Homeostasis

EDEMA
• Increased fluid in the interstitial tissue spaces
• Massive edema is called Anasarca.
• Fluid may also accumulate in body cavities
• These collections of fluid are referred to based on
location as:
– Hydrothorax, hydropericardium, hydroperitoneum (Ascites )
• maintained by opposing effects of vascular hydrostatic
pressure and plasma colloid osmatic pressure
Fluid Homeostasis

Homeostasis
Homeostasisisis
maintained
maintainedbybythe
the
opposing
opposingeffects
effectsof
of
vascular
vascularhydrostatic
hydrostatic
pressure
pressureand
andplasma
plasma
colloid
colloidosmotic
osmotic
pressure
pressure
Either
Eitherincreased
increased Edema
vascular
vascularhydrostatic
hydrostatic Development
pressure
pressureor
ordecreased
decreased Picture
plasma
plasmacolloid
colloid Fig 2.2
osmotic
osmoticpressure
pressurecan
can
lead
leadto
toEDEMA
EDEMA

Inflammatory
Inflammatory
mediators
mediatorscan
canalter
alter
vascular
vascular
permeability
permeabilitycausing
causing
local
localEDEMA
EDEMA
 Edema Fluid = TRANSUDATE

• A transudate is protein-poor (specific gravity

<1.012)
• An exudate is protein-rich (specific gravity
>1.020)
Pathophysiologic Categories of Edema

I. Increased
I. Increased
Hydrostatic
Hydrostatic
Pressure
Pressure
II. Reduced Plasma Oncotic Pressure
III. Inflammation
IV. Other
I. Increased Hydrostatic Pressure:
• Generalized increases in venous pressure, with
resultant SYSTEMIC EDEMA, occur MOST
COMMONLY in CONGESTIVE HEART
FAILURE”
• Thus, Congestive Heart Failure is the most
common cause of EDEMA due to Increased
Hydrostatic Pressure
Types of disease causing Edema:
A. Congestive Heart Failure
B. Portal Hypertension
C. Venous Thrombosis
 Congestive Heart Failure
• The Pump is FAILING!!! (All the blood going in IS
NOT going out!)
• Blood backs up, first into the lungs,
• then into the venous circulation - increasing Central Venous
Pressure (CVP)
• Increased CVP leads to increased capillary pressure
(Hydrostatic Pressure) leading to Edema
 Congestive Heart Failure

Overall, there are TWO main effects...

1. Increased Central Venous Pressure

(we just talked about this one…)
2. Decreased Renal Perfusion
 Congestive Heart Failure
Decreased Renal Perfusion
• Decreased Cardiac Output
• Leads to decreased ARTERIAL blood volume
• Activates the Renal Defense Mechanisms:
– Renin-Angiotensin-Aldosterone Axis
– Renal Vasoconstriction
– Increased Renal Anti-diuretic Hormone (ADH)
 Congestive Heart Failure
Decreased Renal Perfusion
• Decreased Renal Perfusion activates the Renal
Defense Mechanisms:
– Renin-Angiotensin-Aldosterone Axis
– Renal Vasoconstriction
– Increased Renal Anti-diuretic Hormone (ADH)
 Congestive Heart Failure
Renin-Angiotensin-Aldosterone Axis
Decreased Renal Perfusion
Renal Na
Renin Aldosterone
reabsorption

Plasma volume Renal retention of

Na + H2O

Transudation
EDEMA
 Congestive Heart Failure
Renal Vasoconstriction
Decreased Renal Perfusion

Renal Tubular Glomerular Filtration

Vasoconstriction reabsorption of Rate (GFR)
Na + H2O

Plasma volume Renal retention of

Na + H2O

Transudation
EDEMA
 Congestive Heart Failure
Renal Vasoconstriction
Decreased Renal Perfusion

Anti-Diuretic Renal retention of

Hormone (ADH) H2O

Plasma volume Renal retention of

Na + H2O

Transudation
EDEMA
Congestive Heart Failure

Central Renal
Venous Perfusion
Pressur
e Renin Renal ADH
Vasoconstriction
 Portal Hypertension
• Portal Hypertension is “Increased resistance to portal blood flow”
• The most common cause of Portal Hypertension is CIRRHOSIS.
• Pathogenesis of Ascites is complex
– Increased Portal Pressure (hydrostatic pressure) leads to increased liver
sinusoidal hypertension. Fluid moves into the Space of Disse then into
lymphatics
 Pathogenesis of Ascites is
complex
• Cirrhosis leads to hypoalbuminemia sneaking
into the next category
• And ultimately, there is decreased renal
perfusion leading to secondary
hyperaldosteronism (increased renin etc.)
 Cirrhosis
Portal Hypertension

