AZCEP

Go back to page one of the thread and look at the excerpt from Dr. Wall's book. All of your RSI questions will be answered accordingly.

Not unless they are septic.

The brain is failing so the chemoreceptor center is maintaining function at a "pseudo-elevated" rate based on the amount of CO2. If the brain would regain perfusion the respiratory rate would increase accordingly, but because it can't the only drive is from the brain stem, thus the rate that is present.

I'll say commend, but don't you have to be hired before you can be promoted? Tough spot for the department he applied at. This kid could be the least qualified of the pool, and now he has a newsworthy save on everyone else. Oh, right, public safety, helping others, blah, blah, blah :roll:

This knuckle head isn't spending a dime on education! :x He says he is spending the money, then tells us the department picks up the tab for most of it. I read that as, "I find every high-dollar course I can so the chief will pay to get me out of town for a few days." Oh, and, "real soon I will be signing up for a paramedic class so that I can spout useless knowledge when someone asks me a medical question when I am off duty, and wearing my full paramedic garb. You know, hat, glasses, belt buckle, jacket, name tag, patches. I am so cool, maybe I can convince someone that I am the hottest thing since the rotating flashing light." Stay in school and learn some humility, you will need both.

Here is a current version in MS Word that may be easier to cut/paste. Remember to add in your representation's name. Also a good idea to include your name and contact information

Okay, so the pulseless patient received Epi/Atropine down the tube. Dose not important just yet. Code worked, ROSC briefly, then back to cardiac arrest with spontaneous respirations, right? So following the description of events, my thoughts would be: The Epi/Atropine that was given down the tube had little/no effect on the situation immediately following administration. CPR with IV Epi/Atropine/Bicarb got the vascular bed to return more CO2 to the central circulation (heart/brain) Return of spontaneous circulation returned even more of the bodies CO2, and the CO2 that came with the administration of the Bicarb to the heart/brain. The increase in the return of CO2 to the chemoreceptor areas of the brain stem caused the ventilations, not a direct response of the brain stem to the catecholamine. The fact that the patient continued to breath pseudo-normally after returning to cardiac arrest would indicate that there was a significant amount of CO2 that the brain chose to remove through ventilation. I still doubt that Epinephrine, by itself would create and environment in the arrested patient to allow spontaneous respiratory patterns. But, hell, not all patients are willing to read the instruction manual for what they are supposed to do anyway. Sure why not ?

Every letter that is sent is one less that is needed. The links have been provided, the information is there as well. Take a few moments to compose a coherent thought on the subject and send it to your representation.

Make your wheels squeakier than everyone else's. For your next council meeting, have a discussion on funding for the EMS service placed on the agenda. Make sure that all of the members that can are in attendance. Nothing like showing up en masse to rattle the cages. You know your situation better than anyone here, but taking the information that the feds have generated can be some powerful ammunition for your cause. This might lead to newspaper articles, or other local media coverage for your service. The first step is the hardest. You have the support of the City, if it helps.

The toughest situations are the ones you happen upon. You don't have time to adjust your mindset, and change the plan that you made before arriving. Even worse in the middle of the night.

One slight problem with that description whit: Class room + Field experience = Education You can't really have one without the other to consider yourself "educated" Take a student out of the classroom with no experience, what will you end up with? Take an EMT with 20 years of field experience, that has not tried to further themselves, and holds to the minimum standard that they learned in class all those years ago, you will end up with the same problem in the end. The information that is presented must be expanded on by field experience. That is why all paramedic classes require as much, if not more clinical/vehicular time than they do classroom time. Even with that, the most new providers will learn comes in the first few weeks they are forced to practice on their own, without a safety net. The learning curve is much steeper for those that did not get exposed to the information in class. You also can't take an EMT class, not apply the information for 15-20 years and expect to have good results either. I'm sure you've come across providers like that in your practice, if not where are you, because I am tired of dealing with them.

The horrible thing for local governments, is the fact that the meetings are open to the public :twisted: Federal representation has been notified, now it is on to the locals.

Letters duly sent to my representation. You would think that with an election coming up, they would be more responsive than normal. Probably have to send one daily for the next millenia to see an effect, but if that is what it takes form letters are not hard to generate.

The risk is there, and should not be minimized. The benefit, however, is often greater than the associated risk. This is what makes the decision making necessary. No one, not even CT/MRI/PET scanned provided neuroradiologists, can definitely rule out the possibility of a hemorrhage based on the image given. So if the physicians can't be 100% sure, and we can do a similar level of risk assessment, why couldn't we use the same tools to do the same job. Before the medication is used, the family has to consent to it as well. They base their decision on what information we provide them. If they decide yes, then why not have it available? If they decide no, why would we be willing to argue? Use for Acute Coronary Syndromes can wait due to the longer treatment window. Use for CVA's, without intraarterial administration can't wait. It is these patients that it could make a huge difference in. The recommendations for use are very clear on when they could be used for CVA. If we can notify a receiving facility of a possible candidate, the next step is, in fact, our being able to use the medication to fix the problem.

