The term ACS is understood as an acute violation of the blood supply to the heart – myocardial infarction and unstable angina. As a rule, acute coronary syndrome develops in people suffering from coronary heart disease and other types of angina pectoris. It can be provoked by physical exertion, emotional experiences, the use of large doses of caffeine, and the use of certain drugs.
Symptoms of ACS, which are possible and diagnosis:
- 1. Pain behind the sternum or on the left side of the chest – pressing, compressing. It is not relieved by taking analgesics and nitroglycerin, it does not pass on its own within half an hour (a hallmark of angina pectoris). Pain is given under the left shoulder blade, in the left shoulder and arm, in the left half of the neck and lower jaw, sometimes in the left half of the abdomen and left leg.
- 2. Shortness of breath, in some cases – suffocation and signs of pulmonary edema.
- 3. Pallor, cold sweat, weakness up to a faint, fear of death.
- 4. Heart rhythm disturbances, weak pulse, drop in blood pressure.
- 5. A less typical case is pain in the stomach (gastralgic form of ACS). A distinctive sign of exacerbation of gastritis or peptic ulcer is shortness of breath and heart rhythm disturbances.
If the patient has a pain characteristic of ACS, even if there are no other signs or they are weakly expressed, it is necessary to call an ambulance. The faster the patient enters the hospital, the more chances he has for subsequent rehabilitation. It is imperative to reassure the patient, because the fear of death that occurs as a symptom of ACS is well founded, and emotional experiences exacerbate the patient’s condition.
There are certain risk factors associated with acute coronary syndrome that are important to be aware of. These include:
- age – age – for men 45 years and older, for women – 55 years and more;
- high blood pressure;
- increased blood cholesterol;
- lack of physical activity;
- diet failure, obesity or being overweight;
- hereditary factors;
Nevertheless, atherosclerosis is the cause of ACS No. 1 – it is found in 70 – 95% of patients.
Acute coronary syndrome is a sudden violation of the blood supply to the myocardium due to thrombosis, embolism, dynamic obstruction, or inflammatory processes in the coronary arteries that feed the heart. This condition is manifested primarily by pain.
A heart attack affects older people, but the disease gets younger every year. This is due to environmental degradation, a decrease in the financial well-being of people, and an increase in physical and psycho-emotional stress.
An important role in the development of pathology is played by hereditary factors, as well as malnutrition. These factors contribute to the appearance of various kinds of vascular disorders that impede the normal flow of blood through them.
The essence of the pathological process is approximately the same, regardless of type. As already mentioned, two types of the described position are distinguished: angina pectoris and heart attack. They are similar in nature.
In both cases, there is a violation of the nutrition of the muscle layer of the heart as a result of stenosis or occlusion (blockage) of the coronary arteries. Often this is a consequence of atherosclerotic changes, less often congenital or acquired defects.
As a result of a drop in blood flow intensity, toxins accumulate in the structures of the organ, which inhibit the normal myocardial contractility.
On the other hand, the muscle layer cannot work due to ischemia. Accordingly, the heart chambers are also not able to function adequately. The left ventricle does not throw blood into a large circle with sufficient force.
Hence the drop in oxygen saturation, poor supply of the brain, distant organs and systems.
This situation is not normal. Over time, death will inevitably occur. Recovery requires urgent action.
The main factor in the development of acute coronary syndrome is atherosclerosis of the corresponding arteries that feed the heart. Depending on the type of deviation from the norm, two forms of the described state are distinguished.
- Stenosis. He is a narrowing of the blood supply structures. It is somewhat less common when compared with the second type of atherosclerosis. Often it becomes the result of prolonged smoking, drinking alcohol, improper treatment of the underlying vascular disease (no matter what). The lumen is narrowed, there is a violation of conductivity. Blood cannot circulate normally. The heart increases the intensity of work to compensate for resistance. Hence the increase in blood pressure, an increase in heart rate. And since there is not enough nutrition, angina also occurs. The result is a generalized dysfunction of the entire system. The treatment is strictly surgical, urgently.
