AZCEP

Right about what exactly? The CT does not tell us it is okay to reduce a hypertensive blood pressure associated with neurologic symptoms with nitrates. No treatment guideline does either. You have to take responsibility for the inappropriate treatment that you are administering regardless of who gives you the order. How can you be so sure? He had a neurologic event, and is now hypertensive. What assessment tool are you using to determine that this is not a bleed? The crisis that the hypertension is causing is neurologic. This alone should make you consider the possibility of an intracranial bleed. The coincidence should alert you to the possibility that this is more than it appears to be. What is it saying? Your reply seems to indicate that you have a gross inability to listen to any one else's opinion of what may be happening. You need to familiarize yourself with the current recommendations on blood pressure management in the neurologic patient before you make statements like these. Very well. Have the neurologic patients that you have treated in this way had good outcomes following this treatment? Have you done follow up to ensure that there have not been increases in the morbidity/mortality associated with the administration of nitrates? Please educate us on how your system allows you to treat neurologic emergencies despite recommendations from many places to the contrary. I do not understand why you feel it is necessary to resort to name calling again. Your system has apparently struck upon a treatment modality that is significantly different than anywhere else. If you could please explain how this came about, without resorting to the epithets, I eagerly await your response. This is not a concern of many others here. I have somehow made you think that I do not believe you know what you are doing. For this I will apologize. I merely want you to explain how it is that your system is capable of not following treatment recommendations. I will be glad to when he decides to ask a question that I have expertise in. There are a great many providers that are willing to help students learn. If he asks me, I will answer as I see fit. PARTS OF THE QUOTE REMOVED TO REFLECT THE REMOVAL OF CONTENT IN ORIGINAL POST - ADMIN

This is a patient that had a neurologic event, and is now hypertensive. What did I miss? I'm still curious how you can be so sure about it not being an intracranial bleed. The prehospital treatment for a hypertensive patient following a neurologic insult is not to reduce the blood pressure through the use of nitrates. You have oversimplified the treatment that this patient needs. Only if you are unable to think outside of your protocols You really need to consider that this patient is not presenting as a black and white case. Perhaps you've not experienced enough to be familiar with the amount of variability that patients will present with. Perhaps you are restricted as to what your medical director will allow you to do. Either way, you have no grounds to question my education or history taking skill. And the question stands. This is not apparent through the modality that you are suggesting be tried. Causing another problem because you've not thought the situation out is not acceptable for anyone. The use of nitrates will not allow you the control you need to ensure that this patient's intracranial pressure doesn't exceed his mean arterial pressure. Hypotension or not, you should not use a vasodilator for this situation in the prehospital environment. Actually, in the management of an intracranial bleed, even one that is hypertensive, fluid challenges are indicated well before nitrates. I will assume that you've not had an opportunity to look it up yet. You have yet to "school" anyone on the proper management of this patient. Very good. You have decided not to wait for your previous poorly thought out treatment to wear off. Perhaps you will be able to use this as your defense when you present your case to a jury of your peers. I'd also be interested in knowing where you were taught that this treatment was appropriate. JPINV is showing a better understanding of the proper management of this patient, and you feel it necessary to belittle him? Why is this?

And why would you do something that you know will cause a problem, when you can avoid it in the first place? You have not "pissed me off". You are not capable of that. I merely wanted a clarification on why you would choose to treat someone with a modality that is not indicated, and potentially dangerous for the circumstances. Hypertension associated with a neurologic event is a reason to NOT treat hypertension in the field with the paucity of agents that are commonly available. Because this patient is on a beta blocker is another reason not to treat with nitrates. It is not a reason to initiate a treatment that will cause harm. You also indicated that an epidural bleed can present like this. So why can't a sub arachnoid bleed? Headaches can, and do, dissipate following a vascular event. Not a common presentation, but one that needs to be considered. Because of the onset, you can reliably rule out a subdural bleed as well? How do you know when it began? Because the patient became symptomatic while cooking dinner is immaterial. This event could well have been evolving over hours to days. The information given is a bit scarce in this regard, and the provider on scene was probably unable to obtain a reliable history from the patient anyway. Before you make intentionally inflammatory, and obviously wrong statements, please take your own advice and think it through.

