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125 Cards in this Set
- Front
- Back
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The BBB separates which compartments?
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BBB isolates brain and extracellular compartment from intravascular compartment
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Which areas of the brain lack BBB?
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Circumventricular organs, e.g., area postrema (chemoreceptor trigger zone), pituitary gland, pineal gland, choroid plexus, portions of hypothalamus.
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List characteristics of CSF.
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Total volume ~ 150 ml
SG: 1.002-1.009, pH 7.32 Bathes brain & spinal cord, cushions structures, controls extracellular milieu for neurons & glial cells Secreted by ependymal cells of choroid plexus w/in ventricular system at ~ 30 ml/hr. |
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Describe blood flow to the brain in terms of anatomy, CO, and metabolic demand.
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Brain receives 15% CO
50 ml/100 g brain/min Anterior circulation: carotids Posterior circulation: vertebrals Arterial systems communicate through circle of Willis |
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Name the CPP equation
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CPP= MAP- ICP or CVP (whichever is greater)
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Name the CBF equation
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CBF = 50 ml/100 g whole brain tissue/min
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What are the parameters of autoregulation?
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Maintained by autoregulation over 50-150 mmHg- brain will still get what it needs
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What is the relationship between CBF and PaC02?
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CBF increases linearly w/↑ PaCO2 in range of 20-80 mmHg
Effect diminishes over 24 hrs |
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What is the relationship between CBF and PaC02?
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Hypoxia is potent cerebral vasodilator
CBF ↑ ↑ when PaO2 < 50 mmHg |
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What are implications of the cerebral perfusion curve?
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Left side of curve, (hypotension), will have a correlatory decrease in cerebral blood flow. Right side has high systemic pressure and is at risk for bleed. In chronically HTN, whole curve is shifted to right. P02 less than critical low will not change anything. In pulmonary disease, big AA gradient, so ETC02 will not equate PaC02. ETC02 normally lower than PaC02 by 5-6 mmHg to facilitate outward diffusion.
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Name factors that influence CMR02.
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Temperature
Hypothermia ↓ CMRO2 7%/1C Seizures- huge increase Anesthetics- decreases it |
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What is normal ICP?
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5-15mm Hg
Relationship between volume of intracranial contents (brain/blood/CSF) & volume of intracranial vault |
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By what mechanism do volatile anesthetics increase ICP?
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w/↑intracranial volume, ↓intracranial compliance rapid ↑ICP
Pts w/ ↓compliance may develop marked ↑ICP w/sm ↑ intracranial volume, e.g., cerebral vasodilation secondary toanesthesia |
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Describe goals of anesthesia treatment in the patient with elevated ICP.
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Meticulous airway management
Hypoxia & hypercarbia can cause cerebral vasodilation Hyperventilation produces cerebral vasoconstriction Venous drainage ↓ intracranial venous blood volume Elevate HOB 30o Avoid excessive neck flexion or rotation |
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What is the relationship between barbituates and ICP?
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Barbiturates- thiopental, pentobarbital
Potent cerebral vasoconstrictors ↓ CBV, ↓ CMRO2 Effectively decrease ICP Maintaining high serum osmolality 305-320 mOsm/L may ↓ cerebral edema & ↓ brain volume Mannitol 0.5-2 g/kg IV & lasix produce hyperosmolar state that helps reduce ICP Reduce CSF volume (drain or ventriculostomy) |
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What can etomidate cause in the neuro patient?
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Etomidate can cause clonus that can be mistaken for a seizure. Also does not lower seizure threshold.
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What are the benefits of thiopental use over other barbiturates in the patient with elevated ICP?
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Selective vasoconstriction. Spares areas that are ischemic.
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What does the cerebral compliance curve tell us about tumors?
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Why brain tumors are asymptomatic. When threshold is reached, you have huge jumps in ICP.
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Name considerations when using volatile anesthetics in those with elevated ICP.
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All potent inhalation agents ↑CBF, CBV & ICP
Regarding cerebral physiology, no one agent better than another Hyperventilation attenuates dose-dependent ↑s in ICP Considered acceptable in all pts except those w/ marked ICH & midline shift |
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What are the effects of volatile anesthetics on ICP and CBF?