Sinusoidal Serum Renal

Hypertensio Albumin Perfusion
n
Overwhelms Aldosterone
Hepatic Lymph Thoracic Duct

ASCITES
 Venous Thrombosis

• Impaired venous outflow increases hydrostatic

pressure
Pathophysiologic Categories of Edema

I. Increased Hydrostatic Pressure

II. Reduced Plasma Oncotic Pressure
III. Inflammation
IV. Other
 Reduced Plasma Osmotic Pressure
• Albumin is the serum protein MOST responsible for the
maintenance of colloid osmotic pressure.
• A decrease in osmotic pressure can result from increased
protein loss or decreased protein synthesis.
• Increased albumin Loss: Nephrotic Syndrome
– Increased protein permeability of the glomerular basement
membrane
• Reduced albumin synthesis
– Cirrhosis
– Protein malnutrition
Pathophysiologic Categories
of Edema
I. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic Pressure
III. Inflammation
IV. Other
 Inflammation

• Both Acute and Chronic Inflammation are

associated with EDEMA
Pathophysiologic Categories
of Edema
I. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic Pressure
III. Inflammation
IV. Other
Lymphatic Obstruction
 Lymphatic Obstruction

• Impaired lymphatic drainage with resultant

lymphedema, usually localized
– Usually due to INFLAMMATION or NEOPLASTIC
OBSTRUCTION
– Inflammatory (Filariasis - A parasitic infection affecting
inguinal lymphatics resulting in elephantiasis
Picture of Elephantiasis
 Neoplastic

• Resection and/or radiation to auxiliary lymphatic

can lead to arm edema
• Carcinoma of breast with obstruction of superficial
lymphatic can lead to an unusual appearance of the
breast - “peau d’orange” (orange peel)
GENERALIZED EDEMA
(Walker’s Law)
• HEART
• LIVER
• KIDNEY
 Edema
Morphology
• Edema of the Subcutaneous
Tissue is most easily detected
Grossly (not microscopically)
• Push your finger into it and a
depression remains
 Edema
Morphology
• Dependent Edema is a prominent feature of
Congestive Heart Failure
• Facial edema is often the initial manifestation of
Nephrotic Syndrome
• Pulmonary Edema is most
frequently seen in Congestive
Heart Failure
– May also be present in Renal
failure, Adult Respiratory
Distress Syndrome (ARDS),
Pulmonary Infections and
Hypersensitivity Reactions.
• The Lungs are typically 2-3
times normal weight
• Cross sectioning causes an
outpouring of frothy,
sometimes blood-tinged fluid
Normal Pulmonary Edema
Edema of the Brain :
• Trauma, Abscess, Neoplasm, Infection (Encephalitis), etc.
• The big problem is: There is no place for the fluid to go!!! The skull is the
limit.
• Herniation into the foramen ovale will kill

Subcutaneous Edema :
Annoying but Points to Underlying Disease
– However, it can impair wound healing or clearance of Infection.

Pulmonary Edema :
• May cause death by interfering with Oxygen and Carbon Dioxide
exchange
• Creates a favorable environment for infection
“Culture Media”
 Hyperemia and Congestion

• Hyperemia : is an active process resulting from

augmented tissue inflow due to arteriolar dilation (e.g.
acute inflammation).
• Congestion is a passive process resulting from
impaired outflows from a tissue
(e.g. cardiac failure or venous obstruction)
 Hyperemia
Infection
in Pneumonia
Hyperemia

