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Why do we want to avoid high CO2 in an ischemic brain injury?
High CO2 levels & vasodilation that impedes the ability to direct flow. In a situation where pt is hypercarbic, the pt would be vasodilated and unable to redirect flow to areas of ischemia. If brain injury, not breathing well, high co2, vasodilation, not able to redirect
Why is having a low CO2 in an ischemic brain injury beneficial?
- Low CO2, hyperventilated pt, or whose metabolism is reduced (by giving Propofol) there is an overall reduction in CBF.
- But the vessels in the ischemic area would be able to dilate. In an ischemic situation the pH is lower and certain metabolites cause vasodilation. If a certain situation we decreased flow by hyperventilation or by decreased metabolism (metabolism and flow are coupled) so overall decreased flow but the ischemic areas would vasodilate, this phenomena is called inverse steal
Why is hyperventilation not a long term solution in reducing cerebral blood flow
- Systemically the PaCO2 goes down and stays down when we hyperventilate a patient. Will have a metabolic alkalosis and lasts until kidneys begin to compensate (a few days).
- However within 6-8hrs the CSF pH and CBF return to normal. So that’s important, active transport of bicarbonate out of brain CSF and happens much more quickly than systemic so hyperventilation is not permanent in effect of CBF.
How long does it take for CSF pH and CBF to return to normal after hyperventilation?
Autoregulation: In pt who are normotensive there is no change in CBF between mean BP of __-___mmHg.
At what PaO2 will CBF increase?
What is normal CBF?
For 1mmHg increase in CO2, there is __1-__ml/100g/min increase in CBF.
CO2 and CBF have a direct or indirect relationship?
How are glucose and bicarb transported across the BBB?
Why is hypoglycemia such an important problem for the brain??
Glucose will only be carried over into the brain if the concentration in the blood exceeds that in the brain. Which is why hypoglycemia is so dangerous particularly in anesthetized patient who you don’t see the mental status changes of hypoglycemia.
What is the normal range for ICP?
- Intracranial normal pressure is 5-15mmHg.
- Cerebral HTN is defined as greater than 20mmHg.
What is the equation for CPP?
CPP = MAP – ICP
What is the Monro-Kellie doctrine?
- 3 areas in brain where we can decrease volume: brain tissue, blood (venous or arterial), and CSF/ECF
- So our goal is to control these three things. We can manipulate the volume of any of these three compartments to stabilize the ICP.
What things will increase the Blood volume compartment in the Monro-Kellie doctrine?
- ↑ airway or intrathoracic pressure
- ↑ jugular venous pressure
- ↑ PaCO2 and ↓ PaO2
- Some anesthetics
What things will increase the cellular compartment, mass, lesions, in the Monro-Kellie Doctrine?
- Hematoma (subdural, epidural, intracerebral)
How can we reduce edema??
Lasix or mannitol: pulls off water and reduces edema. Steroids also limit edema.
The efficacy of steroids in reducing edema is well established and usually steroids are administered ___hrs prior to elective craniotomy
All the volatiles agents are vasodilators. List them in order of vasodilating potency (Most to least)
- Halothane (worst, 200% increase in CBF)
So Sevo is best in terms of least vasodilation but compared to Iso/Des, it's not clinically signficant. The vasodilation is dependent on what?????
- Dose dependent.
- Iso vs. Sevo vs. Des the main thing is the concentration of the agent. The vasodilating properties are dose dependent.
How long does the vasodilation from a volatile last?
returns to normal within 3hrs after exposure (once it’s discontinued)
All volatiles decrease CMR. Which is the worst at doing this?
Halothane is worst because the decrease in CMR is least.
With our usual selection of volatile agents (Iso/Sevo and sometimes Des) the ability to decrease CMR with all these drugs, except Halothane, competes with the direct vasodilation. What is the net efffect on CBF?
So the net effect on CBF depends on the concentration of the agent, the extent of previous CMR reduction, and other factors such as the PCO2.
Why is Enflurane a poor choice for a volatile in neurosurgery?
Enflurane would not be a good choice, because it can cause seizure like electrical activity. That would be deleterious because it would increase CMR and therefore increases flow.
Why is the use of Desflurane controversial in neurosurgery?
Desflurane: is controversial. Those against it say that it may decrease CSF reabsorption and 1 study showed an increase in ICP when Desflurane was used and patients have abnormal compliance. So not good when compliance is abnormal. Unsure how good that science is because some studies advocate use.
Can N2O be used safely in neurosurgery?
- Can be used safely as part of a balanced technique w/a volatile agent and narcotics.
- Used alone can be sympathetic stimulant, Can increase CMR if not using balanced technique w/a volatile.
- Effect on CBF is greatest when administered as a sole anesthetic.
What is the best anesthetic technique if the patient has increased ICP (or s/s of it)?
If pt definitely has increased ICP or s/s of increased ICP (HA, somnolence, N/V, CT shows midline shift) the safest anesthetic technique is TIVA.
