Sudden coronary death definition. Sudden coronary death: causes, how to avoid. Healthy and balanced diet

Sudden cessation of blood circulation (sudden death) - primary circulatory arrest in a healthy person or a patient in a satisfactory condition, in the first 6 (24) hours of the disease due to acute ischemia or myocardial infarction, pulmonary embolism, infections (meningitis), etc. The risk increases sharply against the background of alcohol intoxication.
Symptoms. Sudden loss of consciousness with or without tonic-clonic convulsions, absence of carotid pulse, respiratory arrest or sudden onset of agonal breathing, pupillary dilatation maximizing at approximately 105 s.
In 80% of cases, flutter and ventricular fibrillation (VT, VF) are observed: convulsions, wheezing breathing, asymmetry and cyanosis of the face occur more often. Harbingers of VT and VF can be frequent (> 6 per minute), group, polytopic, allorhythmic, early (where the ratio Q-R’/QT<0,85) желудочковые экстрасистолы; левожелудочковые, альтернирующие, двунаправленные, torsades de pointes желудочковые тахикардии; фибрилляция и трепетание предсердий на фоне синдрома WPW с ЧСС>240 per minute and functional blockade of the legs.

Rice. 1. Continuous electrical stimulation (?) of parasystole (4), R inhibitory stimulator (arrow indicates natural contractions of the ventricles)

Rice. 2. Ventricular flutter (frequency 240 per minute). Ventricular fibrillation, turning into asystole; P waves are recorded

ECG: QRS, ST, T are not differentiated, there is no isoline. In VT, the recorded complexes are rhythmic, sinusoidal in nature, while in VF they are of different amplitudes, arrhythmic. The frequency of complexes is 150-600 per minute.
Electromechanical dissociation (may be caused by a sharp increase in pre- or afterload, observed with hypovolemia, cardiac tamponade, tension pneumothorax, metabolic disorders): the presence of QRS on the ECG and symptoms of clinical death. With asystole (short attacks of asystole against the background of sick sinus syndrome, the appearance of bifascicular blockades, especially bilateral ones, sharply increase its risk): absence of QRS (it is necessary to make sure that the electrocardiograph is working). With asystole, the face is usually pale, convulsions are not characteristic (Fig. 2).
Urgent care. Indirect cardiac massage (frequency of compressions 80-100 per minute) and mechanical ventilation in a ratio of 5:1 (one resuscitator -15:2). If the mechanism of death is not established: EIT 3 J/kg, then take an ECG. With TG and VZh - EIT 200 J, 2-300 J, then 360 J (3-4-5 7 / kg) after 15 compressions. Adrenaline (1 mg / amp.) After three EITs (with the amplitude of VF waves< <10 мм перед ЭИТ 1 мг адреналина, 1 мг атропина, 30 мг преднизолона в/в) - 7,5-15 мкг/кг (05-1 мг) каждые 5 мин в/в. Дополнительно вводится 1 мг/кг лидокаина в/в, повторять по 05 мг/кг каждые 3-5 мин до общей дозы 3 мг/кг, или 5 мг/кг орнида в/в (препараты сочетаются), повторять по 10 мг/кг каждые 5 мин до общей дозы 30-35 мг/кг.
After the introduction of drugs - EIT after 1-2 minutes of massage. After 3-4 EIT - tracheal intubation (endotracheal administration of adrenaline, atropine, lidocaine in a double dose per 10 ml of saline). Calcium chloride (10% 10 ml, g / amp.) 02 g IV (max 2-4 mg / kg at 10-minute intervals) with an overdose of verapamil or other calcium blockers, potassium preparations If a defibrillator is not available, lidocaine and ornid applied independently; in their absence, novocainamide is used - 250-500 mg IV or 100-200 mg IV, propranolol - 5-10 mg IV or IV. With ineffective ventilation in / in 1 ml / kg (1 meq / kg) of trisamine (in the absence of trisamine - 1 meq of base which contains 2 ml of 4.2% sodium bicarbonate solution) once or 0.5 ml / kg with repetition every 10 min. If, after EIT, atrial fibrillation or flutter is recorded with a hemodynamically ineffective rhythm or ventricular tachycardia, repeat EIT.
After restoration of a hemodynamically significant rhythm - infusion of 1 g / h of potassium chloride, 2 g / h of magnesium sulfate (10 ml of panangin in a stream for 5-10 minutes), 30-50 mcg / kg / min of lidocaine, which is approximately 2-4 mg / min (if lidocaine was not administered - first 15 mg/kg IV bolus), 50-100 mg/kg sodium hydroxybutyrate (20% 10 ml, 2 g/amp.) or 10 mg to 03 mg/kg sibazon (10 mg / amp.) in / in the jet.
With asystole and electromechanical dissociation and the impossibility of pacing - intravenous bolus 05-1 mg of adrenaline every 3-5 minutes [for asystole, it can be replaced with orciprenaline in / in 05 mg every 3-5 minutes or intravenous infusion of isadrin (isolroterenol) 1-4 mcg / min, with electromechanical dissociation - mezaton in / in 5-10 mg every 3-5 minutes]. After a single injection of adrenaline, pulmonary intubation. Atropine - 1 mg IV every 5 minutes up to 0.04 mg / kg (more effective in reflex cardiac arrest). If resuscitation is ineffective - the introduction of 1 ml / kg of trisamine, repeated every 10 minutes at 05 ml / kg. Rhythmic blows to the middle part of the sternum with a frequency of 60 per minute can be used.
If more than 5 minutes have passed since the moment of circulatory arrest, then alternative methods of adrenaline administration can be recommended in all cases of sudden clinical death: intermittent doses - 2-5 mg every 3-5 minutes, increasing - 1-3-5 mg every 3 minutes, high doses - 0.1 mg / kg, but not more than 8 mg, every 3-5 minutes.
Intracardiac administration of drugs - only in the absence of the effect of intravenous administration
Hospitalization: as fast as possible to the intensive care unit, bypassing the emergency room, on a stretcher with the provision of intravenous administration of drugs, oxygen therapy and resuscitation in the car.

