Other

Terminal states. What is the agonal state? Biological death ICD code

Terminal states

Terminal states- pathofunctional changes, which are based on increasing hypoxia of all tissues (primarily the brain), acidosis and intoxication with products of impaired metabolism.

During terminal conditions, the functions of the cardiovascular system, respiration, central nervous system, kidneys, liver, hormonal system, and metabolism collapse. The most significant is the decline of the functions of the central nervous system. Increasing hypoxia and subsequent anoxia in brain cells (primarily the cerebral cortex) lead to the replacement of the oxidative type of metabolism with a glycolytic one. In this case, a disruption in the synthesis of ATP and ion gradients is observed, free radicals are formed, and the permeability of cell membranes increases. These metabolic changes entail destructive changes in cells, which manifests itself in the form of cloudy swelling and hydropic degeneration.

In principle, these changes are reversible and, when normal oxygen supply to tissues is restored, do not lead to life-threatening conditions. But with continued anoxia, they turn into irreversible degenerative changes, which are accompanied by protein hydrolysis and, ultimately, autolysis develops. The least resistant to the glycolytic type of metabolism are the tissues of the brain and spinal cord; only 4–6 minutes of anoxia are necessary for irreversible changes to occur in the cerebral cortex. With the glycolytic type of metabolism, the subcortical region and the spinal cord can function somewhat longer. The severity of terminal conditions and their duration depend on the severity and speed of development of hypoxia and anoxia.

Terminal conditions include:
- severe shock (IV degree shock)
- extreme coma
- terminal pause

Terminal conditions include 3 stages:
- 1. Preagonal state;
- – Terminal pause (since it does not always happen, it is not included in the classification, but it is still worth taking into account);
- 2. Agonal state;
- 3. Clinical death.

Preagonal state: characterized by respiratory distress, rapid pulse, feeling bad, pale skin. Consciousness is confused.

Terminal or agonal pause doesn't always happen. Clinically, it is manifested by respiratory arrest and transient periods of asystole from 1–2 to 10–15 seconds.

When there is agony: severe pallor of the skin, arrhythmic breathing. The pulse is not detected. The pupils are dilated. Preagonal and agonal states can last from several minutes to several hours (sometimes they can be very short-lived, so it is not always possible to track them).

Clinical death: there is no breathing; the pulse is not detectable, the skin is pale; Pupils are dilated and do not respond to light.

Severe shock, extreme coma, collapse can turn into a state of clinical death or other terminal conditions. While the preagonal state, terminal pause, agony and clinical death do not necessarily have to be preceded by shock, coma or collapse. During the terminal period, severe pathofunctional disorders occur in all tissues and organs. Sometimes the terminal period is so long and severe that a state of irreversibility develops in the cerebral cortex, when resuscitation measures are meaningless and reviving a person is impossible even after several seconds of clinical death.

Anesthesiology and intensive care of children. Practical guide, V.V. Kurek, A.E. Kulagin. The manual presents modern data on the clinical physiology of the respiratory and cardiovascular systems, water and electrolyte balance and the acid-base state of the body...
Terminal states. Algorithm for basic (elementary) cardiopulmonary resuscitation + DVD, Borisova Svetlana Yurievna. This educational and visual aid has been prepared taking into account modern requirements for conducting basic (elementary) cardiopulmonary resuscitation in order to consolidate theoretical knowledge and…

Table of contents of the topic "Convulsive syndrome. Agony. Death. Cessation of cardiac activity.":
1. Convulsive syndrome. Cramps. Causes of seizures. Pathogenesis of seizures. The mechanism of convulsive syndrome.
2. Epilepsy. Epileptic seizure. Epistatus. Causes (etiology) of epileptic seizures. Clinic (signs) of a seizure.
3. Emergency care for an epileptic seizure (convulsions). First aid for status epilepticus (epistatus, convulsions).
4. Convulsive states during hysteria. Convulsions during hysteria. Causes (etiology) of a hysterical attack. Clinic (signs) of a hysterical attack (convulsions).
5. Emergency care for a hysterical attack (convulsions). First aid for hysterical convulsions.

7. Agony. Agonal state. Clinic (signs) of agonal state (agony). Clinical death. Clinic (signs) of clinical death.
8. Biological death. Clinic (signs) of biological death. Brain (social) death. Clinic (signs) of brain death.
9. Termination of cardiac activity. Asystole. Causes (etiology) of asystole.
10. Ventricular fibrillation. Causes (etiology) of ventricular fibrillation. Clinic (signs) of ventricular fibrillation. Myocardial atony.

Reanimatology- the science of revitalization (re - again, animare - to revive), studying the etiology, pathogenesis and treatment of terminal conditions, which mean various pathological processes characterized by syndromes of extreme depression of the vital functions of the body.

Reanimation- a set of methods aimed at relieving these syndromes. The survival rate of victims in critical condition depends on 3 factors:

1. Early diagnosis of circulatory arrest.
2. Immediate initiation of basic resuscitation measures.
3. Calling a resuscitation team to carry out specialized resuscitation measures.