What medication should we avoid in neurosurgery?
What is nice about Propofol and Etomidate?
- In a situation of intracranial HTN, tight brain, we can purposefully decrease CMR with hypnotic agents such as propofol.
- Propofol decreases CMR and therefore because of the coupling decreases CBF.
- Etomidate would have the same effect, decreasing CMR. Etomidate can decrease CMR without decreasing the MAP.
There is a barbiturate that does not decrease CMR, what is it and what could it be used for?
- Methohexital (Brevitol) is often used for ECT, because it tends to increase seizure activity.
- When you’re doing ECTs, you want to have the seizure activity, why you’re using the methohexital.
- Timing it and want the seizure to last a certain amount of time. The methohexital promotes seizures
Benzodiazepines do reduce CMR and CBF. Is it more or less than Propofol?
to a lesser extent than drugs like propofol.
How do opioids effect CMR?
- Opioids have either no effect or a mild reduction in CMR.
- If the patient has pain, an opioids would reduce CMR and therefore reduce CBF.
Succinylcholine will increase ICP transiently. How do we avoid this?
avoid this by defasiculation.
Some drugs can release histamine and cause increased CBF. Give an example of a muscle relaxant
Atracuriuum, should be avoided or given in small incremental doses.
What is important to think about in treating HTN in someone with increased ICP?
- For tx of HTN, think twice about giving Nipride, a vasodilator, because it could potentially increase CBF and increase ICP.
- So use a drug that has combined effects rather than pure vasodilation. Because the vasodilation could be deleterious
On the CT. What is obliterated in edema?
Basal cistern is obliterated in edema
What is on the high-intracranial pressure/"tight brain" checklist?
- 1. Are the relevent pressures being controlled? (Jugular venous pressure, Airway pressure, pp CO2 & O2, and arterial pressure)
- 2. Is the metabolic rate controlled?
- 3. Are there any potential vasodilators in use?
- 4. Are there any unrecognized mass lesions?
How do we prevent intracranial hypertension?
- Adequate anxiolysis & analgesia pre-op
- Pre-induction, hyperventilate on demand, head up and midline, avoid jugular compression
- Avoid overhydration
- Osmotic diuretics and steroids
- Optimize HD (use BB, clonidine or lido if necessary)
- Ventilate (PaCO2 ~35, PaO2 >100) low intrathoracic pressure
- IV induction and maintenance
How can we treat intracranial HTN?
- CSF drainage
- Osmotic diuretics
- Augment depth of anesthesia using IV anesthetics (Propofol, Etomidate, Thiopental)
- Muscle relaxation
- Improve cerebral venous drainage (head up, no PEEP, reduced inspiratory time)
- Mild controlled hypertension if autoregulation intact (MAP ~100)
What is a supratentorial tumor?
supratentorial tumors are tumors in brain other than the brain stem.
What is the goal of anesthesia for a patient with supratentorial tumors?
- To reduced intracranial volume. Main thing w/supratentorial tumors is controlling blood volume. Avoid excessive dehydration, give diuretics.
- When tumor is opened the goal is to maintain optimal operating conditions→a decreased ICP (slack brain, nice soft compressed brain tissue). That is a decreased volume and decreased pressure. Slack brain facilitates surgical dissection
How do we control the volume? (Fluid)
- Restricing fluid. Maintain euvolemia to control the brain water content.
- In addition diuretics are also give to control volume
How do we give mannitol
- Mannitol is an osmotic diuretic, dose is 0.25-1g/kg given over 10min or more) at peak effect removes about 90mls of brain water.
- Give slow because it transiently increases blood volume. But then it will draw brain water because there is an osmotic diuretic, big molecule sitting on BBB. Will draw water out and helps us decrease blood volume
What two diuretics are commonly given to control volume?
Mannitol and Lasix
Why must we use caution in pre-medicating patients for neurosurgery?
Compliance may be low and so sedation could cause respiratory depression, increased CO2, increased CBF and increased ICP
What types of fluids would we give to maintain normovolemia in patients with supratentorial tumors?
- NS is SLIGHTLY hypertonic and LR are SLIGHTLY hypotonic but they are close. Alternate the NS and LR.
- 3% NS is given rarely and specifically to pull water from the brain.
- Hetastarch is hypertonic.
What would we NEVER give for fluid in a neurosurgery patient?
Glucose administration has been demonstrated to increase the risk of neurologic injury. So never give these Neurosurg pt D5W, the glucose is deleterious and can increase injury. After metabolism, it’s free water and hypotonic.
What is a risk of working on an infratentorial or posterior fossa tumor?
It's near the brain stem and often operated on in SITTING POSITION so could have air embolism
What are our concerns for the pins used in neurosugery?
- Pin placement=give Fentanyl (1-2mcg/kg)
- Have pins secured to part of bed that allows patient to be moved quickly if CPR needs to be preformed (head of bed)
What are the pros of the sitting position for neurosurgery?
