Heart Attack Symptoms
Mar 05, 2018
Myocardial infarction is an acute heart muscle disease characterized by one or more foci of necrosis due to circulatory disorders. This is the most severe form of ischemic heart disease. The patient needs bed rest. The diagnosis is based on three clinical signs: a characteristic severe anginal pain that lasts for more than 30 minutes, not abating after taking nitroglycerin;ECX data( abnormal Q or QS complex as a sign of necrosis, elevation of the ST segment and a negative T wave);increase in the enzyme FK-MB in the blood serum. How to apply folk remedies for an infarction, see here.
It is observed more often in men aged 40-60 years. In men myocardial infarction of is more common than in women, especially at a young age. At the age of 41-50 years this ratio is equal to 5: 1, and in the period of 51-60 years - 2: 1.Later, the difference disappears due to the increase in the frequency of infarction in women. It is believed that the townspeople suffer from myocardial infarction more often than the villagers, but here the role, apparently, of a different level of diagnostic capabilities seems to play a role. Maximum mortality is in the autumn-winter period. Read here in detail how to provide first aid to increase a patient's chances of surviving. Typically, myocardial infarction occurs as a result of the destruction of coronary arteries of the heart in atherosclerosis, when the narrowing of their lumen occurs. Often, this process involves the obstruction of the vessel in the area of its defeat, as a result of which the blood completely or partially ceases to flow to the corresponding portion of the heart muscle, and foci of necrosis( necrosis) are formed in it.
Risk of myocardial infarction( based on materials of the American Heart Association)
The risk of myocardial infarction is low - 6-13, average - 14-22 points, high - 23 points.
People with stroke who have diabetes mellitus genetically predisposed to heart disease are much more likely to develop myocardial infarction.
1. Localization( right ventricular, left ventricular, septal, etc.);
2. The depth of necrosis of the myocardium( penetrating, non-penetrating, focal, widespread);
3. In stages of myocardial infarction:
4. By the presence of complications:
5. By the depth of the lesion: transmural myocardial infarction( the process captures the entire thickness of the heart muscle), intramural( with localization of the dead center in the heart muscle), as well as subepia- Cardiac and subendocardial infarction( adjacent to the endocardium or epicardium).
6. Three main zones of cardiac muscle changes in a heart attack: a necrosis focus, a prenecrotic zone and a zone distant from necrosis. The outcome of the necrosis of the muscle is the formation of connective tissue scar.
7. Clinical variants of myocardial infarction: typical( or painful) and atypical, including: asthmatic, abdominal, arrhythmic, cerebrovascular and painless( malosymptomatic), as well as with atypical localization of pain.
Most often the infarction develops in the anterior wall of the left ventricle, in the blood supply pool most often affected by atherosclerosis of the anterior descending branch of the left coronary artery. The second most frequent place is the infarction of the posterior wall of the left ventricle. Further, the lesions of the interventricular septum and papillary muscles follow.
1. Pain form( typical development variant)
In the typical course of a severe myocardial infarction, five periods are distinguished: prodromal, acute, acute, subacute and post-infarction.
The prodromal period, or the so-called pre-infarction, is observed in more than half of the patients. Clinically, it is characterized by the appearance or significant increase and increase in the severity of angina attacks, as well as changes in the general condition( weakness, fatigue, decreased mood, anxiety, sleep disturbance).The action of conventional painkillers in patients receiving them becomes, as a rule, less effective
The sharpest period( the time from the onset of myocardial ischemia to the first manifestations of its necrosis).
Characteristics of a typical attack of pain in myocardial infarction:
1. Pain characteristics: suddenly, the pain behind the sternum is very intense, burning with irradiation in the left arm, left shoulder blade, abdomen, back.
