CENTRAL NERVOUS SYSTEM DISEASE Flashcards
What is the arterial blood supply to the brain?
- The arterial blood supply to the brain is from three blood vessels, including the right and left internal carotids and the vertebrobasilar artery. Anastomoses between these vessels form the circle of Willis, and provide for a collateral blood supply forcerebral protection against ischemia. (476)
In what proportion of human brains is the classic depiction of the circle of Willis
found?
- The classic depiction of the circle of Willis is found in less than half of human
brains and collateralization may not be complete in all individuals. (476-477,
What makes up the blood-brain barrier?
- The blood-brain barrier is composed of capillary endothelial cells with tight
junctions. This barrier allows the passage of lipid-soluble substances such as carbon
dioxide, oxygen, and some anesthetic agents but prevents the passage of large
macromolecules such as proteins. (476)
Name conditions in which the blood-brain barrier may be disrupted.
- The blood-brain barrier may be disrupted in conditions such as acute systemic hypertension, head trauma, infection, arterial hypoxemia, severe hypercapnia,intracranial tumors, and sustained seizure activity. (476)
Name some factors that influence cerebral blood flow.
- Factors that influence cerebral blood flow include the cerebral metabolic rate,
cerebral perfusion pressure and autoregulation, the PaO2, the PaCO2, and
anesthetic drugs.
What is normal cerebral blood flow?
- Normal cerebral blood flow is 50 mL per 100 g of brain tissue per minute and
represents approximately 15% of cardiac output. Although the brain is a very small
percent of body weight, its high metabolic rate and inability to store energy account
for the high percent of cardiac output it receives
What is the relationship between cerebral metabolic rate and cerebral blood flow?
- The cerebral metabolic rate directly affects cerebral blood flow through cerebral
flow-metabolism coupling. Increases or decreases in metabolic rate result in
a proportional increase or decrease in cerebral blood flow
- For every 1 C decrease in temperature below normal body temperature, what is thecorresponding decrease in cerebral blood flow?
- For every 1 C decrease in temperature below normal body temperature there is
a corresponding decrease in cerebral blood flow by about 7%. This effect is due to the
decrease in the cerebral metabolic rate caused by the decrease in temperature. (477)
Define cerebral perfusion pressure.
- Cerebral perfusion pressure is defined as the difference between mean arterial
pressure and central venous pressure or intracranial pressure, whichever is
greater. (
Within what range of mean arterial pressures will cerebral blood flow remain
relatively constant?
- In healthy, normotensive individuals cerebral blood flow remains relatively
constant between cerebral perfusion pressures of 50 to 150 mm Hg. Within this
range the cerebral vasculature is able to vasodilate or vasoconstrict in response to
changes in mean arterial blood pressure to maintain a constant cerebral blood flow.
Below a cerebral perfusion pressure of 50 mm Hg (mean arterial pressure of
about 65 mm Hg assuming an intracranial pressure of 15 mm Hg) cerebral blood
flow decreases proportionally to mean arterial pressure. Above a cerebral perfusion
pressure of about 150 mm Hg, cerebral blood flow increases proportionally to
the mean arterial pressure. This response of the cerebral vasculature to alterations in the mean arterial pressure to maintain a constant cerebral blood flow is termed
“autoregulation.”
What is the time course within which cerebral vasculature changes in response to alterations in mean arterial pressure? What is the clinical implication of this?
- The time course within which cerebral vasculature changes in response to
alterations in mean arterial pressure is 1 to 3 minutes. That is, within 1 to 3 minutes
of an alteration in the mean arterial pressure, the cerebral vasculature is able torespond appropriately to maintain a constant cerebral blood flow. In the interim,
with drastic increases or decreases in mean arterial pressure, there may be a
brief period of respective cerebral hyperperfusion or hypoperfusion.
What are factors that impair the autoregulation of cerebral blood flow?
- Autoregulation of cerebral blood flow may be impaired in the presence of
intracranial mass lesions, head trauma, intracranial surgery, subarachnoid
hemorrhage, severe hypothermia, or volatile anesthetics. Chronic arterial
hypertension or sympathetic nervous system stimulation results in a shift of the
autoregulatory curve to the right, such that cerebral blood flow is maintained
between pressures higher than 60 to 150 mm Hg. This effect is believed to occur
after 1 to 2 months of hypertension.
Describe the relationship between PaCO2 and cerebral blood flow.
