Collapse heart disease. Collapse as a pathological state of the body

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 sudden death vary, but most of them 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 system. However, at 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 inefficiency resuscitation); 2) a pronounced sharp decrease cardiac output, which is observed when there is a mechanical obstruction to blood circulation [massive pulmonary thromboembolism and cardiac tamponade are two examples of this form; 3) acute sudden ventricular, pumping failure, which may occur due to acute myocardial infarction, "non-arrhythmic cardiac death", with or without ventricular rupture or critical aortic stenosis; 4) activation of vasodepressor reflexes, which can lead to an unexpected decrease blood pressure and decrease in heart rate and that is observed in various situations, including pulmonary embolism, 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 appears that the majority of patients with ischemic disease of the heart, it is precisely the acute obstruction of the lumen of the coronary vessel that is the starting point for sudden death. In other cases, sudden death may be the result of a functional electrophysiological instability that is diagnosed by a provocative invasive electrophysiological study and may persist for a long time or indefinitely after myocardial infarction. In those who die as a result of sudden death younger than 45 years, platelet thrombi are often found in the coronary microvasculature. Approximately 60% of patients who died from myocardial infarction died before admission to the hospital. Indeed, in 25% of patients with coronary heart disease, death acts as the first manifestation of this disease. Based on the experience of the activities of the emergency departments, it could be assumed that the incidence of sudden death could be significantly reduced by using preventive measures carried out primarily in populations with a particularly high risk, if it were shown that such interventions are effective, have low toxicity and do not cause great inconvenience to patients. However, sudden death may be one of the manifestations of coronary heart disease, and effective prevention sudden death requires, among other things, the prevention of atherosclerosis. The risk of sudden death, which is a manifestation of a previous myocardial infarction, is increased in patients with severe left ventricular dysfunction, complex ectopic ventricular activity, especially when these factors are combined.

Factors related to increased risk sudden death

When recording an electrocardiogram within 24 hours during normal daily activities, supraventricular premature 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 ectopic ventricular beats high degrees(repeating 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 of the cardiac cycle are especially often combined with malignant ventricular arrhythmias. High-frequency, low-amplitude potentials arising during registration of the final part of the complex QRS and segmentST,which can be identified using the frequency analysis of the signal-averaged electrocardiogram (ECG), also allow the identification of patients with a high risk of sudden death.

Premature ventricular contractions can be a trigger factor for fibrillation, especially against the background of myocardial ischemia. On the other hand, they may be manifestations of the most common fundamental electrophysiological disorders that predispose to both ventricular premature contractions and ventricular fibrillation, or may be a completely independent phenomenon associated with electrophysiological mechanisms other than those that cause fibrillation. Their clinical significance varies from patient to patient. Ambulatory electrocardiographic monitoring has shown that an increase in the frequency and complexity ventricular arrhythmias within 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 sudden deaths. 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 spicy emotional stress may 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 recurrences, possibly reflecting the electrical instability of the myocardium that led to the initial episode, as well as a relatively high mortality in the subsequent 2 years, reaching 50%. Clearly, these patients can only be saved if there is a responsive cardiac service capable of providing vigorous diagnosis and treatment using pharmacological preparations, if surgery is needed, implantable defibrillators or programmable pacing devices. Pharmacological prophylaxis is likely to improve survival. The second, smaller group includes patients who, after successful resuscitation, show signs of acute myocardial infarction. These patients are characterized by prodromal symptoms (retrosternal pain, dyspnea, syncope) and a significantly lower rate of relapses and deaths during the first two years (15%). Survival in this subgroup is the same as in patients after resuscitation for ventricular fibrillation complicating acute myocardial infarction in the coronary care unit. The predisposition to ventricular fibrillation at the time of the development of an acute infarction persists in them only for a short time, in contrast to patients in whom fibrillation occurs without an acute infarction, after which the risk of relapse remains elevated for a long time. However, in some patients who have had a myocardial infarction, the risk of sudden death remains quite high. The factors that determine this risk are the vastness of the infarct zone, severe ventricular dysfunction, persistent complex ectopic ventricular activity, prolongation of the interval Q-Tafter acute attack, loss after recovery of the ability to respond normally to physical activity by increasing blood pressure, maintaining long time positive results of myocardial scintigrams.

