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II. General anesthesia

1. Medicamentous:

1) mononarcosis:

a) inhalation:

— mask (including oro- and nasopharyngeal, with laryngomask);

— intubation;

b) noninhalation:

— intravenous;

— peroral;

— rectal;

— intramuscular;

— subcutaneous;

— intraosteal;

— intracavitary;

2) mixed:

— two and more inhalation anesthetics;

— two and more noninhalation anesthetics;

— inhalation and noninhalation anesthetics;

— anesthetics and other neurotropic substances (analgetics, ataractics, myorelaxants et al.);

— neurotropic agents without anesthetics.

2. Nonmedicamentous:

— electroanesthesia;

— hypnonarcosis.

A classification of forms of anethesia given in the official medical documents (Form of the Ministry of Public Health of Ukraine No. 003-3/o): LOCAL:

— regional;

— conduction;

— epidural;

— subdural;

— caudal. GENERAL: Inhalation:

— mask;

— endotracheal. Intravenous:

— with ALV;

— without ALV. MIXED:

— with ALV;

— without ALV.

It is of interest that an up-to-date anesthesiology having taken a step far head, particularly, for the last decades, in the development of different tiedicamentous agents and methods of their application, is noticeably behind n the development of the theory of anesthesia. Possibly, it is explained by the ibjective reason the absence of prerequisites in the nature to create a unitary heory of anesthesia not only on the systemic, but even on the cellular and, lerhaps, molecular level (T.M. Darbinyan, 1976).

Mechanism of anesthetic action lies in the influence on transmission of terve impulses at the synapses of the brain, though it is not yet completely tudied. Probably, they achieve this, having dissolved in lipid membrane of he pre- and post-synapses and, interfering with ionic transmembrane transport, lossibly, act upon membrane proteins, playing the role of receptors, though hat fact, that anesthesia may be caused by a whole number of substances liferent in their chemical nature (inert gas, alcohols, carbohydrates, steroids) nakes the existence of a unified receptor for all anesthetics extremely doubtful. Tie areas of the brain responsible for unconsciousness are not unequivocal: hese may be both a thalamus and a reticular formation or cortex.

Pharmacokinetics of inhalation anesthetics is determined by a number of actors:

— a partial pressure of anesthetic in the form of gas (vapour) in the inhaled mixture, the value of which is determined by the volume of this gas in the mixture or by fractional concentration of gas given in vol.%. A difference between partial pressure in the media, separated by a semipermiable membrane, makes the gas to move from the side with greater concentration to the side with lesser concentration, until the concentration is being equalized on both sides of the membrane. The processes of induction, maintenance and recovery from anesthesia are based on this principle;

— patient's respiratory volume. The greater is it, the greater is the area of contact of inhalation anesthetic with blood and it is dissolved in it;

— respiratory minute volume. The greater is it, the greater amount of anesthetic will be dissolved per time unit in the blood in the induction and released from the organism during recovery from narcosis;

— residual air. Fresh portions of inhalation anesthetic are diluted with residual air and this slows down the onset of anesthesia, for example, in emphysema;

— solubility of anesthetic in the blood. The greater is anesthetic solubility, the sooner a partial pressure is equalized in the alveolar mixture and blood, the shorter a period of induction continues;

— condition of blood circulation in the pulmonary circuit. In case of congestion and heart defect with a discharge of blood from the right to the left (blue defects), a saturation of blood is being slowed down, while

the circulation in the pulmonary circuit is increased (Botallo's duct patency) and accelerated;

— systemic circulation. In blood loss a blood supply of cerebral tissue is relatively maintained, therefore a narcotic effect advances quickly, but the blood supply of tissues is decreased and equilibrium between a partial pressure of anesthetic in blood and tissues comes on slower;

— anesthetic solubility in tissues.Inhalation anesthetics are the most soluble in fatty tissue, and less in the blood, muscles and practically insoluble in poorly vascularized tissues.

First of all a great amount of anesthetic gets into well-vascularized tissues (brain, heart, liver, kidneys and endocrine organs).

