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IV RUS could you pause the IV and then close the rollerclamp to prevent backflow? I get that pausing IV and then clamping ext set prevents backflow but wouldnt pausing and then closing rollerclamp do the same?

I meant if tube is disconnected from unit use 2in of sterile water to place it in...

Ok... love your detail. So, if I'm assessing for a leak 1. Clamp with 1 clamp closest to the patient, if there is still a leak then use the 2nd clamp to clamp a small ways down from the patient? If the leak has still not been found do i move both sets of clamps downward or just the one farthest from the patient? Also, if cdu is full and needs changed where do i clamp tube at? I thought if tube was pulled out it should be placed in 2in of water.

Hi all, Just a few questions: 1. Why do we need two sets of clamps at bedside for a chest tube? 2. If we use them to assess for a leak where are they placed? If we use them to change the system (full cdu) where do we place them? 3. Whwn changing a cvad one must wear a mask, but is this also true for a picc dressing? Why shouldn't we wear a mask to change a regular periphereal line dressing also as all 3 devices provide direct entry for bacteria into the bloodstream and heart? Thanks in advance

Two sets lol

Hi all, I have a few questions about chest tubes and CVAD dressing changes: 1. Why do we need to sets of clamps bedaide for a chest tube? 2. If the clamps are for leak assessment, how are they placed? 3. Where do you clamp the tube when changing the CDU (full) 4. Whwn changing a CVAD a mask must be worn yet is this also true for a PICC? Also, why wouldn't one also wear a mask for a periphereal IV site? As they all provide bacteria direct access to the bloodstream and heart? Thanks in advance

So, I'm studying for my boards and have a few questions: 1. What is the purpose of having two hemostats or clamps at the bedside? I've read a few conflicting things. 2. How do you actually assess for a system leak? Do you use both clamps? Read conflicting things about that. 3. If the pneumo- is healed, will tidying disappear, and if so, please explain the physiology as I've read that it's because the eyelets on the tube become occluded by an expanded lung, but I just wondered if this were the reason because having the tube on suction up against parenchyma seems like it'd cause damage. Please help. Thanks in advance to anyone taking the time to respond. Have a great day.

Ok, but how does the protein leave vascular volume? It states protein remains within vascular spaces to keep osmotic pressure and endothelial cells do not permit their passage except in cases of burns and such when inflammatory substances cytokines are present. How and why is protein getting in there? I understand ascites in cases of malnutrition makes perfect sense: low blood protein=low osmotic pull= fluid in peritoneal cavity but the cirrhosis ascites which states is a protein rich fluid I'm lost

If protein is what "keeps" fluid in vascular spaces and a lack of protein causes ascites as in malnutrition, then how is ascitic fluid caused by portal hypertension "protein rich"?

Hi, I have been reading up on ascites and have a few questions. With liver damage and portal hypertension I've read that the ascitic fluid is "protein rich" yet a patient with a nutrition and protein deficiency has ascites from a lack of protein to create osmotic pressure. If protein is what holds fluid in the vascular space and a lack of protein causes ascites then how does ascitic fluid in portal hypertension yield "protein rich" fluid? How is the protein crossing into the vascular space?

See, that's what I would think also. Like a complete blockage of flow... in which case increasing moms BP and O2 isn't going to matter. Maybe once a nurse pushes on the presenting part to relieve compression, the O2 and bolus would help... idk

So, if it mirrors a CTX in respect to timing but appearance is rapid onset and recovery ud still call it a variable rather than an early? Also ATI suggests 8-10 L of O2 to mom for a prolapsed cord... um I hardly see the necessity. If moms o2 sat are fine, which I'd imagine they are, giving her excess O2 isn't going to help the baby or increase her sat level. It also suggests bolus fluids, and while this will raise moms BP, I'm not making a connection of how this will help the fetus. The kinked cord is still gonna be kinked and baby is still only gonna have some much flow toward the placenta to be oxygenated by mom. I mean u could raise moms bp 200 over 150 and if babys cord is kinked and only sending minimal rbc and flow to the placenta ur in the same mess?????? Please help I'm gonna scream

Ok, so if the decel is happening with the CTX as the cause wouldn't it then be classified as either late or early?

Also, if a CTX is causing the compression, then why would it be a variable decel which I thought had nothing to do with a contraction??? Like variable decels aren't related to ctx and can happen anytime...

See, that's my thought but my teacher said "cord compression" causes variable decels and threw prolapse on the list. Welp, I've researched and variable decels actually resolve and the FHR returns to baseline meaning perfusion is restored. So, I was like if the cord is continuously compressed, as I imagine it would be in prolapse, how does it return to baseline? What the crap. I believe ATI also has prolapse in the variable decel mix. Leaves me confuses