Neuro Flashcards
Normal CMRO2-and what is that?
Normal-3-3.5 mL
It is the rate of O2 consumption by the brain
Formula for CBF- Normal CBf? Impairment? Isoelectric? Irreversible brain damage?
CPP/CVR (cerebral vascular resistance) Normal-50mL/100g/min Impairment-20-25 Isoelectric-15-20 Irreversible-10
CBF is _____ proportional time Pa____.
When is CO2 responsiveness lost?
CBF is directly proportional to PACO2 between PACO2 of 20-80.
KIM that hyperventilation causes vasoconstriction, but that hypocarbia can lower BP.
CO2 responsiveness lost 24-48 hrs due to increase in CSF HCO3
How does O2 affect cerebral blood flow?
O2 at PaO2 less than 59, CVF markedly increases. PaO2 greater than 300, it slightly decreases
CBF is coupled to what?
How does temp affect CBF? When does CBF become isoelectric with regard to temp?
Hct less than 30 or less than 50 and CBF?
Coupled to CMRO2
CBF decreased 5-7% with hypothermia, isoelectricity iccurs at 20 degrees Cel
Less than 30-increases CBF. Less than 50-decreases CBF
Formula for CPP
Normal values
MAP-ICP (or CVP-whichever is greater) Normal-100 Slowing-50 mmHg Isoelectric-40-25 Irreversible brain damage-sustained <25
Compensation for increases in volume of brain:
Movement of CSF into spinal compartment, increase in CSF absorption, decrease in CSF production, decrease in Venus cerebral blood volume
What crossed the BBB?
O2, CO2, H2O, lipid soluble drugs
Severe HTN, rumors, CVA, hypercapnea, seizures
What do inhalational agents do to CMRO2? Volatiles are uncouplers-explain-
What do all agents do to ICP?
All decrease CMRO2. Isoflurane-the most can actually produce isoelectric EEG.
Volatiles decrease CMRO2 and increase CBF, they can also import auto regulation
In general, all agents increase ICP. N20 mood, but still does this
What do barbiturates do to CMRO2, CBF, ICP, CSF?
Reverse steal and barbiturates?
Barbiturates decrease CMRO2 and CBF, decrease ICP, increases resorption of CSF.
Robin Hood-by constricting normal areas, blood can be diverted to areas that have maximal vasodilation and are unresponsive to other stimuli (reverse steal)
Narcotics and CMRO2, CBF, ICP, CSF
Decreases ICP, CMRO2, CBF. Increases CSF resorption
Benzos and CMRO2, CBF, ICP, CSF
Decrease in everything- including CSF resorption
Ketamine and CMRO2, CBF, ICP, CSF
Unchanged CMRO2
Only agent that INCREASES CBF
ICP-increases
Impedes resorption if CSF
Etomidate and CMRO2, CBF, and ICP and CsF
CMRO2, CBF, ICP CSF resorption-decreased. KIM Etomidate should be avoider in pts with seizure disorders and myoclonus is seen
Propofol CMRO2, CBF, ICP, CSF
CMRO2-decreases,
CBF decreases,
ICP decreases
Lidocaine- CBF, CMRO2, ICP
CMRO2-decreases
CBF decreased usually without hypotension
ICP decreased
Do muscle relaxants affect CMRO2, CBF or ICP?
What about sux?
No-not directly, but the ones that release histamine (at Tacuri I’m, mivacarium) a can increase ICP by causing vasodilation, or decrease it by causing vasodilation.
Sux can cause a minor increase in ICP-can be pretreated with defasicykating dose of roc
Why maintain CbF?
Brain is one of the most metabolically active organs and is very sensitive to hypoperfusion and hypotension. Irreversible damage can occur within minutes or loss of CBF
What exactly is auto regulation?
It’s the maintenance of CBF over a given range it CPPs (usually a MAP between 50-150)
Both are important, but CBf is usually most important because CBF is maintained over a wide range of CPP
Advantage of etomidate
More hemodynakicbinstability die to its critical effect and less of a brain stem effect.