In pharmocokinetics of inhalation anesthetics the minimal alveolar concentration (MAC) of inhalation anesthetic is of great significance, at which a pain response to a skin incision does not come in 50% of patients. It is considered that 1.3 MAC of any inhalation anesthetic prevents a pain response to a skin incision in 95% of patients, and 0.3-0.4 MAC causes a recovery from anesthesia. MAC values may be summed up to estimate the power of the mixture. For instance, a mixture of 0.5 MAC N₂0 and 0.5 MAC fluothane is equal to 1 MAC of enflurane, i.e. the action of 53% nitrous oxide and 0.37% of fluothane is comparable to the effect of 1.7% of enflurane. The lesser is MAC, the higher is the power of anesthetic.

There is a number of factors having their influence on MAC. A young age, chronic consumption of alcohol and narcotics increase it, hypo- and hyperthermia, old age, acute alcoholic intoxication, anemia, respiratory failure, hypotension,pregnancy, intake of sedatives and other sympathomimetics decrease it;

— total anesthetic capacity of tissues that is in direct proportion to the
anesthetic solubility in tissue and to tissue volume.

In the first turn, anesthetics enter well-vascularized tissues (brain, heart, liver, kidneys, endocrine glands). These tissues are fast saturated, since their total anesthetic capacity is not great.

Total anesthetic capacity of muscular tissue is greater and it needs several hours for its saturation. Anesthetic capacity of adipose tissue is the greatest, so several days are required for its complete saturation. Poorly vascularized tissues (bones, ligaments, teeth, hair, cartilages) practically do not require anesthetic. A clearance of inhalation anesthetics is the most slowed-down after a prolonged anesthesia in patients with pronounced fatty tissue.

A variety of the mechanism of action of different anesthetics causes some difference in clinical manifestation of their effect. However, a contemporary anesthesiology widely uses in practice a classic division of clinical picture of anesthesia into stages and levels suggested by Gwedell in 1920 and supplemented later by Artusio (Table 2). And though in description of anesthesia

stages the authors had in mind a mononarcosis with ether, the basic principle, jsed by them to recognize stages and levels of anesthesia, the principle based jn determining a degree of CNS functional activity in accordance with manifestation of reflex activities, remains valid for other forms of general anesthesia as well. In applying different ways and methods of anesthesia the;xpression and duration of separate stages are only being changed up to a;omplete disappearance of some of them.

Table 2 Stages and levels of anesthesia

level III₃ and stage IV (agonal) should be considered, from a viewpoint of the up-to-date anesthesiology, as a complication owing to an overdosage of narcotic substances and they must be excluded from anesthesiologic practice. It is justly to consider stage IV as the stage of waking, in which, to the extent of decrease of anesthesia depth, all the stages are repeated in the reverse order, starting from that level, at which a supply of anesthetic was discontinued. However, patient's recovery from anesthesia should not be let to take its course, but requires an active participation of anesthesiologist in order to avoid possible complications.

A continued monitoring of functional indices of respiration and blood circulation, as far as they may reflect a degree of activities of respiratory and vasomotor centers also helps to recognize anesthesia stages along with the signs that are directly associated with neuro-reflex activity. Stages of anesthesia as a representation of deepness of CNS inhibition can be made more precise by EEG indices.

Modern arsenal of agents for anesthesiologic support is rather varied that is the result of progress of world's chemico-pharmaceutical industry:

INHALATION ANESTHETICS: Gaseous

— nitrous oxide;

— xenon. Liquid volatile

— fluofhane;/ \\-^\o\ko^<i

— enflurane;

— isoflurane;

— desflurane;

— sevoflurane.

NONINHALATION ANESTHETICS:

— barbiturates;

— ketamine;

— etomidate;

— propofol.

For premedication, receiving a sedative and amnestic effects, as well as additional agents to general anesthetics, benzodiazepins are applied:

— midazolam;

— diazepam;

— lorazepam.

For anesthesia, primarily, in combination with other agents of premedication or for maintenance of general anesthesia they use: Neuroleptics:

— droperidol;

— haloperidol.

Narcotic (opioid) analgetics:

— morphine;

— meperidin;

— fentanyl;

— sufentanyl;

— alfentanyl;

— remi fentanyl.

Antagonists of narcotic analgetics:

— naloxon;

— nalorphine.