1. Mechanisms of sudden death:

1.1. ventricular fibrillation (in 80% of cases), asystole or electromechanical dissociation. Ventricular fibrillation develops gradually, the symptoms appear sequentially: the disappearance of the pulse in the carotid arteries, loss of consciousness, a single tonic contraction of the skeletal muscles, respiratory failure and cessation. The response to timely cardiopulmonary resuscitation is positive, to the termination of cardiopulmonary resuscitation - fast negative;

1.2. electromechanical dissociation in massive pulmonary embolism develops suddenly (often at the time of physical exertion) and is manifested by cessation of breathing, lack of consciousness and pulse on the carotid arteries, severe cyanosis of the upper half of the body, and swelling of the cervical veins. With myocardial rupture and cardiac tamponade, it develops suddenly, usually against the background of a protracted, recurrent anginal attack. There are no signs of the effectiveness of cardiopulmonary resuscitation. Hypostatic spots quickly appear in the underlying parts of the body.

In favor of circulatory arrest, not associated with ventricular fibrillation, data on drowning, a foreign body in the airways, and hanging speak.

2.1. Statement of the state of clinical death.

2.2. Precordial stroke.

2.3. Ensure airway patency:

Safar's reception (extension of the head, removal of the lower jaw);

clean the oral cavity and oropharynx from foreign bodies, if necessary - the Heimlich maneuver;

tracheal intubation;

Cricothyreotomy for permanent blockade of the upper respiratory tract.

mouth to mouth;

Ambu bag;

Ambu bag through the endotracheal tube with an air-oxygen mixture.

the patient lies on a hard flat surface;

compression of the middle third of the sternum;

the resuscitator's arms are straight, positioned vertically;

help massage with your body weight;

frequency of compressions in adults 80-100 per minute;

stop the massage only for inhalation;

slightly delay the massage movements in the position of maximum compression.

5. The ratio between IVL and VMS:

one rescuer - 2:15 (2 breaths - 15 compressions);

two or more resuscitators 1:4 (1 breath - 4 compressions).

6. Provide permanent venous access.

7. The introduction of epinephrine 1 ml of 0.18% solution in / in or endotracheally for 10 ml of 0.9% sodium chloride solution.

8. ECG recording and/or cardiac monitoring.

9. Differentiated therapy.

immediate electrical impulse therapy (hereinafter referred to as EIT) (according to paragraph 16 of chapter 3);

if immediate EIT is not possible, apply a precordial strike and start CPR, ensure the possibility of EIT as soon as possible;

if EIT is ineffective or asystole, inject 1 ml of a 0.18% solution of epinephrine in 10 ml of a 0.9% solution of sodium chloride into the main vein (if the veins were catheterized before resuscitation) or into a peripheral vein (through a long catheter reaching a large vein) , or intracardiac followed by EIT. The introduction of epinephrine can be repeated every 3-5 minutes;

if VF persists or recurs after the above measures, intravenous lidocaine (hereinafter referred to as IV) slowly 120 mg (6 ml of a 2% solution) followed by drip administration (200-400 mg per 200 ml of 0.9% sodium chloride solution - 30- 40 drops per minute) or amiodarone according to the scheme: slowly at a dose of 300 mg (5 mg / kg) (5% -6 ml per 5% glucose) for 20 minutes, then IV drip at a rate of up to 1000-1200 mg / day;

in the absence of effect - EIT again after the introduction of lidocaine 0.5-0.75 mg / kg (2% - 2-3 ml) intravenously slowly, or against the background of the introduction of magnesium sulfate 2 g (20% solution 10 ml) intravenously in slowly;

in the absence of effect - EIT again after the introduction of lidocaine 0.5-0.75 mg / kg (2% - 2-3 ml) intravenously slowly;

with acidosis or prolonged resuscitation (more than 8-9 minutes) - 8.4% solution of sodium bicarbonate IV, 20 ml;

Interrupt CPR for no more than 10 seconds to administer drugs or defibrillate.

Alternate drug administration and defibrillation.

exclude or treat the cause (hypovolemia, hypoxia, cardiac tamponade, tension pneumothorax, drug overdose, acidosis, hypothermia, PE), diagnosis and immediate action - according to the relevant chapters;

in case of an overdose of calcium antagonists, with hyperkalemia, hypocalcemia, inject a 10% solution of calcium chloride 10 ml IV (calcium preparations are contraindicated in case of poisoning with cardiac glycosides).

