Figure 21.2. Magnetic resonance image of a bite wound on the top of the skull of a Pomeranian. Brain matter protrudes into the wound.

If the brain becomes enlarged, initially some blood and cerebrospinal fluid (CSF) escape to avoid the concurrent rise in intracranial pressure. CSF production may decrease as well, in order to maintain a normal ICP. If the pathological process continues to cause increasing pressure within the cranial vault, eventually this compensatory response will reach its limit. Cerebral swelling may lead to herniation of the brain. If cerebral perfusion pressure (CPP) falls to a point where there is no cerebral blood flow, death occurs.

CPP is defined as the difference between mean arterial pressure (MAP) and intracranial pressure (ICP):

CCP = MAP − ICP

To perfuse the brain, the mean arterial blood pressure must be greater than the intracranial pressure. As previously stated, constant cerebral blood flow is maintained when mean arterial pressure is between 50 mm Hg and 150 mm Hg. Cerebral blood flow may become blood pressure dependent in a patient with abnormal brain pathology or in a patient receiving vasodilator agents such as the inhaled halogenated agents. As arterial pressure rises, cerebral blood flow will rise, causing an increase in cerebral volume. As arterial pressure falls, cerebral blood flow will decrease, along with intracranial pressure; but this may lead to inadequate perfusion to the brain. Therefore, it is critical to maintain normal blood pressure during the anesthetic period. The use of fluid therapy and drugs that support blood pressure may be indicated.

The Cushing Reflex

Cerebral perfusion pressure declines as intracranial pressure increases. When arterial pressure is less than intracranial pressure, a reflex called the CNS ischemic response is initiated by the hypothalamus in the brain. The sympathetic nervous system causes peripheral vasoconstriction and increased cardiac output. These two effects increase arterial blood pressure, thus restoring blood flow to the brain. The increased arterial blood pressure stimulates baroreceptors in the carotid bodies, slowing the heart rate, often to the point of bradycardia. The presence of hypertension and bradycardia associated with increased intracranial pressure is referred to as the Cushing reflex. As the condition becomes more life threatening, decreased perfusion to the brainstem may cause respiratory abnormalities. If irregular respiration accompanies the hypertension and bradycardia, the term Cushing’s triad applies (Bledsoe 2007).

Effects of CO₂ and O₂ on Cerebral Blood Flow

Carbon dioxide causes cerebral vasodilation. When a patient experiences hypercapnea (PaCO₂ > 60 mm Hg), cerebral blood flow increases along with intracranial pressure. Therefore, controlled ventilation is necessary to maintain a normal PaCO₂ in anesthetized patients. PaCO₂ can be measured through serial arterial blood gases. Additionally, the measurement of end-tidal CO₂ through capnography is extremely useful. Patients exhibiting severe signs of increased ICP should be hyperventilated to an end-tidal CO₂ of 25–30 mm Hg (Wilson 1992). Controlled hyperventilation also counteracts the effects of inhalation anesthetics (at lower concentrations) on ICP and is useful for reducing brain size during neurosurgery. Excessive hyperventilation (PaCO₂ < 25 mm Hg) leading to low cerebral perfusion pressure can be detrimental to patient survival. In addition, positive pressure ventilation should be carefully adjusted to minimize the side effects (increased intrathoracic pressure leading to decreased cardiac output) that may lead to a low mean arterial pressure.

Low arterial oxygen tension also has a profound effect on cerebral blood flow. Hypoxia (PaO₂ < 50 mm Hg) increases cerebral blood flow, which in turn can cause an increase in ICP.

Other things to consider

Several other factors can cause an increase in intracranial pressure that may be detrimental to the patient. Neck leashes, application of pressure on the jugular veins, and placement of jugular catheters should be avoided (Harvey et al. 2007). Excitement, struggling, straining, or coughing may also increase intracranial pressure. Patient position is also important to consider, because the head-down position or excessive flexion and rotation will increase ICP or occlude jugular venous drainage. Patients should be placed at a slight incline (10–20°) with the head level slightly above the level of the heart. Excessive fluid therapy, positive pressure ventilation, and pain can also increase intracranial pressure. Seizures should be controlled because epileptic activity causes an increase in cerebral metabolism, which in turn increases blood flow, and cerebral swelling.

Effects of Anesthetic Agents on Intracranial Pressure

The anesthetic agents used in veterinary medicine today have different effects on cerebral metabolic rate, cerebral blood flow and intracranial pressure. Most injectable anesthetics cause a reduction in these parameters, with ketamine being an exception. Inhalant anesthetics increase cerebral blood flow and intracranial pressure.

Injectable Anesthetics

The direct effects of opioids on cerebral blood flow and intracranial pressure are minimal, however, respiratory depression caused by the use of opioids indirectly increase CBF and ICP by raising PaCO₂

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