Đang tải... (xem toàn văn)
(BQ) Part 2 book Morgan & mikhail’s clinical anesthesiology has contents: Kidney physiology & anesthesia, anesthesia for genitourinary surgery, anesthesia for orthopedic surgery, obstetric anesthesia, pediatric anesthesia, geriatric anesthesia, peripheral nerve blocks,... and other contents.
CHAPTER 27 Anesthesia for Neurosurgery KEY CONCEPTS Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, location, and intracranial pressure Slowly growing masses are frequently asymptomatic for long periods (despite relatively large size), whereas rapidly growing ones may present when the mass remains relatively small Computed tomography and magnetic resonance imaging scans should be reviewed for evidence of brain edema, midline shift greater than 0.5 cm, or ventricular displacement or compression Operations in the posterior fossa can injure vital circulatory and respiratory brainstem centers, as well as cranial nerves or their nuclei Venous air embolism can occur when the pressure within an open vein is subatmospheric These conditions may exist in any position and during any procedure whenever the wound is above the level of the heart Optimal recovery of air following venous air embolism is provided by a multiorificed catheter positioned at the junction between the right atrium and the superior vena cava Confirmation of correct catheter positioning can be accomplished by intravascular electrocardiography, radiography, or transesophageal echocardiography In a patient with head trauma, correction of hypotension and control of any bleeding take precedence over radiographic studies and definitive neurosurgical treatment because systolic arterial blood pressures of less than 80 mm Hg predict a poor outcome Sudden, massive blood loss from injury to the great vessels can occur intraoperatively with adjacent thoracic or lumbar spine procedures downloaded from www.medicalbr.com Anesthetic techniques must be modified in the presence of intracranial hypertension and marginal cerebral perfusion In addition, many neurosurgical procedures require patient positions (eg, sitting, prone) that further complicate management This chapter applies the principles developed in Chapter 26 to the anesthetic care of neurosurgical patients Intracranial Hypertension Intracranial hypertension is defined as a sustained increase in intracranial pressure (ICP) above 15 mm Hg Intracranial hypertension may result from an expanding tissue or fluid mass, a depressed skull fracture if it compresses a venous sinus, inadequate absorption of cerebrospinal fluid (CSF), excessive cerebral blood volume (CBV), or systemic disturbances promoting brain edema (see next section) Multiple factors may be present For example, tumors in the posterior fossa usually not only are associated with some degree of brain edema and mass effect, but also readily obstruct CSF outflow by compressing the fourth ventricle (obstructive hydrocephalus) Although many patients with increased ICP are initially asymptomatic, they typically develop characteristic symptoms and signs, including headache, nausea, vomiting, papilledema, focal neurological deficits, and altered consciousness When ICP exceeds 30 mm Hg, cerebral blood flow (CBF) progressively decreases, and a vicious circle is established: ischemia causes brain edema, which in turn, increases ICP, resulting in more ischemia If left unchecked, this cycle continues until the patient dies of progressive neurological damage or catastrophic herniation Periodic increases in arterial blood pressure with reflex slowing of the heart rate (Cushing response) can be correlated with abrupt increases in ICP (plateau waves) lasting 1 to 15 min This phenomenon is the result of autoregulatory mechanisms periodically decreasing cerebral vascular resistance and increasing arterial blood pressure in response to cerebral ischemia Eventually, severe ischemia and acidosis completely abolish autoregulation (vasomotor paralysis) CEREBRAL EDEMA An increase in brain water content can be produced by several mechanisms Disruption of the blood–brain barrier (vasogenic edema) is most common and allows the entry of plasma-like fluid into the brain Increases in blood pressure enhance the formation of this type of edema Common causes of vasogenic downloaded from www.medicalbr.com edema include mechanical trauma, high altitudes, inflammatory lesions, brain tumors, hypertension, and infarction Cerebral edema following metabolic insults (cytotoxic edema), such as hypoxemia or ischemia, results from failure of brain cells to actively extrude sodium, causing progressive