collapse state. Sudden cardiovascular collapse and death

Collapse is an acute vascular insufficiency, which is characterized by a sharp decrease in vascular tone and a drop in blood pressure.

The collapse is usually accompanied by a violation of the blood supply, hypoxia of all organs and tissues, a decrease in metabolism, depression of vital important functions organism.

Causes

Collapse can develop due to many diseases. Most often, collapse occurs in pathologies of the cardiovascular system (myocarditis, myocardial infarction, pulmonary embolism, etc.), as a result of acute loss of blood or plasma (for example, with extensive burns), dysregulation vascular tone with shock, severe intoxication, infectious diseases, in diseases of the nervous, endocrine systems, as well as with an overdose of ganglioblockers, neuroleptics, sympatholytics.

Symptoms

The clinical picture of collapse depends on its cause, but the main manifestations are similar in collapse different origin. There is a sudden progressive weakness, chilliness, dizziness, tinnitus, tachycardia (rapid pulse), weakening of vision, and sometimes a feeling of fear. The skin is pale, the face becomes earthy, covered with sticky cold sweat, with cardiogenic collapse, cyanosis (bluish color of the skin) is often noted. The body temperature drops, breathing becomes superficial, speeded up. Arterial pressure decreases: systolic - up to 80-60, diastolic - up to 40 mm Hg. Art. and below. With the deepening of the collapse, consciousness is disturbed, disorders often join heart rate, reflexes disappear, pupils dilate.

Cardiogenic collapse, as a rule, is combined with cardiac arrhythmia, signs of pulmonary edema (respiratory failure, cough with copious froth, sometimes with a pink tinge, sputum).

Orthostatic collapse occurs with a sharp change in body position from horizontal to vertical and quickly stops after the patient is transferred to the prone position.

Infectious collapse, as a rule, develops as a result of a critical decrease in body temperature. Moisture of the skin, pronounced weakness of the muscles is noted.

Toxic collapse is often combined with vomiting, nausea, diarrhea, signs of acute kidney failure(edema, urinary incontinence).

Diagnostics

The diagnosis is made on the basis of the clinical picture. The study of hematocrit, blood pressure in dynamics give an idea of ​​the severity and nature of the collapse.

Types of disease

• Cardiogenic collapse - as a result of a decrease cardiac output;
• Hypovolemic collapse - as a result of a decrease in the volume of circulating blood;
• Vasodilation collapse - as a result of vasodilation.

Patient's actions

In the event of a collapse, you should immediately contact the ambulance service.

Collapse treatment

Therapeutic measures are carried out intensively and urgently. In all cases, the patient with collapse is placed in a horizontal position with raised legs, covered with a blanket. A 10% solution of caffeine-sodium benzoate is administered subcutaneously. It is necessary to eliminate the possible cause of the collapse: the removal of toxic substances from the body and the introduction of an antidote for poisoning, stop bleeding, thrombolytic therapy. With thromboembolism of the pulmonary arteries, acute myocardial infarction, the paroxysm of atrial fibrillation and other cardiac arrhythmias are stopped with medication.

Pathogenetic therapy is also carried out, which includes intravenous administration saline solutions and blood substitutes for blood loss or thickening of the blood in patients with hypovolemic collapse, the introduction hypertonic saline sodium chloride during collapse against the background of indomitable vomiting, diarrhea. If necessary, an urgent increase in blood pressure is administered norepinephrine, angiotensin, mezaton. In all cases, oxygen therapy is indicated.

Complications of collapse

The main complication of collapse is loss of consciousness. varying degrees. Light fainting is accompanied by nausea, weakness, pallor of the skin. Deep fainting may be accompanied by convulsions, increased sweating, involuntary urination. Also, due to fainting, injuries are possible when falling. Sometimes the collapse leads to the development of a stroke (impaired cerebral circulation). Possible various damage brain.

Repetitive episodes of collapse lead to severe cerebral hypoxia, aggravation of concomitant neurological pathology development of dementia.

Prevention

Prevention consists in the treatment of the underlying pathology, constant monitoring of patients in serious condition. It is important to take into account the peculiarities of the pharmacodynamics of drugs (neuroleptics, ganglionic blockers, barbiturates, antihypertensives, diuretics), individual sensitivity to drugs and nutritional factors.

They can develop abruptly, catching a person and the people around him by surprise. Such pathological conditions can be relatively harmless, but in some cases they can carry serious threat health and life. Therefore, in no case should they be left unattended, the victim should be given first aid. Quite common disorders of this type include vascular collapse, causes, symptoms and treatment in a little more detail.

What is vascular collapse?

The term vascular collapse means a variety, with such a pathological condition, a sharp decrease in vascular tone occurs, which in turn causes a sharp decrease in arterial and venous pressure and loss of consciousness.

Causes of vascular collapse

There are a number of factors that can cause vascular collapse. These can be infectious diseases represented by pneumonia, meningoencephalitis, typhoid fever and some other pathological conditions. Sometimes collapse occurs with ailments of the nervous and, it can be caused by poisoning and sudden loss blood. Also, such a pathological condition is provoked by damage to the heart muscle, the use of certain drugs (for example, with an overdose of insulin), anesthesia (especially spinal anesthesia). In addition, it can be provoked by taking an excessive amount alcoholic beverages and developed peritonitis. In some cases, vascular collapse occurs during an attack.

How does vascular collapse manifest itself, what are its symptoms?

The collapse manifests itself characteristic symptoms. Patients suddenly feel severe weakness and fatigue, they are worried about severe dizziness (sometimes it simply does not allow the patient to stay on his feet). Pathological decline vascular tone is accompanied by chills, a decrease in temperature (the limbs of the victim become cold to the touch). The patient has pale skin and choroids. In some cases, cyanosis occurs.

It is worth noting that the deterioration in the collapse occurs quite sharply. Many patients complain of tinnitus and headache. They may be disturbed by darkening in the eyes. The sight of the victim at the same time becomes dull, and the pulse weakens. Sweating is often observed, convulsions may occur.

In the absence of timely assistance, collapse can turn into loss of consciousness.

How is vascular collapse corrected, what is its treatment?

If a collapse is suspected, the patient needs emergency care, so others should immediately call ambulance. And before her arrival, the patient must be given first aid. First, lay him on his back, on a fairly hard surface and slightly raise his legs. So you will ensure a full flow of blood to the area of ​​\u200b\u200bthe heart and brain. With the development of collapse, it is necessary to organize the supply of fresh air to the victim, so open the window wider. But the patient should not freeze - warm him up.

If you have a first aid kit on hand, let the patient sniff the ammonia. If there is no such medicine, rub the victim's temples, as well as the hole that is located directly above the upper lip, and the earlobes.

If the cause of the collapse was bleeding from an external wound, when providing first aid, measures should be taken to stop the bleeding.

In the event that a loss of consciousness has occurred, it is not necessary to give the patient any drink or medicine. In no case should you try to bring him to consciousness by hitting him on the cheeks.

If there is a suspicion of vascular collapse, the patient should not be given valocordin, validol, and. All these drugs dilate blood vessels.

Further treatment of vascular collapse

After the arrival of the ambulance, the doctors put the victim down, slightly raising his lower limbs, and also cover him with a blanket. Next, a subcutaneous injection of two milliliters of a ten percent solution of caffeine-sodium benzoate is carried out. If an infectious collapse has occurred, such therapy is often sufficient. And with orthostatic collapse, the introduction gives a stable positive effect. However, it should be noted that the patient without fail it is necessary to correct the causes of the development of such a violation.

Such etiological treatment is aimed at stopping bleeding if the collapse is hemorrhagic. The poisoning that has occurred requires the elimination of toxic elements from the body, as well as specific antidote therapy. In addition, thrombolytic treatment can be carried out.

If a patient is diagnosed with acute myocardial infarction or pulmonary embolism, an appropriate correction is carried out.

Doctors may infuse the patient with blood, plasma, or a blood-substituting fluid. In the event that indomitable vomiting and diarrhea are observed, one cannot do without the introduction of a hypertonic solution of sodium chloride. The same treatment is indicated for adrenal insufficiency, in which case adrenal hormones are also used.

If there is a need to quickly increase blood pressure, intravenous drip introduction norepinephrine or angiotensin. Slightly slower, but at the same time more stable effect gives the use of injections of methasone and fetanol. Almost all patients receive oxygen therapy.

Alternative treatment

Facilities traditional medicine can be used only as general strengthening. Collapse correction can only be carried out under the supervision of a doctor, using medications.

So, in the event of a loss of blood, the patient may need funds based on nettle. You can brew a couple of tablespoons of crushed nettle leaves with a glass of just boiled water. Insist for two to three hours, then strain. Drink the received medicine for a day in three-four receptions. Nettle, by the way, is advised to add to different dishes such as salads, soups, etc.

You can also cope with bleeding and their consequences with the help of an infusion based on. Brew a couple of tablespoons of such raw materials in a thermos with half a liter of boiling water. Insist for one to two hours, strain and take a third or half a glass twice or thrice a day. It is best to take the reception twenty to thirty minutes before a meal.

Folk remedies will also help patients with impaired activity of the heart muscle. To strengthen such a site, you can brew a glass of crushed fresh fruits of viburnum with a liter of hot water. Boil on a fire of minimum power for eight to ten minutes, then strain and sweeten with honey. Take half a glass three to four times a day.

If you suffer from a weakening of the heart, a medicine based on St. John's wort will come in handy. Brew one hundred grams of dried grass with two liters of water and boil over a fire of minimum power for ten minutes. Remove the prepared medicine from the heat, strain and sweeten with honey. Pour the finished broth into a convenient bottle and refrigerate for storage. Take half a glass three times a day.

