An attack of coronary heart disease. Coronary heart disease (CHD)

Chest pain may indicate diseases of the heart, respiratory system, gastrointestinal tract, spine, mediastinum, central nervous system. All internal organs humans are innervated by the autonomic nervous system, the trunks of which extend from spinal cord. When approaching chest nerve trunk gives branches to individual bodies. This is why sometimes pain in the stomach can feel like pain in the heart - they are simply transmitted to common trunk, and from it to another organ. Moreover, the roots spinal nerves contain sensory nerves that innervate musculoskeletal system. The fibers of these nerves are intertwined with the fibers of the nerves of the autonomic nervous system, and therefore completely healthy heart may respond with pain various diseases spine.

Finally, chest pain may depend on the state of the central nervous system: when constant stress and high neuropsychic stress, a malfunction occurs in its work - neurosis, which can also manifest itself as pain in the chest.

Some chest pains are unpleasant, but not life-threatening, but there are chest pains that need to be relieved immediately - a person’s life depends on it. In order to figure out how dangerous chest pain is, you need to see a doctor.

Chest pain caused by obstruction of the coronary (heart) arteries

The coronary arteries bring blood to the heart muscle (myocardium), which works nonstop throughout life. The myocardium cannot survive even for a few seconds without a new portion of oxygen and nutrients, delivered with blood, its cells immediately begin to suffer from this. If blood delivery stops for several minutes, myocardial cells begin to die. The larger the coronary artery suddenly becomes obstructed, the more of the myocardium is affected.

Spasms (compression) of the coronary arteries usually occur against the background coronary disease heart (CHD), the cause of which is partial blockage blood vessels atherosclerotic plaques and narrowing of their lumen. Therefore, even a minor spasm can block blood access to the myocardium.

A person feels such changes in the form of acute piercing pain behind the sternum, which can radiate to left shoulder blade and in left hand, right down to the little finger. The pain can be so severe that the patient tries not to breathe - breathing movements increase pain. At severe attacks the patient turns pale, or, on the contrary, turns red, and his blood pressure, as a rule, increases.

Such chest pain may be short-lived and occur only with physical or mental stress(angina pectoris), and can occur on their own, even during sleep (angina pectoris at rest). Angina attacks are difficult to get used to, so they are often accompanied by panic and fear of death, which further intensifies the spasm coronary vessels. Therefore, it is so important to clearly know what to do during an attack and to have everything you need at hand. The attack ends as suddenly as it began, after which the patient feels a complete loss of strength.

The peculiarity of these pains is that a person should under no circumstances endure them - they must be relieved immediately. You can’t do this without consulting a doctor - he will prescribe both the course of basic treatment and the medicine that needs to be taken when pain occurs (the patient should have it with him at all times). Usually in in case of emergency Take a nitroglycerin tablet under the tongue, which relieves pain within 1 to 2 minutes. If after 2 minutes the pain does not go away, then the tablet is taken again, and if this does not help, then you must immediately call an ambulance.

What can happen if you endure chest pain? The cells of the myocardial area, which is supplied by the affected artery, begin to die (myocardial infarction) - the pain intensifies, becomes unbearable, and a person often experiences pain shock With sharp decline blood pressure and acute heart failure (the heart muscle cannot cope with its work). Such a patient can only be helped in a hospital setting.

A sign of the transition of an angina attack to myocardial infarction is an increase in pain and the lack of effect from the use of nitroglycerin. The pain has a pressing, squeezing, burning character, begins behind the sternum, and then can spread to the entire chest and abdomen. The pain can be continuous or in the form of repeated attacks one after another, increasing in intensity and duration. There are cases when the pain in the chest is not very severe, and then patients often suffer a myocardial infarction on their legs, which can cause immediate disruption of the heart and the death of the patient.