cellular swelling Interstitial cerebral edema is the result of obstructive hydrocephalus and entry of CSF into brain interstitium Cerebral edema can also be the result of intracellular movement of water secondary to acute decreases in serum osmolality (water intoxication) TREATMENT Treatment of intracranial hypertension, cerebral edema, or both, is ideally directed at the underlying cause Metabolic disturbances are corrected, and operative intervention is undertaken whenever appropriate Vasogenic edema— particularly that associated with tumors—often responds to corticosteroids (dexamethasone) Vasogenic edema from trauma typically does not respond to corticosteroids Blood glucose should be monitored frequently and controlled with insulin infusions (if indicated) when steroids are used Osmotic agents are usually effective in temporarily decreasing brain edema and ICP until more definitive measures can be undertaken Diuresis lowers ICP chiefly by removing intracellular water from normal brain tissue Moderate hyperventilation (PaCO2 of 30–33 mm Hg) is often very helpful in reducing CBF, CBV, and ICP acutely, but may aggravate ischemia in patients with focal ischemia Mannitol, in doses of 0.25 to 1 g/kg, is particularly effective in rapidly decreasing intracranial fluid volume and ICP Its efficacy is primarily related to its effect on serum osmolality A serum osmolality of 300 to 315 mOsm/L is generally considered desirable Mannitol can transiently decrease blood pressure by virtue of its weak vasodilating properties, but its principal disadvantage is a transient increase in intravascular volume, which can precipitate pulmonary edema in patients with borderline cardiac or renal function Mannitol should generally not be used in patients with intracranial aneurysms, arteriovenous malformations (AVMs), or intracranial hemorrhage until the cranium is opened Osmotic diuresis in such instances can expand a hematoma as the volume of the normal brain tissue around it decreases Rapid osmotic diuresis in elderly patients can also occasionally cause a subdural hematoma due to rupture of fragile bridging veins entering the sagittal sinus Rebound cerebral edema may follow the use of osmotic agents Hypertonic saline (3% NaCl) is sometimes used to reduce cerebral edema and downloaded from www.medicalbr.com ICP Hypertonic saline should be administered with care to avoid central pontine myelinolysis or osmotic demyelination syndrome in hyponatremic patients (see Chapter 49) Serum sodium concentration and osmolality should be frequently monitored In patients with traumatic brain injury, interventions in addition to mannitol to lower intracranial pressure include head elevation, CSF drainage via ventriculostomy, moderate hypocapnia, and metabolic suppression with barbiturates Decompressive craniectomy has been shown to decrease mortality in patients with sustained increases in ICP (> 25 mm Hg) following traumatic brain injury Anesthesia & Craniotomy for Patients with Mass Lesions Intracranial masses may be congenital, neoplastic (benign or malignant), infectious (abscess or cyst), or vascular (hematoma or arteriovenous malformation) Craniotomy is commonly undertaken for neoplasms of the brain Primary tumors usually arise from glial cells (astrocytoma, oligodendroglioma, or glioblastoma), ependymal cells (ependymoma), or supporting tissues (meningioma, schwannoma, or choroidal papilloma) Childhood tumors include medulloblastoma, neuroblastoma, and astrocytoma Regardless of the cause, intracranial masses present symptoms and signs according to growth rate, location, and ICP Slowly growing masses are frequently asymptomatic for long periods (despite relatively large size), whereas rapidly growing ones may present when the mass remains relatively small Common presentations include headache, seizures, a general decline in cognitive or specific neurological functions, and focal neurological deficits Symptoms typical to supratentorial masses include seizures, hemiplegia, or aphasia, whereas symptoms typical of infratentorial masses may include cerebellar dysfunction (ataxia, nystagmus, and dysarthria) or brainstem compression (cranial nerve palsies, altered consciousness, or abnormal respiration) PREOPERATIVE MANAGEMENT The preoperative evaluation for patients undergoing craniotomy should attempt to establish the presence or absence of intracranial hypertension Computed tomography (CT) and magnetic resonance imaging (MRI) scans should be reviewed for evidence of brain edema, midline shift greater than 0.5 cm, or ventricular displacement or compression Imaging studies