How to calm the vagus nerve

Angina is based on acute myocardial ischemia due to functional spasm (or insufficient expansion) of the coronary arteries.

In the further course of the disease, their anatomical lesion — coronarosclerosis (atheromatosis of the coronary arteries) develops very often, which was well known to the first authors, who described this disease as “ossification of the coronary arteries”. Thus, the presentation of angina in the section on atherosclerotic lesion of the heart is essentially insufficiently substantiated, and it is more correct to attribute the early stages of the disease to neurogenic functional vascular diseases. GF Lang describes the thoracic toad in the section "Diseases of the neurohumoral apparatus regulating blood circulation", and atherosclerosis of the coronary arteries in the section "Diseases of the blood vessels"; However, the close connection of functional disorders of the coronary circulation with organic lesions of the arteries of the heart makes it more reasonable to describe both forms within a single disease.

This disease, popularly referred to as sometimes “angina pectoris,” was first described by an English physician V. Geberden in 1768. According to some data, angina develops in men 3-4 times more often than in women.

Angina pectoris develops due to acute insufficiency of the coronary blood supply, that is, the discrepancy between the blood flow to the heart and its need for it. As a result of impaired blood supply to the heart muscle, myocardial ischemia can develop – exsanguination of a portion of the heart muscle tissue, which, in turn, provokes a disturbance of metabolic processes in the myocardium and contributes to an excessive accumulation of metabolic products in it.

The most common causes of angina are the following factors:

  • atherosclerosis of the coronary arteries;
  • blood pressure disorder;
  • infectious and infectious-allergic lesions (much less).

Chest pain in angina is characterized by the fact that the time of its occurrence and remission is clearly expressed. In addition, pain occurs, as a rule, in certain conditions, circumstances – when walking, especially accelerating movement, when climbing uphill, in a sharp headwind, as well as during other significant physical effort and / or significant emotional stress. With the continuation or increase of physical effort, the tension increases and the pain, and with relaxation, the pain subsides and disappears within a few minutes. The duration of the attack is usually 1-15 minutes. Angina pain quickly subside and stop after taking nitroglycerin. However, seizures can sometimes occur, which last from 30 minutes to 1 hour. Such attacks in some cases lead to myocardial infarction. Therefore, if an attack of angina continues for 20-30 minutes or there is an increase or an increase in attacks of angina, an electrocardiographic examination should be carried out soon (within a day). In the future, the patient must be under constant medical supervision, that is, the patient must be hospitalized.

Attacks of angina may not appear for a long time, and they can occur quite often. In patients with a long history of illness, there is a risk of developing cardiosclerosis, the occurrence of cardiac arrhythmias, and the appearance of symptoms of heart failure.

There are a number of recommendations, the observance of which may help to postpone or avoid an attack of angina.

  1. During an attack, you should take a calm, sedentary position, and put 1 nitroglycerin tablet on a sugar cube or on a validol tablet under the tongue. In the absence of the effect of the drug must be taken again after 2 to 3 minutes. As a sedative, it is better to take 30-40 drops of Corvalol (Valocordin).
  2. As a prophylaxis of strokes, it is necessary to avoid strong physical and emotional stress.
  3. Equally important is the treatment of concomitant diseases, prevention of atherosclerosis, etc.
  4. Take nitroglycerin in the presence of signs of stress that can trigger an attack of angina. In addition to nitroglycerin, which suppresses acute manifestations of strokes, but with a short duration of action, it is necessary to take long-acting drugs (nitromasin, nitrosorbid, trinitrolong, etc.). These drugs are taken during the courses determined by the doctor, and with the stabilization of the patient’s condition, that is, the long absence of seizures, for example, before exertion, travel, etc.

Symptoms and signs of angina pectoris

It should be noted that pronounced features of angina – paroxysmal nature of pain, a clear relationship between the occurrence of chest pain and physical (as well as emotional) loads, as well as the rapid relief of pain with nitroglycerin – are sufficient grounds for diagnosis and separation of the disease from other pain sensations in the region of the heart and chest related to other causes.

It is important to remember that not all chest pain is a sign of angina pectoris.

Pain in the heart, associated with other causes, but not with angina, is often combined under the general term "cardialgia." Similar manifestations are found in other diseases such as the cardiovascular system (for example, heart defects, aortitis, etc.).

