cbf & its regulation-1.2

8/6/2019 CBF & Its Regulation-1.2

1/47

Cerebral circulationerebral circulation


2/47

Adult human brain weighs approx : 1350 gmabout 2% of body weight

Cranial vault rigid structure with a fixed total volumeBrain Tissue (80 %)Blood (12%)CSF (8%)

Recieves 12-15% of cardiac outputReflects brains high metabolic rate


3/47

Normally brain consumes- 20% of total body O60% - to support neuronal activityto generate ATPS

Cerebral metabolic rate (CMR) measured interms of O consumption (CMR O )

Approx 3- 3.8mL/100g/min OR 50mL/min

Greatest in gray matter of cerebral cotrex


4/47

CEREBRALCEREBRAL

METABOLISM:METABOLISM: 2% of body weight

17% of Cardiac output consumption at rest

20% of inspired oxygen

60% - for neuronal activity

40% - to maintain cellular integrity

CMR / CMRO 2 - 3-3.8ml/100g/min50ml/min

Cerebral glucose consumption - 5mg/100g/min


5/47

cerebral blood flow

80% - Internal carotid arteries

20% - Vertebral arteries

Anterior n posterior communicatingarteries

Circle of Willis Communication between exl & int

carotids opthalmic arteries


6/47

Circle of willis


7/47

Physiology of CBF

Parallels with metabolic activity

Can vary from 10 300 ml/100g/min

Average 50ml/100g/min

Gray matter 80ml/100g/min

White matter- 20ml/100g/min

Total CBF- averages 750ml/min

< 20-25ml/100g/min- ischemia


8/47


9/47 Time (min )

C BF

( m l / 1 0 0 g / m

i n )


10/47

FACTORS CONTROLLING CBF

Intrinsic factors Myogenic Regulation

Metabolic Regulation

Neuronal Regulation

Hormonal Regulation


11/47


Extrinsic factors Respiratory gas

Arterial BP Hematocrit Temperature


12/47

SAFETY FACTOR

Normal brain receives

3x required oxygen

7x required glucose

Anoxia is the initial component of ischemia.

Hippocampus

cerebellem

Most sensitive to

hypoxic injury


13/47

Cerebral perfusion pressure

CPP is the difference between Meanarterial pressure and intracranialpressure (or central venous pressure,which ever is greater)

CPP = MAP ICP


14/47

CPP = MAP - ICP

Normal CPP 80 to 100mmHgMore dependent on MAP

ICP > 30mmHg compromise CPPCPP

< 50mmHg slowing of EEG25 40 mmHg flat EEG< 25 mmHg irreversible brain damage


15/47

Cerebral auto regulation

Ability of the cerebral blood vessels to

alter their caliber in order to maintain aconstant flow in face of variations in

blood pressure


16/47


CBF is kept constant over a wide range of

MAP ( 50 160 mm Hg )

CPP = MAP CVP = MAP - ICP

MAP Cerebral vasoconstriction

MAP Cerebral vasodilatation

Constant CBF is maintained


17/47


graphPressures above160mmHg

Disrupts BBB

Cerebral edema

Haemorrhage

40 C B F

( m l / 1 0

0 g / m i n

)

60 120 180MAP (mmHg)


18/47

Auto regulation

Autoregulatory changes take time

up to 60 sec

Large MAP changes may cause increasedCBF even in presence of intact autoregulation

In Hypertensive persons autoregulatory rangeshifts to higher pressure levels : 180 200mm Hg


19/47

Dynamic v s Static

Dynamic auto regulation describes the

CBF response that takes place over

seconds in response to a sudden drop in

CPP.

Static / slower auto regulation is thesteady state achieved over 1 5 min


20/47

Changes in autoregulation

Absent ( Vasomotor paralysis )brain traumasurgical retraction

high ICPbrain tumor seizures

Shift to rightSystemic hypertension

States of sympathetic activationShift to left

Volatile anesthetic agents


21/47


Intrinsic factorsMyogenic Regulation

Metabolic Regulation

Neuronal Regulation

Hormonal Regulation

Extrinsic factorsRespiratory gas

Arterial BPHematocritTemperature


22/47

Myogenic factors

Is the intrinsic response of smooth muscle cells in cerebralarterioles to changes in MAP

Protective mechanism againstexcessive pressure fluctuationat capillary level


23/47

Metabolic regulation

NO

Hydrogen ions

potassium

adenosine

prostanoids


24/47

Innervation

The sympathetic fibers arise mainly from thesuperior cervical ganglion

The parasympathetic from the sphenopalatineand otic ganglia

Sensory fibers from the trigeminal ganglion

The functional significance of neural innervationshas yet to be elucidated.


