Cerebral Blood Flow

What is the function of the Circle of Willis?

The Circle of Willis provides collateral blood flow to the brain if a major vessel carrying blood to the brain becomes obliterated.

What is cerebral blood flow in mL/min? In mL/100g/min? As % of cardiac output?

Cerebral blood flow is 750 mL/min, 50 mL/100 g/min, and 15% percent of cardiac output.

Below what cerebral blood flow does cerebral ischemia occur?

EEG evidence of cerebral ischemia appears when cerebral blood flow has fallen to about 50% of normal.

What are the two determinants of cerebral blood flow?

The two determinants of cerebral blood flow are cerebral vascular resistance and cerebral perfusion pressure. Cerebral blood flow (CBF) is inversely proportional to cerebral vascular resistance (CVR) and directly proportional to cerebral perfusion pressure (CPP). CBF = CPP/CVR.

Cerebral perfusion pressure normally is equal to what?

Cerebral perfusion = MAP-ICP.

Note: MAP is mean arterial pressure and ICP is intracranial pressure.

When is cerebral perfusion pressure not equal to the difference between mean arterial pressure and intracranial pressure (MAP-ICP)?

If right atrial pressure (RAP) is abnormally elevated and greater than intracranial pressure (ICP), cerebral perfusion pressure = MAP-RAP, not MAP-ICP.

What is the cerebral perfusion pressure when intracranial pressure (ICP) is 15 mm-Hg, right atrial pressure (RAP) is 5 mm-Hg, and the mean arterial pressure (MAP) is 110 mm-Hg?

95 mm-Hg. Cerebral perfusion pressure, in this case, is MAP - ICP. Thus, cerebral perfusion pressure = 110-15 = 95 mm-Hg.

Identify three factors that alter cerebral vascular resistance and hence cerebral blood flow.

Changes in PaCO2, Pa02 or temperature alter cerebral vascular resistance.

The single most important determinant of cerebral blood flow, so far as the anesthetist is concerned, is what?

PaCO2. Cerebral blood flow is proportional to PaCO2 when PaCO2 varies between 20 and 80 mm-Hg.

How does hypercarbia alter cerebral blood flow? Hypocarbia?

Cerebral blood flow is increased by hypercarbia (the cerebral vascula-ture dilates) and is decreased by hypocarbia (the cerebral vasculature constricts).

How would hyperventilation affect cerebral vessels and blood flow? Hypoventilation?

Hypocapnia associated with hyperventilation causes constriction of cerebral blood vessels and a decrease cerebral blood flow. Hypercapnia associated with hypoventilation causes dilatation of cerebral blood vessels and an increase in cerebral blood flow.

How much does cerebral blood flow (CBF) decrease, in mL/100g tissue/ min, for each mm-Hg decrease in PaCO2? How much does it increase for each mm-Hg increase in PaCO2?

The relationship between cerebral blood flow and PaCO2 is nearly linear for PaCO2 ?_ 20 mm-Hg. Thus a cerebral blood flow will decrease 1 mL/100g/min for each mm-Hg decrease in PaCO2 down to about 20 mm-Hg. Accordingly, cerebral blood flow will increase 1 mL/100g/min for each 1 mm-Hg increase in PaCO2.

What substance is the most potent vasodilator of the cerebral vascular system?

CO2.

What is the only intravenous anesthetic agent that dilates cerebral vas-culature and increases cerebral blood flow by 50-60%?

Ketamine dilates the cerebral vasculature and increases cerebral blood flow by 50-60%.

For each 1 degree C decrease in temperature, cerebral metabolic rate (CMR) decreases by what percent?

Cerebral metabolic rate (CMR) decreases by 6 to 7percent for each 1 degree C decrease in temperature.

Does acute metabolic acidosis or alkalosis alter cerebral blood flow? Why or why not?

No. Alterations in cerebral vascular resistance occur when pH of the cerebrospinal fluid is altered (which occurs quickly with changes in PaCO2). Since ions including H+ and HCO3 ó do not cross the blood-brain barrier, neither acute metabolic acidosis nor acute metabolic alkalosis alters cerebral blood flow.

When PaO2 falls below what level will cerebral blood flow increase?

Cerebral blood flow will increase substantially only when Pa02 falls below 50 mm-Hg.

Normally, how does a change in cerebral perfusion pressure affect cerebral blood flow (CBF)?

