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Neuroanesthesia 565
| Question | Answer |
|---|---|
| N2O effect on CBF, CMRO2, ICP, CPP | CBF=↑, CMRO2=↑↓ ICP=none, CPP=↓ |
| Halothane effect on CBF, CMRO2, ICP, CPP | CBF=↑↑, CMRO2=↓, ICP=↑, CPP=↓ |
| Sevo, Iso, Des effect on CBF, CMRO2, ICP, CPP | CBF=↑, CMRO2=↓, ICP=↑, CPP=↓ |
| Barbiturate effect on CBF, CMRO2, ICP, CPP | CBF=↓↓, CMRO2=↓↓, ICP=↓↓, CPP=0/↓ |
| Etomadate effect on CBF, CMRO2, ICP, CPP | CBF=↓↓, CMRO2=↓↓, IPC=↓, CPP=0 |
| Propofol effect on CBF, CMRO2, ICP, CPP | CBF=↓ CMRO2=↓, ICP=↓, CPP=↓ |
| Ketamine effect on CBF, CMRO2, ICP, CPP | CBF=↑, CMRO2=↑, ICP=↑↑, CPP=↓ |
| Benzos effect on CBF, CMRO2, ICP, CPP | CBF=↓, CMRO2=↓, ICP=↓, CPP=0/↓ |
| Opiates effect on CBF, CMRO2, ICP | CBP=0/↓, CMRO2=↓, ICP=↓ |
| Morphine effect on CPP | CPP=↑↓ |
| Fentanyl effect on CPP | CPP=0/↓ |
| Afentanil, sufentanil, remifentanil effect on CPP | CPP=↓ |
| What cerebral vascular function is impaired in the use of inhalation anesthetics | Autoregulation |
| What advantage does desflurane have in neuroanesthesia and why? | It is fast on/Fast off and allow for immediate postop neuro evaluation. It is fast on/fast off because of its low blood gas solubility |
| What ventilation technique can be used to attenuate the increase in ICP associated with volitile agents? | Hyperventilation leaing to hypocapnea which causes cerebreal vasoconstriction |
| What situations would cause a CRNA to not use N20 in neuroanesthesia? (5) | Resences of intracranial air (recent crainiotomy or crainiofacial trauma), When signal quaility during intraoperative evoked poatential monitoring is inadequeat, patient has clinical evidence of ↑ICP, tight brain noted by surgeon, case longer than 8 hrs |
| Describe "inverse Steal" in relation to barbiturate use | Barbs cause decrease in CBF only to normal, healthy areas of the brain, but the ischemic areas remain maximally vasodilated causing blood to be shunted to these areas |
| What are some benefits of barbiturates in neuroanesthesia? | reduction of free-radical formation which may prevent futher injury in ischemic zones, reduced ATP depletion, and provision of effective anticonvulsant activity), decrease in cytotoxic cerebral edema |
| What are some advantages of etomidate in for neuroanesthesia? | rapid elimination allowing a mor prompt postop neuro eval, it's not a CV depressant which results in unchagned or mildly increased CPP |
| What are some disadvantages of etomidate in neuroanesthesia? | high incidence of non-purposeful movements, thrombophlebitis, n/v, and supression of adrenocortical response to stress |
| Which opioid should be avoided in neuroanesthesia and why? | Meperidine because its metabolite normeparidine is a known convulsant |
| What can happen if opioids are abruptly reversed with narcan? | hypertension, cardiac dysrhythmias, pulmonary edema, intracranial hemorrhage |
| Why is ketamine not a good choice in neuroanesthesia? | it has a stormy emergence which can lead to increased ICP, it increases CBF and ICP, it increases CSF reabsorption which may lead to ↑ICP, |
| WHat type of muscle relaxant is preferred in neuroanesthesia? | nondepolarizers because sux can cause increased ICP, CBF, and CMRO2 |
| If a patient has uppermotor neuron disease, which side should you monitor their twitches on? | The unaffected side |
| Why is sux contraindicated in patients with denervated or muscle? | It can cause life-threatening hyperkalemia |
| Are SNP or Nitro recommended in neuroanesthesia and why? | No they are not recommended because they are direct acting cerebrovasodilators that increase CBV resulting in increased ICP |
| Does the pre-induction administration of beta-blockers have an effect on ICP | No, but they are good at blocking the expected increase in HR and BP associated with direct laryngoscopy |
| Which calcium channel blocker is often used to prevent cerebral vasospasm after trauma or hemorrhage? | Nimodipine |
| What are the signs and symptoms of intracranial hypertension?? | HA, N/V, papilledema, focal neuro deficits, altered ventilatory function, deceasing consciousness, seizures, and coma |
| What is considered the last ditch effort to decrease intractable elevations in ICP | Surgical decompression |
| How is hypothermia useful in intracranial hypertension? | It decreases CMRO2 by 7% for every 1 degree C the core temp is decreased which allows the brain to use less O2 |
