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:

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