- Better surgical exposure
- -Less tissue retraction and damage
- -Less Bleeding
- -Less cranial nerve damage
- -More complete resection
- -ready access to chest, airway, extremities
- Modern monitoring gives early warning of air embolism and brain stem compromise
- Serious problems d/t air embolism are uncommon
What is a paradoxic air embolism
(when it goes from R to L heart) PEEP will preferentially increase pressure in RA and allow air to go to LA.
What can cause macroglossia?
Macroglossia and airway obstruction came from a case study or few reports. Of pt who is sitting and head flexed with an oral airway in place for hours. Tongue damage
How can the spinal cord be damaged in the sitting position?
Neck is flexed, and if overly flexed, could have disruption of spinal cord.
What is Pneumocephalus most associated with?
most often associated with posterior fossa procedures in the sitting position. So air is entrained in the cranium.
During neurosurgery, when is N2O ok and when should it NOT be used?
- So when the cranium is opened then N2O shouldn’t make a difference because there is no closed space, but N2O can expand the volume of a closed space.
- N2O is NOT contraindicated when the Dura is open but when the dura is being closed and the intracranial space is sealed from the atmosphere, we should avoid N2O
What can cause a tension pnumocephalus ?
Unrelated to the use of N2O, there can be a tension pnumocephalus post-op. When dura is open, air is entering the cranium. Surgeon has resected tumor, big empty space, and closed the dura. What happens post-op there will be edema, fluid accumulation and a tension pneumocephalus can occur w/ or w/out N2O. This can cause delayed recovery of consciousness.
List the monitors for venous air embolism from most sensitive to least sensitive
- Transesophageal ECHO
- Precordial Doppler
- Increased PAp
- Decreased EtCO2
- Increased end tidal N2 (this is very specific though!)
AFTER THE INDUCTION OF ANESTHESIA AND THE STARTOF SURGERY, INTRACARDIAC AIR IS DETECTED BYTHE PRECORDIAL DOPPLER AND THE ETCO2 SUDDENLY DECREASES. What would you do?
- Tell the surgeon, he would pack the field to prevent further air entry
- Jugular compression can help to keep more air from being entrained.
- Lower Head.
- Aspirate the RA catheter (HUGE benefit to having CVP line)
- Stop N2O
- *Increased risk of using N2O in sitting position and especially in the posterior fossa surgery.
- FiO2 100%
What hormones does the pituitary secrete?
What two ways can you resect a pituitary tumor?
M&M is much lower if they are transphenoidal than craniotomy incision (But it must be less than 10mm)
What risk factors are involved in transphenoidal approach for pituitary tumors?
Risk of infection (must have abx) because going through the patients nose.
Describe the Hunt and Hess classifications for patients with subarachnoid hemmorhage
What pre-induction monitoring would you need for cerebral aneurysm surgery?
How do you induction for cerebral aneurysm surgery?
- Oxygen, thiopental, fentanyl, w/or w/out lido
- Hypotension (DL, Ephedrine, Neo)
- Hypertension (Thiopental, Fentanyl, Nipride, Esmolol)
- Laryngoscopy (Succs, Vec)
How do you do maintenance for cerebral aneurysm surgery?
- Normocapnia (O2,N2O,Fentanyl,Iso, vecuronium/pancuronium/doxacurium)
- Reduce intracranial volume (osmotic diuretics, CSF drainage, hyperventilation)
- During clipping=slight hypotension
- During dissection=reduce BP to low limit of autoregulation w/thiopental or Iso
- After clipping=elevate BP slightly above normal
How do you manage a ruptured aneurysm?
- During rupture- reduce blood flow with NIPRIDE and ipsilateral carotid compression, replace blood loss, ventilate w/100%
- After controlling hemorrhage- cerebral preservation so elevate BP and give barbiturates or Iso. Then reduce edema w/osmotic diuretics & CSF drainage
- Post-op- control ventilation and monitor ICP
Because the surgeon has worked on the vessel, there is a high probability of post-op vasospasm (it’s related to the resection of the aneurysm). How do we prevent this?
use triple Hs (hypervolemia, hypertension, hemodilution to keep the patient full) Hypercarbia-keep on higher side to keep vessels full of volume
True or False. Blood must ALWAYS be available during dissection of an aneurysm?
What are some complications of induced hypotension?
- Cerebral thrombosis or ischemia
- Coronary artery thrombosis
- Renal insufficiency
- Hepatic failure
- Post-op pulmonary dysfunction
- Rebound hypertension
- Increased bleeding at operative site
How do you do a pre-anesthesia assessment of a head-injured patient?
- Airway (C-spine)
- Breathing (Ventilation and oxygenation)
- Circulatory status
- Associated injuries
- Neuro status (Glascow coma scale)
- Pre-existing chronic illness
- Circumstances of the injury: (time, duration of unconsciousness, & associated ETOH/Drug use)
What TWO things are needed to clear C-spine
Name the point system in the GCS