What is agonal state? Biological death Agony ICD code 10.
TOod etcabouttabouttoola: E-003
Ceeh ehtandpand: restoration of the function of all vital systems and organs.
TOod (toaboutds) pabout MTOB- 10:
R96 Drathie inandds innebehindmonoh frommertand pabout neandsineutnoh prandhnot
Istolyuhenabout:
sudden cardiac death, so described (I46.1)
sudden death infant (R95)
Deffoodlenore:
Death occurs suddenly or within 60 minutes after the onset of symptoms of deterioration in well-being in persons who were previously in a stable state, with
no signs of a specific disease.
The sun does not include cases of violent death, death as a result of trauma, asphyxiation,
drowning and poisoning.
VS can be of cardiogenic and non-cardiogenic origin.
The main cardiac causes of OEC: 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 am feludabouthtoov.
Discoordinated and disintegrated contractions of myocardial fibers, leading
to the impossibility of the formation of SV.
It accounts for 60-70% of all OEC cases.
VF is more often observed in acute coronary insufficiency, drowning in fresh water, hypothermia, and electric shock.
VF precursors: early, paired and polytopic ventricular extrasystoles.
Prefibrillatory forms of VT: alternating and pirouette VT, polymorphic VT.
Feludabouthtonew tandxukandrdandi am bes patlbsa
The incidence of ventricular tachycardia is so high that during diastole the cavities
the ventricles are unable to fill with enough blood, which leads to a sharp decrease in cardiac output (no pulse) and, consequently, inadequate blood circulation.
Pulseless ventricular tachycardia is predicted to be equivalent to fibrillation
ventricles.
Aceandfromtoland I
Lack of heartbeat and signs of electrical activity
confirmed in three leads on the ECG.
It accounts for 20-25% of all cases of stopping effective blood circulation.
They are divided into sudden (especially unfavorable in the prognostic plan) and
delayed (arising after previous rhythm disturbances).
Eletotrohmexandnorsancheztoand I dandssaboutqiandqii am (EMD)
Severe suppression of myocardial contractility with a drop in cardiac output and blood pressure, but with persisting cardiac complexes on the ECG.
It accounts for about 10% of all OEC cases.
P e r in and h n and I E M D - the myocardium loses the ability to perform effective contraction when
the 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 his bottom wall);
2) condition after repeated, depleting myocardium, episodes of fibrillation,
eliminated by SLMR;
3) the final stage of severe heart disease;
4) suppression of the myocardium with 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 and I E M D - a sharp reduction in cardiac output, not associated with
direct violation of the processes of excitability and contractility of the myocardium.
Reasons for secondary EMD:
1) pericardial tamponade;
2) thromboembolism pulmonary artery;
4) severe hypovolemia;
5) occlusion of the prosthetic valve by a thrombus.
EMD can be caused by:
sinus bradycardia, atrioventricular block, slow idioventricular rhythm. FROM me w and nna e f op m s E MD
They are noted during the progression of toxic-metabolic processes:
1) severe endotoxemia;
2) hypoglycemia;
3) hypo- and hypercalcemia;
4) severe metabolic acidosis;
Principles beholdrdechnabout- lerabouthnabout- mozrnew reandnandmaqiand (SLMR)
The brain experiences a lack of blood flow only for 2-3 minutes - it is for this period of time that there are enough glucose reserves in the brain to provide
energy metabolism during anaerobic glycolysis.
Resuscitation should begin with prosthetics of the heart, the main task is
provide the brain with perfusion!
ABOUTfromnovnth behinddandhand perhowl reandnormaqiaboutnnoh pomouand:
1. Restoration of effective hemodynamics.
2. Restoring breathing.
3. Restoration and correction of brain functions.
4. Prevention of recurrence of the terminal state.
5. Warning possible complications.
ABOUTfromnovnth fromandmptohms innebehindmonoh aboutfromtandnovtoand ehffetotandinnaboutrabout crovoobranduenori am:
1. Loss of consciousness develops within 8-10 seconds from the moment the blood circulation stops.
2. Convulsions usually appear at the time of loss of consciousness.
3. Absence of pulsation on the large main arteries.
4. Cessation of breathing often occurs later than other symptoms - about 20 -
30 - 40 p. Sometimes agonal breathing is noted for 1-2 minutes or more.
5. The dilation of the pupils appears after 30-90 seconds from the beginning of the arrest of blood circulation.
6. Pallor, cyanosis, "marbling" of the skin.
Pabouttoazanori am to reuatssandtandqiand:
1. Absence and severe weakness of pulsation in the carotid (or femoral and brachial) arteries.
2. Lack of breathing.
dying breath).
4. Lack of consciousness.
5. Lack of photoreactions and dilated pupils.
Etcabouttandinpabouttoazanandi am to reuatssandtandqiand:
1. Terminal stages of an incurable disease.
2. Significant traumatic brain damage.
3. Early (drying and opacity of the cornea, a symptom of "cat's eye") and late ( cadaveric spots and rigor mortis) signs of biological death.
4. Documented refusal of the patient from resuscitation.
5. Being in a state of clinical death for more than 20 minutes before arrival
qualified assistance.
TOandkie manipulyaqiand ne fromlunitsatet etcovodandtb inabout andzbefandnore Paboutterand inremenand:
1. Auscultate the heart.
2. Search for ripple on radial artery.
3. To carry out the algorithm - “I feel, I see, I hear”.
4. Determine the corneal, tendon and pharyngeal reflexes.
5. Measure blood pressure.
Dlavanth crandteriand etcaboutdolfenori am reuatssandtandtions:
1. Pulse on the carotid arteries, synchronous with chest compressions -
indicates the correctness of performing heart massage and maintaining tone
myocardium.
2. Change in the color of the skin (pinking).
3. Constriction of the pupil (improvement of oxygenation in the midbrain).
4. High "artifact-complexes" on the ECG.
5. Recovery of consciousness during resuscitation.
Pabouttoazatewhether beuperfrompetotandinnaboutfromtand dalbnethweth reuatssandtandqiand:
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 heart massage" is invalid, because by pushing the sternum 4-5 cm in the anteroposterior direction, it is impossible to squeeze 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.
When compressing the chest, the effect of the thoracic
pumps, i.e. increased intrathoracic pressure during compression and decreased intrathoracic pressure during decompression.
Etcetoaboutrdandalbnth atdar
1. The patient is inflicted with 4-5 sharp blows with a fist in the border zone of the middle and lower
a third of the sternum from a distance of at least 30 cm.
2. The punch should be strong enough, but not extremely powerful.
3. Indications for precordial strokes are ventricular fibrillation and pulseless ventricular tachycardia.
4. The effectiveness of a blow with a ventricular tachycardia without pulse ranges from 10
5. With ventricular fibrillation, rhythm restoration occurs much less frequently.
6.Used only in the absence of a prepared defibrillator and
patients with reliable circulatory arrest.
7. Precordial strike should not be used in place of electric shock
defibrillation of the heart (EMF).
