Vascular collapse: symptoms and emergency care for a life-threatening condition. Sudden cardiovascular collapse and death Collapse causes symptoms

With this disease, vascular tone drops sharply, so the cells receive much less blood. Emergency assistance in case of collapse is provided immediately, since in the absence necessary actions Death may occur due to insufficient oxygen reaching the brain.

When is it appropriate to provide first aid for a collapse?

If a person has vascular collapse, should be carried out as quickly as possible. This condition is expressed very clearly, it cannot be confused with any other disease. The symptoms are as follows:

A sudden and sharp deterioration in a person’s well-being, while there may not have been any external prerequisites for this phenomenon.
The appearance of causeless and very intense headache.
The darkness before the patient's eyes is expressed by the strong dilation of his pupils.
A person notices the appearance of tinnitus.
Pain syndrome in the heart area. Moderate discomfort may occur.
Severe weakness, often loss of orientation in space. This condition differs from fainting, since even when the person comes to his senses, he does not have the strength to get up quickly.
Demotion blood pressure.
The skin turns pale. This phenomenon occurs as quickly as the appearance of other signs of collapse. After several minutes without assistance, the skin becomes very moisturized and becomes cold. Then they become cyanotic.
There is a sharpening of facial features.
Changes in breathing appear. It becomes very frequent, and its sound is clearly audible, since it is carried out at an impetuous pace.
It is very difficult to feel the patient's pulse.
Often a person loses consciousness for a long time, and without rehabilitation measures he may not come to his senses.

First aid

Every person is capable of providing first aid in case of collapse. You don't have to be a doctor to do this. You should know how it turns out urgent Care during collapse. The algorithm of actions is quite extensive. You need to learn it and be able to implement it so as not to get confused when another person develops a critical condition.

If you don't do it correct actions, a negative condition will most likely end in death. When performing all the points, you must remember that any delay has a detrimental effect on the patient, so assistance should be provided quickly and decisively.

If a person collapses in a crowded place and it is inconvenient to provide first aid, it is necessary to position him correctly. The patient is placed in a supine position. He needs to be placed on his back and ensure balance. It is advisable to choose a hard surface without protrusions so as not to injure a person.

It is not advisable to transfer the patient to the bed, since its softness will interfere with further actions. If nothing even is found, you can lay the person on the floor, having first covered the surface with a cloth. You should bend your head a little. You can place a small pillow or other soft thing under it. The legs should be raised and locked in this position. You can place a bundle of some material under them by rolling up a voluminous roller. If there are no suitable things, one of those present can independently hold their legs in an elevated position.

List of necessary actions

Emergency care for collapse requires that everything that can compress the patient’s body and prevent him from breathing calmly must be removed or unfastened. It is necessary to remove the belt, unfasten the cuffs, and also the collar. You can remove as much clothing as possible, but you should do it all quickly.
Someone needs to call an ambulance while emergency care for the collapse is being carried out. If among those present there is a doctor or a person with experience in providing first aid, it is necessary that he be the one to deal with rehabilitation measures. If a person who is able to provide assistance is alone, then it is advisable to simultaneously call an ambulance and continue to perform necessary measures upon the return of consciousness to the patient.
There should be a lot of fresh air in the room. The window should be opened. If possible, inhale oxygen.
The patient benefits from warmth. Before the doctors arrive, it is necessary, if possible, to make the air in the room warm using a heater, and cover the patient with heating pads on all sides of the body.
It is brought to a person's nose. This can bring him to consciousness. If this tool out of stock, you can perform other actions aimed at activating brain activity. This is a massage of both earlobes, temples, and also the area where the depression is located above the upper lip.

Features of the assistance process

In case of collapse, which is a consequence of large blood loss, it is necessary to eliminate the cause heavy bleeding as fast as possible. A tourniquet is usually applied to prevent death once collapse occurs. The clinic where emergency care will take place after the doctors arrive is responsible for further therapeutic measures. When the patient comes to his senses, he should be given complete rest. You should not constantly ask him about his well-being. It is better to observe his condition from the side.

Prohibited actions

When emergency care is provided for collapse, the patient should not be asked to drink painkillers or take any medications that affect the dilation of blood vessels. This can lead to dire consequences and even death.
Try to mechanically push liquid or any liquid into the patient’s esophagus medications, if he is sleeping, it is impossible. If the attempt is unsuccessful, a reflex cessation of breathing may occur.
Slap a person in the face, bringing him to consciousness. Often these actions do not improve the situation, but only increase the patient’s stress.

Relevance of medications for collapse

Drug treatment is usually prescribed by a doctor, but if those around you have the proper qualifications or if it is impossible to go to the hospital, you can choose the drugs yourself. When shock or collapse occurs, emergency care is very important. If medications are not available, you should immediately send someone to the pharmacy to get them. First, substances are introduced into the body aimed at normalizing blood circulation processes.

Basic medications for collapse

Typically, the first step is an intravenous infusion using drugs such as sodium chloride or Ringer's solution. There is no fixed quantity assigned. When determining the dose, you should be guided by the external signs of the patient:

The general condition of a person, a set of indicators that determine the viability and prognosis of the disease.
Skin tone. The complexion, in particular the nasolabial triangle, is especially important. It shouldn't be too pale. If the color is close to white, more vasodilator solution will be required.
Absence or presence of diuresis.
Blood pressure.
The frequency of heart beats, as well as the intensity of the pulse in different parts bodies.

Additional drugs

Anti-inflammatory drugs are needed. In case of collapse, it is advisable to administer the following drugs: "Metypred", "Triamcinolone" or "Prednisolone".
Vasopressors can also be administered intravenously.
The spasm should be relieved quickly. To do this, you can even introduce a regular solution of novocaine. If it is more convenient to give an injection intramuscularly, it is advisable to use Aminazine.

Emergency care in case of collapse is necessary, since an ambulance cannot always get there quickly. In order to be able to provide real help to a person, you should remember the set of instructions and, if necessary, follow them accurately. Often, providing assistance when collapse occurs is the only way through which a person’s life can be saved.

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

Sudden cardiac death in the United States alone annually claims about 400,000 lives, i.e., approximately 1 person dies every minute. Definitions sudden death vary, but most include the following: death occurs suddenly and immediately or within 1 hour of the onset of symptoms in a person with or without pre-existing heart disease. Typically, only a few minutes pass from the development of sudden cardiovascular collapse (no effective cardiac output) to irreversible ischemic changes in the central nervous system. However, with timely treatment of some forms of cardiovascular collapse, an increase in life expectancy can be achieved without subsequent functional damage.