typically will be downloaded from www.medicalbr.com performed before the patient receives dexamethasone, so the mass effect may be less acute when patients who have already received dexamethasone present in the operating room The neurological examination should document mental status and any sensory or motor deficits Medications should be reviewed with special reference to corticosteroid, diuretic, and anticonvulsant therapy Laboratory evaluation should rule out corticosteroid-induced hyperglycemia, electrolyte disturbances due to diuretics, or abnormal secretion of antidiuretic hormone Anticonvulsant blood concentrations may be measured, particularly when seizures are not well controlled Premedication Sedative or opioid premedication is best avoided, particularly when intracranial hypertension is suspected Hypercapnia secondary to respiratory depression increases ICP Corticosteroids and anticonvulsant therapy should be continued until the time of surgery INTRAOPERATIVE MANAGEMENT Monitoring In addition to standard monitors, direct intraarterial pressure monitoring and bladder catheterization are used for most patients undergoing craniotomy Rapid changes in blood pressure during anesthetic procedures, positioning, and surgical manipulation are best managed with guidance from continuous invasive monitoring of blood pressure Moreover, arterial blood gas analyses are necessary to closely regulate PaCO2 We zero the arterial pressure transducer at the level of the head (external auditory meatus)—instead of the right atrium—to facilitate calculation of cerebral perfusion pressure (CPP), and we document this practice in the anesthetic record End-tidal CO2 measurements alone cannot be relied upon for precise regulation of ventilation; the arterial to end-tidal CO2 gradient must be determined Central venous access and pressure monitoring may be considered for patients requiring vasoactive drugs Use of the internal jugular vein for access is theoretically problematic because of concern that the catheter might interfere with venous drainage from the brain The external jugular, subclavian, or other peripheral veins may be suitable insertion sites for central venous catheters A bladder catheter is necessary because of the use of diuretics, the long duration of most neurosurgical procedures, and the utility of downloaded from www.medicalbr.com bladder catheterization in guiding fluid therapy and measuring core body temperature Neuromuscular function should be monitored on the unaffected side in patients with hemiparesis because the twitch response is often abnormally resistant on the affected side Monitoring visual evoked potentials may be useful in preventing optic nerve damage during resections of large pituitary tumors Additional monitors for surgery in the posterior fossa are described later in this discussion Management of patients with intracranial hypertension may be guided by monitoring ICP perioperatively Various ventricular, intraparenchymal, and subdural devices can be placed by neurosurgeons to provide measurements of ICP The transducer should be zeroed to the same reference level as the arterial pressure transducer (usually the external auditory meatus, as previously noted) A ventriculostomy catheter provides the added advantage of allowing removal of CSF to decrease ICP Induction Induction of anesthesia and tracheal intubation are critical periods for patients with compromised intracranial pressure to volume relationships, particularly if there is an elevated ICP Intracranial elastance can be improved by osmotic diuresis or removal of small volumes of CSF via a ventriculostomy drain The goal of any technique should be to induce anesthesia and intubate the trachea without increasing ICP or compromising CBF Arterial hypertension during induction increases CBV and promotes cerebral edema Sustained hypertension can lead to marked increases in ICP, decreasing CPP and risking herniation Excessive decreases in arterial blood pressure can be equally detrimental by compromising CPP The most common induction technique employs propofol together with modest hyperventilation to reduce ICP and blunt the noxious effects of laryngoscopy and intubation All patients receive controlled ventilation once the propofol has been injected A neuromuscular blocker (NMB) is given to facilitate ventilation and prevent straining or coughing, both of which can abruptly increase ICP An intravenous opioid given with propofol blunts the sympathetic response, particularly in young patients Esmolol (0.5–1.0 mcg/kg) is effective in preventing tachycardia associated with intubation