There are also atypical (atypical) forms of myocardial infarction, when pain begins, for example, in the anterior or posterior surface of the neck, lower jaw, left hand, left little finger, left shoulder blade area, etc. Most often, such forms occur in older people and are accompanied by weakness, pallor, blueness of the lips and fingertips, heart rhythm disturbances, and a drop in blood pressure.

Another atypical form myocardial infarction is abdominal form when the patient feels pain not in the heart area, but in the abdomen, usually in its upper part, or in the area of ​​the right hypochondrium. Such pain is often accompanied by nausea, vomiting, loose stools, bloating. The condition sometimes closely resembles intestinal obstruction.

In this topic we will look at what ischemic attacks are. Ischemic attacks occur acutely and are characterized by unstable focal and general cerebral symptoms, their duration does not exceed 24 hours. Ischemia, insufficient blood flow or, conversely, hyperemia, cerebral edema, and small focal hemorrhages may be their basis.

Ischemic attacks causes

Etiological factor transient transient ischemic attacks are atherosclerosis, hypertension and their combination. Much less commonly, this pathology is caused by vasculitis (collagenous, syphilitic, rheumatic), thromboangiitis, blood diseases, diabetes mellitus.

In the pathogenesis of this pathology, the leading place is occupied by microembolisms emanating from atheromatous masses of ulcerating plaques located along the blood flow in main vessels neck. Emboli of this origin consist of cholesterol crystals, as well as platelet conglomerates. Blood platelets release adenosine diphosphoric acid, an intense aggregator, the moment they come into contact with a rough area vascular wall in the area of ​​ulceration of an atheromatous plaque. Under the influence of this acid, platelet aggregation occurs with the formation of emboli, which are carried by the blood flow to the brain, and, reaching small vessels, the emboli get stuck in them. As a result of irritation of the vascular endothelium by a foreign substrate, spasm of the surrounding vessels occurs, followed by perivascular edema. medulla, which is accompanied by the emergence focal symptoms. The so-called platelet emboli are quite loose, they are easily subject to lysis, or disintegration, the swelling they cause is eliminated, and clinical symptoms undergo reverse development. Microemboli can also be of cardiogenic origin. Development transient disturbances cerebral circulation with focal symptoms may be due to the vascular mechanism brain failure. It occurs when, in the presence of an atherosclerotic vessel or extravasal compression with symptoms of partial occlusion, accompanied chronic failure blood supply to the brain, any extracerebral factor (weakened cardiac activity, massive blood loss, decreased blood pressure of any origin) causes an additional decrease in blood supply to the brain. As a result of insufficient blood supply in the corresponding areas of the brain, symptoms of ischemia develop, manifested by certain focal symptoms. Restoring blood flow due to increased cardiac activity or other factors leads to the elimination of the symptoms that have arisen. For example, the cause of the disorders described above in vestibulobasilar insufficiency is often cervical osteochondrosis, in which the posterior osteophytes in the area of ​​the uncovertebral joints are compressed vertebral artery. With simultaneous deficiencies carotid arteries a sudden throw back of the head can cause a short-term fainting state with a fall muscle tone in the legs, the so-called drop attack state. The clinical picture of vestibulo-basilar insufficiency occurs approximately 2 times more often than insufficiency in the carotid region. This is explained by the fact that in brain stem, in a much smaller volume than in the cerebral hemispheres, there are formations, damage to which gives clear symptoms, while significant areas of the hemispheres are clinically mute. Transient cerebrovascular accidents may also result from changes in physical and chemical properties blood – increased viscosity, development of hypoxia, decreased sugar levels.

