Anesthesia during neurosurgical operations is one of the most difficult sections of anesthesiology, which is due to the following factors:<br />Damage to the central nervous system violates the natural defense mechanisms and mechanisms of regulation of the functions of vital organs and systems. Even before surgery, severe lesions can be observed: dehydration and pulmonary edema, with damage to the hypothalamic-pituitary system; epistatus, with damage to the corresponding parts of the cortex, subcortex and brain stem; uncontrolled hypotension and, as a result, multiple organ failure, with spinal injuries.<br />Very often, the condition of animals worsens under the influence of iatrogenic factors: dehydration therapy to combat cerebral edema, anticonvulsant therapy, etc.<br />Knowledge of the physiology of the CNS is necessary for the anesthetic management of neurosurgical operations. Many anesthetics have significant effects (both undesirable and beneficial) on brain metabolism, cerebral blood flow, cerebrospinal fluid production and absorption, intracranial content volume, and intracranial pressure.<br />Physiology of the CNS<br />brain metabolism<br />At rest, the brain receives up to 20% of the oxygen received by the body. The main consumer of energy in the brain is the enzyme ATPase, which maintains the electrical activity of neurons. The brain's need for oxygen is extremely high compared to other organs, and there are no oxygen reserves in it. If blood does not enter the brain within 10 seconds, the oxygen tension drops and the animal loses consciousness. If cerebral blood flow is not restored within 3-8 minutes, then ATP stores are depleted, and irreversible damage to neurons occurs. The neurons of the hippocampus and cerebellum that are most sensitive to hypoxia.<br />Neurons are provided with energy mainly due to the utilization of glucose. In the CNS, almost all glucose undergoes aerobic breakdown, so oxygen uptake and glucose uptake change in parallel. During fasting, ketone bodies, acetoacetate and beta-hydroxybutyrate, become the main source of energy for the brain. Although the brain is able to absorb lactic acid from the blood, its metabolism does not play a significant role in energy supply. No less than hypoxia, acute hypoglycemia is dangerous for the brain. Studies by Cottrell J. E., Smith D. S. revealed a paradoxical phenomenon: in total cerebral ischemia, hyperglycemia contributes to intracellular acidosis and exacerbates neuronal damage.<br />cerebral blood flow<br />The brain makes up only 2% of the total mass, about 15% of cardiac output is obtained. This ratio reflects the high level of brain metabolism. Regional cerebral blood flow (MR) depends on the level of metabolism and increases significantly with an increase in the level of oxygen consumption by the brain.<br />Changes in cerebral blood flow occur in parallel with changes in the partial pressure of carbon dioxide (PaCO2). An increase in PaCO2 doubles UA, while a decrease in PaCO2 cuts it in half.<br />Body temperature<br />Hypothermia reduces cerebral blood flow, while hyperthermia has the opposite effect. A decrease in temperature leads to a decrease in metabolism, while vascular resistance increases and cerebral blood flow decreases, respectively, venous and CSF pressure decreases. A decrease in body temperature by 1 degree lowers the metabolic rate by 7-8%, respectively, and the consumption of oxygen by the brain decreases. At a temperature of 30 degrees, oxygen consumption by the brain is reduced by 50%. A decrease in the rate of metabolic processes during hypothermia inhibits the initial components of ischemic reactions and contributes to the conservation of ATP reserves.<br />Blood viscosity<br />In healthy animals, blood viscosity does not significantly affect UA. Blood viscosity is most dependent on hematocrit. Therefore, a decrease in hematocrit decreases viscosity and increases UA. A decrease in hematocrit reduces the oxygen capacity of the blood and, consequently, oxygen delivery. High hematocrit increases blood viscosity and lowers UA. Studies have shown that for better oxygen delivery to the brain, the hematocrit should be 30-35%.<br />Blood-brain barrier (BBB)<br />There are practically no pores between the endothelial cells of the cerebral vessels. Few pores are the main morphological feature of the BBB. The lipid barrier is permeable to fat-soluble substances, but significantly limits the penetration of ionized particles and large molecules. Thus, the permeability of the BBB for a molecule of any substance depends on its size, charge, lipophilicity and the degree of binding to blood proteins. Carbon dioxide, oxygen and lipophilic substances (which include most anesthetics) easily pass the BBB, while for most ions, proteins and large molecules (for example, mennitol) it is practically impermeable.<br />Water freely penetrates the BBB through the volumetric current mechanism, and the movement of even small ions is difficult. As a result, rapid changes in plasma electrolyte concentration (as well as osmolarity) cause a transient osmotic gradient between the plasma and the brain. Acute hypertonicity of the plasma leads to the movement of water from the substance of the brain into the blood. In acute hypotonicity, on the contrary, there is a movement of water from the blood into the substance of the brain. Therefore, significant violations of the concentration of sodium and glucose in plasma must be eliminated immediately.<br />The integrity of the BBB is violated by severe arterial hypertension, brain tumors, craniocerebral injuries, severe hypercapnia, hypoxia, and persistent convulsive activity.