in lightly anesthetized patients The actual induction technique can be varied according to individual patient responses and coexisting diseases Succinylcholine may theoretically increase downloaded from www.medicalbr.com ICP, particularly if intubation is attempted before deep anesthesia is established Succinylcholine, however, remains the agent of choice for rapid sequence induction or when there are concerns about a potentially difficult airway, as hypoxemia and hypercarbia are much more detrimental than any effect of succinylcholine to the patient with intracranial hypertension Hypertension during induction can be treated with β1-blockers or by deepening the anesthetic with additional propofol Modest concentrations of volatile agents (eg, sevoflurane) may also be used, provided that hyperventilation is also used Sevoflurane best preserves autoregulation of CBF and produces limited vasodilation; it may be the preferred volatile agent in patients with elevated ICP Because of their potentially deleterious effect on CBV and ICP, vasodilators (eg, nicardipine, nitroprusside, nitroglycerin, and hydralazine) are avoided until the dura is opened Hypotension is generally treated with incremental doses of vasopressors (eg, phenylephrine) Positioning Frontal, temporal, and parietooccipital craniotomies are performed in the supine position The head is elevated 15° to 30° to facilitate venous and CSF drainage The head may also be turned to the side to facilitate exposure Excessive flexion or rotation of the neck impedes jugular venous drainage and can increase ICP Before and after positioning, the tracheal tube should be secured and position verified, and all breathing circuit connections checked The risk of unrecognized disconnections is increased because the patient’s airway cannot be easily assessed after surgical draping; moreover, the operating table is usually turned 90° or 180° away from the anesthesia provider Maintenance of Anesthesia Anesthesia can be maintained with inhalation anesthesia, total intravenous anesthesia techniques (TIVA), or a combination of an opioid and intravenous hypnotic (most often propofol) with a low-dose inhalation agent Even though periods of stimulation are few, neuromuscular blockade is recommended— unless neurophysiological monitoring contradicts its use—to prevent straining, bucking, or other movement Increased anesthetic requirements can be expected during the most stimulating periods: laryngoscopy–intubation, skin incision, dural opening, periosteal manipulations, including Mayfield pin placement and closure TIVA with remifentanil and propofol facilitates rapid emergence and downloaded from www.medicalbr.com immediate neurological assessment Likewise, the α2-agonist dexmedetomidine can be employed during both asleep and awake craniotomies to similar effect Hyperventilation should be continued intraoperatively to maintain PaCO2 at roughly 30 to 35 mm Hg Lower PaCO2 tensions provide little additional benefit and may be associated with cerebral ischemia and impaired oxygen dissociation from hemoglobin Ventilatory patterns resulting in high mean airway pressures (a low rate with large tidal volumes) should be avoided because of a potentially adverse effect on ICP by increasing central venous pressure and the potential for lung injury Hypoxic patients may require positive end-expiratory pressure (PEEP) and increased mean airway pressure; in such patients, the effect of PEEP on ICP is variable Intravenous fluid replacement should be limited to glucose-free isotonic crystalloid Hyperglycemia is common in neurosurgical patients and has been implicated in increasing ischemic brain injury Hyperglycemia should be corrected preoperatively Neurosurgical procedures are often associated with occult blood loss (underneath surgical drapes or on the floor) Hypotension and hypertension should both be expeditiously corrected Emergence Most patients undergoing elective craniotomy can be extubated at the end of the procedure Patients who will remain intubated should be sedated to prevent agitation Extubation in the operating room requires special handling during emergence Straining or “bucking” on the tracheal tube may precipitate intracranial hemorrhage or worsen cerebral edema As the skin is being closed, the patient may resume breathing spontaneously Should the patient’s head be secured in a Mayfield pin apparatus, care must be taken to avoid any patient motions (eg, bucking on the tube), which could promote neck or cranial injuries After the head dressing is applied and full access to the patient is regained (the table