Is sux contraindicated for neurosurgery? Why or why not?
No, but the main concern with using Sux in a Neurosurgery case is the potential to increase ICP. ICP increases with six due to activation of gamma motor afterward with fasiculatuons causing increased metabolic activity of the sensory cortex and concomitant CBF increases are small.
Lidocaine and neurosurgery-
1-1.5 mg/kg 3 minutes before intubation can help blunt the sympathetic response to laryngoscopes and intubation
Types of waves and their amplitudes
How does ischemia appear on EEG?
Beta 13-30 Hx alert, open eyes state
Alpha-8-12 alert, closed eye state
Theta-4-8 drowsy or anesthetize state
Delta 0-4, deep sleep or deep anesthetize date
Ischemia appears as slowing, then complete loss of amplitude
Anesthetic agents-which type of response of activation happens and at which doses? What about Isofkurane and desfkurane and secofkurane? What about barbiturates, etomidate and Propofol? What is unique about their suppression?
Usually produce biphasic response of activation at sub anesthetic doses, followed by dose-dependent depression.
Isoflurane is the only volatile agent that produces burst suppression at clinical doses. Des does burst suppression at 1.2 and 1.5 MAC. Nitrous oxide depends on the anesthetic with which it is used. Barbiturates etomidate and propofol typical biphasic pattern and only agents capable of producing burst suppression and electrical silence at high doses
Opiates and amplitude changes
At high doses, amplitude slowing is observed.
Benzo and eeg
Initial increased amplitude and decreased frequency but no electrical silence.
Ketamine and EEG
High amplitude theta activity at low doses, followed by high amplitude Sigma and low amplitude beta activity to high doses.
Which factors cause slowing on an EEG?
Hypoxia, hypothermia, extreme hypo or hypercapnea, hypocalcemia, hepatic encephalopathy and renal failure.
Indications and limitations of the EEG
Indication-absolute-none
Relative-EEG can be used to detect cerebral ischemia during carotid endarterectomy and CPB. Can also be used to assess attainment of electrical silence or burst suppression.
Limits: artifacts, only cortical tissues are monitored so subcritical injury could happen, only certain cortical areas monitored, regional injury may be missed, lack of conclusive proof of efficiency
What is an evoked potential?
A recording of the neuromuscular responses to neural stimulation.
Somatosensory-it’s measuring which nerves?
Anesthetics (gas) do what to amplitude and latency?
All IV anesthetics ____ latencyband ____ amplitude except-
Peripheral nerves
Gas increases latency and decreases amplitude ILDA
All IV anesthetics increase latency and decrease amplitude except prop which has no effect on amplitude. Etomidate and ketamine which increase amplitude. Fentanyl has minimal effects.
Which factors affect SSEP monitoring?
Temp, ischemia, hypotension, anemia, and hypercapnea. TIHAH
BAEP and anesthetics
Very resistant to anesthetics, but not sensitive to hypoxia or intracranial HTN
VEPs
Most sensitive to anesthetics. Visual pathway including retina, optic chiasm, optic radiations, and occipital cortex
MEPs-are they more or less sensitive to anesthetics?
Less sensitive than visual, but still very affected by anesthetics. It involves stimulation of the motor cortex above site of surgery.
How does ischemia appear in EPS?
Increase in post stimulus latency or decrease in amplitude
N2O and EPs?
Reduces amplitude but doesn’t affect latency
What exactly is an EEG monitoring?
Spontaneous electrical activity in the cortex for signs of cerebral ischemia.
For which procedures would you consider using an EEG? Does every carotid need an EEG?
Those in which cerebral ischemia is likely, and that detection would lead to treatment, and that treatment would improve outcome.