8. Precordial beat can translate ventricular tachycardia into asystole,
ventricular fibrillation or EMD, respectively VF - in asystole or EMD.
9. In asystole and EMD, the precordial shock is not used.
Texnickand etcovfoodnori am taboutrandtoandlbnoh pohmps:
1. The palmar surface of the right hand fits in the middle of the sternum or 2-3
cm above the xiphoid process of the sternum, and the palm of the left hand on the right.
2. You can not take your palm from the chest during pauses.
3. Compression is carried out due to the weight of the rescuer's torso.
4. The depth of the excursion of the sternum towards the spine should be 4-5
see in adults.
five . The rate of pressing should be 60-80 per minute.
6. To assess the effectiveness of the thoracic pump, the pulse of the carotid arteries is periodically palpated.
7. Resuscitation is suspended for 5 seconds by 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 treatment measures and for 25-30 sec for tracheal intubation.
9. Compression-inhalation ratio should be 20: 2 for any number of rescuers
before tracheal intubation, then 10: 1.
INfrompomorandtelbnth priewe,povawandyuuande effetottaboutrandtoandlbnoh pohmps:
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 limbs... This leads to the centralization of blood circulation and an increase in the BCC by 600-700 ml. The inflowing blood accelerates the slamming aortic valves in the phase of cessation of chest compressions, thereby improving coronary blood flow.
Trendelenburg's position is dangerous, because it promotes the development of hypoxic cerebral edema.
1. Infusion of plasma substitutes increases venous pressure and increases venous back pressure.
2. Inserted abdominal compression consists of compressing the abdomen after the compression of the chest has ceased. By this action, it is as if squeezed
blood from the vascular bed of the abdomen. It is performed only in intubated patients because of the danger of regurgitation.
Mexandnorgm taboutrandtoandlbnoh pohmps:
1. Thoracic pump - compression of the chambers of the heart and lungs due to increased pressure throughout
chest cavity.
2. In the phase of chest compression, all chambers of the heart, coronary
arteries and large vessels.
3. The pressure in the aorta and the right atrium is equalized and the coronary
blood circulation stops.
4. When the chest is expanded, blood flow to the heart improves,
a small pressure gradient is established between the aorta and the right atrium.
5. An increase in pressure in the aortic arch leads to the closure of the semilunar valves, behind which the mouths of the coronary arteries depart, and, consequently, to restoration
blood flow through the coronary arteries.
Effetotandinnaboutfromtbtaboutrandtoalbnoh pohmps:
1. Creates a low pressure gradient and low diastolic pressure (the driving force for coronary blood flow) by evenly distributing pressure across
structures of the chest cavity.
2. The heart index is less than 20-25% of the norm, which is lower than that observed
with severe cardiogenic shock.
3. The performance of the thoracic pump rapidly decreases, which, even in the absence of severe myocardial damage, leads to the disappearance of efficiency in 30-40 minutes. Increasing hypoxia and mechanical trauma to the heart in a short time lead to a drop in myocardial tone.
4. Provides no more than 5-10% of normal coronary
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 soft tissues heads.
6. The minimum blood circulation in the brain that a thoracic pump is able to 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 its tone and becomes flabby.
Effetotandinnaboutfromtb abouttcrstaboutrabout massandfand beholdrdcand (ABOUTMFROM) :
1. OMS provides greater survival with full recovery of function
brain. Most patients recover with recovery of cerebral life even after 2 hours of CPMR.
2. Infection is not a serious problem after thoracotomy, even under non-sterile conditions.
3. Compulsory health insurance provides more adequate cerebral (up to 90% of the norm) and coronary (more than 50% of the norm) blood flow than a thoracic pump. the last
increases intrathoracic pressure, blood pressure and venous pressure.
4. OMS creates a higher arteriovenous perfusion pressure.
5. With thoracotomy, the heart can be directly observed and palpated, which helps to assess the effect of drug therapy and PED in CPMR.
6. An open chest helps to stop intrathoracic bleeding.
7. In case of intra-abdominal bleeding, it allows you to temporarily clamp the chest
the aorta above the diaphragm.
8. Mechanical irritation of the heart rendered by direct massage
promotes the appearance of myocardial contractions.
Compulsory health insurance should be started as early as possible in cases where an adequately conducted thoracic pump does not restore spontaneous circulation. Discrediting CHI depends on the delay in its use.
After an unsuccessful long-term production of a thoracic pump, the transition to OMS
is equivalent to massage of a dead heart.
ABOUTfromnovnth Pabouttoazanori am to etcovfoodnoryu etcpitrabout massandfand beholdrdcand:
1. Pericardial tamponade in most cases can be eliminated only by direct emptying of the pericardial cavity from the fluid.
2. Extensive pulmonary thromboembolism.
3. Deep hypothermia - persistent VF occurs. Thoracotomy allows you to rewarm
heart with warm saline during direct massage.
4. Penetrating chest and abdominal, blunt trauma with clinical
picture of cardiac arrest.
5. Loss of chest elasticity - deformity 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 the aortic aneurysm.
12. Severe pulmonary emphysema.
13. Multiple fractures of the ribs, sternum, spine.
Fandtotaboutrs atfrompexand defandbrillyacandand:
1. Efficient production of a thoracic pump, ventilation of the lungs with a maximum supply of oxygen in the respiratory mixture.
2. Defibrillation after adrenaline is more effective. Small-wave fibrillation is converted into large-wave fibrillation with the help of adrenaline. Defibrillation
with small-wave fibrillation, it is ineffective and can cause asystole.
3. With the introduction of cardiotonic or antiarrhythmic drugs, the discharge should
applied no earlier than 30-40 seconds after drug administration. Follow the pattern: medication → thoracic pump and ventilator → defibrillation → medication → thoracic pump and ventilator → defibrillation.
4. It is necessary to observe 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, averaging 70-80
Ohm, and receiving more energy by the heart is applied three discharges with increasing
energy: 200 J → 300 J → 360 J.
7. The interval between discharges should be minimal - only for the time of control
pulse or ECG (5-10 sec.).
8. The polarity of the supplied pulse is not critical.
9. The discharge should be performed in the patient's expiratory phase. This reduces lung occlusion of the heart and reduces ohmic resistance by 15-20%, which increases the efficiency of defibrillator discharge.
9. When repeated episodes of fibrillation occur, apply that energy
discharge that previously had a positive effect.
10. If ECG control is not possible, apply a "blind" discharge in the first minute
cardiac arrest is quite acceptable.
11. Avoid placing electrodes over an artificial pacemaker.
12. With a significant thickness of the patient's chest wall, the initial discharge of EIT
should be 300 J, then 360 J and 400 J.