Ischemic attacks symptoms

Transient disorders of cerebral circulation of the ischemic type usually occur against the background of atherosclerosis and are manifested by focal symptoms, the nature of which is determined by the part of the brain in which circulatory decompensation occurs. With circulatory disorders in the carotid arteries, the most common feeling is numbness. upper lip, one half of the face along the ulnar edge of the arm, less often - in the leg. Short-term mono- or hemiparesis and aphasic symptoms may also develop. When disorders are localized in the area of ​​the vertebrobasilar system, patients complain of attacks of dizziness, sometimes with nausea and to varying degrees incoordination of movements (from the lightest to the inability to walk), as well as occipital pain, noise in the ear, hearing loss, light stimulation in one half of the visual field, up to short-term hemianopia. A number of psychotic disorders may also occur, e.g. different kinds disturbances of consciousness, a peculiar disturbance of voluntary activity in the form of inhibition of action, emotional disorders, hallucinatory syndromes, as well as amnestic syndrome. General cerebral symptoms in these cases are either absent or mildly expressed, relatively in rare cases On examination, nystagmus can be detected. Transient cerebrovascular accidents occurring against the background of hypertension, in to a large extent differ from those described above. They are primarily accompanied by general cerebral symptoms - severe headache, nausea, vomiting, non-systemic dizziness, sometimes psychomotor agitation, and epileptic seizures. Clinical picture complement the expressed autonomic symptoms– sweating, facial flushing. Focal transient symptoms of brain damage may occur. So, for a few minutes the patient experiences disorientation in the environment, a twilight state of consciousness, fainting, difficulty speaking, paresis, hemianesthesia or hemianopsia as symptoms of a short-term cerebrovascular accident or hypertensive cerebral crisis. These phenomena can persist for several hours and days. Apparently, at the basis of a significant part of transient brain disorders it's not a blockage cerebral vessel, and its spasm with subsequent symptoms of stasis. A slight antispasmodic vasoconstriction is enough to cause swelling and temporary anemia of this part of the brain. All these phenomena can quickly pass without leaving a trace, and impaired brain function can soon recover. More persistent paresis or other focal symptoms are based on changes in the form of small foci of softening or pinpoint hemorrhages around precapillaries and arterioles. As a result of cerebral vascular crisis in those suffering hypertension may also develop acute edema brain It begins with a sharp headache, which is accompanied by nausea and vomiting, sometimes dizziness and a feeling of blurred vision. Soon there comes stupor, lethargy, soporous state, sometimes with a period psychomotor agitation or epileptic seizure. Symptoms focal lesion there is no brain, but neck rigidity, Kernig’s sign, and increased blood pressure are clearly visible cerebrospinal fluid, increased protein content in it with normal cytosis. This syndrome, called acute hypertensive encephalopathy, consists of general cerebral and meningeal symptoms, accompanied by increased blood pressure and increased heart rate. In the fundus there is sclerosis of the retinal vessels and the “crossover phenomenon”, or the Hun-Salus symptom, which is quite characteristic of arterial hypertension. After 4–5 days, usually all symptoms disappear, but in some cases, as they increase, they can lead to death. The described conditions may be repeated.

Ischemic attacks diagnosis

Diagnosis can often be difficult. In most cases, certain disorders occur for the first time in a patient, and what their genesis is cannot always be quickly determined. Significant difficulties arise in the diagnosis of fainting conditions. A clear boundary between syncope (fainting) and clinical manifestations violations cerebral blood supply does not exist. However, the young age of patients and the instability of vegetative parameters make it possible to diagnose with a certain degree of confidence fainting states, rather than transient cerebrovascular accidents. Impaired blood circulation in the brainstem in the area of ​​the vestibular nuclei may be accompanied by attacks of systemic dizziness, which should be distinguished from damage to the labyrinth. A thorough otoneurological examination and medical history can help make the diagnosis. Detection of additional neurological symptoms in the form of hearing impairment, balance, sensitivity damage and will indicate the vascular genesis of the lesion. On the other hand, identifying indications of poor tolerance riding in transport, riding on a swing suggest the presence of congenital vestibulopathy. Some difficulties may arise when differential diagnosis transient cerebrovascular accidents with the first manifestations multiple sclerosis. The young age of the patients, the dispersion of symptoms, which do not allow the symptoms to be attributed to any one vascular system, allow us to come to the correct conclusion about multiple sclerosis.