Isngadi

Wiwi Jaya

Departement of Anesthesiology & Reanimation
Dr Saiful Anwar Hospital, Brawijaya University
Malang


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

Cerebral Blood Flow (CBF)
Cerebral metabolic rate (CMR)
Electrophysiologic function (EEG, evoked responses).
Normal cerebral physiologic values
The intracranial contents :
brain (80%),
blood (12%)
CSF (8%).
Any increase in one component
must be offset by an equivalent decrease
in another to prevent a rise in ICP
ICP
Major compensatory mechanisms include :

(1) displacement of CSF from the cranial to the spinal
compartment,
(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 component
must be offset by an equivalent decrease
in another to prevent a rise in ICP
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 glucose
are met by maintaining CBF


Autoregulation : the maintenance of a constant level
of CBF in the precence of alterations in the
perfusion pressure.
Changes : Intracranial phatology
Volatile anaesthetic agents
Chronic hypertention or symphatetic
activation shifts the auotoregulatory
curve to the right.
Normal cerebral autoregulation curve.
Incresed neuronal aktivity causes an increase in CMR.

Increses CBF
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 68 hours, the CBF returns to baseline values because
CSF pH gradually normalises as a result of the extrusion of
bicarbonate

Arterial oxygen tension
Arterial oxygen was previously not thought to effect CBF unless PaO2
fell below 50 mmHg
the threshold for hypoxic vasodilatation exists at arterial saturations
of 9092%.
Localised hypoxia may cause vasodilatation and an increase in CBF
The relationship between cerebral blood flow and arterial respiratory gas tensions.
(McCalla, 2006)




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 role
in cerebral vasodilatation caused by hypercapnia, ischaemia,
increased cerebral metabolic rate, excitatory amino acids and volatile
anaesthetic agents.
Schematic representation of the effect of increasing concentrations of
a typical volatile anesthetic on utoregulation of cerebral blood flow.
Agent CMR CBF CSF Production CSF Absorption CBV ICP
Halothane

Isoflurane



Desflurane

Sevoflurane

? ?

Nitrous oxide



Barbiturates



Etomidate



Proprofol

? ?

Benzodiazepines



Ketamine



Opioids


Lidocaine

? ?


Cerebral blood flow measured in the present of normocapnia and
in the absence of surgical stimulation
Effect of volatile anesthetics on cerebral blood flow (CBF)
Effect of volatile anesthetics on cerebral metabolic rate of oxygen
(CMRO2 )
Effect of anesthetics on cerebral blood flow (CBF) and cerebral
blood volume (CBV).