Transcript Disturbances of Blood Flow

Weeks 4 and 5
Disturbances of Blood Flow
Dr.İ.Taci Cangül
Bursa-2008
Disturbances of Blood Flow
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Hyperemia and congestion
Hemorrhage
Ischemia
Thrombosis
Postmortem clots
Disseminated intravascular coagulation
Embolism
Infarction
Edema
Shock
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
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
Can the increased blood flow
(active hyperemia) in acute
inflammation be a defense
mechanism of the body?
Passive Congestion
• Blood leaving an organ or part is impeded
(impaired venous drainage)
• Grossly, the involved tissues appear
bluish-red because of the poorly
oxygenated venous blood
• Microscopically, congestion is similar to
hyperemia (capillaries and veins are
dilated and filled with blood)
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).
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)
Naming Hemorrhage-1
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Petechiae
Ecchymoses
Purpura
Agonal hemorrhages
Linear hemorrhages
Paint-brush hemorrhages
Hemothorax
Hemopericardium
Naming Hemorrhage-2
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Epistaxis
Hemoptysis
Enterorrhagia
Metorrhagia
Hematuria
The Significance of Hemorrhage
Depends on:
(1) The volume of blood loss
(2) The rate of blood loss, and
(3) The site of hemorrhage
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
Effects of Ischemia
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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
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)
Factors Effective in Thrombosis
(1) Injury to vascular endothelium
(2) Alterations in normal blood flow
(3) Alterations in the blood
(hypercoagulability)
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)
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
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.
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
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
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
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.
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)
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
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
Edema is caused by …
(1) Decreased plasma osmotic pressure
(2) Increased hydrostatic pressure
(3) Increased permeability of vascular
endothelium
(4) Lymphatic obstruction
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
Decreased Plasma Osmotic
Pressure-I
• Malnutrition (starvation, emaciation)
• Severe or advanced liver diseases
(cirrhosis, etc.)
• The loss of plasma proteins (intestine and
kidneys)
Decreased Plasma Osmotic
Pressure-II
• In 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
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
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)
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
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
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
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
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)