Sudden cardiovascular collapse may be a consequence of: 1) heart rhythm disturbances (see Chapters 183 and 184), most often ventricular fibrillation or ventricular tachycardia, sometimes occurring after bradyarrhythmia, or severe bradycardia or ventricular asystole (these conditions are usually are harbingers of ineffectiveness resuscitation measures); 2) pronounced sharp decrease 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 pump failure, which may occur due to acute myocardial infarction, "nonarrhythmic cardiac death", with or without ventricular rupture or critical aortic stenosis; 4) activation of vasodepressor reflexes, which can lead to an unexpected decrease in blood pressure and a decrease in heart rate and is observed in different situations, including pulmonary embolism, syndrome hypersensitivity carotid sinus and primary pulmonary hypertension. Among primary electrophysiologic abnormalities, the relative incidence of ventricular fibrillation, ventricular tachycardia, and severe bradyarrhythmia or asystole is approximately 75%, 10%, and 25%.

Sudden death due to atherosclerosis of the coronary arteries

Sudden death is primarily a complication of severe coronary atherosclerosis affecting multiple coronary vessels. During pathological examination, the detection rate of fresh coronary thrombosis ranges from 25 to 75%. Rupture of an atherosclerotic plaque, which caused vascular obstruction, was detected in a number of patients without thrombosis. Thus, it seems that most patients with coronary heart disease have acute luminal obstruction coronary vessel is the trigger point for sudden death. In other cases, sudden death may result from functional electrophysiological instability, which is diagnosed by provoking invasive electrophysiological testing and may persist for a long time or indefinitely after myocardial infarction. In victims of sudden death under 45 years of age, 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 is the first manifestation of this disease. Based on the experience of emergency cardiology departments, it could be assumed that the incidence of sudden death could be significantly reduced by preventive measures carried out primarily in populations at particularly high risk, if such measures were shown to be effective and have low toxicity and do not cause great inconvenience to patients. However, sudden death may be one of the manifestations of coronary heart disease, and effective prevention sudden death also requires the prevention of atherosclerosis. The risk of sudden death, which is a manifestation of a previous myocardial infarction, is increased in patients with severely impaired left ventricular function, complex ectopic ventricular activity, especially when these factors are combined.

Factors associated with increased risk sudden death

When recording an electrocardiogram for 24 hours during normal daily activities, supraventricular premature contractions can be found in most Americans over 50 years of age, and ventricular premature contractions occur in nearly two-thirds. Simple ventricular premature contractions in individuals with an otherwise healthy heart are not associated with an increased risk of sudden death, but conduction disturbances and bigeminy or high-grade ectopic ventricular contractions (repetitive patterns or complexes) R -on-T) are an indicator high risk, especially among patients who have had a myocardial infarction within the previous year. In patients who have suffered acute myocardial infarction, ventricular ectopic contractions that occur in the late period 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 segmentS.T.which can be identified using frequency analysis of a signal-averaged electrocardiogram (ECG), also allow the identification of patients at high risk of sudden death.

Premature ventricular contractions can be a trigger for fibrillation, especially against the background of myocardial ischemia. On the other hand, they may be a manifestation of the most common fundamental electrophysiological abnormalities that predispose to both ventricular premature beats and ventricular fibrillation, or they may be a completely independent phenomenon associated with electrophysiological mechanisms different from those that cause fibrillation. Their clinical significance varies among patients. 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 of much greater importance and significantly worsen the prognosis in the case of acute ischemia and severe left ventricular dysfunction due to coronary artery disease or cardiomyopathy than in their absence.

Severe coronary heart disease, not necessarily accompanied by morphological signs of acute infarction, hypertension or diabetes mellitus, is present in more than 75% of people who suddenly died. 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 without previous coronary heart disease who die suddenly have at least two of the following four risk factors for atherosclerosis: hypercholesterolemia, hypertension, hyperglycemia, and smoking. Excess body weight 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 nonsmokers, possibly due to higher circulating levels of catecholamines and fatty acids and increased production of carboxyhemoglobin, which circulate in the blood and reduce its oxygen-carrying capacity. The predisposition to sudden death caused by smoking is not permanent, but, apparently, can undergo reverse development when smoking is stopped.

Cardiovascular collapse during exercise occurs in rare cases in patients with coronary artery disease performing an exercise test. With trained personnel and appropriate equipment, these episodes can be quickly controlled with 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 behavioral characteristics, and experimental observations of increased susceptibility to ventricular tachycardia and fibrillation during artificial coronary occlusion after placing animals in a state of emotional stress or increasing their sympathetic activity. nervous system. In experimental animals, the protective effect of the administration of certain 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 completely unexpectedly and without any previous symptoms or prodromal signs. This syndrome is not associated with acute myocardial infarction, although most patients may experience sequelae of previous myocardial infarction or other types of organic heart disease. After resuscitation, there is a predisposition to early relapses, possibly reflecting the electrical instability of the myocardium leading to the initial episode, as well as the relatively high mortality in the subsequent 2 years, reaching 50%. It is clear that these patients can only be saved if there is a responsive cardiac service capable of vigorously diagnosing and treating using pharmacological drugs, if surgery is necessary, implantable defibrillators or programmable cardiac 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 (chest pain, shortness of breath, fainting) and a significantly lower incidence 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 department. The predisposition to ventricular fibrillation at the time of 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 increased for a long time. However, in some patients who have suffered a myocardial infarction, the risk of sudden death remains quite high. Factors determining this risk are the vastness of the infarction zone, severe impairment of ventricular function, 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 with an increase in blood pressure, preservation 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. The cause may be severe aortic stenosis, congenital or acquired, with a sudden disturbance in the rhythm or pumping function of the heart, hypertrophic cardiomyopathy and myocarditis or cardiomyopathy associated with arrhythmias. Massive embolism pulmonary vessels leads to circulatory collapse and death within minutes in approximately 10% of cases. Some patients die after some time due to progressive right ventricular failure and hypoxia. Acute circulatory collapse may be preceded by small embolisms that occur at varying intervals before a fatal attack. In accordance with this, prescribing 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