- Cerebral blood flow is linearly related to the PaCO2, such that increases in the PaCO2
result in increases in cerebral blood flow and vice versa. This effect of the PaCO2
occurs as a result of the effect of the arterial carbon dioxide tension on the pH
of the cerebrospinal fluid. An increase in PaCO2 leads to acidosis, which in turn leads
to cerebral vascular vasodilation. The duration of this effect is 6 to 8 hours,
after which cerebral blood flow normalizes through the transfer of bicarbonate out
of the cerebrospinal fluid. This effect is only in response to respiratory acidosis.
The cerebral vasculature is not affected by metabolic acidosis, owing to the
blood-brain barrier protection against the diffusion of hydrogen ions from the
vascular space. (477-478, Figure 30-2
How much does cerebral blood flow change for every 1 mm Hg increase or decrease
in PaCO2 from 40 mm Hg?
- Cerebral blood flow increases by 1 mL/100 g of brain tissue per minute for every
1 mm Hg increase in the PaCO2 from 40 mm Hg. Conversely, cerebral blood flow
decreases by 1 mL/100 g of brain tissue per minute for every 1 mm Hg decrease
in the PaCO2 from 40 mm Hg. The impact of this can be marked, given that a decreasein the PaCO2 from 40 to 25 mm Hg can lead to approximately a 33% decrease in
cerebral blood flow. (478)
What is a potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than 30 mm Hg?
- A potential risk of prolonged, aggressive hyperventilation to a PaCO2 of less than
30 mm Hg is cerebral ischemia. Prolonged aggressive hyperventilation following
traumatic brain injury has been shown to be associated with a poorer neurologic
outcome. (478)
Below what PaO2 will cerebral blood flow increase?
- Cerebral blood flow increases dramatically when the PaO2 falls below 50 mm Hg.
(478,
What are the effects of volatile anesthetics on cerebral blood flow and intracranial
pressure?
- Volatile anesthetics are potent cerebral vasodilators. At concentrations above
0.5 MAC, these anesthetic agents increase cerebral blood flow in a dose-dependent
manner, most likely through the direct relaxation of vascular smooth muscle
leading to vasodilation. In contrast, volatile anesthetics decrease the cerebral
metabolic oxygen requirement profoundly. Normally, a reduction in cerebral
metabolic rate would produce a reduction in cerebral blood flow through
flow-metabolism coupling. However, the net effect of volatile anesthetics is to
increase cerebral blood flow, particularly at high doses. Therefore, volatile
anesthetics uncouple the normal physiologic relationship between cerebral blood
flow and metabolism. These effects may lead to increases in intracranial pressure
and cerebral edema.
What are the effects of nitrous oxide on cerebral blood flow and intracranial
pressure?
- Nitrous oxide increases cerebral blood flow through cerebral vasodilation. The
effect of nitrous oxide appears to be blunted in the presence of intravenous
anesthetics and increases cerebral blood flow less than the volatile anesthetics.
Limitation of the inspired concentration of nitrous oxide to less than 0.7 MAC
minimizes its effect of cerebral vasodilation and intracranial pressure
What are the effects of ketamine on cerebral blood flow and intracranial pressure?
- The effect of ketamine on cerebral blood flow and intracranial pressure is
controversial. In isolation, ketamine appears to increase PaCO2, cerebral blood
flow, and intracranial pressure, limiting its use for patients with increased
intracranial pressure. These effects appear to be attenuated, however, in the
presence of other anesthetic agents and controlled ventilation. (478)
What are the effects of thiopental on cerebral blood flow and intracranial pressure?
- Thiopental decreases cerebral blood flow via cerebral vasoconstriction. It also
decreases cerebral metabolic oxygen requirements and reliably decreases the
intracranial pressure.
What are the effects of propofol on cerebral blood flow and intracranial pressure?
- Propofol decreases cerebral blood flow via cerebral vasoconstriction in a manner
similar to thiopental. It also decreases cerebral metabolic oxygen requirements and
reliably decreases the intracranial pressure.
- What are the effects of etomidate on cerebral blood flow and intracranial pressure?
- Etomidate decreases cerebral blood flow and cerebral metabolic oxygen
requirements in the absence of myoclonus or seizure activity.
What are the effects of benzodiazepines on cerebral blood flow and intracranial
pressure?
- Benzodiazepines minimally decrease cerebral blood flow and cerebral metabolic
rate and do not appear to cause an increase in intracranial pressure. (478)
What are the effects of opioids on cerebral blood flow and intracranial pressure?
- Studies evaluating the effects of opioids on cerebral blood flow and intracranial
pressure have yielded inconsistent results. Opioids either very minimally decrease
cerebral blood flow and intracranial pressure or produce no effect at all in the
absence of respiratory depression and elevated PaCO2