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All anesthetic agents affect ICP by ↓ cerebrovascular resistance, dose-dependent ↓ autoregulation ↑ ICP, CBV, & CBF w/ ↓ CMRO2
Changes in ICP > in pts w/underlying ↑ ICP Inhalation agents ↓ MAP & ↑ ICP ↓ CPP |
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Name the volatile anesthetics in order of worst to best in patients with high ICP
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Halothane > isoflurane > sevoflurane > desflurane
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Which inhalation agent has no affect on ICP?
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N02
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Which gas causes the highest increase in CBF?
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Halothane
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What do all gasses cause?
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Lower CPP
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Describe considerations of N02 in neuro anesthesia
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Some practitioners d/c N2O before dural closure to ↓ development of pneumocephalus
Potent? (with high percentages) cerebral vasodilator ↑ CBF, ↑ ICP 2o cerebral vasodilation |
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Which gas can increase CMR02?
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N20
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How can you use N20 in neuro anesthesia?
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IV agents (barbiturates, propofol, benzos, opioids) w/hyperventilation can ↓ effects of N2O on CBF & CMRO2
Volatile agents < 1 MAC may ↓ CBF & CMRO2 w/50% N2O, < 1 MAC volatile: ↑ CBF, ↑ CMRO2 Cerebral vasodilation w/N2O ↑ when > 1 MAC volatile agent used (in addition to using >1 MAC) Ali says don’t use > 1 MAC |
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When might you avoid using N20?
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Intracranial air (recent craniotomy, cranial-facial trauma)
When signal quality during intraop evoked-potential monitoring inadequate Evidence of mod/severe ↑ ICP “tight brain” intraoperatively |
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What are benefits of barbiturate use?
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↓ CMRO2 2o ↓ CNS neuronal activity coupled ↓ CBF & ICP
↓ CBF only in normal regions, not ischemic regions Vasomotor paralysis causes vessels in injured or ischemic zones to remain maximally dilated Results in shunting from normal to ischemic areas, called inverse steal ↓ free radical formation prevents further injury in ischemic areas |
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What are free radicals?
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Cascade of events from ischemia to infarction will lead to hyper reactive species/ free radicals/ unpaired electrons. Will react with whatever it comes in contact with to (damage, cellular death) create an electron pair. Thiopental is also a free radical scavenger.
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Name effects of etomidate.
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↓ CMRO2, CBF, ICP in normal brains
Rapid elimination compared to barbiturates More prompt postop neurologic evaluation Direct vasoconstricting effect Minimal C-V depression so CPP unchanged or slightly increased |
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Name effects of opioids.
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Opioid techniques popular for neurosurgical procedures
Hemodynamic stability Predictable emergence Synthetics have all been used successfully Dose related ↓CBF (25 ml/100 g/min) & CMRO2 (40-50%) Induction doses (e.g., 0.5-1 µg/kg sufenta) may cause ↓ MAP, ↓ CPP & ↑ ICP |
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Name the effects of benzos
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Anxiolytic, anticonvulsant, amnestic
Dose-dependent ↓ CMRO2, ↓ CBF Minimal effects on ICP Antagonist Flumazenil: no effect on cerebral dynamics when given alone May produce seizures in large doses |
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What is a benefit of precedex use?
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No respiratory depression
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In which neuro cases do you use precedex?
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1o anesthetic for brain mapping of cortical speech area. Provided adequate sedation & analgesia throughout surgery & allowed pt to complete necessary neuropsych tests
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Name effects of ketamine
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Possible advantage may be in hypovolemic multisystem trauma pt w/head injury
But ↑ CBF 60-80%, ↑ ICP ↑ resistance to CSF reabsorption further ↑ ICP |
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Name effects of succ
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Succinylcholine may produce ↑ ICP, ↑ CBF, ↑ CMRO2
UMN disease alters PNS response Resistance to PNS on hemiparetic/plegic side ↓ sensitivity to nondepolarizers in 1st 3 wks of UMN disease |
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How could you avoid succ complications?
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Consider IV Lidocaine/pretreatment with nondepolarizer/naroctic
Rocuronium 1.2 mg/kg avoids succinylcholine-related complications |
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Which two antihypertensives increase cerebral blood volume and ICP?
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nipride and NTG
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Which antihypertensive has minimal effects on ICP?