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

Variant Prinzmetal angina; spasm of the coronary arteries Congenital coronary disease heart, including malformations, coronary arteriovenous fistulas Coronary embolism

Acquired non-atherosclerotic coronary disease, including aneurysms due to Kawasaki disease

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

Hereditary or acquired prolongation of the interval Q-T,with or without congenital deafness

Damage to the sinoatrial node

Atrioventricular block (Adams-Stokes-Morgagni syndrome) Secondary damage to the conduction system: amyloidosis, sarcoidosis, hemochromatosis, thrombotic thrombocytopenic purpura, dystrophic myotonia

Toxicity or idiosyncrasy of pharmacological drugs, e.g. digitalis, quinidine

Electrolyte disturbances, especially magnesium and potassium deficiency in the myocardium Heart valve lesions, especially aortic stenosis Infective endocarditis Myocarditis

Cardiomyopathies, in particular idiopathic hypertrophic subaortic stenosis

Modified dietary programs to combat excess body weight based on fluid and protein intake

Pericardial tamponade

Mitral valve prolapse (an extremely rare cause of sudden death) Heart tumors

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 reasons sudden death. Sudden cardiac death may be associated with modified dietary programs aimed at reducing body weight using fluids and proteins. Distinctive features these cases are prolongation of the interval Q - T, andalso the 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 cause chronic AV block in adults. However, the risk of sudden death is much higher with conduction disorders combined with coronary heart disease than with isolated primary damage to the conduction system. Electrocardiographic signs of interval prolongation Q-T,hearing loss of central origin and their autosomal recessive inheritance (Jervel-Lange-Nielsen syndrome) occur in a large number of people who have suffered 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 people with these disorders is approximately 1% per year. Congenital deafness, history of fainting, belonging to female, confirmed tachycardia by type torsades de pointes (see below) or ventricular fibrillation are independent risk factors for sudden cardiac death. Although removal of the left stellate ganglion has a transient preventive effect, healing does not occur.

Other conditions associated with prolongation of the interval Q -Tand increased temporary dispersion of repolarization, such as hypothermia, taking a number of drugs (including hnnidine, disopyramide, procainamide, phenothiazine derivatives, tricyclic antidepressants), hypokalemia, hypomagnesemia and acute myocarditis, are combined with sudden death, especially if episodes also develop torsades de pointes , a variant of rapid ventricular tachycardia with distinct electrocardiographic and pathophysiological signs. Arrest or blockade of the sinoatrial node with subsequent inhibition of downstream pacemakers or sick sinus syndrome, usually accompanied by dysfunction of the conduction system, can also lead to asystole. Sometimes fibroids and inflammatory processes in the area of the sinoatrial or atrioventricular nodes can lead to sudden death in people without pre-existing signs of heart disease. Sudden ruptures of the papillary muscle, interventricular septum, or free wall occurring within the first few days after 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, sudden change in intracranial pressure or brain stem damage. It can also occur with asphyxia. Poisoning with digitalis preparations can cause life-threatening cardiac arrhythmias, leading to sudden cardiovascular collapse, which, if not treated immediately, results in death. Paradoxically, antiarrhythmic drugs may aggravate 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 result from activation of the recirculation mechanism (reentry, re-entry ), automaticity disorders, or both. It seems that the recirculation mechanism plays a dominant role in the genesis of early arrhythmias, for example, during the first hour, and disturbances in automaticity are the main etiological factor in later periods.

It is possible that several factors are involved in setting the stage 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, and 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 slowing of conduction, which is a necessary condition for the occurrence of recirculation soon after the onset of ischemia.

Another mechanism involved in maintaining recycling in early dates after ischemia, there is focal repetitive excitation. Anoxia leads to a shortening of the duration of the action potential. In accordance with this, during electrical systole, repolarization of cells located in the ischemic zone may occur earlier than cells of adjacent non-ischemic tissue. The resulting difference between the prevailing transmembrane potentials may cause unstable depolarization of neighboring cells and, consequently, contribute to the appearance of rhythm disturbances that depend on recirculation. Concomitant pharmacological and metabolic factors may also predispose to recirculation. For example, quinidine may suppress conduction velocity disproportionately to the increase in refractoriness, thereby facilitating the occurrence of recirculation-dependent arrhythmias soon after the onset of ischemia.

The so-called vulnerable period corresponding to the ascending knee of the toothT,represents that part of the cardiac cycle when the temporal dispersion of ventricular refractoriness is greatest, and therefore the 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 stimulus intensity required to cause recurrent tachycardia or ventricular fibrillation is reduced. Temporal dispersion of refractoriness may be enhanced in non-ischemic tissues in the presence of a slow heart rate. Thus, profound bradycardia caused by decreased sinus node automaticity or atrioventricular block may be especially dangerous in patients with acute myocardial infarction because it potentiates recirculation.

Ventricular tachycardia, which occurs 8-12 hours after the onset of ischemia, appears to be partly dependent on a disorder of automaticity or triggered activity of Purkinje fibers, and possibly myocardial cells. This rhythm resembles slow ventricular tachycardia, often occurring within several hours or in the first days after ligation coronary artery in experimental animals. As a rule, it does not progress to ventricular fibrillation or other malignant rhythm disorders. The decrease in diastolic transmembrane potential in response to regional biochemical changes caused by ischemia may be related to disorders of automaticity due to the facilitation of repeated depolarizations of Purkinje fibers provoked by a single depolarization. Since catecholamines facilitate the propagation of such slow responses, increased regional adrenergic stimulation may play an important role here. The apparent effectiveness 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 automaticity.

Asystole and/or profound bradycardia are less common electrophysiological mechanisms underlying sudden death caused by coronary atherosclerosis. They may be manifestations of complete occlusion of the right coronary artery and, as a rule, indicate the failure of resuscitation measures. Asystole and bradycardia are often the result of the inability to generate impulses in sinus node, atrioventricular block and the inability of auxiliary pacemakers to function effectively. Sudden death in persons with these disorders is usually largely a consequence of diffuse damage myocardium than AV block itself.