Any terminal condition, regardless of the root cause, is characterized by a critical level of disorders of the basic vital functions of the body: breathing, cardiovascular system, metabolism, etc., up to a complete stop of the heart. The following stages are distinguished in its development: preagonal state, terminal pause (not always noted), agony, clinical and biological death.

Pregonal state. Clinic (signs) of the pregonal state.

Consciousness is sharply depressed or absent. The skin is pale or cyanotic. Blood pressure progressively decreases to zero, there is no pulse in the peripheral arteries, but it is still preserved in the carotid and femoral arteries. At the initial stages, tachycardia is noted, followed by a transition to bradycardia. Breathing quickly changes from tachy to bradyform. Stem reflexes are disrupted and pathological ones may appear. The severity of the condition is quickly aggravated by increasing oxygen starvation and severe metabolic disorders. The central genesis of the above disorders should be especially emphasized.

Terminal or agonal pause doesn't always happen. Clinically, it is manifested by respiratory arrest and transient periods of asystole from 1-2 to 10-15 seconds.

This class includes symptoms, signs and abnormalities identified by clinical or other investigations, as well as ill-defined conditions for which no diagnosis classified elsewhere is indicated.

Signs and symptoms on the basis of which a fairly definite diagnosis can be made are classified under the headings of other classes. The headings of this class, as a rule, include less precisely defined conditions and symptoms that may equally relate to two or more diseases or to two or more body systems, in the absence of the necessary research to establish a definitive diagnosis. Almost all conditions included in this class can be defined as “unspecified,” “not otherwise specified,” “unknown etiology,” or “transient.” In order to establish whether certain symptoms and signs belong to this class or to other sections of the classification, you should use the Alphabetical Index. The remaining subcategories with .8 are usually reserved for other reportable symptoms that cannot be classified elsewhere in the classification.

Conditions, signs and symptoms included in R00-R99 include:

a) cases in which a more accurate diagnosis was not possible even after studying all the available evidence;
b) cases of transient symptoms or signs the cause of which could not be determined;
c) cases of a preliminary diagnosis that could not be confirmed due to the patient’s failure to appear for further examination or treatment;
d) cases of referral of a patient to another institution for examination or treatment before a final diagnosis is made;
e) cases where a more accurate diagnosis was not established for any other reason;
f) some symptoms for which additional information is provided, which in itself has no value for the provision of medical care.

Excluded:

abnormalities detected during antenatal examination of the mother (O28.-)
selected conditions occurring in the perinatal period (P00-P96)

This class contains the following blocks:

R00-R09 Symptoms and signs related to the circulatory and respiratory systems
R10-R19 Symptoms and signs related to the digestive and abdominal systems
R20-R23 Symptoms and signs related to the skin and subcutaneous tissue
R25-R29 Symptoms and signs related to the nervous and musculoskeletal systems
R30-R39 Symptoms and signs related to the urinary system
R40-R46 Symptoms and signs relating to cognition, perception, affect and behavior
R47-R49 Symptoms and signs related to speech and voice
R50-R69 General symptoms and signs
R70-R79 Deviations from the norm identified during blood tests, in the absence of a diagnosis

COMA

ICD-10 code(s):

I61 Intracerebral hemorrhage (hemorrhagic stroke)

I62.0 Subdural hemorrhage

I63 Cerebral infarction (thromboischemic stroke)

I64 Stroke, unspecified (Stroke unspecified)

E14.1 Ketoacidotic coma

E14.2 Hyperglycemic coma

E15 Hypoglycemic coma

T40.9 narcocom

K72 Hepatic coma

N19 Uremic coma

E14.3 other comas

R-40.2 coma, unspecified (excluded: hypoglycemic. diabetic. liver)

COMA (from the Greek koma - deep sleep) is a state of central nervous system insufficiency, characterized by a violation of its coordinating activity, the autonomous functioning of individual systems that, at the level of the whole organism, lose the ability to self-regulate and maintain homeostasis; clinically manifested by loss of consciousness, disturbance of motor, sensory and samotic functions, including vital ones.

Classification com depending on the etiology: primary and secondary.

Most causes of coma are associated either with direct destruction of cerebral structures, or with cerebral ischemia, or with insufficiency of carbohydrate metabolism. Comas in which a violation of brain metabolism (as a result of hemorrhagic or ischemic stroke) or its mechanical destruction are caused by primary cerebral processes (traumatic brain injury, stroke, tumor, meningoencephalitis) are classified as primary cerebral.

Comas that develop as a result of secondary brain damage against the background of somatic pathology, exogenous (overdose of hypoglycemic drugs, fasting, intoxication, overheating) or endogenous intoxication (failure of function of internal organs, diseases of the endocrine system, formations) are called secondary cerebrogenic.

Clinical picture: the clinical picture of any coma is dominated by impaired consciousness with loss of perception of the environment and oneself, suppression of reflexes to external stimuli and disorders of the regulation of vital functions. The following forms of changes in the level of consciousness are distinguished: stupor (superficial and deep), stupor, coma (moderate, deep, extreme).

The severity of consciousness disorders is assessed using the Glasgow scale, according to which the patient’s condition is described by three parameters: eye opening, verbal and motor responses to external stimuli.

