Transcript Neurology seminar - Selam Higher Clinic

Neurology Seminar
Cerebral Blood Flow
Cerebral Perfusion
Cerebral Metabolism
Outline
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Anatomy of the vascular system
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Arterial
Venous
Physiology of the vascular system
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Cerebral blood flow
Cerebral perfusion
Cerebral metabolism
Anatomy of the vascular system
Overview
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Brain has two major arterial systems
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Carotid = cerebral hemispheres
Vertebrobasilar = post fossa, occipital lobe, part
of the temporal lobe
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Interconnections
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Circle of Willis
Surface of the neuraxsis= large circumferential
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arteries
Deep structures = smaller penetrating arteries
and arterioles
Anatomy of the vascular system
Anatomy of the vascular system
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Internal carotids in the cranium
Carotid siphon
Lies within the cavernous sinus
Subarachnoid space->ophthalmic a.
Ant. and middle cerebral a.
Anatomy of the vascular system
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Vertebral a. branch of subclavian a.
Trans. cervical foramen
Foramen magnum
Frequent anatomic variation
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Lt. vertebral a. directly from aorta
Unequal caliber b/n the 2 vertebral a.
Ventrolateral surface of medulla
Unite at pons->basilar a.
Rt and Lt post cerebral a. at midbrain
Anatomy of the vascular system
Anatomy of the vascular system
Circle of Willis
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At the base of the brain
Surrounds the optic chiasm and pit.
stalk
Frequent anatomic variations 50%
Anatomy of the vascular system
Anatomy of the vascular system
Blood supply of cerebral hemispheres
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Anterior cerebral a.
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Middle cerebral a.
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Most of the lateral surface of
cerebral h.
Lateral frontal lobe
Sup and lat temporal lobe
Deep structures of frontal and
parietal lobe
Posterior cerebral a.
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Medial surface of cerebrum
Superior border of frontal and
parietal lobe
Occipital lobe
Inferior and medial temporal lobe
Penetrating branches of big a supply
deeper struct.
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Lenticulostriate a. of MCA for BG and
Int. cap
Perforating br of PCA for thalamus
Anatomy of the vascular system
Anastomoses and collateral circulation
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Circle of Willis
Corticomeningeal anastomoses
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The 3 major a. on the surface of hemis.
b/n extra and intracranial a.
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Ophthalmic a. of internal carotid with
superficial temporal and facial branch
of ext. carotid at face region.
Ext carotid and vertebral a. at the neck
Anatomy of the vascular system
Blood supply of posterior fossa
Neurologic signs
Carotid system
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Hemiparesis
Vertebrobasilar
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(contralateral body and face)
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Hemisensory loss
(contralateral body, ipsilateral face)
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(contralateral body and face)
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Homonymous
hemianopia
Monocular visual loss
Aphasia
Hemiparesis
Hemisensory loss
(contralateral body, ipsilateral face)
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Diplopia
Dysphagia
Dysarthria
Dysequilibrium
Anatomy of the vascular system
Venous system
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Superficial and deep system
SSS
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Lateral Sinus
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Inferior half
Deep system
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Superficial v. of sup half of brain
(great v. of Galen and inferior sagittal and strait sinus)
Deep white matter & deep brain nuclei
Cavernous sinus
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Inferior cerebral surface
Carotid a., cranial n.,
Anatomy of the vascular system
Venous system
Anatomy of the vascular system
Venous system
Physiology of the vascular system
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Cerebral Blood Flow (CBF)
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Amount of blood that enters the brain.
Brain is 2% of body weight
About 10% of the intra cranial space
About 15% of Cardiac output
50 ml Bl. per 100 gm of brain tissue/min
750 ml/ min
About 20% of Ox used at basal state
Total Ox used 50ml/min, 3.7ml/100gm
There is an oxygen metabolic reserve of only
8-10 seconds
Physiology of the vascular system
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Cortical gray matter has 6X bl. flow than
the white matter due to metab.demand
CBF is tightly regulated and maintained
within narrow limits
too little blood causes ischemia,
results if blood flow to the brain is below
18 to 20 ml per 100 g per minute,
 tissue death occurs if flow dips below
8 to 10 ml per 100 g per minute
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Too much blood can raise ICP
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CBF > 55 to 60 ml per 100 g per minute
Physiology of the vascular system
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Cerebral Perfusion Pressure (CPP)
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net pressure of blood flow to the brain
CPP = MAP − ICP
NL b/n 70-90 mmHg in an adult human,
Below 70 mmHg for a sustained period
causes ischemic brain damage
Children have pressure of at least 60
mmHg
Physiology of the vascular system
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Autoregulation
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Physiologic response where by CBF
remains constant and brain maintains
proper CPP over a wide range of Blood
pressures variations.
to lower pressure, arterioles dilate, and to
raise pressure they constrict.
At their most constricted, pressure of 150
mmHg,
At their most dilated the pressure is 60
mmHg.
Physiology of the vascular system
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Autoregulation
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When pressures are outside 50 to 150
mmHg, the blood vessels' ability to
autoregulate pressure through dilation
and constriction is lost, and cerebral
perfusion is determined by blood pressure
alone,
pressure-passive flow
Physiology of the vascular system
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Factors affecting CBF (the ff equation)=
Mean arterial pressure - central venous pressure
Cerebro-vascular resistance
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Extra cerebral
 Systemic
BP
 CV function
 Blood Viscosity
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Intra cerebral
 Cerebral
vasculature
 CSF pressure
 Auto regulatory mechanisms
Physiology of the vascular system
Physiology of the vascular system
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Regulation of CBF
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Metabolic regulation
Auto regulation
Chemical factors
Neurogenic factors
Physiology of the vascular system
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Metabolic regulation
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CBF is coupled directly to neuronal
metabolic activity
Occurs with short latency of 1-2 sec.