9.3. Asystole:

continue CPR;

inject 1 ml of a 0.18% solution of epinephrine again intravenously after 3-4 minutes;

inject atropine 1 mg (0.1% solution - 1 ml) intravenously per 10 ml of 0.9% sodium chloride solution after 3-5 minutes (until the effect or a total dose of 0.04 mg / kg is obtained);

inject sodium bicarbonate 8.4% solution of 20 ml intravenously with acidosis or prolonged resuscitation (more than 8-9 minutes);

inject a 10% solution of calcium chloride 10 ml IV in case of hyperkalemia, hypocalcemia, overdose of calcium blockers;

conduct external or internal pacing.

Continue CPR measures for at least 30 minutes, constantly assessing the patient's condition (cardiomonitoring, pupil size, pulsation of large arteries, chest excursion).

Termination of resuscitation measures is carried out in the absence of signs of cardiac activity on the ECG, against the background of the use of all possible measures for at least 30 minutes in normothermic conditions.

Refusal of resuscitation measures is possible if at least 10 minutes have passed since the moment of circulatory arrest, with signs of biological death, in the terminal stage of long-term incurable diseases (documented in the outpatient card), diseases of the central nervous system (hereinafter referred to as the CNS) with damage to the intellect injury incompatible with life.

Transportation of the patient to the intensive care unit is carried out after the restoration of the efficiency of cardiac activity. The main criterion is a stable heart rate with sufficient frequency, accompanied by a pulse in the large arteries.

10. When restoring cardiac activity:

do not extubate the patient;

continuation of mechanical ventilation with a breathing apparatus with inadequate breathing;

maintaining adequate blood circulation - 200 mg of dopamine (5-10 mcg / kg / min) intravenously in 400 ml of 5% glucose solution, 0.9% sodium chloride solution;

to protect the cerebral cortex, for the purpose of sedation and relief of seizures - diazepam 5-10 mg (1-2 ml of a 0.5% solution) intramuscularly or intramuscularly (hereinafter referred to as intramuscular injection).

11. Features of CPR.

All drugs during cardiopulmonary resuscitation must be administered intravenously quickly. Following the administered drugs for their delivery to the central circulation, 20-30 ml of 0.9% sodium chloride solution should be administered.

In the absence of access to a vein, epinephrine, atropine, lidocaine (increasing the recommended dose by 1.5-3 times) is injected into the trachea (through an endotracheal tube or cricothyroid membrane) in 10 ml of 0.9% sodium chloride solution.

Antiarrhythmic drugs: lidocaine at the above dose or amiodarone at a dose of 300 mg (6 ml of a 5% solution) intravenously is recommended to be administered after 9-12 defibrillator discharges against the background of epinephrine administration.

Intracardiac injections (with a thin needle, with strict observance of the technique) are permissible only in exceptional cases, if it is impossible to use other routes of drug administration (contraindicated in children).

Sodium bicarbonate 1 mmol / kg body weight IV, then 0.5 mmol / kg every 5-10 minutes, apply with prolonged cardiopulmonary resuscitation (after 7-8 minutes after its start), with hyperkalemia, acidosis, overdose tricyclic antidepressants, hypoxic lactic acidosis (adequate mechanical ventilation is required).

Calcium preparations do not improve the prognosis and have a damaging effect on the myocardium, therefore, the use of calcium chloride (at a dose of 2-4 mg / kg intravenously) is limited to situations of well-established situations: hyperkalemia, hypocalcemia, intoxication with calcium channel blockers.

With asystole or electromechanical dissociation, treatment options are limited. After tracheal intubation and administration every 3 minutes of epinephrine 1.8 mg (0.18% solution - 1 ml) and atropine 1 mg (0.1% solution - 1 ml) IV per 10 ml of 0.9% sodium solution chloride (until the effect or a total dose of 0.04 mg / kg is obtained), if the cause cannot be eliminated, decide on the termination of resuscitation, taking into account the time elapsed from the onset of circulatory arrest (30 minutes).

- this is asystole or ventricular fibrillation, which arose against the background of the absence in the anamnesis of symptoms indicative of coronary pathology. The main manifestations include the absence of respiration, blood pressure, pulse on the main vessels, dilated pupils, lack of reaction to light and any kind of reflex activity, marbling of the skin. After 10-15 minutes, the appearance of a symptom of a cat's eye is noted. Pathology is diagnosed on the spot according to clinical signs and electrocardiography data. Specific treatment is cardiopulmonary resuscitation.

ICD-10

I46.1 Sudden cardiac death, as described

General information

Sudden coronary death accounts for 40% of all causes of death in people over 50 but under 75 years of age without diagnosed heart disease. There are about 38 cases of SCD per 100,000 people annually. With the timely start of resuscitation in the hospital, the survival rate is 18% and 11% with fibrillation and asystole, respectively. About 80% of all cases of coronary death occur in the form of ventricular fibrillation. More often, middle-aged men with nicotine addiction, alcoholism, and lipid metabolism disorders suffer. Due to physiological reasons, women are less prone to sudden death from cardiac causes.

