Causes of collapse during surgery. Vascular collapse: symptoms and emergency care for a life-threatening condition

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 the central nervous systems e. However, when timely treatment In some forms of cardiovascular collapse, an increase in life expectancy can be achieved without subsequent functional damage.

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 the ineffectiveness of resuscitation measures); 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 that is observed in various situations, including pulmonary thromboembolism, syndrome hypersensitivity carotid sinus 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 seems that in the majority of patients with coronary heart disease, 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 departments of emergency cardiology, it could be assumed that the frequency of sudden death could be significantly reduced with the help of preventive measures, carried out primarily in populations with a particularly high risk, if such measures were shown to be effective, have low toxicity. and do not cause much 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 associated with an increased risk of sudden death

When recording an electrocardiogram within 24 hours during normal daily activities, supraventricular premature beats can be detected in most Americans over 50 years old, and ventricular premature beats in almost two-thirds. Simple ventricular premature beats in people with a healthy heart are not associated with an increased risk of sudden death, but conduction disturbances and bigeminy or high-grade ectopic ventricular beats (repetitive forms or complexes R -to-T) are an indicator high risk, especially among patients who have had a myocardial infarction during the previous year. In patients with acute myocardial infarction, ventricular ectopic contractions that occur in the late period cardiac cycle, 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 you to identify 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 beats and ventricular fibrillation, or may be a completely independent phenomenon associated with electrophysiological mechanisms other than those that cause fibrillation. Their clinical significance varies among different 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 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 coronary heart disease, not necessarily accompanied by morphological signs of acute infarction, hypertension or diabetes mellitus, 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 syndrome may be isolated from 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 recurrence, 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 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 positive results of myocardial scintigrams for a long time.

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 violation of the rhythm or pumping function 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

Mitral valve prolapse (an extremely rare cause of 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. hallmarks these cases are interval lengthening 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, 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 node has a transient preventive action, 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 with subsequent 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 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, but antiarrhythmic drugs may 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 resulting 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, profound bradycardia caused by reduced automatism of the sinus node or atrioventricular block 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 automaticity disorders 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 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 myocardial damage than the actual AV blockade.

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 an ejection fraction of 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 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. It also identifies patients who are refractory to conventional therapies and facilitates the selection of candidates for vigorous treatments such as the administration of investigational drugs, implantation of automated defibrillators, or surgery.

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 persons who had suffered sudden death, if during acute trials this drug could stop or reduce the severity of high-grade premature ventricular contractions, early or recurring forms. In sudden death survivors with 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 of 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 needed or not gastrointestinal disorders or electrocardiographic signs of toxicity, the dosage of quinidine may 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. Although the antifibrillatory efficacy of amiodarone is generally recognized, its use 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 high variability of spontaneous disturbances heart rate, recorded during Holter monitoring, which should be interpreted individually for each patient, suppression of ectopic activity (at least .80% within 24 hours) must be achieved before one can talk about the pharmacological effectiveness 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 parts of the United States, the time from the onset of symptoms of an acute heart attack to hospital admission is on average 3 to 5 hours. Patient denial of the possibility of developing a serious disease and the indecision of both the doctor and the patient delay care the most.

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 discomfort during discharges of the device and the likelihood of non-physiological discharges are serious disadvantages of 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. The availability of special transport, mobile coronary care units equipped with the necessary equipment and staffed by trained personnel capable of providing adequate care in the corresponding emergency cardiological situation, can reduce 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 an increase in the proportion of patients discharged from the hospital in good condition who underwent cardiac arrest for prehospital stage: 30-35% compared to 10-15% without such a program. Long-term survival, within 2 years, can also be increased from 50 to 70% or more. Proponents of a casual resuscitation program are currently investigating 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. Physical 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, has developed a sudden collapse caused by a heart rhythm disorder, 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) lack of pulse in the peripheral arteries; 3) absence of heart sounds. Because the outdoor massage heart provides only a minimum cardiac output (no more than 30% of lower bound normal value), the true recovery of the effective rhythm should be 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. Immediate strong blow to the precordial region chest(shock defibrillation) can sometimes be effective. It should be attempted, since it only takes seconds to do so. In rare cases, 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 applied strongly to the body and the shock is applied immediately, without waiting for an 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 ineffectively 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 an effective heart rate is restored, then 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. to restore perfusion important 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. If there is no pulse on the carotid arteries for 5 seconds, 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 femoral or carotid arteries, but 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, you should quickly perform tracheal intubation, interrupting external chest compressions for no more than 20 seconds.

