OzMedic

Hey Bushy you wombat rooting, sheep shagging Vexican! Empty your inbox so I can send you a message or send me one with a current email address.

G'day there blokes, yup crawled out from under the study rock for a few breaths. Last semester at the moment so looking forward to being free. Just started 6 weeks leave so I might be be about for a while, hope to catch up in the chat some time. Later shagga's!

You cockroachs aren't worth the money you get now let alone ask for more!

In threads such as this and others I rarely see succinylcholine mentioned as a prehospital induction agent in the US. Is there a reason for this?

Not saying that I disagree but just out of interest how would you go about cardioverting this patient? Would you sedate them and if so with which drug and what dose? What are you aiming for with sedation LOC wise? I'm just interested to hear your views as I often find this scenario difficult from a decision making perspective. Remember we are talking about a patient that is poorly perfused but still conscious say GCS 13-15. How do other people go about preparing these patients for cardioversion?

Thanks for posting the info and for the feedback Doc. For some reason your link would not work for me but if you could please mention the article title and journal I will be able to find it from there as I have access to most online journals. Where do you think this research sits in relation to the way we use morphine in the treatment of pre-hospital ACS. Are we killing them with kindness? Or do you feel it is just the inappropriate prioritisation of morphine instead of aspirin, nitrates, thrombolytics and/or angioplasty in a more timely manner?

Thanks for looking anyway dude! I'm pretty much ready to put this one down to BS as I tend to believe basically what you said, that is is simply a flow-on from decreased sympathetic activity. Oh by the way, did you read about morphines effects on the sphincter of oddi? heh heh heh, happy reading :twisted:

I've posted my views and research about the excessive and inappropriate use of oxygen in EMS in other forums so I won't bore everybody again when a simple search will reveal the info if somebody is interested. Is oxygen helpful?........common sense would dictate that is is but where is the evidence? Can it be harmful?............when administered inappropriately, yes (and I am not talking about the "hypoxic drive" theory in COPD patients). The one thing I think I can offer people reading this thread is perhaps a different perspective on the threads original question. Does oxygen save lives? I say no! The reason I say no is that I feel that inexperienced people in EMS are lead to believe wrongly that it does. Supplemental oxygen therapy buys you time, it is a stop-gap until you can fix the real problem. The mistake that people make is they think that the oxygen is actually correcting something. They see their patient improve after administering a little oxygen and think they have fixed the problem. Often the patients own body may have fixed the problem while the oxygen was being applied. A possible exception being the example of carbon-monoxide poisoning where high oxygen concentrations may help to displace the carbon monoxide from haemoglobin. I guess the message I want to get across is, sure put some oxygen on a patient if you think they need it but don't stop there. Think about why the patient needs it and try to resolve that problem or get the patient to someone who can. Think about the underlying problem people and fix it because the oxygen can't! :wink:

Thanks for that, I have seen this and other similar canine studies however they do not seem to demonstrate the stated effect of morphine slowing AV conduction. Like I said it may be an old wives tale but it is mentioned in our morphine protocol as well as some other readings I have seen but I am yet to hear a plausible cause. :?

I knew the evidence was poor supporting it's use but this article came as a bit of a shock. Sorry I have not been able to locate the links to the original study as yet (feel free to add them if you are familiar with their location). Any comments? Morphine for chest pain increases death risk While patients hospitalized for a heart attack have long been treated with morphine to relieve chest pain, an analysis by researchers from the Duke Clinical Research Institute has shown that these patients have almost a 50 percent higher risk of dying. The researchers call for a randomized clinical trial to confirm their analysis. Meanwhile, they advise cardiologists to begin treatment with sufficient doses of nitroglycerin to relieve pain before resorting to morphine. In their analysis of the clinical data and outcomes of more than 57,000 high-risk heart attack patients -- 29.8 percent of whom received morphine within the first 24 hours of hospitalization -- the researchers found that those who received morphine had a 6.8 percent death rate, compared to 3.8 percent for those receiving nitroglycerin. The increase in mortality persisted even after adjustment for the patients' baseline clinical risk. The results of the Duke were published as a fast-track article in the American Heart Journal. "The results of this analysis raise serious concerns about the safety of the routine use of morphine in this group of heart patients," said Duke cardiologist Trip Meine, M.D., the study's lead author. "Since randomized clinical trials evaluating the safety or effectiveness of morphine for these patients have not been conducted, official guidelines for its use are based solely on expert conjecture. Given the adverse outcomes associated with morphine use found in our analysis, a randomized clinical trial is in order." Morphine was first used to relieve the chest pain associated with heart attacks in 1912 and has been used regularly ever since. Nitroglycerin has been used for more than 130 years for the relief of chest pain, also known as unstable angina. It works by relaxing blood vessels and allowing blood flow to increase. "Nitroglycerin has a physiological effect that may, at least temporarily, influence the underlying ischemia," Meine said. "Morphine, on the other hand, doesn't do anything about what is actually causing the pain. It just masks it, and may, in fact, make the underlying disease worse. "Morphine has the well-known and potentially harmful side effects of depressing respiration, reducing blood pressure and slowing heart rate," he continued. "These side effects could explain the worse outcomes in patients whose heart function has already been compromised by disease." For their analysis, the researchers consulted the nationwide quality improvement initiative named CRUSADE (Can Rapid Risk Stratification of Unstable Angina Patients Suppress Adverse Outcomes with Early Implementation of the American College of Cardiology and AHA Guidelines) The registry continually collects data from more than 400 hospitals on outcomes and on the use of proven drugs and procedures used to restore blood flow to the heart. From this registry, the researchers identified 57,039 high-risk patients with non-ST-segment elevation myocardial infarction (non-STEMI), a categorization of heart attack based on electrocardiogram (ECG) readings. These patients typically arrive at emergency rooms with chest pain, but often will not have telltale signs of a heart attack on the initial ECG. They might be diagnosed with a heart attack only when the results of the blood tests are reported a few hours later. The researchers found that patients who were given morphine had 48 percent higher risk of dying and 34 percent higher risk of suffering another heart attack while in the hospital. "This increase in mortality was present in every subgroup of patients we studied," Meine said. "What we found interesting was that patients given morphine were more likely to receive evidence-based medicine, were more likely to be treated by a cardiologist and were more likely to receive an invasive cardiac procedure." Meine recommended that physicians with hospitalized heart attack patients should begin with nitroglycerin therapy to control pain. "Our recommendation is that patients should receive the full dose of nitroglycerin," he said. "Based on our analysis, morphine should be the last resort after else has been tried." While patients with acute STEMI are at higher risk of dying within 30 days of their hospital stay, patients with non-STEMI actually have a higher risk of dying six months and one year after initial hospital presentation. It is estimated that about 1.3 million Americans are hospitalized each year with non-STEMI. CRUSADE continuously gathers data from participating U.S. hospitals on treatments for patients with non-STEMI and provides quarterly feedback to hospitals with the ultimate goal of improving adherence to the ACC/AHA treatment guidelines and patient outcomes.

