Intensive Care of Emergency Conditions - V. M. Zaporozhan 2006

Anesthetic Management

Unlike previous periods, when the primary task of the person administering anesthesia was limited to general or local pain relief, the main hallmark of the modern, scientific era in The Development of anesthesiology is the management of vital bodily Functions in defiance of surgical aggression striving to disrupt them.

The specific tasks (components) of anesthetic care for surgical interventions are defined as follows:

— loss of consciousness — suppression of mental perception (general anesthesia, Sleep);

— pain relief — blockade of painful impulses (analgesia);

— neurovegetative blockade;

— immobility (myorelaxation);

— maintenance of adequate gas exchange;

— maintenance of adequate Blood Circulation;

— maintenance of normal METABOLISM.

Undoubtedly, accomplishing all these tasks by administering a single anesthetic agent, i.e., via single-agent anesthesia (mononarcosis), is impossible in most cases and impractical to pursue. Therefore, the core principle of modern anesthesia is its combined nature, meaning The Use of various agents (drugs) and Methods (manipulations) to achieve adequate anesthesia. Below is a list of various options for these agents and methods. We propose their systematization:

I. General Anesthesia

Medicated:

1. Single-agent anesthesia can be inhalational (mask, intubation) and non-inhalational (intravenous, oral, intramuscular, subcutaneous, intraosseous, intracavitary).

2. Combined anesthesia refers to:

— two or more inhalational anesthetics;

— two or more non-inhalational anesthetics;

— inhalational and non-inhalational anesthetics;

— anesthetics and other neurotropic substances (analgesics, ataractics, Muscle relaxants, etc.);

— neurotropic substances without anesthetics.

Non-medicated:

— electronarcosis;

— hypnonarcosis.

II. Local Anesthesia

Medicated:

— topical (terminal);

— infiltrative;

— conduction: truncal, plexus, paravertebral;

— regional: epidural, spinal.

Non-pharmacological:

— acupuncture;

— electro- and pharmacopuncture;

— cryotherapy.

For clinical practice, the Classification of analgesia types is provided according to official medical documents (Form No. 003-3/o, approved by the Order of the Ministry of Health of Ukraine No. 184 dated July 26, 1999).

Interestingly, while modern anesthesiology has made significant strides, especially over recent decades, in developing various pharmacological agents and administration methods, it noticeably lags behind in formulating a theory of anesthesia. This may be due to an objective limitation: the absence of natural prerequisites for establishing a unified theory of anesthesia not only at the systemic level, but even at the cellular and apparently molecular levels (T. M. Darbinyan, 1976).

Until the 20th century, it was believed that anesthetic agents depress The activity of various CNS structures more or less uniformly. However, in recent years, it has been established that various general anesthetics exert selective effects on different functional areas of the CNS. For instance, ether has a pronounced effect on the cortex while having virtually no impact on the thalamic and bulbar regions or the reticular formation. Barbiturates and propanidid primarily depress the reticular formation, whereas ketamine and electronarcosis activate the limbice system (hippocampus), thereby causing reciprocal inhibition of other systems.

At the CELLULAR AND MOLECULAR levels, The Mechanism of anesthesia is likewise not explained unambiguously. Several historical theories attempted to explain the state of anesthesia through physicochemical or physiological phenomena (Claude Bernard's coagulation theory, 1885; Meyer-Overton lipid theory, 1899–1901; Verworn's "asphyxiation of Nerve Cells" theory, 1912; Traube's adsorption theory, 1904–1913; Warburg, 1914–1918; Pauling's microhydrate crystal theory, 1961).

Recently, the membrane theory has gained widespread acceptance, explaining anesthesia As a result of anesthetics dissolving in Cell membranes, which impairs their permeability to sodium ions, disrupts excitation generation, and lowers the Action Potential. However, even at THE MOLECULAR LEVEL, the effects of various anesthetics are not identical.

The diversity in the Mechanisms of action of different anesthetics determines the differences in their clinical manifestations. Nevertheless, modern anesthesiology widely utilizes in practice the classical division of the clinical picture of anesthesia into stages and planes, proposed by A. Guedel in 1920 and later supplemented by Artusio. Although the authors originally described these stages based on single-agent ether anesthesia, the fundamental principle they used to identify the stages and planes of anesthesia—based on assessing the functional activity of the CNS through reflex manifestations—remains valid for Other types of general anesthesia as well. When using different agents and methods, only the intensity and duration of individual stages change, up to the complete disappearance of some of them:

Stage I — analgesia (dullness):

І₁ — initial intoxication;

І₂ — partial analgesia and complete amnesia;

І₃ — complete analgesia and amnesia;

Stage II — excitement (confusion of consciousness);

Stage III — surgical (loss of consciousness):

ІІІ₁ — Eyeball movement;

ІІІ₂ — corneal reflex;

ІІІ₃ — pupil dilation;

ІІІ₄ — diaphragmatic Respiration;

Stage IV — agonal.