is turned back to its original position as at induction), any anesthetic agents are discontinued and the neuromuscular blockade is reversed Rapid awakening facilitates immediate neurological assessment and is generally expected Delayed awakening may be seen following opioid or sedative overdose, when the end-tidal concentration of the volatile agent remains greater than 0.2 minimum alveolar concentration (MAC), or when there is a metabolic derangement or a perioperative neurological injury Patients may need to be transported to the CT scanner directly from the operating room for evaluation when they do not respond as predicted Immediate reexploration may be downloaded from www.medicalbr.com required Most patients are taken to the intensive care unit postoperatively for close monitoring of neurological function Anesthesia for Surgery in the Posterior Fossa Craniotomy for a mass in the posterior fossa presents a unique set of potential problems: obstructive hydrocephalus, possible injury to vital brainstem centers, pneumocephalus, and, when these procedures are performed with the patient in the sitting position, an increased risk of postural hypotension and venous air embolism Obstructive Hydrocephalus Infratentorial masses can obstruct CSF flow through the fourth ventricle or the cerebral aqueduct of Sylvius Small but critically located lesions can markedly increase ICP In such cases, a ventriculostomy is often performed under local anesthesia to decrease ICP prior to induction of general anesthesia Brainstem Injury Operations in the posterior fossa can injure vital circulatory and respiratory brainstem centers, as well as cranial nerves or their nuclei Such injuries may occur as a result of direct surgical trauma or ischemia from retraction or other interruptions of the blood supply Damage to respiratory centers is said to nearly always produce circulatory changes; therefore, abrupt changes in blood pressure, heart rate, or cardiac rhythm should alert the anesthesia provider to the possibility of such an injury Such changes should be communicated to the surgeon Isolated damage to respiratory centers may rarely occur without premonitory circulatory signs during operations in the floor of the fourth ventricle Historically, some clinicians have employed spontaneous ventilation during these procedures as an additional monitor of brain function At completion of the surgery, brainstem injuries may present as an abnormal respiratory pattern or an inability to maintain a patent airway following extubation Monitoring brainstem auditory evoked potentials may be useful in preventing eighth nerve damage during resections of acoustic neuromas Electromyography is also used to avoid injury to the facial nerve but requires incomplete neuromuscular blockade intraoperatively downloaded from www.medicalbr.com Positioning Although most explorations of the posterior fossa can be performed with the patient in either a modified lateral or prone position, the sitting position may be preferred by some surgeons The patient is actually semirecumbent in the standard sitting position (Figure 27–1); the back is elevated to 60°, and the legs are elevated with the knees flexed The head is fixed in a three-point holder with the neck flexed; the arms remain at the sides with the hands resting on the lap Figure 27–1 The sitting position for craniotomy Careful positioning and padding help avoid injuries Pressure points, such as the elbows, ischial spines, heels, and forehead, must be protected Excessive neck flexion has been associated with swelling of the upper airway (due to venous obstruction), and, rarely, quadriplegia (due to compression of the cervical spinal cord) Preexisting cervical spinal stenosis probably predisposes patients to the latter injury Pneumocephalus The sitting position increases the likelihood of pneumocephalus In this position, downloaded from www.medicalbr.com intravenous regional anesthesia, 1022 median nerve block, 1016–1017 musculocutaneous nerve block, 1018–1019 radial nerve block, 1018 ulnar nerve block, 1017–1018 Testicular tumors, 706–707 Tetany, 204 Tetracaine, 265t, 269t Tetralogy of Fallot, 431 Therapeutic window, 147 Thermodilution, 101–106 Thermodilution curve, 101, 102f, 104f Thermoregulation, 1214–1215 Thiamylal, 172f Thiazide diuretics, 390t Thiazide/thiazide-like diuretics, 668–669 edematous disorders (sodium overload), 668 hypercalciuria, 668 hypertension, 668 intravenous dosages, 668 nephrogenic diabetes insipidus, 668 side effects, 669 Thiocyanate, 256 Thiopental, 172f, 174t, 1220, 1249 Third-degree burns, 834 “Third-space” loss, 