2. Duration of pain: painful syndrome lasts on average more than 30 minutes, sometimes even 1-2 days.
3. Reaction to medicines: pain is not stopped by nitroglycerin or Validol, for the anesthesia you need medical help.
4. Reaction to physical stress: pain is aggravated, bed rest and reduction of any physical exertion is necessary.
5. Other signs of pain: a painful attack can be accompanied by a feeling of fear, severe weakness, a feeling of lack of air, a fear of death, usually marked profuse sweat, dyspnea at rest, and nausea and vomiting are frequent( especially with the lower location of myocardial infarction).Often this happens in patients in a state of strong psychoemotional stress, alcoholic intoxication.
Myocardial infarction occurs at any time of the day, especially in night, pre-weaning hours. Very rarely, pain is absent.
When examining a patient, the pallor of the skin and the symptoms associated with intense pain( a painful facial expression, motor anxiety or stiffness, cold sticky sweat) are determined. In the first minutes, blood pressure rises, then progressively decreases as a manifestation of developing cardiac and reflex acute vascular insufficiency. A sharp drop in blood pressure is usually associated with the development of cardiogenic shock.
The acute period occurs immediately after the end of the acute period and lasts for about 2 days until the final delimitation of the necrosis foci( during this period, one part of the myocytes located in the perianfarric acid zone dies and the other recovers).With a recurrent course of myocardial infarction, the duration of an acute period may extend to 10 or more days.
In the first hours of the acute period, anginal pain disappears. Preservation of pain is possible with the development of pericardial inflammation, as well as with continued or recurrent myocardial infarction. Heart failure and arterial hypotension, as a rule, remain and can even progress, and in some cases they occur even after the end of the acute period. Violations of the rhythm and conductivity of the heart are determined in the overwhelming majority.
The resorption syndrome, which develops in the acute period of myocardial infarction, is characterized by the onset of a febrile reaction( with body temperature only rarely exceeding 38.5 ° C) and an increase in ESR.
Subacute period, corresponding to the time interval from complete delimitation of the necrosis foci until replacement with a tender connective tissue, lasts approximately 1 month. The clinical symptoms associated with a decrease in the mass of the functioning myocardium( heart failure) and its electrical instability( cardiac arrhythmia) during this period are manifested in different ways. The general well-being of patients, as a rule, improves. Dyspnea at rest, as well as auscultatory and radiologic signs of blood congestion in the lungs decrease or disappear.
The sonority of cardiac tones gradually increases, but it is not completely restored in most patients. Systolic blood pressure in most patients gradually increases, although it does not reach the initial value. If the myocardial infarction developed against the background of arterial hypertension, systolic blood pressure remains significantly lower than before myocardial infarction, whereas the diastolic does not change significantly( "decapitated" arterial hypertension).
It is necessary to know that angina attacks may be absent;their disappearance in a patient suffering from angina pectoris before myocardial infarction, indicates a complete blockage of the artery, in the basin of which, until infarct, myocardial ischemia periodically appeared.
The post-infarction period following acute is terminating the course of myocardial infarction, since at the end of this period the final formation of a dense scar is expected in the infarction zone. It is generally accepted that in the typical course of a large-heart attack of myocardial infarction, the post-infarction period ends within a period corresponding to approximately 6 months after the onset of the necrosis foci. During this period, compensatory hypertrophy of the surviving myocardium is gradually developing, due to which heart failure, if it originated in earlier periods of myocardial infarction, can be eliminated in some patients. However, with large lesions of the myocardium, full compensation is not always possible, and signs of heart failure persist or increase.
Of the atypical forms of myocardial infarction, the most common asthmatic variant, proceeding according to the type of cardiac asthma or pulmonary edema. It is observed with extensive damage to the heart muscle, with repeated heart attacks, against the already existing circulatory failure, in the presence of cardiosclerosis. Occurs in 5-10% of patients. In half of cases, asphyxiation is combined with chest pains. The development of cardiac asthma can contribute to an acute increase in blood pressure.