The reasons

Risk factors for VCS do not differ from those for ischemic disease. Among the provocative effects include smoking, eating a large amount of fatty foods, arterial hypertension, insufficient intake of vitamins in the body. Non-modifiable factors - old age, male gender. Pathology can occur under the influence of external influences: excessive power loads, diving into ice water, insufficient oxygen concentration in the surrounding air, and acute psychological stress. The list of endogenous causes of cardiac arrest includes:

Atherosclerosis of the coronary arteries. Cardiosclerosis accounts for 35.6% of all SCD. Cardiac death occurs immediately or within an hour after the onset of specific symptoms of myocardial ischemia. Against the background of an atherosclerotic lesion, AMI is often formed, which provokes a sharp decrease in contractility, the development of a coronary syndrome, and flicker.
Conduction disorders. Sudden asystole is usually observed. CPR measures are ineffective. Pathology occurs with an organic lesion of the conduction system of the heart, in particular the sinatrial, atrioventricular node or large branches of the His bundle. As a percentage, conduction failures account for 23.3% of total cardiac deaths.
Cardiomyopathy. They are detected in 14.4% of cases. Cardiomyopathies are structural and functional changes in the coronary muscle that do not affect the coronary artery system. They are found in diabetes mellitus, thyrotoxicosis, chronic alcoholism. May have a primary nature (endomyocardial fibrosis, subaortic stenosis, arrhythmogenic pancreatic dysplasia).
Other states. The share in the overall structure of morbidity is 11.5%. These include congenital anomalies of the cardiac arteries, left ventricular aneurysm, and cases of SCD, the cause of which could not be determined. Cardiac death can occur with pulmonary embolism, which causes acute right ventricular failure, in 7.3% of cases accompanied by sudden cardiac arrest.

Pathogenesis

The pathogenesis directly depends on the causes that caused the disease. With atherosclerotic lesions of the coronary vessels, one of the arteries is completely occluded by a thrombus, the blood supply to the myocardium is disturbed, and a focus of necrosis is formed. The contractility of the muscle decreases, which leads to the onset of an acute coronary syndrome and the cessation of cardiac contractions. Conduction disorders provoke a sharp weakening of the myocardium. Ned residual contractility causes a decrease in cardiac output, stagnation of blood in the chambers of the heart, and the formation of blood clots.

In cardiomyopathies, the pathogenetic mechanism is based on a direct decrease in myocardial performance. In this case, the impulse propagates normally, but the heart, for one reason or another, reacts poorly to it. The further development of the pathology does not differ from the blockade of the conduction system. With PE, the flow of venous blood to the lungs is disrupted. There is an overload of the pancreas and other chambers, stagnation of blood is formed in the systemic circulation. A heart overflowing with blood in conditions of hypoxia is unable to continue working, it suddenly stops.

Classification

Systematization of SCD is possible due to the causes of the disease (AMI, blockade, arrhythmia), as well as the presence of previous signs. In the latter case, cardiac death is divided into asymptomatic (the clinic develops suddenly against the background of unchanged health) and having previous signs (short-term loss of consciousness, dizziness, chest pain an hour before the development of the main symptoms). The most important for resuscitation is the classification according to the type of cardiac dysfunction:

ventricular fibrillation. Occurs in the vast majority of cases. Requires chemical or electrical defibrillation. It is a chaotic erratic contraction of individual fibers of the ventricular myocardium, unable to provide blood flow. The condition is reversible, well stopped with the help of resuscitation.
Asystole. Complete cessation of heart contractions, accompanied by a cessation of bioelectric activity. More often it becomes a consequence of fibrillation, but it can develop primarily, without prior flicker. Occurs as a result of severe coronary pathology, resuscitation measures are ineffective.

Symptoms of sudden cardiac death

40-60 minutes before the development of a stop, the appearance of previous signs may occur, which include fainting lasting 30-60 seconds, severe dizziness, impaired coordination, a decrease or increase in blood pressure. Characterized by pain behind the sternum of a compressive nature. According to the patient, the heart seems to be clenched in a fist. Precursor symptoms are not always observed. Often the patient simply falls during the performance of any work or exercise. Sudden death in a dream without previous awakening is possible.

Cardiac arrest is characterized by loss of consciousness. The pulse is not determined both on the radial and on the main arteries. Residual breathing can persist for 1-2 minutes from the moment the pathology develops, but breaths do not provide the necessary oxygenation, since there is no blood circulation. On examination, the skin is pale, cyanotic. There is cyanosis of the lips, earlobes, nails. The pupils are dilated and do not react to light. There is no reaction to external stimuli. With tonometry of blood pressure, Korotkoff's tones are not auscultated.

Complications

Complications include a metabolic storm that occurs after successful resuscitation. Changes in pH due to prolonged hypoxia lead to disruption of the activity of receptors and hormonal systems. In the absence of the necessary correction, acute renal or multiple organ failure develops. The kidneys can also be affected by microthrombi, which are formed during the onset of DIC, myoglobin, the release of which occurs during degenerative processes in the striated muscles.

Poorly performed cardiopulmonary resuscitation causes decortication (brain death). In this case, the patient's body continues to function, but the cerebral cortex dies. Recovery of consciousness in such cases is impossible. A relatively mild variant of cerebral changes is posthypoxic encephalopathy. It is characterized by a sharp decrease in the mental abilities of the patient, a violation of social adaptation. Somatic manifestations are possible: paralysis, paresis, dysfunction of internal organs.

Diagnostics

Sudden cardiac death is diagnosed by a resuscitator or other specialist with a medical background. Trained representatives of emergency response services (rescuers, firefighters, policemen), as well as people who happened to be nearby and have the necessary knowledge, are able to determine circulatory arrest outside the hospital. Outside the hospital, the diagnosis is made solely on the basis of clinical signs. Additional techniques are used only in the ICU, where they require minimal time to apply. Diagnostic methods include:

hardware allowance. On the heart monitor, to which each patient of the intensive care unit is connected, large-wave or small-wave fibrillation is noted, ventricular complexes are absent. An isoline may be observed, but this rarely happens. Saturation indicators quickly decrease, blood pressure becomes undetectable. If the patient is on assisted ventilation, the ventilator signals that there are no spontaneous breath attempts.
Laboratory diagnostics. It is carried out simultaneously with measures to restore cardiac activity. Of great importance is a blood test for acid-base balance and electrolytes, in which there is a shift in pH to the acid side (a decrease in the pH value below 7.35). To exclude an acute infarction, a biochemical study may be required, in which increased activity of CPK, CPK MB, LDH is determined, and the concentration of troponin I increases.