Other causes of sudden death

Sudden cardiovascular collapse can result from a variety of disorders other than coronary atherosclerosis. 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 embolism lung vessels leads to circulatory collapse and death within minutes in about 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 (very rare cause sudden death) Tumors of the heart

Rupture and dissection of aortic aneurysm Pulmonary thromboembolism

Cerebrovascular complications, in particular bleeding

In recent years, a number of conditions have been identified that are less common causes sudden death. Sudden cardiac death may be associated with modified diet 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. General Risk sudden death in persons with similar disorders is approximately 1% per year. congenital deafness, history of syncope, belonging to female gender, confirmed tachycardia by type torsades de pointes (see below) or ventricular fibrillation are independent risk factors for sudden cardiac death. Although the removal of the left stellate 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, followed by inhibition of downstream pacemakers, or sick sinus syndrome, usually accompanied by dysfunction of the conduction system, can also lead to asystole. Occasionally, fibroids and inflammation of the sinoatrial or atrioventricular nodes can lead to sudden death in individuals without preexisting evidence of heart disease. Sudden ruptures of the papillary muscle, interventricular septum or free wall that develop during the first few days after an acute myocardial infarction can sometimes cause sudden death. Sudden cardiovascular collapse is also a serious and often fatal complication of cerebrovascular disorders; in particular subarachnoid hemorrhage, a sudden change in intracranial pressure or damage to the brain stem. It can also occur with asphyxia. Digitalis poisoning can cause life-threatening cardiac arrhythmias leading to sudden cardiovascular collapse, which, if left untreated, ends in death. Paradoxically, 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 recycling in early dates after ischemia, is focal repetitive excitation. Anoxia shortens the duration of the action potential. In accordance with this, during electrical systole, repolarization of cells located in the ischemic zone can occur earlier than cells of the adjacent non-ischemic tissue. The emerging difference between the prevailing transmembrane potentials can cause unstable depolarization of neighboring cells, and therefore contribute to the appearance of rhythm disturbances that depend on recirculation. Concomitant pharmacological and metabolic factors may also predispose to recirculation. For example, quinidine can inhibit the rate of excitation disproportionately to the increase in refractoriness, thereby facilitating the onset of recirculation-dependent arrhythmias soon after ischemia has developed.

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

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

Asystole and/or profound bradycardia are among the less common electrophysiological mechanisms underlying sudden death due to coronary atherosclerosis. They may be manifestations of complete occlusion of the right coronary artery and, as a rule, indicate the failure of resuscitation. Asystole and bradycardia are often the result of sinus node failure, atrioventricular block, and the inability of accessory pacemakers to function effectively. Sudden death in individuals with these disorders is usually more a consequence of diffuse 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 ejection fraction less than 40% or overt heart failure; 4) in patients with an extended interval Q-Tand frequent premature contractions, especially when a history of syncope is indicated. Although the identification of patients at high risk of sudden death is extremely important, the choice of effective prophylactic remains an equally difficult task, and none of them has proven unequivocally effective in reducing risk. Induction of arrhythmias by stimulation of the ventricles using a catheter with electrodes inserted into the heart cavity and the choice pharmacological agents to prevent such provocation of arrhythmias is probably an effective method for predicting the possibility of preventing or reversing recurrent malignant arrhythmias, in particular ventricular tachycardia, using specific drugs in patients who have experienced prolonged ventricular tachycardia or fibrillation. In addition, this method allows the identification of refractory patients. conventional methods treatment, and to facilitate the selection of candidates for vigorous methods such as administration of drugs under investigation, implantation of automated defibrillators, or surgical intervention.

Medical treatment

Treatment with antiarrhythmic drugs at doses sufficient to maintain therapeutic blood levels has been considered effective for recurrent ventricular tachycardia and/or fibrillation in sudden death survivors if during acute trials this drug could stop or reduce the severity of premature ventricular contractions of high degrees, early or repetitive 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 effectiveness 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 necessary and in the absence of gastrointestinal disorders or electrocardiographic signs of toxicity, the dosage of quinidine can be increased to 3 g / day. Amiodarone (a US trial drug at 5mg/kg IV over 5-15 minutes or 300-800mg per day orally with or without loading dose of 1200-2000mg per day divided over 1 or 4 weeks) has a strong antifibrillatory effect, but a very slow onset of the maximum effect, which manifests itself only after a few days or weeks of continuous administration. Toxicity can occur in 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 overt protective action still not installed. The incidence of sudden death was significantly reduced compared with the overall reduction in mortality over several years of follow-up for a group of people who had myocardial infarction who were treated R-blockers were started a few days after the infarction.