<br />Non-inhalation anesthetics<br />All inhalational anesthetics, except for ketamine, reduce brain metabolism and UA or do not affect these parameters. Barbiturates, propofol, and benzodiazepines reduce MC, as well as brain oxygen consumption. Opioids have minimal effect on these parameters (the exception is butorphanol, which slightly increases ICP).<br /><br />The effect of muscle relaxants on the central nervous system<br />Muscle relaxants act on the central nervous system indirectly. They cause vasodilation of the brain (resulting in the release of histamine) and increase blood pressure, which leads to an increase in ICP. On the other hand, muscle relaxants can cause arterial hypotension (due to blockade of the autonomic ganglia), which leads to a decrease in central perfusion pressure. An adequate dose of thiopental or propofol and hyperventilation significantly reduce the severity of ICP volume when using succinylcholine. With prolonged apnea, hypercapnia and hypoxia occur, which also leads to a significant rise in ICP.<br />Protecting the brain from ischemia<br />Due to the high demand for oxygen and glucose, the brain is extremely sensitive to ischemia. Impaired brain perfusion, hypoglycemia, and hypoxia rapidly cause neuronal damage; a decrease in perfusion, in addition, leads to the accumulation of toxic metabolic products. If PaO2, UA and blood glucose levels do not return to normal within 3-8 minutes, then ATP stores are depleted and irreversible brain damage occurs.<br />In ischemia, the state of water and electrolyte balance is of particular importance. So, for example, an increase in intracellular calcium concentration is carried out as a result of the following processes: phospholipase 2, due to a lack of oxygen and glucose, is not able to move calcium ions out of the cytosol or into intracellular tanks. A steady increase in intracellular calcium concentration activates lipases and proteases, which leads to structural damage to neurons. Phospholipase 2 also acts on the phospholipids of cell membranes, causing the release of arachidonic acid, the oxidation of which leads to the formation of prostaglandins and leukotrienes. They increase the permeability of the blood-brain barrier for macromolecules and water, which contributes to the development of cerebral edema.<br />Anti-ischemic agents<br />Calcium antagonists nimodipine is indicated for ischemia caused by traumatic brain injury or subarachnoid hemorrhage. This drug expands the cerebral vessels and improves blood circulation in the affected areas of the brain. It is administered in/in drip 0.1-0.5 mg/hour up to 10 mg/day.<br />Lidocaine can be used to block sodium channels and thus reduce cerebral edema. In low concentrations (0.5-1.0 mg/kg), it does not block the electrical activity of the brain and protects it from hypoxia.<br />Circulatory-metabolic disorders that occur 2-8 hours after injury to the spinal cord or brain, contributing to the development of cerebral edema, are a consequence of the activation of lipid peroxidation. To protect nerve cells from free radicals, Mexidol 50-200 mg/live is used. 2 times a day, or emicidin 1 ml / 10 kg. These drugs activate microcirculation, eliminate tissue hypoxia and accelerate reparative processes.<br />cerebral edema<br />The increase in brain water content may be due to several mechanisms. Most often, vasogenic edema caused by an increase in the permeability of the BBB. The cause of vasogenic edema can be inflammatory diseases of the brain, mechanical damage, brain tumors, arterial hypertension. In hydrocephalus, cerebrospinal fluid extends into the extracellular space of the brain, causing interstitial edema. With metabolic disorders (hypoxia, systemic ischemia), the active transport of sodium from the cell into the interstitial fluid is disrupted, which leads to a progressive swelling of the brain cells (cytotoxic edema).<br />Treatment<br />Treatment of cerebral edema should be aimed at eliminating the cause. Vasogenic edema associated with brain tumors is successfully treated with corticosteroids at a dose of 15-30 mg/kg. With the introduction of diuretics, ICP decreases due to a decrease in intracellular fluid from healthy brain tissue.<br />Mannitol (1-2 g/kg) significantly reduces ICP, its action comes quickly. By increasing plasma osmolarity, it causes osmotic diuresis. The main side effect is an increase in BCC, which, if the function of the heart and kidneys is impaired, is fraught with pulmonary edema.<br />Loop diuretics (furosemide 1-4 mg/kg) are also used to treat cerebral edema, although their action is weaker and slower compared to that of osmodiuretics. Loop diuretics have an additional positive property, they suppress the formation of CSF. In our opinion, it is advisable to use mannitol in combination with furosemide (synergism). The negative aspects of this synergism are hypotension and hypokalemia.<br />An effective means of combating cerebral edema is artificial lung ventilation (ALV) in hyperventilation mode. The hypocapnia that occurs in this case causes vasospasm in healthy parts of the brain with preserved regulation, which improves blood circulation in damaged areas where autoregulation is impaired. During hyperventilation, CSF formation decreases, hypocapnia occurs, and saturation also increases, indicating adequate oxygenation.<br />Hypertonic saline solutions have a beneficial effect on patients with traumatic brain injury, as they reduce ICP and may improve regional cerebral blood flow. Hypertonic saline solutions extract fluid from brain tissue in a manner similar to other hyperosmolar solutions (eg, mannitol). Apparently, hypertonic saline solutions will soon be included in the standard protocols for intensive care. Hypertonic saline solutions increase the concentration of sodium in the plasma, so the question of the advisability of their use is still open.<br /><br />MSc Sura Hasan Al-Zubaidi