hemodynamic disorders (disorders of blood flow)
DESCRIPTION
Hemodynamic Disorders (Disorders of blood flow). Dr. Abdelaty Shawky Dr. Gehan Mohamed. * Topics:. 1. Hyperemia 2. Thrombosis 3. Embolism 4. Ischemia. 5 . Infarction 6. Hemorrhage 7. Edema 8 . shock. Learning objectives. - PowerPoint PPT PresentationTRANSCRIPT
Hemodynamic Disorders(Disorders of blood flow)
Dr. Abdelaty Shawky Dr. Gehan MohamedDr. Abdelaty Shawky Dr. Gehan Mohamed
* Topics:* Topics:1. Hyperemia
2. Thrombosis
3. Embolism
4. Ischemia
5. Infarction
6. Hemorrhage
7. Edema
8. shock
Learning objectivesLearning objectives• Identify definition, types, causes and effect of both hyperemia
& congestion.• Understand definition, causes, composition, types, sites and
fate of thrombosis.• Discuss definition, causes, composition, types, sites and fate
of emboli.• Understand definition, causes, types and effect of ischemia.• Discuss definition, causes, types of infarction.• identify definition, causes and types of hemorrhage.• Understand definition, causes,types of edema.• Discuss definition and types of shock.
HyperemiaHyperemia
- Means local increase in volume of blood in a particular tissue.
a. Active Hyperemia (arterial):a. Active Hyperemia (arterial): is an active process resulting from increased arterial blood inflow because of arteriolar dilatation. - The affected tissue is reddened because of engorgement of tissues with oxygenated blood.
b. Passive hyperemia (Congestion)b. Passive hyperemia (Congestion) is a passive process resulting from impaired venous outflow from a tissue. - The affected tissue has a red-blue color due to accumulation of deoxygenated blood.
* Types:
1. Physiological:
- Hyperemia in skeletal muscles during exercise ,in the
gut following a meal.
2. Pathological: e.g. in acute inflammation.
a. Active Hyperemiaa. Active Hyperemia
* Definition: - Increase in venous blood in an organ as result of obstruction of venous outflow. - The veins, venules & capillaries in the organ become passively dilated (passive hyperemia).* Types:a. Localized: acute, chronicb. Generalized: acute, chronic
b. Passive Hyperemia b. Passive Hyperemia (venous congestion)(venous congestion)
* Causes: Sudden complete venous obstruction by: thrombosis or ligature.
* Effects: - Edema. - Hemorrhage due to rupture of veins and capillaries.
Acute localized venous congestionAcute localized venous congestion
* Causes: Gradual incomplete venous obstruction by: Venous compression by: a tumor, enlarged lymph node
or pregnant uterus. * Effects: Chronic dilatation of the veins, venules and
capillaries proximal to the obstruction resulting in:
1. Edema. 2. Stasis of the blood: predisposes to thrombosis. 3. Development of varicoses.
Chronic localized venous congestionChronic localized venous congestion
* Causes: - Acute heart failure
* Effects: Rapid generalized congestion in the all viscera.
Acute generalized venous congestionAcute generalized venous congestion
* Definition: Gradual congestion affecting the whole venous
system in the body.
* Causes: chronic Right sided heart failure
* Effects: 1- Dyspnea (due to pulmonary Congestion). 2- Chronic venous congestion in different organs.
3- Generalized edema.
Chronic generalized venous Chronic generalized venous congestioncongestion
ThrombosisThrombosis
* Thrombosis is:- Formation of a solid mass (compact mass), composed of the circulating blood elements, inside CVS system (blood vessels or heart) during life.
*Causes of thrombosis:- There are 3 major factors which predispose to
thrombosis (Virchow’s triad):
1. Endothelial damage.
2. Slowing & turbulence of blood flow.
3. Changes in blood composition.
1. Endothelial damage:- Endothelial damage may be:
a. Mechanical: trauma, repeated tourniquet…
b. Inflammatory: arteritis, phlebitis and endocarditis.
c. Degenerative: atherosclerosis, hypertension.. - The injured endothelium becomes swollen with rough surface.
2. Slowing & turbulence of blood flow.There is slowing of blood flow in the heart as in mitral stenosis
and in blood vessels as in varicose veins.
3. Changes in composition of blood:- ↑ platelets e.g. after operations.- ↑ fibrinogen as in pregnancy.- ↑ R.B.Cs. (polycythemia) → ↑ viscosity of blood →
stasis → thrombosis. - ↑ W.B.C. as in leukemia → ↑ viscosity of blood →
stasis → thrombosis.
• Endothelial injury leads to:1. Exposure of sub-endothelial collagen:
promote platelet aggregation.2. Release of tissue factor: promote fibrin
formation.
* Pathogenesis (Mechanism) of thrombosis:
I. Exposure of sub- endothelial collagen:
a. Platelets adhesion to the exposed collagen (this is
mediated by factor VIII released from endothelial
cells).
b. Platelet activation and release of Thromboxane
A2 (potent vasoconstrictor and induce platelet
aggregation)
II. Release of the tissue factor (from
endothelial cells) that stimulate the coagulation
cascade to form thrombin that convert
fibrinogen into fibrin.
•The end result is fibrin network entangling
aggregated platelet (Thrombus)
• The lumen of blood vessel is occupied by a red
mass which is adherent to the vessel wall by an
area called the head of the thrombus .
Gross picture of the thrombus
Left atrial Thrombus
Microscopic picture of thrombus:
ThankThankss