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• W2469909968 abstract "INTRAOPERATIVE MANAGEMENT INTRAOPERATIVE MANAGEMENT OF VENTILATION By changing the PaCO2, cerebral blood flow (CBF), cerebral blood volume (CBV), and intracranial pressure can be modified. A high PaCO2 causes cerebral vasodilation, increasing CBF and to a lesser extent CBV. Between a PaCO2 of 18 mmHG and a PaCO2 of 80 mm Hg, CBF varies directly with the PaCO2. The lowest CBF that can be obtained by hyperventilation occurs at a PaCO2 of 18 20 mmHg. In INR procedures, PaCO2 control has two objectives: (1) to modify cerebral blood flow: A decrease in cerebral blood flow is useful for imaging since contrast transit time is decreased, and better contrast visualization will result. In embolization of intracerebral AVM’s, lowering of the CBF can decrease shunt flow and allow the embolic liquid adhesive more time to polymerize inside the AVM, decreasing the possibility of distal embolization. If the neuroradiologist requests it, ventilation can be increased, preferably by increasing respiratory rate, until he or she is satisfied with the velocity of contrast flow, or until the PaCO2 is 20 to 25 mmHg. When controlled hypotension and hyperventilation are used concurrently, cerebral ischemia will occur at a higher level of blood pressure than it would if the PaCO2 was normal. Hyperventilation also augments the CBVlowering effects of hypotension induced by bblockers. Accordingly, we avoid using hyperventilation simultaneously with controlled hypotension, and maintain either normocapnia, or mild hyperventilation (PaCO2 30 to 35 mmHg) during controlled hypotension. (2) to control intracranial pressure In cases of cerebral edema or in the presence of mass lesions, hyperventilation is used to decrease the ICP. The PaCO2 should be maintained close to 20 mmHG to effect the maximum decrease in CBV. Hyperventilation, however, will not reduce the ICP if there is cerebral venous outflow obstruction. Thus, all constrictions around the neck, such as crossing EKG cables, or gowns, must be loosened. If possible, the head of the bed should be raised in cases of elevated ICP to facilitate venous outflow. All inhalation anesthesia agents, to different degrees, cause a dose-dependent increase in CBF; however, when hyperventilation is begun prior to the introduction of the inhaled anesthetic, and the end -tidal anesthetic concentration is kept close to 1 MAC, the ICP is not increased. To manage ventilation, the PaCO2 can be obtained from a blood gas, or deduced from the PetCO2. Ventilatory adjustments should be made by changing respiratory rate, keeping tidal volume constant, because changes in tidal volume can alter physiologic dead space and change the PetCO2 PaCO2 relationship. Increasing the ventilation by using large tidal volumes can also elevate intracerebral venous pressure. Most patients for INR are ventilated to a PaCO2 of around 35 mmHg. However, we change the level of ventilation in conjunction with blood pressure control to fit the clinical situation. Anesthesia For Interventioanl Neuroradiology, Part IV: Intraoperative management, Anticoagulation, Management of neurologic complications, Conclusions 2 of 8 DELIBERATE HYPERCAPNIA According to Young et al,(75) hypercapnia, to a PaCO2 of 50 to 60 mmHg has been used in cases of facial AVM’s or dural fistulas to decrease the possibility of inadvertent intracerebral embolization when embolic agents are injected from the venous side into the malformation. The elevated PaCO2 increases CBF and cerebral venous outflow to a greater degree than extracranial venous outflow. Presumably, pressure gradients, clinically demonstrable but not measured, are created that impede extracranial to intracerebral flow. INTRAOPERATIVE CONTROL OF BLOOD PRESSURE The most important physiological goals in the management of arterial pressure during INR procedures are to maintain cerebral perfusion pressure, to prevent vessel rupture, and to avoid cerebral edema. A secondary goal, to assist the neuroradiologist to perform the procedure, is met by adjusting hemodynamics. In most INR procedures, a normal or high blood pressure is needed initially to assist in floating the superselective catheter to the lesion. On reaching the lesion, induced hypotension is used for embolization and then, postoperatively, the blood pressure is increased above hypotensive levels, but kept below control. During the initial diagnostic angiography, the mean arterial pressure (MAP) is kept close to basal levels. Next, during the phase of superselective catheterization, the neuroradiologist often requests an increase in pressure to pre-induction or slightly higher than normal levels, in order to float the thin superselective catheter into place. It is usually not necessary to induce hypertension with vasoactive drips at this time. In our team’s experience, all that is needed is a decrease in the depth of anesthesia, but rarely we have to use small boluses of ephedrine or neosynephrine. Once the radiologist reaches the AVM or aneurysm, we begin controlled hypotension, to a MAP of 50 to 70 mmHg, and continue until embolization is complete. This is the most critical part of the procedure. During AVM embolization with liquid adhesive, we have been empirically using a Valsalva maneuver (to 20mm Hg) during, and for a few seconds after, adhesive injection into the AVM nidus. We believe that the increase in cerebral venous pressure produced by the Valsalva decreases AVM venous outflow, and lessens the amount of distal embolization of the adhesive. It is very critical that the patient does not “buck” during the Valsalva maneuver. Deepening the level of anesthesia may not be well tolerated during controlled hypotension; therefore, we recommend administering an additional dose of muscle relaxant prior to Valsalva in order to avoid movement or coughing during this crucial phase of the procedure. Although no research data is yet available, there is clinical angiographic evidence that a Valsalva maneuver with controlled hypotension, during injection of liquid adhesive, significantly decreases circulation time through AVMs,(76) and allows time for the adhesive to solidify without distal embolization. After the embolization is complete, we allow the MAP to increase, but keep it 10 20 percent lower than basal levels during emergence and in the neurological intensive care unit." @default.
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• W2469909968 title "Anesthesia For Interventioanl Neuroradiology, Part IV: Intraoperative management, Anticoagulation, Management of neurologic complications, Conclusions" @default.
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