Neuro Flashcards
Why is the CNS so sensitive to ischemia and hypoxia?
Highly metabolically active with little oxygen reserve
Contents of the supratentorial compartment of the cranium
The cerebral hemispheres and the diencephalon (thalamus and hypothalamus)
Contents of the infratentorial compartment of the cranium
Brainstem and cerebellum
Anterior blood supply to the brain
Internal carotid arteries
Posterior blood supply to the brain
Vertebral arteries
What types of molecules cannot permeate the blood brain barrier?
Macromolecules and proteins
What types of molecules can penetrate the blood brain barrier?
Lipid-soluble substances including CO2, O2, and anesthetic drugs.
Normal cerebral blood flow rate
50 mL/100 g/min
What percent of cardiac output does the brain receive?
15%. It makes up 2% total body weight.
Describe the concept of neurovascular coupling (aka cerebral metabolism-flow coupling)
An increase or decrease in CMRO2 results in a proportional increase or decrease in CBF
By what percent does CBF decrease for every 1 degree Celsius drop in temperature below 37?
7%
How is CPP calculated?
MAP-ICP
What does the lower limit of the cerebral autoregulation curve signify?
The CPP level below which the CBF decreases linearly with decreasing CPP. Basically, the point where vasoconstriction can no longer compensate adequately to maintain CPP.
What does the upper limit of the cerebral autoregulation curve signify?
The CPP level above which the CBF increases linearly with increasing CPP. Basically, the point where vasodilation can no longer compensate adequately for increased CBF.
What are the lower and upper limits of cerebral autoregulation?
60 mmHg and 150 mmHg
What does the plateau phase of the autoregulation curve signify?
The CPP range at which CBF remains stable d/t compensatory changes in blood vessels.
What effect do volatile anesthetics have on cerebral autoregulation?
At high concentrations, volatiles cause a direct vasodilatory effect on cerebral blood vessels, thus impairing cerebral autoregulation.
What effect do IV anesthetics have on cerebral autoregulation?
No effect. Autoregulation is preserved.
How do changes in PaCO2 affect CBF?
Changes in PaCO2 produce corresponding and same-directional changes in CBF when PaCO2 is between 20 and 80 mmHg.
How does a 1 mmHg increase or decrease in PaCO2 from 40 mmHg affect CBF?
Each 1 mmHg change in PaCO2 above 40 increases CBF by 1 mL/100 g/min. Each 1 mmHg decrease in PaCO2 below 40 produces a decrease in CBF by 1 mL/100 g/min. (About a 2% change in flow)
What is the relationship between PaO2 and CBF?
Decreases in PaO2 less than a threshold of 50 mmHg result in an exponential increase in CBF.
Formula for cerebral oxygen delivery
Arterial blood oxygen content x CBF
IV anesthetic effect on CMRO2 and CBF
Decrease both
Exception: there is debate about ketamine and it is usually avoided in pts with known intracranial disease. (In ventilated pts there is no known effect. In spontaneously ventilating pts ketamine can cause hypercarbia which leads to increase in CBF and ICP)
What drugs should be used cautiously in spontaneously ventilating patients with intracranial disease?
Opioids and benzos can lead to respiratory depression and hypercarbia resulting in increased CBF and ICP. Ketamine can also cause hypercarbia.
Alpha-2 agonist effects on CBF and ICP
Decrease CBF with no effect on ICP.
Nitrous oxide effect on CMRO2 and CBF
Increases both.
Three components of the intracranial compartment
Blood
CSF
Brain matter
Definition of elevated ICP
ICP > 15 mmHg
Onset and time to peak mannitol
Onset 5-10m
TTP 20m
Why is the use of PEEP discouraged during intracranial surgeries?
Excessive PEEP can impair cerebral venous drainage and increase ICP
Why are dextrose-containing solutions avoided in intracranial surgeries?
Dextrose solutions are rapidly distributed throughout body water and if BG concentrations decrease more rapidly than brain glucose concentrations then water will cross the BBB and cause cerebral edema.
Also, hyperglycemia augments ischemic neuronal fell damage by promoting neuronal lactate production.
Why is labetalol often the preferred beta blocker in the setting of intracranial surgeries?
It reduces MAP without causing cerebral vasodilation
Tension pneumocephalus
A neurosurgical emergency that occurs when subdue always air causes mass effect over the underlying brain parenchyma, often from a ball-valve mechanism causing one-way entry of air into the subdural space
Most common cause of intracranial hemorrhage
Intracranial aneurysm rupture
What percent of pts with SAH will develop vasospasm?
35%
Treatment of post-aneurysmal vasospasm
Triple H therapy
Hypertension, Hypervolemia, Hemodilution
+ CCB (nimodipine)
Fluids and inotropes targeted to goal CVP 10-12 and goal SBP 160-200 (if aneurysm clipped) or SBP 120-150 (if not clipped)
Angioplasty also an option
Time course of cerebral vasospasm
3-5d after SAH
What is the foremost cause of morbidity and mortality after SAH?
Vasospasm
Gold standard treatment of symptomatic carotid artery atherosclerosis
Carotid endarterectomy
Regional anesthetic option for CEA
Deep or superficial cervical plexus block
BP goal during carotid clamping in CEA procedures
20% above pt baseline to ensure adequate collateral flow through the Circle of Willis
What type of fluid should be avoided in TBI pts?
Albumin