From the standpoint of maintaining the safety of vital organ and system functions in the patient, anesthesia should not be deepened below the ІІІ₂ plane. Only in the case of single-agent ether anesthesia, out of extreme necessity for adequate muscle relaxation, is a short-term deepening (no more than 10 minutes) to the initial phase of ІП₃ permitted. From the perspective of modern anesthesiology, the classical ІІІ₃ plane and Stage IV (agonal) must be regarded as complications resulting from anesthetic overdose and should be excluded from anesthetic practice. Stage IV is correctly viewed as the recovery stage, during which, as the depth of anesthesia decreases, all stages repeat in reverse order, starting from the level at which the anesthetic administration was terminated. However, bringing a patient out of anesthesia should not be left to chance; it requires active management by the anesthesiologist to prevent potential complications.

The identification of the stage of anesthesia, along with signs directly related to neuro-reflex activity, is also facilitated by continuous monitoring of functional parameters of respiration and circulation, as they can reflect the activity level of the respiratory and vasomotor centers. The stages of anesthesia, as a reflection of the depth of Central Nervous system depression, can be further clarified using EEG data.

The modern arsenal of anesthetic agents is quite diverse, which is a result of progress in the global chemical and pharmaceutical industry.

Inhalation anesthetics: nitrous oxide, halothane, enflurane, isoflurane, desflurane, sevoflurane.

Non-inhalation anesthetics: barbiturates, sodium oxybutyrate, ketamine, etomidate, propofol.

Thus, as the list of anesthetics shows, nitrous oxide is still used today—one of the agents with which the use of surgical anesthesia began in the mid-19th century. Agents that are still mentioned in modern surgery textbooks (chloroform, cyclopropane, methoxyflurane, trichloroethylene, propanidid, predione) are no longer used at all due to dangerous side effects and high toxicity.

There are also agents with which domestic anesthesiologists are familiar mostly through foreign literature. They are of interest to students because they may appear in the arsenal of domestic anesthesiology at any time as economic ties with distant foreign countries expand (enflurane, isoflurane, desflurane, sevoflurane, etomidate).

Below is a Brief Overview of the agents most commonly used in modern anesthesiology.

Agents for general inhalation anesthesia

Nitrous oxide is a colorless and odorless gas. It does not enter into any compounds in the body, does not break down, and is rapidly excreted unchanged by the Lungs.

To prevent Hypoxia, nitrous oxide is administered in a mixture with oxygen, in which its proportion must not exceed 80%, and after inhalation is stopped, pure oxygen is administered for 1-5 min (to prevent diffusion hypoxia).

Advantages. It does not affect the function of vital Organs and systems. Well-controlled depth of anesthesia. Pronounced analgesic capacity. Absence of nausea and vomiting in most cases. Non-flammable. Potentiates the action of other anesthetics ("second gas effect").

Disadvantages. Low anesthetic potency. Risk of hypoxia. Mandatory use of oxygen due to the threat of diffusion hypoxia. Absence of muscle relaxation. Bone Marrow suppression with prolonged use.

Indications. Single-component anesthesia; used only for analgesia during painful Procedures, childbirth, and in outpatient practice, though recently it has been largely displaced in these cases by non-inhalation anesthetics and regional anesthesia/analgesia techniques. Widely used as a component of combined anesthesia.

Contraindications. Pronounced hypoxia; situations requiring an increased fraction of oxygen.

Halothane is a volatile liquid with a sweetish odor. It decomposes under The Influence of light to form hydrobromic acid; it is stored in a dark bottle with a stabilizer (0.01% thymol). It is excreted by the lungs mostly unchanged and partially metabolized in the Liver, with biotransformation (dechlorination, debromination) stimulated by phenobarbital.

Advantages. Rapid induction (1-5 min) and rapid emergence (5-15 min) without unpleasant sensations; post-anesthetic depression lasts 30-60 min. No irritation of the Upper Respiratory Tract. Relaxation of the Larynx and Bronchi. Non-flammable and non-explosive. Possibility of using a high concentration of oxygen. Good muscle relaxation. Moderate ganglion-blocking effect.

Disadvantages. Narrow therapeutic index. Parasympathomimetic effect. Depresses myocardial contractility. Increases cardiac sensitivity to catecholamines. Suppresses

respiration. Decreases blood pressure. Hepatotoxic. Weak analgesic. Causes chills and metabolic acidosis in the postoperative period.

Indications. Tracheal intubation when relaxants cannot be used. Used as the primary anesthetic or in combination with nitrous oxide and non-inhalation agents during surgeries involving electrical equipment, for respiratory diseases and pulmonary surgeries, in outpatient settings, and during short procedures (though non-inhalation anesthesia is preferred).

Contraindications. Liver disease. Pronounced Heart failure with hypotension. Hypovolemia. Lack of specialized vaporizers and anesthesia equipment. Insufficient qualification of the anesthesiologist. Must not be used during surgeries for pheochromocytoma.

Recently, indications for the use of halothane have been increasingly narrowing, as it—like other inhalation anesthetics—is being replaced by intravenous agents. It is most appropriate to use halothane in combination with nitrous oxide and non-inhalation agents (e.g., analgesics, muscle relaxants), which makes it possible to use low concentrations of halothane ("traces") and thereby mitigate some of its negative properties.

Isoflurane (forane) has a weak analgesic effect. A moderate muscle relaxant. Has minimal effects on The Cardiovascular system and respiration, causing vasodilation and a decrease in blood pressure. Does not alter sensitivity to catecholamines. Does not affect cerebral blood flow or increase intracranial pressure.