ABOUTwandbtoand and aboutfromlofnenori am ehletotraboutandmpatlbfromnoh terandpiand (EIT)
1. It is impossible to carry out EIT with asystole.
2. Accidental exposure to electrical shocks can be fatal.
3. After EIT (cardioversion), there may be a temporary or permanent disruption in the work of the artificial pacemaker.
4. Do not allow extended breaks in intensive care while preparing the defibrillator for shock.
5. Loose pressing of the electrodes is not allowed.
6. Do not use electrodes without sufficient moisture to their surface.
7. Do not leave tracks (liquid, gel) between the defibrillator electrodes.
8. Do not be distracted during EIT.
9. Do not apply low or overvoltage discharge.
activities that increase the energy resources of the myocardium.
11. It is impossible to provide resuscitation at the time of EIT.
Pabouttoazanori am and etcabouttandinpabouttoazanandi am to etcovfoodnandyu manipulyations
Whenmenenore Peraboutrandlbnaboutrabout wHOdatxovodand ne Retoohmendatetfromi am at:
1) unrepaired upper airway obstruction;
2) trauma to the oral cavity;
3) fracture of the jaw;
4) loose teeth;
5) acute bronchospasm.
ABOUTfromlofnenori am etcand andfrompolbthe callnandand peraboutralbnaboutrabout wHOdatxovodand:
1) bronchospastic reaction;
2) vomiting followed by regurgitation;
3) laryngospasm;
4) aggravation of airway obstruction.
Pabouttoazanori am to andntubaqiand trandxeand:
1. Inefficiency of ventilation of the lungs by other means.
2. High resistance to air blowing (unrepaired laryngospasm, large weight of the mammary glands with obesity, with 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 mouth, in the trachea,
bronchus.
5. Inadequate sanitation of the tracheobronchial tree in the presence of consciousness.
6. Lack of pharyngeal reflexes.
7. Multiple rib fractures.
8. Transition to outdoor massage hearts.
9. The need for long-term mechanical ventilation.
Pohmnorte, htabout:
If a defibrillator is available with VF, shocks are applied before
intravenous access.
If peripheral veins are available, catheterization of the great veins is not performed
to avoid complications (tension pneumothorax, injury of the subclavian artery and thoracic lymphatic duct, air embolism and etc.).
If the patient's ribs and / or sternum are fractured, the frame of the chest is disturbed,
which dramatically reduces the effectiveness of the thoracic pump.
Medicines (adrenaline, atropine, lidocaine) can be injected into the endotracheal tube or directly into the trachea by conicopuncture, increasing the dose by 2-3 times and diluting 10-20 ml of isotonic sodium chloride solution, followed by 3-4 forced breaths to spray the drug.
Intracardiac injections "blindly" are not used, due to the risk of damage to the coronary vessels and pathways, the development of hemopericardium and tension pneumothorax, the injection of the drug directly into the myocardium.
TOlassandfukandqii am:
Sudden death:
1. Cardiogenic: asystole, ventricular fibrillation, ventricular tachycardia without
pulse rate, electromechanical dissociation;
2. Noncardiogenic: asystole, ventricular fibrillation, ventricular tachycardia
pulseless, electromechanical dissociation.
Dandandgnaboutfromtandsanchezkie crandteriand:
Signs of a sudden stop of effective blood circulation:
1. Consciousness is absent.
2. The pulsation on the large main arteries is not detected.
3. Breathing is agonal or absent.
4. Pupils are dilated, do not react to light.
5. Skin pale gray, occasionally with a cyanotic tinge.
Perechenb aboutfromnovnoops dandandgnaboutfromtandsanchezkix meraboutprii amtandth:
1) identify the presence of consciousness;
2) check the pulse on both carotid arteries;
3) establish the patency of the upper respiratory tract;
4) determine the size of the pupils and their response to light (during the course of resuscitation);
5) determine the type of stopping effective blood circulation on the monitor
defibrillator (ECG) (during resuscitation);
6) assess the color of the skin (during the resuscitation).
Tandtotukand abouttoazandnori am neabouttlofnoh pomouand:
Principles lechenori am:
1. The effectiveness of restoring the effective work of the heart depends on the start time
SLMR and on the adequacy of the activities.
2. Creation of rigid support under the patient's head and torso improves the efficiency of the chest pump.
3. Raising the legs by 30-40 ° increases the passive return of blood to the heart -
increases preload.
4. Inserted abdominal compression between successive chest compressions increases preload and increases coronary perfusion pressure.
5. Open heart massage after tracheal intubation creates an effective gradient
pressure and significantly increases the perfusion of the brain and heart, which makes it possible to prolong CPMR up to 2 hours or more with the restoration of biological and social life. P ro and s in about d and t from i am n and d about r about from p and t and l b n ohm eh t and p e t about l b to about about study nna m me dicin from to them work t n and to about m !
Fandbrandllyaqii am feludabouthtoov
1. Precordial strikes should be applied during the preparation of the defibrillator for work, if
no more than 30 seconds have passed since the effective circulation was stopped. Remember,
that the precordial shock itself can lead to the development of asystole and EMD!
100% oxygen.
6. A defibrillator shock is delivered only in the presence of coarse fibrillation:
200 J - 300 J - 360 J. The shocks should follow each other without continuing the CPMR and checking the pulse.
7. On failure: epinephrine (0.1%) IV 1.0 ml (1 mg) per 10 ml isotonic solution
NaCl, after which SLMR is performed and EIT is repeated - 360 J.
8. In case of failure: intravenous stream amiodarone (cordarone) 300 mg per 20 ml of 5% glucose; if amiodarone is unavailable - lidocaine 1.5 mg / kg IV stream. SLMR - EIT (360 J). Search for a removable cause of VF.
9. In case of failure: epinephrine 3.0 mg i.v., sodium bicarbonate 2 ml of a 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. In case of failure: magnesium sulfate 5-10 ml of a 25% solution in / in and / or propranolol 0.1% - 10
ml i.v. SLMR - EIT (360 J).
11. In case of failure: thoracotomy, open heart massage with medication and EIT.
12. If VF is eliminated: assess hemodynamics, determine the nature of the post-conversion rhythm. Continue maintenance infusion
an antiarrhythmic agent that has a positive effect.
Feludabouthtonew tandxukandrdandi am bes patlbsa
Treatment is similar to that for ventricular fibrillation.
Aceandfromtoland I
1. Do not use precordial strikes with established or suspected asystole!
2. Compression of the chest (60-80 per minute).
3. Mechanical ventilation. First, "mouth to mouth", with an Ambu bag. After tracheal intubation, use
100% oxygen.
4. Venipuncture or venous catheterization.
6. Epinephrine (0.1%) in / in 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 does not work. CPMR between injections.
7. Atropine (0.1%) in / in 1.0 ml (1 mg), repeat every 3 minutes. Increase the dose to 3 mg,
if the standard does not give an effect up to a total dose of 0.04 mg / kg. SLMR.
8. Eliminate possible reason asystole (hypoxia, acidosis, hypokalemia and
hyperkalemia, drug overdose, etc.).
