Cerebral Circulation

Charles NKURUNZIZA,MD 1st ENT Head&Neck Surgery NUR

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PLAN
Introduction Arterial blood supply Venous drainage Cerebral blood flow

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INTRODUCTION
The

brain has for thousands of years been considered as a noble organ. Its blood supply is of a paramount importance to maintain its function. The brain has an increased blood flow comparing to other organs(700ml/min= 15%) whereas it represent 2.% of the whole body weight. This remarkably large cerebral blood flow reflects the high metabolic rate of the brain of 3.3ml/100g/min (50ml/min in total) which is 20% of the total body consumption. .
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INTRODUCTION(contd)
Cerebral

blood flow and metabolic rate are closely linked and are approximately 4 times greater in gray compared with white matter. Thus, the cerebral cortex has a substantially greater blood flow and metabolic rate than subcortical regions(CBF = 50ml/100g/min ranging from 20ml/100g/min in white matter to70ml/100g/min in grey matter)
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INTRODUCTION(contd)
The

brain is unusual in that it is only able to withstand very short periods of lack of blood supply (ischaemia).

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INTRODUCTION(contd)
This

is because neurons produce energy (ATP) almost entirely by oxidative metabolism of substrates including glucose and ketone bodies, with very limited capacity for anaerobic metabolism. Without oxygen, energy-dependent processes cease leading to irreversible cellular injury if blood flow is not re-established rapidly (3 to 8 minutes under most circumstances).
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Blood Supply of The Brain

The brain receives its arterial supply from two pairs of vessels, the vertebral and internal carotid arteries which are interconnected in the cranial cavity to produce an arterial circle (of Willis).
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Internal Carotid Artery

Begins bifurcation of Com Carotid A Perforates base of skull carotid canal Enters middle cranial fossa beside dorsum sellae In the cavernous sinus

Horizontal

Emerge out medial side of Ant clinoid process perforates dura & arachnoid mater enters subarachnoid space Turns posteriorly below optic nerve Turns upward lateral to optic chiasma

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Internal Carotid Artery

Its main branches: Middle cerebral a. Anterior cerebral a. Anterior communicating artery a. Posterior communicating artery

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Posterior communicating artery

Middle cerebral artery

Anterior cerebral artery Internal carotid artery in cavernous sinus

Posterior cerebral Posterior cerebral artery artery Basilar artery Basilar artery Internal carotid artery In temporal bone

External carotid artery

Vertebral artery Common carotid artery

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Vertebral Artery
Branch of first part of subclavian A Passes foramen transvesarium C6 C1 Enters through foramen magnum perforates dura & arachnoid mater enters subarachnoid space Turns upward, forward, medially medulla oblongata Lower border of pons joins opposite side

BASILAR artery which gives Posterior cerebral arteries

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Posterior communicating artery

Middle cerebral artery

Anterior cerebral artery Internal carotid artery in cavernous sinus

Posterior cerebral Posterior cerebral artery artery Basilar artery Basilar artery Internal carotid artery In temporal bone

External carotid artery

Vertebral artery Common carotid artery

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Anterior communicating artery

Anterior cerebral artery

Posterior communicating artery Posterior cerebral artery

Internal carotid artery

Middle cerebral artery

Basilar A

Vertebral arteries
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Branches of :

VERTEBRAL
Basilar PCA Pontine Labyrinthine Ant Inf CA Sup cerebellar Choroidal

INTERNAL CAROTID
ACA MCA Ant ComA Post Com A Choroidal Ophthalmic

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PCA
Supply: Occipital lobe(Mainly) Parietal lobe Temporal lobe

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MCA
Supply: Mainly the temporal lobe Parietal lobe Occipital lobe Frontal lobe

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ACA
Supply: Mainly the Frontal lobe Some branches for the parietal lobe

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Blood Supply of The Brain

Substances injected into one carotid artery are distributed almost exclusively to the cerebral hemisphere on that side. Normally no crossing over occurs, probably because the pressure is equal on both sides. Even when it is not, the anastomotic channels in the circle do not permit a very large flow.

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Blood Supply of The Brain

There are precapillary anastomoses between the cerebral arterioles, but flow through these channels is generally insufficient to maintain the circulation and prevent infarction when a cerebral artery is occluded.

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D. Venous drainage

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Venous drainage(contd)

The deep veins and dural sinuses empties principally into the internal jugular veins A small amount of venous blood drains through the ophthalmic and pterygoid venous plexuses, through emissary veins to the extra cardiac veins.

