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CEREBRAL CIRCULATION

& AUTO-REGULATION

By: Dr. Salah Al-Shawi


UKMMC
24/June/2010
Anatomy of the cerebral circulation
 The brain, though representing 2% of the total
body weight, it receives about one fifth of the
resting cardiac output. This blood supply is
carried by the two internal carotid arteries (ICA)
and the two vertebral arteries that anastomose at
the base of the brain to form the circle of Willis.
 Carotid arteries and their branches (referred to
as the anterior circulation) supply the anterior
portion of the brain while the vertebrobasilar
system (referred to as posterior circulation)
supplies the posterior portion of the brain.
Cerebral Circulation
 The carotid system.
 The vertebrobasilar system.
 The collateral blood supply of the brain.
 Venous drainage
A: The carotid system
 1. Common Carotid artery (CCA): The left CCA arises from
the aortic arch while the right arises from the bifurcation of
the innominate artery.
 2. External carotid artery (ECA): It starts at the CCA
bifurcation. Its branches supply the jaw, face, neck and
meninges. The bulk of the meningeal circulation is supplied
by the middle meningeal artery, the most important branch
of the maxillary artery which is one of the two terminal
branches of the ECA (the other terminal branch is the
superficial temporal artery). These two terminal branches in
addition to the occipital artery can serve as collateral
channels for blood supply to the brain in instances of
obstruction of the ICA. The ascending pharyngeal artery
can serve as a source of blood in instances of occlusion of
the ICA.
CAROTID SYSTEM
1.Common Carotid A.
2.External Carotid A.
 3. Internal carotid artery (ICA): It starts at the
carotid sinus at bifurcation of CCA at the level
of the upper border of the thyroid cartilage at
the level of the fourth cervical vertebra. It
ascends just behind and lateral to the
hypopharynx where it can be palpated. It passes
up the neck without any branches to the base of
the skull where it enters the carotid canal of the
petrous bone. It then runs through the
cavernous sinus in an S-shaped curve (the
carotid siphon), then it bifurcate into anterior
cerebral artery and the larger middle cerebral
artery.
3.Internal Carotid A.
B. Vertebrobasilar System
 1. Vertebral artery : It arises from the proximal
subclavian artery and ascends through the
transverse foramina of the cervical vertebrae. It
then passes posteriorly around the articular
process of the atlas to enter the skull through
the foramen magnum. The two vertebral
arteries join each other to form the basilar
artery. The vertebral artery gives rise to
anterior and posterior spinal arteries, the
posterior inferior cerebellar artery and
branches to the medulla.
B. Vertebrobasilar
System

 1. The Vertebral A.
 2. Basilar artery : It is formed by the two
vertebral arteries joining each other in the
midline. It ascends along the ventral aspect of
the pons. It ends at the ponto-midbrain
junction where it divides into two posterior
cerebral arteries. It gives rise to anterior inferior
cerebellar artery, superior cerebellar artery and
numerous paramedian, short and long
circumferential penetrators.
 3. Posterior cerebral artery (PCA): The basilar
artery ends by dividing into the two posterior
cerebral arteries. They anastomose with the
posterior communicating arteries to complete
the circle of Willis. Many small perforating
arteries arise from PCA to supply the midbrain,
the thalamus, hypothalamus and geniculate
bodies.
C.Circle Of Willis
 It is a network of blood vessels present at the
base of the brain. This polygon of blood vessels
is formed by the proximal parts of the two
anterior cerebral arteries connected by the Ant.
Communicating A. and the proximal parts of the
two posterior cerebral arteries connected to the
distal internal carotid arteries by the posterior
communicating arteries. However fifty per cent
of circles have hypoplastic or absent segments
and the potential for collateral flow is not always
as good as it might first appear.
D. Venous drainage
 Venous blood flows peripherally via superficial
cerebral veins and centrally via the deep cerebral
veins into the venous sinuses (which lie between
the outer endosteal and the inner meningeal layer
of the dura) which drain into the internal jugular
vein. The cerebral veins are thin walled and have
no valves. There are numerous venous
connections between cerebral veins and dural
sinuses and venous systems of the meninges,
skull, scalp and nasal sinuses so facilitating
propagation of thrombus or spread of infection
between these vessels.
CEREBRAL CIRCULATION
AUTOREGULATION
Cerebral Blood Flow
 The cerebral blood flow, represent 15-20% of the
cardiac output. This is equal to 750ml/min or
50ml/100g/min.
 Although, the adult brain weighs only 1.4 kg
but, it’s uses 20% of the basal oxygen
consumption of the body. This is equal to 50 mls
O2/min or 3-3.5 mls/100g/min.
 Cerebral Blood Flow (CBF) = Cerebral Perfusion
Pressure (CPP) divided by the Cerebral Vascular
Resistance (CVR).
 CBF=CPP / CVR
Cerebral Blood Flow
 CPP:- Is the pressure driving the flow of blood
through the brain.
 CPP= MAP – (The greater of the ICP or Cerebral

