Anesthesia PDF

ANESTHESIOLOGY This chapter has been edited by doctor Vakhtang Shoshiashvili MD.Ph.D Anesthesiology (is greek for,,without sensation’’) is the field of medicine about anesthesia and regulation of vital functions of organisms in pre-, intra- and postoperative periods. It may include...

ANESTHESIOLOGY This chapter has been edited by doctor Vakhtang Shoshiashvili MD.Ph.D Anesthesiology (is greek for,,without sensation’’) is the field of medicine about anesthesia and regulation of vital functions of organisms in pre-, intra- and postoperative periods. It may include some or all of analgesia (prevention of pain), paralysis (muscle relaxation), amnesia (loss of memory) and unconsciousness. The American Board of Anesthesiology defines anesthesia as a discipline that is dealing with: Assessment, preparation and consultation of patients for anesthesia It provides relief and prevention of pain during and following surgery or therapeutic and diagnostic procedures Monitoring patients in the perioperative period Diagnosis, treatment of acute and chronic pain The History of Anesthesia 1200 Liulius /Spain/: discovery of ether; 1589 Dela Porta /Italy/: inhalation of ether; 1771 Priestly /English/, Shele /Sweden/: discovery of the oxygen; 1772 Priestly /English/: discovery of nitrous oxide (N2O, gas of fun); 1806 Serturner /Germany/: received the morphium from the opium; 1819 Faraday /English/: narcotic action of ether; 1831 Suberan /France/: discovery of the chloroform; 1842 Long /U.S.A./: excision of the cystic tumor from the neck under the ether narcosis; 1844 Harris Welles /U.S.A./: tooth extraction under the nitrous oxide narcosis; 1845 W. T.G. Morton /U.S.A./: tooth extraction under ether narcosis; 1846 W. T.G. Morton anesthetised the patient (Gilbert Abbott) and surgeon Warren /U.S.A./ made angiogenic tumor excision from the neck under ether narcosis; October 16 is a world anesthesia day 1846 Pirogov /Russia/: mastectomy under ether narcosis; 1847 Y. Simpson /Scotland/: narcosis with chloroform; 1853 A.Woody /Scotland/, C. Pravatz /France/-> invention of the syringe with hollow needle; 1879 Anrep /Russia/: narcotic action of cocaine; 1884 Dr. K. Koller /Austria/ introdused cocaine as an anesthetic for eye surgery; 1894 Med. Students E. A. Codman and H. Cushing develop the first anesthesia record using observed respiratory rate and palpated pulse rate. By 1901, Cushing will add blood pressure measurement by Riva Rocci sphygmomanometry; by 1903, respiratory rate and heart rate as auscultated by precordial stethoscope; 1898 Conducts the first spinal (subarachnoid) anesthetic using cocaine; 1899 August Bier: Spinal (subarachnoidal) anesthesia; 1902 Lemon /France/: electronarcosis; 1904 Einhorn: invention of Novocain (Procaine); 1929 Dr. J. S. Lundy used the intravenous anesthetic thiopental (Pentothal); 1937 Professor Macintosh introduced his curved laryngoscope blade; 1942 Griffith and Johnson /Canada/: using of muscular relaxants, drugs, separated from curare (intocostrin). 1950 Labari and Hugenar: artificial hibernation and neuroplegia; 38  1956 Dr. M. Johnstone /UK/ clinically introduces halothane, the first modern-day brominated general anesthetic. Theories of Narcosis General anesthetics have been widely used in surgery since 1842 when C. Long for the first time used diethyl ether to a patient and performed a painless operation. It has long been belived that general anesthetics exert their effects by modulating the activity of membrane proteins in the neuronal membrane. However, the exact mechanism of this action are still largely unknown althrough much research has been done in this area. There are a number of theories, both outdated and modern, that attempt to explain anesthetic action. Lipoid Theory [Mayer (1889), Overtone (1910)] explains the action of the narcotic drugs with ability to dissolve the fats and lipoids, lecithin and cholesterol in the nervous tissue. Adsorbtional Theory [Traube (1904),Varburg (1914)] explains the action of narcotic drugs with their ability to be absorbed on the surface of membranes of the nervous cells and break the enzymatic processes. Theory of Penetration [Heber (1924)] and Coagulation of the protoplasm [Claud Bernard (1875)] explains the action of narcotic drugs with their ability to enter into the nervous cell and cause the dehydration and coagulation of the protoplasm and induration of the colloid membrane of the cell. Theory of Asphyxia (suffocation) [Ferworn (1912), Mackintosh and Anokhin (1959)] explains the action of the narcotic drugs with breaking of the oxygenation processes. Molecular Theory of Poling (1961) affirms that narcotic drugs are able to form microcrystals in the water, which stops the electric oscillations. Types of Anesthesia 1. General anesthesia (narcosis); 2. Iv/monitored Sedation; 3. Local (topical) 4. regional: (peripheral nerve blocks, neuroaxial anesthesia) General Anesthesia (Narcosis) General anesthesia (narcosis) is condition of central nervous system, put on the brakes and accompanied with reversible loses of consciousness, sensitivity, movement, conditional and some unconditioned reflexes. The term "narcotic" is believed to have been coined by the Greek physician Galen to refer to agents that numb or deaden, causing paralysis or loss of feeling. Inhalational anesthesia: Face mask or laryngeal mask narcosis; Endotracheal (orotracheal, nasotracheal) narcosis; Endobronchial (one-lung) narcosis. ❖ Non-Inhalation anesthesia: 39  Intravenous; Intraosseous; Intramuscular; ❖ Monitored anesthesia care and sedation is used for performing of short manipulations or some surgeries which are performing under local anesthesia Inhalation Anesthesia Means the introduction on of the vapors of the volatile liquid narcotic drugs and air anesthetics into the respiratory tract by inhalation. Inhalational anesthetics which are using for induction of anesthesia must have pleasant odor (halothane, sefoflurane). Inhalational aneshetics are used for the induction and maintenance of general anesthesia as well as sedation. The exact mechanisms by which they act are still unknown. The most widely used inhalational anesthetics are: ♦ Desflurane; ♦ Sevoflurane; ♦ Isoflurane; ♦ Nitrous oxide: Specific characteristics Nitrous oxide Can cause expansion of gas trapped in a cavity; Usually insufficient if used alone → often combined with a more potent inhalational anesthetic to achieve the “second gas effect”; Rapid onset and recovery; Desflurane Very rapid onset and recovery; Pungent odor; irritates airways; Most commonly used inhalational anesthetic; Sevoflurane Rapid onset and recovery; Nonpungent → suitable for induction of anesthesia; Isoflurane Relatively slow onset and recovery; Pungent odor; Methoxyflurane Nephrotoxicity; Can be used as a patient-controlled short-term pain relief; Enflurane Proconvulsive; Medium speed of onset and recovery; Halothane Hepatotoxicity; Medium speed of onset and recovery; Liquid anesthetic remedies for inhalation anesthesia (out of use): 40 1. Ether-Oxygen Anesthesia: (not currently using) According to P. Guedel (1920) there are 4 main clinical stages of the ether narcosis duration: There are four stages of the general anesthesia First stage – analgesia; Second stage – Delirium; Third stage - surgical; Fourth stage – Respiratory arrest, Medullary paralysis. Stage 1: Analgesia stage - In 1954, Artusio distinguished 3 phases of I stage: Beginning of sleep – non complete analgesia and no amnesia; Complete analgesia and partial amnesia; Complete analgesia and amnesia. I stage appears when ether concentration is 2.0-3 vol.