Every carotid does not need an EEG-someone needs to be able to interpret it and there needs to be a plan for if ischemia were detected-I.e., shunt placement and hypertension
Somatosensory measures:
Measures function of the sensory tract, from peripheral nerve to cortex, including dorsal spine.
BAEPs measure
Measures function of the auditory tract, from the eighth cranial nerve to the brainstem.
Visual:
Measures function of the optic tract, from the retina to the occipital cortex, including the optic chiasm
Motor:
Measure function of the motor pathway, from cortex to muscle, including anterior spine
Processed va unprocessed EEG
Unprocessed-offers note info but difficult to interpret
Processed-simpler to use, but loses some info. Which ever modality it is important that there is a qualified personnel member capable of interpreting significant findings
What is the spectral edge?
Another way to visually depict processed EEG data in which the frequency below which 95% of the power is found represented by a line
What is aperiodic analysis?
A simple form of. Amplitude analysis in which the EEG is analyzed by examining the amplitude of waves over certain periods of time. Each wave is represented as a vertical line the height of which corresponds to the amplitude and frequency of which is indicated by its position along the horizontal axis
What anesthetic technique would you use with EEG monitoring?
I would use a balanced technique with low-dose potent inhalational agent. Other anesthetic agents and techniques including high-dose potent inhalational agents barbiturates etomidate and propofol produce a bye phasic response consisting of activation at sub anesthetic doses followed by dose-dependent depression. Ketamine produces high amplitude slow wave activity. Narcotics however given in typical doses cause minimal change
Would you personally feel comfortable using processed EEG in the OR?
Since I have not had specific experience with the device, I would say no. But if an anesthesiologist were specifically trained and experienced and it’s used or if I receive such a training, and it’s used did not interfere with more important intraoperative responsibilities, then I believe anesthesiologist my monitor EEG as part of an overall plan of managing neurologic ischemia
What if depression of the EEG, decrease in the EP amplitude, increase in the EP latency occurred intraoperatively?
All of these signs are suggestive of ischemia. first I would inform the surgeon to determine if there was any surgical for the change such as excessive bleeding and I would also let the surgeon know that I would now begin to go down my own checklist. That check list includes reviewing the ABCs. I would examine the patient’s pulse oximeter in color, ET CO2, ABG, and hematocrit. As well as blood pressure and peripheral pulses. Next, I would determine the patient’s temperature and make certain the level or type of anesthetic could not change suddenly.
Does use of the SSEP mean that the wake up test is a necessary?
Not necessarily. The problem with the SSEP is that false negatives can still occur, even though the incidence of such an event is rare. The SSEP tells you what is going on at that moment but does not tell you about ischemia happening before that moment or anytime afterwards.
How would intraoperative EEG or EP changes affect your post operative management?
I would have to do a quick neurologic exam for example mental status motor sensory function cranial nerves reflexes and make sure the patients oxygenation been elation ABG temperature in anesthetic level where appropriate I would also consider obtaining a neurologic or surgical consult
What is normal I CP
15
What is Cushing’s Triad and when would you see it?
Cushing’s try out his hypertension, bradycardia, and bradypnea in association with intracranial hypertension
What do you want to do with a patient that just has ICH?
First treat the underlying cause, then ABCs. Assure adequate oxygenation, ventilation, and CBF. In adequate oxygenation and hypertension are devastating combo in terms of cerebral ischemia.
Next you could place a CSF drain, it is the fastest and most effective means if a catheter is available.
Then you could do a burn hole. Lastly you could hyperventilate to a C02 of 25 to 30, but be careful because that can cause cerebral ischemia.
You could also give mannitol, or furosemide, you could elevate the head of the bed to 30°
What is the dosing of mannitol and reducing ICP and how does it work? What are you concerned about? What about in the elderly?
Minotaurs dose is .25-1.0 mg per kilogram. It is effective in reducing I CP by increasing serum osmolality in producing cerebral desiccation. The issue is that the transient increase in intravascular volume can increase the blood pressure, creating a potential hazard with unruptured intracranial aneurysms or expanding hematoma. In the elderly rapid osmotic diuresis can shrink the brain tear the bridging veins and lead to a sub dural hematoma.