Folk remedies will also help patients who have had a myocardial infarction. They will improve the general condition, speed up recovery after a heart attack. So a good effect is given by the collection of equal parts of valerian roots, motherwort grass and cumin fruits. Brew a tablespoon of this mixture with a glass of boiling water, soak in a water bath for a quarter of an hour. Insist for half an hour, then strain. Squeeze out the vegetable raw materials, and take the infusion in a glass before going to bed.

After a heart attack. Even after a myocardial infarction, you can take medicine from rose hips. We will complement it with a few strawberry leaves. Combine fifty grams of such raw materials, brew half a liter of boiling water and heat in a water bath for a quarter of an hour. Next, completely cool the broth, strain it, and squeeze the plant mass. You need to take such a remedy for half a glass twice a day shortly before a meal.

Collapse is a rather serious condition that requires close attention and adequate timely therapy. The feasibility of using folk remedies after suffering a vascular collapse must be discussed with the doctor.

Ekaterina, www.site
Google

- Dear our readers! Please highlight the found typo and press Ctrl+Enter. Let us know what's wrong.
- Please leave your comment below! We ask you! We need to know your opinion! Thank you! Thank you!

barton E. Sobel, E. Braunwald (Burton E. Sobel, Eugene Braunwald)

Sudden cardiac death in the USA alone claims about 400,000 lives annually, i.e., approximately 1 person dies in 1 minute. Definitions of sudden death vary, but most include next feature: death occurs suddenly and instantly, or within 1 hour of the onset of symptoms in a person with or without preexisting heart disease. Usually only a few minutes pass from the moment of development of a sudden cardiovascular collapse (there is no effective cardiac output) to irreversible ischemic changes in central nervous systems e. Nevertheless, with the timely treatment of some forms of cardiovascular collapse, an increase in life expectancy without subsequent functional damage can be achieved.

Sudden cardiovascular collapse may be due to: 1) cardiac arrhythmias (see Chapters 183 and 184), most often ventricular fibrillation or ventricular tachycardia, which sometimes occurs after bradyarrhythmia, or severe bradycardia or ventricular asystole (these conditions are usually are harbingers of inefficiency resuscitation); 2) a pronounced sharp decrease in cardiac output, which is observed when there is a mechanical obstruction to blood circulation [massive pulmonary thromboembolism and cardiac tamponade are two examples of this form; 3) acute sudden ventricular, pumping failure, which may occur due to acute infarction myocardial infarction, "non-arrhythmic cardiac death", with or without ventricular rupture or critical aortic stenosis; 4) activation of vasodepressor reflexes, which can lead to unexpected decline blood pressure and decrease in heart rate and what is observed in different situations including pulmonary embolism, carotid sinus hypersensitivity syndrome, and primary pulmonary hypertension. Among the primary electrophysiological disorders, the relative incidence of ventricular fibrillation, ventricular tachycardia, and severe bradyarrhythmia or asystole is approximately 75%, 10%, and 25%.

Sudden death in atherosclerosis of the coronary arteries

Sudden death is primarily a complication of severe atherosclerosis of the coronary arteries affecting several coronary vessels. In pathoanatomical examination, the frequency of detection of fresh coronary thrombosis ranges from 25 to 75%. Rupture of an atherosclerotic plaque, which caused vascular obstruction, was found in a number of patients without thrombosis. Thus, it appears that the majority of patients with ischemic disease of the heart, it is precisely the acute obstruction of the lumen of the coronary vessel that is the starting point for sudden death. In other cases, sudden death may be the result of a functional electrophysiological instability that is diagnosed by a provocative invasive electrophysiological study and may persist for a long time or indefinitely after myocardial infarction. In those who die as a result of sudden death younger than 45 years, platelet thrombi are often found in the coronary microvasculature. Approximately 60% of patients who died from myocardial infarction died before admission to the hospital. Indeed, in 25% of patients with coronary heart disease, death acts as the first manifestation of this disease. Based on the experience of the activities of the emergency departments, it could be assumed that the incidence of sudden death could be significantly reduced by using preventive measures conducted primarily in populations with especially high risk if it were shown that such measures are effective, have low toxicity and do not cause great inconvenience to patients. However, sudden death can be one of the manifestations of coronary heart disease, and effective prevention of sudden death requires, among other things, the prevention of atherosclerosis. The risk of sudden death, which is a manifestation of a previous myocardial infarction, is increased in patients with severe left ventricular dysfunction, complex ectopic ventricular activity, especially when these factors are combined.

Factors related to increased risk sudden death

When recording an electrocardiogram within 24 hours during normal daily activities, supraventricular premature contractions can be found in most Americans over 50, and ventricular premature beats in nearly two-thirds. Simple ventricular premature beats in persons with a healthy heart are not associated with an increased risk of sudden death, however, conduction disturbances and high-grade bigeminy or ectopic ventricular beats (repetitive forms or complexes R -on-T) are a high-risk indicator, especially among patients who have had a myocardial infarction within the previous year. In patients with acute myocardial infarction, ventricular ectopic contractions that occur in the late period of the cardiac cycle are especially often combined with malignant ventricular arrhythmias. High-frequency, low-amplitude potentials arising during registration of the final part of the complex QRS and segmentST,which can be identified using the frequency analysis of the signal-averaged electrocardiogram (ECG), also allow the identification of patients with a high risk of sudden death.

Premature ventricular contractions can be a trigger factor for fibrillation, especially against the background of myocardial ischemia. On the other hand, they may be manifestations of the most common fundamental electrophysiological disorders that predispose to both ventricular premature contractions and ventricular fibrillation, or may be a completely independent phenomenon associated with electrophysiological mechanisms other than those that cause fibrillation. Their clinical significance varies from patient to patient. Ambulatory electrocardiographic monitoring has shown that an increase in the frequency and complexity of ventricular arrhythmias over several hours often precedes ventricular fibrillation.

In general, ventricular arrhythmias are much more important and significantly worsen the prognosis in the case of acute ischemia and severe left ventricular dysfunction due to coronary heart disease or cardiomyopathy than in their absence.

Severe ischemic heart disease, not necessarily accompanied by morphological signs of acute infarction, hypertension, or diabetes, is present in more than 75% of suddenly deceased persons. But perhaps more importantly, the incidence of sudden death in patients with at least one of these diseases is significantly higher than in healthy individuals. More than 75% of men with no previous coronary heart disease who die suddenly have at least two of the four risk factors for atherosclerosis listed below: hypercholesterolemia, hypertension, hyperglycemia, and smoking. Overweight and electrocardiographic signs of left ventricular hypertrophy are also associated with an increased incidence of sudden death. The incidence of sudden death is higher in smokers than in non-smokers, possibly due to higher levels of circulating catecholamines and fatty acids and increased production of carboxyhemoglobin, which, when circulating in the blood, leads to a decrease in its ability to carry oxygen. Sudden death susceptibility induced by smoking is not permanent, but seems to be reversed with smoking cessation.

Cardiovascular collapse during physical exertion occurs in rare cases in patients with ischemic heart disease performing a stress test. With trained personnel and appropriate equipment, these episodes are quickly controlled by electrical defibrillation. Sometimes acute emotional stress can precede the development of acute myocardial infarction and sudden death. These data are consistent with recent clinical observations indicating that such conditions are associated with type A behaviors, and experimental observations of increased susceptibility to ventricular tachycardia and fibrillation with artificial coronary occlusion after placing animals in a state of emotional stress or increased activity of the sympathetic nervous system. systems. In experimental animals, the protective effect of the introduction of individual precursors of neurotransmitters of the central nervous system has also been shown.

Two main clinical syndromes can be distinguished in patients who die suddenly and unexpectedly; both of these syndromes are generally associated with coronary heart disease. In most patients, rhythm disturbances occur quite unexpectedly and without any previous symptoms or prodromal signs. This syndrome is not associated with acute myocardial infarction, although most patients can detect the consequences of a previous myocardial infarction or other types of organic heart disease. After resuscitation, there is a predisposition to early recurrences, possibly reflecting the electrical instability of the myocardium that led to the initial episode, as well as a relatively high mortality in the subsequent 2 years, reaching 50%. Clearly, these patients can only be saved if there is a responsive cardiac service that can provide vigorous diagnosis and treatment with pharmacological agents, if necessary surgery, implantable defibrillators or programmable pacing devices. Pharmacological prophylaxis is likely to improve survival. The second, smaller group includes patients who, after successful resuscitation, show signs of acute myocardial infarction. These patients are characterized by prodromal symptoms (retrosternal pain, dyspnea, syncope) and a significantly lower rate of relapses and deaths during the first two years (15%). Survival in this subgroup is the same as in patients after resuscitation for ventricular fibrillation complicating acute myocardial infarction in the coronary care unit. The predisposition to ventricular fibrillation at the time of the development of an acute infarction persists in them only for a short time, in contrast to patients in whom fibrillation occurs without an acute infarction, after which the risk of relapse remains elevated for a long time. However, in some patients who have had a myocardial infarction, the risk of sudden death remains quite high. The factors that determine this risk are the vastness of the infarct zone, severe ventricular dysfunction, persistent complex ectopic ventricular activity, prolongation of the interval Q-Tafter acute attack, loss after recovery of the ability to respond normally to physical activity by increasing blood pressure, maintaining long time positive results of myocardial scintigrams.

Other causes of sudden death

Sudden cardiovascular collapse can result from a variety of disorders other than coronary atherosclerosis. Causes include severe aortic stenosis, congenital or acquired, with sudden rhythm or pumping failure of the heart, hypertrophic cardiomyopathy, and myocarditis or cardiomyopathy associated with arrhythmias. Massive pulmonary embolism leads to circulatory collapse and death within minutes in approximately 10% of cases. Some patients die after some time against the background of progressive right ventricular failure and hypoxia. Acute circulatory collapse may be preceded by small emboli at various intervals before a lethal attack. In accordance with this, the appointment of treatment already in this prodromal, sublethal phase, including anticoagulants, can save the patient's life. Cardiovascular collapse and sudden death are rare but possible complications of infective endocarditis.