Each external compression of the chest inevitably limits the venous return by some amount. Thus, the optimally achievable heart index during external massage can reach only 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.

One gets the impression that the classical method of conducting cardiopulmonary resuscitation(CPR) in the near future will undergo certain changes aimed at: 1) an increase in intrathoracic pressure during chest compressions, for which positive pressure will be used in respiratory tract; simultaneous ventilation and external massage; pulling of the anterior abdominal wall; the beginning of chest compression at the final stage of inspiration; 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 coughing 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, the necessary drugs should be administered through the veins of the upper limb or central veins, but not through the femoral one (preferably by bolus rather than infusion). Isotonic preparations 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 stopped 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 terminated 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 the general hospital is significantly 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 proper 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

Many disruptions of cardio-vascular system arise suddenly, against the background of relative well-being. One such acute life-threatening condition is vascular collapse. We will talk about the mechanisms of development, symptoms and emergency care for this pathology in our review and video in this article.

The essence of the problem

Vascular collapse is a form of cardiovascular insufficiency that develops against the background of a sudden decrease in the tone of arteries and veins. Translated from the Latin word collapsus, the term is translated as "fallen".

The basis of the pathogenetic mechanisms of the disease is:

• decrease in BCC;
• decreased blood flow to the right side of the heart;
• a sharp drop in pressure;
• acute ischemia of organs and tissues;
• inhibition of all vital functions of the body.

The development of collapse is always sudden, rapid. Sometimes only a few minutes pass from the onset of pathology to the development of irreversible ischemic changes. This syndrome is very dangerous because it often leads to lethal outcome. However, thanks to timely first aid and effective drug therapy, the patient can be saved in most cases.

Important! The terms "collapse" and "shock" should not be confused. Unlike the first, shock occurs as a response of the body to superstrong irritation (pain, temperature, etc.) and is accompanied by more severe manifestations.

Causes and mechanism of development

There are many factors that influence the development of pathology. Among them:

• massive blood loss;
• acute infectious diseases (pneumonia, meningitis, encephalitis, typhoid fever);
• some diseases of the endocrine, nervous systems (for example, syringomyelia);
• the effect on the body of toxic and poisonous substances (organophosphorus compounds, CO - carbon monoxide);
• side effects of epidural anesthesia;
• overdose of long-acting insulin, ganglionic blockers, agents for lowering blood pressure;
• peritonitis and acute infectious complications;
• acute violation of myocardial contractility in myocardial infarction, arrhythmias, dysfunction of the AV node.

Depending on the cause and mechanism of development, four types are distinguished.

Table: Types of collapse

Type of collapse	Description
	Caused by decreased cardiac output
	Provoked by a sharp decrease in circulating blood volume
	The cause of the acute condition is a sudden decrease
	Violation of the redistribution of blood with a sharp change in body position in space

Note! Orthostatic collapse at least once developed in most people on the planet. For example, many are familiar with mild dizziness, which develops with a sharp rise from bed in the morning. However, in healthy people, all unpleasant symptoms disappear within 1-3 minutes.

Clinical symptoms

A person develops:

• a sharp rapid deterioration in well-being;
• general weakness;
• severe headache;
• darkening in the eyes;
• noise, buzzing in the ears;
• marble pallor of the skin;
• respiratory disorders;
• sometimes loss of consciousness.

Principles of diagnosis and treatment

Collapse is a dangerous and highly unpredictable state. Sometimes, with a sharp decrease in blood pressure, the count goes on for minutes, and the cost of delay may be too high. If a person develops symptoms acute insufficiency circulatory system, it is important to call an ambulance as soon as possible.

In addition, everyone should know the algorithm for providing first aid to patients with collapse. To do this, WHO specialists have developed a simple and understandable instruction.

Step one. Assessment of vital signs

To confirm the diagnosis, it is enough:

1. Conduct a visual inspection. The patient's skin is pale, with a marble tint. She is often covered in clammy sweat.
2. Feel the pulse on the peripheral artery. However, it is weak, filiform or not defined at all. Another sign of acute vascular insufficiency is tachycardia - an increase in the number of heartbeats.
3. Measure blood pressure. The collapse is characterized by hypotension - a sharp deviation of blood pressure from the norm (120/80 mm Hg. Art.) to the lower side.

