Pathophysiology of CvD

D!SEASE PROCESS












ACENT
unknown
HOST
Predisposing factors
Cender:Nale
Age:Elderly
Smoker
Alcoholic
family history of
hypertension
high fat diet
sedentary lifestyle

ENv!RONNEN'
none
Organ affected the heart and the right side of
the brain (Basal Canglia)
Altered cerebral
metabolism
!ncreased
intracellular calcium
and released in
glutamate

ysfunction of vascular endothelial cells, increase fat deposit on the wall of the
blood vessels.
asoconstriction
Some fragments joins in
circulation then it goes
to small vessels and
clog. 'here will be an
obstruction/ interruption
of O2 supply due to
decrease blood supply.
Acute intracerebral hemorrhage of blood
vessel at the left basal ganglia
Blockage of the blood
vessel, as a result there is
insufficient oxygen and
nutrients supply carried by the
blood (hypoxia) and there will
be a decreased in cerebral
perfusion.
estruction of cell
membrane and
asoconstriction and
generation of free
radicals

Enlarges the area of
infarction into the
penumbra (loss of
inadequate supply of
oxygen and glucose),
Cell injury, necrosis
(hemorrhage),
'emporary neurologic
defects
Strokeleft sided
paralysis
CONPL!CAT!ONS
unstable BP
sensory impairment
acute infection
(Hyperthermia)

Arterioles constrict, then the heart has to

work harder to pump blood through the
smaller space, and the pressure inside
the vessels grows. As compensation the
heart will increases its pumping workload
as to supply the body.
Patient's
manifestations:
Headache
Hemiplegia
Ataxia
ysphagia
ysarthria
Expressive aphasia
Cognitive eficits
Book Base
izziness, Homononymous hemianopsia,
, Loss of peripheral vision, iplopia,
Hemiparesis, Hemiplegia, Ataxia
ysphagia, ysarthria, Paresthesia,
Expressive aphasia, Receptive aphasia,
Clobal aphasia, Cognitive eficits,
Emotional eficits