Camulos

I'm looking for a little help here. I've come up with an idea for a new EMS product, but I don't know where to start. It's a simple, low-tech, cheap answer to an on-going problem. Has anyone here taken an idea and turned it into a reality? Ever get something patented? Marketing isn't the problem so much as getting it manufactured. Where do I start?

Email me all your ideas and plans immediately and I'll see to it that it gets manufactured and on the market.

Just jokes - Good luck with it and let us know when we can buy it.

Stay safe,

Curse

Ok someone leaves a large some of cash or expensive gift card in an envelope with your name on it. What do you do with it since you have no way of knowing who left it?

What cash? What envelope?

OK who is coming out on the town? I'm buying!!!!!

Stay safe,

Curse

I'm still trying to catch my firefighter. Slippery those men are! But I wont give up!

You are familiar with the firefighters' motto aren't you?

Find em hot

Leave em wet

Maybe that's why they are so slippery!!

Stay safe,

Curse

I started doing all this stuff when I was pretty young. Twenty to be exact.

The biggest difference between then and now is,

When I first started I knew what I knew

These days I know what I don't know

I'm sure the experienced people know what I'm talking about here. And if you don't get it - you will one day

Stay safe,

Curse

Never mind the staff but can we please start putting a weight limit on the patient's?

Stay safe,

Curse

Apart from the ECG criteria I am unaware of any other test that would confirm or differentiate the diagnosis of MAT. There is a paucity of evidence regarding the clinical significance of MAT however what does exist tells us that it is a transient rhythm (usually) that is a secondary effect of a clinical syndrome. The most common culprits here are COPD, CHF, hypoxemia, PE and theophylline toxicity. Considering this, I guess pt history and present diagnosis may sometimes provide that differentiating factor. As the rhythm is a transient secondary phenomenon, the cornerstone of treatment is to treat the causative condition, which should normalise the rhythm.

I have personally never seen clinically significant MAT that required treatment in itself. I understand the drug of choice in this case is metoprolol however its use may be contraindicated in the setting of some of the main causes of MAT (COPD, CHF, hypoxemia) due to beta blocker induced bronchoconstriction. I have heard magnesium may have some role but I really don’t know much about this.

It would be great to hear others’ experience with this or indeed if there is a definitive test for MAT (apart from ECG).

Stay safe,

Curse

Funny one I had quite a few years ago that caused me some embarrassment to say the least.

C/T fifty something year old female with abdo pain. On arrival pt rolling around on the ground in distress. Reports sudden onset of abdominal pain which she described as “the worst pain I’ve ever had and it goes through to my back”. Pt looks terrible – pale, diaphoretic, short of breath etc. Obs were equally as bad – pulse around 130bpm and BP around 80 systolic. My partner and I are thinking AAA and pretty much load and go.

On starting up the truck the lady says she wants to go to the toilet to open her bowels. I remember being told once, from somewhere, that this can be an ominous sign in these sorts of cases. So I tell her to hold on – both because I don’t want her to bear down and rupture and also because I want to keep my truck clean. Obs don’t really improve en route and we rush her into the ED. Handover given and I tell them I’m thinking AAA. ED staff rush her onto a monitored bed and I go back to the truck to finish paper work and restock.

I go back into the ED to drop my paperwork off and am hit by the most offensive smell I have ever encountered to this day. Get back to where the pt is and one staff member is mopping something off the floor whilst others are cleaning the pt . Pt has just done one of the biggest bowel motions known to man and now is thanking me, of all people, because she feels “so much better”. I drop my paperwork off and run out the door whilst all the ED staff stare at me with utter contempt.

Check with a nurse the next day what the story was and ends up the pt just really needed to do a huge shit!!! She was discharged two hours later very happy that she had been “cured” by the kind ambulance man. Turns out she hadn’t opened her bowels in the past nine days and when she finally did certainly did it in fine fashion. In my haste to get this lady to hospital, and as I had my “diagnosis”, I had not even asked. I still can’t believe to this day that a need to crap caused such derangement of her observations to the point where I thought she had a AAA. These days I always check and I’m sure quite a few AAA pt’s have died hearing the last word’s “When did you last open your bowels?”

The partner I was working with that day has now retired however we still catch up occasionally. Every time, without fail, he manages to fit that story into the conversation. I guess you never live some things down.

Stay safe,

Curse

a) Dial back the attitude.

The reasons for choosing atropine over pacing were covered in my previous post. That's not to say you would never pace someone who is possibly dig toxic.

c) I phrased the question this way because I didn't want the dogmatic answer that anyone would come up with who has taken ACLS of "atropine, pacing" or "pacing, because atropine never works on heart blocks". This is one of those cases where not all bradycardias are the same, and it's important not to do something simply because the algorithm says so. It's not enough to know to do it; you should know why you are doing it. By putting someone to a choice, and having them justify it, you see who really knows why one is appropriate over another.

