Circulatory disturbances
Venous side
Arterial side
CIRCULATURY DISTURBANCES
In circulatory disturbances, the amount of blood in the tissues
may be increased or it may be decreased.
Increased blood content
Arterial
Venous
Hyperemia
ac1ve dilata1on of the arterioles &
capillaries in response to
metabolic ac1vity
Decreased blood
content
Ischemia
Physiological
Hyperemia
Congestion
Complete
Partial
during muscular
exercised
Pathological
acute
in6amma7on
Conges7on
Physiological hyperemia
• Because the increased oxygen consump1on of during
muscle contrac1on s1mulates the produc1on of
vasoac1ve substances that dilate the vessels in the
skeletal muscle. Other examples include the increase
in gastrointes1nal blood >ow during diges1on of
food
Passive dilata1on of the veins &
capillaries in response to
obstruc1on of the venous ouAlow
General
acute
local
Chronic
acute
Chronic
Ischemia
Generalized conges7on:
 Acute as acute heart failure
 Chronic ( gradual) e.g. chronic RT sided HF.
Localized conges7on:
 Acute:
Sudden complete venous obstruc7on due to thrombosis
 Chronic:
Gradual incomplete venous obstruc7on e.g. venous compression
It is decrease of blood supply to an
organ due to occlusion of its arteries:
These occlusion may be:
Partial : usually gradual
Complete : usually sudden
Causes of Ischemia
Generalized ischaemia :
Due to low cardiac output
Localized ischaemia :
Due to arterial or venous obstruction
Venous obstruction --- cong. & oedema --increase in the tissue pressure ------- arterial
obstruction ------ ischemia
INFARCTION
Is an area of coagulative
necrosis (liquefactive in the
brain) due to sudden occlusion
of either arterial or venous
supply (ischemia)
1-Sudden Ischemia (Acute ischemia):
Sudden complete arterial occlusion by:
 Thrombosis or embolism
 Surgical ligature of the artery
EFFECTS:
sudden occlusion----- infarc1on (coagula1ve necrosis)
and gangrene
2-Gradual Ischemia (Chronic ischemia)
Gradual incomplete occlusion:
• Atherosclerosis
• Pressure on the artery
EFFECTS:
Cellular degenera1on, atrophy, degenera1on and
replacement Jbrosis
TYPES OF INFARCTION
RED INFARCTION: (Hemorrhagic)
Its occur in soM and vascular organs as lung,
liver and intes1ne, early – red due to
hemorrhage and late – pale in color
 PALE INFARCTION:
Are more common and occur in Jrm and less
vascular organs as kidney, heart and spleen
Bed Sores:
 It is ischemic necrosis with subsequent sloughing of skin as a
result of pressure of prolonged recumbency
 It is of special clinical importance.
 It is the name given to ulcers occurring over
bony prominence (sacrum) as a complica7on
of prolonged recumbency specially in old or
debilitated pa7ents.
- Prolonged pressure over bony prominence
interferes with the circula7on of the 7ssues 
necrosis of 7ssues  sloughing and ulcera7on
 secondary bacterial infec7on
with putrefac7on.
Veins are the commonest site of thrombus
formation due to :
1.
2.
3.
4.
5.
Thin wall : easily comprisable
Superficial :easily traumatized
Inactive :lack of muscular pumping action
Low blood pressure
Slower blood flow
Thrombosis
Thrombosis
It is formation of a solid mass from the
constituent of the circulating blood within
the cardiovascular system.
Site :
Veins
Arteries Capillaries Heart
3 factors that predispose to thrombosis (Virchow’s Triad)
Stasis
Injury to the
vessel wall
Hypercoagulability
Pathogenesis of thrombosis
Stasis of blood: (slow blood >ow) as
• In case of local venous conges7on
• Heart failure
• Prolonged recumbency.
 Injury of blood vessels: as in case of
• Repeated venous injec7on
• In6amma7on of vessels wall
• Atherosclerosis.
factor VIII
Platelets adherent to the injured endothelium
Endothelial cells produced von willebrand (factor VIII) which act as a bridge
between platelet surface receptor & collagen
 Hypercoagulability of blood: as in cases of
• Decrease plasma of blood……dehydra7on
• Increase blood cells…………polycythemia and leukemia
Types( classiJca1on ) of thrombi
Fate of the Thrombus
According to
Extent of
thrombus
•Mural
•Occlusive
•Propagated
Present of
organisms
•Sep7c
•Asep7c
Thromboplas7n liberate from damaged 7ssue& platelet
Convert Ubrinogen into Ubrin which deposit on pale thrombus
Color &
cons7tuent
•Red
•Pale
•Mixed
1-Septic thrombus----- fragmented by
the proteolytic enzymes into septic
emboli causes pyaemic abscesses
2-Aseptic thrombus
If mass is small it dissolves by
fibrinolysis
If mass is large it undergoes:
If mass is large it undergoes:
Organization(fibrosis): the thrombus is invaded by capillaries
and fibroblast --- change to fibrous mass– lead to permanent
vascular occlusion
Organization and Canalization; some time capillaries dilated
and allow Passage of blood through the thrombus;
Incorporation : the fibrosed thrombus shrinks from the
vascular wall leaving a space which gets lined by endothelium
Dystrophic calcification----- phlebolith (stone in blood
vessels)
Detachment--- aseptic emboli--- infarctions
Propagating thrombus--- due to spread of venous thrombosis
Main differences between Clot & Thrombosis
Clot
Thrombosis
Vital or not ,during live or
after death
Vital process (occurring
only during life )
In vivo or vitro
Only in vivo (inside blood
vessels)
Fibrin is the main lement
Platelet are essential
Blood is stagnant
Blood is in motion
Not adherent to vessel wall
Adherent to vessel wall
Wet & elastic
Dry & friable