Hemodynamic Disorders Disorders of blood flow Dr Abdelaty

Hemodynamic Disorders (Disorders of blood flow) Dr. Abdelaty Shawky Dr. Gehan Mohamed

* Topics: 1. Hyperemia 5. Infarction 2. Thrombosis 6. Hemorrhage 3. Embolism 7. Edema 4. Ischemia 8. shock

Learning 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.

Hyperemia

- Means local increase in volume of blood in a particular tissue. 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) 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.

a. Active Hyperemia * Types: 1. Physiological: - Hyperemia in skeletal muscles during exercise , in the gut following a meal. 2. Pathological: e. g. in acute inflammation.

b. Passive Hyperemia (venous congestion) * 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, chronic b. Generalized: acute, chronic

Acute localized venous congestion * Causes: Sudden complete venous obstruction by: thrombosis or ligature. * Effects: - Edema. - Hemorrhage due to rupture of veins and capillaries.

Chronic 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.

Acute generalized venous congestion * Causes: - Acute heart failure * Effects: Rapid generalized congestion in the all viscera.

Chronic 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.

Thrombosis

* 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.

* Pathogenesis (Mechanism) of thrombosis: • Endothelial injury leads to: 1. Exposure of sub-endothelial collagen: promote platelet aggregation. 2. Release of tissue factor: promote fibrin formation.

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 A 2 (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:

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