HYPERAEMIA

The term hyperaemia literally means "too much blood", and refers to a volume and flow change. It can occur in two ways:

1) Active hyperaemia - active  arteriolar engorgement of the  vascular bed
2) Passive hyperaemia (Congestion) -  too little blood is being  removed by the venules.

Hyperaemia may be either physiological or pathological. Physiologic hyperaemia occurs following an increase in demand for blood as in increase blood flow to stomach and intestines during digestion, or congestion as in erectile tissues during stimulation. Pathological hyperaemia on the other hand occurs as a manifestation of some alterations in blood flow characteristics. It is however not the cause of this alteration, but the result of some underlying pathological process.

Three factors are considered in the classification of pathological hyperaemia:

1) Duration of hyperaemia
2) Extent of hyperaemia
3) the mechanism by which it occurred.

Thus, pathological hyperaemia is classified as follows:

I. Based on Duration:
 1) Acute - abrupt onset, rapid   development.
 2) Chronic - slow developing,   present for a long time.

II. Based on Extent of Hyperaemia:

 1) General - throughout an organ   or system.
 2) Local - confined to discrete   area.

III. Based on the Mechanism involved:

 1) Active - increased arteriolar   inflow.
 2) Passive - engorgement of   vascular bed; venous   obstruction (impedance).

Based on the above scheme of classification, there occur four basic patterns of hyperaemia and are as follows:

 1) Acute Local Active Hyperaemia
 2) Acute Local Passive Hyperaemia
 3) Chronic Local Passive  Hyperaemia
 4) Chronic General Passive Hyperaemia

Acute local active hyperaemia occurs in inflammation, and is due to engorgement of the vascular bed following an increase in arteriolar blood flow into the area. The increase in arteriolar blood flow opens new capillary beds and newly dilated small vessels extend the arteriolar blood pressure into smaller vascular channels. This is a chemically mediated response of the microvasculature to histamine, bradykinins, and other vasoactive amines.

Acute local passive hyperaemia refers to passive engorgement of the drainage area due to obstruction to the venous drainage. As a result, blood backs up into the microvasculature and local venous engorgement occurs. In contrast to acute local active hyperaemia, the tissues involved are dark red in colour than bright red, as they are engorged with poorly oxygenated blood.

Chronic local passive hyperaemia occurs when an organ or organ systems develop chronic inflammatory lesions which progresses to fibrosis and therefore obstruction or impediment in the tissue's venous drainage. As a result, oedema, collateral venous channels and arterio-venous anastomoses develop, which usually are dilated and tortuous.

Chronic general passive hyperaemia involves either the heart or the lungs as the major site of underlying pathological change. If the heart is the source of the problem, the generalised passive hyperaemia that result is called Congestive Heart Failure. Depending on the nature of the lesion and its location in the heart, the tissues that will suffer will either be the liver or the lungs. It may also occur in certain types of pulmonary lesions in which there is progressive loss of pulmonary vascular bed, as in chronic pneumonia.

OEDEMA

 Oedema is the accumulation of too much extracellular water in the interstitial fluid space (outside the vascular fluid compartment and the cellular fluid compartment). To understand the process by which excess fluid accumulates in the interstitial fluid space, it is best to review the fluid dynamics in the capillary bed. A brief description of which follows.
 

Figure 7. Diagram of the microcirculation and the  forces involved in the flow of tissue fluid.

The relationship between the various forces at work in the microcirculatory bed is described by the STARLING EQUILIBRIUM. This equilibrium is achieved by the balance of filtration pressure exerted across the filtering membrane (capillary endothelia) of the terminal vascular bed. A balance exists between the net filtration pressure and net absorption pressure, meaning all fluid being filtered out from the vascular wall and into the interstitium is again reabsorbed. The net filtration pressure is the difference between plasma hydrostatic pressure and interstitial tissue colloid osmotic pressure in the arterial end of capillary vascular bed. The net absorption pressure on the other hand is the difference between plasma colloid osmotic pressure and the tissue hydrostatic pressure at the venous end of the capillary bed. Disturbances resulting to alterations in the balance of forces operating in the vascular bed lead to the accumulation of fluid in the interstitial spaces.

Figure 8. Forces governing the flow of fluid in the  vasculature

The mechanisms in oedema formation include the following:

1) Decreased plasma colloid osmotic  pressure
2) Increased blood hydrostatic  pressure
3) Increased vascular permeability
4) Lymphatic obstruction.

Decreased plasma colloid osmotic pressure results when there is a decrease in plasma protein concentration in the blood. Albumin is the most important plasma protein. Disease processes that manifest either a decrease in production or loss of albumin at a rate greater than it is being synthesized cause oedema formation. These include disease conditions such as hypoproteinaemia (hypoalbuminaemia) following liver disease and starvation; loss of albumin during renal disease (particularly glomerular lesions), and enteric diseases including parasitism.

Increases in blood hydrostatic pressures occur in disease conditions that increase the capillary pressure by raising the venous pressure. The pressure at the capillary level is influenced mostly by the venous pressure and not by the arterial pressure. Thus, the increase in  venous back pressure negates the absorptive function of the venous end. This results to a condition where fluids filtered at the arterial end fail to return to the circulation. Disease conditions by which this may occur include obstructions in the venous flow of blood which may be local (example occlusion of veins by thrombosis or emboli, or compression as in pregnancy), or generalised (example cardiac failure with attendant leakiness of the vessels and increased sodium retention due to increased aldosterone secretion.

An increase in vascular permeability occurs as oedema of inflammation (localised). Various mediators of inflammation are vasoactive and increase vascular permeability. However, some toxins may also produce an increase in vascular permeability (e.g., bee sting venom). The oedema fluid here is of high protein concentration for besides water, plasma proteins leak out of the damaged endothelial wall.

Lymphatic obstructions usually result to local oedema. This may occur in disease conditions such as obstruction of lymphatics by growing neoplasms, obstruction by emboli, and damage to lymphatics following surgical intervention.

The changes produced by oedema are dependent on the following factors:

1) Severity of oedema
2) Rapidity of onset
3) Extent on oedema
4) Anatomic location of oedema
5) Underlying cause of oedema

Oedema fluid collect in the lowermost portions of the body such as the ventral abdomen and the limbs in a pattern referred as Dependent oedema. When such oedema is severe and generalised, it is possible to push a finger against such oedematous tissue and produce a dent. Such an oedematous change is called Pitting oedema.

Special terms are used to refer to oedema fluid accumulation in body cavities as Ascites in peritoneal cavity, Hydrothorax in thoracic cavity, and Hydropericardium or Pericardial effusion in the pericardial sac.