Identification of high risk individuals

The challenges posed by ambulatory electrocardiographic monitoring or other mass population screening efforts to identify individuals at high risk for sudden death are enormous, since the population at risk for sudden death is concentrated in men aged 35 to 74 years. and ventricular ectopic activity occurs very often and varies greatly in different days in the same patient. The maximum risk was noted: 1) in patients who previously suffered primary ventricular fibrillation without connection with acute myocardial infarction; 2) in patients with coronary heart disease who experience attacks of ventricular tachycardia; 3) for 6 months in patients after acute myocardial infarction, in whom regular early or multifocal premature ventricular contractions are recorded, occurring at rest, during physical activity or psychological stress, especially in those who have severe left ventricular dysfunction with an ejection fraction of less than 40% or overt heart failure; 4) in patients with an increased interval Q -Tand frequent premature contractions, especially when indicating a history of fainting. Although identifying patients at high risk of sudden death is extremely important, selecting effective prophylactic agents remains an equally difficult task, and none of them has proven to be clearly effective in reducing risk. Induction of rhythm disturbances by stimulation of the ventricles using a catheter with electrodes inserted into the heart cavity and choice pharmacological agents, allowing to prevent such provocation of arrhythmias, is probably an effective method for predicting the possibility of preventing or stopping recurrent malignant arrhythmias, in particular ventricular tachycardia, using specific drugs in patients who have suffered prolonged ventricular tachycardia or fibrillation. In addition, this method allows the identification of patients refractory to the use of conventional methods treatment, and to facilitate the selection of candidates for aggressive methods such as administration of investigational drugs, implantation of automatic defibrillators, or surgical intervention.

Drug treatment

Treatment with antiarrhythmic drugs in doses sufficient to maintain therapeutic levels in the blood has been considered effective for recurrent ventricular tachycardia and/or fibrillation in persons who have suffered sudden death if, during acute trials, the drug could stop or reduce the severity of high-grade premature ventricular contractions, early or recurring forms. In persons who have suffered sudden death and have frequent and complex ventricular extrasystoles occurring between episodes of ventricular tachycardia and/or fibrillation (approximately 30% of patients), prophylactic treatment should be carried out individually, after determining the pharmacological effectiveness of each drug, i.e. the ability to suppress existing rhythm disturbances. Usual doses of long-acting procainamide (30-50 mg/kg per day orally in divided doses every 6 hours) or disopyramide (6-!0 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 drug currently being tested in the USA, at a dose of 5 mg/kg administered intravenously over 5-15 minutes or 300-800 mg per day orally with or without a loading dose of 1200-2000 mg per day in divided doses over 1 or 4 weeks) has a strong antifibrillatory effect, but a very slow onset maximum effect, which only appears after several days or weeks of continuous administration. Toxicity can occur with both acute and chronic administration. Although the antifibrillatory efficacy of amiodarone is well established, its use should be reserved for conditions refractory to less toxic agents 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 treatment 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 rational choice of drugs and their dosage difficult, and prescribing steroid regimens to all patients makes prevention unfeasible. However, due to the large variability of spontaneous heart rhythm disturbances recorded during Holter monitoring, which must be interpreted individually in each patient, suppression of ectopic activity must be achieved (at least 80% within 24 hours) before it is possible to speak about the pharmacological effectiveness of a particular treatment regimen. Even after such effectiveness has been proven, this does not mean at all that the chosen regimen will be able to have a similar protective effect against ventricular fibrillation. Some patients require simultaneous administration of several drugs. Since the profound electrophysiological abnormalities underlying ventricular fibrillation and premature contractions may vary, 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 patients randomized to acute myocardial infarction has been shown in several double-blind prospective studies using R-adrenergic blockers, despite the fact that the antiarrhythmic effect of treatment has not been quantified and the mechanisms of obvious protective action have not yet been established. The incidence of sudden death was significantly reduced compared with the overall reduction in mortality during several years of follow-up in a group of treated myocardial infarction survivors. R-blockers were started a few days after the heart attack.

Delay in hospitalization of the patient and provision of qualified care after the development of acute myocardial infarction significantly complicates the prevention of sudden death. In most areas of the United States, the time from the onset of symptoms of an acute heart attack to hospitalization averages 3 to 5 hours. The patient's denial of the possibility of developing a serious illness and the indecisiveness of both the doctor and the patient are the greatest delays in the provision of care.

Surgical approaches

Surgical treatment may be indicated for a carefully selected group of people who have suffered sudden death and subsequently have recurrent malignant arrhythmias. In some patients, prophylaxis with automated implantable defibrillators may improve survival rates, although the discomfort of the device and the potential for nonphysiological shocks are major disadvantages of this method.

Community Effort.Experience gained in Seattle, Washington, shows that in order to effectively address the problem of sudden cardiovascular collapse and death on a broad public basis, it is necessary to create a system that can provide fast reaction in such situations. Important elements of this system are: the presence of a single telephone for the entire city, by which you can “launch” this system; 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 persons among 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 after the collapse resuscitation measures are started. The availability of special transport, mobile coronary care units, equipped with the necessary equipment and staffed with trained personnel capable of providing adequate care in the corresponding emergency cardiac situation, can reduce the time spent. In addition, the presence of such teams increases medical awareness and preparedness 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 of well-trained citizens in the public program “Cardiopulmonary Resuscitation by People” increases the likelihood of a successful outcome of resuscitation. This is confirmed by an increase in the proportion of patients discharged from hospital in good condition who suffered prehospital cardiac arrest: 30-35% compared to 10-15% in the absence of such a program. Long-term survival, at 2 years, can also be increased by 50 to 70% or more. Proponents of bystander CPR are currently exploring the use of portable home defibrillators designed for safe use by the general population with only minimal skills.

Patient education. Instructing persons at risk for myocardial infarction on how to induce medical care V urgent situation when symptoms of the disease appear, it is extremely important factor prevention of sudden cardiac death. This policy assumes that patients are aware of the need to urgently seek effective emergency care and that physicians expect the patient to do so, regardless of the time of day or night, if the patient develops symptoms of myocardial infarction. This concept also means that the patient can communicate directly with the emergency care system without informing the doctor. Exercise, such as jogging, should be discouraged in the absence of medical supervision in patients with established coronary artery disease and should be completely prohibited in those at particularly high risk of sudden death, as described above.