Conditions associated with cardiovascular collapse and sudden death in adults

Ischemic heart disease due to coronary atherosclerosis, including acute myocardial infarction

Prinzmetal's variant angina; spasm of the coronary arteries coronary disease heart, including malformations, coronary arteriovenous fistulas embolism of the coronary vessels

Acquired non-atherosclerotic coronary disease, including aneurysms in Kawasaki disease

Myocardial bridges that markedly impair perfusion Wolf-Parkinson-White syndrome

Hereditary or acquired interval lengthening Q-Twith or without congenital deafness

Damage to the sinoatrial node

Atrial-ventricular blockade (Adams-Stokes-Morgagni syndrome) Secondary lesion of the conduction system: amyloidosis, sarcoidosis, hemochromatosis, thrombotic thrombocytopenic purpura, dystrophic myotonia

Drug toxicity or idiosyncrasy to drugs, e.g. foxglove, quinidine

Electrolyte disorders, especially magnesium and potassium deficiency in the myocardium Valvular heart disease, especially aortic stenosis Infective endocarditis Myocarditis

Cardiomyopathies, in particular idiopathic hypertrophic subaortic stenosis

Modified weight loss diet programs based on fluid and protein intake

Packing of the pericardium

Prolapse mitral valve(extremely rare cause sudden death) Tumors of the heart

Rupture and dissection of aortic aneurysm Pulmonary thromboembolism

Cerebrovascular complications, in particular bleeding

In recent years, a number of conditions have been identified that are less common causes of sudden death. Sudden cardiac death may be associated with modified dietary programs aimed at reducing body weight with the use of fluids and proteins. Distinctive features of these cases are the lengthening of the interval Q - T , andalso detection at autopsy of less specific morphological changes in the heart, typical, however, for cachexia. Primary degeneration of the atrioventricular conduction system, with or without calcium or cartilage deposits, can lead to sudden death in the absence of severe coronary atherosclerosis. Trifascicular atrioventricular (AV) block is often detected in these conditions, which in more than two-thirds of cases can be the cause of chronic AV block in adults. However, the risk of sudden death is significantly higher in conduction disorders associated with coronary heart disease than in isolated primary damage to the conduction system. Electrocardiographic signs of interval lengthening Q-T,Hearing loss of central origin and their autosomal recessive inheritance (Ervel-Lange-Nielsen syndrome) occur in a large number of individuals who have had ventricular fibrillation. There is evidence that the same electrocardiographic changes and electrophysiological instability of the myocardium, not combined with deafness (Romano-Ward syndrome), are inherited in an autosomal dominant manner.

Electrocardiographic changes in these conditions may appear only after exercise. The overall risk of sudden death in individuals with these disorders is approximately 1% per year. Congenital deafness, history of syncope, belonging to female gender, confirmed tachycardia by type torsades de pointes (see below) or ventricular fibrillation are independent risk factors for sudden cardiac death. Although the removal of the left stellate ganglion has a transient preventive effect, healing does not occur.

Other conditions associated with interval prolongation Q-Tand increased temporal dispersion of repolarization, such as hypothermia, a number of drugs (including hnnidine, disopyramide, novocainamide, phenothiazine derivatives, tricyclic antidepressants), hypokalemia, hypomagnesemia, and acute myocarditis, are associated with sudden death, especially if episodes also develop. torsades de pointes , a variant of rapid ventricular tachycardia with distinct electrocardiographic and pathophysiological signs. Stopping or blockade of the sinoatrial node, followed by inhibition of downstream pacemakers, or sick sinus syndrome, usually accompanied by dysfunction of the conduction system, can also lead to asystole. Occasionally, fibroids and inflammation of the sinoatrial or atrioventricular nodes can lead to sudden death in individuals without preexisting evidence of heart disease. Sudden ruptures of the papillary muscle, interventricular septum or free wall that develop during the first few days after an acute myocardial infarction can sometimes cause sudden death. Sudden cardiovascular collapse is also a serious and often fatal complication of cerebrovascular disorders; in particular subarachnoid hemorrhage, a sudden change in intracranial pressure or damage to the brain stem. It can also occur with asphyxia. Digitalis poisoning can cause life-threatening cardiac arrhythmias leading to sudden cardiovascular collapse, which, if left untreated, ends in death. Paradoxically, antiarrhythmic drugs can exacerbate arrhythmias or predispose to ventricular fibrillation in at least 15% of patients.

Electrophysiological mechanisms

Potentially lethal ventricular arrhythmias in patients with acute myocardial infarction may be the result of activation of the recirculation mechanism (re-entry, re - entry ), automatism disorders, or both. It seems that the mechanism of recirculation plays a dominant role in the genesis of early arrhythmias, for example, during the first hour, and violations of automatism are the main etiological factor in later periods.

It is possible that several factors are involved in preparing the ground for the development of ventricular fibrillation and other recirculation-dependent arrhythmias after the onset of myocardial ischemia. Local accumulation of hydrogen ions, an increase in the ratio of extra- and intracellular potassium, regional adrenergic stimulation tend to shift diastolic transmembrane potentials to zero and cause pathological depolarization, apparently mediated through calcium currents and indicating inhibition of fast, sodium-dependent depolarization. This type of depolarization is most likely associated with slow conduction, which is a necessary condition for the appearance of recirculation soon after the onset of ischemia.

Another mechanism involved in maintaining recirculation early after ischemia is focal repetitive excitation. Anoxia shortens the duration of the action potential. In accordance with this, during electrical systole, repolarization of cells located in the ischemic zone can occur earlier than cells of the adjacent non-ischemic tissue. The emerging difference between the prevailing transmembrane potentials can cause unstable depolarization of neighboring cells, and therefore contribute to the appearance of rhythm disturbances that depend on recirculation. Concomitant pharmacological and metabolic factors may also predispose to recirculation. For example, quinidine can inhibit the rate of excitation disproportionately to the increase in refractoriness, thereby facilitating the onset of recirculation-dependent arrhythmias soon after ischemia has developed.

The so-called vulnerable period, corresponding to the ascending knee of the prongT,represents that part of the cardiac cycle when the temporal dispersion of ventricular refractoriness is maximal, and therefore a recirculating rhythm leading to prolonged repetitive activity can most easily be provoked. In patients with severe myocardial ischemia, the duration of the vulnerable period is increased, and the intensity of the stimulus necessary for the occurrence of recurrent tachycardia or ventricular fibrillation is reduced. The temporal dispersion of refractoriness can be increased in non-ischemic tissues in the presence of a slow heart rate. Thus, deep bradycardia caused by reduced automatism of the sinus node or atrioventricular blockade may be especially dangerous in patients with acute myocardial infarction, since it potentiates recirculation.

Ventricular tachycardia that occurs 8-12 hours after the onset of ischemia, apparently, depends in part on the disorder of automatism or trigger activity of Purkinje fibers, and possibly myocardial cells. This rhythm resembles slow ventricular tachycardia, which often occurs within a few hours or on the first day after coronary artery ligation in experimental animals. As a rule, it does not turn into ventricular fibrillation or other malignant arrhythmias. Decrease in diastolic transmembrane potential in response to regional biochemical changes caused by ischemia may be related to disorders of automatism due to facilitating repeated depolarizations of Purkinje fibers provoked by a single depolarization. Because catecholamines facilitate the propagation of such slow responses, increased regional adrenergic stimulation may play a role here. important role. The apparent efficacy of adrenergic blockade in suppressing some ventricular arrhythmias and the relative ineffectiveness of conventional antiarrhythmic drugs such as lidocaine in patients with increased sympathetic activity may reflect the important role of regional adrenergic stimulation in the genesis of increased automatism.

Asystole and/or profound bradycardia are among the less common electrophysiological mechanisms underlying sudden death due to coronary atherosclerosis. They may be manifestations of complete occlusion of the right coronary artery and, as a rule, indicate the failure of resuscitation. Asystole and bradycardia are often the result of sinus node failure, atrioventricular block, and the inability of accessory pacemakers to function effectively. Sudden death in individuals with these disorders is usually more a consequence of diffuse lesions myocardium than AV block itself.

Identification of high-risk individuals

The difficulties posed by ambulatory electrocardiographic monitoring or other measures aimed at mass screening of the population in order to identify individuals at high risk of developing sudden death are enormous, since the population at risk of developing sudden death is more in men aged 35 to 74 years, and ventricular ectopic activity occurs very frequently and varies greatly from day to day in the same patient. The maximum risk is noted: 1) in patients who have previously suffered primary ventricular fibrillation without association with acute myocardial infarction; 2) in patients with ischemic heart disease who experience attacks of ventricular tachycardia; 3) within 6 months in patients after acute myocardial infarction who have regular early or multifocal premature ventricular contractions that occur at rest, during physical activity or psychological stress, especially in those who have severe left ventricular dysfunction with ejection fraction less than 40% or overt heart failure; 4) in patients with an extended interval Q-Tand frequent premature contractions, especially when a history of syncope is indicated. Although the identification of patients at high risk of sudden death is extremely important, the choice of effective prophylactic agents remains an equally difficult task, and none of them has proven unequivocally effective in reducing risk. Induction of arrhythmias by stimulation of the ventricles using a catheter with electrodes inserted into the heart cavity and the choice pharmacological agents to prevent such provocation of arrhythmias is probably an effective method for predicting the possibility of preventing or reversing recurrent malignant arrhythmias, in particular ventricular tachycardia, using specific drugs in patients who have experienced prolonged ventricular tachycardia or fibrillation. In addition, this method allows the identification of refractory patients. conventional methods treatment, and to facilitate the selection of candidates for vigorous methods such as administration of drugs under investigation, implantation of automated defibrillators, or surgical intervention.