In order to relax skeletal cross-striated muscles in performing tracheal intubation, carrying out ALV and providing optimal conditions for surgical operations myorelaxation drugs of peripheral action, i.e. having their effect in the area of neuromuscular synapse, are applied.

Below we give information of some medicamentous agents the most widely used in today's anesthesiology.

NITROUS OXIDE (N₂0, "laughing gas") a gas without scent, colour, it is not explosible and inflammable and does not sustain combustion. It is produced in cylinders of gray colour in liquid form under the pressure of 50 atm.

MAC— 101 vol.%. It is poor anesthetic and good analgetic. Its distribution coefficient — blood/gas is 0.47. It is eliminated through the lungs, diffuses, in insignificant amount, through skin, and less than 1.01% is subject to biotransformation in GIT under the action of anaerobic bacteria.

It is applied in the mixture with oxygen. When it is used as "mononarcosis" in the concentration of 50 vol.% (N₂0: 0₂ = 1:1), it causes analgesia without loss of consciousness and disturbance of reflexes in the concentration of 50-70 vol.% (2:1) — excitation, 80 vol.% (4:1) — in some patients (children, women, weakened patients), it may cause general anesthesia at the level III,. Application of higher concentrations is impermissible in view of inevitable hypoxia.

Side effects: cardiodepression, inhibition of bone marrow function, increase of intracranial pressure (ICP), nausea, vomiting in the postoperative period. It diffuses slowly into a cuff of intubation tube causing its overdistension in prolonged anesthesia. It increases a hypertension of pulmonary vessels and penetrates pneumatic cavities that is dangerous in air embolism, pneumothorax, acute intestinal obstruction, pneumocephalus, air pulmonary cysts, intraocular air bubbles, myringoplasty, therefore it is contraindicated in presence of pneumatic cavities, multiple fractures and injuries. When a supply of N₂0 is stopped at the end of anesthesia, an inhalation of high concentrations of oxygen is being continued for 5-10 min to avoid hypoxia as a result of diffusion (dilution of alveolar air with released N₂0).

XENON (Xe) — it is an inert gas, narcotic properties of which have been proved in the experiment by N.V. Lazarev in the 30-ties of the XX century and by Americans Cullen and Gross in 1946. In 1999 Russia became the first country in the world where an official permission was received to use Xe (N.E. Burov, 2000). Clinic trials have shown that xenon in the concentration of 30% (Xe: 0₂ = 30:70) as the variant of mask monoanesthesia and combined endotracheal anesthesia ensures an adequate anesthesia in the most traumatic and long (up to 6 hrs.) operations. Economical use of Xe lies in the repeated application of exhaled air after its thorough purification (Xe recycling).

FLUOTHANE (halothane, narcotan, fluotan) is a liquid in dark glass small bottles, stabilized with thymol. It is not inflammable and explosive.

MAC is 0.7-0.8 vol.% in oxygen, 0.3 vol.% in oxygen-nitrous oxide mixture,

in children — 1.0 vol.% in oxygen. Distribution coefficient blood/gas is 2.3. It is released, mainly, (80-85%) in the unchanged form by the lungs, and a little with bile. It is partially (up to 15-20%) oxidized in the liver to trifluoroacetic acid and bromide. In case of hypoxia it forms hepatotoxic products. Biotransformation is induced by phenobarbital. Metabolites are excreted by the liver and kidneys; and enterohepatic circulation of fluothane and metabolites is possible, contributing to their delay in the blood.

It is a potent anesthetic providing a rapid induction without pronounced excitation, necessary deepness of anesthesia and fast recovery from narcosis.

It inhibits a respiratory center, dilates bronchi, suppresses evacuation of bronchial secretion by ciliated epithelium. It decreases AP dose-dependently (inhibits myocardium, ganglia and vasomotor center), heart rate (HR) (rise of vagal tone), sensibilizes myocardium to catecholamines, that may lead to myocardial fibrillation in case of endogenic rise of adrenaline or its introduction from the outside. It decreases blood flow and hepatic function. From time to time (1:35000 of anesthesias with fluothane) a halothane hepatitis may develop. It diminishes renal blood flow and glomerular filtration, relaxes the uterus that may be the cause of atonic hemorrhage. It relaxes cross-striated musculature decreasing the need in myorelaxants. It is able to cause malignant hyperthermia.