(Pneumonia)
 Hemorrhage
• extravasation of blood due to rupture of blood vessels
– Rupture of a large vessel: Trauma, Atherosclerosis, Inflammatory or
Neoplastic Erosion
– Rupture of small vessels: hemorrhagic diathesis.
• May be external, into a body cavity or into a tissue
• hematoma: accumulation of blood enclosed or confined within
tissue
• petechiae: minute hemorrhages into skin or lining surface
 Hemorrhage
• Purpura (slightly larger hemorrhages than petechia)
• Ecchymoses (over 1-2 cm subcutaneous hematoma aka ‘bruise’).
• Accumulation of blood in a body cavity:
– Hemothorax
– Hemopericardium
– Hemoperitoneum
– Hemarthrosis
• The RBC’s in a hemorrhage are broken down:
– hemoglobin (red) → bilirubin (blue-green) → hemosiderin (golden-brown)
– That’s why bruises change color as they resolve
 Clinical Effects of
Hemorrhage
• <20% blood loss, little health effect in otherwise
healthy individuals
– But suppose you have heart or lung disease - could
decrease critical oxygen carrying capacity and →
‘heart attack’
 Clinical Effects of
Hemorrhage
• >20% blood loss, hemorrhagic shock
• Bleeding into the brainstem is fatal while same
blood loss from a finger cut is trivial
• Chronic recurrent bleeding can lead iron
deficiency anemia!
 Anemia from Blood Loss

• This may be the only hint of Occult Cancer

– Carcinoma of the Colon
– Gastric Carcinoma (less common)
 Hemostasis & Thrombosis
• Hemostasis is the normal, rapid formation of
a localized “plug” at the site of vascular
injury
• Thrombosis is the pathologic formation of a
blood clot within the non-interrupted
vascular system in a living person
 Hemostasis

• Normal - blood is flowing and not clotting

• Injury - blood is clotting and not flowing
• This works due to a daily interaction between the
vascular wall, platelets and the coagulation
cascade
 Thrombosis

• Abnormal activation of the normal hemostatic

process
• Thrombosis is Pathologic
 Hemostasis
• after initial injury, there is a brief period of
arteriolar vasoconstriction (neurogenic
reflex augmented by local factors such as
endothelin)
Vasoconstriction A transient effect
 Hemostasis

• Endothelial injury exposes the blood to the

extracellular matrix (ECM)
– The ECM is highly thrombogenic
– Platelets adhere, flatten and then activate
– To form hemostatic plug (primary hemostasis)
 vWF = von Willebrand Factor

summary
Flatten Recruit
Activate
Adhere Hemostatic
Plug
 Secondary Hemostasis

• Tissue factor together with platelet factors

activate the coagulation cascade with fibrin
deposition. Thrombin activation induces further
platelet recruitment and granule release
(secondary hemostasis)
 Secondary Hemostasis

• Polymerized fibrin and platelet aggregates to

form permanent plug
Secondary Hemostasis Pic
Anti-thrombotic Regulation
 Components of Normal
Hemostasis
• Endothelium
• Platelets
• Coagulation Cascade
 Endothelium

• Anti-thrombotic and Procoagulant Properties

– Anti-thrombotic - Anti-platelet, anti-coagulant and
fibrinolytic effects
– Procoagulant - Tissue Factor, vWF attachment
Figure 4-5 pro- anti coag
effects of endothelium
 Endothelial Anti-platelet Effects

• Physical Barrier
– prevent platelet contact with ECM;
• Endothelial production of prostacyclin and nitric
oxide inhibits platelet adhesion to normal
endothelium
 Endothelial Anticoagulant Effects

• Mediated by membrane-associated, heparin-like

molecules and thrombomodulin and anti-
thrombin III
 Endothelial Fibrinolytic Effects

• Synthesize tissue type plasminogen activation

(t-PA) promoting fibrinolytic activity
 Pro-thrombotic Properties
- Normal endothelium produces : von Willebrand factor
(vWF) facilitates adhesion of platelets to ECM
- Tissue Factor secretion by endothelium is induced by
cytokines or bacterial endotoxin
– Tissue Factor activates the extrinsic clotting pathway.
- Endothelial cells secrete plasminogen activator
inhibitors (PAIs) which depress fibrinolysis thus
promoting thrombosis
 Platelets
• When circulating are (membrane-bound smooth discs)
• They contain two specific types of granules:
alpha granules and delta granules.
1- Alpha: contain fibrinogen, fibronectin, factors V and VIII,
platelet factor 4, platelet-derived growth factor (PDGF), and
transforming growth factor ß (TGF- ß) .
2- Delata: contain adenine nucleotides (ADP and ATP), ionized
calcium, histamine, serotonin and epinephrine
 Platelet Activation

• On contact with ECM, platelets undergo:

(1) Adhesion and shape change
(2) Secretion (release reaction)
(3) Aggregation
 Platelet Adhesion

• Adhesion to ECM is mediated largely via

interactions with vWF which acts as a bridge
between platelet surface receptors and exposed
collagen.
 Platelet Secretion
• Both granules Explode soon after adhesion
• Calcium and ADP: potent mediators of
coagulation and platelet aggregation
 Platelet Aggregation

• ADP and thromboxane A2 (TXA2) stimulate further

platelet adhesion
• This sets up an autocatalytic reaction leading to an
enlarging platelet mass(the primary hemostatic plug)
• This is a ‘reversible’ collection of platelets
 Platelet Aggregation

• With activation of the coagulation cascade, thrombin is

generated, causing further aggregation then platelet
contraction constituting the secondary hemostatic plug
• This is an ‘irreversible’ fusion of platelets
Prostaglandin Balancing Act
• PG12 (endothelium)
– vasodilator
– inhibits platelet aggregation
• TXA2 (platelets)
– vasoconstriction
– Stimulates platelet aggregation
 Clinical Use of ASPIRIN in
Cardiac Patients
• Inhibits TXA2 Synthesis by platelets
• Benefits Patients at risk for Coronary Artery
Thrombosis
 “New”
Coagulation
Activates Activates

Cascade
Factor XII Tissue
Factor
Activates Activates
X
Xa

Prothrombin

Thrombin
Fibrinogen

Fibrin
 Coagulation Cascade
• Conversion of Pro-Factors to Activated Factors , ending in the
formation of Thrombin, Thrombin converts Fibrinogen to Fibrin,
Fibrin is critical for hemostasis.
• Each reaction is the result of the assembly of:
– Enzyme (activated) coagulation factor
– Substrate (pro-enzyme form of a coagulation factor)
– Co-Factor (reaction accelerator).
• Occurs on a phospholipid substrate
– Such as on the surface of activated platelets
– Held together by calcium ions
• This helps to Localize the thrombus
– To sites of platelet aggregation
Fig 4-7 Thrombosis
on a phospholipid
surface
Thrombosis
 Pathogenesis Of Thrombosis

Virchow’s triad
– endothelial injury
– stasis or turbulence of blood flow
– blood hypercoagulability
 Endothelial Injury
• exposure of subendothelial collagen and other
platelet activators
• adherence of platelets
• release of tissue factor
• local depletion of postacyclin (prostaglandin)
and plasminogen activator (PA)
 ALTERATIONS IN
NORMAL BLOOD FLOW
• turbulence of blood flow (arterial and cardiac
thrombosis); stasis of blood flow (venous
thrombosis)
• disrupt laminar flow and brings platelet in
contact with endothelium
• prevent dilution of activated clotting factors
 ALTERATIONS IN NORMAL BLOOD FLOW

• Retard the inflow of clotting factor inhibitors and

permit thrombi build-up
• Promote endothelial cell activation
• Aneurysms, mitral valve stenosis, hyperviscosity
syndromes (e.g. polycythemia)
 HYPERCOAGULABILITY

• any alterations of the coagulation pathways that

predispose to thrombosis
• primary (genetic) or secondary (acquired)
disorders
 HYPERCOAGULABILITY
(cont’d)
• mutation of factor V gene with functional deficiency
of protein C, and other anticoagulants (protein S,
antithrombin III). Patient will have venous
thrombosis and recurrent thromboembolism
• smoking, obesity, lupus anticoagulant with lupus
erythematosis (arterial and venous thrombosis)
 ARTERIAL THROMBI
• usually begin at site of endothelial injury and grow
in a retrograde direction from point of attachment
• typically are firmly adherent to the injured arterial
wall (atherosclerotic plaque) and are gray-white and
friable (mesh of platelets, fibrins, RBC, and
leukocytes)
 Arterial thrombi

• Usually begin at site of endothelial injury and

grow along flow of blood
• Typically are firmly adherent to the injured
arterial wall (atherosclerotic plaque)
Clinical Settings for Cardiac/arterial
Thombus Formation

• Myocardial Infarction (MI)

• Rheumatic Heart Disease
• Atherosclerosis
 Morphology of Thrombi

• Arterial Thrombi Are Usually Occlusive

• Venous Thrombi Are Almost Always Occlusive
– 85-90% of Venous Thrombi Form in Lower
Extremities
• Walker’s Law :-)
VENOUS THROMBOSIS (PHLEBOTHROMBOSIS)

