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Physiology of anesthesia mechanism

The first reports of the mechanism of anesthesia appeared in 1903. N.E. Vvedensky was the first to indicate a close relationship between excitation and inhibition. According to him, the state of deep, persistent, not fluctuating local excitement can be described by the term parabiosis. In this case, the nervous tissue is not able to respond to any effect. This condition is reversible and to eliminate the causes returns to normal. With the development of parabiosis, nerve cells sequentially go through three stages: balanced, paradoxical and inhibitory. The patterns related to the peripheral nervous system, domestic physiologists extended to the physiology of the nerve centers, revealing the effect of drugs on the cells of the central nervous system. In 1928, E.Pick proposed, depending on the place of application of the substance, to divide all narcotic and hypnotic drugs into cortical and subcortical. Numerous studies conducted by I.P. Pavlov and his collaborators have shown that narcotic drugs primarily affect the cells of the cerebral cortex, causing outrageous inhibition. Narcotic inhibition does not immediately radiate to subcortical formations. As a result, the restraining effect is removed, and the subcortex is positively induced. “Subcortical riot” and explains the stage of excitement. Subsequent inhibition in the subcortical structures leads to the onset of narcotic sleep.

In 1953, V.S. Talkin, based on the binary theory of inhibition, put forward the proposition that drugs of one series cause inhibition such as Catholic depression, others (barbiturates) - anodic depression. However, many physiologists disagree with this opinion, citing the fact that parabiosis is accompanied by a phase of increasing lability and a phase of a progressive decrease in it.

Thus, the narcotic effect, first of all, is the result of the central influence of the drug, developing inhibition primarily in cortical cells, i.e., anesthesia cannot develop without suppressing the activity of the cortex, but a decrease in cortical activity is achieved by the direct effect of the drug on cortical cells, indirectly through other structures of the brain, functionally closely interconnected with the cortex and the simultaneous effect on the cortex and subcortical structures of the brain.

The clinical manifestation of any type of anesthesia has its own specific features inherent in it. At the same time, there are the most common symptoms characteristic of all types of anesthesia. Anesthesia period is the period of time from the start of anesthesia (saturation of the body with a narcotic drug) to the complete elimination of the latter (awakening).

Moreover, each stage of anesthesia is characterized by a specific clinical picture.

Stage I of anesthesia - analgesia, in which consciousness remains. All reflexes are elevated. The phase of analgesia ends with a loss of consciousness.

II stage of anesthesia - agitation. At this stage, the sensitive and inhibitory parts of the cerebral cortex are inhibited and the corticothalamic pathways are interrupted. Breathing becomes uneven, frequent, irregular, there is an increase in blood pressure, tachycardia, an increase in muscle tone and reflexes. Pupils in this period are dilated, do not respond to light. The transition from one stage of anesthesia to another is not always pronounced. So stage I can be determined by loss of consciousness and the transition to stage II. The transition to stage III is always gradual, it can be described as the "interstitial phase." At this stage, excitement passes and the resting stage sets in.

Stage III anesthesia is surgical, which is divided into four levels (III1, III2, III3, III4). The most acceptable is a gradation of 3 levels. All levels of transition are peculiar and differ one from another in the state of respiration, the cardiovascular system, the degree of relaxation of skeletal muscles and reflex activity.

In stage III, breathing becomes dynamic, exhalation and inhalation are the same. Breathing does not change when deepening anesthesia to III2. Sometimes breathing excursions are accelerated and become superficial, i.e., the difference between the beginning of level III1 and the end of level III2 is barely distinguishable.

At the end of stage III3, paralysis of the costal muscles and diaphragm is noted. It should be emphasized that the use of muscle relaxants in laparotomy also leads to complete immobility of the diaphragm.

The depth of anesthesia is determined by the degree of relaxation of the smooth transverse cavity muscles and tendon reflexes. So, at stage II, muscle tone increases, at stage Ш1 or III2, muscle tone on the hands decreases, on the legs it increases. At stage III3, atony of all muscles occurs. It should be emphasized that the masticatory muscles relax later than other muscle groups.

Eye reflexes are relatively easy to detect on the operating table. Of the eye reflexes, the corneal and pupillary are most often checked. By the end of stage II, the eyeball tends to move away from its central position (a "floating" eyeball). As stage III1 sets in, the eyeball takes on a central position. The condition of the pupil is also an important indicator of the depth of anesthesia, especially in stage III, when in all cases a narrow pupil is noted. In stage III3, the pupil progressively expands and decreases in size with a decrease in the depth of anesthesia. With hypoxia, hypoxemia, the pupil is always dilated, even in the initial stages of anesthesia. In this regard, the anesthetist needs to check the state of the respiratory tract, the concentration of O2. The conjunctival reflex is checked by touching a moistened sterile cloth to the eyeball. In this case, the contraction of the circular muscles of the eyelids occurs. The reflex weakens and disappears at the end of stage III1 – III2. Reflex of the eyelids is determined by the tip of the finger by touching the upper eyelid. A positive reaction indicates contraction of the circular muscle. Its disappearance indicates the onset of an average depth of anesthesia (III2).

