Case 14 - intracranial mass, ICP, venous air embolism, autoregulation Flashcards
what is cerebral autoregulation?
Cerebral autoregulation
- cebral blood flow (CBF) is maintained constant over a wide range of CPP
- CPP = MAP - ICP (or CVP)
- normal CBF = 50 ml/100g of tissue/min
what are the major determinants of CBF, and what happens at the extremes of each determinant?
CBF components
1) cerebral autoregulation
- CBF = CPP/cerebral vasc resistance
- 50-150mm Hg
- in extremes, CBF becomes CPP dependent
- 50 mm Hg - max cerebral vasodilation
- 150 mm Hg - max cerebral vasoconstriction
2) PaCo2
- 20-80 mm Hg
- low PaCo2 = cerebral vasoconstrict
- lasts temporary; eventually CSF bicarb levels decrease to compensate for induced CSF alkalosis -> no more cerebral vasoconstrict
- high PaCO2 = cerebral vasodilate
3) PaO2
- PaO2 < 50 mmHg = cerebral vasodilation
- CBF increases lineraly with decreasing PaO2
4) CMRO2
* increase CMRO2 = cerbral vasodilation (supply more blood to brain for nutrients and O2 supply)
what is normal ICP, what contributes to increase ICP, how does tumors increase ICP? What mechanism are there to prevent ICP increase?
Normal ICP = 5-13 mm Hg
Components = brain tissue, blood, CSF
Tumor
- inc ICP 2 ways:
- increase parenchymal tissue (increase brain tissue volume)
- associated with surrounding edema (inc brain water content)
ICP increase
- crainal vault = closed -> poor intracranial compliance
- increase in one leads to a decrease in the others
-
mechanisms to prevent ICP =
- shift CSF from cranial vault to spinal SA
- increase absorption of venous blood into sinuses and then into systemic circ (dec blood volume),
- increase absorption of CSF into systemic circ (dec CSF volume
- once these mech are exhausted, see inc ICP
what is the effect of the following in terms of CMRO2 and CBF:
- voltaile anes
- N2O
- bartiurates
- propofol
- Ketamine
- Etomidate
Volatile anes
- dose dependent
- decrease CMRO2
-
increase CBF 2/2 cerebral vasodilation
- decoupling of CRMO2 to CBF
- **inhibit cerebral autoreg at > 1 MAC**
N2o
- increase CBF
- increase CMRo2
Barbiturates *
- decrease CBF 2/2 cerebral vasoconstriction
- decrease CMRO2
- maintains coupling between CMRO2 and CBF
Propofol/Etomidate *
- same as barbiturates
Ketamine
- increase ICP
- increase CBF
- increase MAP
- no change in CMRo2
* = recommended for pts with inc ICP
what is the effect of the following in terms of CMRO2 and CBF:
- BZD
- SNP/NTG
- Labetolol/Nicardipine
- fentanyl
BZD *
- decrease CBF
- decrease CMRo2
SNP/NTG
- Decrease MAP
- cerebral vasodilators
- increase CBF
- increase CBV
Labetolol* or Nicardipine *
- decrease MAP
- **NO EFFECT ON CBV**
fentanyl
- no effect
* = recommended for pts with inc ICP
*
what are s/sx of increased ICP? Why are we seeing these symptoms/
symptoms of ICP
- inc ICP will decrease CPP -> cerebral ischemia -> symp
- inc ICP will shift brain contents, possible herniation through foramen magnum
s/sx of increased ICP
- headache
- n/v
- mental status change (drowsy, coma)
- Cushing triad
- HTN, brady, abnormal respiratory pattern
- absent brianstem reflexes
- CN dysfunction
- fixed and dilated pupils
How is ICP measured, what are the pros/cons of each?
1) ventriculostomy
- most common tool
- catheter placed through burr hole in ventricle
- measure ICP, drain CSF
2) subdural bolt
- device placed via twist drill hole in skull, into dural space
- cannot drain CSF
- only measures local ICP, does not provide global info
3) lumbar SA Drain
- proper measurement involves patient lying supine (avoids gravitational effect on CSF pressure with spinal SA)
- abrupt withdrawl of CSF -> brain herniation
How is increased ICP treated?
ICP: brain tissue, CSF, Blood
Goals: lower blood volume, lower brain water content, lower CSF volume
1) Lower blood volume
Venous
- raise head - promote venous drainage
-
avoid venous outflow obstruction
- patient head is neutral, check for improperly placed tape or devices around neck
-
prevent straining or coughing on ETT
- increases CMRo2 and CBF (inc CVP 2/2 backflow of venous pressure into brain)
- opioid, propofol, deep anesthesia, muscle relax
Arterial
-
hyperventilate to EtCO2 27-30 mm Hg (PaCO2 30-35 mmHg; gradient b/w etco2 and paco2
2) reduce CSF Volume - drain CSF via ventric or lumbar SA catheter
3) reduce brain water content - Mannitol (takes 30 min onset)
- loop diuretics (lasix)
- steroids (Decadron)
What is the mechanism for venous air embolism in a sitting patient?
VAE
- higher association with sitting position
- air enters venous system via noncollapsible venous channels (like dural sinuses)
- head elevated above heart -> see pressure gradient (atm pressure exposed to low venous pressure) -> facilitates entrainment of air (high to low pressure)
how can you monitor for VAE?
- TEE
- Most sensitive (0.1 mL of air detected)
- precordial doppler
- second most sensntive (0.25 mL of air)
- pulmonary artery pressure
- increased 2/2 air embolism -> inc PVR
- SaO2
- dec 2/2 air embolism -> v/q mismatch (dead space ventilation)
- ETCO2
- decrease 2/2 decrease pulm blood flow
- EtN2
- due to air escaping from blood into lungs into alveoli (gas)
intra-op, you notice a patient in the sitting position undergoing posterior craniotomy for tumor resection all of a sudden has acute hypotension. You are suspecting VAE, what do you do?
Tx of VAE
1) notify surgeons to flood surgical field with saline, apply bone wax
2) Increase venous pressure in head
- lower head relative to heart or T-berg
- jugulary vein compression
3) discontinue N2O (avoid further air expansion)
4) left lateral decub or tilt tabel to left
- moves air away from RVOT
5) Cardiovascular support
- fluids
- inotropes
- pressors
- FiO2 100%
6) aspirate from multiorfice catheter
resident suggests to use PEEP in an attempt to increase CVP during treatment of VAE, what are your thoughts?
PEEP in tx of VAE = controversial
- decreases venous return -> decrease SV -> hypoten
-
paradoxical air embolism
- PEEP causing decrease SV will result in low LA pressure.
- right atrial pressure may be increased (RV strain + backflow of blood 2/2 acute pulm HTN from pulm air emboli),
- and in the face of low LA/LV filling pressure, can see paradoxical emboli
are there contraindications to sitting position?
no absolute contraindications
relative contraindications
- PFO
- ventriculoatrium shunt
- cervical pathology (sitting up results in dec spinal cord perfusion pressure)
- hemodynamicaly unstable patient
what are your anesthetic goals for a patient coming for brain tumor resection, who is showing signs of increased ICP (n/v, headache, vision changes)?
Anesthetic Goals/considerations:
1) Avoid increase in ICP:
- avoid inc blood volume, csf volume, brain water
- deep anesthesia (avoid symp stimulation during intubation, incision)
- hyperventilate
- mannitol
- maintain normal MAP (avoid cerebreal ischemia -> cebreal edema -> worsen ICP)
2) avoid hypotonic solutoins, avoid glucose containing solutoins
3) fast emergence -> post-op neurologic eval
how will you induce and maintain anesthesia? what additional IV access do you need?
Pre-op: assess mental status and s/sx of inc ICP
Induction
- goal - avoid excessive symp stimulation, avoid hypotension
- bzd, opioid, lido
- blunt airway reflex (cough), avoid symp with intubation, lower iv anes induction dose (lessen hypotension)
- IV anes induction (prop, etom) + muscle relax
- ensure patient is deep prior to intubation
IV access
- large bore IV and arterial line
- potential for blood loss
maintenance anes
- balance anesthesia
- low dose volatile anes < 1 MAC + propofol infusion or opioid infusion (remi)
- think about quick emergence
- avoid inc in ICP
- hyperventilate
- mannitol
- avoid hypotonic solutions
- normovolemia
- IVF + blood products as needed
