PATHOPHYSIOLOGY OF LEFT CEREBRAL INFARCTION

Legend: Etiology Disease process

Signs and symptoms

Modifiable risk factor: Diabetes mellitus

Non-modifiable risk factors: Genetics: Family Hx of HPN Age: 70 Race : Asian

Laboratory Studies Therapeutic intervention

X-ray Aorta is calcified Impression: Atheromatous aorta

serum lipid in the bloodstream Lipid accumulate in the blood vessel wall Diameter of the blood vessel wall narrows blood flow through the blood vessel blood supply to the kidney blood supply to the myocardium SA node is damaged Prolonged low blood supply Electrical impulse is affected Cardiac rhythm is altered Lipid buildup in the blood vessel wall Heart pumps harder to meet bodys O2demand pressure exerted by the blood on the blood vessel wall

Damage to glomeruli permeability of glomeruli membranes RBC passes through the glomeruli membrane glomerular filtration

PACEMAKER INSERTION

kidney tubular reabsorption sodiumreabs orption

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Atrial fibrillation

Atheroma is dislodged

RBCescape into the urine

urine output

Na retains fluid

Embolus travels through the blood vessel Passes through the internal carotid artery

Urinalysis: RBC : 6-10/hpf

Fluid accumulates in the interstitial space

Edema

Embolus reaches the Left middle cerebral artery

CT Scan Impression: Left middle cerebral artery districution

Embolus occludes the vessel Blood supply is disrupted O2 supply to brain cells is diminished Cells cannot proceed with aerobic respiration Mitochondria switches to anaerobic respiration Less ATP is produced Lactic acid is produced

Less ATP to power cellular activities Membrane pump fails

Sodium and calcium ions will rush into the cell

Glutamate will exit the cell

Cerebral cells begin to die Damage to brain stem

Brocas area is affected

Damage to Left Frontal Lobe

Gag reflex is diminished

Motor control is diminished

Control of speech is diminished

Level of Consciousness is altered

Gastric acid aspiration

Aspiration pnemonia

Right sided paralysis

Aphasia

Stupor

Unproductive Cough