• Superficial venous thrombi, usually occur in

saphenous system, may cause local congestion,
swelling, and pain; rarely embolize
• Deep thrombi, usually in large leg veins at or above
knee joint (e.g. popliteal, femoral, and iliac veins);
cause edema of foot and ankle; may embolize
• Characteristically occur at
site of stasis and extend in
the direction of blood
flow (towards heart);
contains more enmeshed
erythrocytes (red)
• Superficial Veins of the Lower Extremities
– Cause Pain, Swelling - Rarely with emobolization
– Associated With Varicosities
• Varicose Veins - Abnormally Dilated, Tortuous Veins
– Increased Risk of Infections
– Increased Risk of Varicose Ulcers.
• Thrombi in Deep Veins (Femoral, Iliac) More Likely to show
emobolization
• About 50% Are Asymptomatic (Formation of Collaterals)
• May Produce Edema, Pain and Tenderness
 Clinical Settings for Venous Thrombus Formation

• Cardiac Failure (CHF)

• Trauma
• Surgery
• Burns.
• 3rd Term Pregnancy and Postpartum
• Cancer
– Migratory Thrombophlebitis (Trousseau’s Syndrome)
• Bed Rest
• Immobilization
 Valvular Thrombi

• Infective Endocarditis
• Non-bacterial Thrombotic Endocarditis
• Verrucous Endocarditis (Libman-sacks)
– Lupus Related
 FATE OF THROMBOSIS

• Propagation and obstruction

• Embolization
• Dissolution
• Organization and recanalization
 Dissolution of Thrombi

• Recent Thrombi Can Undergo Total Lysis

• After the First 2-3 h, Thrombi won’t undergo
Lysis
– Thus the Use of TPa Is Only Effective in the First 1-
3 Hours
 Organization/Recanalization

• Granulation Tissue Followed by Capillary

Channel Formation or may heal so totally As to
Leave Only a Small Fibrous ‘Lump’ As
Evidence of a Previous Thrombus
Disseminated Intravascular Coagulation (DIC)
• Sudden Widespread Fibrin Deposition in Microcirculation
• Rapid Consumption of Platelets and Coagulation Proteins
• Secondary Massive Fibrinolysis, all the little thrombi
dissolve
• Clotting Disorder Turns Into a Bleeding Disaster
 EMBOLISM

• An embolus is a detached intravascular solid, liquid

or gaseous mass that is carried by the blood to a site
distant from its point of origin
• 99% are dislodged thrombus
• potential consequence: ischemic necrosis (infarction)
 PULMONARY THROMBOEMBOLISM

• Generally originates from deep leg veins

• Usually pass through the right heart into
pulmonary vasculature and may occlude main
pulmonary artery, across the bifurcation (saddle
embolus) or pass into the smaller, branching
arterioles; multiple emboli may occur
 Paradoxical Embolism

• An embolus pass through an interarterial or

intraventricular defect to gain access to the
systemic circulation( from vein to artery)
• Most pulmonary emboli (60-80%) are clinically
silent because of small size
 PULMONARY THROMBOEMBOLISM

• When 60% or more of the pulmonary circulation is obstructed, sudden

death may occur as caused by right heart failure .
• Embolic obstruction of medium-sized arteries may result in hemorrhage
without infarction because of intact bronchial circulation (unless
bronchial circulation is compromised - left heart failure).
• multiple pulmonary emboli over time may cause pulmonary
hypertension and right heart failure
 SYSTEMIC THROMBOEMBOLISM

• emboli traveling within the arterial circulation

• 80% arise from intracardiac mural thrombi, others
from ulcerated atherosclerotic plaques, aortic
aneurysm, or from fragmentation of valvular
vegetation
• major sites are lower extremities (75%), brain
(10%), intestines and kidneys
 FAT EMBOLISM SYNDROME
• characterized by pulmonary insufficiency, neurologic
symptoms, anemia, and thrombocytopenia. 10% of
cases are fatal

• typically are caused by microscopic fat globules

derived from long bone fractures (fatty marrow), or
rarely from soft tissue trauma and burns
 AIR EMBOLISM
• gas bubbles within the circulation can obstruct vascular
flow to cause distal ischemic injury