25/47

Neuronal regulation

-Adrenergic receptors in arterial smooth muscle

Postganglionic sympathetic fibers releasenoradrenaline

Causes smooth muscle contraction and

arterial constriction

Sympathetic innervation is responsible for vascular tone


26/47

Sympathetic

Large & Medium sized arteries

normally overridden by autoregulation

Historically thought to have no role in cerebral circulation

Comes into play in states of excessive circulatoryactivity / pathologic states

Role in prevention of cerebral hge cerebral vasospasm


27/47

Effect of CO 2 on CBF

CBF directly proportional to PaCO2 between tension 20 80 mmHg

1mmHg PaCO2- CBF by 1-2ml/100g/min

After 24 48 hrs CSF HCO 3 - compensation limits theeffects of hypocapnia/ hypercapnia

Persistent hyperventilation L/ODC cerebralimpairment


28/47

Hypercarbia - CBF

The relationshipbetween PaCO2 andCBF is sigmoid

with plateaus below25 mmHg and above75 mmHg.

The slope isapproximately linear


29/47

Mechanism of CO 2 on CBF

The mechanism of CO 2 induced changes in vessel caliber

An increase in perivascular H+ concentration

Associated NOS activation

An increase in intracellular cGMP

K+ efflux

A reduction in intracellular Ca + + resulting in dilation

NOS inhibition attenuates the

Cyclooxygenase inhibition CBF response to CO 2


30/47

Effect of oxygen

Hyperoxia minimal decrease in CBF

10%

Severe hypoxia PaO 2 < 50mmHg

Increases CBF


31/47

Haematocrit

in haematocrit

viscosity CBF

O 2 carrying capacity

haematocrit viscosity

CBF

Optimal haematocrit

30% to 34%


32/47

Temperature

CBF changes 5- 7% per OC

Hypothermia CBF & CMR

Pyrexia has reverse effect


33/47

Clinicalapplication


34/47

Applied aspects

Effects of anesthetic drugs on CBFVolatile anesthetics

Induction agentsAnesthetic adjunctsVasopressorsVasodilatorsNeuromuscular blocking agents


35/47

Volatile agents

Volatile agents dose dependent dilatation of

cerebral vessels

Impair auto regulation

Response to CO 2 retained

May increase cerebral blood volume

May result in elevated ICP


36/47

HalothaneHas greatest effect onCBFCon.> 1% -abolishes auto

regulationGeneralized increasein CBFAt equivalent MACCBF up to 200%Prior hyperventilationto be initiated

IsofluraneCBFAuto regulation maintained upto 1 MAC

is > in sub cortical thanneocortical areas

At equivalent MACCBF up to 20%Simultaneous hyperventilationcan prevent in ICP


37/47

Sevoflurane :CBF effects similar to isofluraneProduce slightly less vasodilationAuto regulation maintained up to 1.5 MAC

Desflurane:CBF similar to isofluranebut at >1 MAC > sevoflurane.Autoregulation progressively abolished as doseincreases


38/47

Nitrous Oxide:When administered on its own- increasesboth CBF and metabolism.

when added to a background of another anesthetic, it increases CBF withoutchanging metabolism

It is a direct acting and potent cerebralvasodilator


39/47

IV induction agents

Intravenous anesthetics reduce CBF ina dose dependent fashion

coupled to the reduction in metabolism

Once maximal suppression of

metabolism occurs, no further reductionin CBF occurs


40/47

Barbiturates

Barbiturates maximal 50% reduction in CBFand metabolism

CO2 reactivity is maintained but is quantitativelyreduced compared to the awake response

Cerebral auto regulation maintained

intact


41/47

Propofol

Propofol produces a coupled dose dependentreduction in CMRO 2 and CBF

High doses vasodilator effect overcomes thecoupling & CBF increases

Both CO2 responses and auto regulation are

maintained intact in the normal brainIn head injured patients static auto regulationmay be impaired by high propofol infusion rates


42/47

Ketamine

Dilates the cerebral vasculature andincreases CBF ( 50 60%)

Increases in CBF, CBV, CSF volume canincrease ICP markedly in patients withdecreased IC compliance


43/47

Opioids

Opioids at low doses produce very little effect onCBF (provided CO2 is not allowed to rise)

Auto regulation remains intactBP vasodilatation to maintain CBF

cerebral blood volume

increase intracranial pressure.


44/47

Vasopressors

With intact auto regulation & BBB

in CBF occurs when

MAP150 160mmHg

In the absence of auto regulation,

vasopressors CBF


45/47

Vasodilators

In the absence of hypotension

Cerebral vasodilatation

CBFWith Hypotension

CBF is maintained

CBV & ICP in patients with ICcompliance


46/47

NMBD

No direct effect on CBF

Histamine releasing agents can causehypotension , CPP


47/47

Thank you

cbf & its regulation-1.2

Documents