Urgent care

Assistance to the victim is provided on the spot, transportation to the ICU is carried out after the restoration of the heart rhythm. Outside the hospital, resuscitation is carried out by the simplest basic techniques. In a hospital or ambulance setting, complex specialized electrical or chemical defibrillation techniques may be used. For revival, the following methods are used:

Basic CPR. It is necessary to lay the patient on a hard, flat surface, clear the airways, tilt the head back, and protrude the lower jaw. Pinch the victim's nose, put a tissue napkin over his mouth, clasp his lips with his lips and take a deep breath. Compression should be done with the weight of the whole body. The sternum should be pressed through by 4-5 centimeters. The ratio of compressions and breaths is 30:2 regardless of the number of rescuers. If the heart rate and spontaneous breathing are restored, you need to lay the patient on his side and wait for the doctor. Self-transportation is prohibited.
Specialized assistance. In the conditions of a medical institution, assistance is provided in a comprehensive manner. If ventricular fibrillation is detected on the ECG, defibrillation is performed with discharges of 200 and 360 J. It is possible to administer antiarrhythmics against the background of basic resuscitation. With asystole, adrenaline, atropine, sodium bicarbonate, calcium chloride are administered. The patient must be intubated and transferred to mechanical ventilation, if this has not been done before. Monitoring is shown to determine the effectiveness of medical actions.
Help after rhythm recovery. After the restoration of sinus rhythm, IVL is continued until consciousness is restored or longer if the situation requires it. According to the results of the analysis of acid-base balance, the electrolyte balance, pH is corrected. It requires round-the-clock monitoring of the patient's vital activity, assessment of the degree of damage to the central nervous system. Rehabilitation treatment is prescribed: antiplatelet agents, antioxidants, vascular drugs, dopamine for low blood pressure, soda for metabolic acidosis, nootropics.

Forecast and prevention

The prognosis for any type of SCD is unfavorable. Even with timely CPR, there is a high risk of ischemic changes in the tissues of the central nervous system, skeletal muscles, and internal organs. The probability of successful rhythm recovery is higher in ventricular fibrillation, complete asystole is less favorable prognostically. Prevention consists in the timely detection of heart disease, the exclusion of smoking and alcohol consumption, regular moderate aerobic training (running, walking, jumping rope). Excessive physical activity (weightlifting) is recommended to be abandoned.

Sudden coronary death is sudden, unexpected death due to the cessation of the functioning of the heart (sudden cardiac arrest). In the US, it is one of the leading causes of natural death, claiming about 325,000 adult lives each year and accounting for half of all deaths from cardiovascular disease.

Sudden coronary death occurs most frequently between the ages of 35 and 45 and affects men twice as often. It is rare in childhood and occurs in 1-2 out of 100,000 children each year.

Sudden cardiac arrest is not a heart attack (myocardial infarction) but can occur during a heart attack. A heart attack occurs when one or more of the arteries in the heart become blocked, preventing enough oxygenated blood from being delivered to the heart. If insufficient oxygen is supplied to the heart with blood, damage to the heart muscle occurs.

In contrast, sudden cardiac arrest occurs due to a malfunction of the electrical system of the heart, which suddenly begins to work irregularly. The heart begins to beat at a life-threatening rate. Fluttering or blinking of the ventricles (ventricular fibrillation) may occur, and the blood supply to the body stops. In the first minutes of the greatest importance is such a critical decrease in blood flow to the heart that the person loses consciousness. If medical attention is not provided immediately, death may occur.

The pathogenesis of sudden cardiac death

Sudden cardiac death occurs with a number of heart diseases, as well as with various rhythm disturbances. Heart rhythm disturbances can occur against the background of structural anomalies of the heart and coronary vessels or without these organic changes.

Approximately 20-30% of patients have bradyarrhythmia and episodes of asystole before the onset of sudden cardiac death. Bradyarrhythmia may appear due to myocardial ischemia and then it can become a provoking factor for the occurrence of ventricular tachycardia and ventricular fibrillation. On the other hand, the development of bradyarrhythmias may be mediated by pre-existing ventricular tachyarrhythmias.

Despite the fact that many patients have anatomical and functional disorders that can lead to sudden cardiac death, this condition is not recorded in all patients. The development of sudden cardiac death requires a combination of various factors, most often the following:

The development of severe regional ischemia.

The presence of left ventricular dysfunction, which is always an unfavorable factor in relation to the occurrence of sudden cardiac death.

The presence of other transient pathogenetic events: acidosis, hypoxemia, vascular wall tension, metabolic disorders.

Pathogenetic mechanisms of development of sudden cardiac death in IHD:

Reducing the ejection fraction of the left ventricle is less than 30-35%.

Left ventricular dysfunction is always an unfavorable predictor of sudden cardiac death. The assessment of the risk of arrhythmia after myocardial infarction and SCD is based on the determination of left ventricular function (LVEF).

