Chief1C Posted October 7, 2009 Posted October 7, 2009 6 LPM/NRB is what our medical director suggests, for hyperventilating patients that can't be easily coached into slowing their breathing. As for regular administration of oxygen, I use the "To Keep The Bag Full" theory.. On NRB's 10 or 12.. NC gets 2 or 3.. Nebs get 6 or 8. People that are getting road sickness, but are otherwise okay; I use the "dog in a car" theory. 2 by NC, tell them it may keep them from getting sick. I hope my white lie distracts them, and like a sugar pill, they feel better. Or just don't vomit. 2
VentMedic Posted October 7, 2009 Posted October 7, 2009 6 LPM/NRB is what our medical director suggests, for hyperventilating patients that can't be easily coached into slowing their breathing. Here you can run into some problems with "interpretation". The NRBM manufacturers have provided recommendations for safe liter flow when using their product. Many publications and protocols have published their recommendations for the usage of O2 devices and liter flow. Do you have the medical director's suggestions in writing? If not, when an adverse incident occurs, the MD might say in the depo "that's not what I said and especially not in that circumstance". Your charting and that of the rec'g ED will have the documentation to which you may have to defend your actions. 1
tniuqs Posted October 7, 2009 Posted October 7, 2009 There ya go buddy! Cheers! Take care, chbare. Whoo Hoo thanks Lord chbare, back at you and one for medicv83 for just starting the thread, good learning post from all, and its hard to keep up with the other oxygen pple. As for 4c6 .... I think a negative rep just to piss him off wtf is the "dog in a car" theory ? Do you talk to dogs or watch to many episodes of the Dog Whisperer ? .... cheers ps the rule of thumb(s) or now referred too as the 4cmk6 Protocol/ Guidelines aint a bad way to go using a Pulse Ox, but I sense a repremand with the A/a gradient vent introduced ... oh well live and learn. 1
VentMedic Posted October 7, 2009 Posted October 7, 2009 bad way to go using a Pulse Ox, but I sense a repremand with the A/a gradient vent introduced ... oh well live and learn. Now, now... The A-a gradient thing is more likely to be an issue with a NRBM. I had thought the "dog in car" theory was like my "cat in carrier" theory when I lie to them. However dogs will believe anything their humans tell them and cats want evidence based proof. 1
RavEMTGun Posted October 7, 2009 Posted October 7, 2009 What a great thread! ps in passing did you know that 15 liters per minute on a BVM can actually cause iatrogenic PEEP, and lead to Dynamic Hyperinflation and dump a intubated patients BP ... ok enough of that, but the point being you want to deliver 1.0 Fio2 ...use a BVM, talk to your patients and watch the reservoir bag ...if its not deflating a bit your wasting O2 bottom line and could be causing some more issues. Can you expound on this more, especially the iatrogenic PEEP? Yes and no. If you are unsure, I see no problem with a cautious approach and supplemantal oxygen. However, sustained exposure to high fractions of inspired oxygen can lead to problems. You can have nitrogen washout and collapse of the alveoli, you can have damage to type I and type II alveolar cells, and even free radical concerns. Therefore, I can see your point; however, health care does nor stop at the door to the ER. Therefore trying to look at the big picture is helpful. Take care, chbare. Wouldn't alveoli collapse from N2 displacement followed by a return to indadequate TV or at least high deadspace? Alveolar cell damage? I have also seen patients with an SpO2 of 100% on a NRBM come back with an A-a gradient of 300+ mmHg and get intubated. Hence, the reference to the flu and the PNA associated with it. Can you explain this further, especially the A-a gradient? 1
