hotcoffee

I will be working at Mission Bay and Parnassus.

It weird how everyone keeps using benzos even when there is evidence they are bad news. I have even had a hospitalist refuse to order precedex because she didnt want the patient "to get intubated" (??) and order ativan instead. Lots of better optioms- Precedex, zyprexa, haldol, etc. propofol and pain meds if intubated.

Anybody?

I am going to be commuting from the peninsula to ucsf. What is the deal with parking? I checked out the website and the lots all have waitlists. Also it looks like the caltrain to N Judah is an option but the muni sounds unreliable. Anybpdy do that? thanks

This is the highest-paying area for nurses, and we have unions so you almost always get to eat lunch (cheers for unions!). It is a hard place to get a job. Lots of new grads move out of town to get experience. If you have teaching hospital experience that will help. Also, some of the hospitals don't pay as well so its easier to find work there.

Sounds like you know more than I do about hemodynamics. But my point was that I don't think it's clinically accurate to say that in all situations an increase in cvp = a drop in stroke volume. There are definite situations in which rising cvp and falling stroke volume occur (tamponade, too much peep, PE, etc). But there are also scenarios in which you might see the opposite relationship- cvp rises and stroke volume increases also (i.e: during blood transfusion to a bleeding patient or after you start norepinephrine and increase venous return on a septic patient).

Use a jaw thrust when bagging a patient, or on someone who is obstructing. most RTs and RNs I have seen bagging don't do it. Emergency Ventilation in 11 Minutes on Vimeo

One thing I have to add- obviously I was not there so I don't know what was happening- but i am reluctant to pull the plug on people who are fully functional prior to admission. Sounds like your patient was super sick. Sometimes people pull through even when the odds are stacked against them. Depends on a lot of factors/ age, comorbidities, etc. you can be surprised how people turn around occasionally.

Regarding the first response- I don't think it's accurate to describe high cvp as an impediment to venous return. But I think I get your point. Cvp is often used as a measure of preload but lots of current info says it's inaccurate. People still use it. the thing is cvp is a pressure measurement not volume measurement. in a normal healthy person a cvp of 8 might reflect adequate preload. put the same person in ARDS and add 14cm PEEP and 8 mm cvp is dry. compliance will be down in ARDS and with peep so you will have less change on volume per mm of increase in cvp. compliance is change in volume / change in pressure http://www.cvphysiology.com/Blood%20Pressure/BP004.htm

Wow that's a lot of questions. you need to look those meds up. sounds like you already have a handle on the clinical implications/applications it will help you if you understand the mechanisms of action get clinical anesthesia by Morgan it's the book you want

Every once in a while this comes up and it bugs me. I have read in a few different studies that really high pao2 is harmful (after cardiac arrest, MI, etc). So to me it seems logical to try and minimize fio2 as long as the saturation is adequate. and typically our orders are to wean 02 for spo2>=90% occasionally when I ask the RT to frm down the fio2 because the patients spo2 is in the high 90s, they ask me for a blood gas because they are concerned about the pao2. who cares what the pao2 is as long as the sat is good? o2 delivery equation is CO x sao2 x hgb x 1.34 + pao2(.003) pao2 barely matters n terms of arterial o2 content. Maybe that's just what they are taught to follow? Rant over

Bicarb isn't in the ACLS algorithm. Does that mean the docs who wrote the guidelines don't know what they are doing too? im not saying we don't give it where I work. just saying that there is no evidence I have seen that it works. treating the underlying problem makes more sense to me than "fixing" the pH

From what I have read there is no evidence that pushing bicarb is helpful. We do it at my job fairly often. I don't have a good grip on the physiology. After you inject the nahco3 you get h20 and co2 and the patient gets a bunch of sodium. this link is interesting 8.7 Use of Bicarbonate in Metabolic Acidosis

I just started advanced Pathophysiology at umass Boston online no exams yet but it seems good

You can get lots of old editions used for cheap on Amazon. clinical anesthesia by Morgan, mikhail is really good. Covers lots of Icu info even though it's an anesthesia text

i think the pass ccrn questions are great. i think some of the questions on the test I took came from Morgan and mikhail clinical anesthesia. I learned a lot from reading that book. also maybe you were just unlucky, it's possible. Or maybe multiple choice tests aren't your strong suit. You can still do it! Keep going and you will pass it.

Actually it does matter where it is positioned vertically when transducing but not horizontally

Very interesting that BIS isn't useful. i read that somewhere else also

My patient's rhythm was juncitonal/3degree block so I doubt there was much atrial kick. I imagine VVI wouldn't cause a drop in output. thanks for the responses

That's what I was saying! Thank you. so the capture threshold is the lowest possible mA at which you have capture. i think you need mechanical as well as electrical capture which can be verified via art line, pulse ox or just a finger on the pulse.

Took care of a CT surgery patient with an epicardial pacer connected but on backup rate of 35 VVI. She was alert and doing great. At shift change we check thresholds. The patients intrinsic rate was about 60 so we set the rate at 70 and were checking the capture threshold. As we turned down past 1.5 mA I could see the EKG rate drop from 70 to the 60s and the pulse ox "pulse" rate drop to 60. Also the Qrs narrowed and changed morphology (looked intrinsic rather than LBBB/paced). so to me we had lost capture and 1.5 was the threshold. The other nurse said that because there were pacing spikes followed by a Qrs we still had capture at 1.3mA even though the patients rate dropped to 60!? what do you think Internet?

Why have a carrier fluid at 100? That doesn't make sense. i believe if you have a drip going slowly (less than 10) it makes sense to run it with a kvo (saline at 10). I don't know of any evidence for the practice but I have heard that line will clot if the drip is going slowly (less than 10). never seen carrier fluids at 100.

Makes sense

Yep you're right. You can zero close to the floor and it does t matter. weird how when you lower the transducer it reads a higher pressure. i do t understand the physics of it.

Of course it depends on the patient. There are lots of conditions besides coronary occlusion that can cause trop elevation- PE, sepsis, other bad stuff. In my experience with a big Stemi you'll see it go high in whole numbers. lots of patients in the hospital for non cardiac reasons will be diagnosed with note I but the trop won't go big also it's a trend and will usually peak I think 6-8 hrs (?) after the event