captainstandup Posted October 15, 2007 Share Posted October 15, 2007 Based on the presentation and progression of this case I feel he is suffering from CHF. Although most of the folks we see with CHF have either a much higher or much lower blood pressure. You said frothy sputum, is it pink or clear? Anyway we need to get a V-4 R before we start slamming him with nitro in the event he is having an MI with primarily RV involvement. We also need a second IV in case this fellow needs to go to the interventional cath lab, but we want to limit fluid admin to KVO for now. Also I didn't notice if anyone asked if this guy was taking viagra, levitra or cialis as this is more common in diabetics. It would also be nice to know if he has dependant edema or a distended abdomen suggesting hepatic engorgement with fluid. In absence of RV involvement this guy needs nitro q5 as long as his pressure will stand it or in our case a NTG drip. He also need 120 mg of lasix. Since he is getting really tired and lethargic I think we are likely beyond the point of being able to use CPAP therefore we are going to be forced to RSI him. akroeze is spot on in that this person needs high flow diesel fuel. It would be really nice to have a chest x-ray and labs but obviously these aren't available in the field. Link to comment Share on other sites More sharing options...
EMS_Cadet Posted October 15, 2007 Share Posted October 15, 2007 Hmmm...Very interesting scenario! I'm very tempted to think that this is acute pulmonary edema. I am, however, reminded that no patient is "normal" or "textbook". As an EMT (and EKG guru) waiting to state test, this is my line of thinking: More than likely, this patient has suffered a previous anteroseptal MI, causing acute heart failure. The presence of the Q waves in the septal and anteroseptal leads leads me to believe there was an old infarction. Also, since the bundle branches are contained in the septal area, an old infarction could possibly damage the LBBB. The septal damage is probably causing LV dysfunction, resulting in acute pulmonary edema. As for the presentation, it sounds like a classic CHF case with the exception of the BP. However, this patient could be one of those "odd" people that has a fairly normal BP even during a major cardiac event. Also, does the patient have any edema, JVD, or abnormal cardiac tones? I also would LOVE to get a BGL on this man. I don't think anyone has asked for one, despite his NIDDM. Link to comment Share on other sites More sharing options...
chbare Posted October 15, 2007 Author Share Posted October 15, 2007 V4R is negative for any acute changes. So, we can tell that this patient has had an MI at some point. How long ago? Hard to tell based on the information we have. However, if the pulmonary edema developed as a direct complication from the MI, would we not have seen it occur during the acute phase of the MI? So, the question still remains. What is going on with this guy? It looks like we may need to RSI. If he is not awake and alert, BIPAP will most likely not be an option. NTG is not a bad idea. We are looking to reduce both preload and afterload with NTG? Lasix may be an option, perhaps we could discuss the rationale for using it with this patient? Any other meds to consider? Is there something that may help us figure out what is going on with this patient? The BGL is 175 mg/dl. The frothy sputum is white in color. Link to comment Share on other sites More sharing options...
DwayneEMTP Posted October 15, 2007 Share Posted October 15, 2007 Apparently tongue-in-cheek humour is not appreciated. I shall try to remember that. Anyway, from what I'm seeing so far I want to immediately get this guy on a high FiO2. I would have my partner attempt to assist his respirations (if possible) while I auscultate the chest, get a full set of V/S (BP, Pulse, Resp, GCS, Saturation) and a rhythm strip. You know what is completely stupid? I read that and thought "Hell, he usually has great posts, I'll bet he's right. It pisses me off that he cheated me out of tracking it down on my own!" My next thought...."Ok...syphillis...what is the physiology of syphillis getting to the lungs...??" Sorry akroeze...Lately I'm having trouble keeping all my plates spinning, and it's evidently got me a little grumpy, I should have thought it through before acting like an ass. Dwayne Link to comment Share on other sites More sharing options...
captainstandup Posted October 15, 2007 Share Posted October 15, 2007 Damn, now I have to research syphillis infections and the associated pathophysiology. Thats what I really enjoy about these threads, they really make you think. With that said I doubt its related to syphillis hmmm back to you in a few. Link to comment Share on other sites More sharing options...