• air may enter circulation in chest wall injury or in

individuals exposed to sudden atmospheric pressure
changes (decompression sickness)
 AIR EMBOLISM (cont’d)

• Caisson Disease: chronic form of decompression

sickness in which persistent of gas emboli in the
bones (heads of femora, tibia, and humera) leads
to multiple foci of ischemic necrosis
 Amniotic Fluid Embolism

• Torn placental membrane - amniotic fluid

release
• Rupture of uterine veins
• Infusion of amniotic fluid into maternal venous
circulation
 Amniotic Fluid Embolism

• Lungs show squamous cells, lanugo hair, fat

from vernix caseosa
• Pulmonary edema, diffuse alveolar damage
• DIC
 Amniotic Fluid Embolism

• Present with dyspnea, cyanosis, shock, seizures

and coma
• Mortality of 80%
– Walker’s Law :-)
 Embolism
• Potential Consequences
– Ischemic Necrosis (Infarction)
– Though Pulmonary Emboli Are Common and
Important, Secondary Pulmonary Infarction Is Not
Common
– Lung Is Protected by a Dual Blood Supply
– The Brain Is Not So Protected and Gets Infarcts
(Stroke) LIQUEFACTIVE NECROSIS
 INFARCTION

• An infarct is an area of ischemic necrosis caused

by occlusion of either the arterial supply or
venous drainage in a particular tissue

• nearly 90% of all infarcts result from thrombotic

or embolic events in arterial vasculatures
• Venous infarcts are more
likely in organs with a
single venous outflow
channel (testis, ovary)

• All infarcts tend to be

wedge-shaped, with the
occluded vessel at the
apex
 RED INFARCTS
Occur:
– with venous occlusions (e.g. ovarian torsion)
– in loose (spongy) tissues (e.g. lung) that allow blood to collect in
the infarcted zone
– in tissues with dual circulations (e.g. lung and small intestines)
– in tissues that were previously congested
– when the occluded site is re-perfused
 WHITE OR PALE
INFARCTS

• occur with arterial occlusions in solid organs

(e.g. heart, spleen, kidney) where the solidity of
the tissue limits the amount of hemorrhage into
the ischemic area
 FACTORS THAT INFLUENCE
DEVELOPMENT OF AN
INFARCT
• nature of the vascular supply (dual arterial
supply?)
• rate of development of occlusion
• vulnerability of the tissue to hypoxia
• oxygen content of blood
 SHOCK
• Constitutes systemic hypoperfusion due to reduction either in cardiac
output or in the effective circulating blood volume. The end results are
hypotension, followed by impaired tissue perfusion and cellular hypoxia
• Three main categories: cardiogenic, hypovolemic, and septic
• Others: neurogenic shock and anaphylactic shock
 CARDIOGENIC SHOCK

• Results from myocardial failure (infarction),

ventricular arrhythmia, extrinsic compression
[cardiac tamponade, or outflow obstruction
pulmonary embolism)]
 HYPOVOLEMIC SHOCK

• Results from loss of blood or plasma volume

(hemorrhage, fluid loss from severe burns or
trauma)
 SEPTIC SHOCK

• Caused by systemic microbial infection, most

often by gram-negative infection (endotoxic
shock) but can also occur with gram-positive and
fungal infections
 PATHOGENESIS OF
SEPTIC SHOCK

• Endotoxic shock: endotoxins are bacterial wall

lipopolysaccharides (LPS) which consists of a
toxic fatty acid (lipid A) core and a complex
polyssacharide cost (including O antigen)
 PATHOGENESIS OF
SEPTIC SHOCK (cont’d)
• LPS → TNF (macrophages) → 1L-1 → 1L6/1L8
• systemic vasodilation (hypotension), diminished
cardiac contractility, endothelial injury and
activation (alveolar capillary damage), activation
of coagulation system
 ANAPHYLATIC SHOCK

• IgE mediated hypersensitivity response

associated with systemic vasodilatation and
increased vascular permeability
 NEUROGENIC SHOCK

• Occur in esthetic accident or spinal cord injury

with loss of vascular tone and peripheral pool of
blood
 STAGES OF SHOCK
1- Initial non-progressive stage: compensatory
reflex, perfusion of vital organs maintained
2- Progressive stage: characterized by tissue
hypoperfusion and onset of circulatory and
metabolic imbalance
3- Irreversible stage: tissue and organ damage