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Hemodynamic Disorders
Hening P. Syahrin
Basic Science and Fundamental of Nursing Group
Faculty of Nursing Universitas Indonesia
2009

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Disturbances of Blood Flow

Hyperemia and congestion

Hemorrhage
Ischemia
Thrombosis
Postmortem clots
Disseminated intravascular coagulation
Embolism
Infarction
Edema
Shock

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Hyperemia and Congestion

Increased volume of blood in an affected
tissue or part

Hyperemia (active hyperemia): Arterial and
arteriolar dilatation produces an increased
flow of blood into capillary beds

Congestion (passive congestion or venous
congestion): Impaired venous drainage

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Active Hyperemia
Too much arterial blood is brought to an
organ or tissue by dilated arterioles and
capillaries
Sympathetic neurogenic mechanisms or
The release of vasoactive substances
Inflammatory reaction
Heat applied locally to a part
Increased physiological activity

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Can the increased blood flow

(active hyperemia) in acute
inflammation be a defense
mechanism of the body?

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Passive Congestion

Blood

leaving an organ or part is impeded

(impaired venous drainage)

Grossly,

the involved tissues appear bluishred because of the poorly oxygenated

venous blood

Microscopically, congestion is similar to
hyperemia (capillaries and veins are
dilated and filled with blood)

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Types of Passive Congestion

Localized

passive congestion

Generalized passive congestion
Chronic generalized passive congestion of the

lungs: Reduced left ventricular output (leftsided heart failure).

Chronic passive congestion of the liver: Rightsided heart failure (rarely from obstruction of
the posterior vena cava).

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Hemorrhage
The presence of erythrocytes outside the
blood vessels
The vessel may be physically damaged so that

erythrocytes flow out through a break in the

wall (hemorrhage by rhexis) or
The erythrocytes may pass through an intact
vascular wall by a process called diapedesis
(hemorrhage by diapedesis)

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Naming Hemorrhage-1

Petechiae

Ecchymoses

Purpura

Agonal

hemorrhages

Linear hemorrhages

Paint-brush hemorrhages

Hemothorax

Hemopericardium

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Naming Hemorrhage-2

Epistaxis

Hemoptysis

Enterorrhagia

Metorrhagia

Hematuria

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The Significance of Hemorrhage

Depends on:

(1) The volume of blood loss

(2) The rate of blood loss, and
(3) The site of hemorrhage

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Ischemia
Local anemia or a deficiency of arterial
blood to a portion of an organ or part. The
chief causes of ischemia are:
(1) External pressure upon an artery
(2) Narrowing of the lumen of an artery
(3) A thrombus or embolus

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Effects of Ischemia

The

organ involved

The size of the vessel

The degree of occlusion

The degree of collateral circulation

End

artery (as in kidneys): Acute necrosis

Gradual obstruction: Atrophy

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Thrombosis

Formation

of a clot from elements of the

circulating blood within the vascular system
during life

May decrease or obstruct vascular flow
causing ischemic/hypoxic injury to cells,
tissues and organs

May become dislodged or fragmented to create
emboli (an embolus is an intravascular mass
carried in the bloodstream to some site
remote from its origin)

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Factors Effective in
Thrombosis
(1) Injury to vascular endothelium
(2) Alterations in normal blood flow
(3) Alterations in the blood
(hypercoagulability)

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Arterial vs Venous Thrombus

Grossly: Thrombi are friable, a mixture of red and

gray in irregular layers, dull, and attached to the
endothelium
Arterial thrombus: Dry, friable gray masses
composed of almost regularly arranged layers of
platelets and fibrin, irregularly mixed with small
amounts of darker red coagulated blood
(White or conglutination thrombus)
Venous thrombus: Red, gelatinous
(Stasis or red coagulation thrombus)

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Nomenclature of Thrombi-I

Mural

thrombi - are attached to the wall of the

heart or blood vessel

Occluding thrombi - are attached to the entire
circumference of the vessel

Valvular thrombi - are attached to the heart
valves

Canalized thrombi - occur when new blood
channels form in an organized thrombus

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Nomenclature of Thrombi-II

Saddle

thrombi - straddle the bifurcation of

blood vessels

Septic thrombi - are those which contain
bacteria

Aseptic thrombi - are those that do not
contain bacteria, etc.