% in it’s vapor. In this stage (Rausch-narcosis, torpor) is possible to perform short surgical operations (incision) and manipulations (reposition of the dislocation) - in the combination with muscle relaxants. It is possible to perform big thoracal operations. II Stage: Excitement stage (stage of desinhibition) - Means activation of subcortical structures on the background of the interrupted cortical function. Characteristical signs of this stage are: high arterial pressure, dilated pupils, increased tonus of muscles, some times patient cries, moves and it is very difficult to fix him on the operative table. This stage begins 5-7 min after the starting of narcosis and lasts from 1 up to 12 min. Deeping the narcosis makes the patient quiet and he comes into III stage. III Stage: Surgical stage of anesthesia (stage of narcotic sleep and surgical operation). Cortex and subcortical structures stops their activity, there is no consciousness, no sensitivity to pain, decreased reflexes and muscle tonus. Bulbar function is maintained. There are distinguished 4 planes of the III stage: Plane I - from onset of automatic respiration to cessation of eyeball movements. Eyelid reflex is lost, swallowing reflex disappears, marked eyeball movement may occur but conjunctival reflex is lost at the bottom of the plane Plane II - from cessation of eyeball movements to beginning of paralysis of intercostal muscles. Laryngeal reflex is lost although inflammation of the upper respiratory tract increases reflex irritability, corneal reflex disappears, secretion of tears increases (a useful sign of light anesthesia), respiration is automatic and regular, movement and deep breathing as a response to skin stimulation disappears. Plane III - from beginning to completion of intercostal muscle paralysis. Diaphragmatic respiration persists but there is progressive intercostal paralysis, pupils dilated and light reflex is abolished. The laryngeal reflex lost in plane II can still be initiated by painful stimuli arising from the dilatation of anus or cervix. This was the desired plane for surgery when muscle relaxants were not used. Plane IV - from complete intercostal paralysis to diaphragmatic paralysis (apnea). 41  Stage IV: from stoppage of respiration till death. Anesthetic overdose-caused medullary paralysis with respiratory arrest and vasomotor collapse. Pupils are widely dilated and muscles are relaxed. Gas (vapor) anesthesia Benefits of gas (vapor) anesthesia are: 1. Quick putting on sleep and recovering; 2. No interreactions (they leave the organism without any chemical transformations); 3. Don’t alterate the parenchymatous organs and cells; 4. Safe and simple. Intubation anesthesia Intubation anesthesia means introduction of anesthetic air or vapor into the trachea (endotracheal, intratracheal narcosis) or into the bronchus (endobronchial, intrabraonchal narcosis). The pioneer of this method was Snow in 1852. This method has got following advantages: Possibility to regulate air exchange during the interrupted spontaneous breathing on the background of muscle relaxants (operations on heart, lungs); More precise dosage of drugs; No risk of obstruction of respiratory tract, possibility to remove the mucus, blood, pus from the trachea by the help of the vacuum-suction machine; Reduction of “dead space” during the respiration; Introduction of the anesthetic with the oxygen under the pressure which provides inflation of lungs and good oxygen saturation; It is most controllable and predictable type of narcosis. Indications: operations on the heart, lungs, magistral blood vessels, bilateral pneumothorax, abdominal surgery; when using of the mask makes problems, there is risk of aspiration of blood, mucus (operations on the head, face, neck); it can reduce the dosage of narcotic drugs and is very useful in cases of liver, kidney and metabolic disturbances. Contraindications: diseases of pharynx, larynx, trachea (tuberculosis, purulent processes, tumors), which makes impossible to perform the intubations. Equipment for the Intubation of Trachea: 1. Endotracheal tube (intubation tube) of Hebuner, Murphy, Woodbridge, Gordon-Green, Kiprensky, Koul with stylet (intubation tube guide) and without it. It is preferable to use endotracheal tube with a cuff; 2. Laryngoscopes are two types: a) indirect (curve, Macintosh), b) Direct (Miller). For the adults the length of the endotracheal tube must be not less than 26 cm and it must not reach on 2 cm the bifurcation of trachea. 42  Types of intubation: Orotracheal (blind and under the checking with laryngoscope or video laryngoscope). Preoxygenation (Application of 100% oxygen), head must be thrown back-in Jackson’s position. Intubation of trachea must be done after initial narcosis and injection of muscular relaxants. Adjustment of the vocal cord level using direct or indirect laryngoscopy, Careful passage of the vocal cords with the endotracheal tube. The tip of the tube must be connected to the anesthesia apparatus respiratory hose (tube). Nasotracheal (blindly and under the checking with laryngoscope or bronchoscope)- Adjustment of the vocal cord level using direct or indirect laryngoscopy, Insert the endotracheal tube into one nostril, Advancement into the oropharynx; Supraglottic airway devices: Laryngeal mask, combitube, kingtube; i-gel. Combitube kingtube i-gel Fig 28. 43 Airway complications of tracheal intubation and anesthesia include: 1.Complications during the laryngoscopy and intubation (iatrogenic): Dental and oral cavity injuries; upper airway complications (injuries, bleeding, perforation, spasm); undetected esophageal intubation; Right main bronchus intubation; Can-not intubate, can-not ventilate scenario. 2.Mechanical complications during endotracheal anesthesia: displacement (twist, compression) of the endotracheal tube, or accidental extubation, broncho- and bronchiolospasm; 3. Respiratory complications of the postoperative period (laryngitis, pharyngitis, bronchitis, pneumonia, laryngospasm, unsuccessful extubation respiratory insufficiency, prolonged ventilation). Methods and ways of inhalation anesthesia: Inhalation anesthesia could be performed using the following methods: ♦ Endotracheal intubation; ♦ Endobronchial intubation; ♦ Supraglottice devices (Laryngeal mask, combitube, i-gel, kingtube); ♦ Narcosis (anesthesia) masks (of Schimelsbusch, Giar’s, Ombredan-Sadovenko’s, Phylomaphitsk-Esmarch’s); There are 4 types of breathing circuits Open system: no reservoir and no rebreathing. Semi-open system: has a reservoir but no rebreathing. Semi-closed system: has a reservoir and partial rebreathing. Closed system: has a reservoir and complete rebreathing. Apparatus for inhalation anesthesia Mechanical ventilation: generic term for complete or partial replacement of physiological breathing by a ventilator (respirator). It involves the application of positive pressure, which can be invasive (i.e., in intubated patients) or noninvasive (e.g., CPAP or BiPAP). Positive-pressure ventilation (PPV) is the underlying mechanism of modern mechanical ventilators. Oxygenated air is pushed into the lungs by a mechanical ventilation device that generates a positive pressure gradient. May be administered: invasively (e.g., via endotracheal or tracheostomy tube); noninvasively (e.g., via a