia-reperfusion.
(A) Thrombolytic therapy
Application of a lysozyme activator activates plasminogen to plasmin in the thrombus to dissolve the thrombus.
Currently common drugs include streptokinase and urokinase. Streptokinase is tested before application (1000 Iu). If there is no allergic reaction, 500,000 to 1.5 million u of streptokinase can be added to 100% of 5% glucose solution for intravenous drip, and the drip will be completed within 1 hour.
For intracoronary administration, streptokinase can be injected once in 10,000-30, 000 units, and then instilled at 2000-4000 Iu / min for 60 minutes.
To prevent allergic reactions such as streptokinase, isopropyl can be given half an hour before administration 25 mg intramuscularly or dexamethasone 2, 5-5 mg intravenously.
Urokinase can be added intravenously to glucose-saline saline with 500,000 to 1 million units, which is completed in 30-60 minutes.
Intracoronary administration: the first dose of 40,000 units, followed by the input of 0.6-2.4 million units per minute, the infarct-related angiography is performed every 15 minutes, the dose is halved when the blood vessel is reopened, and the total is continued for 30-60 minutes.
The dose amounts to about 500,000 units. Others such as tissue-type plasminogen activator (rtpa) are also used in clinical thrombolytic therapy. This therapy is limited to less than 6 hours after the onset of acute myocardial infarction.
Continuous ST-segment elevation of more than 2mm in two leads of the electrocardiogram is not accompanied by abnormal Q waves.
People with bleeding tendency, severe hypertension, and severe liver and kidney dysfunction should not be used.
(B) Anticoagulation therapy: Extensive myocardial infarction or infarct scope is expanding, and can be considered for application.
If there is bleeding tendency, severe liver and kidney dysfunction, recent surgical wounds are not healed, and active ulcer disease should be disabled.
Intravenous infusion with 50mg of heparin once every 6 hours for a total of 2 days, and the clotting time (test tube method) was controlled within 20-30 minutes.
At the same time, the first dose of coumarin was 200mg, and the second day was 100mg, and thereafter 25 daily, 75mg maintenance.
The first dose of warfarin is 15-20mg, the second day is 5-10mg tincture, and the daily maintenance is 2.5-5mg.
The prothrombin time is about twice (25-30 seconds) normal, and the course of treatment is at least 4 weeks.
If bleeding occurs during the treatment period, anticoagulant therapy should be immediately discontinued.
Those who are caused by heparin are given an intravenous drip of protamine, and those who are caused by coumarins are given intravenous injection of vitamin K1 at 20 mg each time.