Neurology Seminar

Cerebral Blood FlowCerebral Perfusion

Cerebral Metabolism

Outline

Anatomy of the vascular system Arterial Venous

Physiology of the vascular system Cerebral blood flow Cerebral perfusion Cerebral metabolism

Anatomy of the vascular systemOverview

Brain has two major arterial systems Carotid = cerebral hemispheres Vertebrobasilar = post fossa, occipital lobe, part

of the temporal lobe

Interconnections Circle of Willis

Surface of the neuraxsis= large circumferential arteries

Deep structures = smaller penetrating arteries and arterioles

Anatomy of the vascular system

Anatomy of the vascular system

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

Vertebral a. branch of subclavian a. Trans. cervical foramen Foramen magnum Frequent anatomic variation

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 systemCircle of Willis

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 systemBlood supply of cerebral hemispheres

Anterior cerebral a. Medial surface of cerebrum Superior border of frontal and

parietal lobe Middle cerebral a.

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.

Occipital lobe Inferior and medial temporal lobe

Penetrating branches of big a supplydeeper struct.

Lenticulostriate a. of MCA for BG andInt. cap

Perforating br of PCA for thalamus

Anatomy of the vascular systemAnastomoses and collateral circulation

Circle of Willis Corticomeningeal anastomoses

The 3 major a. on the surface of hemis. b/n extra and intracranial a.

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 systemBlood supply of posterior fossa

Neurologic signs

Carotid system Hemiparesis

(contralateral body and face) Hemisensory loss

(contralateral body and face)

Homonymous hemianopia

Monocular visual loss Aphasia

Vertebrobasilar Hemiparesis

(contralateral body, ipsilateral face)

Hemisensory loss (contralateral body, ipsilateral face)

Diplopia Dysphagia Dysarthria Dysequilibrium

Anatomy of the vascular systemVenous system

Superficial and deep system SSS

Superficial v. of sup half of brain Lateral Sinus

Inferior half Deep system (great v. of Galen and inferior sagittal and strait sinus)

Deep white matter & deep brain nuclei Cavernous sinus

Inferior cerebral surface Carotid a., cranial n.,

Anatomy of the vascular systemVenous system

Anatomy of the vascular systemVenous system

Physiology of the vascular system

Cerebral Blood Flow (CBF) 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

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 Too much blood can raise ICP

CBF > 55 to 60 ml per 100 g per minute

Physiology of the vascular system

Cerebral Perfusion Pressure (CPP) net pressure of blood flow to the brainCPP = 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

Autoregulation 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

Autoregulation 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

Factors affecting CBF (the ff equation)=Mean arterial pressure - central venous pressure

Cerebro-vascular resistance

Extra cerebral Systemic BP CV function Blood Viscosity

Intra cerebral Cerebral vasculature CSF pressure Auto regulatory mechanisms

Physiology of the vascular system

Physiology of the vascular system

Regulation of CBF Metabolic regulation Auto regulation Chemical factors Neurogenic factors

Physiology of the vascular system

Metabolic regulation 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

Adenosine, K+, H+, prostaglandin, free radicals, NO

Physiology of the vascular system

Physiology of the vascular system

Auto regulation 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 systemRegional increase in metabolism

CO2

Local vasodilatationIncreased blood flow

Accommodate metabolic demand

Physiology of the vascular systemRegional ischemia (occlusive disease)

Intra Luminal pressure

oxygen CO2

lactate Acidotic tissue

Vasodilatation of nearby vessels

Increase blood flow to the area of ischemia

Reduce size of infarct

Reduced cerebro-vascular resistance (infarct zone)

Physiology of the vascular systemReduced cerebro-vascular resistance

Little change in CVP

Major determinant of BF to the region

of ischemia will be MAP

Proper maintenance of SBP in Mx of

ischemic stroke

Physiology of the vascular system

Chemical factors 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

Lactic acid is a potent vasodilator

Physiology of the vascular system

Physiology of the vascular system

Neurogenic control Not as strong as the chem. And metab. Composed of

Extrinsic control Intrinsic control Local components

Physiology of the vascular system

Cerebral Metabolism High metabolic activity & high O2 consumption Energy dependant processes

Membrane potential Maintainace of trans-membrane ion gradient Membrane transport Synthesis of cellular constituents

Prot, Nucleic acid, Lipids, NT Energy supplied by high energy phosphate

bond (ATP), synthesized in brain. Glycolytic pathway Krebs cycle 38 moles of ATP/ mole of glucose Respiratory chain (aerobic)

Anaerobic 2 ATP Creatine Phosphate from ADP glycogen

Cerebral Metabolism

Cerebral Metabolism, ischemic cascade

in CBF -> in glucose and Ox. Less impaired function at the periphery

Local auto regulatory mech, response to chemical & metab changes is lost

Anaerobic glycolysis Fall in glycogen and pH Rise in lactate Zone of increased perfusion in the

periphery of ischemic zone

Cerebral Metabolism, ischemic cascade

Substrate depletion->mitoch. failure Leakage of K from cells IC Na, Cl, Ca, free fatty acids Neuronal depolarization

Loss of trans membrane potentialincrease in tissue waterImpaired ATP dependent NT uptake

Cerebral Metabolism, ischemic cascade

release of excitatory NT glutamate which activates NMDA and AMPA receptors 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

IC Ca-> activates Phospholipases Protease membrane Endonuclease mitoch. DNA cell Ox free radical microtubular damage

death Nitric oxide

Ischemic Penumbra

Ischemic Neuronal Injury (cascade)

Ischemic Neuronal Injury (cascade)

Incomplete Ischemia

Local accumulation of AdenosinePotassium

Hydrogen Ion

Lactic acid accumulation

Vasodilatation

Restoration of blood supply

Complete Ischemia

Cell swelling

Infarction

Affection of BBB

Water content of Brain tissue Increases

BRAIN EDEMA

Scavenger cells

Cystic cavity

Enough glucose

Hypoxia

Enough glucose

Lesser degree ofanoxic change

Hypoglycemia

Adequate Ox

Energy maintained By creatinine Phos.

GENERAL MANAGEMENT Resuscitation – Ox and BP Urgent situations - elevated ICP, (GCS)<8 Monitoring and the decision to treat - ICP <20 mmHg

and CPP between 60 and 75 mmHg 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 Mannitol Corticosteroids (Corticosteroid Randomization After Significant Head

injury) trial enrolled 10,008 Hyperventilation 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