secured mask, as in BiPAP or CPAP); 44 Types of noninvasive positive-pressure ventilation: Continuous positive airway pressure (CPAP): The ventilator delivers one constant airway pressure throughout the respiratory cycle (e.g., 5 cm H2O). Bilevel positive airway pressure (BIPAP): The ventilator delivers two pressure levels and cycles between them: Expiratory positive airway pressure and Inspiratory positive airway pressure; Apparatus for inhalation anesthesia, designed for the clinics, contains following parts: 1. System of gas flow meter with enrichment arrangement; 2. Pressure gauges, regulators and ‘’pop-off’’ valves, to monitor gas pressure throughout the system; 3. Vaporizer of volatile anesthetics (agent specific); 4. Respiratory circuit - for gas circulation and carbon dioxide absorber for carbon dioxide reduction (600g works during 6 h). Anesthetic apparates are divided into 2 groups: (a) Universal; (b) Special. Fig 29. Fig. 29 Anaesthetic machine contains: gas supplies pressure gauges. pressure regulators (reducing valves) flowmeters. vaporizers. common gas outlet. a variety of other features, e.g. high-flow oxygen flush, pressure relief valve and oxygen supply failure alarm and suction apparatus. Anesthesia machines /Fig. 29/ makes possible to give anesthesia with liquid and gas anesthetics using semi-open, semi-closed and closed ways circuits. 45  Rules of exploitation of anesthetic apparatus Before starting to work with apparatus it is necessary to check: Gas pressure in the cylinders; Hermetism of all connections; Good repair of gas flow meters; Work of absorber in aim to chaing it in time; Earth of the anesthetic apparatus in aim to avoid effects of static electricity; Fig 30. Dräger AV-E After the finishing of work with anesthetic apparatus it is necessary to: Close the valves of cylinders; All tubes and filters are changing they are not reusing Preoperative Management for the anesthesia 1. Preliminary preparation includes whole preoperative period and is designed for investigation of all systems and correction of existing disturbances (sanation of chronic infection sources, psychotherapy). 2. Preparation before starting of anesthesia means: Fasting: 6 hours before surgery: no milk or solid food, 2 hours before surgery: no drink! If patient is urgent, it is necessary to empty the stomach by the help of a stomach tube; Monitore an Urine outpute by a urine catheter during the operation; Patient should be given a sleeping (sedative) pill before the night. The patient should be given proper premedication (40-60 minutes before operation); After the premedication patient must not leave his bed; The patient must be taken to the operating room on a stretcher; The patient must be placed and fixed on the operating table in the position, assumed for the operation; Fastens apparatus sensors; Monitor blood pressure, pulse, oxygen saturation, temperature; Venipuncture. Adjusts the system for intravenous infusion, after what anesthesia may be started. Stress ulcer prophylaxis with proton pump inhibitors; Thromboprophylaxis with unfractioned heparin before and after surgery, especially for immobile, bedridden patients; Perioperative antibiotic prophylaxis; 46  Complications in Anesthesia and fight against them Complications in anesthesia are divided into 2 groups: 1. Complications during narcosis; 2. Complications of postoperative period. Complications during narcosis: Complications Clinical signs and treatment Prevention 30-50% among postsurgical It’s necessary to remove the Postoperative nausea patients stomach content from the and vomiting (PONV) may be caused by the essential oral cavity with suction- disease (pylorostenosis, intestinal machine and liberation of obstruction) or by the irritation of tracheobronchial branch with the vomiting center with the tracheal catheter, connected narcotic drug. to negative pressure device. Treatment: use an antiemetics; Aspiration of which may cause laryngo- and Empty stomach before stomach content into bronchospasm (bronchiolospasm) and operation. the trachea and lead to the cyanosis, hypoxia and Permanent nasogastric bronchus tachycardia (syndrome of Mendelson). decompression with gastric tube during whole operation in case of peritonitis and bowel obstruction (Ileus). passive passing of the gastric content into the trachea and bronchus during the deep narcosis and relaxation of cardiac Sellick maneuver: cricoid Regurgitation sphincter. Aspiration of stomach content pressure procedure. into the tracheobronchial tract leads to the very grave pneumonia with high mortality. Complications of postoperative period: Complications Clinical signs and treatment Postoperative acute confusional state, is the organically caused decline from a previous delirium baseline mental functioning that develops over a short period of time; Treatment: atypical antipsychotics; Deep vein thrombosis Swelling, dull pain, cyanosis; (DVT) Treatment: Anticoagulation; Thrombectomy; Intraoperatively or within a few hours of surgery -> Temperature > 38°C; Diagnostics: Chest x-ray, blood cultures, urine cultures, and wound Postoperative fever cultures are indicated if nosocomial infections are suspected; (infectious or Treatment: Acetaminophen; Patients who are hemodynamically noninfectious) unstable: broad-spectrum antibiotic therapy; 47 Postoperative ileus Nausea and vomiting, Abdominal distention, Absence of bowel sounds on auscultation; Treatment: konservativ therapy; Prevention: Early mobilization, early initiation of enteral feeding, Nasogastric tube only if abdominal distention is prominent; Respiratory Complications of anesthesia Complications Clinical signs Treatment Hypoventilation Respiratory depression due to excess Oxygen administration; Mask opioids or narcotics; ventilation; Bronchospasm Airway obstruction Spasmolytics; Tachypnoe Increased spontaneous breathing Optimize pain therapy; frequency due to pain; mechanical (foreign bodies, back-tongue In this situation it is necessary: retraction) and central (depression of the Asphyxia To stop to give narcotic respiratory center with respiratory drug; standstill-apnea, arrest of respiration) reasons. To start the artificial pulmonary ventilation it is necessary to remove mechanical (artificial respiration) reasons (in some cases it is indicated to giving fresh air and perform tracheotomy); oxygen; To administer Prophylaxis of laryngospasm and intravenously respiration bronchorrhea includes also injection of 0.5- center stimulators 1.0 ml of 0.1% sol. of Atropine. (respiration analeptic Central asphyxia (paralysis of respiratory drugs) - Lobelin or center) is most dangerous complication. Cititon. Infusion of cardiac Clinical signs: cyanosis, dilated pupils (no remedies, 4% sol. of reaction on light), arrest of respiration, sodium bicarbonate. dark blood. 48  Fig 31. a. Air-ways; b. Laryngoscope 5. Artificial lung ventilation “from mouth into nose”; 6. Artificial lung ventilation with the aid of Ambou breathing sac (12 inspirations per minute); 7. Artificial lung ventilation by supraglottic devices (laryngeal mask, combitube, king tube) 8. Artificial lung ventilation through the endotracheal tube. Respiratory sac may be used for the performing of artificial pulmonary ventilation during the narcosis. 