loafin'

I agree, just adding more info.

Actually, with nitrates and topical anesthetics that you mentioned as well as others can cause methemoglobinemia. They can change the structure of hemoglobin to where it cannot hold o2, thus causing sats to rapidly decrease. If methemoglobin levels are high enough the patient can die. The antidote is methylene blue.

Well SuperRT, I just happen to be a RRT and a RN. This has gotten way off topic, it's supposed to be about whether to give ice to an intubated patient. Nobody has mentioned giving a patient all the ice they could hold. As I stated in previous posts that if the patient is alert enough to ask for ice then they will be extubated soon. Giving a few ice chips is no different than the toothettes we use to do oral care Q2hrs, they have about the same amount of liquid.

If the cuff pressure is high enough to hinder swallowing then the patient has tracheal malacia and/or the trachea in necrosing. Ask your RT if he/she has ever heard of a chronic home ventilator patient who's trached and eats solid foods and drinks liquids at every meal.

Where is your info coming from? When we suction the vent alarms high pressure, it has nothing to do with losing the cuff seal. No, it's not easy to swallow with an ET tube in your mouth. Where do you think the natural oral secretions that a patient produces goes? Either they swallow it or it sets on top of the ET tube. If there were any validity to what you're saying about the cuff not sealing then every single ventilated patient would have VAP. As far as aspirating we make them aspirate every time we lavage. I will agree some patients occasionally aspirate but so do you and I. The last time you took a drink of soda and aspirated how long did you make yourself npo. We're talking about a little ice not a big mac and coke. If the patient is that awake and alert they will surely be extubated shortly, a little ice won't hurt.

Why not give ice? The airway is protected and pt's can't aspirate unless the et tube cuff blows or et tube comes out. On any intubated pt there are secretions setting on top of the et tube and that's one reason we tell them to cough as we extubate as not to aspirate the secretions.

it is actually called winter's formula. bicarb x 1.5 + 8= expected paco2 +/-2

I will address your question regarding the respiratory meds. Both xopenex and albuterol are both beta2 agonist or sympathomimetics. The medications bind to beta2 receptor sites in the bronchial smoothe muscle causing relaxation. I will explain the difference between these two as I understand it. Albuterol is made up of two isomers, an R-isomer(1.25mg) and an S-isomer(1.25mg), making the 2.5mg dose. The S-isomer once thought to be inert is now being shown to have detrimental effects such as causing bronchoconstriction. Xopenex is actually the R-isomer(responsible for bronchodilation) only of albuterol. Essentially the same medication excluding the S-isomer. Now, the decreased cardiac side effects associated with xopenex is the standard adult dose of 0.63mg(also comes in 1.25mg and 0.31mg) which is actually 1/2 albuterol minus S-isomer. Either med may cause cardiac side effects, but 0.63mg xopenex is less likely than 2.5mg albuterol. Ok, atrovent like atropine is an anticholinergic or parasympatholytic. Atrovent blocks the parasympathic response of causing bronchoconstriction, just like atropine blocks it's response of slowing heart rate. A sympathomimetic and a parasympatholytic can be very effective in promoting and prolonging bronchodilation. Hope this helps.

Vanderbilt University has an acute care NP program that after graduation you have an option for early interview to anesthesia school at Middle Tennessee School of Anesthesia. You will be able to practice as both. Vandy is the only one that I've checked out, I'm sure there other schools with similiar options.

I know this, but thank you for clarifying that oxygen does play a very inportmant role in pH. A lactate level would be drawn of course,but we would know that it was lactic acidosis just by doing a venous gas with the p02 being virtually the same as the abg.

Actually oxygenation does affect pH. The most profound acidosis I've ever seen was on a client who had cyanide poisoning who had a pH of 6.6. He had a normal p02 and sat with abg. I drew venous gas and was vertually identical. He was in anearobic metabolism(lactic acidosis).It is called hystotoxic hypoxia,that is cyanide prevents unloading of o2 from hgb to tissues. Any situation that causes anearobic metabolism for long enough will cause acidosis.

BabyMO1, PM me if my reply to asoldierswife05 still did not explain enough.

You understand exactly. There is a formula called winter's formula for expected pco2 with a given hco3. The abg and client on bipap is a big clue Remember HCO3 compensates slower than co2. And actually the bicarb might be slightly lower than client's normal, difficult to know exactly without seeing a normal baseline abg for this client. I wonder if this client had a previous admission with another abg. Give yourself more credit, sounds like you have a pretty good grasp. Sometimes we have to think out of the box and not automatically assume that everything we learned in nursing school is law. I mean we know our normal ranges for our lab values, but sometimes when things fall out of range especially abg's, it's not always as simple as using the arrow system(when co2 is up and hco3 is down, it is this...).

The experienced RT and charge RN were correct. The K+ was low due to the client hyperventilating and lower the hydrogen ion concentration and subsequently pushing K+ from extracellular to intracellar.

I gave my explanation, what is yours. People who have a high bicarb do not slow down respirations to compensate. this is client is a chronic hypercapnic. I don't need any other hx besides abg's to know that.

Actually this is quite simple. I've seen it hundreds of times with chronic hypercapnic's who are very anxious(especially fighting Bipap). You will see the same thing with a client who is a chronic hypercapnic who is place on vent with too high rate. This client's co2 is below his normal. His normal is somewhere around 73 mmhg +or - 2. So it is actually respiratory alkalosis. There is no strange electrolyte imbalance or a drug that caused it. PM me if you would like a more detailed explanation.

At Centennial if you live >50 miles you can stay at a hotel for $10/night and the hospital pays the rest of the bill, they also have nice apartments for the same rate.

$19-20/hr

I don't understand where the info comes from regarding o2 liter flow and client's with COPD. Just because you have COPD doesn't mean that you are a chronic hypercapnic. You can be a chronic hypercapnic and not have COPD. It's not about the Fio2, it's about how much is diffused across the AC membrane and becomes PaO2 and o2 sat. We traditionally like a chronic hypercapnic's sat 88-92%, regardless of Fio2.

elthia, with status asthmaticus subcu epi could have been given or mag sulfate iv. itsybitsy spider, what do you mean PEEP? how was it used?

I work at Centennial Medical Center and love it. It is a 600+ bed hospital and I work in the 32 bed MSICU. They also have a CVIVU and CCU. The ED nurses and floor nurses seem to like their job too. I haven't heard otherwise. Usually people are happy or you will definately hear about it.

Yes it is possible to be NP or CRNA w/out BSN. Vanderbilt has a MSN NP bridge program for AS/AD to MSN and a bachelor's in any field(without prior RN degree) to MSN. There are also CRNA school's that will accept RN's with bachelor's in another field with the required prerequisites.

what is theoretical? Wet crackles are from fluid and dry are not. your first post was asking how to distinguish between the two, there was nothing about a study.

Yes you can distinguish between wet and dry crackles. Wet with chf or patients who have retained secretions and need suctioning. Dry crackles can usually be heard in bases on late inspiration(due to small airway collapse, at the end of ispiration they pop open). You can also hear dry crackles with patients who have pulmonary fibrosis.