Summary: Episode 57: In this episode, Doctor Dan discusses types and causes of edema, Starlings forces of oncotic and hydrostatic pressure, and gives relevant clinical examples that demonstrate each type.<br> Listen to the podcast here…<br> Fluid and Hemodynamics<br> I. Edema – excess fluid in the interstitial space, which is extracellular fluid (ECF); this is outside the vessel.<br> A. Types of Edema<br> 1. Non-Pitting edema<br> Increased vessel permeability with pus in the interstitial space (pus=exudates). Lymphatic fluid is another type of non-pitting edema. Blockage of lymphatics leads to lymphatic fluid in the interstitial space. Pits early, but eventually becomes nonpitting. Exudates and lymphatic fluid does not pit.<br> 2. Pitting edema<br> Transudate with right heart failure, swelling of the lower extremities, fluid in the interstitial space. Transudate does pit.<br> 3. Three causes of edema:<br> Exudates, lymphedema, and transudate. Transudates are the only one that has pitting edema.<br> B. Transudate/Pitting Edema<br> Transudate deals with Starling forces:<br> 1. What keeps fluid in our blood vessels? Albumin, and this is called oncotic pressure.<br> 80% of our oncotic pressure is related to the serum albumin levels. Anytime there is hypoalbuminemia then we will have a leaking of a transudate (protein of less than 3 g/dL) leaking into interstial space via capillaries and venules (pitting edema).<br> 2. Normally, hydrostatic pressure is trying to push fluid out.<br> Therefore, in a normal person, oncotic pressure is winning. Therefore, a decrease in oncotic pressure and an increase in hydrostatic pressure will lead to transudate (pitting edema).<br> 3. Albumin is made in the liver.<br> With chronic liver dz (cirrhosis), have a decreased albumin level. Can you vomit it out? No. Can crap it out (malabsorption syndrome), or can pee it out (nephrotic syndrome), can come off our skin (3rd degree burn b/c losing plasma), another possibility of low protein ct (low-intake) is seen in kids – Kwashiorkor – kid has fatty liver and decreased protein intake, leading to low albumin level.<br> 4. Examples of clinical edema:<br> a. Person with MI<br> MI 24 hrs ago and he died and he has fluid coming out– transudate b/c increased hydrostatic pressure and left HF due to MI so things backed up into the lungs. B/c the CO decreased, the EDV increases and pressure on left ventricle increases, and the pressure is transmitted into the left atrium, to the pul vein, keeps backing up, and the hydrostatic pressure in the lung approaches the oncotic pressure, and a transudate starts leaking into the interstitial space, which leads to activation of the J receptor, which will cause dyspnea. Leads to full blown in alveoli and pulmonary edema, which is what this is.<br> <br> b. Venom from bee sting<br> On arm leads to exudate due to anaphylactic rxn (face swelled), with histamine being the propagator, and type one HPY, causing tissue swelling. Rx – airway, 1:1000 aqueous epinephrine subcutaneously<br> <br> c. Cirrhosis of liver<br> With swelling of the legs: transudate, mechanism: decreased oncotic pressure b/c cannot syn albumin, and increased hydrostatic pressure b/c portal HTN; there is cirrhosis of the liver, and the portal vein empties into the liver; in this case, it cannot, and there is an increase in hydrostatic pressure, pushing the fluid out into the peripheral cavities (so there are 2 mechanisms for ascites). Pitting edema in legs: decreased in oncotic pressure.<br> d. Right heart failure<br> Pt with dependent pitting edema: pt has right heart failure, and therefore an increase in hydrostatic pressure; with right heart failure, the blood behind the failed right heart is in the venous system; cirrhosis of liver is due to decrease in oncotic pressure.<br> e. Modified radical mastectomy<br> With nonpitting edema: lymphedema. Other causes – w. bancrofti,