9. Surgical airways (cricothyreoidotomy, tracheostomy) Cardiovascular Complications of the anesthesia 1.Blood pressure depression (arterial hypotension) may be happen in period of putting on sleep or during the anesthesia and may be caused by the action of the anesthetic on the heart and vasomotor center (overdosage of anesthetic) or low rate of circulating blood volume; 2.Cardiac rhythm disturbance (cardiac arrhythmia) ventricular tachycardia, extrasystole, ventricular fibrillation may be caused with following reasons: O2 insufficiency (hypoxia) and hypercapnia during delayed intubation and inadequate artificial pulmonary ventilation; overdosage of narcotic drugs; introduction of the epinephrine (adrenaline) after the using of fluothane, which increases sensitivity to catecholamines. Monitoring of ECG during anesthesia, makes the treatment correct, following its etiologic nature (arresting of hypoxia, lowing of narcotic drug dosage, preparations of quinine). 3.Miocardial ischemia and infarction ; 49 4.Cardiac arrest, heart failure (syncope) is the most dangerous complication and may be happen suddenly. Clinical symptoms of it are: ▪ Pulse in carotid and femoral arteries are not felt; ▪ Heart sounds can’t be heard; ▪ Respiratory standstill, arrest (apnea); ▪ Cyanotic skin; ▪ Dilated pupils; ▪ Muscles relaxation; ▪ Wound stops to bleed. The reasons of cardiac arrest are: ❖ Narcotic drug overdosage with paralysis of cerebral vasomotoric centers, nervous apparatus of myocardium; ❖ Reflectory cardiac arrest may be caused by irritation of n. vagus as during the anesthesia, so at the very beginning of the narcosis as the result of reflex, coming from the mucosa of respiratory ways; ❖ Oxygen insufficiency (hypoxia) in myocardium. it is necessary to stop giving the ether and start urgent cardiac massage and artificial pulmonary ventilation in the case of cardiac arrest. Postanesthesia Complications Prophylaxis: early activation of the patient in the bed, exercise (therapy) vibration while doing massage, tapping massage, Pneumonia, atelectasis, respirationexercise (blowing into the special apparatus-designed bronchitis for positive pressure at the moment of end of expiration), removal of sputum and mucus, antibioticotherapy. Is a result of toxic action of anesthetics on the nervous apparatus Cardiac insufficiency of the heart; Prophylaxis: introduction of cardiac drugs, EKG-monitoring, desintoxication, treatment of electrolyte imbalance. Risk of lipoid dystrophy of the today is reduced with decreased dosage of the ether on the liver background of muscle relaxants. Transitory oliguria and increased density of urine, leuco- and erythrocyturia disappears, albuminuria: if the kidneys were in good condition before narcosis. may be alter and cause acidosis (headache, nausea, vomiting, Metabolism of carbohydrates sleeplessness, delirium, coma); Prophylaxis and treatment of this condition includes infusion of glucose sol. with insulin, 4% sodium bicarbonate or Trisamin. Disturbance of water and may be caused with profuse sweat (perspiration), vomiting, electrolyte exchange diarrhea. It is necessary to determine content of K+, Na+, Ca²+, Mg²+, Clin the blood and use such blood substituents (hemocorrectors) as are: isotonic (0.9%) solution of sodium chloride, Ringer-Locke’s solution (Ringer-Lactate, Lactasol); 50  Paralysis of peripheral nerves is a result of mechanical trauma of nervous trunks (radial, ulnar, median) during operation and very rare- result of toxic action of the ether on the cerebral centers. Usually this complication passes spontaneously, but some time needs prolonged treatment. Cerebral edema is the result of deep hypoxia. Treatment: dehydratation, hyperventilation, local hypothermia. Myorelaxation, Muscular relaxants, Drugs, separated from Curare Curare was the poison of the South American Indians, which had been used by them for the poisoning of arrows. Victims died with muscle paralysis and asphyxia. The first scientific work about Curare belongs to Cloud Bernard (1851) and Pelikan (1857). Alkaloid Tubocurarin-chloride was separated by King in 1935. All modern myorelaxants act on the neuromuscular impulse transmission unit (synapse) and are divided on 2 groups: a. nondepolarizing myorelaxants block the work of synapse, acetylcholine can’t act, as depolarization is impossible because of block of postsynaptic membrane; b. depolarizing myorelaxants act as acetylcholine, cause the depolarization, but more prolonged and makes impossible repolarization. Using of the muscular relaxants has following advantages: reduces the dose of basic anesthesia; makes possible to stop the spontaneous breathing and take the patient on the artificial pulmonary ventilation, when bilateral pneumothorax exists; for arresting of cramps in case of tetanus; makes easier reposition of dislocations and fractures; enhances of anesthetic and antischock action of drugs. Antidepolarizing (nondepolarizing) muscle relaxants: Binding to acetylcholine receptor (n-choline receptor) on the motor endplate → competitive antagonism → no depolarization (non-depolarization block); Mivacurium A short-acting non-depolarizing neuromuscular blocking agent; Onset of action 2-4 min, duration of action 15-25 min; used to facilitate tracheal intubation and to relax skeletal Rocuronium muscles during surgery. Onset of action 1-3 min, duration of action 60-90 min; Atracurium A non-depolarizing neuromuscular blocker used to facilitate endotracheal intubation and relax skeletal muscles during surgery. Onset of action 2-3 min, duration of action 45-60 min; Cisatracurium A skeletal muscle relaxant used to facilitate tracheal intubation, muscle relaxation in surgery, or mechanical ventilation. Onset of action 3-5 min, duration of action 45-60 min; Vecuronium relax muscles or as an adjunct in general anesthesia during surgical procedures; Onset of action 2-3 min, duration of action 60-90 min; 51  Chloride of Tubocurarin is the relaxant of prolonged action (30-45 min); i.v. Injection of 15- (Tubarin, Tubocuran) 20 mg causes the myerelaxation, 30 mg – apnea. Antagonist of Tubocurarin is Proserin. Use of Tubocurarin is contraindicated in case of kidney insufficiency; Anatruxonium dosage 0.16 mg/kg. relaxation begins 2-5 min after administration. Antagonist is Proserin; Cyclobutonium Dosage - 0.25 mg/kg. Action starts after 3-5 min and lasts 1-3 hours; contraindication - myasthenia; antagonist drug - Proserin; Dioxonium drug with mixed action: at the beginning causes the depolarization and then antidepolarization. Action starts 1.5-3.0 min after and lasts 20-40 min. Dosage - 0.04-0.05 mg/kg; Proserin reduces its action; Complications: recurarization means repeatedly respiratory standstill (apnea) after the beginning of the spontaneous respiration after the finishing of the anesthesia. It may be happened during 24 hours after the drug administration; prophylaxis - at the moment of finishing of the operation it is preferable to administrate 1.0 ml of 0.5% sol. of Proserin, which must be used together with Atropine - 2.5-5 mg in aim to avoid irritation of parasympathetic nervous system (excitement, vomiting, collapse). Depolarizing myorelaxants: Succinylcholin is known as Listhenon, Myorelaxin, Curacite, Anektin, Scolin, Ditilin and is only one depolarizing muscle relaxant): Binding to acetylcholine receptor on the motor end plate → depolarization (muscle tremors) → lack of degradation by acetylcholinesterase → permanent depolarization with lack of excitability (depolarization block). Onset of action 40-60 sec. Duration of action 5-10 min. It is possible to use it in case of renal insufficiency, myasthenia, bronchial asthma. Warning: Risk of cardiac arrest, hyperkalemia, rhabdomyolysis, intracranial and intraocular hypertension, muscle pain, malignant hyperthermia. Complications: 1. Prolonged apnea in case of congenital insufficiency of pseudocholinestherase in the patient’s organism, weakness, liver failure, anemia, disproteinemia. Treatment of this condition is transfusion of fresh conserved blood which contains pseudocholinestherasa, which destroys Succinylcholin. Application of Proserin is prohibited as it decreases activity of cholinesterase. 