916 Thoracic bioimpedance, 107 Thoracic epidural blocks, 982 Thoracic paravertebral nerve block, 1091 Thoracic surgery, 553–582 See also specific surgeries bronchoscopy for, 573–575 case discussion on, 580–581 diagnostic thoracic procedures, 573–577 esophageal surgery, 578–579 lung resection, 563–573 See also Lung resection lung transplantation, 577–578 downloaded from www.medicalbr.com mediastinoscopy, 575–576 one-lung ventilation in, 556–563 anatomic considerations in, 559 double-lumen bronchial tubes in complications of, 562 description of, 558–562 placement of, 559–562 single-lumen tracheal tubes with bronchial blocker in, 562–563 physiologic considerations in anesthesia for, 554–557 lateral decubitus position in, 554f, 554–555, 555f open pneumothorax in, 555–556 tracheal resection, 573 See also Tracheal resection video-assisted thoracoscopic surgery (VATS), 573 Thoracic sympathetic chain block, 1097 Three-limb lead placement, rearranged, 90, 91f Thrombocytopenia, 867 Thromboelastography (TEG), 451, 725, 827, 828f Thromboembolism, 948 Thrombomodulin (TM), 824 Thromboxane A2 (TXA2), 883 Thyroid disorders hyperthyroidism, 759–760 hypothyroidism, 760–761 physiology, 758–759 Thyroid hormone, 759 Thyroid storm, 760 Thyroidectomy, 760 Thyromental distance, 311 Thyrotoxicosis, 647, 760 Thyrotropin-releasing hormone (TRH), 758 Thyroxine (T4), 722, 758 Tibial nerve, 1039f Tibial/common peroneal nerve courses, 1039f Tidal volume, 1268 Time-cycled ventilators, 68 downloaded from www.medicalbr.com cycle, 1339 Time-weighted average (TWA), 16 Timolol, 777 Tissue Doppler, 362f Tissue group composition, 140t Tissue hypoperfusion, 825f Tissue plasminogen activator (tPA), 615–616 Tonometry, for arterial blood pressuring monitoring, 84 Topiramate, 1078t Torsades des pointes, 409 Total hip arthroplasty illustration of, 812f uncemented, 808f Total intravenous anesthesia (TIVA) technique, 171, 180, 461, 605, 948 Total knee replacement intraoperative management, 813–814 preoperative considerations, 813 Total lung capacity (TLC), 538 Total parenteral nutrition (TPN), 1225–1226 infusions, 1227 Tourniquets, 822 Toxic shock syndrome, 1322t Toyota Production System (TPS), 28–29 Tracheal lumen, 561f Tracheal resection, 573, 575f, 576f anesthetic considerations, 573 preoperative considerations, 573 Tracheal tube (TT) description of, 325f, 1260, 1264 disadvantages of wrapping, 790t Tracheobronchial tree, 559f Tracheostomy, 793 Tracheotomy, 1266 Train-of-four stimulation, 134, 204 Tramadol, 1081 Tranexamic acid, 825, 826f downloaded from www.medicalbr.com Transcardiopulmonary thermodilution, 105f Transcranial Doppler (TCD), 459 Transcutaneous cardiac pacing (TCP), 1272 Transcutaneous electrical nerve stimulation (TENS), 1072, 1104–1105 Transdermal fentanyl, 1084 Transesophageal echocardiography (TEE), 96, 96f, 108–109, 357, 404–406, 442, 452f–456f, 607, 708, 741 probes, 1240 Transfusion See also Blood transfusion blood bank practices, 1199 blood groups, 1197–1198 ABO system, 1197 red blood cell antigen systems, 1198 Rh system, 1198 compatibility testing ABO–Rh testing, 1198 antibody screen, 1198 crossmatch, 1198 crossmatching, 1198 emergency, 1198–1199 intraoperative, 1199–1200 fresh frozen plasma (FFP), 1199–1200 granulocyte transfusions, 1200 packed red blood cells, 1199 platelet transfusions, 1200 procoagulant transfusions, 1200 Transfusion-associated circulatory overload (TACO), 827, 1202 Transfusion-associated hyperkalemia, 1156 Transfusion-related acute lung injury (TRALI), 827, 1202 Transient ischemic attacks (TIAs), 488, 621 Transient neurological symptoms (TNS), 994 Transient receptor potential vanilloid 1 (TRPV1), 264 Transjugular intrahepatic portosystemic shunt (TIPS), 739, 955 Transmittance oximetry, 120 Transplanted heart anesthetic management, 432–434 downloaded from www.medicalbr.com patient with, 432–434 preoperative considerations, 432–433 Transpulmonary pressure, 501 Transpulmonary thermodilution, 102–103 Trans-sacral nerve block anatomy, 1093 complications, 1095 indications, 1093 technique, 1094 Transthoracic echocardiography (TTE), 108–109, 357, 404 Transtracheal jet ventilation, 1265 Transurethral bladder resection, 705–706 Transurethral resection of the prostate (TURP) absorption of irrigation fluid, 699 bladder perforation, 700 intraoperative considerations, 698–701 anesthesia, choice of, 700 bladder perforation, 700 coagulopathy, 700 hypothermia, 700 monitoring, 700–701 septicemia, 700 TURP syndrome, 698–700 manifestations of, 699t preoperative considerations, 698 surgical complications, 699t Transversus abdominis plane (TAP), 916 Transversus