| If utilizing intraoperative somatosensory Evoked Potenials (SSEP) monitoring what medications should be avoided in periods of high risk during the surgery and Why? | Ketamine and etmomidate should be avoided because they can increase wave forms by 200-600%; N2O and volitile agents cause dose dependent depression in wave size that may lead to a false positives or negatives in the monitoring |
| What is the advantage of using brainstem auditory evoked response (BAER) over SSEP | Intraoperative factors other than surgical brain damage are relatively unlikely to seriously alter the BAER |
| Clinical signs of supratentorial mass | Seizures, hemi-plegia, aphasia |
| Clinical signs of infratntorial masses | Cerebellar dysfunction (ataxia,nystagmus, dysarthria) brainstem compression (crainial nerve palsies, altered consciousness, abnormal respiration |
| What is the tentorium? | It is an extension of the dura that separates the cerebrum form the cerebellum |
| Preoperative considerations for supratentoria surgery | Review MRI/CT for ventricualr size, edema, presence of midline shift >0.5cm, neuro assess, Electrolyt changes secondary to diuretics or steroids, check anticonvulsant med levels |
| What adverse effect can premedication with benzos or opioids have with neurosurgery? | They cause respiratory depression and hypercapnea which can potentiate intracranial hypertension |
| When transporting a patient to the OR or preop holding what position should they be in if possible? | Head up 15-30 degrees in an attempt to control elevated ICP |
| Monitors required for supratentorial neurosurgery | Typical Monitors; precordial steth, urinary cath, possibly SSEP |
| What is the goal of fluid therapy in supratentorial neurosurgery? | Keep the patient isovolemic, isotonic, and isooncotic (Don't over or under hydrate), maintin peripheral perfusion, but avoid hypervolemia |
| Compared to nonneurosurgery what are the fluid volume requirement for neurosurgery? | Less in neurosurgery (0.5-1 ml/kg) |
| What is the goal of anesthetic induction in neurosurgical patients? | Smooth induction with avoidance of sudden hypothension or hypertension, use fent and/or lido to block sympathetic response |
| Positioning considerations for supratentorial neurosurgery | elevate head 15-30⁰ to facilitate venous and CSF drainage, avoid excessive neck flexion which may impead jugular venous drainage and ↑ ICP |
| ETT and circuit considerations for neurosurgey | Consider reinfoced or armored ETT to avoid kinking, keep ETT cephalad to keep out of surgical field, ensure firm circuit connections, know that patien and circuit are often covered by drape |
| anesthetic maintenance choices for neurosurgery | O2-air-opioed, volitile agents, O2-air-propofol, Opioid-lowdose Iso |
| Opioid use considerations for neurosurgery | stop giving opioids ~45 min prior to end of surgery for faster wake up (if patient becomes hypertensive or tachycardic in last 45 min consider beta blockers instead of opioids |
| Mechanical ventilation considerations for neurosurgery | Hyperventilate patient for CO2 on ABG of 25-30 |
| According to nagelhout what is the optimal volitile agent for maintenance of anesthesia? | Low-dose isoflurane (<1%) along with hyperventiation maintains stable intracrainial dynamics |
| What are some adverse effects associated with N2O use in neurosurgery? | Expansion of pneumocephalus or air embolism |
| What are the advantages of skeletal muscle relaxation in neurosurgical patients? | May decrease ICP by relaxing chest wall, decreasing intrathoracic pressure and facilitating venous drainage (also may want to avoid PEEP) |
| What is a major adverse effect of suddent emergnece from anesthesia? | Uncontrolled hypertension |
| Describe the changes that should take place just prior to closure of the dura and why | Allow PaCO2 to return to normal, Elevate BP to 120% of baseline; Because HTN and is frequently experienced in the postop period the elevation of BP and CO2 allows the surgeon to see how the brain will respond to these changes postoperatively |
| Contraindications for awake crainiotomy | Developmental delay, immaturity, excessive response to pain, communication barrier, failure to obtain consent |
| What are some advantages of awake crainiotomy | they are the most reliable method for sugery if anesthetic supress seizure activity, or the focus is near an area of eloquent cortical fucntion |
| Anesthesia induction and maintenance for awake crainiotomy | Induction by propofol, LMA placement, Scalp anesthetized with marcaine, consider mannitol or hypertonic for edema Patient draped & provided a light, during scalp opening SV is established. Prior to bone flap removal LMA d/c & verbal contact is established |