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The Thrombus may

(1) increase in size and, by its enlargement,
eventually cause obstruction of some
critical vessel
(2) give rise to emboli
(3) be removed by fibrinolytic action or
(4) become organized

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Disseminated Intravascular
Coagulation (DIC)

Widespread

microthrombi formation in
capillaries, arterioles and venules

Composed largely of fibrin and aggregated
platelets

A complication of a diverse group of clinical
diseases in which there is activation of the
intrinsic pathway of blood clotting

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Embolism

Process

of a foreign body moving through

the circulatory system and becoming lodged
in a vessel causing obstruction

An embolus (plural, emboli) is a detached
intravascular solid, liquid or gaseous mass
that is carried by the blood to a site distant
from its point of origin

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Infarction

A

localized area of ischemic necrosis in an

organ or tissue resulting from occlusion of
either its arterial supply or venous drainage

Usually caused by thrombosis and/or
embolism of the arterial blood supply

More rarely, external compression of
vessels by expanding tumors, etc.

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Edema

Abnormal

accumulation of fluid (water) in

the intercellular tissue spaces or body
cavities

Localized (e.g. obstruction of venous
outflow from the leg)

Generalized in distribution (e.g. in chronic
congestive heart failure)

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Nomenclature

Anasarca:

Generalized edema in which fluid in

subcutaneous tissues is especially prominent

Ascites: Collection of edematous fluid in the
peritoneal cavity

Hydrothorax: Collection of edematous fluid in
the thoracic cavity

Hydropericardium or Pericardial Effusion:
Collection of edematous fluid in the pericardial
sac

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Transudate-Exudate

Inflammatory

edema is referred to as an
exudate and it is associated with an
inflammatory reaction

Non-inflammatory edema is referred to as a
transudate

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Edema is caused by
(1) Decreased plasma osmotic pressure
(2) Increased hydrostatic pressure
(3) Increased permeability of vascular
endothelium
(4) Lymphatic obstruction

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Decreased Plasma Osmotic

Pressure

Deficiency

of blood proteins
(hypoproteinemia)

Decreased formation or excessive loss

Albumin

More fluid is pushed into the intercellular
spaces. Also, the force available to pull
fluid into the bloodstream at the venous end
of the capillary is reduced

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Decreased Plasma Osmotic

Pressure-I

Malnutrition

(starvation, emaciation)

Severe or advanced liver diseases (cirrhosis,
etc.)

The loss of plasma proteins (intestine and
kidneys)

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In

Decreased Plasma Osmotic

Pressure-II

the intestine, blood protein loss is usually

the result of hemorrhage over a long period of
time (stomach worms in sheep and cattle,
slowly bleeding stomach ulcers in pigs and
dogs, etc.)

In the kidneys, renal amyloidosis is the only
frequently encountered condition in animals in
which large volumes of blood protein are lost
through the urine

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Increased Hydrostatic
Pressure

Venous

stasis

Subsequent to venous stasis, the capillaries
become more permeable to large molecules
(albumin and globulin), since they are
deprived of their normal supply of oxygen
and other nutrients

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Increased Permeability of
Capillary Endothelium
Occurs subsequent to venous stasis
(resulting in increased hydrostatic
pressure), as well as from direct damage, as
in inflammation. Increased vascular
permeability is the most important
mechanism in the formation of
inflammatory edema (exudate)

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Lymphatic Obstruction
Occurs when any lesion impedes normal
lymphatic drainage by pressure or obstruction.
Under normal conditions, the lymphatics
constantly drain small amounts of fluid from
the intercellular spaces. Thus, in the absence of
lymphatic drainage from a area, fluid
accumulates

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Shock

Peripheral

circulatory failure with pooling

of the blood in the terminal circulatory beds
(small capillaries)

The fundamental disturbance is that blood
volume is too small to fill the vascular
system, resulting in a fall of blood pressure
and cell damage due to anoxia

Hypovolemic, septic, cardiogenic and
neurogenic

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Clinical Signs of Shock

Inconsistent

and vary with the precipitating

cause

Animals are usually inactive and unresponsive
to external stimuli

Muscle weakness is prominent and there is
pallor and coolness of the skin

Body temperature is subnormal and the heart
rate is increased in most types of shock (but it
may be slow and irregular). Depression of
renal function and urine production often occur

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Shock

Hypovolemic

shock: Due to loss of blood

volume (hemorrhage, trauma, loss of fluids
in burns, etc.)

Septic shock: Septicemia or an overwhelming
infection with gram-negative (endotoxic
shock) or gram-positive (exotoxic shock)
organisms. Peripheral dilatation of the
capillary beds which subsequently lead to
shock

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Shock

Cardiogenic

(Cardiac) shock: Pump

failure." Subsequent to the sudden decrease in
cardiac output

Neurogenic shock: A shock state mediated by
the nervous system which induces peripheral
dilatation (dilatation of the capillary bed). It
occurs in animals with severe fright, pain and
trauma (without hemorrhage)