This syndrome is based on the extreme degree of left ventricular failure and stagnation of blood in the lungs. Suddenly, there is a feeling of lack of air, escalating into choking, and the fear of death associated with it. The patient becomes very restless, "can not find a place", takes a forced sitting position, leaning his hands on the bed to strengthen breathing movements. The respiratory rate rises to 80-90 per minute. The character of breathing changes: after a short inhalation, an extended exhalation follows. The facial expression of the patient is painful, exhausted, skin is pale, lips are cyanotic, cold sweat appears.
Breathing becomes noisy, bubbling, wheezing is heard from a distance. Cough appears, soon begins to separate liquid, foamy sputum of a pinkish color or with an admixture of blood.
Abdominal variant of myocardial infarction is observed in 2-3% of patients, mainly with its lower or lower-posterior localization. Pain sensations are concentrated in the epigastric region. Patients are excited, rush, groan, skin at the time of pain intensification sweat. However, the feeling of the abdomen does not cause significant pain, the abdomen remains mild, there are no symptoms of irritation of the peritoneum.
To the pains in the epigastric region, nausea, vomiting, agonizing hiccough, loose stool can join. This can serve as an excuse for erroneous conclusions about food intoxication or gastroenteritis.
The cerebrovascular form may occur as a syncope or stroke. Violation of the cerebral circulation usually has a transient nature. There are signs of vascular damage to the brain( speech disturbance, cerebral stroke).Along with cerebral strokes in the acute period of myocardial infarction, there are also other neurologic disorders: fainting, loss of consciousness.
Brain stroke is often a complication of myocardial infarction. Clarify the situation by careful examination of the heart, ECG recording, biochemical blood tests.
The arrhythmic variant begins with various disturbances of a rhythm - attacks of a ciliary arrhythmia, a tachycardia, a frequent extrasystole. The pain is absent or appears after arrhythmia. AMI can be manifested by severe tachyarrhythmias with lowering blood pressure, sudden clinical death due to ventricular fibrillation( less often asystole).
The diagnosis of myocardial infarction is conclusive when the patient has a clinical picture of an anginal attack, an increase in a number of enzymes( CK, LDH, etc.) in the blood, characteristic changes in the ECG.
1. Violation of the rhythm of conduction( arrhythmic shock).
When myocardial infarction affects not only myocarditis - muscle cells, but the conductive system suffers. The heart finds itself in unusual working conditions, for the optimization of which some adjustment is necessary. But it takes time for this restructuring. Therefore, the heart tries to deliver blood to human organs with more cuts. Arrhythmias that occur with myocardial infarction can be both temporary and permanent. Very dangerous are the so-called atrial fibrillation.
2. The true cardiogenic shock of is the most severe complication of myocardial infarction, which often results in death. The cause of shock is the rapidly emerging and extensive necrosis of the left ventricular muscle( more than half its muscle mass), which is accompanied by a sharp decrease in the volume of ejected blood. At the same time, the patient does not move, is sharply weakened, does not complain about pain, answers questions with difficulty, often falls into a hindered state, there may be a loss of consciousness. The face is pale, with blue lips and mucous membranes, cold extremities, skin integuments acquire a "marble" pattern, covered with copious cold sticky sweat.
One of the main signs of cardiogenic shock is a catastrophic drop in blood pressure - below 80 mmHg. Often the systolic pressure is not determined. Pulse of weak filling, frequent, more than 100-120 beats per minute. With a decrease in blood pressure below 60/40 mmHg.the pulse becomes threadlike, at a lower pressure the pulse is not probed. Respiration is frequent and superficial( 25-35 per minute).In the lungs against the background of a drop in arterial pressure, stagnant phenomena, including swelling, increase. Decreases urination, up to complete absence of urine.
3. Acute heart failure. Weakness of the left ventricle does not always manifest itself in the form of cardiac asthma and pulmonary edema. In many patients, left ventricular failure is more moderate. The patient feels a short breath, he has heart palpitations( more than 100 beats per minute), lips are cyanotic. Blood pressure is maintained at a normal or slightly reduced level. In the posterior-lower parts of the lungs, a small amount of moist, small-bubbling wheezing is often heard. Extreme forms of left ventricular failure are cardiac asthma.