IV stage of anesthesia - awakening. This period requires sufficient professionalism of the anesthesiologist. An experienced anesthetist does not complete anesthesia at the time the surgery ends, but somewhat earlier. The complete restoration of consciousness, muscle activity and reflexes indicates the end of this stage.

At the present stage, anesthesiology is dominated by combined anesthesia, i.e., the combination of a number of drugs with muscle relaxants and other anesthetics.

Determination of the depth of anesthesia when using muscle relaxants is no less important than with a single-component anesthesia in its pure form. Typical for anesthesia with relaxants is stage III1-2

Breathing is one of the most significant indicators of combined anesthesia. Spontaneous breathing with the use of relaxants is absent due to the use of mechanical ventilation. The adequacy of the latter is determined by the appearance of the patient, the color of the skin and mucous membranes, pulse and blood pressure. Important tests for determining the state of respiration are oximetry, carbometry, indicating oxygen saturation of the blood and the concentration of carbon dioxide in the exhaled air.

Pulse oximetry is included in mandatory preoperative monitoring, it is based on the principles of oximetry and plethysmographin.

Pulse oximetry, in addition to oxygen saturation, evaluates tissue perfusion (by pulse amplitude) and measures the heart rate. Normally, O2 blood saturation is approximately 100%.

Deviation from this indicator indicates a complication in the form of respiratory disorders (hypoventilation, bronchospasm, unrecognized intubation of the esophagus, etc.). There are no provocations for pulse oximetry. However, this may cause artifacts due to displacement of the sensor, pulsation of veins in the limb, lowered below body level, low perfusion (high total peripheral resistance, severe anemia, hypothermia, low cardiac output, etc.).

The acid-base state of the blood. Ways to correct their violations

Surgery and intensive care of patients with severe forms of late gestosis, autoimmune disorders, with massive obstetric bleeding, purulent-septic complications, extragenital pathology, etc. requires constant monitoring of not only hemodynamic parameters, but also the gas composition of the blood.

The acid-base state of the blood is a balanced process of formation, buffering and secretion of acids.
The lungs, kidneys and buffer systems (carbonate, phosphate, hemoglobin and protein) are involved in maintaining the constancy of the active reaction of blood (and tissues). The lungs play a role in the excretion of carbon dioxide, the kidneys - the excretion of excess hydrogen ions in the urine, and phosphate buffer is involved in the regulation of the blood reaction by the kidneys. In this case, bicarbonate buffer reacts most rapidly to changes in the blood reaction.

Hemoglobin buffer stabilizes blood pH in pulmonary and tissue capillaries. The protein buffer of the blood binds the excess of hydrogen ions, releasing the cations necessary for the regulation of electrolyte balance.

CBS disorders are divided into acidosis (respiratory and metabolic) and alkalosis (respiratory and metabolic), compensated (pH within normal limits) and uncompensated (pH outside normal values), multidirectional (e.g. respiratory alkalosis and metabolic acidosis) and unidirectional (respiratory acidosis) and metabolic acidosis).

Acute respiratory acidosis develops, as a rule, rapidly due to decompensation of the function of external respiration and is accompanied by an increase in paCO2 and pCO2 in venous blood and all extracellular fluid, a decrease in pH at a constant level of BE (paCO2> 45 mm Hg, pH <7, 35, BE + 2 meq / l).

As the pH decreases, electrolyte shifts occur with a tendency to increase phosphate and potassium in the plasma. The accumulation of CO2 leads to an increase in the frequency of respiration, pulse, arterial and intracranial pressure and the development of coma.

If respiratory acidosis is detected, it is necessary to conduct adequate ventilation of the lungs with treatment of the underlying disease that caused the CBS violation. Using sodium bicarbonate in these situations is pointless. Metabolic acidosis develops due to base deficiency in extracellular fluid.

The causes of metabolic acidosis are an increase in the concentration of lactic, pyruvic, uric acids, and the concentration of acetoacetic and hydroxybutyric acids. The accumulation of inorganic acids HSO4 and Н2РО4, loss of bicarbonate, and an increase in excess lactate occur.

Typically, these changes occur during shock, hypoxia, hypovolemia, respiratory, cardiac, renal and hepatic failure, with purulent-septic complications, massive blood transfusions, infusion of electrolyte solutions that change the ionic composition of extracellular fluid. With uncompensated metabolic acidosis BE <2 meq / l, pCO2 34-35 mm RT. Art., pH - 7.35-7.40.

Due to the increased production of hydrogen ions, buffer therapy (sodium bicarbonate) may be ineffective, as it can lead to a deterioration in the oxygen supply to tissues. Moreover, in diabetes, acidosis is treated mainly with insulin.

In severe forms of uncompensated acidosis, the administration of bicarbonate in a dose of not more than 1 mg / kg of body weight is indicated. A reliable and effective way in this pathology is the infusion of balanced solutions, maintaining adequate hydration and circulation.