- Occlusion. Coronary artery blockage with a cholesterol plaque. Lipid structures are soluble in the early stages. Then they calcify, become hard as a stone. Removal of such formations requires radical surgical measures.
ACS is polyetiological. Scientists and doctors distinguish such reasons:
Atherosclerosis. As a result of the accumulation of low and very low density lipoproteins, triglycerides and cholesterol in the bloodstream, atherosclerotic plaques form in the vessel walls.
The latter are able to break away and block the flow of blood through the coronary arteries of the heart, provoking myocardial ischemia. At the same time, atherosclerotic plaques narrow the lumen of the vessels, reducing blood circulation.
ACS is primarily due to atherosclerosis. In most cases, the disease develops due to the destruction of the density of the atherosclerotic formation on the walls of the coronary artery, which was previously hemodynamically insignificant, but vulnerable to separation. Vulnerable atherosclerotic plaque is considered in the presence of a large number of lipids (fatty inclusions), numerous inflammatory cells and a thin, fibrous cap.
Plaque detachment can occur with active narrowing and expansion of the coronary artery, which is often observed in connection with an increase in oxygen consumption by the myocardium, for example, as a result of physical activity, emotional or physiological stress. The latter develops with dehydration, loss of blood, hypotension, infection, thyrotoxicosis, or after surgery.
After separation, the atherosclerotic plaque tends in the direction of the heart, where the diameter of the vessel is always smaller, and plugs it completely or partially. After this, the process of severe ischemia and unstable angina pectoris begins. In the overwhelming majority of cases, the condition ends in myocardial infarction due to acute lack of blood supply to the heart muscle.
The density of occlusion of the coronary artery, the duration of obstruction, the volume of the affected cells of the heart muscle, the level of load on the heart and the ability of the rest of the heart muscle to compensate for their work are the main factors that determine the clinical picture and prognosis of acute coronary syndrome.
The development mechanisms (pathogenesis) are the same for all ischemic, that is, associated with a lack of oxygen, heart disease, including for acute coronary syndrome. There are only two reasons that violate the normal movement of blood through the arteries: a change in the tone of the arteries and a decrease in their lumen.
1. Spasm of the vascular wall can occur from an increased adrenaline rush, for example, in a stressful situation. The expression “heart sank in the chest” accurately describes a person’s condition with a short-term attack of ischemia. A short oxygen deficiency is easily compensated: heart rate (HR) rises, blood flow rises, oxygen flow increases, well-being and mood become even better.
People who are passionate about extreme sports and recreation constantly get short adrenaline “attacks” on their hearts and the pleasant sensations associated with them – joyful excitement, an influx of energy. The physiological bonus of any, even small loads is a decrease in the sensitivity of coronary vessels to spasm, and hence the prevention of ischemia.
If the stressful situation dragged on (time varies depending on the “fitness” of the heart), then the decompensation phase begins. Muscle cells spend an emergency supply of energy, the heart begins to beat slower and weaker, carbon dioxide accumulates and reduces the tone of the arteries, and blood flow in the coronary arteries slows down.
2. A decrease in the lumen of the coronary arteries is associated either with violations of the normal state of their inner membrane, or with a blockage of blood flow by a blood clot (blood clot, atherosclerotic plaque). The frequency of the problem depends on risk factors, with prolonged exposure leading to metabolic disorders and the formation of blood clots.
The main external factors:
- Smoking – general intoxication, violation of the cells of the inner layer of arteries, an increased risk of blood clots;
- Unbalanced diet – increased blood lipids; inadequate intake of proteins; a change in the balance of vitamins and minerals; imbalance in metabolism;
- Low physical activity – an “untrained” heart, a decrease in the force of contractions of the heart, venous congestion, a deterioration in the supply of oxygen to tissues, and the accumulation of carbon dioxide in them;
- Stress – constantly increased adrenaline background, prolonged arterial spasm.