4. Heart rupture. Gastric muscle tears occur in patients with primary transmural myocardial infarction. Repeated infarctions are rarely complicated by breaks. The lethality in this case is very high. Most breaks occur in the first three days of the disease, often on the first day. There are external and internal ruptures of the heart, external are more common. The rupture usually occurs along the anterior wall of the left ventricle, closer to its apex. Most patients die on the first day of myocardial rupture.
5. Aneurysm of the heart. This complication of a widespread transmural myocardial infarction is a diffuse swelling or a saccular cavity, usually containing a parietal thrombus. Most often an aneurysm is located in the region of the tip of the left ventricle or near it. Aneurysm is formed in 10-15% of patients in the first weeks of myocardial infarction. Chronic aneurysm is the result of scarring of the walls of an acute aneurysm.
Acute cardiac aneurysm may be complicated by a rupture in the first 3 weeks from the onset of myocardial infarction. About 70% of patients with chronic postinfarction aneurysm die within 3-5 years of heart failure, arrhythmia or repeated myocardial infarction.
One of the criteria listed below is sufficient for the diagnosis of acute myocardial infarction.
Typical increase and gradual decrease( cardiac troponins) or faster increase and decrease( MB CK) of biochemical markers of myocardial necrosis in combination with one of the following:
a) clinical picture of ACS;B) appearance of abnormal teeth Q on the ECG;
c) changes in the ECG, indicating the occurrence of myocardial ischemia: the emergence of an upsurge or depression of the ST segment, blockade of LNPG;
d) the appearance of signs of loss of viable myocardium or violations of local contractility with the use of techniques that allow visualizing the heart.
The main clinical and laboratory signs of myocardial infarction are:
1. Increase in body temperature( from subfebrile digits to 38.5-39 ° C).
2. Leukocytosis, usually not exceeding 12-15 x 109 / L.
4. A small stab that shifts the blood formula to the left.
5. Increase in ESR.
Enzyme diagnostics. By the level of activity of enzymes, one can judge the severity of myocardial infarction. For example, the activity of the MB fraction of the enzyme CKK( creatinine phosphokinase) usually rises after 8-10 hours from the onset of myocardial infarction and returns to normal after 48 hours. The activity is determined every 6-8 hours;at least three negative results are necessary to exclude myocardial infarction. Treatment is started without waiting for an increase in the activity of CK.New methods for the determination of CK isoenzymes can speed the diagnosis, but they have not yet been widely used. The activity of the first isoenzyme LDH( LDH;) becomes higher than the activity of LDH2 on the 3-5th day of myocardial infarction. LDH activity is determined daily for 3 days if the patient enters 24 hours after the onset of symptoms of myocardial infarction. If LDH activity reaches the borderline values or if the patient arrives after 3 days or more after the onset of symptoms, myocardial scintigraphy with 99mTc pyrophosphate is shown.
Electrocardiographic study. According to Bayley, the violation of coronary circulation in myocardial infarction leads to the formation of three zones of pathological changes: zones of ischemic damage and ischemia are located around the necrosis site. In leads, the active electrode of which is located directly above the MI region, each of these zones participates in the formation of the following ECG changes.
1. The necrosis zone is a pathological Q tooth( lasting more than 30 ms) and a sharp decrease in the amplitude of the R wave or the QS complex.
2. Zone of ischemic damage - displacement of the RS-T segment above( with transmural myocardial infarction) or below the isoline( with subendocardial damage to the heart muscle).
3. Ischemia zone - "coronary"( equilateral and acute) T wave( high positive for subendocardial MI and negative for transmural myocardial infarction).
Echocardiography is one of the mandatory methods of research that are used to diagnose acute MI and assess hemodynamic and structural disorders in this disease.
The application of the technique of myocardial scintigraphy with technetium is indicated for the verification of myocardial infarction mainly in those cases when there are significant difficulties in interpreting ECG changes, due to the presence of blockade of the bundle of the bundle, paroxysmal disturbances of the heart rhythm or signs of a myocardial infarction in the past.
