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Cool, thanks for the link! I did a whole bunch of Googling and couldn't find an answer.

I've always thought that with a plasma transfusion, blood type is critical, just as with PRBC's, and that therefore a Type A patient, for example, must get only Type A or AB plasma. However, someone told me that in an emergency, a Type A plasma can be given to a Type B patient, and vice versa. Is this correct? The explanation I was told is that although the Type A plasma donated to the Type B patient has antibodies that will attack the recipient's Type B red cells, those antibodies will be so diluted by the recipient's blood that it the transfusion will not harm them.

I know that the recommendation for treating hypertension in a subarachnoid bleed is to keep the BP below 140, but is there any accepted recommendation for traumatic subarachnoid bleeds? Would you treat a BP of 230/120 in a patient with a traumatic brain bleed (not subarachnoid) if you did not know the ICP?

I'm wondering what protocols/decisions strategies the neurologists in your ICU/ER use for deciding to use Keppra prophylacticaly for seizures, and mannitol/hypertonic saline? I ask the question because I don't seem to see uniformity in how certain patients are treated. FYI I'm not a neuro ICU nurse, so perhaps I'm ignorant about something basic. 1) Patient has extensive subarachnoid bleed showing on CT. There is no signs of herniation yet. Is it standard of care to give an anti-epileptic prohylactically? Is there evidence that it really will prevent seizures? Would you give mannitol/hypertonic saline, again prophylacticly for expected clinical course? 2) A patient with an extensive intraparenchymal bleed, again with no signs of herniation yet. Do you give Keppra and mannitol/hypertonic saline? 3) A patient who is ALOC, combative with an obvious traumatic head injury, but no CT has been done. Would you give these treatments? If they were posturing, you would give the mannitol/hypertonic saline, correct?

Thanks for your responses! What do you guys think is the best way to monitor tube placement during transport of a neonate? In adults waveform capnography is great because you get an immediate alert if the tube is dislodged (i.e., into the hypopharanx). With little babies, it is obviously so much easier to dislodge an ET tube and not realize it. What do neonate transport teams use for monitoring?

For a neonate, can waveform capnography be used for ET tube confirmation (post intubation and during transport)? I guess I don't see why it shouldn't be, but I don't see any reference to waveform capnography in my NRP book.

I get that, but my understand is that an arterial occlusion of the leg is going to happen in the femoral artery, or in the popliteal artery proximal to the knee. In either case, you'd have no circulation to the lower leg, and thus neither a pedal pulse nor a posterior tibial pulse.

Thanks for the reply. My understanding is that we are mainly checking pedal or posterior tibial pulses to make sure the patient hasn't developed an arterial clot higher up in the leg, in which case we would find neither pulse. So, as long as we are finding one pulse, it is safe practice to not bother checking for the other pulse, correct? On my unit everyone automatically documents both, and I'm quite sure hardly anyone consistently checks both pulses. It is awfully time consuming when you can feel one of the pulses but can't feel the other, and then have to spend time trying to find it when you already know that there is good circulation.

If you can feel or Doppler a pedal pulse, is there really any need to find a posterior tibial pulse? Likewise, if you can get a posterior tibial pulse, any need to feel for a pedal pulse?

Thanks for your replies. I didn't realize I had gotten any messages, hence this late reply. I've worked in the ER for many years, but I've never seen a seizure due to hyponatremia. We're always ready to treat for this whenever the L.A. marathon comes around.? I'm mostly curious to hear experiences in treating these seizures, and also in how they present. Are these people usually in status? Will they respond to benzos? Of course I understand you want to correct their sodium a bit with hypertonic saline, but I wonder if initially giving them Versed or Ativan will suppress their seizure until you can confirm their sodium level, or until you get that hypertonic saline from the pharmacy since many ER's won't have it immediately available.

Has anyone ever seen a hyponatremic seizure in the ER? I'm just curious on how the patient presented, how long the seizure lasted, if you saw immediate relief from treatments, etc. details.

Taking a two-week paramedic course may certify you on paper, but it will not make you a competent paramedic. You need a bunch of experience working as a medic, not just a little bit of classroom time. I understand that flight programs look more favorably on applicants who have a medic cert, but is it really that important? By the way, I took the online Creighton master's in EMS a few years ago. Maybe you should look into that program. You won't get a paramedic cert out of it, but you will have a master's in EMS, which will look good on your resume.

Thanks for your responses. We didn't want to do amio because she wasn't anticoagulated yet. The obvious thing to me was to do rate control, but I wasn't sure if Cardizem was the right thing to use since it would antagonize the Levophed. The doc didn't want to use it for that reason, though one of my experienced co-workers said she'd seen Cardizem and Levo used together and believed that that was the right thing to do. What do you guys think?