Step two. First aid

While the ambulance is on its way, take urgent measures aimed at stabilizing the patient's condition and preventing acute complications:

1. Lay the victim on their back on a flat, hard surface. Raise your legs relative to the entire body by 30-40 cm. This will improve the blood supply to the heart and brain.
2. Ensure sufficient oxygen supply to the room. Remove clothing that restricts breathing, open a window. At the same time, the patient should not freeze: if necessary, wrap him with a blanket or blanket.
3. Let the victim sniff a cotton swab dipped in ammonia (ammonia solution). If there is no medicine at hand, rub his temples, earlobes, and also the hole located between his nose and upper lip. These activities will help improve peripheral circulation.
4. If the cause of the collapse was bleeding from an open wound, try to stop the bleeding by applying a tourniquet, finger pressure.

Important! If a person is unconscious, it is impossible to bring him to his senses with blows to the cheeks and other painful stimuli. Until he comes to his senses, do not give him food or drink. In addition, if the possibility of vascular collapse is not excluded, drugs that reduce blood pressure should not be given - Corvalol, Validol, Valocordin, No-shpa, Nitroglycerin, Isoket, etc.

Step three. First aid

Upon arrival of the ambulance, briefly describe the situation to the doctors, mentioning what assistance was provided. Now the victim must be examined by a doctor. After assessing vital functions and determining a preliminary diagnosis, the introduction of a 10% solution of caffeine-sodium benzoate in a standard dosage is indicated. With an infectious or orthostatic collapse, this is enough for a stable long-term effect.

In the future, urgent measures are aimed at eliminating the causes that caused vascular insufficiency:

1. With the hemorrhagic nature of the collapse, it is necessary to stop bleeding;
2. In case of poisoning and intoxication, the introduction of a specific antidote (if any) and detoxification measures are required.
3. In acute diseases (myocardial infarction, peritonitis, pulmonary embolism, etc.), life-threatening conditions are corrected.

If there are indications, the patient is hospitalized in a specialized hospital for further treatment and prevention. serious complications. There, depending on the causes of the disease, an intravenous drip of adrenaline and noradrenaline is carried out (for rapid rise blood pressure), infusion of blood and its components, plasma, physiological saline(to increase BCC), oxygen therapy.

Collapse(lat. collapsus weakened, fallen) - acute vascular insufficiency, characterized primarily by a fall vascular tone and 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 serious illnesses 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 reduced content oxygen 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, high ambient temperature (overheating, thermal shock). Collapse observed in some acute diseases internal organs such as acute pancreatitis. Some allergic reactions immediate type, for example anaphylactic shock, flow from vascular disorders, typical for collapse. Infectious To. develops as a complication of meningoencephalitis, typhoid and typhus, acute dysentery, acute pneumonia, botulism, anthrax, viral hepatitis, toxic flu and others 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, is 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 certain diseases of the endocrine and nervous systems (syringomyelia, encephalitis, tumors of the glands internal secretion, nervous system, etc.), postoperative period, with rapid evacuation of ascitic fluid or as a complication of spinal or epidural anesthesia. Orthostatic collapse sometimes occurs when neuroleptics, ganglion 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 in acute massive blood loss (vascular damage, internal bleeding), due to a rapid decrease in the volume of circulating blood. Such a 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 insufficiency that develops in these conditions is considered by some authors not as K. but as the so-called low ejection 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). Arising in response to this reflex spasm small vessels and increased heart rate due to increased release into the blood catecholamines may not be sufficient to maintain a normal level of blood pressure. A decrease in the volume of circulating blood is accompanied by a decrease in the return of blood to the heart through the veins of the systemic 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 vascular wall, increase 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. Under conditions of increased capillary permeability, this contributes to the transfer of water and electrolytes from the blood into the intercellular spaces. are violated rheological properties, hypercoagulation of blood 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, rarely slow, weak filling, often irregular, on radial arteries sometimes difficult or absent. BP is low, sometimes systolic BP drops to 70-60 mmHg st. and even lower, but initial period K. in persons with previous arterial hypertension BP may remain 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 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 due to a decrease in venous inflow and the violation of central hemodynamics associated with this, and sometimes infectious and 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 children early age collapse is more severe) and emotional features sick. A relatively mild degree To. is sometimes called a collaptoid state.