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Inferior sagittal sinus

Superior sagittal sinus

Falx cerebri

Tentorium cerebelli Superior petrosal sinus

*
Confluence of sinus Straight sinus

Inferior petrosal sinus

Sigmoid sinus

Transverse sinus
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Vessels Anatomical features

The capillaries in the brain substance resemble nonfenestrated capillaries. The brain capillaries are surrounded by the endfeet of astrocytes. These endfeet are closely applied to the basal lamina of the capillaries, but they do not cover the entire capillary wall, and gaps of about 20 nm occur between endfeet .
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Vessels Anatomical features(contd)

The tight junctions between capillary endothelial cells in the brain and between the epithelial cells in the choroid plexus effectively prevent some substance to reach the cerebral cells acting as a BBB. The blood-brain barrier is a selective, rather than absolute barrier.

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Vessels Anatomical features(contd)

Nutrients, such as glucose, essential amino acids, and some electrolytes, move passively by facilitated diffusion through the endothelial cell membranes. Blood borne metabolic wastes, such as urea and creatinine as well as proteins, certain toxins, and most drugs, are prevented from entering brain tissue.

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Vessels Anatomical features(contd)

Lipid soluble molecules will cross it High CO2/low O2 produce vasodilation and decrease resistance of BBB Injury or inflammation decreases resistance of BBB.

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Vessels Anatomical features (contd)

Selected brain areas are not protected by the BBB : the circumventricular organs (CVO) bordering on the 3rd and 4th ventricles
parts of the hypothalamus - median eminence neurohypophysis pineal gland area postrema subfornical organ subcommissural organ
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Differences between brain and general capillaries

General capillary
small solutes can diffuse through intercellular clefts Vesicular transport. fenestrated

Brain capillary
tight junctions Reduced vesicular transport no fenestra astrocyte foot processes
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General vs. Brain Capillaries

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Brain capillary
Tight junctions Surrounded by astrocytes Few vesicles Carrier mediated transport of glucose and amino acids

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CEREBRAL BLOOD FLOW

Cerebral blood flow (CBF) is dependent on a number of factors that can broadly be divided into: i. Those affecting cerebral perfusion pressure. ii. Those affecting the radius of cerebral blood vessel.

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CEREBRAL BLOOD FLOW(contd)

Intracranial pressure (ICP) intracranial pressure is important as it affects cerebral perfusion pressure and cerebral blood flow. Normal ICP is between 5 and13mmHg. Constituents within the skull include the i. brain(80%/1400ml), ii. blood(10%/150ml) and
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CEREBRAL BLOOD FLOW(contd)

The skull is a rigid box so if one of the three components increases in volume, then there must be compensation by a decrease in the volume of one or more of the remaining components otherwise the ICP will increase (Monro-Kellie hypothesis). Compensatory mechanisms include movement of CSF into the spinal sac, increased reuptake of CSF and compression of venous sinuses. These mechanisms reduce the liquid volume of the intracranial contents. 9/26/2012 42

CEREBRAL BLOOD FLOW(contd)

For example, an increase in lesion volume (e.g. epidural hematoma) will be compensated by the downward displacement of CSF and venous blood. These compensatory mechanisms are able to maintain a normal ICP for any change in volume less than approximately 100120 mL.

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ICP elastance curve (change in pressure per unit change in volume)

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CEREBRAL BLOOD FLOW(contd)

Stage 1/2 = compensation phase. As one of the intracranial constituents increases in volume, the other two constituents decrease in volume in order to keep the intracranial pressure constant. Stage 3/4 = decompensated phase. When compensatory mechanisms are exhausted, small increases in the volumes of intracranial constituents cause large increases in ICP.

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CEREBRAL BLOOD FLOW(contd)

The slope of the curve is dependent on which intracranial constituent is increasing. If it is blood or CSF, both of which are poorly compressible, then the slope is steeper. If it is brain tissue, such as from a tumour, the curve is less steep as the tissue is compressible.

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CEREBRAL BLOOD FLOW(contd)

Effects of a Raised ICP As ICP rises, CPP falls eventually to a point when there is no cerebral blood flow, no cerebral perfusion and brain death. Prior to this, brain structures begin to herniate(protrude through an opening). Physiological compensatory mechanisms occur to try and maintain
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CEREBRAL BLOOD FLOW(contd)

Temporal lobe herniation beneath tentorium cerebelli (uncal herniation) causes cranial nerve III palsy (dilatation of pupil followed by movement of eye down and out). Herniation of cerebellar peduncles through foramen magnum (tonsillar herniation). Pressure on the brainstem causes the Cushing reflex hypertension, bradycardia and Cheyne-Stokes respiration.