Indications. Monoanesthesia and combined general anesthesia.

Contraindications. Relative (in hypovolemia).

Enflurane (ethrane) is a potent anesthetic, a weak analgesic, and induces muscle relaxation.

Side effects. Cardiodepressive effects are more pronounced than those of other inhalational anesthetics. It does not sensitize adrenoreceptors. It increases cerebral blood flow and intracranial pressure. It is nephrotoxic.

Contraindications. Heart failure. Brain surgery and patients with elevated intracranial pressure. Kidney diseases.

Desflurane is an anesthetic and a potent analgesic (17 times more potent than nitrous oxide). It rapidly saturates the body and is eliminated quickly, allowing the anesthesiologist to control the depth of anesthesia more precisely.

Side effects. Its effects on the cardiovascular system are similar to those of isoflurane. It decreases alveolar ventilation by reducing tidal volume and increasing respiratory rate. The pungent odor and irritation of mucous membranes during induction can cause excessive salivation, breath-holding, coughing, and laryngospasm. It increases intracranial pressure, which can be reduced by hyperventilation. It induces myorelaxation. It has no effect on kidney and liver function. It does not sensitize the myocardium to catecholamines.

Contraindications. Severe hypovolemia, high risk of malignant hyperthermia, intracranial Hypertension.

Sevoflurane is a novel halogenated anesthetic currently undergoing clinical evaluation. It suppresses myocardial function to a lesser extent than previous agents, has a smaller effect on intracranial pressure, and does not affect liver function. However, it generates fluorides which, under certain conditions (high respiratory gas Temperature, low-flow anesthesia), can accumulate and exert nephrotoxic effects.

Contraindications. The same as for desflurane: severe hypovolemia, high risk of malignant hyperthermia, intracranial hypertension.

Agents for non-inhalational general anesthesia

Barbiturates

Thiopental sodium (pentothal sodium, thiopentobarbital, trapanal) is a greenish-tinged porous powder. Its solutions are strongly alkaline; therefore, mixing it with acidic drugs (such as ditilin, aminazine, diprazin, pentamine, arfonad, etc.) results in precipitation.

Hexenal (evipan sodium, hexobarbital sodium, cyclobarbital) is a white or slightly yellowish foam-like mass.

Barbiturates are hygroscopic and readily soluble in Water. Their solutions undergo rapid Hydrolysis, making them unstable. They must be prepared immediately before use. They are supplied in 0.5 g and 1.0 g vials and should be stored in a dry, cool, dark place.

They are used primarily for induction of anesthesia, as well as for short procedures, dressings, and surgeries. Independent, prolonged barbiturate anesthesia is practically never used because barbiturates are poor analgesics, the depth of anesthesia is difficult to control, and administering doses exceeding 1 g is contraindicated.

As a rule, 1–2.5% solutions are used, as more concentrated solutions cause significantly greater respiratory and circulatory depression. Slowly inject 1–3 ml of the solution intravenously and wait 30 seconds to check for accidental subcutaneous administration (which causes burning pain and local redness) or hypersensitivity to the drug (an allergic reaction). Then, continue the administration at a rate of 1 ml of solution per 5–10 seconds until loss of consciousness occurs. On average, this requires 200–500 mg of the drug. The total dose must not exceed 1000 mg. The duration of action of the initial dose is 15–20 minutes; if prolonged anesthesia is required, repeated doses of 100–200 mg should be administered based on clinical signs.

Significant respiratory depression, even mild cyanosis, and fixed dilated pupils indicate excessive depth of anesthesia, requiring immediate artificial pulmonary ventilation (APV) and discontinuation of further barbiturate administration. After the patient emerges from barbiturate anesthesia, prolonged postanesthetic sleep may occur, necessitating continued close monitoring. Considering that thiopental is inactivated mainly by Plasma Proteins and hexenal by the liver, one must be cautious of an excessively prolonged anesthetic effect in relevant clinical situations. Under no circumstances should barbiturate anesthesia be initiated without preparing all necessary equipment for artificial pulmonary ventilation and tracheal intubation.

Advantages. Ease of use. Rapid induction of anesthesia without excitation or unpleasant sensations. Quick recovery from anesthesia without nausea or vomiting. Does not alter myocardial sensitivity to catecholamines.

Disadvantages. Narrow therapeutic window. Absence of analgesia. Difficulty in controlling the depth of anesthesia. Vagal stimulation. Marked depression of respiration and cardiovascular function. Prolonged postanesthetic sleep. Insufficient muscle relaxation. Persistence of pharyngeal and laryngeal Reflexes. Irritant effect if injected subcutaneously or intra-arterially. Increased salivation.

Indications. Induction of anesthesia. Short surgeries, painful therapeutic and diagnostic procedures in an inpatient Setting. Cessation of convulsions and psychomotor agitation. Brain protection against hypoxia in traumatic brain injury. Adaptation to the ventilator during prolonged artificial pulmonary ventilation.

Contraindications:

1. Absolute: allergic reactions to the drug; porphyrinuria (risk of central and peripheral paralysis); lack of equipment for artificial pulmonary ventilation; hypovolemia.