Medical treatment

Treatment with antiarrhythmic drugs in doses sufficient to maintain a therapeutic level in the blood was considered effective in recurrent ventricular tachycardia and (or) fibrillation in people who suffered sudden death, if during acute trials this drug could arrest or reduce the severity of high-grade premature ventricular contractions, early or recurring forms. In persons who have suffered sudden death, who have frequent and complex ventricular extrasystoles that occur between episodes of ventricular tachycardia and (or) fibrillation (approximately 30% of patients), prophylactic treatment should be carried out individually, after determining the pharmacological efficacy of each drug, i.e., the ability to suppress existing rhythm disturbances. Usual doses long-acting novocainamide (30–50 mg/kg per day orally in divided doses every 6 hours) or disopyramide (6–10 mg/kg per day orally every 6 hours) can effectively suppress these rhythm disturbances. If necessary and in the absence of gastrointestinal disorders or electrocardiographic signs of toxicity, the dosage of quinidine can be increased to 3 g / day. Amiodarone (a US trial drug at 5mg/kg IV over 5-15 minutes or 300-800mg per day orally with or without loading dose of 1200-2000mg per day divided over 1 or 4 weeks) has a strong antifibrillatory effect, but a very slow onset maximum effect, which appears only after a few days or weeks of continuous administration. Toxicity can occur with both acute and chronic administration. Despite the fact that the effectiveness of the antifibrillatory action of amiodarone is generally recognized, its appointment should be reserved for conditions refractory to less toxic drugs or alternative approaches.

In most people who have suffered sudden death, frequent and complex ventricular extrasystoles are recorded between episodes of ventricular tachycardia and (or) fibrillation only in rare cases. For such patients, the choice of an appropriate prophylactic regimen should be based on the favorable results of specific therapy, as confirmed by the results of provocative electrophysiological tests. Ambulatory electrocardiographic monitoring with or without exercise may be particularly useful in confirming the effectiveness of treatment, since incomplete knowledge of the pathogenesis of sudden death makes it difficult to rationally choose drugs and their dosage, and prescribing steroid regimens to all patients makes prevention unfeasible. However, due to the large variability in spontaneous heart rhythm disturbances recorded by Holter monitoring, which must be interpreted individually for each patient, suppression of ectopic activity (by at least .80% within 24 hours) must be achieved before speech can be achieved. on the pharmacological efficacy of a particular treatment regimen. Even after such effectiveness has been proven, this does not mean at all that the selected regimen will be able to have such a protective effect in ventricular fibrillation. Some patients require the simultaneous administration of several drugs. Since the profound electrophysiological disturbances underlying ventricular fibrillation and premature contractions may be different, even the desired documented suppression of the latter does not guarantee against the development of sudden death.

A reduction in the incidence of sudden death in randomized selection of patients with acute myocardial infarction has been shown in several prospective double-blind studies using R-blockers, despite the fact that the antiarrhythmic effect of the treatment has not been quantified and the mechanisms of a clear protective effect have not yet been established. The incidence of sudden death was significantly reduced compared with the overall reduction in mortality over several years of follow-up for a group of people who had myocardial infarction who were treated R-blockers were started a few days after the infarction.

The delay in hospitalization of the patient and the provision of qualified assistance after the development of acute myocardial infarction significantly complicates the prevention of sudden death. In most areas of the United States, the average time from the onset of symptoms of an acute heart attack to hospital admission is 3 to 5 hours. most delaying assistance.

Surgical approaches

A carefully selected group of individuals who have experienced sudden death, after which they have recurrent malignant arrhythmias, may be indicated for surgical treatment. In some patients, prophylaxis with an automated implantable defibrillator may improve survival rates, although the discomfort of device shocks and the potential for non-physiological shocks are serious drawbacks to this method.

public efforts.The experience gained in Seattle, Washington shows that in order to deal effectively with the problem of sudden cardiovascular collapse and death on a broad community basis, it is necessary to create a system that can provide a quick response in such situations. Important elements of this system are: the presence of a single telephone for the whole city, by which this system can be “launched”; the presence of well-trained paramedical personnel, similar to firefighters, who can respond to calls; short average response time (less than 4 minutes), and big number individuals in the general population trained in resuscitation techniques. Naturally, the success of the resuscitation performed, as well as the long-term prognosis, directly depend on how soon resuscitation measures are started after the collapse. Availability of special transport, mobile coronary care units equipped with necessary equipment and staffed by trained personnel capable of providing adequate care in the relevant cardiac emergency, reduces the time spent. In addition, the presence of such teams increases the medical awareness and readiness of the population and doctors. Such a system can be effective in providing resuscitation care to more than 40% of patients who have developed cardiovascular collapse. Participation in the public program "Cardiopulmonary resuscitation provided by others" of well-trained citizens increases the likelihood of a successful outcome of resuscitation. This is confirmed by the increase in the proportion of patients discharged from the hospital in good condition who underwent cardiac arrest at the prehospital stage: 30-35% compared with 10-15% in the absence of such a program. Long-term survival, within 2 years, can also be increased from 50 to 70% or more. Proponents of a random resuscitation program are currently exploring the use of portable home defibrillators designed for safe use by the general population with only the bare minimum of necessary skills.

Patient education. Instructing people at risk of developing myocardial infarction how to call for medical help in an emergency situation when symptoms of the disease appear is an extremely important factor in the prevention of sudden cardiac death. This policy assumes that patients understand the need to urgently seek effective emergency care, and that doctors expect the patient to such a call, regardless of the time of day or night, if the patient develops symptoms of myocardial infarction. This concept also implies that the patient can, without informing the doctor, directly contact the emergency care system. Exercise, such as hopping, should not be encouraged in the absence of medical supervision in patients with confirmed coronary artery disease, and should be completely prohibited in those who are at particular risk of sudden death, as described above.

Approach to the examination of a patient with a sudden onset of cardiovascular collapse

Sudden death can be avoided even if cardiovascular collapse has already developed. If a patient under constant medical supervision develops a sudden collapse caused by an abnormal heart rhythm, then the immediate goal of treatment should be to restore an effective heart rhythm. The presence of circulatory collapse should be recognized and confirmed immediately after its development. The main signs of this condition are: 1) loss of consciousness and convulsions; 2) no pulse on peripheral arteries; 3) absence of heart sounds. Because the outdoor massage Since the heart provides only a minimal cardiac output (no more than 30% of the lower limit of normal), the true restoration of an effective rhythm should be a top priority. In the absence of contrary data, it should be considered that the cause of the rapid circulatory collapse is ventricular fibrillation. If the doctor observes the patient within 1 minute after the collapse develops, then no time should be wasted trying to provide oxygenation. Instant swipe to the precordium chest(shock defibrillation) can sometimes be effective. It should be attempted, since it only takes seconds to do so. On rare occasions when circulatory collapse is a consequence of ventricular tachycardia and the patient is conscious at the time of the doctor's arrival, strong coughing movements can terminate the arrhythmia. In the absence of immediate restoration of circulation, an attempt should be made to perform electrical defibrillation without wasting time recording an electrocardiogram using separate equipment, although the use of portable defibrillators, which can record an electrocardiogram directly through the defibrillator electrodes, may be useful. The maximum electrical voltage of conventional equipment (320 V/s) is sufficient even for severely obese patients and can be used. Efficiency is enhanced if the electrode pads are strongly applied to the body and the shock is applied immediately, without waiting for the increase in the energy demand of defibrillation, which occurs with an increase in the duration of ventricular fibrillation. The use of devices with automatic selection of shock voltage depending on tissue resistance is especially promising, since it can minimize the dangers associated with the application of unreasonably large shocks and avoid inefficiently small shocks in patients with higher than expected resistance. If these simple attempts are unsuccessful, then external cardiac massage should be started and full cardiopulmonary resuscitation should be carried out with a quick recovery and maintaining good airway patency.

If collapse is an undeniable consequence of asystole, transthoracic or transvenous electrical stimulation should be given without delay. Intracardiac administration of adrenaline at a dose of 5-10 ml at a dilution of 1:10,000 can increase the response of the heart to artificial stimulation or activate the slow, ineffective focus of excitation in the myocardium. If these primary concrete measures prove to be ineffective, despite their correct technical implementation, it is necessary to carry out a quick correction of the metabolic environment of the body and establish monitoring control. The best way to do this is to use the following three activities:

1) external heart massage;

2) correction of the acid-base balance, which often requires intravenous sodium bicarbonate at an initial dose of 1 meq/kg. Half the dose should be repeated every 10-12 minutes according to the results of regularly determined pH arterial blood;

3) determination and correction of electrolyte disorders. Vigorous attempts to restore an effective heart rate should be made as early as possible (naturally, within minutes). If the effective heart rate is restored, then quickly transforms again into ventricular tachycardia or fibrillation, 1 mg / kg lidocaine should be administered intravenously, followed by its intravenous infusion at a rate of 1-5 mg / kg per hour, repeating defibrillation.

Heart massage

External cardiac massage was developed by Kouwenhoven et al. in order to restore perfusion of vital organs by successive compressions of the chest with the hands. It is necessary to point out some aspects of this technique.

1. If efforts to bring the patient to his senses by shaking his shoulders and calling him by name are unsuccessful, the patient should be laid on his back on a hard surface (a wooden shield is best).

