I think CVC cannot lead to heart failure primarily. So let's think its pathogenesis in skin now only.
I think the pathogenesis is like this
- dilation of veins and capillaries due to impaired venous drainage
- reduced outflow of blood from a tissue
- passive process
- $\to$ local increase in blood volumes
- $\to$ local increase in venous pressure
- pathological
- $\to$ shortage of oxygen and built-up metabolic waste
- $\to$ structural changes in microvasculature
- $\to$ increased venous permeability % hallmark of acute inflammation
- $\to$ increased size of venous caliber
- $\to$ emigration of leucocytes
- $\to$ accumulation at site of injury
- activation of acute inflammation
- $\to$ protein into extravascular space
- $\to$ increased viscosity of blood
- $\to$ deoxygenated blood blood stasis
- $\to$ congested tissue
- $\to$ leucocytes move to endothelial wall (selectins)
- $\to$ roll
- $\to$ adhere (integrin to stop)
- $\to$ migrate
- $\to$ dysky reddish-bluish skin (cyanotic)
- $\to$ healing via fibrosis
- $\to$ scar
- Causes: venous thrombosis; venous compression; heart failure;
I am not sure about the role of leucocytes exactly in this process. I am not sure if they play a big role in the formation of cyanotic skin. I think the outcome is mostly because of increased vascular permeability and its deoxygenated blood in extracellular space.
What is the right pathogenesis of chronic venous congestion in skin?
