Anaphysio 9b Cva Bleed Vs Infarct
Anaphysio 9b Cva Bleed Vs Infarct
Anaphysio 9b Cva Bleed Vs Infarct
Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage ICH (within the
brain) and subarachnoid hemorrhage SAH (between the inner and outer layers of the tissue
covering the brain).
Intracerebral hemorrhage
Bleeding occurs directly into the brain
parenchyma. The usual mechanism is
thought to be leakage from small
intracerebral arteries damaged by
chronic hypertension. Other
mechanisms include bleeding diatheses,
iatrogenic anticoagulation, cerebral
amyloidosis, and cocaine abuse.
Intracerebral hemorrhage has a
predilection for certain sites in the
brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the
brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by
the mass effect of the hematoma. Blood vessels carry blood to and from the brain. Arteries or
veins can rupture, either from abnormal pressure or abnormal development or trauma. The blood
itself can damage the brain tissue. Furthermore, the extra blood in the brain may increase the
pressure within the skull (intracranial pressure (ICP)) to a point that further damages the brain .
Subarachnoid hemorrhage
The pathologic effects of subarachnoid
hemorrhage (SAH) on the brain are multifocal.
SAH results in elevated intracranial pressure
and impairs cerebral autoregulation. These
effects can occur in combination with acute
vasoconstriction, microvascular platelet
aggregation, and loss of microvascular perfusion, resulting in profound reduction in
blood flow and cerebral ischemia.
Internal carotid arteries, which carry blood from the heart along the front of the neck
Vertebral arteries, which carry blood from the heart along the back of the neck
In the skull, the vertebral arteries unite to form the
basilar artery (at the back of the head). The internal
carotid arteries and the basilar artery divide into
several branches, including the cerebral arteries.
Some branches join to form a circle of arteries (circle
of Willis) that connect the vertebral and internal
carotid arteries. When the large arteries that supply
the brain are blocked, some people have no symptoms
or have only a small stroke. But others with the same
sort of blockage have a massive ischemic stroke. Why? Part of the explanation is collateral
arteries. Collateral arteries run between other arteries, providing extra connections. These arteries
include the circle of Willis and connections between the arteries that branch off from the circle.
Some people are born with large collateral arteries, which can protect them from strokes. Then
when one artery is blocked, blood flow continues through a collateral artery, sometimes
preventing a stroke. Small collateral arteries may be unable to pass enough blood to the affected
area, so a stroke results
Commonly, blockages are blood clots (thrombi) or pieces of fatty deposits (atheromas, or
plaques) due to atherosclerosis. Fatty deposits can cause two types of obstruction:
Cerebral thrombosis is a thrombus (blood clot) that develops at the site of fatty plaque
within a blood vessel that supplies blood to the brain.
Cerebral embolism is a blood clot that forms in the heart or large arteries of the upper
chest or neck, or at another location in the circulatory system. Part of the blood clot
breaks loose, enters the bloodstream and travels through the brain’s blood vessels until it
reaches vessels too small to let it pass. A main cause of embolism is an irregular
heartbeat called atrial fibrillation. It can cause clots to form in the heart, dislodge and
travel to the brain.
Blood clots in a brain artery do not always cause a stroke. If the clot breaks up spontaneously
within less than 15 to 30 minutes, brain cells do not die and people's symptoms resolve. Such
events are called transient ischemic attacks (TIAs).