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

Surgical approaches

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

public efforts.The experience gained in Seattle, Washington shows that in order to deal effectively with the problem of sudden cardiovascular collapse and death on a broad community basis, it is necessary to create a system that can provide a quick response in such situations. Important elements of this system are: the presence of a single telephone for the whole city, by which this system can be “launched”; the presence of well-trained paramedical personnel, similar to firefighters, who can respond to calls; a short average response time (less than 4 min), and a large number of people 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 the increase in the proportion of patients discharged from the hospital in good condition who underwent cardiac arrest at the prehospital stage: 30-35% compared with 10-15% in the absence of such a program. Long-term survival, within 2 years, can also be increased from 50 to 70% or more. Proponents of a random resuscitation program are currently exploring the use of portable home defibrillators designed for safe use by the general population with only the bare minimum of necessary skills.

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

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

Sudden death can be avoided even if cardiovascular collapse has already developed. If a patient under constant medical supervision, 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. Instant swipe to the precordium 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 strongly applied to the body and the shock is applied immediately, without waiting for the increase in the energy demand of defibrillation, which occurs with an increase in the duration of ventricular fibrillation. The use of devices with automatic selection of shock voltage depending on tissue resistance is especially promising, since it can minimize the dangers associated with the application of unreasonably large shocks and avoid inefficiently small shocks in patients with higher than expected resistance. If these simple attempts are unsuccessful, then external cardiac massage should be started and full cardiopulmonary resuscitation should be performed with fast 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 acid-base balance, which often requires intravenous administration 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 arterial blood pH;

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

Heart massage

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

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

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

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

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

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

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

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

8. Efficient ventilation must be maintained throughout this time and carried out at a frequency of 12 breaths per minute under the control of the tension of gases in the arterial blood. If these indicators are clearly pathological, 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; onset of chest compression final stage inhalation; 2) reduction of intra-thoracic pressure during relaxation by creating a negative airway pressure in this phase; and 3) reduction of intra-thoracic collapse of the aorta and arterial system during chest compression by increasing intravascular volume and using anti-shock inflatable trousers. One way to put these concepts into practice is called cough CPR. This method consists in the fact that the patient, who is conscious despite ventricular fibrillation, performs repeated, rhythmic cough movements for at least a short time, which lead to a phase increase in intrathoracic pressure, simulating changes caused by ordinary chest compressions. Given the effect of CPR on blood flow, through the veins of the upper limb or central veins, but not through the femoral, should be administered necessary drugs(preferably bolus rather than infusion). Isotonic drugs can be administered after dissolution in saline as an injection into the endotracheal tube, since absorption is provided by the bronchial circulation.

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

The therapeutic approach outlined above is based on following provisions: 1) irreversible brain damage often occurs within a few (approximately 4) minutes after the development of circulatory collapse; 2) the probability of restoring an effective heart rhythm and successfully resuscitating the patient decreases rapidly over time; 3) the survival rate of patients with primary ventricular fibrillation can reach 80-90%, as with cardiac catheterization or exercise testing, if treatment is started decisively and quickly; 4) the survival of patients in a general hospital is much lower, approximately 20%, which depends in part on the presence of concomitant or underlying diseases; 5) out-of-hospital survival tends to zero, in the absence of a specially created emergency service (possibly due to the inevitable delays in the start necessary treatment, lack of proper equipment and trained personnel); 6) external cardiac massage can provide only minimal cardiac output. With the development of ventricular fibrillation, as much as possible early holding electrical defibrillation increases the chance of success. Thus, with the development of circulatory collapse as the primary manifestation of the 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, occult bleeding. However, these complications can be minimized with the correct implementation of resuscitation, timely recognition and adequate further tactics. It is always difficult to make the decision to terminate an ineffective resuscitation. In general, if an effective heart rate is not restored and if the patient's pupils remain fixed and dilated despite external cardiac massage for 30 minutes or more, a successful resuscitation outcome is difficult to expect.

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

Collapse is called acute heart failure, in which the vascular tone drops sharply, which results in a drop in arterial and venous pressure and loss of consciousness. Patients develop cyanosis, the face and mucous membranes turn pale. There may be fainting.

Reasons for the development of collapse

Infectious diseases (most often it is pneumonia, however, collapse can also provoke meningoencephalitis, as well as typhoid fever and some others infectious diseases);

sudden loss of blood;

Diseases of the nervous system;

Work disruptions endocrine system;

poisoning;

Damage to the heart muscle;

Reaction to medicines (for example, with an overdose of insulin);

Anesthesia (especially with spinal anesthesia);

Use a large number alcoholic beverages;

Peritonitis.

