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Cerebral Physiology and the Effects of Anesthetic Drugs

Cerebral Physiology and the Effects of Anesthetic Drugs. Dr abdollahi.

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Cerebral Physiology and the Effects of Anesthetic Drugs

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  1. Cerebral Physiology and the Effects of Anesthetic Drugs Drabdollahi

  2. Anesthesia for neurosurgery requires an understanding of the physiology of the central nervous system (CNS). The relationship between cerebral blood flow (CBF), cerebral metabolic rate for oxygen consumption (CMRO2), and intracranial pressure (ICP) is influenced by physiologic and pharmacologic factors that are often under the control of the anesthesiologist.

  3. The selection of drugs, ventilation techniques, and monitors may have important implications in the care of patients with diseases involving the CNS.

  4. The adult human brain weighs approximately 1350 g and therefore represents about 2% percent of total-body weight. However, it receives 12% to 15% of cardiac output. This high flow rate is a reflection of the brain's high metabolic rate.

  5. Normal Cerebral Physiologic Values

  6. CEREBRAL BLOOD FLOW • CBF: Cerebral perfusion pressure cerebral vascular resistance CPP: MAP-ICP

  7. Approximately 60% of the brain's energy consumption is used to support electrophysiologic function. The depolarization-repolarization activity that occurs and is reflected in the EEG requires expenditure of energy for the maintenance and restoration of ionic gradients and for the synthesis, transport, and reuptake of neurotransmitters. The remainder of the energy consumed by the brain is involved in cellular homeostatic activities

  8. Local CBF and CMR within the brain are very heterogeneous, and both are approximately four times greater in gray matter than in white matter. The cell population of the brain is also heterogeneous in its oxygen requirements. Glial cells make up about half the brain's volume and require less energy than neurons do.

  9. Besides providing a physically supportive latticework for the brain, glial cells are important in reuptake of neurotransmitters, in delivery and removal of metabolic substrates and wastes, and in blood-brain barrier (BBB) function.

  10. Cerebral Blood Flow • An understanding of neurophysiology is important for the management of patients with CNS disease. Normal CBF is 40 to 50 mL/100 g/min and represents about 15% of cardiac output. This disproportionately large CBF is due to the rapid metabolic rate of the brain and the absence of oxygen stores.

  11. Factors Influencing Cerebral Blood Flow

  12. Determinants of CBF include • (1) CMRO2 • (2) Paco2 • (3) cerebral perfusion pressure (CPP) and autoregulation • (4 ) Pao2 • (5) Anesthetic drugs

  13. CEREBRAL METABOLIC RATE FOR OXYGEN • Changes in CBF are directly coupled with CMRO2. Increases or decreases in CMRO2 result in a proportional increase or decrease in CBF. Hypothermia, which reduces CMRO2, also decreases CBF about 7% for every 1°C decrease in body temperature below 37c.

  14. CMR is influenced by several phenomena in the neurosurgical environment, including: • The functional state of the nervous system, • Anesthetic drugs, • Temperature.

  15. Although the precise mechanisms that mediate flow-metabolism coupling have not been defined, the data available implicate local by-products of metabolism (K+, H+, lactate, adenosine, and adenosine triphosphate [ATP]). Glutamate, released with increased neuronal activity, results in the synthesis and release of nitric oxide (NO),a potent cerebral vasodilator that plays an important role in coupling of flow and metabolism.

  16. FUNCTIONAL STATE • CMR decreases during sleep and increases during sensory stimulation, mental tasks, or arousal of any cause. During epileptic activity, increases in CMR may be extreme, whereas regionally after brain injury and globally with coma, CMR may be substantially reduced.

  17. ARTERIAL CARBON DIOXIDE PARTIAL PRESSURE • Changes in Paco2 produce corresponding direcrional changes • in CBF between a Paco2 of 20 to 80 mmHg . • As a guide, CBF increases or decreases I mL/IOO g/min for every I-mm Hg increase or decrease in Paco2 from 40 mm Hg. Such changes in CBF reflect the effect of carbon dioxide-mediated alterations in perivascular pH and lead to dilation or constriction of cerebral arterioles.

  18. These Paco2 induced changes in CBF are transient because because the pH of cerebrospinal fluid (CSF) gradually normalizes as a result of extrusion of bicarbonate. • CBF returns to normal in 6 to 8 hours, even if the altered Paco2 levels are maintained. The ability of decreases in Paco2 (secondary to iatrogenic hyperventilation) to lower CBF and thereby cerebral blood volume and ICP is a critically important principle in neuroanesthesia.

  19. CEREBRAL PERFUSION PRESSURE ANDAUTOREGULATION • CPP is the difference between mean arterial pressure (MAP) and ICP or central venous pressure (CVP), whichever is greater. For example, assuming that ICP or CVP is 15 mm Hg, a MAP of 65 mm Hg would provide a CPP of 50 mm Hg.

  20. Autoregularion refers to the mechanism that maintains CBF constant in the presence of a changing CPP and reflects the ability of cerebral arterioles to constrict or relax in response to changes in perfusion (distending) pressure. • This response normally requires 1 to 3 minutes to develop, so a rapid increase in MAP is associated with a brief period of cerebral hyperperfusion.

  21. Similarly, the converse situation occurs with hypotension. Autoregulation maintains CBF relatively constant between a CPP of 50 and 150 mmHgWith normal autoregulation and an intact blood-brain barrier, vasopressorsaffect CBF only when MAP is below 50 to 60 mm Hg or above 150 to 160 mm Hg.