2. To open and maintain airway patency, the following technique should be used: throw the patient's head back; strongly pressing on the patient's forehead, with the fingers of the other hand, press the lower jaw and push it forward so that the chin rises up.

3. In the absence of a pulse on the carotid arteries for 5 s, compression of the chest should begin: the proximal part of the palm of one hand is placed in the lower part of the sternum in the middle, two fingers above the xiphoid process in order to avoid damage to the liver, the other hand lies on the first, covering it with fingers.

4. Compression of the sternum, shifting it by 3-.5 cm, should be performed at a frequency of 1 per second in order to have enough time to fill the ventricle.

5. The rescuer's torso should be above the victim's chest so that the applied force is approximately 50 kg; elbows should be straight.

6. Compression and relaxation of the chest should take 50% of the entire cycle. Rapid compression creates a pressure wave that can be palpated over the femur or carotid arteries, however, little blood is ejected.

7. Massage should not be stopped even for a minute, since cardiac output increases gradually during the first 8-10 compressions, and even a short stop has a very unfavorable effect.

8. Efficient ventilation must be maintained throughout this time and carried out at a frequency of 12 breaths per minute under the control of the tension of gases in the arterial blood. If these indicators are clearly pathological, tracheal intubation should be performed quickly, interrupting external chest compressions for no more than 20 s.

Each external compression of the chest inevitably limits the venous return by some amount. Thus, the optimally achievable cardiac index during external massage can only reach 40% of the lower limit of normal values, which is significantly lower than those observed in most patients after the restoration of spontaneous ventricular contractions. That is why it is crucial to restore an effective heart rate as soon as possible.

It seems that the classical method of cardiopulmonary resuscitation (CPR) will undergo certain changes in the near future, aimed at: 1) increasing intrathoracic pressure during chest compressions, for which positive airway pressure will be used; simultaneous ventilation and external massage; pulling of the anterior abdominal wall; onset of chest compression final stage inhalation; 2) decrease in intra-thoracic pressure during relaxation by creating negative airway pressure in this phase and 3) decrease in intra-thoracic aortic collapse and arterial system with compression of the chest by increasing the intravascular volume and the use of anti-shock inflatable trousers. One way to put these concepts into practice is called cough CPR. This method consists in the fact that the patient, who is conscious despite ventricular fibrillation, performs repeated, rhythmic cough movements for at least a short time, which lead to a phase increase in intrathoracic pressure, simulating changes caused by ordinary chest compressions. Considering the effect of CPR on blood flow, through the veins of the upper limb or central veins, but not through the femur, should be administered necessary drugs(preferably bolus rather than infusion). Isotonic drugs can be administered after dissolution in saline as an injection into the endotracheal tube, since absorption is provided by the bronchial circulation.

Sometimes there may be organized electrocardiographic activity that is not accompanied by effective contractions of the heart (electromechanical dissociation). Intracardiac administration of adrenaline at a dose of 5-10 ml of a 1:10,000 solution or 1 g of calcium gluconate can help restore the mechanical function of the heart. On the contrary, 10% calcium chloride can also be administered intravenously at a dose of 5-7 mg/kg. Refractory or recurrent ventricular fibrillation can be treated with lidocaine at a dose of 1 mg/kg followed by injections every 10-12 minutes at a dose of 0.5 mg/kg ( maximum dose 225 mg); novocainamide at a dose of 20 mg every 5 minutes (maximum dose 1000 mg); and then its infusion at a dose of 2-6 mg / min; or Ornidom at a dose of 5-12 mg/kg for several minutes, followed by an infusion of 1-2 mg/kg per minute. Cardiac massage can only be stopped when effective cardiac contractions provide a well-defined pulse and systemic arterial pressure.

The therapeutic approach outlined above is based on the following assumptions: 1) irreversible brain damage often occurs within a few (approximately 4) minutes after the development of circulatory collapse; 2) the probability of restoring an effective heart rhythm and successfully resuscitating the patient decreases rapidly over time; 3) the survival rate of patients with primary ventricular fibrillation can reach 80-90%, as with cardiac catheterization or exercise testing, if treatment is started decisively and quickly; 4) the survival of patients in a general hospital is much lower, approximately 20%, which depends in part on the presence of concomitant or underlying diseases; 5) out-of-hospital survival tends to zero, in the absence of a specially created emergency service (possibly due to the inevitable delays in the start necessary treatment, lack of proper equipment and trained personnel); 6) external cardiac massage can provide only minimal cardiac output. With the development of ventricular fibrillation, electrical defibrillation as early as possible increases the likelihood of success. Thus, with the development of circulatory collapse as primary manifestation disease treatment should be aimed at the rapid restoration of an effective heart rate.

Complications

External cardiac massage is not without significant drawbacks, since it can cause complications such as rib fractures, hemopericardium and tamponade, hemothorax, pneumothorax, liver injury, fat embolism, rupture of the spleen with the development of late, latent bleeding. However, these complications can be minimized with the correct implementation of resuscitation, timely recognition and adequate further tactics. It is always difficult to make the decision to terminate an ineffective resuscitation. In general, if an effective heart rate is not restored and if the patient's pupils remain fixed and dilated despite external cardiac massage for 30 minutes or more, a successful resuscitation outcome is difficult to expect.

T.P. Harrison. principles of internal medicine. Translation d.m.s. A. V. Suchkova, Ph.D. N. N. Zavadenko, Ph.D. D. G. Katkovsky

Collapse(lat. collapsus weakened, fallen) - acute vascular insufficiency, characterized primarily by a drop in vascular tone, as well as the volume of circulating blood. At the same time, the flow of venous blood to the heart decreases, cardiac output decreases, arterial and venous pressure drops, tissue perfusion and metabolism are disturbed, cerebral hypoxia occurs, and vital functions are inhibited. The collapse develops as a complication mainly of serious diseases and pathological conditions. However, it can also occur in cases where there are no significant pathological abnormalities (for example, orthostatic collapse in children).

Depending on the etiological factors, K. is isolated during intoxication and acute infectious diseases, acute massive blood loss (hemorrhagic collapse), when working in conditions of low oxygen content in the inhaled air (hypoxic K., etc.). Toxic collapse develops in acute poisoning, including professional nature, substances of general toxic action (carbon monoxide, cyanides, organophosphorus substances, nitro- and amido compounds, etc.). A series of physical factors- electricity, large doses ionizing radiation, heat environment (when overheating, heat stroke). Collapse observed in some acute diseases of the internal organs, for example acute pancreatitis. Some allergic reactions immediate type, For example anaphylactic shock, occur with vascular disorders typical of collapse. Infectious K. develops as a complication of meningoencephalitis, typhoid and typhus, acute dysentery, acute pneumonia, botulism, anthrax, viral hepatitis, toxic influenza, etc. due to intoxication with endo- and exotoxins of microorganisms.

orthostatic collapse. arising from a rapid transition from a horizontal to a vertical position, as well as during prolonged standing, due to the redistribution of blood with an increase in the total volume of the venous bed and a decrease in inflow to the heart; the basis of this condition is the insufficiency of venous tone. Orthostatic K. can be observed in convalescents after serious illnesses and prolonged bed rest, with some diseases of the endocrine and nervous systems (syringomyelia, encephalitis, tumors of the glands internal secretion, nervous system, etc.), in the postoperative period, with rapid evacuation of ascitic fluid or as a complication of spinal or epidural anesthesia. Orthostatic collapse sometimes occurs when neuroleptics, ganglionic blockers, adrenoblockers, sympatholytics, etc. are used incorrectly. In pilots and astronauts, it may be due to redistribution of blood associated with the action of acceleration forces; at the same time, blood from the vessels of the upper body and head moves into the vessels of the organs abdominal cavity and lower extremities, causing cerebral hypoxia. Orthostatic To. is quite often observed at practically healthy children, teenagers and young men. Collapse may be accompanied by a severe form decompression sickness.

Hemorrhagic collapse develops with acute massive blood loss (vascular damage, internal bleeding), due to a rapid decrease in circulating blood volume. A similar condition can occur due to abundant plasma loss during a burn, water and electrolyte disorders due to severe diarrhea, indomitable vomiting, and inappropriate use of diuretics.

Collapse possible with heart diseases accompanied by a sharp and rapid decrease in stroke volume (myocardial infarction, cardiac arrhythmias, acute myocarditis, hemopericardium or pericarditis with rapid accumulation of effusion in the pericardial cavity), as well as with pulmonary embolism. Acute cardiovascular failure, which develops under these conditions, is considered by some authors not as K. but as the so-called small emission syndrome, the manifestations of which are especially characteristic for cardiogenic shock. Sometimes referred to as reflex collapse. developing in patients with angina pectoris or myocardial infarction.

Pathogenesis. Conventionally, two main mechanisms of collapse development can be distinguished, which are often combined. One mechanism is a decrease in the tone of arterioles and veins as a result of the impact of infectious, toxic, physical, allergic and other factors directly on the vascular wall, vasomotor center and vascular receptors (sinocarotid zone, aortic arch, etc.). With insufficiency of compensatory mechanisms, a decrease in peripheral vascular resistance (vascular paresis) leads to pathological increase containers vascular bed, a decrease in the volume of circulating blood with its deposition in some vascular areas, a drop in venous flow to the heart, an increase in heart rate, and a decrease in blood pressure.