When it comes to coronary heart disease, you need to keep in mind the following four points:
1. Coronary artery atherosclerosis is an anatomical concept that indicates the possibility of polymorphic narrowing of the coronary arteries.
2. Coronary heart disease reflects a state of the coronary arteries when morphological( structural) or functional disorders lead to their insufficiency. Stenosis of coronary arteries as a result of concentric or eccentric atheromatous changes in the vessel wall and vasospastic coronary artery disease, reflecting not structural but functional changes( angiospasm) are noted. Perhaps the existence of transitional forms: a combination of stenosis and vasospastic disease of the coronary arteries.
3. Coronary insufficiency is the main pathological mechanism accompanying coronary artery disease.
Occurs as a consequence:
1) imbalance between myocardial oxygen demand and delivery in coronary artery stenosis;
2) reduction of coronary blood flow due to coronary artery vasospasm, as evidenced by a technique with thallium-201 or radionuclide ventriculography during a spontaneous attack or ergonovine-induced
3) disorders in small( intramural) blood vessels of the myocardium. The latter is characteristic of syndrome X( coronary heart disease without proven coronary artery disease).
Thus, there are areas of myocardial ischemia that are supplied through the coronary arteries, stenosed or vasospasm. The area of ischemia is a heterogeneous zone, since it is also supplied from other coronary arteries, and therefore there are also non-ischemic fibers.
4. Coronary heart disease is a clinical syndrome that manifests itself as symptoms and signs of myocardial ischemia. The degree of narrowing of the coronary artery and the functional significance of coronary artery affection, proven by the methods of arteriography, can be studied using electronic-diographic techniques.
If during an exercise test on a veloergometer with a load of 120-150 W for 14 minutes, anginal pain does not appear in the subject( and also equivalent symptoms and specific ECG signs of ischemia), then it is possible to exclude angina with good reason. In cases where doubts remain, it is necessary to resort to coronarography. Negative coronary angiography excludes angina pectoris.
Unlike all other types of chest pain, angina pectoris as a characteristic pain syndrome is established on the basis of a detailed study of the subjective feelings of the patient( the character of anginal pain), which provoke various influences, primarily mental and physical stress. Pain with angina rapidly disappears after stopping the load or taking nitroglycerin( usually already for 1 minute).However, it must be borne in mind that anginal pain sometimes appears atypically.
To atypical manifestations of angina pectoris primarily refers to atypical irradiation of anginal pain: the right shoulder, jaw, tip of the nose, the tip of the tongue, hard palate and throat, eyebrows, nape.
It should also be remembered that the equivalent of typical anginal pain may be shortness of breath of varying severity.
When conducting differential diagnostics, the following are especially helpful: detailed inquiry, positive dynamics of specific ECG changes( ischemia), positive test with nitroglycerin( with simultaneous clinical observation and ECG recording).
If there is no positive dynamics of the ECG, the pains of a protracted character in the left half of the chest indicate either a severe form of ischemic heart disease( IHD) or a lack of their connection with IHD.
Angina is usually indicated by positive ECG data in the form of depression( or elevation) of the ST segment more than 2 mm below or above the isoelectric line. Many authors are of the opinion that the appearance of a negative T wave during the loading test is of similar importance.
A physical sample should not be performed in case of positive ECG data at rest, preferably after taking nitroglycerin, repeat the loading test.
Deterioration of the subjective state of the patient and the dynamics of ECG changes, indicating a severe degree of ischemia, indicate an exacerbation of angina pectoris, which in turn requires special measures. To this end, it is necessary to urgently appoint adequate therapy and bed rest to prevent the development of unstable angina or myocardial infarction.
Unstable angina is a transitional clinical form between stable angina and myocardial infarction.
