Brain Metabolism Flashcards
compensation for additional volume in the skull
-increased CSF drainage
-increased venous drainage
once these compensatory mechanisms are exhausted, we experience rising intracranial pressure
brain compliance
*relationship between intracranial pressure and volume
*as intracranial volume increases, intracranial pressure also increases
*ICP increases slowly due to compensatory mechanisms, but once those mechanisms are exhausted, ICP increases rapidly, leading to decreased CPP (cerebral perfusion pressure) and herniation risk
treatments for increased ICP
-elevate head of bed
-HYPERventilate patient
-osmotic agents (mannitol, hypertonic saline)
-steroids for vasogenic edema (tumors)
-heavy sedation
-surgical options (ventricular catheter to drain ICP; hemicraniectomy)
-avoid hypoxia (low paO2), hypercarbia (high paCO2)
-adequately treat pain, fever, and seizures
cerebral perfusion pressure (CPP) =
CPP = MAP - ICP
*note: in normal people, ICP is < 15, so CPP is only slightly lower than MAP in someone with normal ICP
*if ICP gets too high, it severely limits your ability to perfuse the brain tissue and it starts to die
hyperventilation as treatment for increased ICP
*hyperventilation leads to decreased paCO2
*decreased paCO2 leads to respiratory alkalosis
*respiratory alkalosis leads to VASOCONSTRICTION of intracranial arteries
*vasoconstriction** REDUCES cerebral blood flow and cerebral volume**
*NOTE: hyperventilation works fast but is only temporary, as a short-term bridge to more definitive therapy [because prolonged decrease in CBF can produce ischemia]
should you hyperventilate or hypoventilate a patient with elevated ICP
HYPERventilate them (leads to decreased paCO2 to respiratory alkalosis to vasoconstriction to reduced CBF)
what happens if you hypoventilate a patient with elevated ICP
*hypoventilation causes CO2 retention, leading to higher paCO2, leading to respiratory acidosis, leading to arterial vasodilation, aggravating the high ICP
cerebral blood flow equation
CBF = (CPP * (radius of blood vessel^4) * pi) / (blood viscosity * length of blood vessel)
*blood vessel RADIUS is the key factor for determining CBF
what is the key factor for determining cerebral blood flow (CBF)
RADIUS of blood vessels
-increased radius (dilated vessel) = increased cerebral blood flow = increased ICP (BAD if a patient has elevated ICP)
-decreased radius (constricted vessel) = decreased cerebral blood flow = decreased ICP (GOOD if patient has elevated ICP)
brain metabolism - oxygen and glucose consumption relative to mass of body
*brain weighs ~2% of body weight
*uses glucose as primary energy source
*uses 20% of total oxygen and 25% of total body glucose consumption!
*receives 15-20% of cardiac output at rest
what is the average cerebral blood flow
50cc per 100 grams of brain tissue per minute
which is more metabolically active: gray matter or white matter?
*GRAY matter is more metabolically active
*so, gray matter requires more cerebral blood flow on average than white matter
*so, gray matter is more susceptible to damage with changes in CBF
penumbra
*REVERSIBLE neuronal damage (at risk brain tissue)
*occurs when cerebral blood flow is ~15-20 cc/100g/min
*will become infarction with passage of time
irreversible neuronal damage
*occurs when the cerebral blood flow is below ~10-15cc/100g/min
factors that influence cerebral blood flow
-local neuronal activity
-autoregulation
-raised ICP
-paCO2
-paO2
-hematocrit
-temperature
-autonomic regulation
synthesis and storage of glycogen in the brain occurs primarily in ?
*in astrocytes!
-much smaller amount of glycogen in brain than other organs
-acts as an energy buffer
-would last only a few minutes if glycogen was used exclusively
important glucose transporters in the brain
*GLUT1 and GLUT3
*both are required for transport across the blood-brain barrier
*GLUT1 is primarily in astrocytes and endothelial cells
*GLUT3 is primarily in neurons
neurovascular coupling
*aka flow-metabolic coupling or functional hyperemia
*purpose = increase blood flow to active areas of brain
*supplying necessary oxygen and glucose to regions of high neuronal activity!
how are vasoactive changes in the brain mediated by neurons and astrocytes to regulate cerebral blood flow
*glutamate is a significant regulator of CBF
*other molecules (hydrogen, potassium, adenosine, etc) also mediate blood flow changes
*result = vasoconstriction or vasodilation of intracranial blood vessels to regulate CBF
resistance vessels
*branches of cerebral arteries that run along the SURFACE of the brain
*smooth muscle cells lining the arteries respond to changes in ICP and vasoactive mediators to cause changes in blood vessel diameter
*resistance vessels include: penetrating arterioles, capillaries, venules, and pial arterioles
autoregulation - general concept
*brain maintains constant cerebral blood flow, despite fluctuations in CPP (cerebral perfusion pressure) or MAP (mean arterial pressure) by CHANGING CALIBER (diameter) OF PIAL ARTERIOLES
how is cerebral blood flow impacted by chronic hypertension
*people with a chronically high MAP require a higher CPP to start the autoregulation cascade in order to maintain CBF
*essentially, curve is shifted to the right because there is a higher set point for autoregulation to occur
*can tolerate higher perfusion pressures
what ranges of MAP is autoregulation good for
*autoregulation works well for MAP 60-150 mmHg
*outside this range, CBF varies DIRECTLY with perfusion pressure
*loss of autoregulation can be focal or global in brain injury
what happens if MAP or CPP drop too low (in people with intact autoregulation)
vessels cannot dilate any further to compensate, leading to ISCHEMIC INJURY
what happens if MAP or CPP become too high (in people with intact autoregulation)
*high pressure inside vessels overcomes maximal constriction, so BBB is disrupted
*this leads to HYPERPERFUSION, causing cerebral edema +/- hemorrhage
impact of paCO2 on cerebral blood flow
*decreased paCO2 (hyperventilation) -> vasoconstriction -> decreased CBF
*increased paCO2 (hypoventilation) -> vasodilation -> increased CBF
OVERALL: CBF varies DIRECTLY with paCO2 in physiologic range
impact of paO2 on cerebral blood flow
*low paO2 (< 60 mmHg) = trigger to increase CBF (vasodilate) to maintain O2 delivery
NOTE: paO2 is not as impactful as paCO2 on cerebral blood flow
ways to evaluate CBF and cerebral metabolism
-transcranial doppler (TCD)
-positron emission tomography (PET)
-CT perfusion
-MR perfusion with pulsed arterial spin labeling (PASL)
-cerebral microdialysis
-functional MRI (fMRI)
-Tc-99m radionuclide study
transcranial doppler (TCD)
*ultrasound measurement of blood flow velocities in major vessels
*can evaluate for autoregulation by manipulating paCO2
positron emission tomography (PET)
evaluates cerebral metabolism (usually glucose uptake)
CT perfusion
evaluates blood flow, volume, and mean transit time to look for penumbra (at-risk brain tissue)
MR perfusion with pulsed arterial spin labeling (PASL)
shows cerebral perfusion
cerebral microdialysis
evaluates cerebral metabolism by measuring local metabolites
functional MRI (fMRI)
uses blood oxygenation level dependent (BOLD) imaging to evaluate regional differences in CBF based on activity
Tc-99m radionuclide study
*assess flow of radio-tracer to assess CBF
*can be used to evaluate for brain death