This often quoted side effect of morphine administration is starting to tick me off as I have never been able to find a decent piece of literature that will explain the mechanism of this alleged side effect of morphine. My understanding of the effect of morphine on AV conduction is via secondary mechanisms such as a decrease in sympathetic tone resulting in a decreased stimulus via the SA node or that morphine in large doses can cause bradycardia due to a direct effect on vagal neurones. However, I still hear people mentioning morphine decreasing AV conduction via a direct effect on the AV node but when pressed no-one can explain the mechanism. Am I missing something or is this just another medical old wives tale? I'm pretty sure that if there is any substance to it there will be someone on this site that knows how it works!

Once again in this thread I see one of the major barriers to EMS being people looking for 'black and white' rules that they can apply in all situations. In this as well as most situations I think individual judgement on a case by case basis is what is called for. Should you give 400mcg to a possible right sided MI with a sys BP of 110 with no IV?............ Probably not wise. What if the sys BP is 160?................. Far less risk of dropping too low with one dose. Whether they are already on GTN or not will also influence your judgement. We also need to be mindful of applying hard and fast rules to acceptable sys BP's for the administration/discontinuation of GTN in the first place. I can assure you that a myocardium that is used to being perfused via it's partially occluded arteries by a chronic sys BP of 160 will not thank you for dropping it and keeping it at 105! (nor will their brain in some instances). Get as much information as you can, use judgement, Implement you therapies and constantly reassess for positive or negative responses. Treat the individual patient, not the protocol.

Just LR (we call it Hartmanns solution) here

I think I know what you are saying and I could not agree with you more. So many of the interventions we have performed over the years and still currently are questionable. Many of them go back to the early days of EMS when various groups of good people got together and devised the early ALS systems. A lot of the interventions brought in were based on anecdotal experiences, common sense and the misconception that what was working in the ED at the time will work in EMS. I am not criticising these early pioneers as they had no other information to go on. The problem is that the EMS system as a whole never really moved on from that approach even when the opportunity was there to test the real effectiveness of these interventions. Then as time goes on and technology and EMS education improve we implement a whole raft of new drugs and procedures without really examining the ones we already have. I can think of numerous drugs and procedures that I am authorised to perform that I believe that I could do without. On top of that my service announces another 6 or so that they are rolling out this year. This brings me to why I am happy about the study attached to this post. While it is by no means a radical or definitive study it does examine the benefit of basic ACLS procedures in out of hospital cardiac arrest. When I say basic I mean it is not the examining latest wizz bang device or drug that has landed with a few questionable or flawed studies to be incorporated into our existing ACLS protocols. It is finally demonstrating a positive effect of our core ALS skills in cardiac arrest such as good basic cares, judgement, ETT, adrenaline, ECG recognition etc. While this study in no way quantifies any one of these interventions as an individual it gives us an evidentiary basis for ACLS in the first place which has been sadly lacking. More importantly it proves the benefit of ACLS in areas where rapid access to defibrillation and/or CPR (both of which are poorly available in rural environments). Further studies will try and identify individual contributors to this success but I feel that this original study examining the overall benefit is important as ACLS is more than just an ETT or adrenaline or cardioversion etc. In short my feelings are that we need to prove the benefits of what we have been doing before we move on to the next big thing. There are so many things out there in EMS that probably have no place being there. Let's find out what does so we can trim the fat and focus on what matters.

Sorry I'd like to respond but your post is a bit confusing as you seem to contradict yourself in the next line. I think I know what you are saying but would like you to clarify before I respond