9. Aminophylline (2.4%) in / in 10 ml for 1 min. SLMR.
10. External pacing is effective while maintaining myocardial function.
11. Sodium bicarbonate (4%) 1 mmol / kg IV is indicated if asystole occurs against the background of acidosis.
Eletotrohmexandnorsancheztoand I dandssaboutqiandqii am (EMD)
1. Precordial strikes should not be used with established or suspected EMD!
2. Compression of the chest (60-80 per minute).
3. Mechanical ventilation. First, "mouth to mouth", with an Ambu bag. After tracheal intubation, use
100% oxygen.
4. Venipuncture or venous catheterization.
6. Epinephrine (0.1%) in / in 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 does not work. CPMR 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 / h.
9. At low heart rate - atropine 1 mg IV every 3 minutes, bringing to 3 mg.
10. Sodium bicarbonate (4%) 1 mmol / kg IV with the development of acidosis.
11. Electrocardiostimulation.
Whenmechandnore:
Sodium bicarbonate is injected at 1 mmol / kg (2 ml of 4% solution per 1 kg of body weight), and then
0.5 mmol / kg every 7-10 minutes. It is used for prolonged CPMR (10 minutes or more), the development of sudden death against the background of acidosis, hyperkalemia, overdose of tricyclic antidepressants.
With hyperkalemia, the introduction of calcium chloride is indicated at the rate of 20-40 ml 10%
solution in / in.
Perechenb aboutfromnovnoops and daboutpolnandtelbnoops munitsandtoaments:
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
Yingdukandtaboutrs ehffetotandinnaboutfromtand abouttoazanori am munitsicinfromtooh pomouand:
Dlavanth crandteriand etcaboutdolfenori am reandnormacandand:
1) pulse on the carotid arteries;
This indicates the correctness of performing heart massage and maintaining myocardial tone.
2) a change in the color of the skin (pinking);
3) constriction of the pupil (improvement of oxygenation in the midbrain);
4) high "artifact-complexes" on the ECG.
5) restoration of consciousness during resuscitation.
FROMpifromoK andfrompaboutlbthe callnnoh landterandtatrs:
1. Guide to Emergency Medicine. Bagnenko S.F., Vertkin A.L.
Miroshnichenko A.G., Khabutia M.Sh. GEOTAR-Media, 2006
2. First aid in urgent critical conditions. I.F.
Epiphany. St. Petersburg, "Hippocrates", 2003
3. Secrets of emergency care. P.E. Parsons, J.P. Wiener-Kronisch. Moscow,
"MEDpress-inform", 2006
4. Pulmonary cardiac and cerebral resuscitation. F.R. Akhmerov and others Kazan, 2002
5. Intensive therapy for 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. Kiev, 2004
7. Intensive care. 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. Guidelines... Almaty, 2006, 44 p.
No. 883 “On approval of the List of essential (vital) medicines”.
854 "On approval of the Instruction for the formation of the List of essential (vital) medicines."
FROMpifromoK razrababoutthuks:
Head of the Department of Ambulance and Emergency Medical Care, Internal
diseases No. 2 of the Kazakh National Medical University. S. D. Asfendiyarova - Doctor of Medical Sciences, Professor Turlanov K.M. Employees of the Department of Emergency and Emergency Medical Aid, Internal Medicine No. 2 of the Kazakh National Medical University. S. D. Asfendiyarova: Ph.D., associate professor V.P. Vodnev; Candidate of Medical Sciences, Associate Professor Dyusembaev 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 Training of Doctors - Candidate of Medical Sciences, Associate Professor Rakhimbaev R.S. Employees of the Department of Emergency Medicine of the Almaty State Institute for Advanced Training of Doctors: Candidate of Medical Sciences, Associate Professor YY Silachev; Volkova N.V .; Khairulin R.Z .; Sedenko V.A.
* - drugs included in the list of essential (vital) medicines
RCHD (Republican Center for Healthcare Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2007 (Order No. 764)
Instant death (R96.0)
general information
Short description
Death occurs suddenly or within 60 minutes after the onset of symptoms of deterioration in well-being in persons who were previously in a stable state, in the absence of signs of a specific disease.
Sudden death (SC) does not include violent deaths, deaths due to trauma, asphyxiation, drowning and poisoning.
VS can be of cardiogenic or non-cardiogenic origin.
The main cardiac causes of effective circulatory arrest (OEC): ventricular fibrillation, pulseless ventricular tachycardia, complete AV block with idioventricular rhythm, electromechanical dissociation, asystole, severe vascular dystonia with a critical drop in blood pressure.
Ventricular fibrillation
Discoordinated and disintegrated contractions of myocardial fibers, leading to the inability to form cardiac output (CO). It accounts for 60-70% of all OEC cases. VF is more often observed in acute coronary insufficiency, drowning in fresh water, hypothermia, and electric shock.
VF precursors: early, paired and polytopic ventricular extrasystoles.
Pre-fibrillatory forms of VT: alternating and pirouette VT, polymorphic VT.
Pulseless ventricular tachycardia
The incidence of ventricular tachycardia is so high that during diastole, the ventricular cavities are unable to fill with sufficient blood, which leads to a sharp decrease in cardiac output (no pulse) and hence to inadequate blood circulation.
Pulseless ventricular tachycardia is predicted to be equated with ventricular fibrillation.
Asystole
Absence of heartbeats and signs of electrical activity, confirmed in three leads on the ECG.
It accounts for 20-25% of all cases of stopping effective blood circulation.
They are divided into sudden (especially unfavorable in the prognostic plan) and delayed (arising after previous rhythm disturbances).
Electromechanical dissociation (EMD)
Severe suppression of myocardial contractility with a drop in cardiac output and blood pressure, but with persisting cardiac complexes on the ECG.
It accounts for about 10% of all OEC cases.
Primary EMD - the myocardium loses the ability to perform effective contraction in the presence of a source of electrical impulses.
The heart quickly switches to an idioventricular rhythm, which is soon replaced by asystole.
Primary EMD includes:
Acute heart attack myocardium (especially its lower wall);
Condition after repeated, depleting myocardium, episodes of fibrillation, eliminated by CPMR;
End stage of severe heart disease;
Suppression of the myocardium with endotoxins and drugs in case of overdose (beta-blockers, calcium antagonists, tricyclic antidepressants, cardiac glycosides);
Atrial thrombosis, heart tumor.
Secondary EMD - a sharp reduction in cardiac output, not associated with a direct violation of the processes of excitability and myocardial contractility.
Reasons for secondary EMD:
Pericardial tamponade;
Pulmonary embolism;
Tension pneumothorax;
Severe hypovolemia;
Thrombus occlusion of the prosthetic valve.
EMD can be caused by:
1. Sinus bradycardia.
2. Atrioventricular block.
3. Slow idioventricular rhythm.
Mixed forms of EMD
They are noted during the progression of toxic-metabolic processes:
Severe endotoxemia;
Hypoglycemia;
Hypo- and hypercalcemia;
Severe metabolic acidosis.
Protocol code: E-003 "Sudden Death"
Profile: emergency
Stage goal:restoration of the function of all vital systems and organs.