You must admit that the name “external” is no coincidence, their level can be lowered or increased by a person himself, just by changing his lifestyle, habits and emotional attitude to what is happening.
Over time, the quantitative effect of risks accumulates, transformation into qualitative changes occurs – diseases that already belong to the internal risk factors for acute coronary insufficiency:
- Heredity – structural features of blood vessels, metabolic processes are also transmitted from parents, but as relative risk factors. That is, they can be both aggravated and significantly reduced, avoiding external factors.
- With a sharp increase in blood lipids and atherosclerosis – deposits in the arteries in the form of atherosclerotic plaques with narrowing of the lumen, myocardial ischemia.
- O fatty – an increase in the total length of blood vessels, increased load on the heart, thickening of the muscle wall (myocardial hypertrophy).
- And hypertension – consistently high numbers of blood pressure, changes in the walls of the arteries (sclerosis) with a decrease in their elasticity, congestive manifestations – edema
- With diabetes – blood viscosity and the risk of blood clots increase, changes in arterioles (the smallest arterial vessels) lead to ischemia of organs, including myocardium.
A combination of several factors increases the likelihood of blood clots completely blocking the heart’s own arteries. The consequence of the development of events in this scenario will be sudden coronary death, the second most frequent (after myocardial infarction) outcome of acute coronary syndrome.
Myocardial infarction and its varieties
Typification is carried out on a group of grounds.
Based on the form, they talk about two varieties:
- Unstable angina pectoris. Gradual, chronic malnutrition as a result of narrowing of the coronary arteries (much more often) or their blockage.
Recovery requires continued assistance. The pathological process itself is divided into 4 functional classes, they correspond to the severity of the disease.
The first is treated completely, starting from the second, it will not be able to stop the state drastically. Therapy is lifelong.
Unstable angina as a form of acute coronary syndrome occurs in seizures, usually an trigger factor precedes the episode. From physical overvoltage to hypothermia and others.
- Heart attack. In terms of severity, it is much more dangerous and characteristic. Accompanied by severe pain in the chest, respiratory failure, consciousness.
If angina pectoris gives a slow, stepwise development, cardiomyocytes die in small groups, in this case the process is avalanche-like.
Destruction of significant areas is possible. The wider the area of damage, the more intense the symptoms.
After a certain time from the onset of this form of acute coronary syndrome, the phenomena subside.
Imaginary well-being should be perceived as an alarming sign, as destruction continues at a rapid pace.
The clinical version of the described condition partially affects the severity:
- Primary form. It develops in patients who previously did not survive angina attacks and did not have a history of heart attack.
- A progressive variety. Its essence lies in the aggravation of the main process. Usually the reason for this is a complication of the main disease, for example, atherosclerosis or an improper lifestyle. Also, the lack of treatment or its insufficient effectiveness.
- Postoperative form. It is accompanied by severe symptoms, but usually proceeds over a short period of time. If the intervention is carried out incorrectly, it is possible to become a resistant variety.
- Postinfarction type. Accompanying the rehabilitation period of an emergency. It requires mandatory correction, since it increases the risk of relapse.
- Spontaneous angina pectoris. The most dangerous from clinical vision. Provokes frequent episodes of malnutrition in the short term. Up to 5-8 seizures can occur in a week.
As mentioned above, the diagnosis of MI is made on the basis of the clinical manifestations of the disease, ECG data and the determination of biochemical markers in the blood that reflect necrotic changes in cardiomyocytes. In typical cases, clinical manifestations are quite characteristic:
- Suddenly there are pains behind the sternum and (or) in the heart area of a pressing, compressive or burning nature;
- Often the pain radiates (“gives”) to the upper limbs, neck, lower jaw, back, epigastric region;
- The duration of pain exceeds 20 minutes. Many patients have a feeling of fear and cold sweat. Unlike regular angina pectoris, nitroglycerin does not stop these attacks, or brings only short-term relief.