2. Double block- when the relaxant with depolarizing action acquires the characteristics of antidepolarizing relaxants, after the few fractional administrations of Ditilin, or after the simultaneous using of relaxants of both groups. The first complication appears after the first injection, second complication- after the few injections. 52  Noninhalation anesthesia All types of noninhalation anesthesia are used as initial or basal narcosis when combined anesthesia is given. To the noninhalation anesthesia belongs following types of anesthesia: 1. Intravenous; 2. Intraosseous /fig. 32/; 3. Intramuscular; 4. Rectal; Fig 32. Intraosseus anesthesia 1. Total Intravenous Anesthesia (TIVA) Intravenous anesthetics are a group of fast-acting compounds that are used to induce a state of impaired awareness or complete sedation. Commonly used intravenous anesthetics include propofol, etomidate, ketamine, and barbiturates (e.g., thiopental). Patient’s preparation for the i.v. anesthesia is same as for inhalation anesthesia. Contraindications: Known allergy to anesthetic Techniques of i.v. anesthesia: i.v. administration of i.v. Anesthetics must be slowly, in order to avoid respiratory standstill. Typically for TIVA is using propofol and remifentanyl infusion possible also to use fractional or drip i.v. infusion (3-5ml for each time) if the operation lasts 1.5-2 h. I.v. anesthesia has no excitement (disinhibition) stage. Propofol/remifentany TIVA is characterised with quick recovery. Complications are rare and includes: heart failure, tachycardia, nausea, vomiting (after the recover), dizziness (giddiness, vertigo) and marked, prolonged excitement. i.v. anesthetics Effects, side effects, Indications Propofol (1-2% sol.) - agonist on GABAA receptors and sodium channels of the reticular formation; - Hypnotic effect, bronchodilatation, decreasing intracranial pressure; - Hypotension, respiratory depression; 53  - Standard for anesthesia induction; Etomidate - Acts on the GABA receptors in the reticular formation; - Hypnotic effect, decreasing intracranial pressure; - no effect on the cardiovascular system; no effect on respiration; - Transient acute adrenal insufficiency; myoclonus; - Anesthesia for patients with hemodynamic instability Ketamine - NMDA receptor antagonist; - Dissociative anesthesia: unique anesthetic state with analgesia, intact spontaneous breathing, amnesia, and no complete loss of consciousness; - Sympathomimetic effects: ↑ blood pressure, ↑ heart rate, ↑ cardiac output; - Ideal emergency anesthetic for polytrauma patients and other patients with risk of hypotension; - 2. i.m. anesthesia: it is necessary to administer i.m. 5mg/kg Ketamine is good option for pediatric anesthesia. Neuroleptanalgesia (NLA) This method was introduces in the medical practice by De Castro and Mundeller in 1959 and provides looseness of pain sensation (analgesia) and decreased psychical activity (ataraxia) by the help of very strong narcotic analgesics - Phentanil and neuroleptic - Droperidole. The combined preparation of those 2 drugs is named - Thalamonal. Today NLA is rarely using due to the side effects of neuroleptics. Artificial Controlled Hypotension It is necessary to have “dry” operation area (field) and prevent profuse bleeding during the operation on the brain, major blood vessels in case of hypertonic disease. Controlled hypotension is reached with the administration of ganglioblocker drugs (Arphonad, Higronium, Hexametonium). Balansed general Anesthesia Is a cornerstone of the modern anesthesiology, which has no contraindications. Common scheme of this type of anesthesia is - For induction: Hypnotic (propofol), for analgesia opioid (fentanyl or its analogues) an muscle relaxant (depolarising or non-depolarising). After tracheal intubation anestehsia is maintaining by inhalation anesthetics (isoflurane, sevoflurane or desflurane), also propofol can be added as hypnotic (not usual) For muscle relaxation – non-depolarising muscle relaxants and for analgesia – fentanyle or oits analogues. For recovery, delivery all anesthesia medications (hypnotics, opiods, relaxants) are stoopped and patient must became allert, and active. 54  Local (regional) Anesthesia Indications: are determined with its advantages: 1. Prolonged preoperative preparation of patient isn’t necessary; 2. It may be used with success, when general anesthesia can be harmful; 3. Patient doesn’t need intensive supervision, as after general anesthesia and can be discharged in surgical ward earlier; 4. It is useful in outpatient’s department; 5. It may be used with favorable results, when patient is very old, week, with respiratory and cardiovascular insufficiency when intubation narcosis may be more dangerous for patient’s life, than surgical intervention. Contraindications: 1. Intolerance (individual) of the anesthetic drugs, as a result of individual hypersensitivity; 2. Psychological (mental) disturbance – excitement; 3. Local presence of inflammatory process and scars, which makes impossible to perform infiltration anesthesia; 4. Continuing internal hemorrhage which needs the urgent operation in aim to control the bleeding. It is necessary to explain to the patient, that consciousness, tactile and deep sensitivity, but not pain will be maintained during the operation. Before the operation injection of Promedol, Suprastin (Dimedrol), Maxigan (Baralgin) and Droperidol must be done in aim to reduce neuropsychological stress. Einhorn in 1905 introduced the Procaine (Novocain) into the surgical practice. A.Vishnewsky improved the anesthetic liquid: Novocain - 2.5g, sodium chloride - 5g, potassium chloride - 0.075g, calcium chloride - 0.125g, distilled water - 1000ml and 1:100 - diluted adrenaline (epinephrine) - 2ml. Duration of local anesthesia is up to 1.5h. Periods of action of local anesthetics are divided on following parts: 1. Administration of the local anesthesia preparation; 2. Period of waiting lasts 5-6 min in case of infiltration anesthesia by A. Vishnewsky and 10 min in case of conductive anesthesia. During this period anesthetic drug acts on the receptors and nervous trunks; 3. Period of complete anesthesia lasts 1-2h.It is necessary to repeat injections if this time in not enough to perform the operation. Local anesthesia provides loss of sense of pain but not reflexes and motor activity in case if the thick nervous trunks and plexus; 4. Period of restoration of sensitivity: pain, which occurs in this period must be arrested by means of narcotic analgesics, cold (local hypothermia) and elevated position of the operated region. Complications of local anesthesia includes poisoning with preparation for local anesthesia, allergy, broncho- and laryngospasm are more frequent if Cocaine, Dicain, Sovcain were used. 3 stages of poisoning with local anesthesia remedies are distinguished: 55  I stage (light) - typical symptoms are: cold sweat, weakness, dizziness, tachycardia