Depending on the underlying disease that caused the collapse. the clinical picture may acquire 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 cupping orthostatic collapse. especially in adolescents and young adults, it is usually enough to provide peace in horizontal position the patient's body.

Infectious To. develops more often during a critical decrease in body temperature; this happens at different times, for example, when 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, 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, total plasma protein content increase. 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. The differential diagnosis mainly concerns the causes that caused K., which determines the nature of care, as well as indications for hospitalization and the choice of 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. emergency hospitalization of the patient in the nearest hospital, it is desirable of a surgical profile is necessary. An important section of the course of any collapse is etiological therapy; stop bleeding, removal 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 agents that affect the 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. not associated with ulcerative bleeding, glucocorticoids are used, briefly in sufficient doses (hydrocortisone is 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, the active treatment of acute disorders of heart rhythm and conduction, become essential.

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 increased pressure (see. 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 of respiratory failure, auxiliary artificial ventilation of the lungs is used.

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 full recovery hemodynamics. For severe illnesses 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 special role plays 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 medicines 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 occur with deeper tissue hypoxia, accompanied by loss of consciousness and convulsions. Since the alkaline reserve in tissues is limited in young children, a violation of 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 under 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 of the skin, increasing tachycardia.

Therapy for orthostatic collapse. as a rule, does not require medication; it is enough to lay the patient horizontally without a pillow, raise the legs above the level of the heart, unbutton the clothes. Favorable effect is provided by fresh air, inhalation of vapors of ammonia. 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 in severe 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 a complete picture of the infectious collapse, calling this condition 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 consider them only as different periods of the same pathological process, that is, whether to consider "shock" and "collapse" as synonyms. 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, an unambiguous generally accepted classification of collapse forms has 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– impact electric current, large doses of radiation, high ambient temperature (during overheating, heat stroke), 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 can occur in conditions of low oxygen concentration in the inhaled air, especially in combination with low barometric pressure. The immediate cause of 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 frequent 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 profuse 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 in stroke volume (myocardial infarction, cardiac arrhythmias, acute myocarditis, hemopericardium or pericarditis with rapid accumulation of effusion in the pericardial cavity), as well as pulmonary embolism. 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.

With 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. mild degree collapse is sometimes called the 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:

• depletion of energy resources of the 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 acute decrease in blood pressure, life threatening a condition characterized by a drop in blood pressure and low blood supply 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 sharp decline 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 such a pathological condition are acute diseases of the heart and blood vessels, for example, such as myocarditis, myocardial infarction, and many others. Also, the list of causes can include acute blood loss and plasma loss, severe intoxication (with acute infectious diseases, poisoning ). 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 to collapses various kinds 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.

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

The latter is accompanied by an extension 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, it is necessary immediate appeal to the doctor and mandatory examination and treatment.

Collapse- one of the forms of acute vascular insufficiency, which is characterized by a drop in vascular tone and a decrease in the volume (mass) of circulating blood (BCC), accompanied by a sharp drop in blood pressure and leading to a decline in all life processes.

Such a “simple”, according to many physicians, formulation of the concept of “collapse” can easily be found on the pages of medical profile websites. It's great, really! Of course, everyone understands everything! Since it is clear to us (practicing physicians) that you do not understand anything, we propose to put this “case”, as they say, on the shelves.

If we translate this phrase into a commonly understood human language, it will immediately become clear that collapse is a condition in which the vessels of the human body cannot provide an influx the right amount blood to all organs. The most important thing you need to understand is that the brain and heart do not receive oxygenated blood. And, as it is known from the school bench, the brain of many is “the head of everything”, well, the heart is also a very, very necessary organ.

A natural question arises: “why does a collapse occur?”

Causes of collapse:

sudden massive blood loss. As a rule, this is associated with a rupture of internal organs or serious external injuries to the body.

sudden violation of the rhythm of the heart or a violation of its contractility.

Both reasons lead to the fact that the heart does not push the right amount of blood into the vessels. An example of such diseases is: myocardial infarction, blockage of large vessels of the lungs by a thrombus or air plug (pulmonary embolism), all kinds of sudden cardiac arrhythmias.

a sharp expansion of peripheral vessels. Such a condition can occur against the background of high temperature and humidity of the environment, during illness with various acute infectious diseases (pneumonia, sepsis, typhoid fever, etc.), the strongest allergic reaction, drug overdose.

adolescents in puberty may experience a collapse due to a strong emotional experience, both negative and positive.

a sharp change in body position in debilitated patients.