How would you treat this patient in regards to rate control: Pt has been going in AF for a few days, and now they are in AF RVR with a rate of 130. The patient is also on Levophed at 5 mcg/min. BP is 100/60.

I recently heard of a case (if I remember it was the EmCrit podcast, but it may have been another) where a patient with asymptomatic HTN was given hydralazine IVP for a BP of 175/90 in the ED. The patient was admitted for an unrelated complaint (cellulitis) and after the medication his BP was 130 systolic. He was doing fine prior to being sent up stairs, but when he arrived on the med-surg unit, he had developed hemiplegia, so the floor nurse called the doc, who called the neurologist, and after a CT (negative for a bleed), he was given TPA. The neurologist was unaware that the patient had received the hydralazine. The following morning, the patient was unresponsive and was found to have a bleed, likely due to the TPA. The hemiplegia was thought to have been due to the rapid reduction in BP. So my question is, has anyone seen this before? A rapid lowering of BP causing stroke-like symptoms? I have heard of this but never seen it, and it is very common in our ER to lower patient's blood pressures with IV antihypertensives. My second question is why is it such a widespread practice--to give IV antihypertensives even when the patient is asymptomatic---when the current practice guidelines say not to?

Ok, got it. Thanks for all the responses. I realize now that the dialysis could not have made a significant impact on reducing the respiratory acidosis. Makes sense. At one point after she was intubated, I had a chance to bag her for a little while. Wow, I never realized just how poor the compliance is on a ARDS patient. I thought you could only have such poor compliance with an obstruction or a pneumo. That made me really understand just how damaged these patients are!

The patient was perhaps hypotensive due to sepsis, though she could also have been volume down. She initially came in for chronic pancreatitis, then developed a GI bleed, then came to the ICU because she went into respiratory distress after she got blood transfusions. At first they suspected cardiogenic pulmonary edema and diuresed her, but then suspected TRALI. Her creatinine was still WNL. I don't remember the vent settings, but of course she was on a lung-protective strategy (A/C PC) due to the severe ARDS. The idea behind the dialysis was to reduce the acidosis and thereby allow easier vent settings (less volume). No she was not paralyzed, but she was heavily sedated with fentanyl and propofol.

I had a patient with severe ARDS who had been anuric for 24 hours. She was in a respiratory acidosis, with a PaCO2 of 75 and a bicarb of 18. Her pH was 7.20. The fellow ordered CRRT, but the next day the attending d/c it saying that the pt didn't need CRRT because this was a respiratory acidosis. This didn't make sense to me. First of all, even though the pt's electrolytes were stable, shouldn't anurea itself be an indication for immediately starting dialysis? (She was hypotensive, so she needed CRRT). Also, the bicarb wasn't compensating for the respiratory acidosis. I agreed with the fellow's reasoning which was that by starting dialysis to compensate for the respiratory acidosis we could use lower lung volumes, which would benefit the pt's ARDS. All that made sense to me, but the attending disagreed. I didn't hear his reasoning, but what do you guys think?

What is the point of wearing a mask if you have a patient who is intubated and not coughing anyhow? Is it that you could touch something that has their respiratory secretions on it, and then touch your face?

Thanks. The fact that albumin does not stay in the vasculature makes it much easier to understand some of the other processes involved. I'm half way through the article now. Very interesting so far.

Thanks for all the responses so far. One thing I don't understand is how the albumin gets out of the vasculature. Probably I'm forgetting something from physiology class. I understand how the water that's infused with the albumin goes out of the vasculature into the interstitial space, but aren't the proteins too big to go out? Also I'd like to get some opinions on how the following patients should be treated... 1) Normotensive liver-cirrhosis patient with an albumin of 1.0 and a significant amount of peripheral edema. 2) Hypotensive liver-cirrhosis patient with an albumin of 1.0. His BP is 70 systolic. 3) Hypotensive liver-cirrhosis patient with an albumin of 1.0, BP 70 systolic, who is undergoing CRRT.

Thanks for your reply. Since the sodium is not free but bound up with the bicarb, does it have the same effect as if you gave the patient 1150 of sodium only? In other words, would it immediately raise the sodium level, or would it take time for the sodium and the bicarb to come apart?

How much sodium is in one amp (50 ml) of sodium bicarb? Is it 3735 mg?

What is the result of correcting blood sugar levels to quickly in DKA, and also in HHS? I have trouble finding an answer for this. One source says rebound ketoacidosis, and another says brain edema. Also, in peds, has there been a consensus as to the cause of cerebral edema?

Thanks for your reply. What would you do in this scenario: a vent-dependant patient is 3 days post trach placement, and while turning him his trach becomes fully dislodged somehow. Would it be incorrect to make at least one attempt and replacing it? Wouldn't you know if you the track was improperly placed if, after replacing it, you got poor compliance when bagging the trach?