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IsngadiWiwi Jaya

Departement of Anesthesiology & Reanimation

Dr Saiful Anwar Hospital, Brawijaya University

Malang

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Anesthetics cause dose-related and reversible alterationsin many aspects of cerebral physiology including :

Cerebral Blood Flow (CBF)

Cerebral metabolic rate (CMR)

Electrophysiologic function (EEG, evoked responses).

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Normal cerebral physiologic values

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The intracranial contents :brain (80%),blood (12%)CSF (8%).

Any increase in one componentmust be offset by an equivalent decrease

in another to prevent a rise in ICP

ICP

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Major compensatory mechanisms include :

(1) displacement of CSF from the cranial to the spinalcompartment,

(2) increase in CSF absorption,(3) decrease in CSF production,(4) decrease in total cerebral blood volume (primarily venous).

Any increase in one of the intracranial componentmust be offset by an equivalent decrease

in another to prevent a rise in ICP

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The adult brain constitutes only 2% of body mass.

It accounts for 20% of basal oxygen consumption

CBF = 50 ml/100 g/min

The substantial demands for both oxygens dan glucoseare met by maintaining CBF

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Autoregulation : the maintenance of a constant level

of CBF in the precence of alterations in theperfusion pressure.

Changes : Intracranial phatologyVolatile anaesthetic agents

Chronic hypertention or symphateticactivation shifts the auotoregulatorycurve to the right.

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Normal cerebral autoregulation curve.

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Incresed neuronal aktivity causes an increase in CMR.

Increses CBF

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Arterial carbon dioxide tension (PaCO2) CO2 is a potent vasodilator CBF changes by 12 ml/100 g/min for each 1 mmHg change in PaCO2

within physiological limits. However, after 6

8 hours, the CBF returns to baseline values because

CSF pH gradually normalises as a result of the extrusion ofbicarbonate

Arterial oxygen tension

Arterial oxygen was previously not thought to effect CBF unless PaO2fell below 50 mmHg the threshold for hypoxic vasodilatation exists at arterial saturations

of 9092%. Localised hypoxia may cause vasodilatation and an increase in CBF

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The relationship between cerebral blood flow and arterial respiratory gas tensions.

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(McCalla, 2006)

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Potassium and adenosine Both potassium and adenosine are potent vasodilators. Increased concentrations are detected during seizures, direct cortical

stimulation and hypoxia which causes an increase in CBF.

Calcium is a potent vasoconstrictor in high concentrations. Some calcium antagonists blunt hypoxic vasodilatation and prevent

adenosine release.

Recent evidence suggests that nitric oxide (NO) plays an important rolein cerebral vasodilatation caused by hypercapnia, ischaemia,increased cerebral metabolic rate, excitatory amino acids and volatileanaesthetic agents.

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Schematic representation of the effect of increasing concentrations ofa typical volatile anesthetic on utoregulation of cerebral blood flow.

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Agent CMR CBF CSF Production CSF Absorption CBV ICP

Halothane

Isoflurane

Desflurane

Sevoflurane

?

?

Nitrous oxide

Barbiturates

Etomidate

Proprofol

?

?

Benzodiazepines

Ketamine

Opioids

Lidocaine

?

?

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Cerebral blood flow measured in the present of normocapnia andin the absence of surgical stimulation

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Effect of volatile anesthetics on cerebral blood f low (CBF)

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Effect of volatile anesthetics on cerebral metabolic rate of oxygen

(CMRO2 )

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Effect of anesthetics on cerebral blood f low (CBF) and cerebralblood volume (CBV).

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