Manual of Equine Anesthesia and Analgesia. Группа авторов
Чтение книги онлайн.
Читать онлайн книгу Manual of Equine Anesthesia and Analgesia - Группа авторов страница 52
![Manual of Equine Anesthesia and Analgesia - Группа авторов Manual of Equine Anesthesia and Analgesia - Группа авторов](/cover_pre1034366.jpg)
Most absorption occurs through the subarachnoid villi which protrude into the venous sinuses of the cranium.
The subarachnoid space does not communicate with the subdural space, but is continuous with the ventricles of the brain through medial and lateral connections in the roof of the fourth ventricle. Separations of the arachnoid and pia mater form the cerebro‐medullary cistern or cisterna magna.Samples of CSF can be obtained from lumbar puncture or through the cisterna magna, although the latter technique carries a higher risk.
CSF is exchanged every four hours and absorption helps maintain pressure at a constant level.
CSF acts as a cushion and support for the brain.
Changes in brain volume can be offset by CSF production and absorption.
The composition of CSF is tightly regulated. CSF pH remains about 7.33 even with wide changes in plasma pH. Compared to other extra‐cellular fluids, CSF contains 7% higher sodium and chloride ion, and 30% and 40% lower glucose and potassium concentrations, respectively.
A CSF pH decrease of 0.05 units rapidly results in a fourfold increase in ventilation and reflects the ability of lipid soluble CO2 to cross the blood–brain‐barrier, not hydrogen ions. Active transport of bicarbonate ions returns CSF pH to normal with chronic changes in arterial pH.
A potential difference between CSF and blood of about +5 mV is the result of an active transport system.
O2, CO2, barbiturates, glucose, and lipophilic (anesthetic and sedative) substances effectively cross the blood–brain barrier.
Inorganic ions, highly dissociated compounds, amino acids, and sucrose cross very slowly.
CSF pressure changes with body position, and expiratory efforts such as coughing or straining can sharply increase the pressure.
II Central nervous system pathophysiology
A Seizures
Seizures are not common in horses and classification and diagnosis is reviewed elsewhere.
Accidental injection of drugs into the carotid artery can cause convulsions.
Anticonvulsants raise the seizure threshold, prevent spread of seizure activity, and decrease the level of activity of abnormal neurons while sparing normal cells.
B Intracranial pressure (ICP) increase
As an intracranial mass expands within the bony cranium it can cause an increase in ICP. This increase in ICP can be offset by displacement of CSF, blood flow, and displacement of the brain matter.This effect does not continue, and once a certain point is reached, ICP can rise exponentially (see Figure 6.2).
Sudden increases in ICP can increase the risk of brain herniation.
During neuroanesthesia, steps are taken to reduce brain volume as much as possible to offset increases in ICP.
Figure 6.2 The effects of intracranial volume changes on intracranial pressure. At a certain point, the increase in intracranial volume causes a dramatic increase in intracranial pressure as compensatory mechanisms become exhausted.
III Neuroanesthesia
Anesthetic drugs and manipulations performed during anesthesia can affect:
A Cerebral metabolic rate
In humans, normal O2 consumption is 3–5 ml/100 g/minute, similar to that of working skeletal muscle.
When the level of consciousness is depressed, the cerebral metabolic rate is decreased.
Oxygen consumption decreases by approximately 20% during hypoglycemia, 40% during general anesthesia, 3% during sleep, and 15–20% during hypothermia.
Drugs such as α2 adrenergic agonists and a propofol infusion decrease cerebral metabolic oxygen demand and provide some brain protection.
Isoflurane decreases cerebral metabolic oxygen demand, but causes vasodilation.
B Cerebral blood flow and perfusion pressure
Anesthetic drugs
Anesthetic drugs can modify cerebral blood flow and cerebral metabolic rate (see Table 6.1).
These changes can be affected by the presence or absence of intracranial pathology, and may also be influenced by hypoxemic or hypercapnic states.
Isoflurane increases ICP in normal horses, and this is exacerbated by a prolonged duration of anesthesia, by hypoventilation (increased PaCO2), and if the head is positioned below heart level.
Isoflurane preserves autoregulation even at moderate‐deep levels of anesthesia in healthy horses and a cerebral blood flow of 33 ml/100 g/minute, regardless of mean arterial pressure in the 60–100 mmHg range.
Dobutamine infusion was not found to increase ICP in normal horses.
Spinal cord perfusion was found to decrease during isoflurane anesthesia, and dobutamine infusion may decrease perfusion further.
However, hypotension and decreased ability to autoregulate cerebral perfusion caused by older volatile anesthetics such as halothane may cause rare neurological complications in normal horses.
Cerebral vasodilation with volatile anesthetics is a problem in disease states when high ICP is already present. The increase in blood volume within the cranium could increase ICP further.
Drugs which produce a degree of cerebral vasoconstriction may be more useful, especially if they also decrease cerebral metabolic rate (e.g. α2 agonists and propofol).
Increased PaCO 2
Will increase cerebral blood flow and intracranial volume through vasodilation.
This could be detrimental in animals with existing increased ICP.
Mechanical ventilation is required during anesthesia to ensure PaCO2 values are kept between 35 and 40 mmHg (normal PaCO2 in adult horse is approximately 40 mmHg) to reduce the risk of increasing ICP.Table