Myocardial infarction is the most severe form of IHD.In the classic clinical picture, among the characteristic signs, acute anginal pain predominates, lasting 15 minutes, or a protracted anginal condition lasting for hours and days, which is stopped only by narcotic drugs. It is characterized by classical ECG changes that develop in accordance with morphological changes( ischemia, damage, necrosis), and laboratory data( acceleration of ESR, hyperglycemia, leukocytosis, elevated ACT, ALT, CKF, etc.) and body temperature. These biochemical and ECG signs indicate necrosis of the myocardium in acute myocardial infarction.
In the differential diagnosis of anginal pain and the determination of the clinical form of IHD in favor of angina, a good general condition is better than with myocardial infarction, clinical analyzes, absence of tachycardia, dyspnea, hypertension, biochemical disorders, MI-specific ECG data( pathological Q,elevation of the ST segment and elevated body temperature).
Opposite to it on MI, even at absence of an anginal pain, specify unexpected occurrence( without visible other reasons) of a heart failure and a collapse. However, a more detailed study of the anamnesis suggests the existence of a patient with IHD.The establishment of a definitive diagnosis indicating MI is assisted by specific ECG changes and relevant biochemical data.
An anginal attack can be triggered( in addition to the physical and mental stresses already mentioned) in both coronary artery disease and in the absence of coronary artery atherosclerosis: tachycardia( any cause), bradycardia( especially in the atrioventricular block), high body temperature, metabolic disordersthyrotoxicosis, severe anemia and hypoglycemia), intoxication with nicotine, a sharp change in climatic conditions( cold, hot or humid air) and the environment( stay in high-altitude areas), hopesUse by large doses of alcohol.
Decreased perfusion coronary blood flow with concomitant syndrome of coronary insufficiency also reduces the shock volume of the heart, which is especially significant: pronounced bradycardia, arterial hypotension, heart failure.
Differential diagnosis between angina and other cardiovascular diseases is carried out primarily with those diseases in which coronary insufficiency occurs.
- congenital anomalies of the coronary arteries;
- congenital coronary arterial-venous fistulas;
- embolism of the coronary artery( fat, air, tumor cells, etc.);
- idiopathic dilatation of the pulmonary artery mouth with pulmonary hypertension;
- stenosis of the pulmonary artery or its combination with the tetralogy of Fallot;
- congenital heart disease with left-right shunts;
- transient prolapse of the mitral valve;
- affection of the aortic aorta( aortic stenosis, aortic insufficiency);
- mitral stenosis( severe form);
- hypertrophic obstructive myocarditis and idiopathic hypertrophic subaortic stenosis;
- exfoliating aneurysm of the heart;
- aortitis( including syphilitic aortitis);
- rheumatic carditis and especially complications of acute endocarditis;
- acute and chronic pericarditis;
- disorders of the heart rhythm, primarily paroxysmal supraventricular tachycardia;
- primary and secondary pulmonary hypertension;
- inflammatory-allergic coronary artery;
- panarteritis of the aorta( Takayashi disease);
- obliterating thromboarteritis( Buerger's disease);
- nodular periarteritis;
- almost all systemic connective tissue diseases of collagenosis).
When conducting differential diagnosis it is important to remember that there are great therapeutic options for correcting coronary insufficiency in the aforementioned diseases, primarily by treating the underlying disease.
Among the congenital and acquired heart defects, the following diseases are of particular importance in differential diagnosis:
1. Congenital malformations of the coronary arteries, primarily anomalous coronary artery circulation from the pulmonary artery, already leading to coronary insufficiency in early childhood. Some authors believe that the unexpected "painful cries" of children indicate a similar defect.
2. Congenital coronary arterial-venous fistulas can cause angina pain. In differential diagnosis, the detection of coarse diastolic noise in the precordial region helps. Operative correction( ligation) of the fistula leads to the disappearance of coronary symptoms.
3. Acquired heart defects with the advent of coronary syndrome. According to many authors, various acquired heart defects, especially in the stage of heart failure, can be accompanied by anginal pain, and in some are the main subjective manifestation of the disease.