LVEF less than 40%. The risk of SCD is 3-11%.

LVEF greater than 40%. The risk of SCD is 1-2%.

Ectopic focus of automatism in the ventricle (more than 10 ventricular extrasystoles per hour or unstable ventricular tachycardia).

Cardiac arrest resulting from ventricular arrhythmia can be caused by chronic or acute transient myocardial ischemia.

Spasm of the coronary arteries.

Spasm of the coronary arteries can lead to myocardial ischemia and worsen the results of reperfusion. The mechanism of this action can be mediated by the influence of the sympathetic nervous system, the activity of the vagus nerve, the state of the vascular wall, the processes of activation and aggregation of platelets.

Rhythm disturbances in patients with structural anomalies of the heart and blood vessels

In most cases, sudden cardiac death is recorded in patients with structural anomalies of the heart, which are the result of congenital pathology or may occur as a result of myocardial infarction.

Acute thrombosis of the coronary arteries can lead to both an episode of unstable angina and myocardial infarction, and sudden cardiac death.

In more than 80% of cases, sudden cardiac death occurs in patients with coronary artery disease. Hypertrophic and dilated cardiomyopathy, heart failure, and valvular disease (eg, aortic stenosis) increase the risk of sudden cardiac death. The most significant electrophysiological mechanisms of sudden cardiac death are tachyarrhythmias (ventricular tachycardia and ventricular fibrillation).

Treatment of tachyarrhythmias with an automated defibrillator or implantation of an cardioverter-defibrillator reduces the incidence of sudden cardiac death and mortality in patients who have experienced sudden cardiac death. The best prognosis after defibrillation in patients with ventricular tachycardias.

Rhythm disturbances in patients without structural anomalies of the heart and blood vessels

The causes of ventricular tachycardia and ventricular fibrillation at the molecular level can be the following disorders:

Neurohormonal disorders.

Violations of the transport of potassium, calcium, sodium ions.

Dysfunction of sodium channels.

Diagnosis Criteria

The diagnosis of clinical death is made on the basis of the following main diagnostic criteria: 1. lack of consciousness; 2. lack of breathing or sudden onset of agonal type breathing (noisy, rapid breathing); 3. absence of a pulse in the carotid arteries; 4. dilated pupils (if drugs were not taken, neuroleptanalgesia was not performed, anesthesia was not given, there is no hypoglycemia); 5. change in skin color, the appearance of a pale gray color of the skin of the face.

If the patient is under ECG monitoring, then at the time of clinical death, the following changes are recorded on the ECG:

Ventricular fibrillation is characterized by chaotic, irregular, sharply deformed waves of various heights, widths and shapes. These waves reflect excitations of individual muscle fibers of the ventricles. At the beginning of the wave, fibrillation is usually high-amplitude, occurring at a frequency of about 600 min-1. At this stage, the prognosis for defibrillation is more favorable compared to the prognosis at the next stage. Further, the flicker waves become low-amplitude with a wave frequency of up to 1000 and even more per 1 min. The duration of this stage is about 2-3 minutes, then the duration of flicker waves increases, their amplitude and frequency decrease (up to 300-400 min-1). At this stage, defibrillation is not always effective. It should be emphasized that the development of ventricular fibrillation is often preceded by episodes of paroxysmal ventricular tachycardia, sometimes bidirectional ventricular tachycardia (pirouette type). Often, before the development of ventricular fibrillation, frequent polytopic and early extrasystoles (type R to T) are recorded.

With ventricular flutter on the ECG, a curve is recorded that resembles a sinusoid with frequent rhythmic, rather large, wide and similar waves, reflecting the excitation of the ventricles. It is impossible to isolate the QRS complex, the ST interval, the T wave, there is no isoline. Most often, ventricular flutter turns into their flicker. The ECG picture of ventricular flutter is shown in fig. one.

Rice. one

With asystole of the heart, an isoline is recorded on the ECG, any waves or teeth are absent. With electromechanical dissociation of the heart, a rare sinus, nodal rhythm can be recorded on the ECG, which turns into a rhythm, followed by asystole. An example of an ECG during electromechanical dissociation of the heart is shown in fig. 2.

Rice. 2

Urgent care

In the event of sudden cardiac death, cardiopulmonary resuscitation is carried out - a set of measures aimed at restoring the vital activity of the body and removing it from a state bordering on biological death.

Cardiopulmonary resuscitation should begin before the patient enters the hospital. Cardiopulmonary resuscitation includes pre-hospital and hospital stages.

In order to provide assistance at the prehospital stage, it is necessary to conduct a diagnosis. Diagnostic measures must be taken within 15 seconds, otherwise it will not be possible to resuscitate the patient. As diagnostic measures:

Feel for a pulse. It is best to palpate the carotid artery on the side of the neck and on both sides. There is no pulse during VCS.

Checking consciousness. The patient will not respond to painful blows and pinches.

Check reaction to light. The pupils dilate on their own, but do not react to light and what is happening around.

Check for BP. With VKS, this cannot be done, since it does not exist.

It is necessary to measure the pressure already in the course of resuscitation, since it takes a long time. The first three measures are enough to confirm clinical death and start resuscitating the patient.

Prehospital stage of cardiopulmonary resuscitation

Prior to hospitalization of the patient, measures of cardiopulmonary resuscitation are carried out in two stages: elementary life support (urgent oxygenation) and further actions aimed at maintaining life (restoration of spontaneous circulation).