In addition, collapse can develop during an attack of myocardial infarction.

Diagnostics

A differential diagnosis with heart failure, fainting and shock is mandatory (some experts, especially representatives of European medicine, consider shock and collapse to be the same pathological condition).

collapse symptoms

Sudden unexplained feeling great weakness and fatigue;

Dizziness (some patients cannot stand on their feet);

Chills;

Decrease in temperature (extremities become cold);

Paleness of the skin and mucous membranes;

Loss of appetite

sweating ( cold sweat on the forehead);

Decreased blood pressure;

Seizures.

It is recommended to consult a doctor if at least one of the above occurs listed symptoms. Remember, collapse is extremely serious condition which requires emergency medical care. You are unlikely to succeed in lying down and recovering on your own, and failure to provide assistance in the first hours of the collapse can cause tragic consequences for the patient.

Collapse treatment

First of all, it is necessary to deal with the treatment of the condition that caused the collapse. Also, in parallel with this, it is necessary to carry out symptomatic therapy.

The patient must be warmed and laid in a horizontal position, slightly raising his legs (to ensure normal arterial and venous pressure). Hemodez is dripped or saline solution. In some cases (with medical indications) The patient may be given a blood transfusion.

For stimulation, prednisolone (intravenous, bolus), norepinephrine is put. Oxygen therapy indicated. After the blood volume has been restored, vasopressor drugs (caffeine, cordiamine, etc.) are given.

But in general, therapy will directly depend on the cause of the collapse (as I wrote above).

Forecast

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 one of the forms cardiovascular insufficiency, which 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".

At the core pathogenetic mechanisms disease lies:

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

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, as it often leads to death. 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;
• insulin overdose long-acting, ganglioblockers, agents for lowering blood pressure;
• peritonitis and acute infectious complications;
• acute disorder contractility myocardial infarction, arrhythmias, dysfunction of the AV node.

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

Table: Types of collapse

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, healthy people All unpleasant symptoms pass 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 the first first aid 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 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 the nose and upper lip. These activities will help improve peripheral circulation.
4. If the cause of the collapse was bleeding from 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 evaluation vital functions and determining a preliminary diagnosis, the introduction of a 10% solution of caffeine-sodium benzoate in a standard dosage is shown. For 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. At 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, intravenous drip administration of adrenaline and norepinephrine (for a rapid increase in blood pressure), infusion of blood and its components, plasma, physiological saline(to increase BCC), oxygen therapy.

Description:

Collapse is an acute vascular insufficiency characterized by a sharp decrease in blood pressure due to a drop in vascular tone, a decrease in cardiac output, or as a result of an acute decrease in circulating blood volume. The collapse is accompanied by hypoxia of all tissues and organs, a decrease in metabolism, and inhibition of vital body functions.

Symptoms:

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

Blood pressure is reduced: systolic - up to 80 - 60, diastolic - up to 40 mm Hg. Art. and lower (in persons with prior hypertension, a collapse pattern may be observed at higher blood pressure values). In almost all cases, there is a thickening of the blood, oliguria, rapidly increasing. With the deepening of the collapse, the patient's consciousness is darkened, heart rhythm disturbances often join (or progress); pupils dilate, reflexes disappear. If not carried out effective treatment, death occurs.

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

Infectious collapse most often develops during critical decline body temperature; at the same time, moisture of the skin, as a rule, of the whole body (wet linen), pronounced muscle hypotension, and a soft pulse are noted.

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

The diagnosis of collapse is based on a characteristic clinical picture. Studies of blood pressure in dynamics, and, if possible, also the volume of circulating blood, hematocrit give an idea of ​​its nature and severity. Differential Diagnosis with disorders of consciousness, they are carried out with fainting, which is characterized by a short loss of consciousness. It should be noted that collapse can be integral part pictures of shock, in which deeper hemodynamic disturbances occur.

Causes of occurrence:

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

Treatment:

For treatment appoint:

Therapeutic measures should be carried out urgently and intensively. Patients with a collapse that occurred in an out-of-hospital setting should be urgently taken to a hospital, accompanied by an ambulance team (if it has not provided full effective help on the spot) or paramedics who are proficient in resuscitation techniques.

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

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

Many disorders of the cardiovascular system occur 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, as it often leads to death. 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

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 has developed signs of acute insufficiency of the 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 of serious complications. There, depending on the causes of the disease, intravenous drip of adrenaline and norepinephrine (to quickly increase blood pressure), infusion of blood and its components, plasma, saline (to increase BCC), oxygen therapy are carried out.