Approach to examining a patient with sudden onset 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) absence of pulse in the peripheral arteries; 3) absence of heart sounds. Because the external massage heart provides only minimal cardiac output (no more than 30% of the lower limit of normal value), true restoration of an effective rhythm should be a priority. In the absence of contrary data, it should be assumed that the cause of rapid circulatory collapse is ventricular fibrillation. If the doctor observes the patient within 1 minute after the development of collapse, then no time should be wasted trying to provide oxygenation. Instant swipe into the precordial area of the chest (shock defibrillation) may sometimes be effective. It should be attempted as it only takes seconds. In rare cases, when circulatory collapse is a consequence of ventricular tachycardia and the patient is conscious when the doctor arrives, strong coughing movements can interrupt the arrhythmia. If there is no immediate return of circulation, electrical defibrillation should be attempted without wasting time in recording the electrocardiogram using separate equipment, although the use of portable defibrillators that can record the electrocardiogram directly through the defibrillator electrodes may be helpful. The maximum electrical voltage of conventional equipment (320 V/s) is sufficient even in severely obese patients and can be used. The effectiveness is enhanced if the electrode pads are applied firmly to the body and the shock is applied immediately, without waiting for the increased energy demand of defibrillation, which occurs with increasing duration of ventricular fibrillation. Devices that automatically select shock voltage based on tissue resistance are particularly promising because they can minimize the dangers of delivering unnecessarily large shocks and avoid ineffectively delivering small shocks to patients with higher-than-expected resistance. If these simple attempts are unsuccessful, then external cardiac massage should be started and cardiopulmonary resuscitation should be performed in full with rapid recovery and maintenance of good airway patency.

If collapse is clearly a consequence of asystole, transthoracic or transvenous electrical stimulation should be given without delay. Intracardiac administration of adrenaline in a dose of 5-10 ml at a dilution of 1:10,000 can increase the heart's response to artificial stimulation or activate a slow, ineffective source of excitation in the myocardium. If these primary specific measures turn out to be ineffective, despite their correct technical implementation, it is necessary to quickly correct the metabolic environment of the body and establish monitoring control. It is best to use the following three activities for this:

1) external cardiac massage;

2) correction of acid-base balance, which often requires intravenous administration sodium bicarbonate at an initial dose of 1 mEq/kg. Half the dose should be re-administered every 10-12 minutes in accordance with the results of regularly determined arterial blood pH;

3) identification and correction of electrolyte disturbances. Vigorous attempts to restore an effective heart rhythm should be made as early as possible (within minutes, of course). If the effective heart rhythm is restored, it quickly transforms again into ventricular tachycardia or fibrillation, 1 mg/kg lidocaine should be administered intravenously, followed by an 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 vital perfusion important organs by successive compression of the chest with your hands. It is necessary to point out some aspects of this technique.

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

2. To open and maintain airway patency, use next appointment: throw the patient's head back; pressing firmly on the patient's forehead, press the fingers of the other hand lower jaw and push it forward so that your chin rises up.

3. If there is no pulse in the carotid arteries within 5 seconds, chest compressions 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 to avoid liver damage, the other hand rests on the first, covering it with the fingers.

4. Compression of the sternum, displacing it by 3-.5 cm, should be performed at a frequency of 1 per second to allow sufficient time to fill the ventricle.

5. The resuscitator's torso should be higher than 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 femoral or carotid arteries, but little blood is expelled.

7. The 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 adverse effect.

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

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

It seems that the classical method of carrying out cardiopulmonary resuscitation(CPR) will undergo certain changes in the near future aimed at: 1) increasing intrathoracic pressure during chest compressions, which will be achieved by creating positive pressure in the airways; simultaneous ventilation and external massage; tugging of the anterior abdominal wall; the beginning of compression of the chest at the final stage of inspiration; 2) reducing intrathoracic pressure during relaxation by creating negative pressure in the airways during this phase and 3) reducing intrathoracic collapse of the aorta and arterial system for chest compression by increasing intravascular volume and using anti-shock inflatable trousers. One of the practical applications of these concepts is called “cough CPR.” This method involves the patient, who is conscious despite ventricular fibrillation, performing repeated, rhythmic coughing movements for at least a short time, which lead to a phase increase in intrathoracic pressure, simulating the changes caused by normal chest compressions. Considering the effect of CPR on blood flow, through the veins upper limb or central veins, but not through the femoral, should be entered necessary medications(preferably bolus rather than infusion). Isotonic drugs can be administered after dissolving in saline solution as an injection into the endotracheal tube, since absorption is ensured by the bronchial circulation.

Occasionally, organized electrocardiographic activity may appear that is not accompanied by effective heart contractions (electromechanical dissociation). Intracardiac administration of adrenaline in 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 by infusion at a dose of 2-6 mg/min; or ornid at a dose of 5-12 mg/kg over several minutes followed by an infusion of 1-2 mg/kg per minute. Cardiac massage can be stopped only when effective cardiac contractions provide a well-defined pulse and systemic blood pressure.

The therapeutic approach outlined above is based on the following principles: 1) irreversible brain damage often occurs within a few (approximately 4) minutes after the onset of circulatory collapse; 2) the likelihood 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 rate of patients in a general hospital is significantly lower, approximately 20%, which partly depends 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 inevitable delays in the onset of necessary treatment, lack of proper equipment and trained personnel); 6) external cardiac massage can provide only minimal cardiac output. If ventricular fibrillation develops, performing electrical defibrillation as early as possible increases the likelihood of success. Thus, with the development of circulatory collapse as primary manifestation treatment of the disease should be aimed at quickly restoring an effective heart rhythm.

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, hidden bleeding. However, these complications can be minimized with proper implementation of resuscitation measures, timely recognition and adequate further tactics. It is always difficult to make the decision to stop ineffective resuscitation. In general, if effective cardiac rhythm is not restored and if the patient's pupils remain fixed and dilated despite external cardiac massage for 30 minutes or more, it is difficult to expect a successful resuscitation outcome.

T.P. Harrison. Principles of internal medicine. Translation by Doctor of Medical Sciences A. V. Suchkova, Ph.D. N. N. Zavadenko, Ph.D. D. G. Katkovsky

Description:

Collapse is an acute vascular failure characterized by sharp decline Blood pressure due to a fall vascular tone, decreased cardiac output or as a result of an acute decrease in circulating blood volume. Collapse is accompanied by hypoxia of all tissues and organs, decreased metabolism, and inhibition of vital functions of the body.

Symptoms:

The clinical picture of collapse has features depending on its cause, but in terms of its main manifestations it is similar to collapse of various origins. Patients complain of emerging and rapidly progressing weakness, chilliness, blurred vision, and sometimes a feeling of melancholy and fear. The patient's consciousness is preserved, but in most cases he is indifferent to his surroundings. The skin is sharply pale, the face is sallow in color, covered with cold, sticky sweat; with cardiogenic collapse, cyanosis is often noted. Body temperature is reduced. Breathing is shallow and rapid. The pulse is small, soft, rapid.

