VentMedic Posted October 7, 2009 Posted October 7, 2009 I'll make an educated guess here, but perhaps you should have said "chest pain" instead of "hyperventilation". I am not trying to second guess you, here, I'm just thinking out loud. True. I would have said tachypnea with decreased SpO2 as presenting and then go from there. However, right now if a 24 year old has similar complaints in our ED they will immediately get a nasal swab up the nose and a filter mask until the determination is made they do not have the flu.
chbare Posted October 7, 2009 Posted October 7, 2009 Hey guys, we also need to appreciate the difference between oxygenation and ventilation. Putting somebody on a non-rebreather is not going to change their carbon dioxide. Talking about chemoreceptors and respiratory center activation, we need to realize acids typically tell us to breath. When you hold your breath, the urge to breath is due to carbon dioxide levels increasing. Therefore, I cannot see any harm in the short term by placing a person who is breathing rapidly on a NRB if we are unsure of the cause. However, assuming hyperventilation syndrome is a dangerous mistake without solid evidence to back it up. I have seen many anxious diabetics in DKA breathing rapidly to compensate. You assume a rather benign condition and have them breath in a bag, you just opened a big can of fail. Many other pathological causes can cause "hyperventilation" and must be ruled out. ( overdose, pulmonary embolism, trauma, metabolic acidosis to name a few) Take care, chbare. 2
medicv83 Posted October 7, 2009 Author Posted October 7, 2009 As far as the chest pain is concerned, I personally, in my own mind, felt as if this chest pain was secondary to the tachypneic state this pt had been in for nearly 15 min. Pt wife states that he has no med hx, w/nkda, and does not take any prescription medications. Sounds kinda lame I know, but he has no medical problems. Throughout the day though, the wife states she started accusing him of cheating on her with someone who works at the hospital. She states that he was getting angry throughout the day, and that he did have an earlier episode of this rapid breathing, however it lasted appx 2-3 minutes, and he was crying and very emotional when this happened prior to. She was able to calm his breathing verbally. She states that he walked outside after she suggested that if he wanted to get angry with her, that he should leave and go talk to his "girlfriend". Once he was walking outside he started breathing heavy and it turned into what was present when we got on scene. Vent, I was anxious to hear your response to this, for no other reason than I like the way your responses are worded. I had read those articles prior to posting on here as I was trying to find this out through my own research. However they dont state how the admin of o2 is bad in strictly a hyperventilating pt. As far as the other etiologies of tachypnea, one would think from an EMS point of view, that they all deserve o2 admin correct? 1
tniuqs Posted October 7, 2009 Posted October 7, 2009 (edited) It's not so much about the oxygen but the CO2 blowoff. With the patient passing out, metabolism continues and CO2 slowly increases back to homeostatic levels, whereupon the patient comes to and breathes at more normal rate. Question, was there any spasms noted with the patient? The nurse would probably want to stick the patient's head in a paper sack with that attitude. Agreed, I like how you explained that and laughing .. the old paper bag kill them trick MAJOR RN FAIL. Carpal spasm more correctly (just showing off is all) The OP presented/ painted the picture in Technicolor and with SpO2 of 89% on FiO2 of .21 then O2 admin is required asap, no questions asked, it certainly sounds as if Hyperventilation Syndrome (er increased deadspace ventilation due anxiety) was the underlying patho here .. but these days we should not ever rule out recreational drug use(cocaine or meth) or even excited delirium to this presentation, yet another differential dx could be Central Neurological Hyperventilation Syndrome from the early onset of an inter cranial bleed, and with DOA ie drugs of abuse on board then having an MI associated, yes even at this age this should NEVER be ruled out. Late edit Ventmedic/ chbare "tachypnea" more susintly, dang always a day late and a dollar short with you guys .... YES the RN should be treated for cranio rectal inversion, she knows zip (bitch slapping sounds overheard)so use the info provided to open a dialog and discuss all presented here. Now on to my bro LS ... JPINFV is quite correct there are 4 factors that affect any mask or N/C delivery, the concepts they teach about the concentration and flow in differing delivery devices are JUST optimal and just in the books, Unless one exceeds the patients minute volume by 4 times your kidding yourself that a NRB is actually delivering what the books say, or by definition NRM is a high flow delivery system ... I am going to make a RT out of you guys if it kills me ! Since the patient's SPO2 reading was initially 89 on room air, one would think that the hypoxia was the primary 'drive' behind the hyperventilation. The major drive is NOT hypoxia its CO2(argh as already stated) ... unless documented with ABGS and that is only 5% of KNOWN COPD ers....in this case the drive was higher up like frontal lobes anxiety or drug assisted. Criteria for optimal delivery for Masks or N/C. 1-RR less than 28 2-properly fitting mask (as if the reservoir bag ever collapses with one size fits all) 3- RR is regular. 4- Ok I forgot but I know there is another criteria. 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. cheers Edited October 7, 2009 by tniuqs 1
chbare Posted October 7, 2009 Posted October 7, 2009 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. 2
VentMedic Posted October 7, 2009 Posted October 7, 2009 (edited) Vent, I was anxious to hear your response to this, for no other reason than I like the way your responses are worded. I had read those articles prior to posting on here as I was trying to find this out through my own research. However they dont state how the admin of o2 is bad in strictly a hyperventilating pt. As far as the other etiologies of tachypnea, one would think from an EMS point of view, that they all deserve o2 admin correct? We will sometimes do O2 by SpO2 and titrate from there unless there are other immediately obvious factors. Short term O2 should not present a problem. Quite often that STAT ABG upon arrival to the ED will reset the breathing or be enough push them over the edge. Either way it gets "results". I just make sure they are on the stretcher when I poke them. The presenting SpO2 and symptoms did warrant oxygen. A 24 y/o with the initial SpO2 of 89% would deserve a closer look regardless of what emotional issues were going on. The drama is important information but the onset, length and presentation should be emphasized more than the nitty gritty details. Too many distractions can skew an assessment which is why I do fault the RN here for assuming without at least a closer look. O2 can be titrated as the symptoms and vitals stabilize. However, allowing a patient to remain with a low SpO2 could be worse. 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. Edited October 7, 2009 by VentMedic 2
tniuqs Posted October 7, 2009 Posted October 7, 2009 (edited) 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. Ah the fledgling RRT ... Oxygen absorption micro atelectasis, EXPLAINED, nicely done. Funny we (EMSers) throw everyone on O2 then only to start weaning them off as soon as we introduce ourselves as RTs or as Vent medic states "titrate", got to love it and with newer studies in regard to treatment of CHF maybe down the road this will become a household EMS concept ...one can only hope.... Oxygenation can be far more complex than just looking at a pulse ox and with the now introduction of A/a Gradients ... hey don't hurt anyone Vent ... Oh in passing wtf in the reputation department ... I only warrent a 2 ...sniff Edited October 7, 2009 by tniuqs 4
VentMedic Posted October 7, 2009 Posted October 7, 2009 Oh in passing wtf in the reputation department ... I only warrent a 2 ...sniff Now you have 3.
Recommended Posts