Stun(13-14 points on the Glasgow scale) - drowsiness, disorientation, limited and difficult speech contact, monosyllabic answers to repeated questions, following only simple commands.

Sopor(9-12 points on the Glasgow scale) - complete lack of consciousness, preservation of purposeful, coordinated defensive movements, opening of the eyes to painful and sound stimuli, occasional monosyllabic answers to multiple repetitions of a question, immobility or automated stereotypical movements, loss of control over pelvic functions.

Superficial coma(I degree, 7-8 points on the Glasgow scale) - inability to wake up, chaotic uncoordinated defensive movements to painful stimuli, lack of opening the eyes to stimuli and control of pelvic functions, mild respiratory and cardiovascular problems are possible.

Coma deep(II degree, 5-6 points on the Glasgow scale) - inability to wake up, lack of protective movements, impaired muscle tone, inhibition of tendon reflexes, severe respiratory impairment, cardiovascular decompensation.

Coma beyond the limit (terminal)(III degree, 3-4 points on the Glasgow scale)) - atonal state, atony, areflexia, impaired or absent breathing, depression of cardiac activity.

Depression of consciousness and weakening of reflexes (corneal, pupillary, tendon, skin) progress to complete extinction as the coma deepens.

Assessment of the depth of impairment of consciousness in emergency situations in an adult, without resorting to special research methods, can be carried out using the Glasgow scale, where each answer corresponds to a certain score, and in newborns - using the Apgar scale.

Glasgow scale.

The state of consciousness is assessed by totaling 1 points from each subgroup. 15 points correspond to a state of clear consciousness, 13-14 - stun, 9-12 - stupor, 14-8 - coma, 3 points - brain death.

Differential diagnosis

Comas are differentiated from pseudocomatose states (isolation syndrome, psychogenic unresponsiveness, status abulica, non-convulsive status epilepticus). Below are the features of the most commonly observed comatose states.

INneforMonoh Withmert
TOodprOTOToola: E-003

Cel uhTAnA: restoration of the function of all vital systems and organs.

TOod (ToOds) nO MTOB- 10:

R96 Dratgie VAndds VneforMonOuch WithmerTAnd nO neAndhVEUTnOuch nrAndhotherwise

IsTolyuhenO:

sudden cardiac death, so described (I46.1)

sudden death of an infant (R95)

ODAfoodleneithere:

Death occurs suddenly or within 60 minutes after the onset of symptoms of deterioration in health in persons who were previously in a stable condition, with

absence of signs of a specific disease.

The armed forces do not include cases of violent death, death as a result of injury, asphyxia,

drowning and poisoning.

VS can be of cardiogenic or non-cardiogenic origin.

The main cardiac causes of AEC: ventricular fibrillation, pulseless ventricular tachycardia, complete AV block with idioventricular rhythm, electromechanical dissociation, asystole, severe vascular dystonia with a critical drop in blood pressure.

FAndbrAndllyaqiI andeludOhToov.

Discoordinated and disintegrated contractions of myocardial fibers, leading

to the impossibility of forming SV.

Accounts for 60-70% of all cases of OEC.

VF is more often observed in acute coronary insufficiency, drowning in fresh water, hypothermia, and electric shock.

Precursors of VF: early, paired and polytopic ventricular extrasystoles.

Pre-fibrillatory forms of VT: alternating and torsades VT, polymorphic VT.

ANDeludOhTonewTAXIRArdAndI beh natlbsa

The frequency of ventricular tachycardia is so high that during diastole of the cavity

The ventricles are unable to fill with sufficient blood, which leads to a sharp decrease in cardiac output (absence of pulse) and, consequently, to inadequate blood circulation.

Pulseless ventricular tachycardia is predicted to be equivalent to fibrillation

ventricles.

AceAndWithToland I

Absence of heartbeats and signs of electrical activity,

confirmed in three leads on the ECG.

Accounts for 20-25% of all cases of stopping effective blood circulation.

Divided into sudden (particularly unfavorable in prognosis) and

delayed (occurring after previous rhythm disturbances).

AleToTrohmeXAneitherchesTooh dAndssOqiAqiI (EMD)

Severe depression of myocardial contractility with a drop in cardiac output and blood pressure, but with persistent cardiac complexes on the ECG.

Accounts for about 10% of all cases of OEC.

P e r V And h n oh E M D - the myocardium loses the ability to perform effective contraction when

presence of a source of electrical impulses.

The heart quickly switches to an idioventricular rhythm, which soon changes

asystole.

Primary EMD includes:

1) acute myocardial infarction (especially its lower wall);

2) condition after repeated myocardial depleting episodes of fibrillation,

eliminated with CPR;

3) the final stage of severe heart disease;

4) myocardial inhibition by endotoxins and drugs in case of overdose (beta blockers,

calcium antagonists, tricyclic antidepressants, cardiac glycosides).

5) atrial thrombosis, heart tumor.

IN T op And h n oh E M D - a sharp reduction in cardiac output not associated with

direct disruption of the processes of excitability and contractility of the myocardium.