2. Relative (acceptable only for induction of anesthesia): cardiac decompensation; pronounced arterial hypotension; Liver failure; Addison's disease; hypoproteinemia; metabolic acidosis; extensive Burns; predisposition to bronchospasm or Bronchial Asthma (for thiopental); myasthenia gravis treated with proserine; use of ganglion blockers; outpatient settings; early childhood.

Sodium oxybate (Gamma OH-butyric acid, GHB) is the sodium salt of gamma-hydroxybutyric acid. Most of it is utilized in the body as a metabolic substrate. 98% is excreted through the lungs as СО₂. It readily crosses the blood-brain barrier. It has low toxicity. It increases brain resistance to hypoxia. It potentiates the effects of anesthetics and analgesics without increasing their toxicity. It exhibits strong anesthetic and sedative properties along with weak analgesic effects.

Adrenaline acts as an antagonist to GHB, while Insulin acts as a synergist. It moderately decreases blood pressure and heart rate; deep anesthesia may cause respiratory depression down to apnea. It promotes the development of hypokalemia due to the shift of potassium from the extracellular environment into the cells. It has no effect on parenchymal organs. It increases the body's resistance to hyperoxia and radioactive radiation by acting as an antioxidant.

Available in 10 ml ampoules of a 20% solution.

Advantages. Low toxicity. Almost no adverse effects on hemodynamics and respiration.

Disadvantages. Slow induction and delayed recovery. Poor controllability of anesthesia. Inadequate analgesia (achieved only under deep anesthesia). Potential for hypokalemia. Risk of seizures, particularly upon rapid administration.

Indications. Induction of anesthesia, including oral administration in young children. Basal anesthesia, predominantly in combination with other anesthetics. As a sedative for psychomotor agitation. As an antioxidant in hypoxic and TRAUMATIC BRAIN INJURIES, hyperoxia, and radiation exposure. Hyperkalemia. To facilitate patient adaptation to the ventilator during prolonged mechanical ventilation.

Contraindications. Atrioventricular dissociation. Predisposition to seizures. Hypokalemia.

Following premedication, which must necessarily include atropine, sodium oxybutyrate is administered intravenously for induction at a rate of 4-6 ml of the drug per minute, or by slow drip in a glucose solution with insulin over 10-15 minutes. The adult dose is 70-100 mg/kg, and for children, 60-150 mg/kg. The surgical stage of anesthesia is reached in 12-15 minutes and lasts for 1-1.5 hours after a single dose, occasionally extending to 2-2.5 hours. For young children, the drug may be administered orally (100-150 mg/kg) mixed with sweet syrup, given by the mother.

Sodium oxybutyrate may be combined with neuroleptanalgesia agents, analgesics, and other anesthetics. Recovery is generally smooth, though mild agitation may occasionally occur. Post-anesthetic sleep is possible after consciousness is regained. When sodium oxybutyrate is used as a sedative for psychomotor agitation, combining it with barbiturates is recommended: for example, 50-100 mg/kg of sodium oxybutyrate and 3-4 mg/kg of sodium thiopental.

Ketamine (calipsol, ketalar, ketanest) is a phencyclidine derivative. It is a clear, colorless solution supplied in 20 ml vials as 1% or 5% solutions for intravenous or intramuscular administration, respectively. It is inactivated by The Liver and excreted by the Kidneys as metabolites that retain weak ketamine-like properties. Ketamine is a rapid-acting general anesthetic with a wide therapeutic index.

It has low toxicity. It provides potent anesthetic and analgesic effects, while potentiating the narcotic effect of other anesthetics. It induces the excitation of certain brain regions and the depression of others, a state commonly referred to as dissociative anesthesia. It may provoke hallucinations.

Its effect on respiration is minimal. It exerts a stimulating action on The Heart and Blood Vessels, increasing Cardiac Output, blood pressure, cerebral blood flow, and CEREBROSPINAL FLUID pressure. It enhances salivation. Laryngeal and pharyngeal reflexes, as well as muscle tone, are preserved during deep anesthesia. It increases uterine tone in pregnant women. It does not cross the placental barrier. It suppresses immunogenesis.

Advantages. Absence of arterial hypotension. Low toxicity. Preservation of protective reflexes. Suitability for intramuscular administration.

Disadvantages. Muscle rigidity. Psychomotor agitation during emergence from anesthesia, accompanied by delirium and hallucinations. Exaggeration of pharyngeal and laryngeal reflexes. Increased salivation and bronchorrhea. Elevated intracranial pressure. Stimulation of the sympathoadrenal system. Occasionally, an allergic rash at the injection site.

Indications. Short-term surgical procedures and manipulations that do not require muscle relaxation. Analgesia for labor and Cesarean Section. Anesthesia in children. Induction of anesthesia. Procedures in high-risk patients (hypovolemia, Shock, blood loss).

Contraindications. Arterial hypertension. Preeclampsia, Eclampsia. Aneurysms and certain other vascular Pathologies of the brain, chest, and abdominal cavities. Predisposition to hallucinations. Psychiatric disorders. Elevated intracranial pressure. Heart failure.

Following premedication, which must include atropine and either diazepam or droperidol, 2-3 mg/kg of the drug is administered intravenously regardless of the patient's age. To maintain anesthesia, 1/2 to 1/4 of the initial dose is repeatedly administered every 10-15 minutes. Changes in the rate and depth of respiration, the onset of limb mobility, facial muscle twitching, Eye Movements, and nystagmus signal The Need for repeated doses of ketamine. Administration of diazepam, droperidol, or barbiturates mitigates potential central nervous system disturbances in the post-anesthetic period.