Basic life support (urgent oxygenation)

Restoration of airway patency.

Maintaining breathing (artificial ventilation of the lungs).

Maintaining blood circulation (indirect cardiac massage).

Further actions aimed at maintaining life (restoration of spontaneous circulation)

The introduction of drugs and fluids.

Intravenous route of drug administration.

Perhaps the introduction of drugs into a peripheral vein.

After each bolus injection, it is necessary to raise the patient's arm to accelerate the delivery of the drug to the heart, accompanying the bolus with the introduction of some amount of fluid (to push it).

For access to the central vein, it is preferable to catheterize the subclavian or internal jugular vein.

The introduction of drugs into the femoral vein is associated with their slow delivery to the heart and a decrease in concentration.

Endotracheal route of drug administration.

If tracheal intubation is performed earlier than venous access is provided, then atropine, adrenaline, lidocaine can be passed through the probe into the trachea.

The preparations are diluted with 10 ml of isotonic sodium chloride solution and their doses should be 2-2.5 times greater than with intravenous administration.

The end of the probe must be below the end of the endotracheal tube.

After the introduction of the drug, it is necessary to sequentially perform 2-3 breaths (while stopping the indirect heart massage) to distribute the drug along the bronchial tree.

Intracardiac route of drug administration.

It is used when it is impossible to administer drugs in another way.

With intracardiac injections, large coronary arteries are damaged in 40% of cases.

An ECG recording is performed for the purpose of differential diagnosis between the main causes of circulatory arrest (ventricular fibrillation - 70-80%, ventricular asystole - 10-29%, electromechanical dissociation - 3%).

Optimal for ECG recording is a three-channel electrocardiograph in automatic or manual mode.

Management of ventricular fibrillation and hemodynamically ineffective ventricular tachycardia.

If ventricular fibrillation or hemodynamically ineffective ventricular tachycardia is detected in the absence of a defibrillator, it is necessary to apply an energetic fist to the heart (precordial punch) and, in the absence of a pulse in the carotid arteries, proceed to cardiopulmonary resuscitation.

The fastest, most effective, and generally accepted method of stopping ventricular tachycardia and ventricular fibrillation is electrical defibrillation. Method of electrical defibrillation.

Tactics in electromechanical dissociation.

Electromechanical dissociation is the absence of a pulse and breathing in a patient with preserved electrical activity of the heart (the rhythm is visible on the monitor, but there is no pulse).

Measures to eliminate the causes of electromechanical dissociation.

Tactics in asystole.

Carry out general resuscitation.

Intravenously inject adrenaline at a dose of 1 mg every 3-5 minutes.

Intravenous injection of atropine at a dose of 1 mg every 3-5 minutes.

Perform pacing.

At the 15th minute of resuscitation, inject sodium bicarbonate.

In case of effectiveness of resuscitation measures, it is necessary:

Ensure adequate ventilation of the lungs.

Continue the introduction of antiarrhythmic drugs for prophylactic purposes.

To diagnose and treat the disease that caused sudden cardiac death.

rhythm heart violation resuscitation

Sudden coronary death (SCD) occurs due to complete dysfunction of the heart muscle, leading to its instantaneous stop. The lethal outcome for this reason most often comprehends the male part of the middle-aged population. Coronary death is the most common cause of death due to heart disease.

What is sudden coronary death?

Coronary death is the outcome of cardiovascular diseases, due to severe symptoms of which, within 1 hour after the onset of its manifestation, a heart attack and / or cardiac arrest occurs. This disease is associated with the presence of pathology of the coronary arteries, which play a major role in the blood supply to the myocardium.

The most common manifestation of sudden death is observed in patients with coronary artery disease. Also, the pathological condition is caused by previously transferred and chronic pathologies of the heart muscle.

REFERENCE! Comes, leading in most cases to death, in the morning or during active physical activity.

It is important to consider that sudden death may not occur immediately after a heart attack, but within 24 hours. At the same time, VCS, according to the MBC, is classified into 2 forms of manifestation:

Clinical, at the onset of which there is no breathing and blood supply to the heart, the patient is unconscious. In such cases, it is possible to bring the patient back to life by taking resuscitation measures.
Biological, which is characterized by the full manifestation of the symptoms of coronary death and is not amenable to resuscitation methods.

The reasons

Most often, sudden coronary death occurs due to ventricular fibrillation in the presence of such provoking factors:

physical activity on the body;
severe emotional state, mental disorder;
frequent and excessive consumption of alcoholic beverages;
active smoking;
passive lifestyle.

In addition, the following developing diseases can be causes of cardiac arrest:

, especially recently rescheduled;
regular;
respiratory disorders, shortness of breath;
frequent attacks of ischemia;
pathology of the heart valves;
myocarditis and endocarditis;
all forms and cardiac dysplasia;
thromboembolism;
aortic aneurysm.

IMPORTANT! An attack of VCS provokes a malfunction of the heart and its coronary arteries, often resulting from atherosclerosis.

It is also important to monitor the state of health and avoid cases that cause oxygen starvation of the myocardium, including:

the occurrence of neoplasms;
obstructive airways disease;
respiratory failure;
heart muscle injury;
pain shock;
intoxication of the body, in particular, toxic;
electrical shock.

Diseases of the cardiovascular system, together with factors provoking the risk of death, often end in a sudden death, this danger especially extends to certain groups of the population.

