Outline physiological and metabolic effects of anesthetic drugs and techniques on brain and spinal

cord
Basic concepts
 Global CBF= 50mL/100g brain tissue/min
 White matter blood flow= 20mL/100g/min
 Grey matter blood flow= 70mL/100g/min
 Resting O2 consumption of brain= 50mL/min (20% total body O2 requirements)
 Cerebral blood flow= 15% CO (~750mL/min)
 CPP= MAP- (ICP+CVP)
 Normal CPP= 70-80mmHg
 CBF autoregulated between MAP 50-150mmHg

Cerebral autoregulation theory:

1) Myogenic theory
 Change in perfusion pressure myogenic response in cerebral vascular smooth muscle
 Increase MAP cerebral vasoconstriction maintaining CBF
 Decrease MAP cerebral vasodilatation maintaining CBF
2) Metabolic theory
 CBF and cerebral metabolism are coupled
 Increased CMRO2 cerebral vasodilatation (H+/K+/adenosine/Nitric oxide)
 Decreased CMRO2 cerebral vasoconstriction

Effects of cerebral blood flow

1. PaCO2- increase CBF linearly between 22.5mmHg to 75mmHg
2. PaO2- increases below 60mmHg
3. Temperature- CMRO2 falls by 7% per 1 degree celcius decrease in temperature
4. CMRO2
Effects of anesthetic drugs on CBF
1) Volatiles- all increase CBF and reduce CMRO2 uncoupling CBF from CMRO2
2) N2O- increase CBF and CMRO2
3) NMBA- no effect
 4) Induction drugs- all reduce CMRO2,CBF and ICP EXCEPT ketamine

What is the effect of brain injury on CBF?

 TBI loss of cerebral autoregulation in injury-affected areas of brain development of
pressure-dependent perfusion area
 Fall in CPP leads to secondary ischaemic brain injury

What is Monro-Kellie Doctrine?

 Skull is a rigid box containing
i) Brain tissue (80%)
ii) Blood (12%)
iii) CSF (8%)
 Volume of box is constant
 An increase in volume of any one of the intracranial constituents accompanied by parallel
reduction in volume of another constituent if ICP to remain constant

Normal ICP
 10-15mmHg= normal
 >20mmHg= elevated ICP

Causes of raised ICP

1) CSF- hydrocephalus
2) Brain- tumors, edema, contusions
3) Blood- hematoma, cerebral aneurysm

Effect of intracranial volume on ICP

 As intracranial volume increases (eg: cerebral edema) compensatory mechanism occurs

(reduced intracranial venous blood volume, increase CSF absorption and CSF movement into
spinal compartment)
 When mechanisms exhausted small increase in intracranial volume large increase in ICP
What is the vasodilatory cascade?
 In head-injured patients, vasodilatory cascade describes vicious cycle that develops if there is
reduction in CPP
 Vasoconstriction cascade describes treatment of the situation

Explain the signs, symptoms and management of raised ICP

Discuss principles and strategies of cerebral protection

What are the symptoms and signs of raised intracranial pressure (ICP) in an adult?
Symptoms:
1. Headache: bursting, throbbing. Exacerbated by sneezing, exertion, recumbency. Worse in
morning after a period of recumbency, raised PaCO2 associated with sleep, reduced CSF
reabsorption.
2. Vomiting.
3. Visual disturbance.

Signs:
1. Respiratory irregularity, Cheyne-Stokes breathing, neurogenic hyperventilation due to tonsillar
herniation.
2. Cushing’s triad: hypertension with high pulse pressure, bradycardia and associated irregular
respirations.
3. Eye signs: papilloedema, fundal haemorrhages, pupillary dilatation, ptosis, impaired upward
gaze (midbrain compression), abducens palsy.
4. Progressive reduction in consciousness due to caudal displacement of midbrain.

Describe the physiological principles underlying the management of raised ICP.

  The cranium is a closed compartment (Monroe–Kelly doctrine).
 The sum of its contents (brain, CSF, blood, other) must therefore remain the same.
 If the amount of one component increases, some compensation can occur by reducing the
amount of one of the other components.
 Once these compensatory mechanisms are exhausted, ICP will rise, ultimately causing pressure
on the brain, herniation and thus direct tissue damage.
 Physiological manipulation of the quantity of each of the components can limit ICP rise.

1) Reduce CSF:
 Diuretics, mannitol, hypertonic saline, elevation of head of bed 15–30 degrees, CSF drain.

2) Reduce blood:
 Optimise venous drainage: avoid tight tube ties, head-up tilt 15–30 degrees, paralyse to reduce
valsalva, treat seizures with anticonvulsants, avoid excessive PEEP and peak airway pressures.
 Avoid excessive arterial flow: maintain PaO2, keep PaCO2 low-normal, anaesthetise to reduce
cerebral metabolic rate of oxygen (CMRO2) and avoid pyrexia.

3) Reduce brain:
 Mannitol, avoid hyperglycaemia, avoid hypotonic fluid administration.

4) Reduce other:
 Evacuate clot, excise tumour.

5) Stop the cranium being a closed compartment:

 Decompressive craniectomy.

One of the main issues of a rising ICP is the impact it has on cerebral perfusion pressure (CPP), according
to the equation:
CPP = MAP − ICP (or JVP, whichever is higher)
 Therefore, in the early stages of rising ICP (before direct pressure brain damage occurs), the
effects can be mitigated by maintaining CPP through manipulation of mean arterial pressure
(MAP) and jugular venous pressure (JVP).
 Maintain MAP: avoid dehydration and pyrexia, and use vasopressors to target a MAP of 80 mm
Hg (this value depends on ICP, which may not be known).
 Reduce JVP: as previously, optimise venous drainage.

What methods are used to manage or prevent acute rises in ICP?

1) Airway:
 Intubate.
2) Respiratory:
 Aim PaO2 >13 kPa (98mmHg) and PaCO2 4.5–5 kPa (34-38mmHg), keep PEEP <15.
 Hyperventilation to PaCO2 4–4.5 kPa (30-34mmHg) may be used for short time periods in
emergency situations with refractory intracranial hypertension.
3) Cardiovascular:
  15–30-degree head-up tilt, tube ties not too tight/tape tube, head in neutral position, increase
sedation and paralyse if coughing or straining, ensure that MAP >80 (depends on ICP, if being
monitored).
4) Neurological:
 Adequate sedation to reduce CMRO2, treat seizures, treat pyrexia, monitor for and manage
hyperglycaemia (target 6–10 mmol/l).
5) Pharmacological:
 Mannitol 0.25–1 g/kg.
 Hypertonic saline 5% 2 ml/kg.
6) Surgical:
 Consideration of CSF drain, under expert guidance.
 Decompressive craniectomy in specialist centre.

Brain Trauma Foundation 2016 guideline recommendations

Describe GCS score