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Esmolol- Useful during induction
May be preferred during emergence 2o labetalol-related bradycardia |
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Which antihypertensive is thought to be cerebral protective?
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Nimodipine
Used effectively for periop BP control May have cerebral protective effects Used to prevent vasospasm after neurologic trauma/hemorrhage |
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The majority of intracranial procedures are for which type of lesion?
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supratentoral mass lesions
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What are s/s of a supratentorial mass?
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Nimodipine
Used effectively for periop BP control May have cerebral protective effects Used to prevent vasospasm after neurologic trauma/hemorrhage |
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What are s/s of an infratentorial mass?
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Cerebellar dysfunction (ataxia, nystagmus), brain stem compression (cranial nerve palsies, altered LOC)
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Name early signs of increased ICP
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double vision, headache, projectile vomiting w or w/o nausea.
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What are sensory EPs?
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Electrical potentials generated w/in neuraxis in response to stimulation of peripheral or cranial nerve
Potentials recorded as they travel from periphery to brain by electrodes placed over scalp & along transmission pathway Summation of hundreds of signals with software makes it possible to extract needed signals while “averaging out” background EEG |
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What type of anesthesia would you want for a pt. with EP?
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No nitrous, mac < 0.5 of volatile, no paralytic
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How will a damaged nerve pathway show on EP?
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↓ amplitude or ↑ latency (time from peripheral stimulus to arrival of potentials at recording site) of waveform peaks
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What is a concern regarding EP use?
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Intraop EP monitoring does not guarantee prevention of postop neurologic deficits
False (+) and false (-) EPs exist |
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What is an SSEP?
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Obtained by peripheral nerve stimulation, recording elicited signals over spinal cord (spinal SSEPs)or cerebral cortex (cortical SSEPs)
Used to monitor spinal cord function during spinal cord or verebral column surgery; during thoracic aortic surgery (to detect spinal ischemia during aortic cross-clamping) Monitors posterior cord function. Wakeup test necessary to assess anterior function. |
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Which anesthetics increase the latency of SSEP?
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All of them
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Which anesthetic has no effect on amplitude?
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propofol
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What type of anesthesia is preferred with pts. on SSEP?
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Short acting opioids like remi/su fentanyl. Anything that will have easy wake up and decrease need for gas.
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What is EEG and what can it predict?
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Measures cortical neural activity
Threshold marker for ischemia detection. EEG changes can warn of ischemia before CBF inadequate to maintain tissue viability |
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What does a loss of fast activity mean and what CBF does it correlate with?
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Loss of fast activity (α, β): ↓ amplitude, ↑ slow wave activity (delta, theta) associated w/iscehmia
CBF < 20-25 ml/100 g/min EEG slowing CBF 18 ml/100/g/min EEG isoelectric Sustained CBF 8-10 ml/100g/min tissue infarction |
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What is a concern about EEG?
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May show intraop changes but no neuro defect postop
Blood flow threshold for electrical failure higher than needed to maintain cellular integrity |
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What non anesthesia factors can cause EEG changes?
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Hypothermia, hypotension, hypoxia, tumors, vascular abnormalities, epilepsy
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What are the effects of anesthesia on EEG?
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Global rather than focal
Deeper anesthesia slowing, difficult to detect ischemic changes |
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What are intraoperative fluid therapy goals for a pt. with elevated ICP?
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Judicious fluid administration minimizes cerebral edema, ICP, reduced CPP & cerebral ischemia
Goal: give isotonic solutions sufficient to maintain perfusion avoiding hypervolemia, e.g., 0.5-1 m/kg/hr. Keep pts isovolemic, isotonic, isooncotic |
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What is the effect of hyperglycemia on elevated ICP?
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Glucose: association between preischemic glucose administration & poor neurologic outcome
Hyperglycemia w/anaerobic glucose metabolism produces excess lactate, intracellular acidosis |
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What is the dose of hetastarch? What is optimal H&H for neuro?
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20cc/kg
30-35% |
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Which fluids should be used in pts with elevated ICP?
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NS and colloids. NS has higher osmolarity than LR.
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Name concerns during induction of the neuro pt.