with weak pulse, nausea, dispnea, dilatation of pupils; II stage (moderate) - motoric excitement, hallucinations, fear, delirium, tremor, cramps; III stage (grave) - small, rapid, arrhythmic, sometimes slow (30 per min) pulse, dilation of pupil’s, interrupted respiration, loss of consciousness, paralysis of breathing center and death. Treatment: Oxygenation, sodium bromide i.v., chloral hydrate per rectum, artificial lung ventilation, transfusion of blood (after exfussion) and blood substituents. Methods of Local Anesthesia Classification: by coating; by irrigation; by infiltration; Regional; A. Conductive anesthesia: a. Of neural trunks (Ultrasound-guided peripheral nerve block). b. Of neural plexus; c. Of neural nodules (paravertebral); d. Spinal (subarachnoidal); e. Peridural (epidural); f. Intravenous; g. Intra-arterial; h. Intraosseous; 1. Anesthesia by coating (2. irrigation) is widely accepted in ophthalmology, urology, otorhino- laryngology by the help of 1-10% sol. of Cocaine, Novocain (5-10%), Dicain (0.25-3%), Sovcain (0.1%). For the broncho- and esophagoscopy is used Dicain (0.5%) or Novocain (5-10%); 3. Infiltration anesthesia was introduced by Orlov (1887). Recklus (1889) and Schleich (1891). In the very beginning of infiltration anesthesia it is necessary to make “intradermal bleb of local anesthesia“ (cutis limonarium or cutis anserina) with thin needle in aim to make anesthesia of the skin along the whole length of the incision /fig. 33/. Then subcutaneous fatty tissue, fascia, aponeurosis, muscles and other tissues (more deep layers) must be infiltrated. It is very useful to infiltrate margins of operative area (field) to form rhomb (rhomboid anesthesia) or make circular ”case “ anesthesia of the extremity (when limb amputation is designed). A. Vishnewsky worked Fig 33. Intradermal bleb of local anesthesia 56 was injected under the pressure along fascias and muscles cases. Infiltration must be performed “layer by layer” and surgeon must use scalpel and syringe with Novocain in turn (method of “tight creeper infiltrate”). The positive side of this method is low toxicity of the anesthetic and absence of reabsorptive action (as big amount of Novocain is poured out after the incision), easy dissection of a tissues after hydropreparation with solution of anesthetic. Fig 34. Conductive anesthesia of the fingers by Oberst 4.Regional anesthesia: A. Conductive anesthesia is based on interruption of nervous impulse passing through the nervous fiber with the help of intra- or perineural injection of anesthetic solutions (usually 1-2% of Novocain). It is widely used in the stomatological practice (extraction of tooth) during thoracic operations (symphatic trunk, vagus nerve, celiac nerve blocking) for the operations on fingers. Conductive anesthesia of the fingers by Oberst-Lukashevich: at the basis of the finger tourniquet must be applied and after that into both lateral sides 2-3ml of 1-2% solution of Novocain must be injected deeply up to the bone /fig. 34/. Fig 35. Intercostal anesthesia 5. Intercostal anesthesia is used against the pain in case of ribs fracture. After the anesthesia of the skin, tip of the needle must be inserted to the fractured rib on few centimetres from the site of fracture in the direction to the backbone (spine). 3- 5ml of 1-2% sol. of Novocain must be injected perineurally under the lower margin of the rib, after that with the same needle 2- 3ml 1-2% sol. of Novocain must be injected to the upper border of the rib /fig. 35/. 6. Brachial plexus anesthesia can be performed with interscalene, supraclavicular , infraclavicular and axi- llary approaches, by the using of landmark technique or nerve stimulatory and ultrasound guidance. (landmark technique, 1928) Fig 36. Brachial plexus anesthesia Fig 37. Lumbar (paranephral) block 57  Fig 38. Intravenous anesthesia 8. Intravenous anesthesia. Indications: operations on the limbs (surgical treatment of the wounds, reposition of the fractured fragments and dislocations, arthrotomy). Method is based on the local diffusion and action of Novocain, injected into the vein of the extremity, isolated with the applying of tourniquet from other parts of body. With the help of the venepunction or venesection 150-200ml (for the upper extremity) or 200-250ml (for the lower extremity) of 0.25% Novocain sol. must be injected into the superficial fore-arm or cubital veins or v. saphena magna or v.saphena parva. Arterial blood supply must be renewed after the operation by loosening and removing of tourniquet (not too quickly) /fig. 38/; Spinal (subarachnoid) Anesthesia Spinal anesthesia belongs to the conductive type of anesthesia. It was worked out in 1899 by August Bier. This method is based on the injection of Bupivacaine 0.5% (hyperbaric, hypobaric or isobaric solution)) into the subarachnoid space by the help of special needle and its action on the roots of the spinal cord. Indications of spinal anesthesia : Spinal anesthesia is indicated for surgical procedures involving the lower abdominal area, perineum, and lower extremities Contraindications of spinal anesthesia: Infection at the level of needle placement Mitral and aortic stenosis (lack of compensation after sympathetic block) Coagulation abnormalities (INR>1.5, aPTT>40s, Platelets Agonal state; ->Clinical death. Collapse: is blood pressure fall as a result of sudden cardiac weakness, or decreased tonus of blood vessels. Types of Collapse: ▪ Hemorrhagic; ▪ Hypoxemic (hypoxic); ▪ Septic; ▪ Carcinogenic collapse/shock; ▪ Orthostatic. ▪ Pancreatic collapse/shock; ▪ Semeran-Siemianowsky’s paroxysmal collapse; ▪ Toxic; ▪ Circulatory. 62  Clinical signs of collapse: sudden pallor, small and rapid (sometimes-thread-like) pulse, low blood pressure, shallow and infrequent breathing, cool sweat, cool extremities, low temperature of the body, consciousness is confused or lost (in case of shock it is retained). Clinical signs of collapse and shock are very similar, but in case of collapse initial alterations are in cardiovascular system and in the nervous system in case of shock. Treatment: includes removal of reasons, which caused cardiovascular weakness (blood loss, intoxication), blood transfusion, infusion of hemocorrectors, Coffein, Cordiamin, Strophantin; Syncope, Faint is the sudden losing of consciousness for a short time, caused with transitory ischemia of the brain as a reason of hypoxemia or decreased blood supply of the brain. If the patient has fainted, doctor must be sure that there is no injury of the skull. It is necessary to put the patient down, unbutton the clothes, place the patient’s head lower than the rest of the body, elevate the legs, let him inhale ammonia spirit, give him strong tea or coffee with cognac, injections of Coffein, Cordiamin. Shock: the term “shock” was introduced in medical practice in 1737 by French surgeon Anri Le Dran. P.Savenko determined shock as a grave alteration of central nervous system in 1834. N. Pirogov made classic description of clinical picture of shock and distinguished two phases of shock: a) Erectile b) Torpid. Shock is defined as a critical condition of the organism with marked depression of functions of central nervous system, cardiovascular insufficiency, disturbance of microcirculation and hypoxia of tissues. It is polietiologic pathology. Classification of Shock: 1. Traumatic shock: Mechanical traumas (wounds, fractures of the bones, compression of the tissues); Burn (thermal, chemical); Cold; Electric. 