Causes of secondary EMD:

1) pericardial tamponade;

2) pulmonary embolism;

4) severe hypovolemia;

5) occlusion of a prosthetic valve by a thrombus.

EMD may be caused by:

sinus bradycardia, atrioventricular block, slow idioventricular rhythm. WITH meh w A nny e f op m s E MD

Observed with the progression of toxic-metabolic processes:

1) severe endotoxemia;

2) hypoglycemia;

3) hypo- and hypercalcemia;

4) pronounced metabolic acidosis;

Principles serdechnO- leGOhnO- brainGova reAnAndmaqiAnd (SLMR)

The brain experiences a lack of blood flow for only 2-3 minutes - it is for this period of time that the glucose reserves in the brain are sufficient to provide

energy metabolism during anaerobic glycolysis.

Resuscitation should begin with prosthetics of the heart, the main task is

provide blood perfusion to the brain!

ABOUTWithnovns fordAhAnd nerhowl reAneithermaqiONNOuch nomoschAnd:

1. Restoration of effective hemodynamics.

2. Restoration of breathing.

3. Restoration and correction of brain functions.

4. Prevention of relapse of a terminal condition.

5. Prevention of possible complications.

ABOUTWithnovns WithAndmnTohms VneforMonOuch OWithTAnovToAnd uhffeToTAndVnOGO crovoobrAscheneitherI:

1. Loss of consciousness develops within 8-10 seconds from the moment blood circulation stops.

2. Convulsions usually appear at the moment of loss of consciousness.

3. Absence of pulsation in large main arteries.

4. Stopping breathing often occurs later than other symptoms - about 20 -

30 - 40 s. Sometimes agonal breathing is observed for 1-2 minutes or more.

5. Pupil dilation appears 30-90 seconds after the start of circulatory arrest.

6. Paleness, cyanosis, marbling of the skin.

POToazaneitherI To rEUatssAndTAqiAnd:

1. Absence and severe weakness of pulsation in the carotid (or femoral and brachial) arteries.

2. Lack of breathing.

fading breath).
4. Lack of consciousness.

5. Lack of photoreactions and dilated pupils.

PrOTAndinnOToazanAndI To rEUatssAndTAqiAnd:

1. Terminal stages of an incurable disease.

2. Significant traumatic destruction of the brain.

3. Early (drying and clouding of the cornea, cat's eye symptom) and late (rigor spots and rigor mortis) signs of biological death.

4. Documented refusal of the patient to resuscitate.

5. Staying in a state of clinical death for more than 20 minutes before arrival

qualified help.

TOAkie manipulyaqiAnd ne WithlunitsateT provodAndTb VO AndzbeandAneitherenOTerAnd VremenAnd:

1. Auscultate the heart.

2. Search for pulsation on the radial artery.

3. Carry out the algorithm - “I feel, I see, I hear.”

4. Determine corneal, tendon and pharyngeal reflexes.

5. Measure blood pressure.

GlavanscrAndTeriAnd prOdolandeneitherI rEUatssAndTAtions:

1. Pulse in the carotid arteries, synchronous with chest compressions -

indicates the correctness of performing cardiac massage and maintaining tone

myocardium.

2. Change in skin color (pinkness).

3. Constriction of the pupil (improved oxygenation in the midbrain area).

4. High “artifact complexes” on the ECG.

5. Restoration of consciousness during resuscitation.

POToazaTewhether bEUnerWithneToTAndVnOWithTAnd dalbnethweth rEUatssAndTAqiAnd:

1. Reactivity of dilated pupils.

2. Absence or steady decrease in muscle tone.

3. Lack of reflexes from the upper respiratory tract.

4. Low deformed “artifact complexes” on the ECG.
The term “closed cardiac massage” is inappropriate, because By pushing the sternum 4-5 cm in the anteroposterior direction, it is impossible to compress the heart between the sternum and the spinal column - the indicated size of the chest is 12-15 cm, and the size of the heart in this area is 7-8 cm.

With chest compression, the effect of the thoracic

pumps, i.e. increased intrathoracic pressure during compression and decreased intrathoracic pressure during decompression.

PreToOrdAndalbnth atdar

1. The patient is given 4-5 sharp blows with a fist in the area of the border of the middle and lower

third of the sternum from a distance of at least 30 cm.

2. The blow should be strong enough, but not extremely powerful.

3. Indications for precordial beats are ventricular fibrillation and pulseless ventricular tachycardia.

4. The effectiveness of the shock for pulseless ventricular tachycardia ranges from 10

5. With ventricular fibrillation, rhythm restoration occurs much less frequently.

6. Used only in the absence of a defibrillator prepared for operation and

patients with reliable circulatory arrest.

7. Precordial shock should not be used instead of electric shock.

cardiac defibrillation (EDS).

8. Precordial beat can convert ventricular tachycardia into asystole,

ventricular fibrillation or EMD, respectively VF - in asystole or EMD.

9. For asystole and EMD, the precordial stroke is not used.

TeXNickA provfoodneitherI TOrAToAlbnOuch nohmns:

1. The palmar surface of the right hand is placed in the middle of the sternum or 2-3

cm above the xiphoid process of the sternum, and the palm of the left hand is on the right.