Regardless of the cause that caused the collapse, the manifestations of the signs of this condition in people of any age are almost always similar.

Clinical manifestations of collapse:

deterioration in well-being occurs suddenly.

there are complaints of headache, tinnitus, weakness, discomfort in the region of the heart, darkening in the eyes.

consciousness is preserved, but some lethargy is possible, in the absence of help, loss of consciousness is possible.

blood pressure drops sharply and by significant numbers.

the skin becomes wet, cold, pale.

facial features are sharpened, the look becomes dull.

breathing becomes shallow, frequent.

the pulse is palpable.

Emergency first aid for collapse:

Whatever the reason was the impetus for the development of the collaptoid state, a doctor's examination is needed in any case. The patient himself may object to the examination, but you must remember that the collapse is the result of a serious problem in the body. A momentary improvement in the patient's well-being is not at all a guarantee of well-being in the future. Calling a doctor is a prerequisite for full assistance. In the meantime, you are waiting for the ambulance team to do the following:

lay the patient on a hard surface. A flat and hard surface is the best platform for resuscitation should the need arise.

raise your legs (put a chair or things under them). This is done to increase blood flow to the brain and heart.

provide fresh air. Simply open a window or balcony door.

loosen tight clothing. To improve overall blood flow, you need to unfasten the belt, collar and cuffs of clothing.

give a sniff of cotton wool with ammonia. The absence of ammonia can be replaced by stimulation (light massage) nerve endings earlobes, temples, dimples of the upper lip.

if the collapse is caused by blood loss from an external wound, try to stop the bleeding.

Remember!

In no case do not give the patient nitroglycerin, validol, no-shpu, valocordin, corvalol. These drugs dilate the vessels, which in this case are already not in good shape.

It is impossible to give medicines and drink to the victim through the mouth if he is unconscious!

It is impossible to bring the patient to life with blows on the cheeks!

Indications for hospitalization:

This issue is considered in each case by physicians.

Addition:

There are differences between the concepts of "collapse" and "shock". We will separately consider briefly this issue, because often people confuse these concepts. Perhaps this is not of practical importance for the provision of first aid, but this information will not hurt the overall development.

Shock is, like collapse, a general reaction of the body to a powerful damaging factor. This factor can be all kinds of injuries, poisoning, death of a large section of the heart muscle, loss of most of the blood, severe pain. The state of shock begins to develop from the phase of excitation of the patient, and then abruptly gives way to a pronounced depression of consciousness and motor activity of a person. Blood pressure during shock decreases to such an extent that the excretory function of the kidneys stops. On my own without drug treatment blood pressure does not rise.

The human body can be called a well-coordinated mechanism. That is why the slightest failures in its work lead to the appearance of diseases, each of which has its own symptoms and characteristics.

Knowledge of the clinical picture of a certain disease, the causes of its occurrence, as well as the ability to provide first aid in case of collapse to oneself or others in difficult situation increase the chances of a successful recovery, and in some cases, save lives.

Collapse is a very serious pathological condition that requires immediate medical attention. A sick person should be given first aid in case of collapse (first aid). In addition, you need to call an ambulance.

What is collapse?

This pathological condition is an acute vascular insufficiency. The victim has a sharp decrease in venous and arterial pressure, which is due to a decrease in the volume of blood circulating in the body, a deterioration in vascular tone, or a decrease in cardiac output. As a result, metabolism significantly slows down, hypoxia of organs and tissues occurs, and vital functions are inhibited.

As a rule, collapse is a complication of serious diseases or pathological conditions.

Causes, symptoms, types and first aid for fainting and collapse

In medicine, there are two main reasons that provoke a threat: the first is a sharp profuse blood loss, which leads to a decrease in the amount of blood in the body; the second is the impact of pathogenic and toxic substances, when the tone of the walls of blood vessels worsens.

Progressive acute vascular insufficiency provokes a decrease in the volume of blood circulating in the body, which, in turn, leads to acute hypoxia (oxygen starvation). Then the vascular tone drops, which affects blood pressure(it goes down). That is, the pathological condition progresses like an avalanche.

It is worth noting that there are several types of collapse, and they differ in their triggering mechanisms. We list the main ones: general intoxication; internal/external bleeding; a sharp change in body position; acute pancreatitis; lack of oxygen in the inhaled air.