When ketamine is administered intramuscularly for anesthesia, the dosage depends on age: newborns receive 12-14 mg/kg, infants 10-12 mg/kg, children aged 1-2 years 9-11 mg/kg, aged 3-6 years 8-10 mg/kg, aged 7-14 years 7-9 mg/kg, and adults 5-6 mg/kg. To maintain anesthesia, 1/2 to 1/4 of the initial dose is given after 20-30 minutes. The final dose is administered 30-40 minutes before the end of the surgery. In the post-anesthetic period, the patient does not require analgesics for 2-3 hours.

Etomidate (hypnomidate) is ethyl 2-(1-methylbenzyl)imidazole-5-carboxylate. It is a yellowish-white crystalline or amorphous powder. It is available as an aqueous solution in 10 ml ampoules containing 2 mg/kg of the active substance. It is characterized by a rapid onset of anesthesia and recovery within 4-8 minutes. Dosage: for induction, 0.2-0.3 mg/kg; for maintenance of anesthesia for 5-10 minutes, 0.1 mg/(kg·min), followed by 0.01 mg/(kg·min). The concurrent use of nitrous oxide significantly reduces the required doses of etomidate.

Advantages. Good controllability of anesthetic depth. Minimal impact on respiration and circulation. Minimal toxicity.

Disadvantages. Occasional myoclonic jerks. Hyperalgesia (increased pain sensitivity). Suppression of corticosteroid production.

Propofol (diprivan, recofol, profol) is supplied in 20 ml ampoules containing 10 mg/ml of diisopropylphenol in intralipid. Dosage: for induction, a single bolus of 2.5 mg/kg is administered, followed by continuous infusion During the first 15 minutes at a rate of 12 mg/(kg·h), after 30 minutes at 9 mg/(kg·h), and after 45 minutes at 6 mg/(kg·h). Induction in children requires a higher dose of 3-5 mg/kg.

Propofol decreases myocardial contractility, depresses respiration up to apnea following induction, lowers blood pressure, and in the post-anesthetic period, may cause hyperalgesia, nausea, vomiting, and headache.

Neuroleptanalgesia (NLA) is a state combining elements of neurolepsis (motor and psychic sedation) and analgesia, induced by the combined action of a neuroleptic (most commonly droperidol) and an analgesic (most commonly fentanyl).

Droperidol is a butyrophenone neuroleptic, supplied in 10 ml vials of a 0.25% solution. It exhibits mild hypnotic activity, blocks alpha-adrenoceptors, does not depress respiration, reduces myocardial sensitivity to catecholamines, lowers blood pressure, improves peripheral circulation, and increases heart rate.

It possesses antiemetic and anti-shock properties. In conventional doses, it is non-toxic. It potentiates the action of analgesics and muscle relaxants. It undergoes biotransformation into imidazole, with 10% excreted unchanged by the kidneys.

Fentanyl is a piperazine derivative, a potent synthetic analgesic and moderate M-cholinomimetic (causing bradycardia and decreased respiratory rate). It is inactivated in the liver. It is supplied in 2 and 5 ml ampoules of a 0.005% solution. It does not impair hepatic or renal function, depresses respiration and the cough reflex, and induces muscle rigidity, predominantly in the chest and abdominal walls. Vomiting and bronchospasm may occur.

Advantages of NLA. Wide therapeutic index and minimal toxicity. Good controllability. Full analgesia and neurovegetative protection. Hemodynamic stability. Synergism with anesthetics, analgesics, and muscle relaxants.

Disadvantages of NLA. Muscle rigidity. Increased airway resistance. Potential extrapyramidal disturbances.

Indications for NLA. Premedication. Used as an independent method of anesthesia as well as in combination with other anesthetic techniques. Diagnostic cardiac examinations. Thermal blockade aimed at controlling hyperthermia or inducing hypothermia.

Contraindications to NLA. Pronounced hypovolemia. Outpatient surgeries. Extramyramidal side effects. Pulmonary hypertension. Bronchospasm or a predisposition to it. Cesarean section prior to fetal delivery.

The method of NLA represents a successive stage in the development of "ataralgesia"—a term first proposed by Du Cailar et al. in 1958 (derived from the Greek tarache meaning soul, and ataraxie meaning absence of soul). Clinically, it refers to The Effect of central relaxation accompanied by complete mental and emotional indifference to the environment, along with an absence of fear and anxiety, while the patient remains conscious. Pain and tactile stimuli are perceived and reacted to, but without emotional coloring, which is suppressed or entirely absent. THE CONCEPT OF "ataralgesia" evolved, in turn, from the concept of balanced anesthesia, which involves targeted action on the Main Components of general anesthesia, namely: 1) suppression of consciousness; 2) neurovegetative blockade; 3) analgesia; 4) myorelaxation utilizing novel psychotropic agents developed through psychopharmacology, pioneered by Laborit and Huguenard ("hibernation" in the 1950s).