Code (codes) according to ICD-10:
R96 Other sudden death of unknown cause
Ruled out:
Sudden cardiac death, so described (I46.1)
Sudden infant death (R95)
Classification
Sudden death:
1. Cardiogenic - asystole, ventricular fibrillation, pulseless ventricular tachycardia, electromechanical dissociation.
2. Noncardiogenic - asystole, ventricular fibrillation, pulseless ventricular tachycardia, electromechanical dissociation.
Diagnostics
Diagnostic criteria
Signs of a sudden stop of effective blood circulation:
1. Consciousness is absent.
2. The pulsation on the large main arteries is not detected.
3. Breathing is agonal or absent.
4. Pupils are dilated, do not react to light.
5. The skin is pale gray, occasionally with a cyanotic tinge.
List of main diagnostic measures:
Reveal the presence of consciousness;
Check the pulse in both carotid arteries;
Establish the patency of the upper respiratory tract;
Determine the size of the pupils and their response to light (in the course of resuscitation);
Determine the type of stopping effective blood circulation on the defibrillator monitor (ECG) (during resuscitation);
Assess the color of the skin (during the course of resuscitation).
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Treatment
Principles of Cardiopulmonary Resuscitation (CPRM)
The brain experiences a lack of blood flow only for 2-3 minutes - it is for this period of time that there are enough glucose reserves in the brain to ensure energy metabolism during anaerobic glycolysis.
Resuscitation should begin with prosthetics of the heart, the main task is to provide the brain with perfusion!
The main tasks of the first resuscitation aid:
1. Restoration of effective hemodynamics.
2. Restoring breathing.
3. Restoration and correction of brain functions.
4. Prevention of recurrence of the terminal state.
5. Prevention of possible complications.
The main symptoms of a sudden stop of effective blood circulation:
1. Loss of consciousness develops within 8-10 seconds from the moment the blood circulation stops.
2. Convulsions usually appear at the time of loss of consciousness.
3. Absence of pulsation on the large main arteries.
4. Cessation of breathing often occurs later than other symptoms - about 20-30-40 seconds. Sometimes agonal breathing is noted within 1-2 minutes. and more.
5. The dilation of the pupils appears after 30-90 seconds from the beginning of the arrest of blood circulation.
6. Pallor, cyanosis, "marbling" of the skin.
Indications for resuscitation:
1. Absence and severe weakness of pulsation in the carotid (or femoral and brachial) arteries.
2. Lack of breathing.
3. Inadequate breathing (pathological forms of breathing, shallow, rare, fading breathing).
4. Lack of consciousness.
5. Lack of photoreactions and dilated pupils.
Contraindications to resuscitation:
1. Terminal stages of an incurable disease.
2. Significant traumatic brain damage.
3. Early (drying and opacity of the cornea, a symptom of “cat's eye”) and late (cadaveric spots and rigor mortis) signs of biological death.
4. Documented refusal of the patient from resuscitation.
5. Being in a state of clinical death for more than 20 minutes before the arrival of qualified assistance.
What manipulations should not be carried out in order to avoid wasting time:
1. Auscultate the heart.
2. Search for pulsation in the radial artery.
3. To carry out the algorithm - “I feel, I see, I hear”.
4. Determine the corneal, tendon and pharyngeal reflexes.
5. Measure blood pressure.
The main criteria for continuing resuscitation are:
1. The pulse on the carotid arteries, synchronous with chest compressions - indicates the correctness of the cardiac massage and maintenance of tone
Myocardium.
2. Change in the color of the skin (pinking).
3. Constriction of the pupil (improvement of oxygenation in the midbrain).
4. High "artifact-complexes" on the ECG.
5. Recovery of consciousness during resuscitation.
Indicators of the futility of further resuscitation:
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 heart massage" is invalid, because by pushing the sternum 4-5 cm in the anteroposterior direction, it is impossible to squeeze 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.
When compressing the chest, the effect of the thoracic pump is mainly important, i.e. increased intrathoracic pressure during compression and decreased intrathoracic pressure during decompression.
Precardiac beat:
1. The patient is inflicted 4-5 sharp blows with a fist in the zone of the border of the middle and lower third of the sternum from a distance of at least 30 cm.
2. The punch should be strong enough, but not extremely powerful.
3. Indications for precordial strokes are ventricular fibrillation and pulseless ventricular tachycardia.
4. The effectiveness of a stroke for pulseless ventricular tachycardia ranges from 10 to 25%.
5. With ventricular fibrillation, rhythm restoration occurs much less frequently.
6. Used only in the absence of a prepared defibrillator and in patients with reliable circulatory arrest.
7. A precordial blow should not be used instead of electrical defibrillation hearts (EMF).
8. A precordial stroke can translate ventricular tachycardia into asystole, ventricular fibrillation or EMD, respectively, VF - into asystole or EMD.
9. In asystole and EMD, the precordial beat is not used.
Thoracic pump technique:
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 on the right.
2. You can not take your palm from the chest during pauses.
3. Compression is carried out due to the weight of the rescuer's torso.
five . The rate of pressing should be 60-80 per minute.
6. To assess the effectiveness of the thoracic pump, the pulse of the carotid arteries is periodically palpated.
7. Resuscitation is suspended for 5 seconds. by the end of 1 minute and then every 2-3 minutes to assess whether spontaneous breathing and blood circulation have been restored.
8. Resuscitation should not be stopped for more than 5-10 seconds. for additional therapeutic measures and for 25-30 sec. for tracheal intubation.
9. Compression-inspiratory ratio should be 20: 2 for any number of rescuers before tracheal intubation, then 10: 1.
Auxiliary techniques that increase the effect of the thoracic pump:
1. Carrying out the thoracic pump only on a solid base.
2. Raising the legs by 35-40 ° reduces the “functioning” vascular bed at the expense of the lower extremities. This leads to the centralization of blood circulation and an increase in the BCC by 600-700 ml. The inflowing blood accelerates the collapse of the aortic valves in the phase of cessation of chest compressions, thereby improving coronary blood flow.
Trendelenburg's position is dangerous, because it promotes the development of hypoxic cerebral edema.
3. Infusion of plasma substitutes increases venous pressure and increases venous back pressure.
4. Inserted abdominal compression consists of compressing the abdomen after the compression of the chest has ceased. By this action, as it were, blood is squeezed out of the vascular bed of the abdomen. It is performed only in intubated patients because of the danger of regurgitation.
Thoracic pump mechanism:
1. Thoracic pump - compression of the chambers of the heart and lungs by increasing pressure throughout the chest cavity.
2. In the phase of chest compression, all chambers of the heart, coronary arteries and large vessels are compressed.
3. The pressure in the aorta and right atrium is equalized and the coronary circulation stops.
4. With the expansion of the chest, blood flow to the heart improves, a slight pressure gradient is established between the aorta and the right atrium.
5. An increase in pressure in the aortic arch leads to the closure of the semilunar valves, behind which the mouths of the coronary arteries depart, and, consequently, to the restoration of blood flow through the coronary arteries.