Blood pressure is reduced: systolic - up to 80 - 60, diastolic - up to 40 mm Hg. Art. and lower (in persons with pre-existing hypertension, the collapse pattern can be observed at higher blood pressure levels). In almost all cases, thickening of the blood and oliguria, rapidly increasing, are noted. As the collapse deepens, the patient’s consciousness becomes darkened, and cardiac arrhythmias often develop (or progress); Pupils dilate, reflexes disappear. If not carried out effective treatment, death occurs.

Cardiogenic collapse is usually combined with cardiac arrhythmia, pulmonary edema or signs of acute right ventricular failure (for example, with pulmonary embolism), and is severe. Orthostatic collapse occurs only when the body is in an upright position and quickly stops after transferring the patient to a lying position.

Infectious collapse most often develops during a critical decrease in body temperature; At the same time, there is moisture in the skin, usually the whole body (wet underwear), severe muscle hypotension, and a soft pulse.

Toxic collapse, especially in case of poisoning, is often combined with nausea, vomiting, diarrhea, signs of dehydration, etc.

Diagnosis of collapse is based on a characteristic clinical picture. Dynamic studies of blood pressure, and, if possible, also the volume of circulating blood and hematocrit, give an idea of its nature and severity. Differential diagnosis in case of disorders of consciousness, it is carried out with fainting, which is distinguished by the short duration of loss of consciousness. It should be borne in mind that collapse may be part of the picture of shock, in which deeper hemodynamic disturbances occur.

Causes:

Among the diverse causes of its occurrence, the most common are diseases of the heart and blood vessels, especially acute (myocardial infarction, thromboembolism of the pulmonary arteries, etc.), acute blood loss and plasma loss (for example, with extensive burns), severe in various poisonings and infectious diseases, disturbances in the regulation of vascular tone in shock of various origins, as well as in a number of diseases of the central nervous system and endocrine system, in case of overdose of neuroleptics, ganglion blockers, sympatholytics.

Treatment:

For treatment the following is prescribed:

Therapeutic measures must be carried out urgently and intensively. Patients with collapse that occurred in out-of-hospital conditions should be urgently taken to the hospital, accompanied by an ambulance team (if they do not provide full effective assistance on the spot) or medical workers who are proficient in resuscitation techniques.

In all cases, the patient is placed in a horizontal position with slightly elevated lower limbs, cover with a blanket, and 2 ml of a 10% solution of caffeine-sodium benzoate is injected subcutaneously. For infectious collapse, this therapy is sometimes sufficient; for orthostatic collapse, it is always effective, but if blood pressure does not tend to increase, it is necessary, as with collapses of other origins, to carry out etiological and more comprehensive pathogenetic therapy. Etiological treatment involves stopping hemorrhagic collapse, removing toxic substances from the body and specific antidote therapy for poisoning, thrombolytic therapy for acute myocardial infarction and pulmonary embolism, stopping paroxysms or other cardiac arrhythmias, etc.

Pathogenetic therapy includes intravenous administration of blood for hemorrhagic collapse, plasma and blood-substituting fluids for blood thickening in patients with toxic, infectious and any hypovolemic collapse, administration hypertonic solution sodium chloride for collapse against the background of indomitable diarrhea, as well as in patients with adrenal insufficiency, along with the administration of adrenal hormones. If it is necessary to urgently increase blood pressure, norepinephrine or angiotensin is administered intravenously; injections of mezaton and fethanol give a slower but also longer-lasting effect. In all cases, oxygen therapy is indicated.

In medicine collapse om (from the Latin collapse - fallen) characterizes the patient’s condition with a sharp drop in blood pressure and vascular tone, as a result of which the blood supply to vital organs deteriorates. In astronomy there is a term “gravitational collapse", which implies hydrodynamic compression of a massive body under the influence of its own gravity, which leads to a strong decrease in its size. Under "transport" collapse om" is understood traffic jam, in which any violation of the movement of vehicles leads to a complete blocking of vehicles. On public transport - when one vehicle is fully loaded, the number of waiting passengers is close to the critical point. Economic collapse- this is an imbalance between supply and demand for services and goods, i.e. a sharp decline in the economic condition of the state, which appears in the decline of the production economy, bankruptcy and disruption of established production relations. There is a concept “ collapse wave function,” which means an instantaneous change in the description of the quantum state of an object.

In other words, the wave function characterizes the probability of searching for a particle at any point or period of time, but when trying to find this particle, it ends up at one specific point, which is called collapse om.Geometric collapse om is a change in the orientation of an object in space, fundamentally changing its geometric property. For example, under collapse ohm rectangularity is understood as an instant loss of this property. The popular word “ collapse” did not leave computer game developers indifferent. So, in the game Deus Ex collapse This is the name of an event taking place in the 21st century, when a crisis of power has matured in society with the very rapid development of science, the creation of revolutionary nanotechnologies and intelligent cyber systems. In 2009, the film “Collapse” by the American director K. Smith was released on television. The film is based on a television interview with Michael Rupert, the author of acclaimed books and articles and an accused conspiracy theorist.

Collapse

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

Collapse is usually accompanied by impaired blood supply, hypoxia of all organs and tissues, decreased metabolism, and inhibition of vital functions of the body.

Causes

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

Symptoms

The clinical picture of collapse depends on its cause, but the main manifestations are similar to collapse of different origins. There is a sudden progressive weakness, chilliness, dizziness, tinnitus, tachycardia (rapid pulse), blurred vision, and sometimes a feeling of fear. The skin is pale, the face becomes sallow in color, covered with sticky cold sweat; with cardiogenic collapse, cyanosis (bluish color of the skin) is often noted. Body temperature decreases, breathing becomes shallow and rapid. Blood pressure decreases: systolic - to 80-60, diastolic - to 40 mm Hg. Art. and below. As the collapse deepens, consciousness is disrupted, heart rhythm disturbances often occur, reflexes disappear, and the pupils dilate.

Cardiogenic collapse, as a rule, is combined with cardiac arrhythmia, signs of pulmonary edema (breathing difficulties, cough with copious foamy, sometimes pink-tinged, sputum).