That is an interesting read. Apparently someone has been watching some of our discussions. They actually realized the volunteer system is failing, and that a transition to a paid service is the answer. :shock: Making more money available to upgrade equipment is a good thought, but I don't see it actually happening anytime soon. Too many providers, too little money, too much bureaucracy to get it. :roll: If it works out this way, it will be good, but that is a big if. Another letter to Congress, coming up.

The pharmacology of Epinephrine doesn't lend itself to the action you describe. Now, the cardiologist that you spoke to may have some greater insight into this mechanism than I do, but he also wouldn't be the first to be contradicted by this paramedic. Renal dose Dopamine, prehospital 12 lead interpretation, prehospital CHF management, even ETT verification, and bradycardia management are all topics that I have taken doctors to task over. If this doctor is willing to discuss the mechanism, I am willing to listen, but I have not seen any evidence that it would. The other code drugs would likely have less direct effect on the respiratory centers than epinephrine would. Unless the antidysrhythmic was able to convert the rhythm, and work with epinephrine to restore pulses, I would doubt they had much of an effect.

History and physical exam is the short answer. How do bleeds present? What conditions will a patient complain of when a bleed happens versus an occlusion? What historical factors make the presence of a bleed more likely? NO this assessment is not 100%, but it can give you pretty clear indications of whether a bleed is happening or not. Here is some technology that might make it even easier to tell the difference.

Grassroots level involvement? Good plan Ace. Now the lazy, scared, or indifferent among us have to make their voices heard. Letters to Congressmen and Senators people. For admin: If we put together a letter to Congress, could you post the links to the senators/representatives so we could do a mass mailing? One voice type solidarity.

And every couple of months, the same discussions are revisited. I'm beginning to think that some law of physics is being applied to the information as well. Bonus points to the one that can name which law it is. Except you Ace, you know too much as it is.

Honestly, it was probably directed at wanting to see what kind of response we got out of you. You are not the first, and you won't be the last. Keep in mind that not all share your enthusiasm, and judging from the age you posted, you will grow out of most of it. Probably shortly after you get asked to help someone you don't know at a most inopportune moment. Anytime the public can identify that you are a medical provider, they will ask you for free advice that you shouldn't be giving, or help for something you aren't ready for. Get a job with a professional organization that doesn't rely on volunteer responses in private vehicles, so you can learn more.

With an ischemic event we can assume that it involved a plaque, since the formation of a clot would be difficult following tPA. "multiple ischemic lesions in both patients suggests the disintegration and subsequent scattering of cardiac or aortic thrombi as the underlying etiology." My guess, since the article doesn't specifically address it, would be the vulnerable plaque starts to break down following the tPA. Because the blood flow is increased, the plaque embolizes to the distal vascular bed. The fact that 2 of the 341 patients experienced the ERIS indicates an incident but not statistical significance. The more interesting point of the article was the fact that there is a call for a revision in the usage of the fibrinolytics.