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Smooth & gentle induction more important than drugs used. One possibility:
preoxygenate Thiopental 2-4 mg/kg or propofol 1-2 mg/kg Nondepolarizer Hemodynamic response to intubation blunted with fentanyl (~1 µg/kg total dose) +/or lidocaine 1.5 mg/kg 3 min before intubation |
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Name positioning concerns
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Head elevated 15-30o
Facilitates venous & CSF drainage If head turned to side for better exposure Excessive neck flexion impedes venous drainage and elevates ICP Stabilize ETT w/hand during positioning Verify BBS present after positioning Double-check that circuit connections secure; table may be turned 90-180o away from anesthetist |
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Which craniotomies are performed supine?
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Frontal, temporal, and parietooccipital craniotomies performed supine (duh)
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Why does the sitting position have a higher chance of venous air embolism?
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Sitting craniotomy a bigger problem for air entrainment because wound is above level of heart. Dura cannot colapse and will continue to suck air when pressure in venous dural sinus drops
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What is a common anesthetic technique for craniotomy?
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Typically “balanced” low-dose inhalation +/- narcotic infusion, +/- N2O, +/- Precedex
If potential for air embolus/pneumocephalus exists, N2O contraindicated Large air embolus can cause c-v collapse Hyperventilation to PaCO2 of 25-30 Confirm w/ABG |
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By what mechanism could muscle relaxants be beneficial in decreasing ICP?
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May decrease ICP by relaxing chest wall, decreasing intrathoracic pressure, facilitating venous drainage
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Name anesthetic considerations during maintenance phase
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Anesthetic requirements less after craniotomy & dural opening
No sensation from brain parenchyma Long-acting narcotics/sedatives avoided during last 1-2 hrs of case Facilitates neuro exam at end of surgery Prevents postop obtundation/hypoventilation |
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What are anesthetic considerations during emergence?
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If intracranial HTN not present, may be able to extubate
Must be slow/controlled Straining, bucking may precipitate intracranial hemorrhage or worsen cerebral edema Brief cough or gag may not be problem if BP controlled Uncontrolled HTN hemorrhage Esmolol, labetalol, hydralazine, nimodipene |
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Name considerations during a posterior cranial fossa surgery
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Neuropathology w/in post fossa may impair airway control, respiratory function, C-V function, autonomic function and consciousness
Major motor and sensory pathways, primary c-v and respiratory centers, reticular activating system and nuclei of lower cranial nerves all in brainstem Tight space w/little room for edema, tumor or blood |
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What do you do if you suspect a VAE?
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1st thing to do is to tell the surgeon and have them wet field. Whatever air is sucked in needs to stay on the right side of the heart where is can become reabsorbed. Place in trendelenberg position, left side down.
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What are s/s of VAE?
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VAE- everything drops, ETC02 first, C02 still in body and will be high in serum. BP dropping
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What is a paradoxical air embolism?
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Paradoxical air embolism is air on the left side of the heart that may lead to stroke.
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Name clinical situations related to VAE
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Position-Seated, prone, steep Trendelenburg
Surgical- urologic, post spinal, bone marrow harvest, laproscopy, radical pelvic, any catheter insertion, liver, transfusion rx |
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Name factors that predispose one to paradoxical embolism
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Existing connection between R & L heart
ASD, VSD, PFO especially at risk PFO in 30-35% of population- no flow If R sided pressures > L sided, systemic air may embolize & enter arterial circlation If preop murmur, pts who require seated position should have echo to r/o presence of intracardiac defect |
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What is RV airlock?
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Continued air entry can produce RV airlock
Pulm HTN, hypoxemia, CO2 retention, ↑ deadspace ventilation, ↓ETCO2 Large alveolar air volume: sudden appearance of end-tidal N2 |
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How can you detect small air entrainment rates?
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Precordial doppler can detect small entrainment rates
Placed over R heart along R sternal border between 3rd and 6th intercostal spaces Placement confirmed w/change in Doppler signal when 10 ml saline bolus given through CVP |
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What is the first sign of RV airlock?