  22. With respect to inhaled anesthetics, autoregulation is maintained at anesthetic concentrations less than 1 minimum alveolar concentration (MAC).At higher concentrations, inhaled anesthetics abolish autoregulation, and CBF becomes proportional to MAP. In contrast, intravenous anesthetics do not disrupt autoregulation.

  23. The autoregulation curve in patients with chronic hypertension is shiftedto the right such that a lower MAP is less well tolerated.

  24. The anesthetic state shifts the autoregulatory response to the left, which provides for some safety from the decreases in MAP that can occur intraoperatively.

  25. Autoregulation may be impaired in patients with • Poorly controlled systemic hypertension • May also be impaired in the proximity of intracranial tumors

  26. AUTOREGULATION • A drop in CPP produces vasodilatation • A rise in CPP produce vasoconstriction • autoregulation fails when the CPP falls below 60mmhg or rises above 160. • in damaged brain the autoregulation is impaired.

  27. ARTERIAL OXYGEN PARTIAL PRESSURE • Decreases in Pao2 result in an exponential increase in CBF • below a threshold value of about 50 mm Hg .

  28. INHALED ANESTHETICS • Volatile anesthetics administered during normocapnia at concentrations higher than 0.5 MAC rapidly produce cerebral vasodilation and result in dose-dependent increases in CBF. CBF remains increased relative to CMRO2 during administration of halothane, isoflurane, or sevoflurane.

  29. This drug-induced increase in CBF occurs despite concomitant decreases in CMR02. The largest increase in CBF occurs with halothane, with less of an effect seen with isoflurane, desflurane, and sevoflurane. • Nitrous oxide also increases CBF.

  30. INTRAVENOUS ANESTHETICS • All intravenous drugs except ketamine reduce CMR02 and CBF in a dose-dependent fashion, and this decrease is associated with a reduction in ICP. There is controversy about the effects of ketamine, which probably reflects differences in the conditions of the research study.

  31. When ketamine is given on its own without control of ventilation, Paco2, CBF, and ICP all increase, whereas when given in the presence of another sedative/anesthetic drug in patients whose ventilation is controlled, these effects are not noted. Because of this controversy, however, ketamine is not usually selected for patients with known intracranial disease.

  32. Thiopental, propofol, and etomidate are cerebral vasoconstrictors • that decrease CMR02, CBF, and ICP. These drugs may be administered to patients with intracranial hypertension to decrease ICP. Large doses of propofol or thiopental may decrease systemic blood pressure sufficiently to also decrease CPP.

  33. Autoregulation of CBF is not altered by propofol or thiopental. Myoclonus may accompany the administration of etomidate. An increased frequency of excitatory peaks on the electroencephalogram of patients receiving etomidate, as compared with thiopental, suggests caution in the administration of etomidate to patients with a history of epilepsy..

  34. Benzodiazepines decrease CMR02 and CBF, analogous to thiopental and propofol.

  35. Opioids decrease CBF and possibly ICP in the absence of hypoventilation. These drugs should be used with caution in patients with intracranial disease because of their • depressant effects on consciousness, • production of miosis, • depression of ventilation with associated increases in ICP if Paco2 increases.

  36. Although opioids do not usually increase ICP, there is evidence that modest and transient increases in ICP may accompany administration in patients with acute head injury despite maintenance of normocapnia or even hypocapnia.This is probably related to reductions in arterial blood pressure with autoregulatory-mediated cerebral vasodilation.

  37. a2-agonists(clonidine and dexmedetomidine) have sedative, sympatholytic, and analgesic properties. They are unique sedatives in that: • They do not cause significant respiratory depression • They have no effects on ICP • Because they reduce arterial blood pressure without having an effect on ICP, they reduce CPP. • a2-agonists reduce CBF • Only slightly attenuate the cerebrovascular response to changes in Paco2.

  38. Clinically, a2-agonists can be usedintraoperativelyto reduce the dose of other anesthetics and analgesics or postoperatively as sedatives and to attenuate postoperative hypertension and tachycardia.

  39. NEUROMUSCULAR BLOCKING DRUGS • Neuromuscular blocking drugs do not usually affect ICP unless they induce release of histamine or hypotension. • Histamine can cause cerebral vasodilation leading to an increase in ICP. Succinylcholine may increase ICP through stimulation of muscle spindles, which in turn either directly or indirectly results in increased CMR02.Because CBF is coupled to CMR02, the increase in CMR02 is responsible for increasing CBF and thus ICP. However, the increase in ICP has not been a consistent observation.

  40. Extrinsic Mechanisms for control ofCBF:Viscosity • • Polycythemia is detrimental to CBF and can cause a CVA • • HCTs less than 30 improve CBF but at the expense of decrease O2 carrying capacity • • Studies suggest the optimal HCT to be between 30 and 40

  41. Systemic vasodilators (nitroglycerin, nitroprusside, hydralazine, calcium channel blockers) vasodilate the cerebral circulation and can, depending on mean arterial pressure, increase CBF.

  42. Vasopressors such as phenylephrine, norepinephrine, ephedrine, and dopamine do not have significant direct effects on the cerebral circulation. Their effect on CBF is dependent on their effect on systemic blood pressure.

  43. When mean arterial pressure is below the lower limit of autoregulation, vasopressors increase systemic pressure and thereby increase CBF. If systemic pressure is within the limits of autoregulation, vasopressor-induced increases in systemic pressure have little effect on CBF.

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