Changing perfusion pressure does not normally alter CBF, because CBF is autoregulated over the range of mean arterial pressure from about 50 to 150 mm-Hg.

When is autoregulation of cerebral blood flow lost?

Autoregulation of CBF ceases when mean arterial pressure (MAP) falls below 50 mm-Hg or rises above a mean arterial pressure (MAP) of 150 mm-Hg.

The range for autoregulation of cerebral blood flow is 50 to 150 mm-Hg.

Note: Miller emphatically emphasizes that the autoregulatory range for cerebral blood flow is 70 to 150 mm-Hg. Morgan and Mikhail suggest the autoregulatory range is 50-175 mm-Hg.

What happens to autoregulation in patients with chronic arterial hypertension?

The range of pressures for autoregulation increases. Whereas the normal autoregulatory range for cerebral blood flow is about 50-150 mm-Hg, the autoregulatory range maybe 90-190 in the hypertensive patient.

Point: The range of pressures for autoregulation increases in the patient with hypertension.

Where in the brain may autoregulation of blood flow be diminished/ impaired?

Autoregulation may be absent in diseased or traumatized regions of the brain. For example, autoregulation is absent in tissue surrounding brain tumors, in the acute phase of subarachnoid hemorrhage, and after brain trauma.

Distinguish between focal and global cerebral ischemia.

Global ischemia occurs when the entire brain is unperfused, such as would occur during cardiac arrest. In focal ischemia, which may occur with a stroke or a trauma (blow to the head), there are three zones of brain tissue:

(I) an inner zone, which is ischemic and the tissue is necrotic (dead),

(2) the penumbra, a zone of tissue that surrounds the ischemic core of tissue (the penumbra is perfused by collateral vessels and is partially, not completely, starved for blood), and

(3) normally perfused tissue. Inverse steal (Robin Hood effect) can increase blood flow to, and survival of, tissue in the penumbra.

At what intracranial pressures does focal ischemia occur? At what intra-cranial pressures does global ischemia occur?

Focal ischemia develops when intracranial pressure is between about 25 and 55 mm Hg. Global ischemia occurs when intracranial pressure exceeds approximately 55 mm Hg.

How is cerebral "steal" syndrome triggered during anesthesia?

Cerebral steal, also known as luxury perfusion, could be triggered if the patient is given a vasodilator (nitroglycerin, nitroprusside or hydralazine) or if the patient is hypoventilated.

If the patient is hypoventilated, PaCO2 increases, pH decreases, arterioles in non-ischemic brain dilate, and blood flow to the non-ischemic brain increases. This vasodilation in non-ischemic brain tissue could theoretically result in "steal" of blood flow from the ischemic areas that require oxygen.

What two actions can the anesthetist take to prevent cerebral steal?

The anesthetist can hyperventilate the patient or reduce metabolism by giving an agent such as a barbiturate.

What is Robin Hood effect? What are other names for the Robin Hood effect?

Shunting of blood from adequately perfused cerebral tissues to compromised, potentially ischemic areas is referred to as the Robin Hood effect. Other names for the Robin Hood effect are a reverse steal and inverse steal.

What triggers the Robin Hood (inverse steal or reverse steal) effect? Explain.

Hypocarbia. Hypocarbia constricts cerebral vessels in nonischemic tissues. Blood is diverted from nonischemic to ischemic (maximally dilated) regions.

What happens to cerebrovascular tone (increased, decreased, unchanged) and blood flow (increased, decreased, unchanged) in ischemic and nonischemic regions of the brain when the patient is hyperventilated?

Hyperventilation decreases PaCO2. Decreased PaCO2 produces an increased cerebrovascular tone, which decreases blood flow to non-ischemic areas of the brain. Blood vessel diameters in ischemic areas remain unchanged; they remain maximally dilated because of the presence of local metabolic factors so blood flow to ischemic tissue increases (inverse steal, reverse steal or Robin Hood effect).

What happens to cerebrovascular tone (increased, decreased, unchanged) and blood flow (increased, decreased, unchanged) in ischemic and nonischemic regions of the brain when the patient is hypoventilated?

Increased PaCO2 in a hypoventilated patient causes a decreased cerebrovascular tone and a corresponding increase in blood flow in non-ischemic regions of the brain. The cerebrovascular tone in ischemic areas remains unchanged, but blood flow decreases because blood is diverted to non-ischemic regions (steal effect or luxury perfusion).