Name the four intracranial monitors in briefly tell me about them.
Intro ventricular catheter: allows direct measurement of ICPCSF drainage and determination of compliance risk include damage to brain, bleeding, infection and occlusion. This is the gold standard.
Sub dural/sub arachnoid bolt inserted through a burn hole it does not penetrate the brain; but it’s unable to withdraw CSF the number one problem is infection.
Epidural transducer: extra dural location, so brain is protected from infection but unable to withdraw CSF or determine compliance rarely used.
Fiber optic: measures pressure by reflection of light off a pressure sensitive diaphragm. Less infection unable to calibrate in vivo. Insertion possible and intraventricular sub dural epidural or intraparenchymal spaces
Why is a rapid decrease in ICP dangerous?
Because it may increase the transmural pressure across the vascular structure, leading to aneurysm or a VM rupture.
What are your goals preop intra-op and postop and patience with intracranial hypertension?
Preop I want to determine the chronicity and severity of any ICH, and if necessary optimized CPP by decreasing ICP or increasing MAP before surgery.
Intra-op – implement measures to decrease ICP/increase CPP at least until the door is open. Once opened conditions that lead to cerebral swelling such as an increase in CBF Or CMRO2 should be avoided.
Postoperatively, continue ICP reduction as necessary and assess neurologic status.
Which findings are concerning on imaging for intracranial hypertension?
Slit like ventricles or a greater than .5 cm midline shift
When can drainage of CSF cause brain stem herniation?
Brain stem herniation could happen if Hydro Cephalus is obstructive
Where would you place your Adaline transducer in a patient with ICH? Sidenote consider using atomic date during intubations because it will help decrease hemodynamic instability in patients with ICH
I would place the arterial line at the level of the external auditory canal which approximates the level of the circle of Willis. If it were not there I would simply subtract 7 mmHg for every 10 cm the transducer was below that level to obtain the map perfusing the brain
What is the benefit of isoflurane in patients who have intracranial hypertension?
Iso flooring decreases the CMR02 and lowers the cerebral blood flow
What emergency airway preparations must always be available in patients with difficult airway?
LMA, glide scope, notification of surgeons about possible need for a STAT cricothyrotomy
The surgeons are saying that they cannot close the school because of a swollen brain can you help them?
First the cause must be determined.
First I would check the ABCs. If the swelling is due to hypoxia hypercarbia hypertension or an adequate Anesthesia I would correct these. Secondly if it were due to the use of vasodilator such as nitroglycerin sodium nitroprusside or inhalational agents I would need to discontinue them. Third if there were the possibility of bleeding beneath the brain surface that should be addressed by the surgeons. Lastly once all these possibilities have been excluded I would remove CSF from a ventriculostomy or lumbar drain. Possibly hyperventilate if the PAC02 is above 25
What would you do if hypotension occur during removal of CSF from the ventriculostomy?
I would immediately stop the drainage. Rapid drainage of CSF for my ventriculostomy can cause brain stem herniation resulting in hypertension or hypotension, tachycardia or bradycardia. It has been recommended that CSF drainage not exceed 5 mL per minute
How would you asked to be a patient with ICH?
First I may not activate if the patient’s mental status were already impaired or if they were significant disruption of brain parenchyma cerebral edema or significant hypercapnia or were likely.
Otherwise the criteria should be no different than for an otherwise healthy patient.
What is the vicious cycle of uncorrected ICH?
The vicious cycle is I CH leading to ischemia which leads to Adema in further ICH.
When is the time you would give steroids with intracranial hypertension?
If there is a tumor.
What are the types of cerebral edema and what does cerebral edema due to the intracranial hypertension?