4. Intermittent mitral valve prolapse may be accompanied by coronary insufficiency due to spasm of the coronary arteries. In favor of this, the research of IK Shkhvatsabai( 1982) also says that during coronary angiography and ventriculography, as a result of touching the tip of the catheter to the mouth of the coronary arteries, a spasm appeared, which in turn causes ischemia of the papillary muscles and mitral valve insufficiency.
In patients with intermittent mitral valve prolapse, anginal pains occur spontaneously at rest, often accompanied by fainting, shortness of breath, and ECG changes indicating ischemia and rhythm disturbances.
According to numerous studies, including those conducted in Yugoslavia, a favorable therapeutic effect in the treatment of this disease is achieved with the help of calcium antagonists.
Acquired and congenital heart defects, most often leading to an increase in the requirements for coronary blood flow, or relative( secondary) coronary insufficiency, are as follows:
- mitral stenosis,
- pulmonary artery stenosis,
- heart defects with left-right shunts,
- hypertrophic obstructive myocarditis and idiopathic hypertrophic subaortal stenosis,
- primary and secondary pulmonary hypertension.
For various types of acquired heart defects, pains of an anginous character occur with different frequencies.
- aortic and aortic-mitral defects - 40%,
- mitral stenosis, especially in children, 6.4%.
The greater the severity of heart failure, the more angina pain occurs.
According to IK Shhvatsabay( 1982), the use of the coronary angiography method really makes it possible to detect stenosing coronary atherosclerosis with different heart defects. In this way it was found that it is equally represented in patients with aortic( 17%) and mitral( 20%) heart defects. IK Shkhvatsabai explains these differences by the fact that the main role in the pathogenesis of coronary syndrome with acquired heart defects is due to hemodynamic insufficiency, and not the degree of atherosclerotic changes in coronary vessels.
In aortic insufficiency, the appearance of anginal pain in the chest is caused by low diastolic pressure and a "suction" effect on the coronary arteries of the reverse blood flow in the hypertrophied myocardium of the left ventricle of the heart.
In aortic stenosis, including subaortic stenosis, anginal pain is more pronounced as a result of a decrease in systolic and minute blood volume in conditions of increased need for hypertrophied left ventricular myocardium, which causes a decrease in coronary blood flow.
With mitral malignancy, anginal pains are caused by a stasis of blood in the coronary sinus as a result of increased pressure in the right atrium, as well as a reduced stroke volume and its inadequate increase in physical activity.
Pericarditis( acute and chronic) can be accompanied by pain in the left half of the chest, which simulates angina.
The sharp onset and persistent intense pain of atypical localization in the chest with acute pericarditis can simulate angina, especially since ECG signs indicate this( ST segment elevation and negative T wave, even the appearance of Q wave in some cases).
In differential diagnosis, difficulty represents not only pain syndrome, but also acceleration of ESR, an increase in the number of leukocytes, which is also characteristic of severe ischemic heart disease, myocardial infarction and pericarditis. However, a clear clinical definition of pericarditis, especially the corresponding angiographic data( silhouette of the heart in the form of a trapezoid) and the above ECG changes that do not reflect the dynamics, help the differential diagnosis of acute pericarditis.
Chronic pericarditis, accompanied by partial atresia or lime deposition, may also resemble angina due to:
- pain in the left half of the chest, which manifests itself in the form of prolonged compression or tingling, and aggravated when body position changes or weather conditions change;
- changes in ECG, representing known difficulties( persistently negative tooth T, "corrected" to positive when loaded and immediately after it returns to baseline).
In differential diagnosis, along with the above indications in favor of this type of pericarditis, the corresponding results of angiography( the presence of adhesion and lime deposits) also testify.
Embolism of the coronary arteries( fat, air, tumor cells) leads to coronary insufficiency. Therefore, in differential diagnosis, it is necessary to remember the etiological factors that lead to a similar embolism of the coronary arteries.
The present system for the treatment of patients with myocardial infarction includes:
Basic therapy, which is performed in all patients with Q-wave infarction, regardless of the presence or absence of any complications, includes the following activities: