Neuroanesthesia Flashcards
What is the normal cerebral blood flow?
50 ml/100 g/min
<20 ml/100 g/min - ischemic changes
<10 ml/100 g/min - neuronal death
How is cerebral blood flow regulated?
Cerebral autoregulation:
(1) blood pressure
(2) PaCO2
(1) ensures constant blood flow over a wide range of blood pressure ~60-160 mmHg: above or below, autoregulation is lost and CBF becomes solely dependent on MAP
(2) cerebral vasculature reacts from 20-80 mmHg: vasoconstriction - hypocarbia
vasodilation - hypercarbia
How does hypertension affect cerebral autoregulation?
Shifts to the right - requires higher pressure to maintain adequate perfusion
e.g. 100-180 mmHg
Over time, treated hypertension may revert back to the usual range
Describe CBF/CMRO2 relationship
Under normal conditions, the CMRO2 is directly related to CBF
Cerebral vasculature dilate or constrict to supply for the demand aka coupling
How does PaCO2 affect cerebral perfusion in normal and ischemic regions?
(1) hypercarbia - vasodilation
(2) hypocarbia - vasoconstriction
(1) normal tissues vasodilate more –> more blood shunted to non-ischemic area aka Steal Phenomenon
(2) normal tissues vasoconstrict more –> more blood shunted away from non-ischemic aka Reverse Steal or Robin Hood Phenomenon
Describe the use of hyperventilation in neuroanesthesia
(A) aims to rapidly decrease ICP and ‘relax’ the brain
ETCO2 25-30 mmHg ~PaCO2 30-35 mmHg
Short-term effect of 6-10hrs only, afterwards bicarbonate ions start to compensate
Prolonged hyperventilation –> respiratory alkalosis –> oxyhemoglobin curve shifts to the left –> decreased unloading of O2 –> further ischemia
(B) lowers seizure threshold
How to manage increased ICP?
– hyperventilation (most rapid)
– diuresis: mannitol, furosemide, hypertonic saline
– head elevation: at least 15 deg to facilitate drainage
– control BP: nicardipine
– if ventilated: use lower PEEP - higher intrathoracic pressure may block venous drain
What are the expected nociceptive stimuli in cranial surgery?
- laryngoscopy, intubation
- placement of pins
- scalp incision
- opening of skull up to dura
- High-dose opioid: e.g. fentanyl 5-10 ug/kg
- lidocaine 1.5 mg/kg to help blunt response to laryngoscopy/intubation
Basic principles in providing anesthesia during neurosurgery
- maintain cerebral perfusion
- manage ICP (keeping the brain relaxed during surgery)
- burst suppression if needed (propofol, thiopental): usually during temporary clipping
- monitor serum glucose, acid-base balance, temperature
- use short-acting agents (to facilitate early neurologic assessment)
- blunt response to nociceptive stimuli
- smooth emergence
- upright/sitting position: at-risk for VAE
Options for preinduction anxiolysis
- individualized
- dexmedetomidine > BZD
Dexmedetomidine - respiratory function is preserved, reduced interference with EP monitoring; can be continued as infusion intra-op
BZD - disinhibition, can delay awakening and interfere with postoperative assessment
Sudden drop in ETCO2, sudden hypotension in a craniotomy patient positioned upright
T/C VAE - air entrainment whenever operating field is higher than the right atrium
What is the most sensitive modality in detecting VAE?
- TEE - <0.25ml
- Doppler
- PA catheter, ETCO2
- Cardiac output, CVP, BP
What are the steps to do if VAE is suspected?
- alert surgeon
- stop further air entrainment: flood the field with saline, press neck veins to increase JVP
*Durant maneuver - left lateral decubitus - prevent expansion of entrained air - D/C N2O
- support CV function: inotropes, vasopressors, fluid
- aspirate air (if with RA catheter)
Complications associated with VAE
a) stroke or MI - especially if with patent foramen ovale
b) pulmonary hypertension - secondary to INC pulmonary vascular resistance
c) CV collapse
d) bronchoconstriction
Most common causes of nontraumatic SAH
Cerebral aneurysm, AVM