Vasogenic is the most common it means that there’s been a disruption of the blood brain barrier. Then there is osmotic which comes from interstitial hyperosmolality. Then there is compressive which is from obstruction of interstitial fluid flow pathways. In hydrocephalus which is from obstruction of CSF blood flow
Cerebral edema causes intercranial hypertension
What is the treatment for cerebral edema
The treatment for cerebral edema is similar to the treatment for intracranial hypertension since cerebral edema causes intracranial hypertension. First ABCs and then you want to address the underlying cause.
ABC’s, then address the underlying cause. This may include antihypertensive therapy to reduce hydrostatic pressure contributing to fluid translation through Adema. Next elevation of the head of the bed to 30° C hyperventilation moderate just 25 to 30. Then diuretics including mannitol and furosemide and lastly steroids which may be affected for vasogenic Adema but are not effective for acute head trauma
What is the primary determinant of water flux a cross the blood brain barrier?
Oncotic pressure is the primary determinant since under normal conditions of sodium concentrations in the brain interstitium in the blood are equal. However should the blood become hyper or hypo natremia with respect to the brain cerebral dehydration or Adema could result.
What are four conditions that start with the letter H that can cause cerebral edema? What exactly is cerebral edema?
Hypoxia, hypotension, hypertension, hypo osmolality
Cerebral edema is an increase in extra cellular brain water
What are your goals for MAP and I CP during cerebral edema?
Our goals include maintaining MAP and possibly even making it elevated, and reducing ICP as much as possible.
Which fluids would you use in cerebral edema?
I would start with an isotonic or slightly hyper tonic Krystle Lloyd solution. NS may be preferable to LR because it has an osmolarity of 308 where is that for Ella is 273. Since normal serum osmolarity is approximately 285 the slightly hypotonic LR could call cerebral edema. I would also avoid dextrose containing solutions under conditions of cerebral ischemia glucose worsens neurologic outcome presumably by acting as a substrate for the production of intracellular lactate an intracellular acidosis
How is the formation of cerebral edema different than that of peripheral Edema?
It is different because the brain cannot offset is water entry because it is less permeable to sodium. The peripheral Adema is a little less due to the fact that sodium crosses from the peripheral interstitium in to the blood the opposite direction of water movement offsetting the net amount of edema formed.
What are some problems with using colloids for cerebral edema?
How do you feel about hypotonic solutions and cerebral edema?
Had a starch can cause coagulopathy, pentastarch can cause more rapid rental excretion, dextran can cause problems with coagulopathy anaphylaxis in renal failure. Albumin has been shown to have worse outcomes.
Hypotonic solutions can also cause more cerebral edema by allowing for fluid to go into the brain
What is a concern if CSF is removed to quickly from a lumbar drain? What about from a ventriculostomy?
Trans tentorial or tonsillar herniation is a concern.
If you remove fluid to quickly from a ventriculostomy, then the concern will be brain stem herniation
What are some pros and cons of the sitting position when removing brain tumors?
Pros include decreased bleeding improve surgical access improve in elation and access to extremities. Cons include lower extremity pooling with decreases in cardiac output increases in SVR, PVR and cerebral perfusion pressure.
Other kinds include increased incidence of vie a E, cervical cord injury from excessive neck flexion and owner nerve compression or sciatic nerve stretching. As well as pneumocephalus
Other cons of the sitting position include ischemia of the cervical spine which can occur from neck flexion in the sitting position which can lead to quadriplegia as well as hyperflexion causing jugular venous obstruction leading to ICP and swelling of the face and tongue, compression of the owner nerve from pressure on the OR table leading to neuropathy. Sciatic nerve damage from flexion of the hips with the knees held straight
What are relative contraindications to the sitting position?
Right to left shunt, pulmonary a v-mail formations, severe hypovolemia, and severe hydrocephalus, but not the use of beta blockers
How does the brain compensate for an expanding mass lesion
First bite his placement of blood Venus, then by his placement of CSF, and finally by this placement of the brain
In a patient with a brain tumor would you place them in Trendelenburg to place a central line? And what is the difference between a supra and infratentorial tumor?