When did I say anything about not having control in giving them? You have the control of giving 400 micrograms without the ability to titrate the response. If the patient becomes hypotensive, you have to wait the 3-5 minutes before you can give any more. If you were one of the very few to be blessed with IV infusions of NTG, then perhaps you would have more control. Even with this remote possibility, you do not want to use nitrates because of the reflex tachycardia they induce. I said, you have less control over the effects they exert. Widespread vasodilation is not something you want to cause to a potential intracranial bleed. CHF is a significantly different disease process. Perhaps you should re-read the "book". While you are looking, perhaps you could look for the time frame that it takes to cause irreprable damage to the brain. Drop the blood pressure, decrease the mean arterial pressure, worsen the ischemia, further damage the brain. The vasodilatory effects of NTG do not allow the heart to slow down. They do allow for greater oxygen supply, not demand. Think this one through for a moment. Create a relative hypovolemia, through vasodilation. How is the body going to respond? Through tachycardia, and a further attempt to vasoconstrict. Why do you insist on name calling? You're not any better than anyone else that has an opinion on how to manage this situation. ERDoc, Rid, chbare, and I have all suggested that this patient should be transported with as little pharmacologic administration as possible based on the best available evidence. Look for some literature that suggests it is appropriate to actively reduce a blood pressure with associated neurologic complaints, even transient ones, with nitrates. Until you do, please keep the insults to yourself.

Nitrates will worsen the ischemic prenumbra of the nervous tissue. Careful control over how much you decrease the blood pressure has to be taken. This patient may be a candidate for more aggressive therapy, but until a CT is done you should not aggressively lower the pressure. A beta blocker would be a decent option for prehospital, if they are available. Nitrates should not be considered for this patient due to the lack of control you would have.

Treading dangerously on the urban myth ground there. :roll: The patient that is experiencing a respiratory problem bad enough to seek treatment is already dumping their endogenous epinephrine stores into their circulation. You would have to throw them off a bridge to get a big enough change to have a clinical effect. The coffee can work as a way to prevent needing any rescue maneuvers. Once the bronchoconstriction happens, you need something that will work much faster than the GI tract will allow.

I wouldn't call this a "hypertensive emergency" per say, but would consider doing something for the vitals. Do you have a beta blocker available? That may be the best route to take, if you are going to.

Will the ambulance company's course allow for college credits down the road? If not you might consider taking the college program. It may not be that big of a benefit now, but at some point you may see a need to have some additional college credits. The EMT class I took was 17 years ago, so it's not really going to compare. The paramedic program that I run has been steadily increasing it's price to cover the costs involved. We include books and clinical rotations for $1600 U.S. Since it is through a non-profit facility, this is just enough to cover the total cost of the program with 20 students enrolled. The local community college will run roughly $3-4000. They do offer the same credits for our program once completed. You just have to pay for the credit/hours.

How about not using so much Narcan that the patient will wake up enough to need restraint? We use just enough of the antagonist to get them breathing, but not so much to make them combative. I've also liked the limited results I've gotten with Revex (Nalmefene) and Revia (Naltrexone). Longer lasting, and less of the sudden responses.

Unless you are in an enclosed bay with the doors closed and the lights off, there will still be enough ambient light to limit the utility of the device. Leave this one for use in the batcave, and you will find it useful. Otherwise, save your money for something else.

No it is not worth the money. I have one, and in most ambient light situations it does nothing to help you. It does not require another hand to use, you just have to be sure to place it a bit away from where you make your stick. It takes some practice to become proficient with, like any other tool. It's a nice idea that doesn't really have a place for most EMS providers that work in daylight.

I've had this type of schedule for the last 7 years. This is the first I've heard of it being called something special. :shock: No, I don't get anything beyond the standard overtime pay after the forty hours. I work from 0800 Saturday morning to 0800 Tuesday. I can't imagine working during the week when the chief is looking over your shoulder all the time.

The mantra from the sources you commonly see will be "You can't identify an AMI with a LBBB", and you will be left to ponder why this is so. The ACLS doesn't spend any time on the topic at all. The Mosby and Brady paramedic books regurgitate the ACLS information almost verbatim. The steps you seek: First: identify the BBB. This is the easy part. QRS wider than 0.10 sec indicates a conduction delay at best. QRS wider than 0.12 indicates the BBB. Second: identify which BB is blocked. Still not so tough, right? It's either right or left. Third: Look for ST changes in leads that the BBB does not directly influence. Lateral and inferior leads have a different view of the events. They will be useful in identifying the presence of other changes that may be masked by the BBB. Fourth: Look for ST changes in the direction of the QRS complex. If the patient is having an anterior/septal wall MI the BBB will not hide the ST change. Due to the direction the QRS deflects, which direction would you expect the ST segment to go? It does become more difficult to identify ischemia using this criteria, but the injury/infarction patterns hold up pretty well.