Venous Pressure). This type of situation referred


to as “Starling Resistor mechanism”.
 In normal conditions the ICP is higher than the

Cerebral Venous Pressure). So


CPP = MAP – ICP.
Control of cerebral blood flow
 Autoregulation is the maintenance of a constant
blood flow to an organ in the face of changing
arterial pressure.
 Cerebral Autoregulation mainly concerns with the
alteration in CVR (cerebral vascular resistance).
 Alteration in CVR is achieved by:
 Vasoconstriction and vasodilatation of vessels.
Control of cerebral blood flow
 Principal mechanisms responsible for the control
of cerebral vascular resistance (CVR):

 Myogenic hypothesis.
 Metabolic hypothesis.
 Chemical factors.
 Neurogenic Regulation.
MYOGENIC- PRESSURE
AUTOREGULATION
 The myogenic hypothesis states that when
vascular smooth muscle is stretched, it contracts.
 Thus, if arterial pressure is suddenly increased,
the arterioles are stretched and the vascular
smooth muscle in their walls contracts in response
to this stretch.
 Contraction of arteriolar vascular smooth muscle
causes constriction (i.e., increased resistance),
thereby maintaining a constant flow in the face of
increased pressure. Remember the hydrulic
equation of ohm’s law Q = ΔP/R.
MYOGENIC- PRESSURE AUTOREGULATION
 Response begin within seconds of a change in CPP and
is complete between 10s and 2 minutes.
MYOGENIC- PRESSURE AUTOREGULATION
 In chronic hypertensive patients, the curve will be shifted
to the right. The main point to know here that the lower
limit of the autoregulation is also shifted to the right.
MYOGENIC- PRESSURE AUTOREGULATION

 In neonates, the pressure autoregulation is left-


shifted in comparison to the adult curve.
 The plateau is narrower (from 30-90 mmHg),
and slops upward to the right.
 The neonates have a lower BP so it’s
physiologically appropriate that the curve is
left-shifted.
 The decrease in the upper limit means that the
neonate is less able to tolerate high BP.
Metabolic hypothesis
 It refers to the ability of a tissue to adjust it’s blood
supply so that it receives sufficient blood flow to
carry out it’s functions.
 Increase metabolic activity in the brain is
associated with an appropriate increase in
perfusion to supply increased oxygen and other
metabolite and to remove wastes.
 This relationship between flow and metabolism is
known as Flow-Metabolism Coupling.
 Metabolic regulation is important for minute to
minute regulation of regional CBF even though
global CBF may remain relatively constant.
 As a result of metabolic activity, the tissues
produce various vasodilator metabolites (e.g.,
CO2, H+, K+ lactate, and adenosine). The
greater the level of metabolic activity, the
greater the production of vasodilator
metabolites.
 These metabolites produce vasodilation of
arterioles, which decreases resistance and,
therefore, increases flow to meet the increased
demand for O2.
CHEMICAL FACTOR
PaCo2

 The cerebral circulation is most sensitive to PaCO2.


 Co2 is very potent cerebral vasodilator.
 The curve is almost linear between an arterial Pco2 from
20-80mmHg.
 The normal Pco2 is at about the midpoint of the steep part
of the curve allowing maximal sensitivity in both direction.
CHEMICAL FACTOR:
Arterial Po2
 The reason that the CBF does not increase until
the arterial Po2 falls down below 50 mmHg is
related to the shape of the ODC (O2 dissociation
curve) for hemoglobin.
 The blood oxygen content is not much altered,
while we are still on the flat upper part of the
ODC.
 As Pao2 falls below 50 mmHg, the o2 content of
the blood falls rapidly.
 So, there is no much decrease in cerebral O2
supply until this level is reached.
 Cerebral arterioles start to vasodilate and CBF
increases to maintain adequate O2 delivery.
NEUROGENIC REGULATION
 The sympathetic nervous system is not very important in
the cerebral circulation for causing changes in CVR.
 Changes in the CBF due to autonomic stimulation can at
best alter CVR about (5-10%).
 Despite this, the nervous system is extremely important
in CBF regulation, because of it’s effect on the CPP.
 The carotid baroreceptors monitor the MAP, if the
pressure falls, the signal firing from the carotid sinus
decrease, and this will result in powerful sympathetic
stimulation to the heart (increase HR & contractility) and
to peripheral circulation (vasoconstriction) in attempt to
maintain MAP sufficient for brain and other tissue.
Thank you…
References
 Linda S. Costanzo physiology 3rd edition.
 Kerry Brandis, The Physiology Viva.
 Medical Physiology, Guyton 11th edition.
 http://www.doctorslounge.com
 http://www.anaesthetist.com
 http://www.medscape.com

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