If the ICP were critically elevated I would try to avoid the Teebird position. If I were unable to place a central line any other way in the for moral or long arm and he would over in adequate then I would consider a brief period of Tieberg. For infratentorial tumors, There is a greater likelihood of brain stem involvement, more frequent intraoperative hemodynamic instability from brainstem manipulation and the need for sitting or prone positioning
In the sitting position of a tumor removal the patient becomes hypoxemic what is your differential diagnosis and what would you do?
I am concerned about the usual causes of hypoxemia as well as VE. I will confirm hypoxemia by looking at the pulse ox and checking the patients color, then I would look at the cat in a gram for changes in the pattern in amount of exhale CO2. VE would be confirm that only by decreasing and title but the appearance of entitle nitrogen next I would look at the airway pressure’s and title volumes. Finally I would hand finally feel the patient’s airway compliance an exam in the chest for symmetric wall excursion and equal breath sounds flexion of the head while in the sitting position can cause call dad this placement of the endotracheal to buy 2 cm leaving to Endobronchial intubation.
What is the significance of bradycardia during posterior fossa surgery? And would you allow spontaneous ventilation during posterior fossa Surgery?
Bradycardia during posterior fossa surgery could be a primary dysrhythmia anesthetic or drug affect or I could represent brain stem or cranial nerve manipulation. Tachycardia and PVCs are asystole can also result from brain stem herniation or stimulation. I would not allow spontaneous been elation during posterior fossa surgery due to the fact that it can risk hypercapnia patient movement in Venus air in trapment from an open
What kind of things would you see in an AC TH secreting tumor?
ACTH stimulates the adrenal release of cortisol. We would see Cushing’s disease which is osteoporosis proximal myopathy high blood pressure diabetes and accelerated atherosclerosis.
What kind of things would you see in a GH secreting tumor?
Acromegaly, macroglossia, enlargement of the lips, nose, and nasal turbinates. Glottic stenosis from tissu overgrowth vocal cord palsy impaired cricoarytenoid mobility obstructive sleep apnea arthritis diabetes hypertension and Exceller rated atherosclerosis.
What kind of things would you seen the prolactin secreting tumor
Infertility amenorrhea galactorrhea women loss of libido and men and women
Why are you concerned about a total spinal with surgery on the pituitary tumor?
Because of the fact that there can be systemic absorption of intramucosal he injected epinephrine or cocaine as well as a total spinal from local anesthetic inject into the preform plate.
What happens to pituitary hormones during surgery?
It is variable and can be difficult to predict. GH, prolactin, and AC TH and cortisol may be released during surgical stimulation ATH is released during surgery and anesthesia especially with the use of narcotics TSH release is inconsistent
Cushing’s disease versus syndrome
The disease differs from the syndrome and that even though the symptoms are the same the syndrome is due to hyper cortisol is them from any cause exogenous or endogenous
What are you thinking about when a patient has a growth hormone producing tumor?
I’m thinking about the fact that they could have hypertension, accelerated atherosclerosis, possibly CHF. Their airway – mask ventilation may be difficult to do large nose lips and mandible. Intubation may be difficult due to a large town, hypertrophied soft palate, tonsils, epiglottis and larynx. Perry operative strider may be related to vocal cord palsy. Make an attempt to elicit a history of obstructive sleep apnea, patients may also have insulin resistance.
Where would you place the intra-arterial catheter in a patient with acromegaly?
If the patient had signs of carpal tunnel syndrome, I would prefer the dorsalis pedis artery to avoid the possibility of hand ischemia
During topical is Asian of the nasopharynx you notice PVCs. What would you do
This could be due to infiltration of the nasal mucosa with epinephrine. If so, I would ask that they stop. If the associated tachycardia and hypertension was well tolerated, I would allow the epinephrine to wear off. Other factors include hypoxia, myocardial ischemia, electrolyte abnormalities, mechanical stimulation of the myocardium via catheter.
