Page 536 - Clinical Application of Mechanical Ventilation

502 Chapter 15

General Principles of HIE

The brain occupies about 2% of the total body weight but uses 15% of the energy
Causes of acute cerebral generated by the body. Unlike the muscle cells in the body, the brain does not
hypoxia include inadequate
ventilation or oxygenation, hold or store any energy of its own except for a small amount of glycogen in the
inadequate perfusion, and astrocytes. Furthermore, the brain cells cannot utilize fatty acids because they are
decrease in cerebral perfusion
pressure. not transported across the brain capillaries. The brain is highly dependent on the
constant supply of oxygen and glucose provided by the blood. For these reasons, a
severe deprivation of oxygen (e.g., respiratory/cardiac arrest, shock, severe anemia,
decrease in CPP) or lack of glucose (e.g., hypoglycemia, starvation) can severely
affect the normal functions of the brain (Agamanolis, 2011).
A lack of cerebral circulation depletes the neuronal oxygen stores within 20 seconds
A lack of cerebral circula- and leads to unconsciousness. Within 5 minutes of complete cerebral anoxia, brain
tion depletes the neuronal
oxygen stores within 20 glucose and ATP stores are lost, and energy depletion is the end result (Madl et al.,
seconds and leads to uncon- 2004). The mechanism of cerebral cellular injury and death as a result of energy depri-
sciousness. Within 5 minutes
1
of complete cerebral anoxia, vation is complex. The first event following energy depletion is failure of the Na and
brain glucose and ATP stores 1
are lost, and energy depletion K pumps, leading to depolarization of the neuronal membrane. Depolarization causes
is the end result. neurons to release excessive glutamate into the synaptic cleft. Since some glutamate
receptors are nonselective cation-permeable ion channels, influx of excessive Ca 11 into
neurons leads to activation of catabolic (destructive) enzymes, as well as activation of ni-
tric oxide synthase and increase of nitric oxide production. Furthermore, passive influx
2
1
of Cl (and Na ) into the cells can cause osmotic edema and rapid death of the cells
(Agamanolis, 2011). Figure 15-2 outlines the mechanism of cerebral cellular injury as a
result of energy depletion to the brain.

Energy Failure

Depolarization Loss of Function

Excessive Glutamate Discharge in Synaptic Cleft

Opening of Ca 11 Channels

Influx of Ca 11 into Neurons

(1) Activation of Catabolic Enzymes
(2) Activation of NO Synthase and Increase
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NO Production

Cerebral Cellular Injury

Figure 15-2 Mechanism of cerebral cellular injury as a result of energy depletion to the brain.

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