Pain in the heart with angina can last for many hours and even days. Sometimes patients feel lightning, piercing pain, which is localized in the apex of the heart. The use of nitroglycerin in such cases does not work. Relief of the patient’s condition, as a rule, occurs under the influence of sedatives (sedatives) and painkillers. It should be noted that when neuralgia along the intercostal nerves pain points are palpable.

The following symptoms, which are not necessarily accompanied by stenocardia, can also complement the picture of the disease manifestations:

  • localization of pain in the retrosternal region, which is quite typical; pain can be given to the neck, lower jaw, teeth, to the arm (usually left), shoulder girdle and scapula (usually to the left);
  • oppressive, constricting, less often burning nature of pain;
  • simultaneously with the onset of the disease, there is an increase in blood pressure, a feeling of irregularities in the heart area.

These signs characterize the so-called exertional angina resulting from exercise. It should be noted that patients often do not focus on a number of typical symptoms of angina, believing that these manifestations do not relate to the heart, and do not report them to the attending physician, which may make it difficult to make a diagnosis.

Unlike exertional angina, rest angina pectoris attacks are not associated with physical exertion and often occur at night. However, the rest of the manifestations of these two types of the disease are very similar. Attacks of rest angina are often accompanied by a feeling of lack of air, suffocation.

For the first time, angina pectoris can develop in one of three directions: go into stable exertional angina, develop into a myocardial infarction, or disappear.

Most patients with angina have a stable form of the disease, that is, the severity of the frequency and severity of attacks remains approximately the same for quite a long time, the attacks occur under similar conditions and subside under conditions of rest, as well as when taking nitroglycerin.

Depending on the intensity of the manifestations of the disease, four functional classes of stable angina are distinguished.

  • I functional class – Patients with rare angina attacks that occur only under the influence of excessive physical exertion.
  • II functional class – patients in whom angina attacks occur during normal physical exertion.
  • III functional class – attacks arise at small household loads.
  • IV functional class – Seizures in patients occur with minimal exertion and even in its absence.

Angina pectoris can be considered stable if the symptoms of the disease show up for several weeks without significant worsening. As a rule, bouts of stable angina are associated with an increase in myocardial oxygen demand.

How to calm the vagus nerve

Sometimes, against the background of stable angina, asymptomatic ("silent", painless) ischemia can develop, which is not accompanied by pain and any discomfort. Such a pathology can be identified only by conducting a special study – an electrocardiogram and some other methods.

Angina in a brighter form is more common in men after 40 years of age, when coronary sclerosis is usually found.

Attacks of simple angina pectoris (angina pectoris), not complicated by acute necrosis of the heart muscle, usually occur when walking or other physical exertion — the so-called ambulatory angina pectoris, or angina pectoris, as well as at other times characterized by increased requirements for coronary circulation, such as with agitation.

The classic description of angina pectoris (from ango — squeeze) was given as early as the 18th century.

As soon as the patient stops, the pain stops. Beyond these signs, the patient feels completely healthy. The pain is localized sometimes in the upper part, sometimes in the middle or at the base of the sternum and often to the left of the sternum. The pulse on the radial artery does not change during a seizure, the disease has nothing to do with shortness of breath. ”

All these signs are extremely valuable for the characteristics of simple (ambulatory) angina pectoris. An attack of pain occurs due to physical stress, mental agitation, in the cold, after lunch, relief gives complete rest, taking nitroglycerin, etc.

In severely ill patients with advanced atherosclerotic cardiosclerosis, simple angina may also occur in the quiescent state, when patients lie in bed — rest angina.

Severe painful attacks can alternate, with a feeling of numbness or tingling in the fingers of the left hand, with uncertain pains in the left shoulder and neck, etc., where skin areas of hypersensitivity respectively in the VIII cervical and five upper thoracic segments ( hyperesthesia zones).