It is contraindicated in hepatic function disorders, in danger of ICP elevation, in hypovolemia, cardiac diseases, pheochromocytoma.

ENFLURANE (ethrane).

It is a liquid in dark glass bottles with a weak, sweetish ether scent, noninflammable.

In adults MAC is 1.7 vol.% in oxygen, 0.6 vol.% in the oxygen-nitrous oxide mixture. Distribution coefficient blood/gas is 1.8. Metabolism with formation of fluoride-ion is so insignificant that, in contrast to methoxiflurane, inefficacy of enflurane is meaningless; it does not display, unlike fluothane, a hepatotoxicity.

It is a potent anesthetic with a rapid induction and recovery from anesthesia.

Side effects are similar to those observed in fluothane, but pronounced in a lesser degree. This is a myocardial inhibition, a decrease of AP, cardiac output and oxygen consumption by myocardium. It is an inhibition of breathing, muscular relaxation, ICP increase, in which connection a development of epileptiform fits is possible in high doses of anesthetic and hyperventilation, that is why to decrease ICP one cannot, as usual, use hyperventilation.

It is contraindicated in the early terms of pregnancy, increased ICP, predisposition to malignant hyperthermia, disturbance of renal function, epilepsy.

It is not recommended: to mix enflurane with other anesthetics in one vaporizer, to decrease a dose of myorelaxants. In case of need adrenaline may be used.

ISOFLURANE (forane).

It is contraindicated in IHD (a danger of "steal syndrome", when intact coronary vessels are dilated, a blood flow is decreased in the area of ischemia) and hypovolemia.

DESFLURANE (suprane).

It is a liquid with sharp, irritating scent and so strong evaporation that at room temperature it boils and requires a special vaporizer.

Its MAC is 0.6 vol.%, i.e. 4 times weaker than enflurane and isoflurane, but 17.5 times more potent than N₂0. Distribution coefficient blood/gas is 0.42, it means that the induction of anesthesia and recovery from it are achieved quickly.

It is eliminated in the unchanged form by the lungs, its biotransformation is insignificant.

It decreases ventilation at the expense of shallower, though hurried, breathing. It irritates mucous membranes, increases salivation and causes laryngospasm. Deflurane inhibits myocardial activity as isoflurane, but it is not a coronarolytic. It increases ICP, responding to correction by hyperventilation. It relaxes cross-striated muscles, depending on the dose, and potentiates the effect of nondepolarizing myorelaxants. It is not toxic for the liver and kidneys.

It is contraindicated in the expressed hypovolemia, ICP increase and risk of malignant hyperthermia.

It is a liquid with sharp ether scent, noninflammable.

In adults MAC is 1.5 vol.% with oxygen-nitrous oxide mixture, and in children — 1.4-1.6 vol.% with oxygen. Distribution coefficient blood/gas is 1.4.

Its biotransformation to trifluoroacetic acid is 10 times less intensive than that of enflurane, in so doing it forms so small amount of fluoride-ions that it is not nephrotoxic.

It is a potent anesthetic, powerful analgetic.

Side effects are less expressed than in fluothane: it inhibits myocardium insignificantly, a blood flow is compensated by HR increase. Isoflurane is a moderate /?-adrenomimetic: increases a blood flow in skeletal musculature, decreases AP and TPVR; a moderate coronarolytic. It increases ICP less than fluothane and enflurane, that may be eliminated by hyperventilation; relaxes skeletal musculature, decreases hepatic and renal blood flow, but it is not toxic for these organs. It potentiates the effect of nondepolarizing myorelaxants.

SEVOFLURANE (ultane).

Liquid is without a sharp scent.

Its MAC is 2.0 (a little weaker than desflurane), a gas/blood distribution coefficient — 0.65 (rapid induction and recovery).

It acts on the respiratory system analogous to isoflurane.

It inhibits insignificantly myocardial function, decreases TPVR and AP in a lesser extent than isoflurane and desflurane, does not cause a "steal syndrome", and increases ICP insignificantly.

It relaxes musculature allowing the intubation without myorelaxants.

It is metabolized with formation of fluorides having a nephrotoxic effect.

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