Thoracic pump efficiency:
1. Creates a low pressure gradient and low diastolic pressure (the driving force for coronary blood flow) by evenly distributing pressure across the chest cavity structures.
2. The cardiac index is less than 20-25% of the norm, which is lower than that observed in severe cardiogenic shock.
3. The performance of the thoracic pump rapidly decreases, which, even in the absence of severe myocardial damage, leads to the disappearance of efficiency in 30-40 minutes. Increasing hypoxia and mechanical trauma to the heart in a short time lead to a drop in myocardial tone.
4. Provides no more than 5-10% of normal indicators of coronary circulation.
5. Cerebral blood flow during the production of a thoracic pump does not exceed 10-20% of the norm, 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 is able to 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 its tone and becomes flabby.
Effectiveness of open heart massage (OMS):
1. OMS provides greater survival with full recovery of brain function. Most patients recover with recovery of cerebral life even after 2 hours of CPMR.
2. Infection is not a serious problem after thoracotomy, even under non-sterile conditions.
3. Compulsory health insurance provides more adequate cerebral (up to 90% of the norm) and coronary (more than 50% of the norm) blood flow than a thoracic pump. the latter increases intrathoracic pressure, blood pressure and venous pressure.
4. OMS creates a higher arteriovenous perfusion pressure.
5. With thoracotomy, the heart can be directly observed and palpated, which helps to assess the effect of drug therapy and PED in CPMR.
6. An open chest helps to stop intrathoracic bleeding.
7. In case of intra-abdominal bleeding, it allows to temporarily clamp the thoracic aorta above the diaphragm.
8. Mechanical stimulation of the heart, rendered by direct massage, promotes the appearance of myocardial contractions.
Compulsory health insurance should be started as early as possible in cases where an adequately conducted thoracic pump does not restore spontaneous circulation.
Discrediting CHI depends on the delay in its use.
After an unsuccessful long-term production of a thoracic pump, switching to OMC is equivalent to massage a dead heart.
The main indications for direct heart massage:
1. Pericardial tamponade in most cases can be eliminated only by direct emptying of the pericardial cavity from the fluid.
2. Extensive pulmonary thromboembolism.
3. Deep hypothermia - persistent VF occurs. Thoracotomy allows the heart to be warmed with warm saline during direct massage.
4. Penetrating wounds of the chest and abdominal cavity, blunt trauma with clinical picture cardiac arrest.
5. Loss of elasticity of the chest - deformation and rigidity of the chest and spine, displacement of the mediastinum.
6. Unsuccessful attempts (within 3-5 minutes) of external defibrillation (not less than 12 maximum energy discharges).
7. Sudden asystole in young people and ineffectiveness of the thoracic pump.
8. Massive hemothorax.
10. Exudative pleurisy.
11. Rupture of the aortic aneurysm.
12. Severe pulmonary emphysema.
13. Multiple fractures of the ribs, sternum, spine.
Defibrillation success factors:
1. Efficient production of a thoracic pump, ventilation of the lungs with a maximum supply of oxygen in the respiratory mixture.
2. Defibrillation after administration of adrenaline is more effective. Small-wave fibrillation is converted into large-wave fibrillation with the help of adrenaline. Defibrillation with small-wave fibrillation is ineffective and can cause asystole.
3. With the introduction of cardiotonic or antiarrhythmic drugs, the discharge should be applied no earlier than 30-40 seconds after drug administration. Follow the pattern: medication → thoracic pump and ventilator → defibrillation → medication → thoracic pump and ventilator → defibrillation.
4. It is necessary to observe the density and uniformity of pressing the electrodes to the skin - the pressure is about 10 kg.
5. The location of the electrodes should not be close to each other.
6. To overcome the resistance of the chest, averaging 70-80 Ohm, and to receive more energy in the heart, three discharges with increasing energy are applied - 200 J → 300 J → 360 J.
7. The interval between shocks should be minimal only for the time of pulse control or ECG (5-10 sec.).
8. The polarity of the supplied pulse is not critical.
9. The discharge should be performed in the patient's expiratory phase. This reduces lung occlusion of the heart and reduces ohmic resistance by 15-20%, which increases the efficiency of defibrillator discharge.
9. In the event of repeated episodes of atrial fibrillation, apply the same discharge energy that previously had a positive effect.
10. If ECG control is not possible, a “blind” discharge in the first minute of cardiac arrest is quite acceptable.
11. Avoid placing electrodes over an artificial pacemaker.
12. With a significant thickness of the patient's chest wall, the initial EIT discharge should be 300 J, then 360 J and 400 J.
Errors and complications of electro-pulse therapy (EIT):
1. It is impossible to carry out EIT with asystole.
2. Accidental exposure to electrical shocks can be fatal.
3. After EIT (cardioversion), there may be a temporary or permanent disruption in the work of the artificial pacemaker.
4. Do not allow extended breaks in intensive care while preparing the defibrillator for shock.
5. Loose pressing of the electrodes is not allowed.
6. Do not use electrodes without sufficient moisture to their surface.
7. Do not leave tracks (liquid, gel) between the defibrillator electrodes.
8. Do not be distracted during EIT.
9. Do not apply low or overvoltage discharge.
11. It is impossible to provide resuscitation at the time of EIT.
Indications and contraindications for manipulation
The use of an oral airway is not recommended for:
Unrepaired upper airway obstruction;
Oral trauma;
Jaw fracture;
Loose teeth;
Acute bronchospasm.
Complications when using an oral duct:
Bronchospastic reaction;
Vomiting followed by regurgitation;
Laryngospasm;
Worsening airway obstruction.
Indications for tracheal intubation:
1. Inefficiency of ventilation of the lungs by other means.
2. High resistance to air blowing (unrepaired laryngospasm, large weight of the mammary glands with obesity, with 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 mouth, trachea, bronchi.
6. Lack of pharyngeal reflexes.
7. Multiple rib fractures.
8. Transition to open heart massage.
9. The need for long-term mechanical ventilation.
Remember, that:
If a defibrillator is available for VF, shocks are delivered prior to creating an intravenous access.
If peripheral veins are available, catheterization of the great veins is not performed in order to avoid complications (tension pneumothorax, injury of 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 dramatically reduces the effectiveness of the thoracic pump.
Medicines (adrenaline, atropine, lidocaine) can be injected into the endotracheal tube or directly into the trachea by conicopuncture, increasing the dose by 2-3 times and diluting 10-20 ml of isotonic sodium chloride solution, followed by 3-4 forced breaths to spray the drug.
Intracardiac injections "blindly" are not used, due to the risk of damage to the coronary vessels and pathways, the development of hemopericardium and tension pneumothorax, the injection of the drug directly into the myocardium.
Emergency tactics
Treatment principles:
1. The effectiveness of restoring the effective work of the heart depends on the time of the onset of CPMR and on the adequacy of the measures taken.