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CEREBRAL BLOOD FLOW(contd)

Subfalcine herniation occurs when the cingulate gyrus on the medial aspect of the frontal lobe is displaced across the midline under the free edge of the falx cerebri and may compress the anterior cerebral artery.

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CEREBRAL BLOOD FLOW(contd)

Upward, or cerebellar herniation occurs when either a large mass or increased pressure in the posterior fossa occurs. The cerebellum is displaced in an upward direction through the tentorial opening and causes significant upper brainstem compression.

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CEREBRAL BLOOD FLOW(contd)

If ICP is not measured directly, we can estimate it and therefore make changes in MAP to maintain CPP: Patient drowsy and confused (GCS 913) ICP ~ 20mmHg GCS = 8 ICP ~ 30mmHg

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CEREBRAL BLOOD FLOW(contd)

Measuring ICP ICP is traditionally measured by use of a ventriculostomy, which involves a catheter that is placed through a small hole in the skull (burr hole) into the lateral ventricle. ICP is then measured by transducing the pressure in a fluid column. Ventriculostomies also allow for drainage of CSF, which can be
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CEREBRAL BLOOD FLOW(contd)

An epidural monitor can also be used but becomes increasingly unreliable at extremes of pressure.

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CEREBRAL BLOOD FLOW(contd)

Cerebral Perfusion Pressure Perfusion of the brain is dependent on the pressure gradient between the arteries and then veins and this is termed the cerebral perfusion pressure (CPP). This is the difference between the mean arterial blood pressure (MAP) and the mean cerebral venous pressure.
i.
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CEREBRAL BLOOD FLOW(contd)

The mean cerebral venous pressure is difficult to measure and approximates to the more easily measured intracranial pressure (ICP). CPP = MAP ICP MAP can be estimated as equal to: diastolic blood pressure + 1/3 pulse pressure and is usually around 90mmHg.

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CEREBRAL BLOOD FLOW(contd)

In a normal brain, CBF remains constant over a wide range of CPPs. This is achieved by autoregulation.

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CEREBRAL BLOOD FLOW(contd)

ii.The radius of cerebral arterial blood vessels This is regulated by four primary factors: A. Cerebral metabolism B. Carbon dioxide and oxygen C. Autoregulation D. Neurohumeral factors
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CEREBRAL BLOOD FLOW(contd)

The radius of the arterial vessels is doubly important because: a) As well as having an effect on CBF, b) An increased radius (vasodilatation) leads to an increase in cerebral blood volume which in turn increases ICP and reduces CPP.

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CEREBRAL BLOOD FLOW(contd)

Cerebral metabolism Changes in CBF and metabolism tend to follow each other; local or global increases in metabolic demand are met rapidly by an increase in CBF and substrate delivery and vice versa (often referred to as flow-metabolism coupling)
A.

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CEREBRAL BLOOD FLOW(contd)

These changes are thought to be controlled by several vasoactive metabolic mediators including hydrogen ions, potassium, CO2, adenosine, glycolytic intermediates, phospholipid metabolites and, nitric oxide (NO).

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Graph illustrating coupling between CBF and CMRO2

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CEREBRAL BLOOD FLOW(contd)

B.Carbon dioxide and oxygen At normotension, the relationship between partial pressure of carbon dioxide in arterial blood (PaCO2) and CBF is almost linear and At a PaCO2 80mmHg CBF is approximately doubled. No further increase in flow is possible at this point as the arterioles are maximally dilated.
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CEREBRAL BLOOD FLOW(contd)

Conversely at 20mmHg flow is almost halved and again cannot fall further as the arterioles are maximally vasoconstricted. These effects are regulated by a complex and interrelated system of mediators.

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CEREBRAL BLOOD FLOW(contd)

The initial stimulus is a decrease in brain extracellular pH bought about by the change in PaCO2, further mediated by nitric oxide, prostanoids, cyclic nucleotides, potassium channels, and a decrease in intracellular calcium concentration as a final common mediator.

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Relationship between CBF and PaC02

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CEREBRAL BLOOD FLOW(contd)

Arteriolar tone has an important influence on how PaCO2 affects CBF. Moderate hypotension impairs the response of the cerebral circulation to changes in PaCO2 and severe hypotension abolishes it. Oxygen has little effect on the radius of blood vessels at partial pressures used clinically.

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CEREBRAL BLOOD FLOW(contd)

CBF increases once PaO2 drops below 50mmHg so that cerebral oxygen delivery remains constant. Hypoxia acts directly on cerebral tissue to promote the release of adenosine, and in some cases prostanoids contribute significantly to cerebral vasodilatation.