captainstandup Posted October 15, 2007 Share Posted October 15, 2007 Is it possible he is reacting to something he was using to wash dishes? Exposure to certain toxins will cause "non-cardiac" pulmonary edema. Of special nastiness are chlorine, ammonia or nitrogen dioxide. I know, this is grasping at straws but this is an unusual presentation. What about considering an albuterol HHN tx earlier in the case. Another concern would be a massive lung infection but ordinarily this would have been know by the patient and would have been of gradual onset. Link to comment Share on other sites More sharing options...
Just Plain Ruff Posted October 15, 2007 Share Posted October 15, 2007 For Akroeze An article on syphillis and respiratory illness http://www.aegis.com/conferences/hiv-glasgow/2002/P257.html But CHBARE, wheres the twist? You said there was a twist. I'm leaning towards Pulmonary Edema but there's something else going on here too if you go specificaly with the chest pain with a twist topic title. What is his LOC now? Is it to the point where this guy is so tired that we have no choice but to RSI him and ventillate him? I think that we may be to this point. Or is he becoming so obtunded that he would not fight off attempts to nasally intubate or orally intubate him? Has anyone mentioned Morphine or is his BP too low now? Do we have access to the following: Nesiritide (Natrecor) -- Recombinant DNA form of human B-type natriuretic peptides (hBNP), which dilate veins and arteries. Human BNP binds to particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells. Binding to receptor causes increase in cyclic GMP, which serves as second messenger to dilate veins and arteries. Reduces pulmonary capillary wedge pressure and improves dyspnea in patients with acutely decompensated congestive heart failure. Here’s a little statistic regarding sub-optimal care in the acute setting • Based on data from 4606 patients hospitalized with CHF between 1992-1993, the total in-hospital mortality rate was 19%, with 30% of deaths occurring from noncardiac causes. These patients, however, were noted to have had suboptimal use of proven efficacious therapy, compared with those who survived hospitalizations, particularly among women and the elderly. Thirty-year data from the Framingham heart study demonstrated a median survival of 3.2 years for males and 5.4 years for females. source http://www.emedicine.com/EMERG/topic108.htm Link to comment Share on other sites More sharing options...
chbare Posted October 15, 2007 Author Share Posted October 15, 2007 -There is a twist. Everything points to your run of the mill massive MI left sided failure type patient. However, the 12 lead indicates that the patient may not actually be actively infarcting. What if the MI may only be part or a contributing factor to the problem at hand? Are we able to gather any more information on this patient? -You did not notice any chemicals at the scene otrhan dish soap. -His blood pressure is still 120/72. You are able to RSI and intubate without difficulty. You still have about 15 minutes to the hospital. Take care, chbare. Link to comment Share on other sites More sharing options...
Just Plain Ruff Posted October 15, 2007 Share Posted October 15, 2007 well let's see, I'm suspecting the big one. Are we sure we have the leads in the right places??? It could happen. What about this scenario WE had a patient one night who when they had chest paiin they showed an MI yet when their chest pain resolved they showed a normal ekg. I was pretty new at the time and I didn't believe it but the cardiologist said at the time(I hope I get this correct) - that the clot was right on where the artery branched and split. When the clot was covering the opening of one of the arteries the MI appeared but when the clot was not on the opening then there was no MI. (Can this even happen? I was skeptical). The patient was given Eminase and the MI symptoms resolved. It sounds like this guy is too far into his MI but I just thought this was pretty hinky, I mean my patient. Link to comment Share on other sites More sharing options...
chbare Posted October 15, 2007 Author Share Posted October 15, 2007 -The leads are placed properly. -Think about conditions that cause acute pulmonary edema. The guy had pretty sudden onset pulmonary edema, so you may consider that perhaps he developed an acute problem. -Would you assess anything else? Think about things you want to assess in a CARDIAC patient. Take care, chbare. Link to comment Share on other sites More sharing options...
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