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Rising ET N2
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Name clinical situations related to VAE
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Position-Seated, prone, steep Trendelenburg
Surgical- urologic, post spinal, bone marrow harvest, laproscopy, radical pelvic, any catheter insertion, liver, transfusion rx |
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Name factors that predispose one to paradoxical embolism
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Existing connection between R & L heart
ASD, VSD, PFO especially at risk PFO in 30-35% of population- no flow If R sided pressures > L sided, systemic air may embolize & enter arterial circlation If preop murmur, pts who require seated position should have echo to r/o presence of intracardiac defect |
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Name clinical situations related to VAE
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Position-Seated, prone, steep Trendelenburg
Surgical- urologic, post spinal, bone marrow harvest, laproscopy, radical pelvic, any catheter insertion, liver, transfusion rx |
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What is RV airlock?
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Continued air entry can produce RV airlock
Pulm HTN, hypoxemia, CO2 retention, ↑ deadspace ventilation, ↓ETCO2 Large alveolar air volume: sudden appearance of end-tidal N2 |
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Name factors that predispose one to paradoxical embolism
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Existing connection between R & L heart
ASD, VSD, PFO especially at risk PFO in 30-35% of population- no flow If R sided pressures > L sided, systemic air may embolize & enter arterial circlation If preop murmur, pts who require seated position should have echo to r/o presence of intracardiac defect |
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How can you detect small air entrainment rates?
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Precordial doppler can detect small entrainment rates
Placed over R heart along R sternal border between 3rd and 6th intercostal spaces Placement confirmed w/change in Doppler signal when 10 ml saline bolus given through CVP |
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What is RV airlock?
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Continued air entry can produce RV airlock
Pulm HTN, hypoxemia, CO2 retention, ↑ deadspace ventilation, ↓ETCO2 Large alveolar air volume: sudden appearance of end-tidal N2 |
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What is the first sign of RV airlock?
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Rising ET N2
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How can you detect small air entrainment rates?
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Precordial doppler can detect small entrainment rates
Placed over R heart along R sternal border between 3rd and 6th intercostal spaces Placement confirmed w/change in Doppler signal when 10 ml saline bolus given through CVP |
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What is the first sign of RV airlock?
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Rising ET N2
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Name methods of detecting VAE in order of highest to lowest sensitivity
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TEE, ETC02, PA cath, CO, CVP, EKG change, BP change, precordial stethoscope
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Describe treatment of VAE
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Flood surgical field. D/C N2O, give 100% O2. Perform Valsalva maneuver or compress jugulars. Aspirate air from atrial catheter. Support BP w/volume, pressors. Reposition in L lat decub w/15o head-down tilt if BP continues to fall. Modify anesthetic to optimize hemodynamics
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What does the valsalva maneuver do during treatment of VAE?
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Valsalva to increase intrathoracic pressure and decrease venous return. Will prevent air and blood from returning to the heart.
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How can you modify sitting position to prevent venous pooling?
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Semi-recumbent in standard seated position w/back ↑ 60o, legs elevated w/knees flexed to level of heart
Prevents venous pooling, decreases risk of DVT |
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Name postoperative considerations of a pt. undergoing posterior cranial fossa surgery
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Central apnea- VRG not working
Impaired swallowing HTN Arrhythmias Delayed awakening 2o brain stem compression |
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What is the leading cause of SAH?
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Saccular aneurysm rupture leading cause of SAH
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Name characteristics of a pt. with Hunt's grade I
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Asymptomatic/min headache, sl nuchal rigidity
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What is the leading cause of SAH?
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Saccular aneurysm rupture leading cause of SAH
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Name characteristics of a pt. with Hunt's grade II
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Mod-severe h/a, nuchal rigidity
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Name characteristics of a pt. with Hunt's grade I
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Asymptomatic/min headache, sl nuchal rigidity
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Name characteristics of a pt. with Hunt's grade II
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Mod-severe h/a, nuchal rigidity
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Name characteristics of a pt. with Hunt's grade III
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Drowsiness, confusion, mild focal deficit
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Name characteristics of a pt. with Hunt's grade III
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Drowsiness, confusion, mild focal deficit
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Name characteristics of a pt. with Hunt's grade IV
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Stupor, mod-severe hemiparesis, poss early decerebrate rigidity
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Name characteristics of a pt. with Hunt's grade IV
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Stupor, mod-severe hemiparesis, poss early decerebrate rigidity
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Name characteristics of a pt. with Hunt's grade V
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Deep coma, decerebrate rigidity, moribund appearance
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What is transmural pressure?