Another mechanism is directly related to a rapid decrease in the mass of circulating blood (for example, with massive blood and plasma loss that exceeds the compensatory capabilities of the body). The resulting reflex spasm of small vessels and increased heart rate under the influence of increased release into the blood catecholamines may not be sufficient to maintain a normal level of blood pressure. A decrease in circulating blood volume is accompanied by a decrease in the return of blood to the heart through the veins great circle blood circulation and, accordingly, a decrease in cardiac output, a violation of the system microcirculation, accumulation of blood in the capillaries, a drop in blood pressure. Develop hypoxia circulatory type, metabolic acidosis. Hypoxia and acidosis lead to damage to the vascular wall, an increase in its permeability . The loss of tone of precapillary sphincters and the weakening of their sensitivity to vasopressor substances develop against the background of maintaining the tone of postcapillary sphincters, which are more resistant to acidosis. In conditions of increased capillary permeability, this contributes to the transfer of water and electrolytes from the blood into the intercellular spaces. The rheological properties are disturbed, blood hypercoagulation and pathological aggregation of erythrocytes and platelets occur, conditions are created for the formation of microthrombi.

In the pathogenesis of infectious collapse, an especially important role is played by an increase in the permeability of the walls of blood vessels with the release of fluid and electrolytes from them, a decrease in the volume of circulating blood, as well as significant dehydration as a result of profuse sweating. A sharp rise in body temperature causes excitation and then inhibition of the respiratory and vasomotor centers. With generalized meningococcal, pneumococcal and other infections and the development of myocarditis or allergic myopericarditis on the 2-8th day, the pumping function of the heart decreases, the filling of the arteries and blood flow to the tissues decrease. Reflex mechanisms always take part in K.'s development also.

With a prolonged course of collapse as a result of hypoxia and metabolic disorders, vasoactive substances are released, while vasodilators predominate (acetylcholine, histamine, kinins, prostaglandins) and tissue metabolites (lactic acid, adenosine and its derivatives) are formed, which have a hypotensive effect. Histamine and histamine-like substances, lactic acid increase vascular permeability.

Clinical picture at K. various origins basically similar. The collapse develops more often acutely, suddenly. The patient's consciousness is preserved, but he is indifferent to the environment, often complains of a feeling of melancholy and depression, dizziness, blurred vision, tinnitus, thirst. The skin turns pale, the mucous membrane of the lips, the tip of the nose, fingers and toes become cyanotic. Tissue turgor decreases, the skin can become marbled, the face is earthy in color, covered with cold sticky sweat, the tongue is dry. Body temperature is often lowered, patients complain of cold and chilliness. Breathing is superficial, rapid, less often slow. Despite shortness of breath, patients do not experience suffocation. The pulse is soft, rapid, less often slow, of weak filling, often incorrect, sometimes difficult or absent on the radial arteries. BP is low, sometimes systolic BP drops to 70-60 mmHg st. and even lower, however, in the initial period of K. in persons with previous arterial hypertension BP may remain close to normal. Diastolic pressure also decreases. Superficial veins subside, blood flow velocity, peripheral and central venous pressure decrease. In the presence of right ventricular heart failure, central venous pressure may persist for normal level or decrease slightly the volume of circulating blood decreases. Deafness of heart sounds, often arrhythmia (extrasystole, atrial fibrillation), embryocardia are noted.

The ECG shows signs of insufficiency coronary blood flow and other changes that are secondary in nature and are most often caused by a decrease in venous inflow and the violation of central hemodynamics associated with this, and sometimes by infectious-toxic damage to the myocardium (see. Myocardial dystrophy). Violation of the contractile activity of the heart can lead to a further decrease in cardiac output and progressive impairment of hemodynamics. Oliguria is noted, sometimes nausea and vomiting (after drinking), which, with prolonged collapse, contributes to thickening of the blood, the appearance of azotemia; the oxygen content in the venous blood increases due to shunting of the blood flow, metabolic acidosis is possible.

The severity of manifestations To. depends on the underlying disease and the degree of vascular disorders. The degree of adaptation (for example, to hypoxia), age (in the elderly and young children, the collapse is more severe) and the emotional characteristics of the patient also matter. A relatively mild degree To. is sometimes called a collaptoid state.

Depending on the underlying disease that caused the collapse. clinical picture can buy some specific features. So, with K. coming as a result of blood loss, excitation is often observed at first, sweating often sharply decreases. Collapse phenomena at toxic lesions, peritonitis, acute pancreatitis are most often combined with signs of general severe intoxication. For orthostatic To. suddenness (quite often against the background of good health) and rather easy current are characteristic; and for the relief of orthostatic collapse. especially in adolescents and young men, it is usually enough to ensure peace in the horizontal position of the patient's body.

Infectious To. develops more often during a critical decrease in body temperature; it happens in different dates, for example, with typhus, usually on the 12-14th day of illness, especially during an abrupt decrease in body temperature (by 2-4 °), more often in the morning. The patient lies motionless, apathetic, answers questions slowly, quietly; complains of chills, thirst. The face takes on a pale earthy hue, the lips are bluish; facial features are sharpened, eyes sink, pupils are dilated, limbs are cold, muscles are relaxed. After a sharp decrease in temperature, the forehead, temples, sometimes the whole body are covered with cold sticky sweat. Temperature when measured in armpit sometimes drops to 35°. The pulse is frequent, weak: blood pressure and diuresis are reduced.

The course of infectious collapse is aggravated dehydration of the body hypoxia, which is complicated by pulmonary hypertension, decompensated metabolic acidosis, respiratory alkalosis and hypokalemia. With the loss of a large amount of water with vomit and feces during food poisoning, salmonellosis, rotavirus infection, acute dysentery, cholera, the volume of extracellular fluid decreases, incl. interstitial and intravascular. The blood thickens, its viscosity, density, hematocrit index, content total protein plasma. The volume of circulating blood decreases sharply. Decreased venous inflow and cardiac output. In infectious diseases, K. can last from several minutes to 6-8 h .

With the deepening of the collapse, the pulse becomes threadlike, it is almost impossible to determine blood pressure, breathing quickens. The patient's consciousness gradually darkens, the reaction of the pupils is sluggish, there is a tremor of the hands, convulsions of the muscles of the face and hands are possible. Sometimes K.'s phenomena grow very quickly; facial features sharply sharpen, consciousness darkens, pupils dilate, reflexes disappear, with increasing weakening of cardiac activity, agony.

Diagnosis in the presence of a characteristic clinical picture and relevant history data, it is usually not difficult. Studies of circulating blood volume, cardiac output, central venous pressure, hematocrit and other indicators can complement the idea of ​​the nature and severity of the collapse. what is necessary for the choice of etiological and pathogenetic therapy. Differential Diagnosis concerns, in the main, the reasons that caused K., which determines the nature of the assistance, as well as the indications for hospitalization and the choice of the hospital profile.

Treatment. At the prehospital stage, only collapse treatment can be effective. due to acute vascular insufficiency (orthostatic K. infectious collapse); at hemorrhagic To. it is necessary emergency hospitalization patient to the nearest hospital, preferably a surgical one. An important section of the course of any collapse is etiological therapy; stop bleeding, removal of toxic substances from the body (see Detoxification Therapy) , specific antidote therapy, elimination of hypoxia, giving the patient a strictly horizontal position in orthostatic K. immediate administration of adrenaline, desensitizing agents in anaphylactic collapse. elimination of cardiac arrhythmia, etc.

The main task of pathogenetic therapy is to stimulate blood circulation and respiration, increase blood pressure. An increase in venous flow to the heart is achieved by transfusion of blood-substituting fluids, blood plasma and other fluids, as well as by means that act on peripheral circulation. Therapy for dehydration and intoxication is carried out by the introduction of polyionic pyrogen-free solutions of crystalloids (acesols, disols, chlosols, lactasol). The volume of infusion in emergency therapy is 60 ml crystalloid solution per 1 kg body weight. Infusion rate - 1 ml/kg in 1 min. Infusion of colloidal blood substitutes in severely dehydrated patients is contraindicated. At hemorrhagic To. transfusion of blood is of paramount importance. In order to restore the volume of circulating blood, massive intravenous administration of blood substitutes (polyglucin, rheopolyglucin, hemodez, etc.) or blood is carried out by jet or drip; apply also transfusions of native and dry plasma, the concentrated solution of albumine and protein. Infusions of isotonic saline solutions or glucose solution are less effective. The amount of infusion solution depends on clinical parameters, blood pressure level, diuresis; if possible, it is controlled by determining hematocrit, circulating blood volume and central venous pressure. The introduction of agents that stimulate the vasomotor center (cordiamin, caffeine, etc.) is also aimed at eliminating hypotension.

Vasopressor drugs (norepinephrine, mezaton, angiotensin, adrenaline) are indicated for severe toxic, orthostatic collapse. With hemorrhagic K., it is advisable to use them only after the restoration of blood volume, and not with the so-called empty bed. If blood pressure does not increase in response to the administration of sympathomimetic amines, one should think about the presence of severe peripheral vasoconstriction and high peripheral resistance; in these cases, further use of sympathomimetic amines can only worsen the patient's condition. Therefore, vasopressor therapy should be used with caution. The effectiveness of a-blockers in peripheral vasoconstruction has not yet been sufficiently studied.

in the treatment of collapse. unrelated to ulcer bleeding, use glucocorticoids, briefly in sufficient doses (hydrocortisone sometimes up to 1000 mg and more, prednisone from 90 to 150 mg, sometimes up to 600 mg intravenously or intramuscularly).

To eliminate metabolic acidosis, along with agents that improve hemodynamics, 5-8% sodium bicarbonate solutions are used in the amount of 100-300 ml drip intravenously or lactasol. When K. is combined with heart failure, the use of cardiac glycosides, active treatment acute disorders heart rate and conduction.

Oxygen therapy is especially indicated for collapse. resulting from carbon monoxide poisoning or against the background of anaerobic infection; in these forms, it is preferable to use oxygen under high blood pressure(cm. Hyperbaric oxygen therapy ). With a protracted course of K., when the development of multiple intravascular coagulation (coagulopathy of consumption) is possible, as remedy apply heparin intravenously drip up to 5000 IU every 4 h(Exclude the possibility of internal bleeding!). With all types of collapse, careful monitoring of respiratory function is necessary, if possible with a study of gas exchange indicators. With the development respiratory failure auxiliary artificial ventilation lungs.