What are your concerns in the transphenoidal approach versus the suprasellar approach?
I am concerned for the transphenoidal approach that there will be systemic absorption of intramucosal epinephrine, accumulation of blood and tissue in the pharynx and stomach, bleeding from the cavernous sinus or carotid artery entry, cranial nerve injury to three for V one and six, and pituitary dysfunction such as diabetes insipidus. If a suprasellar surgical approach were playing the chance of bleeding, brain injury, and edema are greater.
The patient who had a pituitary surgery is polyuric post operatively what would you do? What would you do if you found hypoglycemia and hypotension post operatively? After you give a supplemental dose of hydrocortisone the patient has polyuria. Are you surprised? What neurologic complications can result from this operation?
The polyuria could represent diabetes insipidus also be due to overhydration diuretic use osmotic diuresis from hyperglycemia your contract use. I would examine the patient for signs of hyper or hypo kalemia review the history labs and fluid balance. The diagnosis of DI is suggested by the findings of production of dilute urine in urine osmolality less than plasma osmolality. In the absence of diuretic use or hyperglycemia
If I found hypoglycemia and hypotension the differential could be expensive but must include pan hypopituitarism or pituitary apoplexy
After a dose of hydrocortisone polyuria happening. I am not surprised adrenocortical hormones are necessary to facilitate renal excretion of water in massive diuresis from diabetes insipidus often enSues after steroid placement
Neurologic complications that can result from a pituitary operation include ophthalmoplegia, facial Anesthesia, contralateral hemiparesis or hemi plegia from direct pressure or vasospasm.
What is one of the biggest risks for VAE?
It occurs in association with surgeries that I have a greater than 5 cm of water gradient between the open Venus structure in the right atrium. The incidence and severity is greatest and sitting craniotomy’s.
Why does cardiovascular collapse occur in a VAE?
It occurs because in trapped air can cause mechanical obstruction and precapillary arterials or an airlock in the right heart, leading to, increases an RV and PA pressures, impaired L a filling and cardiovascular collapse.
What is a PAE?
Can occur from air bubbles that pass from the Venus to the systemic arterial circulation through a PFO. This can also happen if right sided pressures exceed left-sided pressures.
What are five ways that you can detect a VAE?
TEE – most sensitive monitor. Precordial Doppler – probe should be placed over the right heart at the right parasternal second intercostal space. As little as .25 ML’s of air can be detected. Changes in pulmonary artery pressure has detected by a P a catheter. Changes in entitle CO2, in title nitrogen and perhaps PaO2 or CVP.
A mill wheel murmur is a late finding
How do you prevent a VAE?
Minimize elevation of head, exposure or open Venus channels. Maintain adequate hydration as hypovolemia is a risk factor for VENPAE. Use bone wax. Avoid N2O
Why would you not use nitrous in a patient who is having a sitting craniotomy? Why would you?
I would not because once a patient who has been breathing air breeds a gas mixture containing nitrous but not nitrogen, the nitrous enters close air space is faster than nitrogen can leave this expand the clothes air space decreasing the legal amount that could cause cardiovascular collapse. It also may cause a paradoxical air embolus. My argument for its use is that it may allow earlier detection of a VEA
Treatment of a VAE:
Notify Surgery, pack flooded with saline, Apply bone wax. Discontinue nitrous and use 100% O2 if you are using nitrous. Valsalva maneuver or bilateral compression of the jugular vein’s for 5 to 10 seconds. Attempt aspiration of air from a central venous catheter. Position in the left lateral to cubitus or Trendelenburg position. Cardiovascular support including fluids be so active agents and X ternal cardiac massage. Peep is not recommended for treatment because it may cause a paradoxical air embolism and if you use it prophylactically it may cause decreased cardiac output or blood pressure, increase RA and PA pressures and increase R—L shunting