Risk groups for sudden coronary death

An attack of coronary death is diagnosed in most cases in people who are at high risk, which includes:

People with a family history of diseases of the cardiovascular system and pathological conditions of the heart.
Chronic patients with previous sudden cardiac arrest.
Patients suffering from ventricular disorders (tachycardia, fibrillation) due to heart attacks.
People with congenital anomalies of the heart and blood vessels.
Patients with heart failure.
Patients with any form of cardiomyopathy.
Drug addicts.
People suffering from obesity and diabetes.
Patients actively taking drugs aimed at eliminating arrhythmia.

Symptoms before coronary death

Since sudden death, by definition, cannot be accompanied by symptoms other than the absence of vital signs, it is important to know the preceding symptoms of SCD:

an attack of tachycardia followed by a gradual cessation of heart contractions (read more about how to relieve an attack of tachycardia);
dizziness due to failures in blood pressure and heart rate, turning into an unconscious state;
gradual decrease in heart rate and respiratory arrest;
dilated pupils without reaction to light.

ATTENTION! Such manifestations in a short time without first aid and resuscitation measures can be fatal.

First aid

People at risk of sudden coronary death are advised not to be alone when their health deteriorates. With attacks of VCS, it is important to provide first aid as soon as possible before the arrival of specialists. The right technique for carrying out such events can save a person's life. It includes the following actions:

Move the victim to a safe place.
Check for signs of life in the patient.
An unconscious patient needs to open the airway.
Make sure the victim is able to breathe. It is important to make sure that breathing is not the last breath of a person.
If the victim has breathing problems, a closed heart massage should be performed: put one hand with the palm on the center of the sternum, put the other palm on it as well. With arms straight at the elbows, pressure should be applied to the chest with a frequency of at least 100 such compressions per minute.
Give the victim artificial respiration (if possible and if you have the skills).
Conduct emergency care until the arrival of doctors or until signs of restoration of the heart.

Resuscitation measures

ATTENTION! It is important to perform resuscitation in case of coronary death in hospital conditions.

The main method of resuscitation of an unconscious patient is the use of a defibrillator that delivers electrical shocks to restore cardiac function. The procedure takes place in several stages:

The position of the victim on a flat surface.
Placing a gasket that conducts an electric charge between the patient's body and the electrodes of the device.
Installing electrodes in proper places.
The supply of current discharges with increasing power until the normalization of human cardiac function.

Also, one of the resuscitation methods is the use of ventilation with a mask to restore the patient's ability to breathe. If it is impossible to carry out the procedure, doctors can save the victim's life by resorting to tracheal intubation to ensure airway patency.

Medications are an addition to the resuscitation of the patient. Used for cardiac arrest:

Atropine - for recovery from asystole.
Epinephrine or adrenaline - to increase the heart rate after the heart is restored to working capacity.
Sodium bicarbonate - for prolonged cases of VCS.
Lidocaine or amiodarone - for.
Magnesium sulfate - to stabilize and excite the cells of the heart muscle.
Calcium - to restore its balance in the body.

The use of drugs is also urgently needed to accelerate the recovery of the patient after returning to consciousness.

Treatment of coronary insufficiency

Acute coronary insufficiency in most cases is the main cause of myocardial pathologies and further sudden death, it is important to detect it in time and start treatment. It is especially necessary to undergo a diagnosis of the disease for patients who are at risk, suffering from coronary artery disease.

IMPORTANT! The sooner action is taken, the longer the patient will not die, and he will also have a higher chance of avoiding sudden death.

The main method for determining coronary insufficiency is hardware coronary angiography. This research method allows you to accurately determine the location of damage and narrowing of the coronary artery. The results of coronary angiography allow the doctor to determine the stage of development of the pathology and methods of treatment. Also, to clarify them, an ECG and tests can be prescribed, the results of which are compared with the codes of normal indicators.

With mild stages of the development of coronary insufficiency, it is necessary to change the lifestyle:

observe a correct and normalized diet;
balance the daily routine so as not to overload the body;
when feeling normal;
avoid smoking and drinking alcohol;
normalize body weight.

More severe cases of narrowing of the coronary artery include the need for medical therapy:

antianginal and to prevent heart attacks ("Nitroglycerin", "Verapamil");
anticoagulants for blood thinning ("Dicoumarin", "Warfarin");
vasodilators (Aptin, Iprazid);
a course of lipid-lowering drugs ("Anvistat", "Lipanor");
anabolic drugs ("Albumin", "Rikavit").

REFERENCE! To expand the coronary arteries and subsequently restore the blood supply to the heart muscle, a surgical method such as coronary artery bypass grafting is used.

Prevention

Avoid smoking and drinking alcohol;
reduce weight to normal (in the presence of obesity) and gain weight in case of insufficient weight;
regularly engage in sports as much as possible the load of the body;
change the diet, minimize the amount of fat, cholesterol and salt consumed, increase the amount of fiber in the daily menu;
control blood sugar and cholesterol levels;
maintain blood pressure within normal limits.

A healthy lifestyle and the exclusion of possible risk factors help to stabilize the state of health, prevent the development and complications of heart disease and VCS.

Conclusion

Sudden coronary death is a reversible process with timely first aid and subsequent resuscitation in a hospital setting. It is almost impossible to foresee an attack of VCS, but there is a chance to protect yourself and prevent a pathological condition, which is facilitated by the observance of preventive measures and timely diagnosis of heart diseases.