This excellent question comes from Esther!
Digging back into basic physiology, approximately 2/3 of body fluid is INTRAcellular and 1/3 is EXTRAcellular. We are only talking about EXTRAcellular fluid here. Extracellular fluid is divided into the intravascular space and extravascular space.
As above, fluid shifts are affected by factors like endothelial permeability (which is affected by direct tissue injury or inflammatory cytokines, etc.), hydrostatic pressure (free water in the plasma that goes into the interstitium), and osmotic pressure (proteins in the interstitium that pull water in).
Clinically, patients who are “intravascular dry and extravascularly overloaded” are patients who don’t have enough volume in their vascular system because all their fluid is getting pushed into other parts of the body, like the abdomen, lungs, extremities, and dependent areas. These patients will often have pitting edema on exam or “wet sounding” lungs with crackles or decreased breath sounds indicating pleural effusions.
Severe heart failure is a good example. The heart cannot pump blood effectively (there is poor “forward flow”) so fluid is retained in the veins, leading to fluid leaking out into the interstitium because of increased hydrostatic pressure. These patients develop “volume overload” which refer to the edema and lung findings above, but because there is not enough fluid in the vascular system, they are also “dry” and can be at risk for hypotension and poor perfusion of organs like the brain and kidneys. If a patient has acute kidney injury from poor perfusion, they may have low urine output, but this is not always present.
We use diuretics (like furosemide or bumetanide) to treat heart failure exacerbations because they cause Na/K/Cl loss in the urine, which leads to water getting pulled from the interstitium back into the vascular system. Treatment success is measured in terms of increased urine output (peeing out extra fluid that had built up in the interstitium) and weight loss.