2. You cannot lift your palm from your chest during pauses.

3. Compression is carried out due to the weight of the rescuer’s torso.

4. The depth of excursion of the sternum towards the spine should be 4-5

cm in adults.

5. The rate of pressure should be 60-80 per minute.

6. To assess the effectiveness of the thoracic pump, the pulse in the carotid arteries is periodically palpated.

7. Resuscitation is suspended for 5 seconds at the end of 1 minute and then every 2-3 minutes,

to assess whether spontaneous breathing has been restored and

blood circulation

8. Resuscitation should not be stopped for more than 5-10 seconds to carry out

additional therapeutic measures and for 25-30 seconds for tracheal intubation.

9. The compression-to-inhalation ratio should be 20:2 for any number of rescuers

before tracheal intubation, then 10:1.

INWithnomoGATelbns nrieWe,novswAyuschAnde effeToTTOrAToAlbnOuch nohmns:

1. Carrying out the thoracic pump only on a solid base.

2. Raising the legs by 35-40° reduces the “functioning” vascular bed due to

lower extremities. This leads to centralization of blood circulation and an increase in blood volume by 600-700 ml. The inflowing blood accelerates the closure of the aortic valves in the phase of cessation of chest compressions, thereby improving coronary blood flow.

The Trendelenburg position is dangerous because it contributes to the development of hypoxic cerebral edema.

1. Infusion of plasma substitutes increases venous pressure and increases venous support.

2. Intercalated abdominal compression involves squeezing the abdomen after compression of the chest has stopped. This action seems to squeeze out

blood from the vascular bed of the abdomen. Performed only in intubated patients due to the risk of regurgitation.

MeXAneitherzmTOrAToAlbnOuch nohmns:

1. Thoracic pump - compression of the chambers of the heart and lungs by increasing pressure throughout

chest cavity.

2. In the chest compression phase, all chambers of the heart, coronary

arteries and large vessels.

3. Pressure in the aorta and right atrium is equalized and coronary

blood circulation stops.

4. When the chest is straightened, blood flow to the heart improves,

a small pressure gradient is established between the aorta and the right atrium.

5. Increased pressure in the aortic arch leads to the closure of the semilunar valves, behind which the ostia of the coronary arteries arise, and, consequently, to recovery

blood flow through the coronary arteries.

EffeToTAndVnOWithTbTOrAToalbnOuch nohmns:

1. Creates a low pressure gradient and low diastolic pressure (the driving force for coronary blood flow) by uniformly distributing pressure across

structures of the chest cavity.

2. Cardiac index is less than 20-25% of normal, which is lower than observed

with severe cardiogenic shock.
3. The performance of the thoracic pump decreases rapidly, which, even in the absence of severe myocardial damage, leads to the disappearance of effectiveness within 30-40 minutes. Increasing hypoxia and mechanical injury to the heart in a short time lead to a drop in myocardial tone.

4. Provides no more than 5-10% of normal coronary parameters

blood circulation

5. Cerebral blood flow during the production of a thoracic pump does not exceed 10-20%

norms, while most of the artificial blood flow is carried out in the soft tissues of the head.

6. The minimum blood circulation in the brain that a thoracic pump can create is a 10-minute time barrier. After the specified

period of time, the entire supply of oxygen in the myocardium completely disappears, energy reserves are completely depleted, the heart loses tone and becomes flabby.

EffeToTAndVnOWithTb OTcrsTOGO massAandA serdtsA (ABOUTMWITH) :

1. Compulsory medical insurance provides longer survival with full recovery of function

brain. Most patients recover with restoration of cerebral life even after two hours of CPR.

2. Infection is not a serious problem after thoracotomy even under nonsterile conditions.

3. Compulsory medical insurance provides more adequate cerebral (up to 90% of normal) and coronary (more than 50% of normal) blood flow than a thoracic pump, because last

increases intrathoracic pressure, blood pressure and venous pressure.

4. OMS creates higher arteriovenous perfusion pressure.

5. With thoracotomy, the heart can be directly observed and palpated, which helps to evaluate the effect of drug therapy and EDS during CPR.

6. An open chest helps stop intrathoracic bleeding.

7. In case of intra-abdominal bleeding, it allows you to temporarily compress the chest

the aorta above the diaphragm.

8. Mechanical irritation of the heart caused by direct massage

promotes the occurrence of myocardial contractions.
Compulsory medical insurance should be started as early as possible in cases where an adequately administered thoracic pump does not restore spontaneous circulation. Discrediting compulsory medical insurance depends on the delay in its use.

After unsuccessful long-term production of a thoracic pump, transition to compulsory medical insurance

equivalent to massaging a dead heart.

ABOUTWithnovnsnOToazaneitherI To provfoodneitheryuprpitGO massAandA serdtsA:

1. Pericardial tamponade in most cases can be eliminated only by direct emptying of the pericardial cavity from fluid.

2. Extensive pulmonary thromboembolism.

3. Deep hypothermia - persistent VF occurs. Thoracotomy allows you to warm up

heart with warm saline solution during direct massage.