It is worth noting that modern invasive methods of treating ACS not only improved treatment outcomes, but also greatly diversified the causes that lead to the development of MI.
Types of Myocardial Infarction
Spontaneous myocardial infarction due to myocardial ischemia due to erosion and / or tearing of an atherosclerotic plaque.
Myocardial infarction, which is caused by myocardial ischemia due to increased myocardial oxygen demand or poor blood supply, for example, as a result of spasm of the coronary arteries, their embolism, arrhythmia, anemia, increase or decrease in blood pressure.
Cardiac death with signs of possible myocardial infarction, when it is not possible to evaluate biomarkers of heart damage.
Myocardial infarction, which is associated with percutaneous coronary intervention.
Myocardial infarction associated with stent thrombosis according to angiography or autopsy.
Myocardial infarction associated with coronary artery bypass grafting.
Thrombolysis in patients without ST segment elevation is not indicated.
The clinical course and stages of the disease
Classification of acute coronary syndrome allows you to divide patients into two groups:
- Patients with chest pain lasting more than 20 minutes, which cannot be relieved by taking nitroglycerin. On the ECG – ST segment elevation, which indicates acute coronary artery occlusion. In the future, this leads to the occurrence of Q-infarction.
- Patients with chest pain lasting more than 20 minutes, which cannot be relieved by taking nitroglycerin, and patients with class III angina pectoris that first appeared without a steady ST segment elevation (depression, T change). This condition transforms into non-Q-infarction or into unstable angina.
Direct classification by severity involves taking into account the indicators of electrocardiography:
- ACS without ST segment elevation. Evidence in favor of a relatively mild clinical variant of the pathological process. Recovery is likely, the forecast is relatively favorable. Usually corresponds to angina pectoris or mild heart attack. Therapy in stationary conditions in any case.
- Acute coronary syndrome with ST segment elevation. Accompanying severe organic damage to the heart. Corresponds to an extensive heart attack or rapidly progressing process of destruction of cardiac structures. Recovery is strictly in the conditions of the specialized branch. The prognosis is much worse, urgent medical attention is required.
Despite the difference between the two described forms in terms of results and outcome, the symptoms do not always correspond.
A patient with a potentially lethal variant of ACS may not feel significant changes in well-being, at the same time, minor angina pectoris can lead to intense pain syndrome, falsely prompt a person to think about the severity of the condition.
Not only sensations, but also objective data are subject to evaluation.
There are two main forms of ACS:
- Unstable angina pectoris is a sternal pain characteristic of a heart attack, which appeared for the first time or already repeatedly, immediately after physical or emotional stress, or in a calm position.
- Myocardial infarction – necrosis (necrosis) of the muscle wall of the heart. Depending on the area of the lesion, there is a small focal (microinfarction) and extensive, according to localization – according to the accepted names of the walls of the heart – the anterior, lateral, posterior-diaphragmatic and interventricular septa. The main life-threatening complications are fatal rhythm disorders and rupture of the heart wall.
The classification is important both for assessing the severity of the condition and for analyzing the risk level of sudden coronary death (occurring no more than 6 hours after the onset of the attack).
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the presence of at least one of the signs:
- An attack of angina pectoris for more than 20 minutes to the present;
- Pulmonary edema (shortness of breath, bubbling breath, pinkish foamy sputum, forced sitting position);
- On the ECG: decrease or rise of the ST segment more than 1 mm above the contour;
- Angina pectoris with decreased pressure in the arteries;
- Laboratory: bend level markers of myocardial necrosis.