abdominis plane (TAP) block, 1044, 1045f, 1075, 1105 Trauma anesthesia, 820 Trauma/emergency surgery airway, 820–821 breathing, 821–822 case discussion on, 839–841 circulation, 822 definitive trauma interventions anesthetic induction/maintenance, 829–830 downloaded from www.medicalbr.com damage control surgery, 830 in elderly, 838 head See Head trauma injury assessment, 823 mass casualty incidents, 838 neurological function, 823 resuscitation hemorrhage, 823–824 hemostatic resuscitation, 826–827 massive transfusion protocols, 827–828 trauma-induced coagulopathy, 824–826 Trauma-induced coagulopathy, 825f Traumatic brain injury (TBI), 830–833 diffuse neuronal injury, 831 Glasgow Coma Scale for, 610t intracranial pressure, 831 intraparenchymal injuries, 831 primary brain injuries, 831 secondary brain injuries, 831 Trazodone, 1077t Trendelenburg positions, 696–697 Triamcinolone, 1080t Tricuspid atresia, 431–432 Tricuspid regurgitation, 424–425 anesthetic management choice of agents, 425 monitoring, 425 objectives, 425 pathophysiology, 425 preoperative considerations, 424–425 treatment, 425 Trifluoroacetic acid, 164 Trigeminal nerve block anatomy, 1085 complications, 1088 gasserian ganglion block, 1085, 1086f downloaded from www.medicalbr.com illustration of, 1086f indications, 1085 mandibular nerve, 1087f, 1087–1088 maxillary nerve, 1085–1087, 1087f ophthalmic nerve, 1085 Triiodothyronine (T3), 722, 758 Triple response of Lewis, 1059 Trismus See Masseter muscle rigidity Tromethamine, 447, 1178, 1181 Troponin, 348 Trousseau sign, 763, 1160 True negatives, 300t True positives, 300t Truncus arteriosus, 432 Trunk, peripheral nerve blocks intercostal block, 1040–1041 paravertebral block, 1041–1043 Pecs block, 1043–1044, 1044f superficial cervical plexus block, 1040 transversus abdominis plane (TAP) block, 1044 ultrasound image of, 1045f Tubeless lithotripsy unit, 701f Tubuloglomerular balance, 1149 Tubuloglomerular feedback, 662 Tuffier’s line, 972 Tumor lysis syndrome, 1160 Tumors, 1070 Tuohy needle, 1042 Two-compartment model, 144, 144f Tympanoplasty, 798 U Ulnar artery, blood pressure monitoring via, 87 Ulnar nerve course, 1018f downloaded from www.medicalbr.com stimulation, 134 Ulnar nerve block, 1017–1018 at elbow, 1019f at wrist, 1019f Ultrafiltration, 445–446 Ultrasonic flow sensors, 63 Ultrasound-guided interscalene block, 1008f Ultrasound-guided procedures, 1085 Unanticipated hospital admission, following ambulatory surgery, 952 Unidirectional valves, 42–43, 43f Unstable angina, 395 Upper extremity axillary block, 1012–1015 brachial plexus anatomy, 1004 infraclavicular block, 1010–1012 interscalene block, 1005–1008 intravenous regional anesthesia, 1022 peripheral nerve blocks, 1004–1022 supraclavicular block, 1008–1010 surgery of distal upper extremity surgery, 815–816 shoulder surgery, 815 terminal nerves, blocks, 1015–1022 Upper gastrointestinal bleeding, 1325 Upper respiratory tract infection (URI), 909 Urinary diversion, 706 Urinary output clinical considerations, 133 indications and contraindications, 133 in noncardiovascular monitoring, 133 techniques and complications, 133 U.S Food and Drug Administration (FDA), 77, 285 Use-dependent block, 264 Uterine activity, 853–854 Uterine atony, 854 Uterine muscle, 853 downloaded from www.medicalbr.com Uteroplacental circulation, 847, 848f anesthetic agents, placental transfer of, 850–851 placental function, 848–849 physiological anatomy, 848 placental exchange, 849 respiratory gas exchange, 849–850 uterine blood flow, 847–848 uteroplacental blood flow, anesthetic agents effect, 851 V Vacuum system, in medical gas systems, 13 Vaginal birth after cesarean (VBAC), 867, 881 Vaginal delivery, general anesthesia for, 873t Vagus nerve, 500, 794f Valproic acid, 1078t Valvular aortic stenosis, 421 Valvular heart disease, 414–427, 415–427 anticoagulation, 426–427 aortic regurgitation, 423–424 aortic stenosis, 421–423 endocarditis prophylaxis, 425–426 general evaluation of patients, 414–415 history of, 414 laboratory evaluation, 415 mitral regurgitation, 417–420 mitral stenosis, 415–417 mitral valve prolapse, 420–421 physical examination, 414–415 special studies, 415 tricuspid regurgitation, 424–425 Vancomycin, 1251 Vaporization, 55 Vaporizers, 55–59 copper kettle, 55–56 electronic, 57, 59 modern conventional, 56–57 downloaded from www.medicalbr.com Vaporizing chamber, 57 Vapor-phase humidifier, 66 Vascular surgery, 483–490 anesthetic management of, 485–488 kidney failure, 487 paraplegia, 486–487 postoperative considerations, 488 surgery involving aortic arch, 485–486 surgery involving descending