Resuscitation care for K. is provided by general rules. To maintain an adequate minute volume of blood during external cardiac massage in conditions of hypovolemia, it is necessary to increase the frequency of cardiac compressions to 100 in 1 min.

Forecast. Rapid elimination of the cause that caused the collapse. often leads to complete recovery of hemodynamics. In severe diseases and acute poisoning, the prognosis often depends on the severity of the underlying disease, the degree of vascular insufficiency, and the age of the patient. When not enough effective therapy To. can recur. Patients endure repeated collapses more difficult.

Prevention consists in intensive treatment of the underlying disease, constant monitoring of patients in severe and moderate condition; in this respect plays a special role monitoring observation. It is important to take into account the peculiarities of the pharmacodynamics of drugs (ganglioblockers, antipsychotics, antihypertensive and diuretics, barbiturates, etc.), allergic history and individual sensitivity to certain drugs and nutritional factors.

Features of collapse in children. In pathological conditions (dehydration, starvation, hidden or obvious blood loss, "sequestration" of fluid in the intestines, pleural or abdominal cavities), K. in children is more severe than in adults. More often than in adults, collapse develops with toxicosis and infectious diseases, accompanied by high body temperature, vomiting, and diarrhea. A decrease in blood pressure and impaired blood flow in the brain proceed with deeper tissue hypoxia, accompanied by loss of consciousness and convulsions. Since in young children the alkaline reserve in the tissues is limited, the violation oxidative processes during collapse easily leads to decompensated acidosis. Insufficient concentration and filtration capacity of the kidneys and the rapid accumulation of metabolic products complicate K.'s therapy and delay the restoration of normal vascular reactions.

Diagnosis of collapses in young children is difficult due to the fact that it is impossible to find out the patient's sensations, and systolic blood pressure in children even in normal conditions may not exceed 80 mmHg st. The most characteristic for K. in a child can be considered a set of symptoms: a weakening of the sonority of heart sounds, a decrease in pulse waves when measuring blood pressure, general adynamia, weakness, pallor or spotting skin increasing tachycardia.

Therapy for orthostatic collapse. usually does not require medication prescriptions; it is enough to lay the patient horizontally without a pillow, raise the legs above the level of the heart, unbutton the clothes. Have a beneficial effect Fresh air, inhalation of ammonia vapors. Only with deep and persistent K. with a decrease in systolic blood pressure below 70 mmHg st. shows intramuscular or intravenous administration of vascular analeptics (caffeine, ephedrine, mezaton) in doses appropriate for age. In order to prevent orthostatic collapse, it is necessary to explain to teachers and coaches that it is unacceptable for children and adolescents to stand still for a long time on lines, training camps, and sports formations. With collapse due to blood loss and with infectious diseases, the same measures are shown as in adults.

Abbreviations: K. - Collapse

Attention! Article ' Collapse‘ is given for informational purposes only and should not be used for self-medication

Collapse

Collapse is an acutely developing vascular insufficiency, characterized by a drop in vascular tone and an acute decrease in the volume of circulating blood.

Term etymology collapse: (Latin) collapsus - weakened, fallen.

When collapse happens:

• decreased venous blood flow to the heart
• decrease in cardiac output,
• drop in blood and venous pressure,
• tissue perfusion and metabolism are disturbed,
• brain hypoxia occurs,
• vital functions of the body are inhibited.

Collapse usually develops as a complication of the underlying disease, more often with serious illnesses and pathological conditions.

Forms of acute vascular insufficiency are also syncope and shock.

History of study

The doctrine of collapse arose in connection with the development of ideas about circulatory failure. The clinical picture of collapse was described long before the introduction of the term. So, S. P. Botkin in 1883 at a lecture, in connection with the death of a patient from typhoid fever, presented complete picture infectious collapse, calling this state intoxication of the body.

IP Pavlov in 1894 drew attention to the special origin of the collapse, noting that it is not associated with weakness of the heart, but depends on a decrease in the volume of circulating blood.

The theory of collapse was greatly developed in the works of G. F. Lang, N. D. Strazhesko, I. R. Petrov, V. A. Negovsky, and other Russian scientists.

There is no generally accepted definition of collapse. The greatest disagreement exists on the question of whether collapse and shock should be considered independent states or considered only as different periods of the same pathological process, that is, whether “shock” and “collapse” should be considered synonymous. The latter point of view is accepted by Anglo-American authors, who believe that both terms denote identical pathological conditions, prefer to use the term "shock". French researchers sometimes oppose collapse in an infectious disease to shock of traumatic origin.

G. F. Lang, I. R. Petrov, V. I. Popov, E. I. Chazov and other domestic authors usually distinguish between the concepts of “shock” and “collapse”. Often, however, these terms are confused.

Etiology and classification

Due to differences in the understanding of the pathophysiological mechanisms of collapse, the possible dominance of one or another pathophysiological mechanism, as well as the variety of nosological forms of diseases in which collapse can develop, it is unambiguous generally accepted classification collapse forms have not been developed.

In clinical interests, it is advisable to distinguish between forms of collapse depending on etiological factors. Most often, collapse develops when:

• body intoxication,
• acute infectious diseases.
• acute massive blood loss,
• stay in conditions of low oxygen content in the inhaled air.

Sometimes collapse can occur without significant pathological abnormalities (for example, orthostatic collapse in children).

Allocate toxic collapse. which occurs in acute poisoning. including those of a professional nature, substances of a general toxic effect (carbon monoxide, cyanides, organophosphorus substances, nitro compounds, etc.).

A series of physical factors- exposure to electric current, large doses of radiation, high ambient temperature (due to overheating, thermal shock), in which the regulation of vascular function is disturbed.

The collapse is observed at some acute diseases of the internal organs- with peritonitis, acute pancreatitis, which may be associated with endogenous intoxication, as well as with acute duodenitis, erosive gastritis and etc.

Some allergic reactions immediate type, such as anaphylactic shock. occur with vascular disorders typical of collapse.

infectious collapse develops as a complication of acute severe infectious diseases: meningoencephalitis, typhoid and typhus, acute dysentery, botulism, pneumonia, anthrax, viral hepatitis, influenza, etc. The reason for this complication is intoxication with endotoxins and exotoxins of microorganisms, mainly affecting the central nervous system or precapillary and postcapillary receptors.

hypoxic collapse may occur under conditions reduced concentration oxygen in the inhaled air, especially in combination with low barometric pressure. immediate cause circulatory disorders in this case is the lack of adaptive reactions of the body to hypoxia. acting directly or indirectly through the receptor apparatus of the cardiovascular system on the vasomotor centers.

The development of collapse under these conditions can also be promoted by hypocapnia due to hyperventilation, leading to the expansion of capillaries and blood vessels and, consequently, to the deposition and decrease in the volume of circulating blood.

orthostatic collapse. arising from a rapid transition from a horizontal to a vertical position, as well as during prolonged standing, due to the redistribution of blood with an increase in the total volume of the venous bed and a decrease in inflow to the heart; the basis of this condition is the insufficiency of venous tone. Orthostatic collapse can be observed:

• in convalescents after serious illnesses and prolonged bed rest,
• with some diseases of the endocrine and nervous system (syringomyelia, encephalitis, tumors of the endocrine glands, nervous system, etc.),
• in the postoperative period, with rapid evacuation of ascitic fluid or as a result of spinal or epidural anesthesia.
• Iatrogenic orthostatic collapse sometimes occurs when neuroleptics, adrenoblockers, ganglioblockers, sympatholytics, etc. are used incorrectly.

In pilots and cosmonauts, orthostatic collapse may be due to the redistribution of blood associated with the action of acceleration forces. At the same time, blood from the vessels of the upper body and head moves into the vessels of the abdominal organs and lower extremities, causing hypoxia of the brain. Orthostatic collapse is quite often observed in apparently healthy children, adolescents and young men.

severe form decompression sickness may be accompanied by collapse, which is associated with the accumulation of gas in the right ventricle of the heart.

One of the most common forms is hemorrhagic collapse. developing with acute massive blood loss (trauma, injury to blood vessels, internal bleeding due to rupture of an aneurysm of a vessel, arthrosis of a vessel in the area of ​​a stomach ulcer, etc.). Collapse with blood loss develops as a result of a rapid decrease in the volume of circulating blood. The same condition can occur due to abundant plasma loss during a burn, water and electrolyte disorders in severe diarrhea, uncontrollable vomiting, and inappropriate use of diuretics.

The collapse can be observed heart disease. accompanied by a sharp and rapid decrease stroke volume(myocardial infarction, cardiac arrhythmias, acute myocarditis, hemopericardium or pericarditis with rapid accumulation of effusion in the pericardial cavity), as well as thromboembolism pulmonary arteries. Acute cardiovascular insufficiency that develops in these conditions is described by some authors not as a collapse, but as a low output syndrome, the manifestations of which are especially characteristic of cardiogenic shock.

Some authors call reflex collapse. observed in patients during angina pectoris or anginal attack with myocardial infarction. I. R. Petrov (1966) and a number of authors distinguish collapse syndrome in shock, believing that the terminal phase of severe shock is characterized by collapse phenomena.

Clinical manifestations

The clinical picture in collapses of various origins is basically similar. More often the collapse develops sharply, suddenly.

In all forms of collapse, the patient's consciousness is preserved, but he is indifferent to the environment, often complains of a feeling of melancholy and depression, dizziness, blurred vision, tinnitus, thirst.