4. Penetrating wounds of the chest and abdominal cavity, blunt trauma with clinical

picture of cardiac arrest.

5. Loss of elasticity of the chest - deformation and rigidity of the chest and

spine, mediastinal displacement.

6. Unsuccessful attempts (within 3-5 minutes) of external defibrillation (at least 12

maximum energy discharges).

7. Sudden asystole in young people and ineffectiveness of thoracic

8. Massive hemothorax.

11. Rupture of aortic aneurysm.

12. Severe pulmonary emphysema.

13. Multiple fractures of the ribs, sternum, spine.

FAToTOrs atWithneXA defAndbrillyatsAndAnd:

1. Effective production of a thoracic pump, ventilation of the lungs with maximum oxygen supply in the respiratory mixture.

2. Defibrillation after administration of adrenaline is more effective. Small-wave fibrillation is converted to large-wave fibrillation using adrenaline. Defibrillation

with small-wave fibrillation it is ineffective and can cause asystole.

3. When administering cardiotonic or antiarrhythmic drugs, the shock should

applied no earlier than 30-40 seconds after administration of the medicine. Follow the pattern: medication → thoracic pump and ventilator → defibrillation → medication → thoracic pump and ventilator → defibrillation.

4. It is necessary to maintain the density and uniformity of pressing the electrodes to the skin:

pressure about 10 kg.

5. The location of the electrodes should not be close to each other.

6. To overcome the resistance of the chest, which averages 70-80

Om, and the heart receives more energy, three discharges are applied with increasing

energy: 200 J → 300 J → 360 J.

7. The interval between discharges should be minimal - only for the duration of the control

pulse or ECG (5-10 sec.).

8. The polarity of the supplied pulse is not of fundamental importance.

9. The shock should be applied during the patient’s exhalation phase. This reduces the cover of the heart by the lungs and reduces the ohmic resistance by 15-20%, which increases the efficiency of the defibrillator discharge.

9. If repeated episodes of fibrillation occur, apply the same energy

discharge, which previously had a positive effect.

10. If ECG control is impossible, apply a shock “blindly” in the first minute

cardiac arrest is quite acceptable.

11.The placement of electrodes over the artificial pacemaker should be avoided.

12. If the patient’s chest wall is significantly thick, the initial EIT discharge

should be 300 J, then 360 J and 400 J.

ABOUTwAndbToAnd And OWithloandneneitherIuhleToTrOAndmnatlbWithnOuch TerApiAnd (EIT)

1. EIT cannot be performed during asystole.

2. Accidental exposure of others to electrical discharge can be fatal.

3. After EIT (cardioversion), temporary or permanent disruption of the artificial pacemaker may be observed.

4. Long interruptions in resuscitation should not be allowed when preparing the defibrillator for shock.

5. Loose pressing of the electrodes is not allowed.

6. Electrodes should not be used without sufficiently moistening their surface.

7. Do not leave tracks (liquid, gel) between the defibrillator electrodes.

8. You cannot be distracted when performing EIT.

9. Low or excessively high voltage shocks should not be administered.

measures that increase the energy resources of the myocardium.

11. It is impossible to provide resuscitation at the time of EIT.

POToazaneitherI And prOTAndinnOToazanAndI To provfoodnAndyu manipulyations

AtmeneneitherenerOrAlbnOGO WHOdatXovodA nereToohmendateTWithI at:

1) unresolved obstruction of the upper respiratory tract;

2) trauma to the oral cavity;

3) jaw fracture;

4) loose teeth;

5) acute bronchospasm.

ABOUTWithloandneneitherI prAnd AndWithnolbcallnAndAnd nerOralbnOGO WHOdatXovodA:

1) bronchospastic reaction;

2) vomiting followed by regurgitation;

3) laryngospasm;

4) worsening airway obstruction.

POToazaneitherI To AndnTubaqiAnd TrAXeAnd:

1. Ineffectiveness of ventilation of the lungs by other means.

2. Great resistance to air blowing (unresolved laryngospasm, large weight of the mammary glands in obesity, toxicosis in pregnant women).

3. Regurgitation and suspicion of aspiration of gastric contents.

4. The presence of a large amount of sputum, mucus and blood in the oral cavity, in the trachea,

bronchi.

5. Inadequate sanitation of the tracheobronchial tree in the presence of consciousness.

6. Absence of pharyngeal reflexes.

7. Multiple rib fractures.

8. Switch to open cardiac massage.

9. The need for long-term mechanical ventilation.

PohmneitherTe, hTO:

If a defibrillator is available for VF, shocks are given before creating

intravenous access.

If peripheral veins are accessible, catheterization of the main veins is not performed.

to avoid complications (tension pneumothorax, injury to the subclavian artery and thoracic lymphatic duct, air embolism, etc.).

When a patient’s ribs and/or sternum are fractured, the frame of the chest is disrupted,

which sharply reduces the effectiveness of the thoracic pump.