The perception of The Role of analgesia as a component of general anesthesia has evolved—shifting from a very modest auxiliary role (Du Cailar, 1966) to a decisive one, although obstructed by the side effects of narcotic analgesics, such as vagal reactions, respiratory depression, renal toxicity, and others. The Introduction of lexyr (pentazocine) somewhat shifted this paradigm: it lacks the drawbacks of narcotic analgesics, exhibits properties characteristic of narcotic antagonist agents, and at the same time acts as a potent analgesic. This led to the Development of the concept of central analgesia—utilizing high doses of fentanyl, followed by lexyr at the end of surgery. Neurovegetative blockade can be of two types: neuroplegia—a complete neurovegetative blockade resulting in a loss of regulatory control over the body's primary functions during anesthesia; and neurolepsis—the same effect, but with the preservation of adaptive protective reactions restricted to functional limits.

Consequently, modern anesthetic management is viewed as a combination of components that can be achieved through mononarcosis using traditional anesthetics, though it is more rational and safer to utilize specialized psychotropic agents for each specific component. The resulting psychostasis is no less important than pre- and postoperative Homeostasis ("protecting the patient from themselves and their environment"). Analgesics serve to prevent the body's reaction to pain and trauma, whereas neuroleptics act as a therapeutic measure against reactions that have already occurred.

The methodology of anesthetic management for surgical interventions encompasses several stages, beginning from the moment surgeons decide to perform the operation and extending through the postoperative period. The anesthesiologist's involvement begins with reviewing the patient's diagnostic findings and assessing surgical and anesthetic risk. The degree of risk can be roughly estimated by considering two factors: the patient's physical status and the severity of the upcoming surgery.

Based on the patient's physical status, 5 degrees of risk are distinguished:

I — patients with no organic diseases, or whose disease is localized and causes no systemic disorders;

II — individuals with mild to moderate systemic disorders, whether related or unrelated to the surgical condition, which only moderately impair normal activity and general physiological balance;

III — patients with severe systemic disorders, whether related or unrelated to the surgical condition, which severely impair normal daily functioning;

IV — patients with extreme systemic disorders, whether related or unrelated to the surgical condition, which drastically impair normal functioning and pose an immediate threat to life;

V — individuals whose preoperative condition is so critical that death is expected within 24 hours even without the additional impact of surgery.

Based on the severity of the surgical interventions, there are also 5 risk grades (A, B, C, D, E):

A — minor surgeries on the body surface and in Body Cavities: opening of small abscesses, amputation of fingers and toes, uncomplicated appendectomies and hernia repairs, ligation and removal of hemorrhoids.

B — moderately severe surgeries on the body surface and in body cavities: opening of deep-seated abscesses (Pleural Empyema, interintestinal and appendicular abscesses, etc.), amputation of upper and lower extremity segments, peripheral vascular surgery, complicated appendectomies and hernia repairs requiring extended intervention, exploratory laparotomy and thoracotomy.

C — major surgical interventions: radical surgeries on abdominal organs other than those listed above, radical thoracic surgeries, extensive limb amputations (e.g., interpelviabdominal amputation of the lower extremity).

D — surgeries on the heart and great vessels.

E — emergency surgical interventions.

Preparation of patients for surgery includes:

1) mechanical measures — emptying The Stomach, intestines, and Urinary Bladder; gastric decompression using a tube is mandatory for all emergency surgeries;

2) measures to foster a positive psychological mindset in the patient;

3) premedication — administration of pharmacological agents (analgesics, sedatives, antihistamines, hypnotics, etc.) that potentiate anesthesia, mitigate Adverse effects of narcotics, and prevent potential complications.

For patients with extreme risk grades, hemodynamic status, respiratory function, water-electrolyte balance, and acid-base status must be optimized prior to surgery. This is achieved through infusion therapy, blood transfusions, administration of cardiotonic and vasoactive drugs, corticosteroids, oxygen inhalation, or assisted ventilation, among other measures. Life-saving surgeries (e.g., in the presence of ongoing severe bleeding) may be performed concurrently with resuscitation and intensive care. Significant functional impairments of respiration and circulation may constitute contraindications for elective surgeries, but not for urgent procedures aimed directly at eliminating a threat to the patient's life.

The goal of premedication is to calm the patient, prevent allergic, autonomic, and other potential complications during induction of anesthesia, minimize the side effects of anesthetic agents, and potentiate the action of anesthetics used for maintenance of anesthesia.

In elective surgeries, premedication begins on the eve of the Procedure with the administration of standard doses of medium- or long-acting hypnotics (phenobarbital, sodium amobarbital, glutethimide). On the morning of surgery, 2 hours prior to the scheduled procedure, the patient is given one of the "minor" tranquilizers (trioxazine, meprobamate, seduxen). For infants and young children, preoperative premedication is unnecessary, as they are typically not informed about the upcoming surgery and sleep peacefully. Preliminary premedication is also omitted in emergency surgeries.

30 minutes directly before surgery, M-cholinolytics, narcotic analgesics, and antihistamines are administered subcutaneously or intramuscularly. In emergency surgeries, the same agents are often administered intravenously in appropriate doses immediately before induction of anesthesia on the operating table.

Combinations of premedication drugs and their dosages are adjusted depending on the specific clinical situation. Table 4 lists the most commonly used agents and their dosages for this purpose. Premedication can be considered effective if the patient is calm and drowsy, the heart rate is 80–100 bpm, and blood pressure is not elevated.