2. Creation of rigid support under the patient's head and torso improves the efficiency of the chest pump.
3. Raising the legs by 30-40 ° increases the passive return of blood to the heart - increases the preload.
4. Inserted abdominal compression between successive chest compressions increases preload and increases coronary perfusion pressure.
5. Open heart massage after tracheal intubation creates an effective pressure gradient and significantly increases perfusion of the brain and heart, which allows prolonging CPMR up to 2 hours or more with the restoration of biological and social life. It is performed at the prehospital stage only by a trained medical professional!
* - drugs included in the list of essential (vital) medicines.
Information
Sources and Literature
- Protocols for the diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 764 of 28.12.2007)
- 1. Guide to Emergency Medicine. Bagnenko S.F., Vertkin A.L., Miroshnichenko A.G., Khabutia M.Sh. GEOTAR-Media, 2006 2. First aid for critical emergencies. I.F. Epiphany. St. Petersburg, "Hippocrates", 2003. 3. Secrets of emergency care. P.E. Parsons, J.P. Wiener-Kronisch. 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. Intensive care guidelines. Ed. A.I. Treshchinsky and F.S. Glumcher. Kiev, 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 protocols for diagnosis and treatment, taking into account modern requirements. Guidelines. Almaty, 2006, 44 p. 6. Order of the Minister of Health of the Republic of Kazakhstan dated December 22, 2004 No. 883 "On approval of the List of essential (vital) medicines". 7. Order of the Minister of Health of the Republic of Kazakhstan dated November 30, 2005 No. 542 "On amendments and additions to the order of the Ministry of Health of the Republic of Kazakhstan dated December 7, 2004 No. 854" On approval of the Instruction for the formation of the List of essential (vital) medicines. "
Information
Head of the Department of Emergency and Emergency Medical Care, Internal Diseases No. 2, Kazakh National Medical University. S. D. Asfendiyarova - Doctor of Medical Sciences, Professor Turlanov K.M.
Employees of the Department of Emergency and Emergency Medical Aid, Internal Medicine No. 2 of the Kazakh National Medical University. S. D. Asfendiyarova: Ph.D., associate professor V.P. Vodnev; Candidate of Medical Sciences, Associate Professor Dyusembaev 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 Training of Doctors - Candidate of Medical Sciences, Associate Professor Rakhimbaev R.S. Employees of the Department of Emergency Medicine of the Almaty State Institute for Advanced Training of Doctors: Candidate of Medical Sciences, Associate Professor YY Silachev; Volkova N.V .; Khairulin R.Z .; Sedenko V.A.
Attached files
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Terminal state - a critical level of disability with a catastrophic drop in blood pressure, profound disturbances in gas exchange and metabolism. During the provision of surgical care and intensive care, acute development of respiratory and circulatory disorders of extreme degrees with severe, rapidly progressing cerebral hypoxia is possible.
Code for the international classification of diseases ICD-10:
Classification ... Pre-gonal state. Agony. Clinical death. Note. Often, the concept of a terminal state is narrowed down to clinical death. This approach is justified when clinical death develops as a result of sudden cessation of breathing and / or blood circulation under the influence of external or internal factors associated with the damage itself or with iatrogenic causes.
The reasons
Pathogenesis. When dividing shock according to the parameters of systolic blood pressure, it is important to distinguish levels of 70 and 50 mm Hg. With systolic blood pressure above 70 mm Hg. perfusion is vital important organs (level of relative security). At 50 mm Hg. and below, the blood supply to the heart and brain suffers significantly, and the processes of dying begin.
Symptoms (signs)
Clinical picture
Pre-agonal state .. General lethargy .. Impaired consciousness up to stupor or coma .. Hyporeflexia .. Reduction of systolic blood pressure below 50 mm Hg .. Pulse on the peripheral arteries is absent, but palpable on the carotid and femoral arteries.. Severe shortness of breath .. Cyanosis or pallor of the skin.
Agony .. Consciousness is lost (deep coma) .. Pulse and blood pressure are not determined .. Heart sounds are muffled .. Breathing is shallow, agonal.
Clinical death .. Recorded from the moment of complete cessation of breathing and cessation of cardiac activity .. If it is not possible to restore and stabilize vital functions within 5-7 minutes, then death of the most sensitive to hypoxia cells of the cerebral cortex occurs, and then - biological death.
Primary clinical signs clearly detected in the first 10-15 seconds from the moment of blood circulation stoppage .. Sudden loss of consciousness .. Disappearance of the pulse in the main arteries .. Clonic and tonic convulsions.
Secondary clinical signs. They appear in the next 20-60 s and include: .. Dilation of the pupils in the absence of their response to light. The pupils can remain narrow even after a long time after the development of clinical death: ... In case of poisoning with organophosphates ... In case of an overdose of opiates .. Cessation of breathing .. The appearance of an earthy gray, less often cyanotic color of the skin of the face, especially the nasolabial triangle .. Relaxation of the entire voluntary muscles with relaxation of the sphincters ... Involuntary urination ... Involuntary defecation... The combination is considered quite reliable for an almost indisputable diagnosis of clinical death: .. Disappearance of the pulse in the carotid artery .. Dilatation of the pupils without their reaction to light .. Respiratory arrest.
Treatment
TREATMENT
Management tactics. Revitalization (resuscitation) is a complex of emergency measures used to remove a patient from clinical death. The success of resuscitation care is primarily determined by the time factor. The successful removal of a patient from clinical death is possible only when the first person takes measures to revitalize, in front of whom the blood circulation has stopped and consciousness has disappeared.
Measures to remove the patient from the terminal state.
At the 1st stage - measures of the highest urgency .. IVL .. Heart massage.
The scheme of cardiopulmonary resuscitation (scheme ABC, see also Note) .. The goal is to resume the circulation of blood sufficiently saturated with oxygen, primarily in the basins of the cerebral and coronary arteries .. AND (Air ways). Ensuring the patency of the upper respiratory tract ... Tilting the head back with hyperextension of the neck ... Leading forward lower jaw... Using a breathing tube (nasal or oral S-shaped airway) ... Tracheal intubation (in an operating room or intensive care unit) .. IN (Breath). IVL ... By expiratory methods: mouth-to-mouth, mouth-to-nose, mouth-to-air duct ... Various breathing devices: Ambu bag, ventilators .. FROM (Circulation). Maintaining blood circulation ... Outside the operating room - closed heart massage ... In the operating room, especially with an open chest, - open heart massage ... During laparotomy - heart massage through the diaphragm.
At stage 2: .. Cardiopulmonary resuscitation according to the ABC scheme .. Selective drug and infusion treatment .. Purpose: to consolidate the success of the revitalization, if it is achieved and independent blood circulation is restored as a result of the pumping function of the patient's myocardium.
At stage 3, in conditions of sufficiently effective blood circulation with restoration of heart rate and subnormal or even normal systemic blood pressure .. Medicinal .. Transfusion .. Surgical interventions .. Objectives ... To consolidate the achieved success of resuscitation ... To prevent recurrence of circulatory arrest ... To carry out correction early manifestations of the disease of a revitalized organism.
