Page 58 - JSOM Summer 2022

FIGURE 1 Cerebral autoregulation. to maintain a normal ICP. Since the skull volume is fixed,
any increase in the volume of one content is compensated by
the decrease in the volume of another. It is a zero-sum game.
This volumetric balancing is maintained through a pressure
dynamic. Therefore, an increase in the volume of one com-
ponent will directly lead to an increase in ICP. At some point,
the increase in ICP will exceed the pressure required to force
other components out of the skull. If there is no obstruction at
the foreman magnum, the other components will move down
through it to decrease its intracranial volume until a new equi-
librium is achieved. Thus, as the ICP elevates, CSF will first
The brain uses cerebral autoregulation to maintain cerebral blood relocate from the ventricles and the intracranial subarachnoid
flow through wide ranges of blood pressure by adjusting vascular re- spaces to their counterparts in the spine. Then, the venous
sistance. In healthy individuals, cerebral autoregulation breaks down
outside of this range and the brain becomes ‘pressure passive.’ Trau- blood, which makes up a large proportion of the intracranial
matic brain injury patients may have dysfunctional cerebral autoregu- volume, will move out of the head through the internal jugu-
lation even within the autoregulation thresholds and can easily fail to lar veins. This is why you do not want the cervical collar (or
maintain adequate cerebral blood flow. anything around the neck) too tight, because it will compress
these important veins and cause venous blood to back up into
blood pressure drops and constrict when it rises. How well the head. As the ICP continues to climb, arterial blood will get
cerebral autoregulation works depends on the blood pressure pushed out, CPP will decrease, and the brain becomes isch-
because of the mechanical limits of the arteries in the brain— emic. Once the ICP matches the MAP, no blood will enter the
they can only dilate and constrict so much. In healthy people, skull and the whole brain will die. Many processes can cause
cerebral autoregulation is the most effective and predictable increased ICP (Table 1). Although not part of the CPP equa-
when the mean arterial blood pressure (MAP) is between 60 tion, venous outflow and pressure have an immense contribu-
and 160mmHg (Figure 1). Of note, MAP is a more accurate tion to ICP, and attempting to match one’s arterial inflow with
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measure of blood pressure than systolic blood pressure, which venous outflow may be one of the most effective strategies in
can change based on where in the body one measures. Out- ICP management. 8
side of this ideal MAP range, cerebral autoregulation does not
work well and as a result, CBF becomes directly dependent TABLE 1 Abnormal Processes That Can Increase Intracranial
on the MAP (Figure 1). This ‘pressure-passive’ situation is po- Pressure
tentially dangerous because the blood supply to the brain be- Pathophysiology Examples
comes dependent on the systemic circulatory status, which can Addition of an extra Epidural hematoma, subdural
readily become unstable or inadequate. Because its survival component inside the skull hematoma, foreign body, trapped air
depends on its CBF, the brain constantly monitors many vari- Reduction in the skull Depressed skull fracture
ables including blood pressure, arterial carbon dioxide (CO ) volume
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level, CMRO , autonomic nervous system activities, and body Obstruction of the blood Venous sinus thrombosis,
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posture to fine-tune cerebral autoregulation. Of these, arterial flow out of the skull compression, or obstruction of the
CO or Paco (normal 35–45mmHg) is one of the most potent draining veins by skull fracture;
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influencers of CBF and has a profound, reversible effect on compression of the internal jugular
veins by a cervical collar; increased
the sizes of the blood vessels in the brain; hypercapnia causes intrathoracic or intraabdominal
arterial dilation and an increase in CBF, whereas hypocapnia pressure from agitation or injury
leads to vasoconstriction and lower CBF. These powerful ef- Increase in the brain Brain edema, contusion,
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fects can kick in within minutes. volume hypoventilation
Increase in the cerebral Seizures, agitation
Although CBF is a critical parameter of interest, it is techni- metabolic demand
cally challenging to measure and requires special equipment Increase in cerebral blood Severe hypertension, hypoventilation
typically only found in an intensive care unit (ICU) setting. flow
CBF depends predominantly on cerebral perfusion pressure
(CPP), which, in turn, depends on MAP and intracranial
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pressure (ICP). CPP is calculated using the following simple Pathophysiology
formula: Primary and Secondary Injuries
TBI involves structural injury or physiological disruption of
CPP = MAP – ICP
brain function due to an external force. Brain damage caused
Therefore, CPP is the most commonly used surrogate param- by a TBI can be divided into two separate processes called
eter of CBF. In a normal adult, CPP is > 50mmHg and it will the primary and secondary injuries. Primary injury occurs at
need to drop below 40mmHg before CBF becomes impaired. the time of trauma and manifests as brain bruising, laceration,
compression, bleeding, and diffuse axonal injury. Prehospital
Intracranial Pressure providers cannot influence the impact damage. Therefore,
Intracranial pressure (ICP) is the pressure that is exerted on TBI prevention and head protection remain the most effective
the brain inside the skull. At rest, ICP normally ranges at means to mitigate primary injuries. Secondary injury devel-
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3–7mmHg (pediatrics) and 7–15 mmHg (adults). In adults, ops after the primary injury, and it occurs largely because of
the skull is a rigid container with one hole in the bottom (i.e., the brain’s harmful responses to the shock and trauma. These
foramen magnum) that holds the brain, blood, and the cere- processes, including hypoxemia, ischemia, vasospasm, and
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brospinal fluid (CSF), which exist in a volumetric homeostasis edema, worsen the brain damage and its recovery potential.

56 | JSOM Volume 22, Edition 2 / Summer 2022