Medicines (adrenaline, atropine, lidocaine) can be administered into the endotracheal tube or directly into the trachea by conical puncture, increasing the dose by 2-3 times and diluting 10-20 ml of isotonic sodium chloride solution, followed by 3-4 forced breaths to atomize the medicine.

Intracardiac “blind” injections are not used due to the risk of damage to coronary vessels and conduction tracts, development of hemopericardium and tension pneumothorax, and administration of the drug directly into the myocardium.

TOlassAndfIRAqiI:

Sudden death:

1. Cardiogenic: asystole, ventricular fibrillation, ventricular tachycardia without

pulse, electromechanical dissociation;

2. Non-cardiogenic: asystole, ventricular fibrillation, ventricular tachycardia

no pulse, electromechanical dissociation.

DAndAgnOWithTAndcheskiecrAndTeriAnd:

Signs of a sudden stop in effective blood circulation:

1. There is no consciousness.

2. Pulsation in large main arteries is not detected.

3. Breathing is agonal or absent.

4. Pupils are dilated and do not react to light.

5. The skin is pale gray, occasionally with a cyanotic tint.

Perechenb OWithnovns dAndAgnOWithTAndcheskiX merOnriITAndth:

1) identify the presence of consciousness;

2) check the pulse in both carotid arteries;
3) establish the patency of the upper respiratory tract;

4) determine the size of the pupils and their reaction to light (as resuscitation progresses);

5) determine the type of stoppage of effective blood circulation on the monitor

defibrillator (ECG) (during resuscitation);

6) assess the color of the skin (as resuscitation progresses).

TAToTIRA OToazAneitherI neOTloandnOuch nomoschAnd:

Principles lecheneitherI:

1. The effectiveness of restoring effective heart function depends on the time of onset

Personal protective equipment and the adequacy of the measures taken.

2. Creating a rigid support under the patient's head and torso improves the effectiveness of the breast pump.

3. Raising the legs by 30-40° increases the passive return of blood to the heart -

increases preload.

4. Intercalated abdominal compression between successive chest compressions increases preload and increases coronary perfusion pressure.

5. Open cardiac massage after tracheal intubation creates an effective gradient

pressure and significantly increases the perfusion of the brain and heart, which allows CPR to be extended to 2 hours or more with the restoration of biological and social life. P ro And h V O d And T With I n A d O G O With n And T A l b n ohm uh T A n e T O l b To O about study nny m meh dicin With To them work T n And To O m !

FAndbrAndllyaqiI andeludOhToov

1. Use precordial shocks when preparing the defibrillator for operation if

no more than 30 seconds have passed since the effective blood circulation stopped. Remember

that a precordial stroke itself can lead to the development of asystole and EMD!

100% oxygen.

6. A defibrillator discharge is applied only in the presence of large-wave fibrillation:

200 J – 300 J – 360 J. The shocks should follow each other without continuing CPR and checking the pulse.

7. If unsuccessful: epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml of isotonic solution

NaCl, after which CPR is performed and EIT is repeated - 360 J.

8. If unsuccessful: IV bolus amiodarone (cordarone) 300 mg per 20 ml of 5% glucose; if amiodarone is unavailable, lidocaine 1.5 mg/kg IV bolus. SMR - EIT (360 J). Search for a removable cause of VF.

9. If unsuccessful: epinephrine 3.0 mg IV, sodium bicarbonate 2 ml of 4% solution per 1 kg (1

mmol/kg) IV, amiodarone 300 mg per 20 ml of 5% glucose (lidocaine 1.5 mg/kg IV). SLMR

– EIT (360 J).

10. If unsuccessful: magnesium sulfate 5-10 ml of 25% IV solution and/or propranolol 0.1% - 10

ml i.v. CPR - EIT (360 J).

11. If unsuccessful: thoracotomy, open cardiac massage with drug support and EIT.

12. If VF is eliminated: assess hemodynamics, determine the nature of the post-conversion rhythm. Continue maintenance infusion

antiarrhythmic drug, which gave a positive effect.

ANDeludOhTonewTAXIRArdAndI beh natlbsa

Treatment is similar to that for ventricular fibrillation.

AceAndWithToland I
1. Do not use precordial beats with established or suspected asystole!

2. Chest compression (60-80 per 1 min).

3. Ventilation. First, “mouth to mouth”, with an Ambu bag. After tracheal intubation, use

100% oxygen.

4. Venipuncture or venocateterization.

6. Epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml of isotonic NaCl solution (repeat every 3 minutes). Increase the dose to 3 mg, then 5 mg, then 7 mg if the standard dose does not have an effect. CPR between injections.

7. Atropine (0.1%) IV 1.0 ml (1 mg), repeat every 3 minutes. Increase the dose to 3 mg,

if the standard does not produce an effect up to a total dose of 0.04 mg/kg. SLMR.

8. Eliminate the possible cause of asystole (hypoxia, acidosis, hypokalemia and

hyperkalemia, drug overdose, etc.).