2. Hemorrhagic (hypovolemic) shock caused by: a) Bleeding (hemorrhage) and acute blood loss; b) Acute disturbance of the water balance of the organismdehydration (exicosis). 3. Septic (infective-toxic) - as a result of grave purulent processes; 4. Anaphylactic shock; 5. Cardiogenic shock (myocardial infarction, acute cardiac insufficiency). Most important starting mechanisms of the shock are: vasodilatation, hypovolemia, decrease heart output and microcirculatory disturbance, aggregation of erythrocytes as “coin pillar”, increase blood viscosity, intracapillary blood clotting (microthrombosis of capillaries), disturbances of acid-base balance (metabolic acidosis) increased blood plasma creatinine and blood serum urea nitrogen, decreased synthesis of corticosteroids, blood circulation disturbance in visceral organs (shocked lung, kidney, liver). So, principal, initial pathogenetic factors of the shock are: decreased volume of circulating blood (hemorrhagic, hypovolemic shock) -> Vasodilatation-increased volume of blood vessel’s, bed redistribution of blood (anaphylactic, septic shock) -> Disturbance of cardiac activity with decreased cardiac output. All those factors cause capillary circulation damage, hypoxia and metabolic disturbances in tissues and organs. Factors, which promote the development of shock: avitaminosis, tuberculosis, hypo- and dysproteinemia, cachexia, anemia, cold, nervous stress, incomplete transport immobilization and anesthesia during operation, ionizing radiation. 63 Theories of Etiopathogenesis of shock: 1. Toxic (Quenu); 2. Vasomotor (Crile); 3. Acapnic (Henderson); 4. Blood and plasma loss (Blelock); 5. Sympathetic-adrenal depletion (H.Selye); 6. Neuro-reflector (I.Pavlov). Assessment of the phases and the degree of the shock: phases of the shock (according to N. Pirogov): 1. Erectile phase of the shock is very short, occurs at once after the trauma and is characterized with the hypertonus of sympatheticadrenal system (skin integument and visible mucous membranes are pale, pulse-rapid, blood pressure-elevated, patient is excited, cries, asks to help him); 2. Torpid phase patient is depressed, low blood pressure thread-like pulse. Shock of I degree: consciousness is retained (a little depressed), systolic blood pressure is decreased down to 90mmHg, pulse is a little, rapid, skin is pale, muscular tremor, circulation restores slowly after the compression and decompression of the nail. Shock of II degree: patient is depressed, pallor, viscous sweat, cyanosis of the nails is marked (circulation restores very slowly) systolic blood pressure 90-70mm.Hg, pulse-weak, rapid, 110-120 per min, central venous pressure is decreased, shallow breathing. Shock of III degree: patient’s condition is grave, he is adynamic, very depressed, clouded consciousness, no reaction on pain, skin-cold, pale with cyanotic color, breathing is accelerated, shallow, sometimes-infrequent (bradipnea), pulse 130-140, systolic blood pressure 70-50mm Hg, central venous pressure 0 or negative, no excretion of urine (anuria). Shock of IV degree: means the preagonal state, arterial blood pressure less, than 50 mm Hg, skin and mucosa arepale, pulse - rapid, weak, breathing superficial. Monitoring of the patients with shock: it is necessary to determine general condition of the patient, pulse, arterial blood pressure, respiration (frequency, depth, rhythm), diuresis, central venous pressure, pO2 and pCO2 and Algover’s index of shock (correlation of pulse and arterial blood pressure). 64 Normally Algover’s index is equal: 60 pulse beat/min = 0.5 120 mmHg Conversion from the early stage to the marked shock: 100 pulse beats/min = 1.0 100 mm Hg Developed shock 120 pulse beats/min = 1.5 80 mm Hg As high is above-mentioned index, as worse is prognosis. It is possible to calculate the blood loss, following to this index. If Algover’s index is 1, blood loss compose 20-30% of volume of circulating blood. If Algover’s index is more than 1, blood loss reaches 30-50% of volume of circulating blood. Treatment of the Shock The first aid (before hospitalization) includes: 1. Control of bleeding; 2. Adequate pulmonary ventilation; 3. Anesthesia; 4. Transfusion and infusion therapy; 5. Immobilization in case of fractures; 6. Transportation in adequate region The pathogenic treatment of shock: 1.The removal of the reason, caused the shock; 2.Restoration of blood vessel’s tonus; 3.Substitution of the circulatory blood volume; 4.Normalization of capillary circulation (microcirculation); 5.Removal of hypoxemia and hypoxia of tissues; 6.Treatment of renal, hepatic, respiratory and other complications of shock; 7.Recovery of metabolic disturbances. For correction of hypovolemia, it is preferable to use hemocorrectors (blood substitute liquids) with homodynamic (anti shock) action Macrodex (Polyglukin), Rheomacrodex (Rheopoliglucin), Gelofusin (Gelatinol), crystalloid solutions are also useful, Trisamin (trisbupher) or 4% solution of sodium bicarbonate for the removal of acidosis. As peripheral blood circulation is damaged, all preparations must be administrated intravenously, not i.m. Morphine hydrochloride, Omnopon (Pantopon), Promedol (trimeperidine hydrochloride), Phentanil, Pentazocin (Lexir) may be used for the anesthesia, with monitoring of respiration (narcotic analgesics can decrease the respiratory center activity). Trancvilizators: Seduxen (diazepam) 0.5%- 1-2 ml is also useful. 65  airway tubes must be used for adequate respiration, if patient is in unconsciousness condition. Good transport immobilization, local anesthesia, Novocain-block (vago-sympathetic, paranephral, paravertebral and intercostal) must be discussed as prophylaxis of shock. For the restoration of blood vessel's tonus, dopamine (Dobutrex) sol. is very useful, so as glucocorticoid hormones (prednizollone, hydrocortisone). Hemorrhagic Shock: see “Bleeding”; Burns Shock: see “Burns”; Anaphylactic Shock is based on the immediate reaction antigen - antibody, which happens in the organism with allergic (hypersensitive) state. It is very frequent after the infusion of protein-containing blood substitute liquids, immune drugs, antibiotics and iodine-containing antiseptics among the patients with bronchial asthma, drug-induced dermatitis. Types of anaphylactic shock are: 1. Cardiovascular type with tachycardia, cardiac arrhythmia, atrial and ventricular fibrillation, hypotension and acute cardiac insufficiency; 2. Respiratory type: respiratory insufficiency, dyspnea (shortness of breath, breathlessness), cyanosis, whistling (stridor) breathing with moist râles in the lungs, swelling of the lungs, larynx and epiglottis; 3. Cerebral type: with hypoxia, swelling of brain, coma with local signs of CNS alteration. Anaphylactic shock is divided in to 4 stages following its gravity. I stage (slight) itching of the skin, rashes, headache and vertigo; II stage (moderate) Quincke’s swelling, tachycardia, hypotension, increased Algover’s index joints to the abovementioned symptoms; III stage (grave) unconsciousness, acute cardiovascular and respiratory insufficiency; IV stage (very grave): Unconsciousness, grave cardiovascular insufficiency (no pulse on periphery, low blood pressure). Treatment of the anaphylactic shock: Restoration of circulation (Ephedrine, Adrenaline, Noradrenalin, Dopamine); Substitution of circulation blood mass (colloid solutions, Rheomacrodex, Gelofusin); Antihistamine