Strictly regional effect
Little effect on the total blood flow
E.g.. Sleep, coma, seizure
Vasodilator substances
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+
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Adenosine, K , H , prostaglandin, free radicals, NO
Physiology of the vascular system
Physiology of the vascular system
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Auto regulation
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The ability of brain to maintain its blood
flow constant for all but the widest
extremes in perfusion pressure
MAP 60-150 mmHg
Primarily pressure controlled myogenic
mechanism that operates independently
but synergistically with other neurogenic
and chemical metabolic mechanism.
Both small and large arterioles
Major homeostatic and protective
mechanism.
Physiology of the vascular system
Physiology of the vascular system
Physiology of the vascular system
Regional increase in metabolism
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 CO2
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Local vasodilatation
Increased blood flow
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Accommodate metabolic demand
Physiology of the vascular system
Regional ischemia (occlusive disease)
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 Intra Luminal pressure
 oxygen
 CO2
 lactate
Acidotic tissue
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Vasodilatation of nearby vessels
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Increase blood flow to the area of ischemia
Reduce size of infarct
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Reduced cerebro-vascular resistance (infarct zone)
Physiology of the vascular system
Reduced cerebro-vascular resistance
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Little change in CVP
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Major determinant of BF to the region
of ischemia will be MAP
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Proper maintenance of SBP in Mx of
ischemic stroke
Physiology of the vascular system
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Chemical factors
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Strong influence on CBF
Mech= sm ms, NT, pH
CO2 readily crosses BBB end product of
cerebral metabolism
 PaCO2= Vasodilatation &  CBF
 PaO2= Vasodilatation &  CBF
 pH= Vasodilatation &  CBF
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Lactic acid is a potent vasodilator
Physiology of the vascular system
Physiology of the vascular system
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Neurogenic control
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Not as strong as the chem. And metab.
Composed of
Extrinsic control
 Intrinsic control
 Local components
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Physiology of the vascular system
Cerebral Metabolism
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High metabolic activity & high O2 consumption
Energy dependant processes
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Energy supplied by high energy phosphate
bond (ATP), synthesized in brain.
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Membrane potential
Maintainace of trans-membrane ion gradient
Membrane transport
Synthesis of cellular constituents
 Prot, Nucleic acid, Lipids, NT
Glycolytic pathway
Krebs cycle
Respiratory chain
Anaerobic 2 ATP
Creatine Phosphate
38 moles of ATP/ mole of glucose
(aerobic)
from ADP
glycogen
Cerebral Metabolism
Cerebral Metabolism, ischemic cascade
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 in CBF ->  in glucose and Ox.
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Less impaired function at the periphery
Local auto regulatory mech, response
to chemical & metab changes is lost
Anaerobic glycolysis
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Fall in glycogen and pH
Rise in lactate
Zone of increased perfusion in the
periphery of ischemic zone
Cerebral Metabolism, ischemic cascade
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Substrate depletion->mitoch. failure
Leakage of K from cells
 IC Na, Cl, Ca, free fatty acids
Neuronal depolarization
Loss of trans membrane potential
increase in tissue water
Impaired ATP dependent NT uptake
Cerebral Metabolism, ischemic cascade
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 release of excitatory NT glutamate
which activates NMDA and AMPA
receptors
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permeability to Na ions
Cellular swelling and lysis
Massive entry of Ca into post synaptic
neurons ->more release of excitatory NT
Cerebral Metabolism, ischemic cascade
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 IC Ca-> activates
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Phospholipases
Protease
Endonuclease
Ox free radical
Nitric oxide
membrane
mitoch. DNA
microtubular damage
cell
death
Ischemic Penumbra
Ischemic Neuronal Injury (cascade)
Ischemic Neuronal Injury (cascade)
Incomplete Ischemia
Complete Ischemia
Lactic acid accumulation
Cell swelling
Enough glucose
Local accumulation of
Adenosine
Potassium
Hydrogen Ion
Infarction
Lesser degree of
anoxic change
Hypoxia
Affection of BBB
Vasodilatation
Restoration of
blood supply
Water content of
Brain tissue Increases
BRAIN EDEMA
Hypoglycemia
Scavenger cells
Energy maintained
By creatinine Phos.
Cystic cavity
Adequate Ox
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GENERAL MANAGEMENT
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Resuscitation – Ox and BP
Urgent situations - elevated ICP, (GCS)<8
Monitoring and the decision to treat - ICP <20
CPP between 60 and 75 mmHg
mmHg
and
Fluid management - avoiding all free water
Sedation decrease ICP by reducing metabolic demand, ventilator
asynchrony, venous congestion, and the sympathetic responses of
hypertension and tachycardia
Blood pressure control when CPP >120 mmHg and ICP >20
Position 30o to decrease venous outflow
Fever
Antiepileptic therapy
SPECIFIC THERAPIES
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Mannitol
Corticosteroids
(Corticosteroid Randomization After Significant
injury) trial enrolled 10,008
Hyperventilation
Head
1 mmHg change in PaCO2 = 3 percent
change in CBF, short-lived (1 to 24 hours)
Barbiturates reduce brain metabolism & cerebral blood flow
Therapeutic hypothermia
Removal of CSF 1 to 2 mL/minute, for two to three minutes at a time
Decompressive craniectomy