"Heavy lungs" are generally due to the buildup of fluid, principally caused by pneumonia, or as in this case, heart failure.
In patents with progressive aortic stenosis, adaptation can no longer compensate for the valvular disfunction resulting in "left ventricular failure."
When the left heart no longer pumps blood effectively, fluid builds up in the lungs resulting in "congestive heart failure" or CHF. In early CHF, there is perivascular and interstitial edema which thickens the alveolar septae. Later, the alveolar spaces fill with transudative fluid. Since RBCs are too big to passively move with the transudate, the fluid is clear. However, the chronic congestion can cause the thin walled alveolar capillaries to burst, releasing RBCs into the alveolar spaces. In response, macrophages phagocytose the RBCs and store the iron from their hemoglobin as a brown pigment (hemosiderin). These cells are a telltale sign of CHF and are called "heart failure cells."
During processing of the lung tissue for histology, the transudate is washed away, so usually nothing aside from RBCs and macrophages is seen in the alveolar spaces.
You continue, by removing and examining the lungs.
The lungs weighted 810g (right) and 730g (left).
Normal weights are 450g and 370g, respectively.
Why are the lungs heavy?
Here is a chest X-ray of a similar patient.
Can you correlate the X-ray findings with what you might think the effect of heart failure might be?
Review the histology of the lungs.
Where in the lungs is the section taken from (center, periphery) and why?
There is no massive infiltrate to explain the weight of the lungs. Why not?
What do you notice about the thickness of the alveolar septae compared to the normal lung shown below?
What are ovoid cells in the alveolar spaces filled with brown pigment? What is the pigment and where does it come from?