chbare Posted October 7, 2009 Posted October 7, 2009 What a great thread! Wouldn't alveoli collapse from N2 displacement followed by a return to indadequate TV or at least high deadspace? Alveolar cell damage? The problem is in essence three fold: First, we do not use nitrogen, therefore nitrogen gas is present in our alveoli. Nitrogen is still present after oxygen diffuses out of the alveoli, allowing the alveoli to stay open in part because of the pressure that nitrogen exerts. If we replace nitrogen with oxygen, we can run into a nitrogen washout scenario where oxygen is dissolved, but nothing is left behind to keep the alveoli open. Next, once alveoli collapse, they can be quite difficult to open back up again. It is not a simple matter of inflating with volume or pressure. Finally, if the type I & II cells are damaged, you have damage to the endothilial lining and damage to the cells that produce surfactant, another substance vital to keeping the alveoli open. It is a complex situation. Can you explain this further, especially the A-a gradient? A = Alveoli where a = arterial. The A-a gradient is the difference. (PAO2-PaO2) Normal is around ten or so depending on your patient. High A-a say around 65 or greater indicates some sort of VQ mismatch. You can calculate the Aa gradient by finding you PaO2 on the ABG. Then, you can use the alveolar air equation to give you a good idea of the PAO2: PAO2 = (BP-VP)* FiO2 - (1.25 * PcO2) [ BP = barometric pressure (760 @ MSL), VP = Vapor Pressure (~ 47 at body temperature) So, a generic setup would look like this: PAO2 = (760-47)* 0.21 - (1.25 *40) Take care, chbare. 2
VentMedic Posted October 7, 2009 Posted October 7, 2009 A-a is Alveolar to arterial What you expect for PAO2 at the alveolar level minus the measured PaO2 or arterial level. A-a gradient = PAO2 - PaO2 The normal difference should be about 10 mmHg. Alveolar equation: PAO2 = ( FiO2 * (760 - 47)) - (PaCO2 / 0.8) Now you can also relate the value for the PaO2 and SpO2 (or SaO2) via the Oxyhemoglobin Dissociation Curve. http://www.ventworld.com/resources/oxydisso/dissoc.html The SpO2 or SaO2 can still be near 100% but the A-a gradient might be very wide which could be the result of impaired diffusion or ventilation-perfusion inequality or mismatching (V/Q) or shunting. Of course, once removed from the NRBM the SpO2 will probably drop quickly. 2
Chief1C Posted October 8, 2009 Posted October 8, 2009 aint a bad way to go using a Pulse Ox I didn't say anything about a pulse ox. I personally avoid it's use, b/c I don't think it works properly. If it does.. Even at rest and perfectly calm, I'm tachy. Maybe the end is near? Oh well. Anyhoo, Dog in a car, is what I say when I tell noob responders to open and sit next to the curb window, for air.. when they're getting motion sickness. Kinda of like a dog sticking their head out the window of a car. We were taught to use a plain SCBA bottle, with no fittings, just an open valve, to ward off nasty dogs to get at patients. Blowing in a dogs face, either pisses them off - or they run away, but sticking their head out the window of a car apparently makes them feel good. As fresh air seems to cure ride induced nausea, since sea bands clearly don't work. Dog In A Car, Theory. I didn't mean hot day suffocation. I'd have said head out the window theory, but then you'd be blaming me when your partner got decapitated by a road sign. 2
medicv83 Posted October 8, 2009 Author Posted October 8, 2009 I greatly appreciate all the responses, and I think two things I will take from this thread.... 1) o2 was obviously in order, in at least the short term aspect of the pre-hospital care that was performed. Which I kind of already had figured out, but was looking deeper as to why this Nurse was so adamant that it be taken off 2) I have to do some more research on this A-a gradient/equation that is being talked about. On this note....It can be said now that, if we are not already doing so, we must look deeper into the broad picture of a simple tachypneic patients hx or s/s to take this essentially BLS level call, and identify the true etiologies that may be effecting this pt and his resp rate. Certainly sounds like something we say we do, at least for me, and to be honest with you, I packed this one into my head right from the get go as an anxiety induced sort of hyperventilation. Thanks again for the educational responses~! I need to get on here more often, I almost forget how informative this site can be!
RavEMTGun Posted October 8, 2009 Posted October 8, 2009 When googling VQ I found this great educational read (don't forget to click forward)! http://www.scottishintensivecare.org.uk/education/icm induction/respiratory failure/vent2.htm CBHare: the 100% SpO2 with a high A-a gradient... how does he have a high A-a gradient but still good sats? How does tubing fix the A-a gradient? Additional Question: So how do we avoid alveolar collapse secondary to oxygen displacement of nitrogen? Ensure good TV and MV? Only run high flow for a short time? How common is this problem really? What is the mechanism that causes the damage to the type 1 and 2 cells?
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