Orthostatic collapse occurs when there is a sudden change in body position from horizontal to vertical and quickly stops after transferring the patient to a lying position.

Infectious collapse, as a rule, develops as a result of a critical decrease in body temperature. Skin moisture and severe muscle weakness are noted.

Toxic collapse is often combined with vomiting, nausea, diarrhea, and signs of acute renal failure (edema, difficulty urinating).

Diagnostics

The diagnosis is made based on the clinical picture. Studying hematocrit and blood pressure over time gives an idea of the severity and nature of the collapse.

Types of disease

Cardiogenic collapse - as a result of decreased cardiac output;
Hypovolemic collapse - as a result of a decrease in circulating blood volume;
Vasodilatory collapse - as a result of vasodilation.

Patient Actions

If a collapse occurs, you should immediately contact the ambulance service.

Treatment of collapse

Treatment measures are carried out intensively and urgently. In all cases, a patient with collapse is placed in a horizontal position with legs raised and covered with a blanket. A 10% solution of caffeine sodium benzoate is administered subcutaneously. Needs to be eliminated possible reason collapse: removal of toxic substances from the body and administration of an antidote for poisoning, stopping bleeding, thrombolytic therapy. In case of thromboembolism of the pulmonary arteries, acute myocardial infarction, paroxysm is stopped with medication atrial fibrillation and other heart rhythm disturbances.

Pathogenetic therapy is also carried out, which includes intravenous administration of saline solutions and blood substitutes for blood loss or blood thickening in patients with hypovolemic collapse, administration of a hypertonic sodium chloride solution for collapse against the background of uncontrollable vomiting and diarrhea. If it is necessary to urgently increase blood pressure, norepinephrine, angiotensin, and mesaton are administered. In all cases, oxygen therapy is indicated.

Complications of collapse

The main complication of collapse is loss of consciousness varying degrees. Mild fainting is accompanied by nausea, weakness, and pale skin. Deep fainting may be accompanied by convulsions, increased sweating, and involuntary urination. Fainting can also result in injury from a fall. Sometimes collapse leads to the development of a stroke (a disorder cerebral circulation). Various types of brain damage are possible.

Repeated episodes of collapse lead to severe brain hypoxia, worsening concomitant neurological pathology, and the development of dementia.

Prevention

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

Collapse: what is it?

Collapse is an acute vascular insufficiency, which is characterized by a sharp drop in arterial and venous pressure caused by a decrease in the mass circulating in the blood circulatory system, a drop in vascular tone or a reduction in cardiac output.

As a result, the metabolic process slows down, hypoxia of organs and tissues begins, and the most important functions of the body are inhibited.

Collapse is a complication of pathological conditions or serious illnesses.

Causes

There are two main causes:

Sudden massive blood loss leads to a decrease in the volume of circulation, to its inconsistency with the throughput capabilities of the vascular bed;
Due to exposure to toxic and pathogenic substances the walls of blood vessels and veins lose their elasticity, and the overall tone of the entire circulatory system decreases.

Steadily growing manifestation acute failure vascular system leads to a decrease in the volume of circulating blood, acute hypoxia occurs, caused by a decrease in the mass of oxygen transported to organs and tissues.

This in turn leads to a further drop in vascular tone, which provokes a decrease in blood pressure. Thus, the condition progresses like an avalanche.

Reasons for triggering pathogenetic mechanisms in different types collapse are different. The main ones:

internal and external bleeding;
general toxicity of the body;
sudden change in body position;
reducing the mass fraction of oxygen in the inhaled air;
acute pancreatitis.

Symptoms

The word collapse comes from the Latin "colabor", which means "falling". The meaning of the word accurately reflects the essence of the phenomenon - a drop in blood pressure and the fall of the person himself during collapse.

Basic Clinical signs collapses of various origins are basically similar:

Prolonged forms can lead to loss of consciousness, dilated pupils, and loss of basic reflexes. Failure to provide timely medical care can lead to serious consequences or death.

Kinds

Despite the fact that in medicine there is a classification of types of collapse according to the pathogenetic principle, the most common classification is based on etiology, distinguishing the following types:

infectious - toxic, caused by the presence of bacteria in infectious diseases, which leads to disruption of the heart and blood vessels;
toxic– the result of general intoxication of the body;
hypoxemic, which occurs when there is a lack of oxygen or under conditions of high atmospheric pressure;
pancreatic caused by trauma to the pancreas;
burn occurring after deep burns of the skin;
hyperthermic, occurring after severe overheating, sunstroke;

dehydration caused by loss of fluid in large volumes;
hemorrhagic, caused by massive bleeding, has recently been considered as a deep shock;
cardiogenic associated with pathology of the heart muscle;
plasmorrhagic, arising due to plasma loss during severe forms diarrhea, multiple burns;
orthostatic, which occurs when the body is brought into a vertical position;
enterogenous(fainting) that occurs after eating in patients with gastrectomy.

Separately, it should be noted that hemorrhagic collapse can occur both from external bleeding and from invisible internal: ulcerative colitis, stomach ulcer, spleen damage.

With cardiogenic collapse, stroke volume decreases due to myocardial infarction or angina pectoris. There is a high risk of developing arterial thromboembolism.

Orthostatic collapse also occurs when standing in an upright position for a long time, when the blood is redistributed, the venous part increases and the flow to the heart decreases.

Collapse due to poisoning is also possible medicines: sympatholytics, neuroleeptics, adrenergic blockers.

Orthostatic collapse often occurs in healthy people, in particular in children and adolescents.

Toxic collapse can be caused professional activity associated with toxic substances: cyanides, amino compounds, carbohydrate oxide.

Collapse in children is observed more often than in adults and occurs in a more complex form. may develop against the background intestinal infections, flu, pneumonia, with anaphylactic shock, adrenal dysfunction. The immediate cause may be fear, injury and blood loss.

First aid

At the first sign of collapse, you should immediately call an ambulance. Qualified doctor will determine the severity of the patient,, if possible, establish the cause of the collapsive state and prescribe primary treatment.

Providing first aid will help alleviate the patient’s condition, and possibly save his life.

Necessary actions:

place the patient on a hard surface;
raise your legs with a pillow;
throw back your head, ensure free breathing;
unbutton the collar of the shirt, free it from everything that constrains it (belt, strap);
open the windows to provide fresh air;
bring it to your nose ammonia, or massage the earlobes, dimple of the upper lip, temples;
stop bleeding if possible.