Discrepancy with high-risk points, or the presence of one of the mentioned signs:
- An attack of angina pectoris for less than 20 minutes, stopped when taking nitroglycerin;
- Angina pectoris less than 20 min, stopped after taking nitroglycerin;
- Nighttime attacks of chest pain;
- Severe angina pectoris first appeared in the last 14 days;
- Age over 65;
- On the ECG: dynamic changes of the T wave to normal, Q waves more than 3 mm, a decrease in the ST segment at rest (in several leads).
in case of discrepancy with the criteria for high and medium risk:
- More frequent and more severe than usual seizures;
- Lower level of physical stress causing an attack;
- Angina pectoris first appeared, from 14 days to 2 months;
- On the ECG: a normal curve in accordance with age, or the absence of new changes compared to previously obtained data.
How is ACS developing?
Myocardial cells require oxygen and adenosine 5b-triphosphate (ATP) to maintain contractility and electrical stability. Since they are deprived of it, anaerobic glycogen metabolism occurs, less ATP is formed, which leads to a failure of sodium-potassium and calcium pumps and the accumulation of hydrogen and lactate ions.
Depends on the form of acute coronary syndrome.
- Chest pains. Angina is characterized by the development of moderate discomfort. Moreover, its duration is not more than 30 minutes. Nitroglycerin when taking well stops the sensation. Against the background of a heart attack, the pain is much stronger or lasts longer.
- Lack of oxygen. In complete rest. The patient cannot find a position to alleviate the condition.
- Increased cold sweating.
- Pale skin.
- Cyanosis of the nasolabial triangle as a visiting card of cardiac pathologies in general.
- Panic attack. It is accompanied by a strong sense of fear, anxiety, continues throughout the first phase of the attack, then subsides. It is stopped by tranquilizers, it is better within the hospital. It does not always occur.
- Motor excitement. The patient does not find a place, rushing around.
- Confusion. Disturbed perceptions of reality.
- Fainting or syncope. Indicate involvement in the pathological process of the brain.
The presented moments form the basis of acute coronary syndrome.
The intensity of manifestations and the completeness of the clinical picture is never the same, but depends on the degree of circulatory disturbance and the individual characteristics of the human body.
Acute coronary circulation disorder has the following clinical symptoms:
- sudden pain behind the sternum. Depending on the vastness of the process, painful sensations are localized or diffuse. They can radiate to the back, shoulder blade, neck, hands, stomach and even to the pelvic area;
- the occurrence of cold, sticky sweat on the forehead;
- darkening in the eyes with the appearance of artifacts similar to glowing dots or lightning;
- noise in ears. Some patients experience a ringing or throbbing effect;
- cyanosis of the nasolabial triangle and fingertips. This symptom is due to the fact that with a heart attack, cardiac output decreases sharply and the distal parts of the body stop supplying blood;
- deterioration in mental activity. Temporary impairment of consciousness is also caused by insufficient oxygenation of nerve cells in the brain. Patients sharply worsen memory, attention and other mental functions;
- the appearance of a cough, occasionally accompanied by sputum separation;
- feeling of a sinking heart in the chest.
First of all, the diagnosis of ACS begins with the collection of anamnesis and detailing of complaints: prolonged (more than 20 min.) Intense chest pain of a pressing nature, shortness of breath, fear of death – a similar symptom complex practically does not occur in other heart pathologies. The main purpose of a physical examination is to exclude pains of non-cardiac origin , non-ischemic heart diseases, as well as any pathologies that potentially contribute to the increase in ischemia.
An electrocardiogram (ECG) at rest – is the “golden method” of diagnosing ACS, as well as a screening method for other diseases accompanied by pain. An ECG at rest must be compared with a preliminary cardiogram and with an ECG after the disappearance of pain. Another advantage of this method is the ease of execution – patient management is available both in the hospital, in the clinic, and in the family type outpatient clinic.
During myocardial death, heart cells die. Enzymes from cardiomyocytes enter the bloodstream and continue to circulate in it for some time. Using special tests, you can determine the concentration of these substances, assess the degree of damage, and also establish the fact of necrotic changes in the heart muscle.