Angina is based on a mismatch between the blood supply to the heart muscle and the need for blood increased during physical work, digestion, and. increased resistance to the work of the left ventricle from spasm of peripheral vessels, etc. The coronary vessels, which are unyielding as a result of sclerosis, and most importantly, with impaired neuro-vegetative regulation, do not expand properly with increased oxygen demand; myocardium is insufficiently supplied with blood; as a result, ischemic, or anoxic, pain of an organ that is not sensitive to mechanical trauma, but responds with a specific pain sensation to adequate stimulation in the form of impaired muscle tissue metabolism, appears. Indicative often held analogy of angina with intermittent claudication; in the latter, as a result of sharp angiospasm of the anatomically isolated lower limb vessels, painful cramps of the calf muscles or first numbness, stiffness of the leg and foot, which require an urgent “rest, stop, come on, after which the blood circulation is sufficient and the pain subsides immediately. It is characteristic that gradually, while walking, a certain adaptation may occur, and after a series of forced stops due to pain, the patient can already move much more freely; Apparently, the dystonic factor is reduced due to vasodilating substances formed in the working muscles, and most importantly, due to the establishment of nervous regulation. Thoracic toad was called “intermittent claudication of the heart” (claudicatio intermittens cordis). Primary importance in the origin of angina pectoris should be given to the violation of the coronary circulation due to changes in cortical activity and reflex influences from various internal organs. Changed in their activities, often sclerotic coronary vessels are also a center of irritation, a source of pathological signaling sent to the cerebral cortex. During an angina attack, signs of irritation of the vegetative subtalamic centers were observed, previously considered characteristic mainly for functional angina pectoris (“nervous toad”), such as “ejection of liquid spastic urine, low urge, high blood pressure”, as well as “sharp hyperalgesia integument of the pre-cardiac area. "

Residual, trace reactions in the cerebral cortex and coronary vessels of the heart contribute to the recurrence of strokes.

Diagnosis and differential diagnosis of angina pectoris

A diagnosis of angina on the basis of coronarosclerosis should be made in all cases when the patient may have atherosclerosis, in particular, coronarosclerosis, and there is at least an erased picture of a typical pain syndrome, even without acute severe pain with typical irradiation. The most conclusive for the diagnosis of stenocardia is not the strength of pain and not the classical fear of death (angor), but the appearance of sensations, even if they are not characteristic of walking, physical work, and disappearing completely or after taking nitroglycerin. The power of pain, as said, is of lesser importance; it can range from a feeling of great heaviness in the region of the heart, squeezing with ticks, to an obscure squeezing, numbness behind the sternum or to the left towards the neck or to the shoulder joint. The seizure is often limited to numbness, an unpleasant feeling of stiffness in the left hand in the area of ​​the median nerve branching.

How to calm the vagus nerve

Recently, they are trying to make an objective basis for the diagnosis of angina attacks, conducting a physical dosed load in patients and noting an S – T interval shift at an electrocardiogram removed at this time, which is absent during the workload of a healthy heart (the method does not have any indisputable value).

Having diagnosed the stenocardic nature of the pain, it should further be established whether the patient actually has coronary sclerosis or pain syndrome of similar origin is not associated with coronary sclerosis.

  1. Reflex thoracic toad of vagal origin with lesions of the abdominal organs, especially diaphragmatic hernia in the hiatus oesophageus area, when the cardiac part of the stomach that is herniated in the chest cell irritates the nearby nerve – the beginning of the reflex. Highly located peptic ulcers of the stomach or cancer of the cardia can also be accompanied by reflex angina pectoris, which is eliminated after the removal or mobilization of the cardiac part of the stomach. Inflammation of the gallbladder, hepatic colic can also be accompanied by angina, and the operation of cholecystectomy can lead to the cessation of this reflected pain for years. Apparently, any other hollow organ of the abdominal cavity, especially the stomach and intestines, can become a source of vagal reflex to the coronary circulation of the heart if it is stretched excessively. Thus, Botkin describes a case of sudden death, apparently of such origin, caused by excessive stretching of the stomach with pancakes. True, usually in this kind of patients, such as, for example, in cholelithiasis in obese elderly people, it is more correct to suspect the presence of coronary sclerosis and the leading significance of impaired neurovascular regulation.
  2. Thoracic toad of a hemodynamic-ischemic nature, due to insufficient delivery of oxygen to the heart with unchanged coronary vessels due to small systolic volume, insufficient pressure in the initial part of the aorta, oxygen poor blood with severe anemia, with poison gas, etc., even in young patients with a sharp rheumatic stenosis of the mouth of the aorta, severe angina attacks are possible due to insufficient blood pressure in the Valsalva sinuses, and hence insufficient blood irrigation does not even Changing the coronary arteries, the more dramatically exaggerated in aortic heart defect requires more oxygen. Aortic valve insufficiency also, although less frequently, leads to angina pectoris due to too rapid pressure fluctuations in the arterial system, which do not provide a constant supply of blood to the heart muscle. Excessive tachycardia, for example, paroxysmal tachycardia, tachycardia during crises of graves’ disease, can also disrupt the blood supply to the myocardium and cause ischemic pains. In severe anemia, such as malignant anemia with very low hemoglobin numbers (about 20% or less), painful attacks can equally be associated with insufficient oxygen supply of the myocardium, and with an improvement in the composition of the blood, the attacks stop. Acute blood loss can also cause angina-like pain. Collapse with insufficient blood supply to the heart, for example, in a person recovering from a serious infection during the first steps in the ward or in a patient with hypoglycemic shock, can also be accompanied by ischemic heart pains. Of course, here too it is necessary to think more often about sclerosis of the coronary arteries. So, in patients with malignant anemia, especially in elderly men with symptoms, apparently, of anemic angina, as well as in patients with diabetes mellitus in the presence of seemingly only hypoglycemic angina, is often severe coronary sclerosis. With rheumatism and valvular aortic disease, rheumatic coronaritis and so on can also be present.