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Transmural pressure: difference between MAP and ICP – represents stress applied to aneurysm wall
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What is the primary cause of death in SAH
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Primary bleed
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When do rebleeds often occur after postoperative repair of aneurysm.
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Peak risk on 1st day, another large proportion rebleeds by day 14
50% will rebleed by 6 months (without having it fixed) |
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Describe prevention of rebleeding
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Secure or clip the aneurysm
Stabilize the clot (antifibrinolytics NOT used due to increased risk of vasospasm) Decrease the transmural gradient Transmural gradient = Difference between pressure inside the aneurysm (BP) and outside the aneurysm (ICP) |
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How long can a pt. tolerate temporary arterial occlusion for?
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Up to 15 mins. Older patients/poorer grade patients will be less tolerant
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What are anesthesia goals during temporary arterial occlusion?
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NO HYPOTENSION. Maintain collateral circulation. Decrease CMRO2 with TPL
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What causes vasospasm? What can vasospasm lead to?
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Reactive narrowing of cerebral arteries after SAH
Leads to neurologic deterioration from impaired cerebral perfusion, ischemia, 2o brain infarction Results from trauma to vessels, spasmogenic substances, e.g., oxyhemoglobin, platelets |
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When is the peak onset of vasospasm post operatively?
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Onset of vasospasm is usually by day 5, peaks at about day 7-10, gone in 3 weeks
70% incidence of some vasospasm. Only 30% are symptomatic Up to 50% of them die or suffer damage |
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What EKG changes can occur during vasospasm?
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Pathognomic sign is prolonged QT interval with inverted T waves
May require delaying surgery |
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Which patients are at risk for developing vasospasm?
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Patients who are “critically ill” on admission, have the worst grade
Patients who are hypertensive on admission and have nuchal rigidity Prominent subarachnoid blood on CT with a lot of basal cisternal blood. |
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What causes vasospasm? What can vasospasm lead to?
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Reactive narrowing of cerebral arteries after SAH
Leads to neurologic deterioration from impaired cerebral perfusion, ischemia, 2o brain infarction Results from trauma to vessels, spasmogenic substances, e.g., oxyhemoglobin, platelets |
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When is the peak onset of vasospasm post operatively?
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Onset of vasospasm is usually by day 5, peaks at about day 7-10, gone in 3 weeks
70% incidence of some vasospasm. Only 30% are symptomatic Up to 50% of them die or suffer damage |
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What EKG changes can occur during vasospasm?
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Pathognomic sign is prolonged QT interval with inverted T waves
May require delaying surgery |
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Which patients are at risk for developing vasospasm?
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Patients who are “critically ill” on admission, have the worst grade
Patients who are hypertensive on admission and have nuchal rigidity Prominent subarachnoid blood on CT with a lot of basal cisternal blood. |
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Treatment of vasospasm
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Successful rx r/t maintenance of adeq CPP CPP = MAP – ICP
Volume expansion- want them hypervolemic Avoid hyponatremia Relative hemodilution (hct ~ 32%) Deliberate intraop hypertension Postop HTN not treated aggressively |
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Pharmocological treatment of vasospasm.
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Pharmacologic vasodilation ineffective since vasospasm involves structural alteration in vessel wall rather than spastic contracture of vessel
Nimodipine and nicardipene used to prevent neurologic deficit after SAH. Steroids Drip papaverine on the circulation at the time of operation (done by surgeon) |
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Describe triple H therapy
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Maintenance of cerebral perfusion
Augmentation of BP & CO Administration of inotropes Administration of nimodipine or nicardipine “Triple H Therapy” Hypervolemia, Hypertension, Hemodilution. Correction of hyponatremia, Transluminal angioplasty |
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Name an important difference between nimodipine and nicardipine
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Nimodipine crosses BBB, whereas nicardipine doesn’t
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Eary vs late surgical treatment of SAH
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Edematous hyperemic brain
Autoregulation abolished by SAH. Brain is tense/swollen with a clot. Early surgery allows you to evacuate the clot decreased risk of vasospasm. Early surgery allows more aggressive hemodynamic management. |
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Name anesthetic concerns regarding epilepsy surgery
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Awake craniotomy w/local anesthesia of scalp & IV sedation allows mapping, which requires pt cooperation
Anesthetic techniques chosen based on ability to augment or attenuate the seizure focus |