Respiratory alkalosis develops with excessive removal of CO2 from the body (hyperventilation), while pCO2 decreases, and the pH increases. In this case, respiratory alkalosis is compensated by the development of metabolic acidosis due to the elimination of HCO3 by the kidneys, which leads to a decrease in pH and the content of HCO3. However, with prolonged mechanical ventilation, respiratory alkalosis can lead to serious consequences, namely, decompensated metabolic acidosis, and a violation of the electrolyte composition of the blood. Possible dysregulation of the breath and brain disorders (paresthesia, muscle twitching, cramps). The deficit of bases is growing, the pH is within the normal range or slightly increased, pCO2 <35 mm Hg. Art.

If such violations of CBS are detected, it is necessary to treat the underlying disease that caused hypoxic changes, cerebral edema. With hypocalcemia, the introduction of 10-20 ml of a 10% calcium solution is indicated.

Metabolic alkalosis is characterized by an excess of bases in the extracellular fluid, an increase in buffer bases, pH and HCO3 increase. The cause of metabolic alkalosis are: hypokalemia, hypochloremia, the use of massive doses of corticosteroids, diuretics, sodium bicarbonate.

Treatment with acids (hydrochloric acid or ammonium) in these situations can be harmful. To normalize the pH, the introduction of chlorine and potassium preparations is necessary, i.e., therapy should be aimed at enhancing the ability of the kidneys to retain hydrogen ions and secrete buffers, namely bicarbonate.

Respiratory acidosis can lead to increased intracranial and blood pressure, hyperventilation, increased bronchial resistance, pulmonary hypertension, oliguria, impaired water-salt metabolism.

Respiratory alkalosis, in contrast, causes hypotension, a change in venous return and a decrease in minute release, and insufficient oxygen supply to body tissues.

Metabolic alkalosis leads to a violation of the water-electrolyte composition of the blood, hypoventilation and the development of respiratory acidosis with all the ensuing consequences.

Metabolic acidosis causes an increase in blood flow in the vessels of the brain, a decrease in arterial and venous pressure, MOS, and the development of functional hypovolemia.

For timely diagnosis and correction of CBS disorders, it is necessary to determine it at least once every 2 hours, especially in women with severe forms of late gestosis, with massive bleeding, purulent-septic complications and other pathologies that require intensive therapy and surgical intervention.

Monitoring the concentration of carbon dioxide at the end of exhalation (capnography) allows you to objectively assess the condition and other vital functions of the body, including the cardiovascular system. The stability of hemodynamic parameters indicates the adequacy of anesthesia.

In this regard, information monitoring is of great importance at the present stage, which makes it possible to objectively assess the state of the cardiovascular system and other vital functions of the body during anesthesia. It is very important to determine the difference (gradient) between the concentration of CO2 at the end of exhalation and the partial pressure of CO2 in the arterial blood (normal 2-5 mm Hg). This indicator reflects the alveolar, "dead space". A change in this parameter indicates a significant decrease in lung perfusion and a complication (air embolism, decreased cardiac output, blood pressure, etc.).

Percutaneous monitoring of oxygen and carbon dioxide allows you to indirectly judge pO2 in the artery if cardiac output and perfusion are adequate. It is known that PtcO2 (PsO2) is 75% of PaO2, and PtcCO2 (PSCo2) is 130% of PaCO2. The lack of correlation between PtcO2 and PaO2 should be considered as inadequate tissue perfusion (shock, hypothermia, hyperventilation). The PtcO2 index (ratio of PtcO2 to PaO2) varies in proportion to cardiac output and peripheral flow. At the same time, pulse oximetry and percutaneous monitoring should be considered as complementary techniques.

Monitoring of the central nervous system is carried out by conducting electroencephalography. EEG involves recording electrical potentials generated by cells of the cerebral cortex. Monitoring evoked potentials is a non-invasive method for assessing central nervous system function by measuring the electrophysiological response to sensory stimulation.

The most common monitoring of visual, acoustic and somatosensory evoked potentials. Evoked potentials are affected not only by damage to neurons, but also by other factors. It must be remembered that the lack of response when monitoring evoked potentials is a prognostic sign for central nervous system disorders, which is especially important in women with severe forms of late gestosis, extragenital pathology, with complications of anesthesia, etc.

Thus, monitoring of vital functions of the body in obstetric and gynecological patients during anesthesia, in the postpartum and surgical period, during intensive care ensures high-quality monitoring of patients and allows timely diagnosis and prevention of unforeseen complications.
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Physiology of anesthesia mechanism

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    затянувшееся пробуждение и апноэ - дрожь - судороги - нарушение дыхания и кровообращения - нарушения чувствительности в конечностях - осиплость голоса - отек подсвязочного аппарата - рвота - мышечные боли Затянувшееся пробуждение м б связано с гипоксией головного мозга из-за гипотонии, гиповентиляции, метаболических нарушений – ацидоза, ведущих к отеку мозга.
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