Symptoms

From Latin, collapse can be translated as "fall". The meaning of the word directly reflects the essence of the problem - both arterial / venous pressure falls, and the person himself may faint. Despite the difference in the mechanisms of occurrence, the signs of pathology are almost the same in all cases.

What are the symptoms of a critical condition:

1. Dizziness;
2. Weak and at the same time frequent pulse;
3. Consciousness is clear, but the person is indifferent to the environment;
4. Mucous membranes acquire a bluish tint;
5. Reduced skin elasticity;
6. A cold and clammy sweat is released;
7. The skin turns pale;
8. There is noise in the ears, vision weakens;
9. thirst, dry mouth;
10. Decrease in body temperature;
11. Arrhythmia;
12. Hypotension;
13. Breathing is rapid, superficial;
14. Nausea, which may lead to vomiting;
15. involuntary urination;
16. With a protracted threat, loss of consciousness occurs, pupils dilate, and basic reflexes are lost.

From timely delivery medical care a person's life may depend. At a wrong time Taken measures lead to death. Some people confuse collapse with shock. They differ significantly: in the first case, the state of a person does not change, in the second - first there is excitement, and then a sharp decline.

Types and appearance algorithm

Doctors classify this critical condition according to the pathogenetic principle, but more common is the division into types according to the etiological factor, respectively, they distinguish:

1. Infectious-toxic - provoke bacteria, occurs with infectious diseases;
2. Toxic - a consequence of the general intoxication of the body. It can be triggered by the conditions of professional activity, when a person is exposed to toxic substances, for example, carbohydrate oxide, cyanides, amino compounds;
3. Hypoxemic - appears at high atmospheric pressure or lack of oxygen in the air;
4. Pancreatic - provokes trauma to the pancreas;
5. Burn - due to deep thermal damage to the skin;
6. Hyperthermic - after severe overheating or sunstroke;
7. Dehydration - loss of fluid in a large volume (dehydration);
8. Hemorrhagic - massive bleeding. Now it is also called deep shock. This type can be triggered by both external and internal blood loss, for example, with damage to the spleen, stomach ulcer or ulcerative colitis;
9. Cardiogenic - provoke pathologies of the myocardium, for example, with angina pectoris or myocardial infarction. There is a risk of arterial thromboembolism;
10. Plasmoraggic - loss of plasma in severe diarrhea or multiple burns;
11. Orthostatic - occurs when the body position changes from horizontal to vertical. A similar situation can also occur with a long stay in a vertical position, when the venous current increases and the flow to the heart decreases. Often this phenomenon occurs in healthy people, especially in children and adolescents;
12. Enterogenic, or syncope, often occurs after a meal in people with gastrectomy.

A critical condition can occur when poisoning with medicines: neuroleptics, sympatholytics, adrenoblockers. In children, this is more difficult and can even occur against the background of influenza, intestinal infection, pneumonia, anaphylactic shock, adrenal dysfunction. Even fear and, of course, blood loss and trauma can provoke it.

Collapse emergency

Seeing that a person has an attack, you need to immediately call an ambulance and at the same time help him. Doctors will be able to determine the severity of a person’s condition, if possible, establish the cause and prescribe primary therapy.

Providing first aid can improve the condition of the victim and even in some cases save his life.

What is the correct sequence of first aid for collapse:

1. The patient must be laid on a hard surface;
2. He needs to raise his legs, placing something under them;
3. Then they throw back their head to make it easier for him to breathe;
4. It is necessary to unbutton the collar of the shirt, freeing the person to the maximum from the fettering items of clothing, for example, a belt, a belt;
5. It is necessary to open windows / doors, etc., to provide the room with oxygen;
6. A handkerchief / cotton swab dipped in ammonia should be brought to the person’s nose. You can also massage the whiskey, dimple upper lip, earlobes;
7. If possible, stop bleeding.

In no case do not give the victim drugs that have a pronounced vasodilating effect. For example, these include Glycerin, Valocordin, No-shpa. It is also strictly not recommended to be on the cheeks, shake the head, bringing the person to life.

Collapse: medical emergency care, an algorithm of actions

Non-stationary therapy is prescribed for infectious, orthostatic and other types caused by acute vascular insufficiency. But in the presence of bleeding, which is accompanied by hemorrhagic collapse, emergency hospitalization is necessary.

The sequence of therapy is carried out in several directions at once.