The skin turns pale, the mucous membrane of the lips, the tip of the nose, fingers and toes become cyanotic.

Tissue turgor decreases, the skin can become marble, the face is earthy in color, covered with cold sticky sweat. Dry tongue. Body temperature is often lowered, patients complain of cold and chilliness.

Breathing is superficial, rapid, less often - slow. Despite shortness of breath, patients do not experience suffocation.

The pulse is small, soft, quickened, less often - slow, weak filling, often incorrect, sometimes difficult or absent on the radial arteries. Arterial pressure is lowered, sometimes systolic blood pressure drops to 70-60 mm Hg. Art. and even lower, however, in the initial period of collapse in individuals with previous hypertension, blood pressure may remain at a level close to normal. Diastolic pressure also decreases.

Superficial veins collapse, blood flow velocity, peripheral and central venous pressure decrease. In the presence of right ventricular heart failure, central venous pressure may remain at a normal level or decrease slightly. The volume of circulating blood decreases. On the part of the heart, deafness of tones, arrhythmia (extrasystole, atrial fibrillation, etc.), embryocardia are noted.

On the ECG - signs of insufficiency of coronary blood flow and other changes that are secondary in nature and are most often caused by a decrease in venous inflow and the violation of central hemodynamics associated with this, and sometimes by infectious-toxic damage to the myocardium. Violation of the contractile activity of the heart can lead to a further decrease in cardiac output and progressive impairment of hemodynamics.

Oliguria, nausea and vomiting (after drinking), azotemia, thickening of the blood, an increase in the oxygen content in the venous blood due to shunting of the blood flow, and metabolic acidosis are almost constantly noted.

The severity of manifestations of collapse depends on the severity of the underlying disease and the degree of vascular disorders. The degree of adaptation (for example, to hypoxia), age (collapse is more severe in the elderly and young children) and the emotional characteristics of the patient, etc., also matter. A relatively mild degree of collapse is sometimes called a collaptoid state.

Depending on the underlying disease that caused the collapse, the clinical picture may acquire some specific features.

So, for example, in the event of a collapse as a result of blood loss. instead of oppression of the neuropsychic sphere, excitation is often observed at first, sweating is often sharply reduced.

Collapse phenomena at toxic lesions. peritonitis, acute pancreatitis are most often combined with signs of general severe intoxication.

For orthostatic collapse characterized by suddenness (often against the background of good health) and a relatively mild course. Moreover, to stop orthostatic collapse, especially in adolescents and young men, it is usually enough to ensure peace (in a strictly horizontal position of the patient), warming and inhalation of ammonia.

infectious collapse develops more often during a critical decrease in body temperature; this happens at different times, for example, with typhus, usually on the 12-14th day of illness, especially during an abrupt decrease in temperature (by 2-4 ° C), more often in the morning. The patient is very weak, lies motionless, apathetic, answers questions slowly, quietly; complains of chills, thirst. The face becomes pale earthy, the lips bluish; facial features are sharpened, eyes sink, pupils are dilated, limbs are cold, muscles are relaxed.

After a sharp decrease in body temperature, the forehead, temples, sometimes the whole body is covered with cold sticky sweat. Body temperature when measured in the armpit sometimes drops to 35°C; the gradient of rectal and skin temperature increases. The pulse is frequent, weak, blood pressure and diuresis are reduced.

The course of infectious collapse is aggravated by dehydration of the body. hypoxia. which is complicated pulmonary hypertension, decompensated metabolic acidosis, respiratory alkalosis and hypokalemia.

With the loss of a large amount of water with vomit and feces during food poisoning, salmonellosis, acute dysentery, cholera, the volume of extracellular, including interstitial and intravascular, fluid decreases. The blood thickens, its viscosity, density, hematocrit index, total plasma protein content increase, the volume of circulating blood decreases sharply. Decreased venous inflow and cardiac output.

According to the biomicroscopy of the conjunctiva of the eye, the number of functioning capillaries decreases, arteriovenular anastomoses, pendulum-like blood flow and stasis in venules and capillaries with a diameter of less than 25 microns occur. with signs of aggregation of blood cells. The ratio of the diameters of arterioles and venules is 1:5. In infectious diseases, the collapse lasts from several minutes to 6-8 hours (usually 2-3 hours).

As the collapse deepens, the pulse becomes threadlike. It is almost impossible to determine blood pressure, breathing quickens. The patient's consciousness gradually darkens, the reaction of the pupils is sluggish, there is a tremor of the hands, convulsions of the muscles of the face and hands are possible. Sometimes the phenomena of collapse increase very rapidly; facial features are sharply sharpened, consciousness is darkened, pupils dilate, reflexes disappear, and with increasing weakening of cardiac activity, agony occurs.

Death by collapse occurs due to:

• exhaustion energy resources brain as a result of tissue hypoxia,
• intoxication,
• metabolic disorders.

Big medical encyclopedia 1979

What is mitral valve collapse? The collapse is..

Collapse is a special clinical manifestation of an acute decrease in blood pressure, life threatening a state of falling blood pressure and low blood supply to the most important human organs. Such a condition in a person can usually be manifested by pallor of the face, severe weakness, and cold extremities. In addition, this disease can still be interpreted a little differently. Collapse is also one of the forms of acute vascular insufficiency, which is characterized by a sharp decrease in blood pressure and vascular tone, an immediate decrease in cardiac output and a decrease in the amount of circulating blood.

All this can lead to a decrease in blood flow to the heart, to a drop in arterial and venous pressure, hypoxia of the brain, human tissues and organs, and a decrease in metabolism. As for the reasons that contribute to the development of collapse, there are plenty of them. Among the most common causes of this pathological condition are acute illnesses heart and blood vessels, for example, such as myocarditis, myocardial infarction and many others. Also, acute blood loss and plasma loss, severe intoxication (with acute infectious diseases, poisoning) can also be added to the list of causes. Often, this disease can occur due to diseases of the endocrine and central nervous systems, spinal and epidural anesthesia.

Its occurrence can also be caused by an overdose of ganglionic blockers, sympatholytics, neuroleptics. Speaking about the symptoms of collapse, it should be noted that they mainly depend on the cause of the disease. But in many cases, this pathological condition is similar in collapses of various types and origins. It is often accompanied in patients with weakness, chilliness, dizziness, and a decrease in body temperature. The patient may complain of blurred vision and tinnitus. In addition, the patient's skin becomes sharply pale, the face becomes earthy, the limbs cool, sometimes the whole body can be covered with cold sweat.

The collapse is no joke. In this condition, a person breathes rapidly and shallowly. In almost all cases of various types of collapse, the patient has a decrease in blood pressure. Usually the patient is always conscious, but he may react poorly to his surroundings. The pupils of the patient react weakly and sluggishly to light.

The collapse is unpleasant feeling in the cardiac region with severe symptoms. If the patient complains of an uneven and frequent heartbeat, fever, dizziness, frequent pain in the head and profuse sweating, then in this case it may be mitral valve collapse. Depending on the causes of this disease, there are three types of acute decrease in blood pressure: cardiogenic hypotension, hemorrhagic collapse and vascular collapse.

The latter is accompanied by the expansion of peripheral vessels. The cause of this form of collapse are various acute infectious diseases. Vascular collapse can occur with pneumonia, sepsis, typhoid fever and other infectious diseases. It can cause low blood pressure during barbiturate intoxication using antihypertensive drugs(as a side effect in case of hypersensitivity to the drug) and severe allergic reactions. In any case, you need to immediately consult a doctor and mandatory examination and treatment.

Cardiovascular collapse is a form of heart failure that occurs due to a sharp drop in the tone of blood vessels. At this time, there is a rapid decrease in the mass of circulating fluid, therefore, blood flow to the heart decreases. Arterial-venous pressure falls, which in turn leads to inhibition of the vital functions of the body.

Collapse in Latin means "fallen", "weakened". Its development is sharp and rapid. Sometimes accompanied by loss of consciousness. This manifestation is quite dangerous, as it can lead to sudden death of a person. It happens that it takes only a few minutes after an attack to irreversible ischemic changes, sometimes - hours. However modern methods Treatments for some forms of collapse help prolong the life of patients with this disorder.

Causes of the collapse

Among the main reasons for an unexpected drop in vascular tone are:

• large blood loss;
• acute infections;
• intoxication;
• an overdose of certain drugs;
• consequence of anesthesia;
• damage to the blood organs;
• severe dehydration;
• impaired regulation of vascular tone;
• injury.

Symptoms

The clinical picture is pronounced. Together, the symptoms can immediately identify the pathology, without confusing it with other diseases of the heart and blood vessels.

• sudden and rapid deterioration of health;
• severe and sharp headache;
• noise in ears;
• darkening in the eyes;
• general weakness against the background of low blood pressure;
• pallor;

• the skin quickly becomes cold, becomes moist, acquires a bluish tint;
• violation of respiratory function;
• weak palpation of the pulse;
• body temperature drops;
• sometimes there is a loss of consciousness.

Note that a distinction is made between vascular and cardiac collapses. The first is less dangerous for the patient's life, but it also requires an adequate response.

Therapeutic measures

At the slightest sign of collapse, you should immediately seek qualified help. Compulsory hospitalization is required with further therapy for the underlying disease that causes atony.

First medical measures will be aimed at restoring vascular tone, blood volume, pressure, circulation. Applies conservative method- drug therapy.

And yet, in order to avoid relapse, it is necessary to undergo a course of treatment for the underlying disease that causes collapse.

Staying at home and hoping that everything will pass by itself will not work. Also, do not independently increase the pressure by taking over-the-counter medications. The appointment should be made by a cardiologist based on the results of a qualitative diagnosis. Quick response and timeliness of the provided therapeutic assistance is the key to saving human life!