Prohibited actions:

give drugs with a pronounced vasodilator effect (nosh-pa, valocordin, glycerin);
hit the cheeks, trying to bring him to his senses.

Treatment

Non-inpatient treatment is indicated for orthostatic, infectious and other types of collapse, which are caused by acute vascular insufficiency. In case of hemorrhagic collapse caused by bleeding, urgent hospitalization is necessary.

Treatment of collapse has several directions:

Etiological therapy designed to eliminate the causes that caused the collapsive state. Stopping bleeding, general detoxification of the body, eliminating hypoxia, administering adrenaline, antidote therapy, and stabilizing the heart will help stop further deterioration of the patient’s condition.
Methods of pathogenetic therapy will allow you to return the body to its usual working rhythm as quickly as possible. Among the main methods, it is necessary to highlight the following: increasing arterial and venous pressure, stimulating respiration, activating blood circulation, administering blood substitutes and plasma, blood transfusion, and activating the central nervous system.
Oxygen therapy used for carbon monoxide poisoning accompanied by acute respiratory failure. Operational implementation therapeutic activities allows you to restore the most important functions of the body and return the patient to normal life.

Collapse is a pathology caused by acute vascular insufficiency. Different kinds collapse have a similar clinical picture and require urgent and qualified treatment, sometimes surgical intervention.

A life-threatening condition in which blood pressure drops and blood supply to vital organs deteriorates is called collapse. This condition is manifested by the appearance of severe weakness and pallor in a person, cooling of the extremities and sharpening of facial features.

Collapse also means one of the forms of acute vascular insufficiency, in which there is a sharp drop in vascular tone or a rapid decrease in circulating blood volume, leading to:

Inhibition of vital functions of the body;
Reduced venous flow to the heart;
A drop in venous and blood pressure;
Brain hypoxia.

It is important to correctly determine the cause of the condition and know how to provide first aid in case of collapse, as this can help save a person’s life before being transported to medical institution.

Causes of collapse

Possible causes of collapse may be acute infections, which include meningoencephalitis, abdominal and typhus, pneumonia, etc. The condition also occurs against the background acute blood loss, for diseases of the nervous and endocrine systems, exogenous intoxications resulting from poisoning with organophosphorus compounds or carbon monoxide.

In medical practice, many cases have been recorded in which collapse occurred as a result of orthostatic redistribution of blood resulting from an overdose of drugs such as antihypertensive drugs, ganglion blockers, insulin, etc.

Collapse can develop as a result of complications of low cardiac output syndrome, which occurs during acute myocardial infarction with tachycardia, deep bradycardia and dysfunction of the sinus node.

Collapse of the cardiovascular system can be caused by:

Puberty in girls;
A sharp change in body position in a bedridden patient;
High ambient temperature;
Severe electric shock;
Dehydration of the body;
A strong dose of ionizing radiation.

The causes of collapse are also spinal and epidural anesthesia, acute diseases abdominal organs.

Signs of collapse

The patient suddenly develops a feeling of general weakness, chilliness, dizziness, chills, unquenchable thirst, and a decrease in body temperature. Signs of collapse are manifestations such as:

Sharpness of facial features;
Cooling of extremities;
Paleness of the skin and mucous membranes (sometimes with a cyatonic tint);
The whole body, or just the forehead and temples, is covered with cold sweat;
Weakness of pulse;
Decreased blood pressure.

When examining a patient, it is usually revealed that his heart is not dilated with dull, sometimes arrhythmic, tones, breathing is rapid and shallow, and diuresis is reduced. A blood test reveals that its volume is reduced, the hematocrit is increased, and metabolic acidosis is decompensated.

The patient has a desire to lie down or sit with his head low, he does not experience suffocation despite shortness of breath, his consciousness is preserved or darkened, this state is characterized by complete indifference to what is happening around him.

Signs of collapse are also a sluggish reaction of the pupils to light, convulsions and tremors of the fingers.

Types of collapse

In medicine, there are conventionally three types of collapse:

Hypovolemic;
Cardiogenic;
Vasodilatory.

The occurrence of hypovolemic collapse is caused by dehydration of the body, severe blood loss or plasma loss, due to which the volume of blood in the vessels sharply decreases.

Cardiogenic collapse occurs against the background of:

Heart failure;
Acute cardiac dysfunction;
A sharp decrease in cardiac output.

Vasolidation collapse is characteristic of severe infectious and toxic conditions, deep hypoxia, hyperthermia, hypocapnia, endocrinopathy, and develops with improper use of medications and with an excess of kinins, histamine and adenosine in the blood, leading to general peripheral vascular resistance.

Collapse: first aid and treatment

Depending on the cause of the condition, it is necessary to provide first aid to the patient in the event of collapse in a short time. If the condition is caused by bleeding, it is necessary to stop it; poisoning by toxic substances, remove them from the body using specific antidotes.

Then the patient needs to be taken to a medical facility, where he will be prescribed adequate treatment for collapse - a transfusion of blood substitutes will be carried out using saline solutions, hemodez, polyglucin and reopolyglucin, if necessary and strictly as prescribed, blood components can be used.

Then, when treating collapse, the patient is given a bolus intravenous injection of 60-90 mg of Prednisolone; if the effect of its use is insufficient, the following is added:

10% caffeine solution – 1-2 ml;
1% Mezaton solution – 1-2 ml;
0.2% solution of Norepinephrine – 1 ml;
Cordiamine – 1-2 ml;
10% solution of sulfocamphocaine – 2 ml.

For metabolic acidosis, the patient is given intravenous injection of either 8.4% (50-100 ml) or 4.5% (100-200 ml) sodium bicarbonate solution. If the collapse is caused by low cardiac output syndrome caused by arrhythmia, antiarrhythmic drugs are usually prescribed, diluted 25, 100 or 200 mg of dopamine in an isotonic sodium chloride solution or 5% glucose solution is administered intravenously, and emergency cardiac pacing is also provided.

Collapse is a condition in which the blood supply to internal organs deteriorates and blood pressure drops, which threatens a person’s life. When developing a condition, it is most important to determine what caused its appearance, since subsequent treatment of collapse should be aimed at eliminating the cause. Further, depending on the indications and type of collapse, the doctor prescribes adequate drug treatment, may prescribe blood substitute transfusions and apply cardiac pacing.

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