9. Aminophylline (2.4%) iv 10 ml for 1 min. SLMR.

10. External cardiac pacing is effective in preserving myocardial function.

11. Sodium bicarbonate (4%) 1 mmol/kg IV is indicated if asystole occurs due to acidosis.

AleToTrohmeXAneitherchesTooh dAndssOqiAqiI (EMD)

1. Do not use precordial beats with established or suspected EMD!

2. Chest compression (60-80 per 1 min).

3. Ventilation. First, “mouth to mouth”, with an Ambu bag. After tracheal intubation, use

100% oxygen.

4. Venipuncture or venocateterization.

6. Epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml of isotonic NaCl solution (repeat

every 3 minutes). Increase the dose to 3 mg, then 5 mg, then 7 mg if the standard dose does not have an effect. CPR between injections.

7. Identify the cause (shock, hypokalemia, hyperkalemia, acidosis, inadequate ventilation, hypovolemia, etc.) and eliminate it.

8. Infusion therapy – 0.9% NaCl solution or 5% glucose solution up to 1 l/hour.

9. For low heart rate - atropine 1 mg IV every 3 minutes, bringing up to 3 mg.

10. Sodium bicarbonate (4%) 1 mmol/kg IV in case of acidosis development.

11. Electrocardiostimulation.

AtmechAneithere:

Sodium bicarbonate is administered at 1 mmol/kg (2 ml of 4% solution per 1 kg of body weight), and then at

0.5 mmol/kg every 7-10 minutes. Used for prolonged CPR (10 minutes or more), development of sudden death due to acidosis, hyperkalemia, overdose of tricyclic antidepressants.

For hyperkalemia, administration of calcium chloride is indicated at the rate of 20-40 ml 10%

IV solution

Perechenb OWithnovns And dOnolnAndTelbns munitsAndToamenTov:

1) epinephrine

2) atropine

3) amiodarone

4) aminophylline

5) 0.9% sodium chloride solution

6) 4% sodium bicarbonate solution

7) lidocaine

8) 25% magnesium sulfate solution

9) propranolol

IndIRATOrs uhffeToTAndVnOWithTAnd OToazaneitherI munitsicinWithToOuch nomoschAnd:

GlavanscrAndTeriAnd prOdolandeneitherI reAneithermatsAndAnd:

1) pulse in the carotid arteries;

This indicates the correctness of performing cardiac massage and maintaining myocardial tone.

2) change in skin color (pink);

3) constriction of the pupil (improved oxygenation in the midbrain);

4) high “artifact complexes” on the ECG.

5) restoration of consciousness during resuscitation.

WITHpiWithOK AndWithnOlbcallNNOuch lAndTerATatrs:

1. Guide to emergency medical care. Bagnenko S.F., Vertkin A.L.,

Miroshnichenko A.G., Khabutia M.Sh. GEOTAR-Media, 2006

2. First aid for emergency critical conditions. I.F.

Epiphany. St. Petersburg, “Hippocrates”, 2003

3. Secrets of emergency care. P. E. Parsons, J. P. Wiener-Kronish. Moscow,

"MEDpress-inform", 2006

4. Pulmonary-cardiac and cerebral resuscitation. F.R. Akhmerov et al. Kazan, 2002

5. Intensive therapy of threatening conditions. Ed. V.A. Koryachkin and V.I.

Strashnova. St. Petersburg, 2002

6. Guide to intensive care. Ed. A.I. Treshchinsky and F.S.

Glumcher. Kyiv, 2004

7. Intensive therapy. Moscow, GEOTAR, 1998

8. Henderson. Emergency medicine. Texas, 2006

9. Vital Signs and Resuscitation. Stewart. Texas, 2003

10. Rosen`s Emergency Medicine. Mosby, 2002

5. Birtanov E.A., Novikov S.V., Akshalova D.Z. Development of clinical guidelines and diagnostic and treatment protocols taking into account modern requirements. Methodological recommendations. Almaty, 2006, 44 p.

No. 883 “On approval of the List of essential (vital) medicines.”

854 “On approval of the Instructions for the formation of the List of essential (vital) medicines.”

WITHpiWithOK razrabOThIRov:

Head of the Department of Ambulance and Emergency Medical Care, Internal

diseases No. 2 of the Kazakh National Medical University named after. S.D. Asfendiyarova - Doctor of Medical Sciences, Professor Turlanov K.M. Employees of the Department of Ambulance and Emergency Medical Care, Internal Medicine No. 2 of the Kazakh National Medical University named after. S.D. Asfendiyarova: candidate of medical sciences, associate professor Vodnev V.P.; candidate of medical sciences, associate professor Dyusembayev B.K.; Candidate of Medical Sciences, Associate Professor Akhmetova G.D.; candidate of medical sciences, associate professor Bedelbaeva G.G.; Almukhambetov M.K.; Lozhkin A.A.; Madenov N.N.

Head of the Department of Emergency Medicine of the Almaty State Institute for Advanced Medical Studies – Candidate of Medical Sciences, Associate Professor Rakhimbaev R.S. Employees of the Department of Emergency Medicine of the Almaty State Institute for Advanced Medical Studies: candidate of medical sciences, associate professor Silachev Yu.Ya.; Volkova N.V.; Khairulin R.Z.; Sedenko V.A.

* – drugs included in the list of essential (vital) medicines