Disturbances In Circulation Notes

Disturbances in Circulation

• Hyperemia (active hyperemia)

• Congestion (passive hyperemia)

• Hemorrhage

• Edema

• Thrombosis

• Emboli

• Infarction

1. Active hyperemia (Hyperemia)

Definition: An active process leading to an increased amount blood in the arterial circulation.

Etiology:

*all active hyperemias are acute. There are no chronic active hyperemia!

• Acute local: after a meal, oestrous, exercise (physiologic), inflammation (pathologic)

• Acute general: septicemia, bacteremia (pathologic)

Figure 1 normal arteries

Figure 2 active hyperemia

Signs & Lesions: similar to inflammation (dark red)

Significance & Results: similar to inflammation eg it brings additional amount of nutrient and oxygen to combat irritant, quickly remove waste products, brings more leukocyte.

2. Passive hyperemia (Congestion)

Definition: A passive process leading to an increased amount blood in the venous circulation.

Etiology:

*can be acute or chronic.

• Acute/chronic local: obstruction to flow (within or outside the vessel)

• Acute/chronic general: lesions impeding normal heart, liver & kidney

Signs: darker red or slightly bluish hue

Lesions: often accompanied by oedema

Significance & Results:

• obstruction of principal vein in limbs interfere with locomotion

• fatal if heart, liver, kidney are severely affected

• fibrosis & atrophy

3. Hemorrhage

Definition: Presence of red blood cells (RBC) outside of the blood vessel.

Two types of hemorrhage: (i)by rhexis, (ii) by diapedesis.

Per rhexis: RBC escape through broken wall of blood vessel.

Per diapedesis: RBC escape through intact blood vessel.

• Petechia = pin-point size to 1-2 mm

• Purpura = > 2mm but < 1 cm

• Ecchymotic = > 1 cm

• Suffusion = covers a large area or shape

• Haematoma (haematocyst) = blood clot

Etiology:

*Hemorrhages only occur antemortem!

4. Edema

Definition: Excessive accumulation of fluid in the intracellular spaces or body cavities.

Signs & Lesions:

- usually pale, puffy, raised

- cold, pitting upon pressure

-fluid ooze freely upon incision or yellowish gelatinous mass found

Before knowing the cause, we have to understand the normal fluid exchange. In a normal individual, there is a continuous fluid circulation from arterial end of capillary, through the tissues, and back into the venous end. To accomplish this, blood pressure (BP) must be greater at arterial end than at venous end. Arterial BP is usually 45mmHg, venous BP 15mmHg, oncotic (or osmotic) pressure is 30mmHg. Thus, arterial BP overcomes 30mmHg of oncotic pressure and being forced into the tissues at the rate of 15mmHg. At venous end, the venous BP cannot overcome oncotic pressure thus fluid flow into blood at the same rate of 15mmHg. Therefore, there’s no accumulation of fluid.

Figure 3 Normal fluid exchange

Etiology:

• Deficiency of blood proteins

• Passive hyperemia

• Increased permeability of capillary endothelium

• Obstruction of lymph vessel

Fate of Edema:

• removed via veins & or lymphatics

• space occupying

• chronic organised by fibrous tissue

• depends on the aetiology

5. Thrombosis

Definition: Clot within the vasculature of a living animal.

Aetiology:

• endothelial damage

• alterations in normal blood flow

• hyper-coagulability of the blood

Pathogenesis:

Fate of thrombus:

• Propagation: Thrombus may accumulate more platelets and fibrin eventually obstructing other critical vessel

• Dissolution: Thrombi may be removed by the fibrinolytic activity

• Embolization: Detached as thrombotic emboli

• Organization and recanalization: induce...

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