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Pathophysiology of Hemorrhage

1. The document discusses the pathophysiology of cerebral ischemia and stroke, from initial vascular damage and impaired blood flow, to cellular hypoxia and initiation of the ischemic cascade. 2. It describes the progression from transient ischemic attack to irreversible cerebral damage as tissues are deprived of oxygen and nutrients. 3. The cascade ultimately leads to structural breakdown, loss of neural feedback and physiologic functions, and ultimately cerebral death if perfusion is not restored in time.

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Jubelle Sipalay
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117 views3 pages

Pathophysiology of Hemorrhage

1. The document discusses the pathophysiology of cerebral ischemia and stroke, from initial vascular damage and impaired blood flow, to cellular hypoxia and initiation of the ischemic cascade. 2. It describes the progression from transient ischemic attack to irreversible cerebral damage as tissues are deprived of oxygen and nutrients. 3. The cascade ultimately leads to structural breakdown, loss of neural feedback and physiologic functions, and ultimately cerebral death if perfusion is not restored in time.

Uploaded by

Jubelle Sipalay
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as DOCX, PDF, TXT or read online on Scribd

GIT

Relaxation of
intestines and
sphincters

Loss of bowel
control

GUT

Neurogenic bladder Loss of sphincter


control

Other systems Pulmonary


Cardiovascular GIT GUT
system failure system failure failure failure

Dopami
Systemic failure

Norepinephri

DEATH
Structural integrity loss of brain
tissue and blood vessels

Breakdown of the protective


Blood Brain Barrier
Mgt: Monitor Neuro
Cerebral Edema V/S

Vascular Congestion
Mannit
Compression of tissue
Dexamethas
Increased ICP

Impaired perfusion and function Dobutami

Continued insufficiency of blood

Further compression of tissues

Coma
Dx: GCS 3

Cerebral Death
Sx:
Loss of neural feedbacks Fixed, dilated pupils,
5mm
Cessation of physiologic functions GCS 3 (E1, V1, M1)

Cardiovascular Pulmonary GIT GUT Other systems

Dx: ECG 12 Parac


Leads Cardiovascular etam
ol
Findings:
Diminished S T
Loss of cardiac Relaxation of
waves muscle fxn venous valves
Dopami
Decreased cardiac
output
Dobutami

Cardiopulmonary
arrest

Pulmonary

Failure of Loss of lung


accessory muscles movement
for breathing

Cardiopulmonary Mgt: Intubate under direct


arrest laryngoscopy ETT size 8.0mm
PREDISPOSING FACTORS
PRECIPITATING FACTORS
Age Hypertension
Heredity Non-compliance
Sex (men) to meds
Prior stroke Atherosclerosis
Lifestyle

Dx: CXR AP
Findings:
Atherosclerotic Aorta

Dx: Brain CT Scan


Findings: Massive
Thalamic Bleed (L)
with IV Extension &
Obstructive
Hydrocephalus

Cerebral hypoperfusion

Impaired distribution of O2 &

Tissue hypoxia and cellular

Cerebral Ischemia

Initiation of Ischemic cascade

Damage to the blood vessel

Transient Ischemic Attack

Brain sustains irreversible


cerebral damage

Breakdown of collagen,

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