Induction of anesthesia is a stage of combined general anesthesia that ensures transition into anesthesia without the excitation stage. Non-inhalation anesthetics (barbiturates, sodium oxybutyrate, ketamine, etc.) are primarily used. If mechanical ventilation is anticipated during surgery, muscle relaxants are administered after induction and tracheal intubation is performed.

Maintenance anesthesia is administered throughout the entire surgery. Its main goal—to provide optimal conditions for the surgeon and effective Protection of the patient from surgical stress—is achieved by fulfilling all the components (individual tasks) mentioned above.

Class="center">Table 4 Premedication Agents (L. V. Usenko et al., 1995)

Recovery from anesthesia involves the restoration of vital body functions, primarily adequate spontaneous ventilation, protective reflexes, and consciousness. Sometimes a patient's severe condition and the high invasiveness of the surgery necessitate prolonging anesthesia and mechanical ventilation for several hours postoperatively. In such cases, the patient requires extended intensive monitoring, which is best carried out in intensive care units. For adequate postoperative analgesia, along with injections or infusions of analgesics and potentiating ataractics, local anesthetics are administered via an epidural catheter.

Complications associated with anesthesia may occur during surgery and in the postoperative period. They are minimal during local anesthesia (occasionally, anaphylactic reactions to local anesthetics may be observed). Complications of general anesthesia can arise at various stages of anesthetic management: premedication, induction, maintenance, and the postanesthetic period. However, the induction, emergence, and early postoperative periods are the most critical in this regard. Complications may be triggered by the specific action of the anesthetic, the type and method of anesthesia, the primary or concomitant disease, and The Nature of the surgical intervention.

The foundation of complication Prevention is adequate preparation of the patient for surgery and anesthesia, along with meticulous monitoring of their condition at all stages of anesthetic management. Respiratory complications are the most probable. They arise due to airway obstruction (accumulation of mucus, jaw drop, aspiration of vomit, laryngospasm, bronchospasm, etc.), impaired respiratory regulation (depression of the respiratory center, hyperventilation during mechanical ventilation, hyperoxia, etc.), impaired neuromuscular transmission (effects of muscle relaxants, electrolyte disorders, etc.), and lung damage (Pneumonia, Atelectasis, edema, etc.).

Equally threatening are cardiovascular complications, which may be caused by inadequate gas exchange, alterations due to the effects of anesthetics and other medica

ments used during and immediately after surgery, and shifts in Blood Coagulation and anticoagulation systems. They manifest as Cardiac Arrhythmias, up to cardiac arrest, blood pressure fluctuations, embolism, and thrombosis. Tachycardia may occur due to impaired gas exchange, blood loss, inadequate anesthesia, reflex cardiac irritation, or the use of atropine. Pronounced tachycardia can be a precursor to myocardial fibrillation. Bradycardia may develop as a result of severe hypoxia, vagal stimulation, side effects of halothane or other halogenated anesthetics, or the administration of certain muscle relaxants. Bradycardia can precede cardiac arrest. Arterial hypotension accompanied by tachycardia is most often the result of hypovolemia; with a normal pulse, it indicates vagotonia; and with bradycardia, it points to severe hypoxia, halothane or narcotic analgesic overdosage, or severe vagotonia. Arterial hypertension may occur during hypercapnia, under the influence of ketamine, or due to inadequate depth of anesthesia.

Gastrointestinal complications include vomiting caused by the effect of certain drugs (such as morphine) on the vomiting center and gastric mucosa, irritation of reflexogenic

zones (ROOT of the Tongue, Pharynx) during insufficient depth of induction anesthesia, and hypoxia and hyperhydration in the postoperative period. Against the Background of a weakened laryngeal reflex, this can cause the aspiration of vomit, which is why it is recommended to position the patient without a pillow, with their HEAD turned to the side, and not leave them unattended until they have fully recovered from anesthesia.

During anesthesia, relaxation of the pharyngeal and esophageal Muscles combined with increased gastric pressure can lead to regurgitation—the movement of gastric contents in a direction opposite to the physiological one. Like vomiting, this can result in aspiration accompanied by asphyxia and Mendelson's syndrome. Regurgitation is particularly dangerous because it occurs asymptomatically prior to aspiration.

The best method for preventing vomiting and regurgitation is gastric emptying, as well as the oral administration of antacids before surgery. During induction, extremely careful ventilation prior to tracheal intubation is recommended to avoid forcing air into the stomach, along with the Sellick maneuver (cricoid pressure directed toward the spine) during laryngoscopy and tracheal intubation, and the use of endotracheal tubes with inflatable cuffs.

Nervous system complications may manifest as central nervous system Damage caused by prolonged hypoxia, hypercapnia, or anesthetic overdose (delayed emergence from anesthesia, seizures, psychiatric disturbances), as well as Peripheral Nervous System damage in the form of neuritis, paresis, or paralysis resulting from compression or overstretching of the Brachial Plexus, peroneal nerve, and other nerves due to improper patient positioning during and immediately after surgery.