Sequence of actions after diagnosis of clinical death
Free the respiratory tract from possible obstructions.
Change the filling of the right chambers of the heart, especially if the patient has critical blood loss .. Raise the victim's legs 50-70 cm above the level of the heart (if it lies low) .. Transfer to the Trendelenburg position.
Perform 3-4 blows into the patient's lungs.
Check for signs of circulatory failure.
Apply 1-2 precordial punches to the sternum.
Perform 5-6 chest compressions.
The next working rhythm of the resuscitator is 2 blows and 10 compressions for 10-15 minutes.
On the background of ongoing resuscitation, install an infusion system with a crystalloid solution into an accessible peripheral vein.
Inject into the trachea 1-2 mg of epinephrine, diluted in a crystalloid solution, with a puncture below the thyroid cartilage along the midline.
If by this time the patient is intubated, inject 3-4 mg of epinephrine into the endotracheal tube.
Connect an EKG monitor (if there is one nearby) and evaluate the nature of cardiac disorders .. Asystole .. Ventricular fibrillation.
Only with fibrillation - defibrillation (electrical depolarization).
Due to the high incidence of complications (pneumothorax, damage to the coronary arteries, myocardial necrosis after administration of epinephrine or calcium chloride), intracardiac administration of drugs is used as a last reserve measure.
Signs of the effectiveness of resuscitation. Distinct rhythmic tremors, coinciding with the rhythm of cardiac massage, on the carotid, femoral or radial arteries. The skin of the nasolabial triangle turns pink. The pupils become narrower, passing through the stages of anisocoria and deformation. Recovery of spontaneous breathing against the background of a closed heart massage.
Immediate resuscitation success. Recovery of independent heart contractions. Determination of pulsation in the peripheral arteries. Absence of gross changes in the rhythm of heart contractions .. Significant bradycardia .. Extreme tachycardia. Clear definition of the level of systemic blood pressure. Once immediate success has been achieved, you can: .. Complete the necessary emergency surgical intervention.. Transfer the patient to the intensive care unit.
Ultimate resuscitation success. Recovery: .. Spontaneous breathing .. Reflex activity .. Consciousness of the dying. This option for successful resuscitation may not come to light immediately after the measures taken, but after some time.
ICD-10. R57 Shock, not elsewhere classified. R57 Shock, not elsewhere classified. Note... These codes apply only in the absence of an established or suspected diagnosis. In other cases, the condition is coded for the disease that caused it.
Note to ABC diagram: at the hospital stage, stage D is distinguished (Definitive treatment: defibrillation, drugs, diagnostic aids) - specialized resuscitation measures (defibrillation, drug therapy, diagnostic studies [monitoring cardiac activity, detecting rhythm disturbances, etc.]).
Subject table of contents "Convulsive syndrome. Agony. Death. Cessation of cardiac activity.":1. Convulsive syndrome. Convulsions. The causes of seizures. The pathogenesis of seizures. The mechanism of convulsive syndrome.
2. Epilepsy. Epileptic seizure. Status Episode. Causes (etiology) of epileptic seizures. Clinic (signs) of a convulsive seizure.
3. Emergency care for epileptic seizures (convulsions). First aid for status epilepticus (status epilepticus, seizures).
4. Convulsive states with hysteria. Convulsions with hysteria. Causes (etiology) of a hysterical fit. Clinic (signs) of a hysterical seizure (convulsions).
5. Emergency help for hysterical seizures (convulsions). First aid for hysterical convulsions.
7. Agony. Agonal state. Clinic (signs) of an 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. Cessation of cardiac activity. Asystole. Causes (etiology) of asystole.
10. Ventricular fibrillation. Causes (etiology) of ventricular fibrillation. Clinic (signs) of ventricular fibrillation. Myocardial atony.
Resuscitation - the science of revitalization (re - again, animare - revive), which studies the issues of etiology, pathogenesis and treatment of terminal conditions, which mean various pathological processes characterized by syndromes of extreme depression of the vital functions of the organism.
Resuscitation - a set of methods aimed at arresting these syndromes. The survival rate of critically ill victims depends on 3 factors:
1. Early diagnosis of circulatory arrest.
2. Immediate start of the main resuscitation measures.
3. Calling the resuscitation team for specialized resuscitation measures.
Any terminal state, regardless of the root cause, is characterized by a critical level of disorders of the foundations of the body's vital activity: respiration, CVS, metabolism, etc., up to a complete cardiac arrest. In its development, the following stages are distinguished: pre-agonal state, terminal pause (not always noted), agony, clinical and biological death.
Pre-gonal state. Clinic (signs) of a pre-gonal state.
Consciousness is sharply depressed or absent. The skin is pale or cyanotic. BP decreases progressively down to zero, the pulse is absent in the peripheral arteries, but is still preserved in the carotid and femoral arteries. At the initial stages, tachycardia is noted, followed by a transition to bradycardia. Breath quickly goes from tachy to bradyform. Stem reflexes are disturbed, pathological ones may appear. The severity of the condition is rapidly aggravated by increasing oxygen starvation and severe metabolic disorders. The central genesis of the above violations should be emphasized.
Terminal or agonal pause is not always the case. 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 found in clinical or other studies, as well as ill-defined conditions for which no diagnosis is indicated, classified elsewhere.
Signs and symptoms, on the basis of which it is possible to make a fairly definite diagnosis, are classified under other headings. The headings in this class usually include less well-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 the headings of this class can be defined as "unspecified", "no other indication", "unknown etiology" or "transient". In order to establish whether certain symptoms and signs belong to this class or to other sections of the classification, the Alphabetical Index should be used. The remaining subheadings with an 8 are usually provided for other reported symptoms that cannot be classified elsewhere.
Conditions, signs and symptoms classified under R00-R99 include:
- a) cases in which a more accurate diagnosis was not possible even after examining all the available evidence;
- b) cases of appearance of transient symptoms or signs, the causes of which could not be established;
- 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 the final diagnosis is made;
- e) cases when a more accurate diagnosis was not established for any other reason;
- f) some symptoms for which additional information is provided, which in themselves are not of value for the provision of medical care.
Excluded:
- abnormal findings on antenatal examination of the mother (O28.-)
- certain conditions originating in the perinatal period (P00-P96)
This class contains the following blocks:
- R00-R09 Symptoms and signs involving the circulatory and respiratory systems
- R10-R19 Symptoms and signs involving the digestive and abdominal systems
- R20-R23 Symptoms and signs involving the skin and subcutaneous tissue
- R25-R29 Symptoms and signs involving the nervous and musculoskeletal systems
- R30-R39 Symptoms and signs involving the urinary system
- R40-R46 Symptoms and signs involving cognition, perception, emotional state and behavior
- R47-R49 Symptoms and signs involving speech and voice
- R50-R69 Common symptoms and signs
- R70-R79 Abnormal findings on blood tests without diagnosis