And they never will mention it. It's one of those nuggets of information that can make a world of difference when you need it, but probably never will. I just happened to pick up an advanced 12 lead interpretation book that discussed it. I mean really, how often can EMS know that a LBBB is new or old?

As long as you now understand what you need, the information will always be here to be referenced. I'm glad to help when I can.

To the best of my knowledge, there is no scope of practice involved with a patient assessment. You may be limited in the use of some tools in gathering your information, but the assessment itself isn't typically restricted. Things like ECG, BGL, SpO2, and EtCO2 will be included, or excluded from a given level's scope. You would just have to figure a way to obtain the informational equivalent some other way. You would be in more danger of violating your scope by giving a medical opinion, or advice.

Your argument is not so much with the volunteer system as it is with the creation of add on levels of EMT's then. This is similar to what happened when the big cities decided they all wanted paramedics, and the smaller communities didn't think they could afford the same levels. The intermediate, or enhanced EMT, was the result. This level of care is no longer worth having, as it, much like the volunteer, establishes a measure to provide a stop gap solution to a problem that does not get completely solved. If a community wants to pay for add on skills, why not get all of them in one place? If a community, or region, wants full time EMS service, how does the volunteer system allow for this to happen? Allowing lower levels of care to present themselves as "almost paramedics" cheapens the entire profession.

Given that the narcan was going to have a temporary effect, and the redosing was going to be difficult considering the movement described, wouldn't it be prudent to secure the airway and move the patient to the transporting unit, leaving the titration of the narcan to the ER in a more controlled setting? Once the airway is secured, I'd have a hard time pushing any narcotic antagonist that I knew would wear off before the opiates did.

Does anything change the pain? Position/movement/cough? Any surgical history? Diet? Issues urinating/defecating?

Sustained release morphine with the presentation here probably would not have responded favorably to Narcan. This patient was already feeling the effects of an unknown amount of the narcotic. Reversing it would have been exceedingly difficult/time consuming. It may have been worth a try, if just to get his help walking down the stairs.

Just the definitions of the different waves get bunged up. Many students have the same problem, particularly when they learn interpretation by only looking at lead II. The QRS complex is the same. There may not be a Q, or an R, or an S-wave specifically, but we still call them "QRS". Once this is settled for you, things will become easier.

The only time a professional organization was mentioned was during the PHTLS program. The NAEMT rep spoke for all of 10 minutes on the benefits of membership. Yes, I admit that I joined, and was not the least bit impressed by the representation that was offered. The consensus opinion has been that NREMT is doing the job. Unfortunately, NREMT has never been intended to represent the needs of the providers, and people wonder why there isn't more of it. The provider in the street is more concerned with their paycheck stretching ability, than they are the direction of the profession. Very frustrating.

You need to look to a source other than the ACLS book for your information scope. You can determine the presence of an MI with a co-existing LBBB. It's a bit more challenging, but you owe it to your patients to do the work. Notice the LBBB pattern. Notice the ST elevation in the lateral leads. Notice also that the ST segment moves in the direction of the QRS complex. In this ECG, if there was evidence of ST depression, we could justify treating this patient as an acute MI based on the ECG. The LBBB does not interfere with this mechanism. You are also being a bit empiric with a treatment that can, and does cause harm on occasion. If your patient is tachycardic due to hypoxia, you better make sure why this is happening prior to giving them aspirin. Ever managed an asthmatic that you've given aspirin to? Not something you want to do to a sick heart.

The small positive deflection you see is the Q wave. Remember this is normal in V1 because the wave of depolarization is moving towards the lead as the septum is stimulated. Also, the text said "The left side of the septum depolarises first, and the impulse then spreads toward the right. Lead V1 lies immediate to the right of the septum and thus registers an initial small positive deflection (R wave) as the depolarisation travels ward the lead. " So, I just assumed that little spike was the small positive deflection they were talking about. But you guys are saying that's not what I'm seeing when I look at the V1 examples...

Let's see if I can clear this up. In V1, the normal healthy DEFLECTION of the QRS complex will be predominantly negative (pointing down). If there is some type of disease process at work that will alter the direction of the electricity, then you can get a positively deflected QRS in this lead. Right ventricular hypertrophy, COPD, or a RBBB will cause this pattern to show. If you measure the amount of electricity (amplitude), which is what the ECG measures on the vertical, you can end up with a positive number. Typically, and more accurately, it would be measured as a negative