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The average cerebral blood flow in humans is approximately 55 mL per 100 g of brain tissue per minute. This is a little over 700 mL/min for a 1350-g brain. Thus while the human brain comprises only about 2.5 percent of the body's weight, it receives almost 15 percent of the cardiac output, attesting to the high vascular demands of this organ.

A reliable and frequently used method of determining cerebral blood flow is the method of Kety and Schmidt. It is based on the Fick principle and utilizes the arteriovenous difference of a freely diffusible gas such as N2O as it passes through the brain. Accordingly, the flow of blood through the brain can be determined by measuring the amount of N2O removed from the blood by the brain per minute and dividing this by the arteriovenous difference of N2O as it passes through the brain. The cerebral blood flow is higher in children than in adults, typically exceeding 100 mL per 100 g per minute. However, contrary to popular thinking, the blood flow decreases only slightly with advancing age. The brain utilizes fully 25 percent of the body's total oxygen consumption. The arteriovenous O2 difference is relatively high since the brain receives only 15 percent of the cardiac output. The arteriovenous difference is 6.6 mL per 100 ml., falling from 19.6 to 13 mL per 100 mL as blood passes through the brain (Fig. 17-2). Thus we can calculate a cerebral oxygen consumption of approximately 3.5 mL per 100 g per minute. This value is greater in skeletal muscle, skin. and liver. but less in cardiac muscle and kidney.



The utilization of oxygen by the brain is not uniform throughout its mass. The gray matter consumes as much as 94 percent of cerebral oxygen. while the white matter, which makes up fully 60 percent of the brain's mass. consumes only 6 percent. Oxygen consumption, and hence oxygen need, increases as we move up the neuraxis. It is lowest in the spinal cord and increases through the medulla. midbrain, thalamus, cerebellum, and cerebral cortex. Thus it is not surprising to find that the sensorimotor functions of the cerebral cortex are more sensitive to hypoxic damage than are the vegetative functions of the pontomedullary areas. Progressive decreases in cerebral oxygen consumption are always accompanied by progressive decreases in the level of mental alertness. Compared to the mentally alert young man with an O2 consumption of 3.5 mL per 100 g per minute, the mentally confused states associated with diabetic acidosis, insulin hypoglycemia, and some forms of cerebral arteriosclerosis might typically show O2 consumptions rates down to 2.8 mL per 100 g per minute. Finally, the comatose states of diabetic coma. insulin coma. and anesthesia can show consumption rates as low as 2.0 mL per 100 g per minute. On the other hand. O2 consumption by the brain increases during convulsions.



Almost all of the oxygen consumed by the brain is utilized for the oxidation of carbohydrate. Sufficient energy is released from this process so that the normal level of oxygen utilization is adequate to replace the 12 mmol or so of A TP which the whole brain uses per minute. However, since the normal brain reserve of A TP and creatine phosphate (CrP) totals only about 8 rnmol, less than a minute's reserve of high energy phosphate bonds is actually available if production were to suddenly stop. In the absence of oxygen, the anerobic glycolysis of glucose and glycogen could supply only another 15 mmol of A TP, as these two energy substrates are stored in such low quantities in brain tissue.

A continuous uninterrupted supply of oxygen to the brain is essential in order to maintain its metabolic functions and to prevent tissue damage. The ox­ygen-independent glycolytic pathway (anerobic glycolysis) is insufficient, even at maximum operating levels, to supply the heavy demands of the brain. Thus a loss of consciousness occurs when brain tissue P02 levels fall to 15 to 20 mmHg. This level is reached in less than 10 s when cerebral blood flow is com­pletely stopped

Low tissue oxygen levels in the brain (hypoxidosis) can be caused by de­creased blood flow (ischemia) or with adequate blood flow accompanied by low levels of blood oxygen (hypoxemia). It is important to recognize that decreased P02 caused by ischemia is accompanied by decreased brain glucose and in­creased brain CO2 while hypoxemia with normal blood flow is not accompanied by changes in brain glucose or CO2, with complete cessation of CBF, irreversible damage occurs to brain tissue within a few minutes and the histological ef­fects observed are remarkably similar whether caused by ischemia, hypoxemia, or hypoglycemia.

Experimental studies on rats and mice in which arterial P02 is progres­sively reduced have illustrated some aspects of hypoxemia which are likely to be similar in humans. A drop in arterial P02 to 50 mmHg (normal, 96 mmHg) produces no change in CBF, O2 utilization by the brain, or lactic acid produc­tion. However, as P02 levels drop to 30 mmHg, a 50 percent increase in CBF is observed along with the onset of coma, decreased oxygen utilization, and in­creased lactic acid production. When the P02 drops further to 15 mmHg, 50 percent of the animals die because of cardiac failure. The remainder show a tremendous increase in lactic acid production, but, surprisingly, levels of ATP, ADP, and AMP remain normal. If cerebral perfusion is artificially maintained while the arterial P02 is decreased further, ATP, ADP, and AMP levels still remain normal. The implication is that the coma observed at low oxygen levels may not be due to a decrease in ATP but instead to some still unexplained mechanism. It appears likely that cardiac complications caused by hypoxemia and the subsequent effect on cerebral blood flow may actually be a primary cause of the irreversible pathologic damage to the brain.

Hypoxia, such as that brought on by high altitudes, brings on a number of symptoms, including drowsiness, apathy, and decreases in judgment. Unless oxygen is administered within half a minute or so, coma, convulsions, and depression of the EEG occur.


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