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CEREBRAL BLOOD FLOW(contd)

Hypoxia also acts directly on cerebrovascular smooth muscle to produce hyperpolarisation and reduce calcium uptake, both mechanisms enhancing vasodilatation.

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Relashionship between CBF and PaO2 (Almost no effect on CBF in normoxemic range)

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CEREBRAL BLOOD FLOW(contd)

C.Autoregulation
The brain requires a constant flow of blood over a range of pressures and this is achieved by the process of autoregulation. The stimulus to autoregulation is CPP, not MAP. In adults under normal circumstances (ICP <10mmHg), CPP and MAP are very similar and CBF remains constant with a CPP of 60-160mmHg.

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CEREBRAL BLOOD FLOW(contd)

Clearly the higher the ICP the more CPP deviates from MAP and must be calculated. The autoregulation curve is shifted to the right in chronic hypertensive patients and to the left in neonates.

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CEREBRAL BLOOD FLOW(contd)

Autoregulation is thought to be a myogenic mechanism, whereby vascular smooth muscle constricts in response to an increase in wall tension and to relax to a decrease in wall tension. At the lower limit of autoregulation, cerebral vasodilation is maximal, and below this level the vessels collapse

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CEREBRAL BLOOD FLOW(contd)

At the upper limit, vasoconstriction is maximal and beyond this the elevated intraluminal pressure may force the vessels to dilate, leading to an increase in CBF and damage to the blood-brain-barrier. Metabolic mediators, such as adenosine, may also be involved in the low-pressure range of autoregulation.

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CEREBRAL BLOOD FLOW(contd)

As with all the other mechanisms that affect the radius of the blood vessels, autoregulation will also change the cerebral blood volume and may affect ICP. Pressure autoregulation can be impaired in many pathological conditions including patients with a brain tumour, subarachnoid haemorrhage, stroke, or head injury.

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CEREBRAL BLOOD FLOW(contd)

A loss of CBF regulatory capacity can be attributed either to damage of the control system (eg.cerebral vessels) or of the feedback mechanisms involved in the brains haemodynamic control. At this time, CBF becomes pressuredependent and thus small changes in MAP can have profound changes on CBF

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Relationship between cerebral blood flow and cerebral perfusion pressure.

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CEREBRAL BLOOD FLOW(contd)

D.Neurohumeral factors A major difference between other systemic circulations and the cerebral circulation is the relative lack of humoral and autonomic control on normal cerebrovascular tone. The main action of the sympathetic nerves is vasoconstriction that protects the brain by shifting the autoregulation curve to the right in
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CEREBRAL BLOOD FLOW(contd)

The parasympathetic nerves contribute to vasodilatation and may play a part in hypotension and reperfusion injury (for example after cardiac arrest).

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CEREBRAL BLOOD FLOW(contd)

v.Other factors 1.Blood viscosity: This is directly related to haematocrit. As viscosity falls, CBF increases(see HagenPoiseuille law). However, there will also be a reduction in oxygen-carrying capacity of the blood. The optimal haematocrit is where there is a balance between flow and
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CEREBRAL BLOOD FLOW(contd)

2.Temperature: CMRO2 decreases by 7% for each 1C fall in body temperature and is paralleled by a similar reduction in CBF. At 27C, CBF is approximately 50% of normal. By 20C, CBF is about 10% of the normal
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CEREBRAL BLOOD FLOW(contd)

The reduction of CMRO2 is the factor that allows patients to withstand prolonged periods of reduced CBF without ischaemic damage for example during cardiopulmonary bypass. Again, because of vasoconstriction, cerebral blood volume and ICP are reduced. Although this has been tried to help control high ICP, clinical trials have been disappointingly ineffective in showing an improved outcome. 9/26/2012

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CEREBRAL BLOOD FLOW(contd)

3.Drugs: Cerebral metabolism can be manipulated (reduced) and consequently CBF, cerebral blood volume and ICP is reduced. Infusions of the barbiturate thiopentone are used in this manner to help control high ICP after head injury.

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CEREBRAL BLOOD FLOW(contd)

Anaesthetic drugs have a significant effect on cerebral blood vessels; volatile agents cause a reduction in the tension of cerebral vascular smooth muscle resulting in vasodilatation and an increase in CBF. Interestingly many of the newer drugs (isoflurane, sevoflurane) also reduce neuronal function and metabolic demands and as a result this can lead to uncoupling of flow-metabolism.

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CEREBRAL BLOOD FLOW(contd)

This appears to be dependent on the concentration of volatile anaesthetic given. The vasodilatation can be countered by hyperventilation, without serious risk of cerebral ischaemia.

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