| What is meant by eloquent areas of the brain | Areas important to daily living (speech motor control, visual areas) |
| Describe the awake phase of awake crainiotomy | Sedation is stopped & conversation w/ patient is confined to surgeon & 1 CRNA, Stim of eloquent area is carried out with results noted, seizures controlled w/ propofol, Following stim and mapping of brain, surgical removal of tumor or seizure focci occurs |
| What causes venous air embolisms | Development of a negative pressure gradient betewwn the op site and the right side of the heart |
| What are some risk factors that contribute to the development of venous air embolisms | positioning (sitting, prone steep trendelenberg), transfusion and IVF, CVC, hepatic procedures, Uro procedures, Posterior spine procedures, Epdural or caudal cath, bone marrow harvesting, laproscopy, radical pelvic surgery |
| Treatment of venous air embolism | Tell surgeon (who should flood field w/ saline or pack with saline soaked sponges, D/C N2O, Perform valsalva or compression of jugulars, aspirate air from atrial cath, support BP with volume and pressors, put patient in left lateral head down position |
| What positions are utilized for posterior fossa surgery? | Lateral, Prone, Sitting |
| Why is sitting position sometimes preferred for posterior fossa surgery | It allows for drainage of CSF and a better view of the field |
| What is a common pathophysiology that must be diagnosed and corrected prior to posterior fossa surgery and how to you correct it | Obstructive Hydrocephalus; It's corrected by placement of a intraventricular drainage catheter |
| Should you premedicate a patient with obstructive hydrocephalus? | NO |
| What are the goals of induction, maintenance and emergence of anesthesia with a posterior fossa surgery | Slow deliberate smooth induction and emeregence are desirable (no coughing or bucking) |
| Fluid management of posterior fossa surgery | Only give maintenance fluids and replace deficit |
| What are some clinical symptoms associated with pituitary tumors? | Amenorrhea, galactorrhea, Cushings, Acromegaly |
| What is the most common approache for removal of pituitary tumors? | transphenoidal |
| Patient position for transphenoidal surgical approach | supine with head and back up 10-20⁰. head is positioned within a 3 pin head holder and centered in a C-arm for fluroscopy |
| SHould you hyperventilate a patint who is having pituitary surgy via transphenoidal approach and why? | No, decreased CO2 can cause the pituitary gland to retract into the sella turcica making the surgery more difficult |
| What serious complication can occur with the transphenoidal approach to pituitary surgery? | The carotid arteries may be nicked leading to massive hemorrhage |
| What side effect is often associated with pituitary surgery and how to you fix it? | DI, Treat with DDAVP, but it is usually self limiting to about 10 days post-op |
| ETT management with transphenoidal approach to pituitary surgery | ETT is placed in left side of mouth and taped to chin (consider Right angle ETT), |
| Other considerations preop for transphenoidal approach to pituitary surgery | insert esophageal steth and temp probe, place OG and suction stomach then leave to gravity drainage, pack oropharynx with moist cotton gauze, tape and cover eyes with cotton patches to prevent corneal abrasion and seepage of clensing solution in eyes |
| What steps are taken to prevent nasal mucosal and gingival bleeding in transphenoidal surgery? | cocaine and LA w/epi constric vessels |
| WHat SBP should be maintained prior to aneuysm clipping and why | 120-150. It is enough pressure to help prevent exacerbation of ischemia if a bleed does occur, but a low enough pressure that aneurysm will likely not burst |
| What drugs can help prevent vasospasm following SAH | Nimodipine or Nicaripine |
| Which grade of SAH patients benefit the most from early surgical treatment? | Grades I and II |
| Preop SAH considerations | note neuro status, optimize patient, minimize aspiration risk |
| Induction of SAH patients | Smooth slow deliberate induction with lido, fentanyl, propofol; avoid sympathetic response to laryngoscopy/intubation |
| Intraoperative BP control with SAH patients | Often intentional hypotension is used to decrease potential bleeding and to make the aneuysm softer and more pliable for the clipping (MAP no lower 40% of preop) |
| What is done to prevent vasospasm postoperatively following SAH clipping? | Moderate intentional HTN (MAP of 80-120) |
Created by:
SRNA84