Complications related to thermoregulation disorders during anesthesia occur in newborns and infants as sclerema—hardening of the subcutaneous adipose tissue accompanied by respiratory failure—and spontaneous hypothermia due to increased heat loss against the background of blocked thermoregulation. In young people and children, malignant hyperthermia may occur in the postoperative period, the exact cause of which is not yet fully understood. Prevention of complications involves monitoring and maintaining normal body temperature, and taking a thorough medical history regarding thermoregulation pathology, especially when using halothane, muscle relaxants, etc.

Alongside the widespread use of the general anesthesia methods described above, local and regional anesthesia have played a significant role since the times of V. K. Anrep (1880) and Koller (1884). Their essence lies in blocking the conduction of impulses from the surgical site at various levels: directly in the surgical area for local anesthesia, and proximally to the surgical site for regional anesthesia.

The technique of local anesthesia—both terminal (application of a local anesthetic solution to the mucous membrane) and infiltrative (injection of a local anesthetic solution into the Tissues of the surgical zone)—is straightforward. This type of anesthesia is typically performed by the operating surgeon. Cocaine and dicain were recently used for terminal anesthesia, but they have now been replaced by less toxic anesthetics: pyromecaine, xycaine, trimecaine, and marcaine. Novocaine is widely used for infiltrative anesthesia, including for the so-called Novocaine blockades by A. V. Vishnevsky. Unlike classical conduction anesthesia, these do not involve applying the anesthetic solution directly to the nerve, but rather injecting it into specific closed fascial spaces (fascial compartment Novocaine blockade of the limbs, presacral, cervical vagosympathetic, and lumbar paranephral blockades).

Regional anesthesia techniques require specific skills and are predominantly performed by anesthesiologists. Among these types of anesthesia, interest in conduction anesthesia has grown over recent decades; it is achieved by applying an anesthetic solution directly to a nerve trunk or plexus. Examples include brachial plexus block, nerve blocks at the wrist level, median, ulnar, radial, femoral, obturator, and other nerve blocks, as well as paravertebral block. Xycaine (lidocaine), trimecaine, and marcaine are more commonly used as anesthetics in these procedures, while novocaine is used less frequently, and dicain only rarely.

Varieties of regional anesthesia include intraosseous and intravenous regional anesthesia under a tourniquet, which block sensitivity in an isolated part of the limb excluded from the circulation.

Epidural and spinal anesthesia provide pain relief through the blockade of spinal nerve roots. Spinal anesthesia was the first to be used clinically (A. Bier, 1898). Epidural anesthesia was introduced much later and more slowly (F. Pagés, 1921) due to its more complex technique. With the advent of epidural space catheterization techniques, epidural anesthesia gained advantages over spinal anesthesia.

The techniques of epidural and spinal anesthesia share many similarities. Puncture of the central spinal canal is performed with the patient in a sitting or (more frequently) lateral decubitus position. The back must be maximally flexed, the head brought toward the chest, and the thighs drawn up toward the abdomen. The Skin at the puncture site is prepared as for surgery and draped with sterile sheets. There are two approaches to the spinal canal: median and paramedian. In the median approach, the needle is inserted into the interspinous space along the midline. Having passed through the skin and subcutaneous tissue, the needle encounters resistance from the supraspinous and then the interspinous ligaments. The paramedian approach involves inserting the needle 1.5–2 cm lateral to the midline of the spinous processes in the intervertebral space, directing the needle slightly medially so that its tip emerges into the interarcuate space along the midline.

The technical elements discussed above are common to both epidural and spinal anesthesia, but subsequent steps differ.

In epidural anesthesia, the stylet is then removed from the needle, and a syringe filled with saline and an air bubble is attached to the needle. The needle is advanced through the ligamentum flavum while pressing on the plunger, during which the air bubble is compressed. As soon as the needle passes through the ligament, the bubble expands and the solution flows freely from the syringe, indicating that the tip of the needle is in the epidural space. This is also evidenced by the absence of cerebrospinal fluid leakage from the needle and the aspiration into the needle hub of a "hanging" drop of solution. If prolonged pain relief is planned, a catheter is threaded through the needle into the epidural space to a specific depth. The anesthetic solution administered through it spreads upward, downward, and partially penetrates the paraneural tissue through the lateral intervertebral foramina, producing a targeted zone of anesthesia as needed.

During spinal anesthesia, the needle is advanced until cerebrospinal fluid appears after the stylet is removed. By injecting a hypo-, hyper-, or isobaric anesthetic solution into the subarachnoid space and adjusting the tilt of the operating table and the patient's position, the desired level of anesthesia is achieved. When using novocaine, anesthesia lasts for about 1 hour; with trimecaine and xylocaine, it lasts 1.5 hours; and with dicaine, 2 hours.

Aside from technical failures where the onset of epidural and spinal anesthesia may be delayed, these techniques can be associated with several complications. The most probable complication is dangerous hypotension, which may be combined with respiratory depression ranging up to complete apnea. Therefore, epidural and spinal anesthesia are contraindicated in emergency conditions. If surgery is necessary under such circumstances, general anesthesia methods are employed instead.

Thus, despite significant progress in anesthesiology and pharmacological efforts to improve pain management agents, they remain far from ideal. Anesthetic management still amounts to a more or less controlled temporary intoxication of the body that affects vital functions. This places an extraordinary level of responsibility on the practitioner performing it, which increases significantly when providing anesthesia in emergency situations.

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