drugs (Dimedrol, Suprastin, Tavegil); Glucocorticoids (Dexamethazon, Prednizollon, Hydrocortisone); Calcium chloride or gluconate (10% -10.0 ml); Inactivation of antigen (e.g. inactivation of the penicillin wit penicillinaza or β-lactamaza). Prophylaxis: careful collection of allergic history, performing of allergic tests, using of antihistamine and glucocorticoid drugs. Drowning: for the drowned person the duration of clinical death is reduced until 3 min. Drowned person spends all his stocks of oxygen, because of enormous intensive muscular movements. It is necessary to start artificial pulmonary ventilation and indirect (external) cardiac massage (in case of cardiac arrest) as soon as possible in the boat or on the beach. One must not waist the time on removal of water from the lower airways. It is necessary to empty the stomach by the help of compression of the epigastrium with the hand after that the body of the patient is turned on the side. 66  It is necessary to remove the mucus, slime (salt) and sand from mouth and nose in aim to establish adequate airway and perform urgent artificial respiration by mouth to mouth. In case of drowning in the fresh water, which has low osmollarity than blood, it will easily be absorbed from alveoli into the blood. That’s why it is not necessary to waist the time on removal of the water from the trachea and bronchus. In case of drowning in salt (3,5- 4%) water, liquid part of the blood (plasma) passes into the upper airways and trachea and bronchus could be filled with foam and liquid, which prevents to performing of artificial pulmonary ventilation. This liquid foam partially could be removed by the help of placement of the upper part of the body and the head lower than the rest part of the body. In the case of the drowning in the cold water, effect of hypothermia occurs and resuscitation may be successful after the stay of patient’s body under the water during 20 min and more. All patients must be transported into the resuscitation department after the successfully performed first aid. Coma: is the unconsciousness, areactive state, getting out from which is impossible by the stimulation. There is no simple defense reflexes, in the case of deep coma. Types of coma: ♦ Apoplectic; ♦ Asthmatic; ♦ Hemolytic; ♦ Hyperthermal; ♦ Hypoglycemic; ♦ Hypocorticoid/Adrenal; ♦ Hypoxic/Anoxic; ♦ Alimentary-dystrophic; ♦ Diabetic; ♦ Hepatic; ♦ Respiratory/Hypoxic; ♦ Thyreotoxic; ♦ Eclamptic; ♦ Epileptic; Treatment: should be etiopathogenic and include removal of reasons of coma, normalization of the cardiovascular, respiratory, nervous and metabolic damages. Terminal States Preagonal state: patient is depressed, clouded or confused consciousness, pallor, acrocyanosis, eye reflexes-retained, no pulse, or thread-like pulse, low blood pressure (60- 70 mm Hg) or it is impossible to determine it. Agonal state: Unconsciousness, thread pulse or no pulse, no blood pressure, areflexia (absence of a reflex), pulse may be palpated only on the carotic arteries, heart sounds are dull, bradicardia, irregular, agonal (terminal) breathing (gasp). 67 Clinical death: starts after cardiac arrest and respiratory standstill and lasts 5-6 minutes (according to V. Negovsky, 1969). In this period anaerobic glycolysis occurs. After 5-6 minutes unreversable processes in the brain cause the biological death. The reasons of the cardiac arrest may be: ♦ Myocardial infarction; ♦ Obstruction of upper airways with foreign body; ♦ Reflectory cardiac failure; ♦ Wound of heart; ♦ Anaphylactic shock; ♦ Electric trauma; ♦ Drowning; ♦ Grave metabolic disturbances (hyperkaliemia, metabolic acidosis). The clinical signs of cardiac arrest: ▫ Absence of the pulse on the carotic artery; ▫ Pupil’s dilation, no reaction to light; ▫ Respiratory standstill (apnea, respiratory arrest); ▫ Unconsciousness; ▫ Pallor, sometimes-cyanosis; ▫ Absence of pulse on peripheral arteries; ▫ Absence of the blood pressure; ▫ Absence of the heart sounds. Absolute signs of the cardiac arrest: ❖ Absence of the pulse on the carotic artery; ❖ Respiratory arrest; ❖ Dilation of pupils, no reaction on light; ❖ Resuscitation measures must be started immediately in case of presence of those symptoms. Cardiopulmonary Resuscitation (principal methods of resuscitation). It includes 4 stages of reanimation: o Providing an adequate airway; o Artificial pulmonary ventilation (artificial respiration); o Cardiac massage (1, 2 and 3 stages, see “General anesthesia”); o Differential diagnosis, drug therapy, heart defibrillation must be performed by the physicians in the reanimobiles or in the resuscitation departments (electrocardiography, intracardial drug administration, defibrillation). There are following types of cardiac massage: 1. External (indirect) cardiac massage (König-Maas): Patient must be placed into the supine position on some firm surface; Doctor has put his palm two fingers above the xiphoid and place the second hand on top (fingers should not touch the chest); 68  Press the sternum in pushing movement (sternum goes down on 4-5 cm) with 8-9 kg force; Relax the hands without taking them away from the sternum; Repeat pushing movements 100-120 times per min. External cardiac massage must be combined with artificial ventilation of the lungs in proportion 30 :2 /fig. 45/. If the cardiac massage is effective, the pulse appears, pupils retracts (comes narrow), skin becomes rosy (pink). Fig 45. External cardiac massage combined with artificial pulmonary ventilation 2. Open (direct) cardiac massage may be performed by the following ways: Transthoracal (by the help of left thoracotomy, performed in the IV intercostals space /fig. 46/); Transdiaphragmal (Tuffier); Subdiaphragmal (Lane); Fig 46. Direct transthoracal cardiac massage. Descending aorta is crossclamped with vascular clamp Compression of the heart between I and II-V fingers must be accompanied with i.v. injections of Epinephrine, Calcium chloride, Atropine and intra-arterial blood transfusion In case of non-shockable rithm (asystole or pulsless electrical activity) epinephrine 1mg must be injected by intravenous or intraosseus rout and repeated for each 3-5 min., untill the restoration of spontaneous circulation. In case of shockable rithm (ventricullar fibrillation or pulsless ventricular tachycardia) after 1-2 min of CPR defibrilation is needed, Epinephrine is injected after second defibrillation. After the third defibrillation 300 mg amiodaron infusion is needed and after the fourth defibrllation, if there is no restoration of sinus rithm repeated dose of 150 mg amiodaron is needing. 69 For the best blood supply of the brain the end of the head of operative table (bed) must be lowered (Trendellenburg’s position of the body /fig. 47/). Fig 47. Trendellenburg’s position The methods of artificial pulmonary ventilation (artificial respiration): 1. Artificial pulmonary ventilation “from mouth into mouth” (trough the gauze or S-shape oropharyngeal tube) /fig 30/; 2. Artificial lung ventilation “from mouth into nose”; 3. Artificial lung ventilation with the aid of Ambou breathing sac (12 inspirations per minute); 4. Artificial lung ventilation by supraglottic devices (laryngeal mask, combitube, king tube) ; 5. Artificial lung ventilation through the endotracheal tube. Respiratory sac may be used for the performing of artificial pulmonary ventilation during the narcosis; 6. Surgical aproach for airway control (cricothyreoidotomy, tracheostomy). 70