thoracic aorta, 486–487 surgery on abdominal aorta, 487–488 surgery on ascending aorta, 485 aorta/aortic lesions, 484–485 aneurysms in, 484 coarctation of, 485 dissection of, 484 occlusive disease of, 484–485 trauma in, 485 carotid artery surgery, 488–490 general anesthesia, 489 monitoring cerebral function, 489–490 preoperative anesthetic evaluation and management, 488–489 preoperative considerations, 488 regional anesthesia, 490 Vasoconstriction, 1299 Vasodepressor, 363 Vasodilators, 391t, 472t, 593 Vasopressin, 739, 1275t Vasopressors, 421, 471t, 593, 1324 Vecuronium, 217–218, 683 characteristics of, 211t, 212t chemical structure of, 206f dosage, 218 metabolism and excretion, 217–218 physical structure, 217 side effects and clinical considerations cardiovascular, 218 downloaded from www.medicalbr.com liver failure, 218 Venlafaxine, 1077t Venous air embolism, 606–608 central venous catheterization, 607 monitoring for, 607–608 treatment of, 608 Ventilation, 512–514, 513t distribution of, 513f, 513–514 mechanical See Mechanical ventilation in operating rooms, 16 spontaneous See Spontaneous ventilation time constants of, 514 Ventilation-perfusion (V/Q) scintigraphy, 564 Ventilators, 66–75 alarms, 72 anesthesia ventilators, problems associated with, 74–75 circuit design, 69–72 double-circuit system ventilators, 69–71, 71f piston ventilators, 71 spill valve, 72 expiratory phase, 68–69 function, 67 inspiratory phase, 67–68 mechanics of, 1344–1345 overview, 67–69 pressure and volume monitoring, 72 transition phase from expiration to inspiration, 68 transition phase from inspiration to expiration, 68 ventilator alarms, 72 ventilator circuit design, 69–72 double-circuit system ventilators, 69–71 piston ventilators, 71 spill valve, 72 Ventricular arrhythmias, 409, 410t–411t Ventricular compliance, 355f Ventricular function curves, 357, 357f downloaded from www.medicalbr.com Ventricular hypertrophy, 371 Ventricular pressure-volume diagrams, 358F Ventricular pressure–volume relationships, 369f Ventricular septal defect (VSD), 430 Ventricular systolic function, 353 Ventricular tachycardia (VT), 399, 1270 Verapamil, 376t, 378t, 1276t Vernakalant, 378t Vertebra prominens, 972 Vertebrae, 962 Vertebral column, 963f Vertebroplasty, 1107 Vessel-rich group, 140 Video laryngoscopes, 321–324 Video-assisted thoracoscopic surgery (VATS), 564, 573 Viral DNA, 1253 Vitamin D, 762, 764, 1159 Vitamin D receptors, 762 Vitamin K, 720, 722 Volatile anesthetics, 55, 159, 540, 590 See also Desflurane; Halothane; Isoflurane; Sevoflurane cerebral autoregulation, dose-dependent depression of, 590f cerebral blood flow and volume affected by, 589–590 cerebral metabolic rate affected by, 589 cerebral metabolic rate and blood flow, altered coupling of, 590 cerebrospinal fluid dynamics affected by, 590 intracranial pressure affected by, 590 Volume-controlled ventilation (VCV), 1339 Volume-cycled ventilators, 68, 1339 Volume–pressure loop, 125f von Willebrand factor (vWF), 734 W Waste anesthetic gas disposal (WAGD), 13, 16 Waste-gas scavengers, 75–77 Weak base, 1170 downloaded from www.medicalbr.com Wenger chestpiece See Precordial stethoscope West zones, 515 Wick humidifier, 66 Wide dynamic range (WDR) neurons, 1054 Widened pulse pressures, 253 Widespread Pain Index (WPI), 1066 Wind-up, 1055 Withdrawal of treatment, 1326 Wolff–Parkinson–White (WPW) syndrome, 373–374, 408 Wong-Baker FACES rating scale, 1063 Wood’s metal, 11 World Health Organization (WHO), 10 Wound-related sepsis, 1322 Wright respirometer, 61, 64f X Xenon advantages and disadvantages of, 161t anti-apoptotic effect of, 158 clinical pharmacology of, 169 Y Y-connection, 63 Y-connector, 61 Z Ziconotide, 1075 Zollinger–Ellison syndrome, 278 Zygapophyseal joints, 1070 downloaded from www.medicalbr.com downloaded from www.medicalbr.com downloaded from www.medicalbr.com ... stimulation testing, sedative infusions should be discontinued to facilitate patient participation in determining correct electrode placement (Table 27 –1) TABLE 27 –1 Advantages and disadvantages of drugs used for conscious sedation.1 ,2 downloaded from www.medicalbr.com... cerebral vasospasm and patient outcome (Table 27 –5) TABLE 27 –3 Hunt and Hess grading scale for SAH.1 downloaded from www.medicalbr.com TABLE 27 –4 World Federation of Neurological Surgeons grading scale for aneurismal SAH.1 TABLE 27 –5... Moderate hyperventilation (PaCO2 of 30–33 mm Hg) is often very helpful in reducing CBF, CBV, and ICP acutely, but may aggravate ischemia in patients with focal ischemia Mannitol, in doses of 0 .25 to 1 g/kg, is particularly effective in rapidly