Early Recurrent Stroke Linked to Tissue Plasminogen Activator Caroline Cassels July 27, 2006 — Early recurrent ischemic stroke (ERIS) has been linked to intravenous thrombolysis (IVT) with tissue-type plasminogen activator (tPA) in a report by researchers at the University of Zurich in Switzerland. The prospective, population-based study is the first description of ERIS as the cause of early neurological deterioration in acute stroke patients undergoing IVT. Of the 341 patients included in the study, 2 were deemed to have ERIS. Although the incidence of this complication was low, the researchers note that the presence of "multiple ischemic lesions in both patients suggests the disintegration and subsequent scattering of cardiac or aortic thrombi as the underlying etiology." The study is published in the July 18 issue of Circulation, with first author Dimitrios Georgiadis, MD, from the University of Zurich. Researchers analyzed data from 341 consecutive acute stroke patients treated with tPA at 8 medical centers in Switzerland between January 2001 and November 2004. The study's primary end point was neurological deterioration of 4 or more points on the National Institutes of Health Stroke Scale (NIHSS) occurring within 24 hours of tPA treatment and caused by ERIS or intracranial hemorrhage (ICH). Causative Role? According to the study, ERIS was defined as the occurrence of new neurological symptoms suggesting involvement of initially unaffected vascular territories and evidence of corresponding ischemic lesions on cranial computed tomography (CCT) scans. Administration of tPA was performed according to protocols based on the results of the 1996 National Institute of Neurological Disorders and Stroke (NINDS) study, which, among other guidelines, recommended that tPA be administered within 3 hours of stroke symptom onset and that a CT scan done before thrombolysis not show any major infarction, mass effect, edema, or hemorrhage. Neurological deterioration and evidence of appropriately located ICH on CCT, magnetic resonance imaging (MRI) scans, or both were diagnosed as symptomatic intracranial hemorrhage (SICH). The 2 patients diagnosed with ERIS both worsened within 1 hour of receiving tPA infusion. Brain infarcts and, in 1 patient, renal infarcts were scattered among different vascular territories. These findings, the researchers write, are "highly suggestive of the disintegration and subsequent scattering of cardiac or aortic thrombi as the underlying etiology. Obviously, disintegration of thrombi can occur spontaneously and is not necessarily associated with tPA administration. Still, the fact that neurological deterioration occurred 40 to 50 minutes after tPA initiation in both cases strongly argues for a causative role of tPA." A total of 15 patients were diagnosed with SICH. However, the researchers note that all of these events occurred between 2 and 22 hours after termination of tPA infusion. The only definitive way to determine whether tPA causes ERIS would be to conduct a randomized trial comparing the incidence of ERIS between stroke patients with IVT and controls. Since this is ethically impossible, the authors point out that a registry of patients with ERIS following IVT would provide the neurology community with valuable information. Clinical Implications According to the authors, these findings should alert treating physicians to the fact that deterioration of patients during thrombolysis therapy is not necessarily due to ICH but can also be caused by ERIS. In addition, they write that exclusion of ICH "should by no means prompt a wait-and-see attitude but rather should lead to urgent MRI studies and possibly additional therapeutic interventions such as local thrombolysis." The demonstrated benefit of early IVT treatment and the low incidence of ERIS would not justify a delay in IVT initiation. However, the authors note that the true incidence of ERIS was potentially underestimated because they evaluated only those patients with a deterioration of 4 or more points on the NIHSS — a criterion that constitutes a severe worsening. Call for New Treatment Guidelines In an accompanying editorial, Louis R. Caplan, MD, from Beth Israel Deaconess Medical Center in Boston, Massachusetts, says the study's findings highlight the need to update tPA treatment protocols to reflect advances in imaging technology and current neurological practice. Current treatment protocols, which include recommendations that tPA be administered only within 3 hours of symptom onset; that a CT scan done before thrombolysis not show any major infarction, mass effect, edema, or hemorrhage; and that treatment not be administered in patients with a deficit or minor signs or in patients who are improving, are outdated, he writes. For instance, Dr. Caplan notes, several recent studies have shown that choosing patients using modern MRI protocols can extend patient selection beyond the current recommended 3-hour time limit. Furthermore, he writes that the time delay and severity of the clinical deficit do not reliably predict improvement after thrombolysis. "Two studies showed that giving tPA between 3 and 6 hours after onset to patients with considerable at-risk tissue was an effective strategy," he writes. According to Dr. Caplan, "research, experience, and therapeutic alternatives have come a long way since the NINDS trial was planned and reported. The present guidelines badly need to be updated to reflect these advances." Circulation. 2006;114:237-241, 187-190.

Short answer: No The epinephrine will increase the amount of oxygenated blood that is delivered to the brain. More importantly, the respiratory center in the medulla oblongata. When the heart stops, the brain loses perfusion and the respiratory center shuts down. Retun pulses, return perfusion to the medulla, the signals get sent from the brain, and respirations start up again. Look up the Reticular Activating System for more: Level of consciousness Chemoreceptors-->Respiratory center Baroreceptors-->Blood pressure center Cardiac center-->Changes in heart rate The perfusion of these areas follows a stepwise increase/decrease The level of consciousness drops first, recovers last The respiratory rate and depth next, then the blood pressure, then the heart rate If the level of consciousness is good then the worst the vitals can be is compensated.

Nothing to increase the pucker factor like having your medical director running calls with you. 2nd year residents and nurse externs are doing ride time as we speak. By the time they are done, and actually making decisions or taking reports from us, they will have long forgotten what it was like. In the meantime, it is very useful. The ER staff used to be required to do 12 hrs/year. Not a lot, but at least some. This has since gone away. RN's sucking up hospital department budgets on overtime, doing things that don't directly benefit the hospital isn't supported by administration much. Course, everytime they ask why I've done something, I will offer to take them on some calls to show them what my work environment is like.

On the plus side, the responses are all the same. Kind of a de facto fact checker.