1 Patofisiologi Stroke

7/27/2019 1 Patofisiologi Stroke

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PATHOPHYSIOLOGY OF STROKE


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Perdarahan

Subarahnoid;

5%

Stroke Infark;

85%

Perdarahan

Intraserebral;10%

Stroke Infark

Perdarahan

Intraserebral

Perdarahan

Subarahnoid


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INRODUCTION

STROKE CLASSIFICATION

STROKE

85 %

Ischemic

15 %

Hemorrhagic

80 %

AT Stroke

20 %

Cardioembolic

50 %

ICH

50 %

SAB


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BRAIN INFARCTION

Normal metabolism and blood flow

Brain : A very metabolically active organ

Glucose as a sole substrate

Energy produced depends on oxygen presence

ATP as energy for

maintain neuronal integrity

keep Ca++ outside and K+ within the cells

Brain requirementO2 500 mL

Glucose 75-100 mgEach minute !!


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Cerebral Blood Flow (CBF)

53 ml/100 gm brain/minute (range 50-60)

Cerebral Metabolism Rate for Oxygen (CMRO2)

Cerebral O2 Consumption3.5 ml/mg/minute


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Cerebral Blood Flow (CBF) in 100mg/minute

If CBF decreases to 15-18 electrical failure

Below 15 change in somato-sensory evoked potential

Below 10 ionic failure

Extracellular K+ , Intracellular Ca++

Free fatty acid releases, ATP breakdown, intracellular acidosis

neuronal death


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Cerebral Blood Flow (CBF) in 100mg/minute

In 10-15 ml (between electrical and ionic failure)

Neuron not functioning, but still viable

These neuron appear in the periphery, around

infarcted area (perifocal area).

Their existence is determined by collateral system.

The area is calledPENUMBRA.It is a target of intervention !!.


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Clot

Area of core infarction

Ischemic penumbra Cells at risk but not permanently

20-50% of perfusion from collateral

circulation

Cells die quickly without reperfusion

The Ischemic Cascade

and Secondary Injury


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Metabolic and neuro-chemical changes

K+ moves across the cell membrane into the

extracellular space

potentiate and enhance celldeath

Production of O2 free radicals peroxidation fatty

acid in cell organelles and plasma membrane

damage cell functionAnerobic glycolysis accumulation of lactic acid

and lowering pH acidosis impaire cell

metabolic function


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Production of excitatory neurotransmitter (glutamate,

aspartate, kainic acid) Na+ and Ca++ influx into

cellsWater and Cl- follow Na+

cytotoxic edema


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Subarachnoid Bleeding

The causes :

Ruptured aneurysm

Ruptured AVM

Ruptured angiomaBlood dyscrasia

Aneurysm : found commonly in Willis circle and

its branchesAneurysm ruptures blood fills in subarachnoid

space and brain parenchym close to it.


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Complications of Subarachnoid Hemorrhage

Vasospasm :

Delayed narrowing of large capacitance

arteries at the base of the brain after SAHOften occurs at day 2 to 12 after the onset.

Hydrocephalus

Rebleeding : occurs in a few weeks after the onset

HyponatremiaSeizures

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1 Patofisiologi Stroke