NCM 112: Fluids & Electrolytes

1st Semester A/Y 2020-2021

Hydrostatic Pressure and Colloid Osmotic Pressure

Evaluation

1. Explain how tissue injury secondary to burn causes the disturbance in both the hydrostatic
and colloid osmotic pressures?

When a burn occurs on the skin, it causes changes within the skin. If it's a superficial burn it will
cause damage to the epidermis and the upper dermis only. Superficial burns will damage the keratinocytes
(cells in the epidermis) and will also activate an immune response. The damaged keratinocytes and
immune cells will secrete pro-inflammatory cytokines triggering an immune response. Some cytokines will
cause increase in vascular permeability. The increase in vascular permeability will cause fluid to leak out—
from the intravascular space to the interstitium—and may lead to interstitial edema.

The damage to the structural integrity of capillaries increases vascular permeability. Therefore,
hydrostatic pressure also increases. This action promotes more fluids and solutes to be forced out of the
capillary. Meanwhile, colloid osmotic pressure decreases. Since the capillaries are already damaged and
more fluids and solutes are escaping, there will be a weak countering of pressure that supposed to be,
should return the fluids and solutes back into the capillaries. Decreased plasma COP promotes water
retention in the interstitial space. Thus, the disruption of these pressures will not promote equilibrium
inside the body.

2. How does increased capillary permeability affect the colloid osmotic pressure?

The increase of capillary permeability, which can occur during inflammatory states, makes vessels
become “leaky”. There will be an escape of water and solutes into the interstitial space whenever the
hydrostatic pressure is much higher than the osmotic pressure inside the intravascular space. Osmotic
pressure relies on selective permeability in membranes. Proteins, specifically albumin, may escape the
plasma compartment because of its increase in permeability. Moreover, since albumin is non-diffusible,
the capillaries can’t reabsorb it back to its compartment. Without the albumin, there will be no osmotic
pulling force in the intravascular space resulting in decreased colloid osmotic pressure.

3. What are the possible outcomes of increased pulmonary capillary permeability?

When the heart is not able to pump efficiently, blood can back up into the veins that take blood
through the lungs. As the pressure in these blood vessels increases, fluid is forced to push into the air
spaces (alveoli) in the lungs. This fluid reduces normal oxygen movement through the lungs. This condition
is called pulmonary edema. It is caused by elevated pulmonary capillary hydrostatic pressure and
increased pulmonary capillary permeability leading to transudation of fluid into the pulmonary
interstitium and alveoli.
 4. Explain the effects of right-sided congestive heart failure on the venous circulation and
hydrostatic pressure.

In right-sided CHF, the right ventricle of the heart fails to pump blood forward, and now heavy
fluid backflows into the lungs and/or body. The blood backs up into the systemic venous circulation which
elevates venous pressures and capillary hydrostatic pressures. This leads to fluid retention in the lower
extremities, especially in the feet and legs. This movement is caused by venous stasis that increases
plasma hydrostatic pressure of blood that returns to the heart.

5. How do disturbances in hydrostatic and colloid osmotic pressures affect gas exchange?

Gas exchange occurs in the lungs between the alveoli and a network of capillaries, which are
located in the walls of the alveoli. The walls of the alveoli share a membrane with the capillaries in which
oxygen and carbon dioxide move freely between the respiratory system and the bloodstream.

This movement, often referred to as bulk flow, involves two pressure-driven mechanisms:
hydrostatic and colloid osmotic pressure. When moving from the bloodstream into the interstitium, bulk
flow is termed filtration, which is favored by blood hydrostatic pressure and interstitial fluid oncotic
pressure. When moving from the interstitium into the bloodstream, the process is termed reabsorption
and is favored by blood oncotic pressure and interstitial fluid hydrostatic pressure.

When one pressure is greater than the other, equilibrium will not exist since the fluid leaving the
circulation and the amount of fluid returning are not equal. The huge amount of fluid and solutes coming
out of the vessel will result in hypotension, reducing the amount of blood of the heart that can pump,
affecting the gas exchange, which then leaves a person tired and often short of breath.

6. How do alterations in hepatic and renal functions cause the disturbances in hydrostatic and
colloid osmotic pressures?

In hepatic and renal disfunction, there is an inflammation and damage to the glomerulus which
may be caused by immune cells, antibodies, etc. This will now cause destruction to the podocytes
(normally prevents protein loss), which also causes more protein to diffuse into the tubules. It means that
protein will now be part of the urine output. Mass proteinuria results in hypoproteinemia more
specifically, hypoalbuminemia (less protein, less albumin). This causes the liver to produce more proteins
and thus leading it to and eventual overdrive. Hypoalbuminemia would also result in a decline in plasma
colloid osmotic pressure (oncotic pressure). This means that increase in water and electrolytes will move
in the interstitium from the circulation. This occurs because of colloid osmotic pressure — there are no
solutes or proteins in the vascular compartment to hold the water in the circulation. Thereby, causing
peripheral edema.