Angina pectoris pain can also occur as a result of rapidly developing hypertension in acute nephritis, when the heart muscle cannot cope with a sudden obstacle, often with the same reduced blood flow through the coronary arteries, as well as with an overdose of adrenaline when it is administered intravenously.

Excessive physical exertion with a healthy heart is less likely to cause angina, as increasing shortness of breath causes you to stop working before the lack of blood affects the myocardium; a significant expansion of the heart in these conditions can cause pain in the heart, apparently due to stretching of the pericardium.

Arising from chronic nephritis, and even more so with hypertensive disease, angina pectoris is neurogenic, but usually combined with coronary sclerosis. The so-called tobacco angina pectoris is also functional, but often combined with or leading to coronarosclerosis. Angina pectoris has to be further differentiated from pain of a different origin in the region of the heart, in the chest, which is not dependent on myocardial ischemia.

Aortalgia with syphilitic aortitis is characterized by persistent unsharp pains predominantly behind the grip of the sternum, not associated with walking, not relieved by nitroglycerin and at rest, and is explained by the involvement in the inflammatory process of the nervous elements of the outer membrane of the aorta and neighboring tissues. This nature of pain in the upper part of the chest is revealed with particular evidence clinically with significant mesh aneurysms with periaortitis. In practice, aortalgia is difficult to distinguish from angina pain due to syphilitic aorta with a specific lesion of the orifices of the coronary vessels or a complication of conventional coronary sclerosis.

Pain in acute pericarditis is associated with excessive pericardial distension when its support function is exceeded. When fluid accumulates in the pericardium under high pressure, the coronary arteries with circulatory disturbances in them can also be compressed.

The pathogenesis of pain in the heart in acute myocarditis is unclear. Perhaps, they arise as a result of a cardiopulmonary process or the formation of disturbed metabolism products in the sharply affected myocardium, similar to those occurring in the ischemic muscle tissue of the heart.

Pain in the heart can be a manifestation of diseases of neighboring organs. Such are chest pains with paramediastinal pleurisy, sometimes occurring with dysphagia, different pupil sizes, etc .; pain in the shoulder, disturbing the breathing act, with diaphragmatitis; pain in the left nipple with intercostal neuralgia, fibrositis, myositis, gouty deposits, ribs fractures, osteomyelitis, periostitis, with painful cramps of the diaphragm in neuropaths — so-called frenocardia, or when the diaphragm is high, especially in women during menopause.

In this group of diseases, the localization of pain in the nipple and skin soreness in the same area are often the foremost, although such pain may also occur with typical angina pectoris of varying severity.

Thoracic toad is often mixed, finally, with cardiac asthma, although the classic manifestation of these syndromes has almost nothing in common: however, they are combined largely by the common pathogenesis and, in some cases, can be combined or alternated in the same patient.

Current and prognosis of angina pectoris

Angina, despite the severe subjective feelings and fear of imminent death, experienced by patients, usually ends safely. However, having appeared, the attacks, as a rule, recur, gradually increasing in frequency; for example, first 1-2 times a year, then monthly, and finally, almost daily. Mild seizures, allowing the free movement of the patient over a considerable distance, can occur for decades. Only occasionally, the attacks of pain stop for years and for many years, which usually happens if the patient manages to reduce the excess weight and gradually train in physical activity, stop smoking, etc.

However, the immediate attack of angina can be fatal, accompanied by heart attack. Resting angina,

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