Markers of necrotic changes in the myocardium are:
- Creatine phosphokinase (MV).
Echocardiography – this method is widely used to clarify the diagnosis, but is not suitable for making it, since it does not allow you to see small foci of necrosis.
Signs of ACS are:
- Pathological valve function.
- Enlarged chambers of the heart.
- Turbulent blood flow.
- Enlarged inferior vena cava.
This method is used if it is necessary to determine the exact localization of the necrotic focus. Its essence is that healthy and damaged cells have different biochemical activity. With the introduction of special reagents, the latter will accumulate selectively in either healthy or dead cells (depending on the reagent), which will accurately determine the presence of damaged areas.
Coronarography is a rather complicated, but quite informative method for the study of ACS. Its essence is the implementation of an x-ray image after the administration of a contrast agent into the coronary arteries. Coronarography allows you to determine the exact location and degree of narrowing of the affected artery.
Mandatory (standard) diagnostic measures for suspected ACS are an electrocardiogram and determination of necrosis markers. The rest are prescribed if necessary – depending on the specifics of the disease in each patient.
It is carried out under the supervision of a cardiologist. If the patient was transported to a hospital, the minimum time for examination.
Limited to visual data and blood pressure, heart rate. Occasionally resort to electrocardiography, but more often than not every minute counts.
The task is to first stabilize the patient, then engage in diagnostic research.
An approximate therapeutic regimen after restoration of body functions and relief of an attack:
- Oral questioning of the patient, history taking.
- Measure blood pressure and heart rate. Holter monitoring is much more effective. That is, the registration of indicators within 24 hours. Repeated carrying out is possible.
- Electrocardiography Assessment of the functional activity of the heart.
- Echocardiography. Tissue visualization.
- The blood test is general, biochemical, for hormones.
- Clinical examination of urine. Primarily interested in the work of the kidneys and the presence of sugar, as a sign of diabetes.
Unfortunately, most manifestations are smoothed out in bright moments. Only in the event of a relapse of the coronary syndrome they are again updated.
ACS should be assumed in men over 30 years old and women over 40 years old if the main symptom is discomfort or chest pain. Since the pathogenesis of all forms of ACS is similar and differs mainly in the extent and degree of myocardial damage, clinically (according to the symptoms) different forms of ACS have similar manifestations, mainly anginal pain.
Pain in ACS should be distinguished from pain in pulmonary embolism, pneumonia, pericarditis, pneumothorax, myocarditis, fracture of the ribs, hypertensive crisis, esophageal spasm, diaphragmatic hernia, renal colic, acute aortic dissection, osteochondrosis. In most cases, anginal pain has obvious characteristic features, which allows you to confidently make a preliminary diagnosis:
- According to the patient’s description, the pain is compressive, sometimes burning;
- The pain is localized most often behind the sternum – in its middle and lower parts.
- The pain is spilled, has a large area on the front surface of the chest.
“If you combine the above properties of coronarogenic pain and ask the patient to show it, then the patient with an open palm will describe a circle or several circles at the level of the middle and lower part of the sternum, and then clench his fingers apart. The patient, as it were, subconsciously points to a feeling of compression, compression in the middle-lower part of the sternum and the diffuse nature of the pain. This is the symptom of a clenched fist described by Yushar – one of the reliable signs of coronarogenic pain. “
If we are talking about angina pectoris, then an alternation of attacks of pain and periods when the pain completely disappears is characteristic. Sublingual administration of nitroglycerin (a tablet under the tongue) quickly stops the pain or significantly reduces it. The attack itself has a wave-like character – at first the pain sensations become stronger and then decline.
Myocardial infarction (MI) is characterized by severe pressing or constricting chest pain, often radiating to the left arm and accompanied by fear of death. In general, in terms of their characteristics and localization, pain is similar to angina pectoris, but is more severe, lasts
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