'zilla

a) I apologise if it came across as attitude as that was certainly not my intention. My use of capitals and bold was to emphasise that I wanted you to choose one treatment only - as per your original question. I will desist from using capitals in future and hope I have not caused offense as I have certainly enjoyed reading your replies, both here and on other topics, in the past.

My main reason for choosing pacing over atropine was that I believe there is a high likelihood that atropine will not be effective. There are a lot of case reports of this and as such I believe the numbers support pacing, along with its inherent risks, over atropine. Your earlier post semed to assert that atropine "will" work however I don't believe it's such a sure thing and thought the word "may" would have been better used. It is this "may", this unknown quantity that caused me to choose pacing over atropine. I am guessing that you have anecdotally had some success with atropine in this setting and as such have chosen it over pacing. It would be great to hear of your experience and sucess / failure with both pacing and atropine in these cases.

c) I enjoyed the fact that you worded the question the way you did as it made me really think about what my priority was. As I always have both options at my disposal I have never really had to think outside that square and as such thank you for making me do so. I am happy to be proved wrong but still believe pacing is the way to go.

Keen to hear your responses, here and on other topics Doc.

Stay safe,

curse - note all lower case (jokes)

I'd also call that MAT. P wave morphology seems different from one to another, PRI and RRI are both variable, rate > 100. That certainly fits the criteria for MAT as far as I recall.

I definitely don't think it is AF as earlier stated as the P waves are very easily discernable.

It would be great to hear the three different answers from the ER Docs that were asked by the OP.

Stay safe,

Curse

This looks like electrical alternans that can be noted in all leads except lead III. Whilst not pathognomonic for pericardial tamponade, in the setting of PEA it would certainly have to be at the top of my list of causative factors. Or at least top of the list of causes that are easily reversible any way!!

A good clue here may have been his JVP on the initial assessment.

Stay safe,

Curse

I've read that with dig toxicity patient's are more likely to have a negative reaction from electrical therapy, ie ventricular fibrillation may result.

My understanding is that this is more prevalent in the setting of cardioversion. As was said earlier TCP definitely lowers the fibrillatory threshold though so can cause the same problems. TCP is normally only used after medications have been ineffective. And from what I have read medications are quite frequently ineffective in this setting. Hence my reason to choose TCP over drugs if only given ONE choice. Of course in real life I would have both and would try the atropine first and then progress to TCP if it was ineffective. However Doc's question didn't allow for this and asked us to choose one only.

Stay safe,

Curse

Atropine is therefore DOC in heart block caused by dig toxicity. Don't let some ACLS instructor tell you never to bother with atropine in heart block. In this situation, it will help.

Can you really be so sure it WILL help? After a quick check there are quite a few reports of atropine being ineffective in the setting of digoxin overdose. I am happy to be proven wrong but it was this unknown quantity that provided my main justification for advocating cardiac pacing if I had to only choose ONE treatment - as per your question.

I would be keen hear your answer and justification to your question Doczilla on which ONE you would choose in the scenario - drugs or pacing?

Stay safe,

Curse

Then let's up the stakes.

Same patient, same presentation, different vitals.

Alert, disoriented.

Multifocal Atrial tachycardia with superimposed 3rd degree block (pathognomonic for dig toxicity)

Ventricular rate (and pulse) 30

BP 70/40

What do you want to do?

You get one choice. Pace, or drug. Don't just guess; justify your answer as to why one is better than the other.

'zilla

Although this a bit unrealistic, as I would normally have both, I am happy to play the game. If I only had one to choose from I would choose pacing over medication therapy for this revised scenario. My justification for this is;

• I believe the chance that atropine may have little effect is too high due to the fact that the rhythm is not primarily vagally mediated.

• I have had some success with glucagon in the past however the benefits of this are only transient. Given that we are 45 minutes away from the hospital, I believe the benefit of glucagon would not sustain the patient for this time given its short half life. Please note here that I have no option for continuous infusion in this case due to the amount normally carried.

• This level of hemodynamic instability requires drastic action and as such I believe that cardiac pacing would provide the best chance at a positive outcome given the length of time away from the hospital. In pacing this pt though I am cognisant of the risk of decreasing the fibrillatory threshold. I have also had difficulty pacing some of these pt’s in the past due to the inability to capture despite the use of high voltage settings.

Good scenario though. I believe in these cases it always comes down to a risk v benefit analysis (for me anyway). In this particular scenario I simply believe that the risk of medication only therapy MAY either not be effective or not buy me enough time to get to the hospital. Whilst pacing alone is not ideal I believe it is the best option if forced to choose only one. Of course though this is my prehospital treatment as my decision in hospital would be different. Keen to hear others views on this.

Stay safe;

Curse

There is a theoretical problem with aggressive beta blockade and increasing hypertension due to unopposed alpha blockade.

Sorry missed that my question on beta blockers had been answered earlier.

Here's a link on this topic that may be useful

http://circ.ahajournals.org/cgi/reprint/117/14/1897

Go to the section that states BEGIN DOWNLOAD and you can then access the article

Stay Safe,

Curse

Cocaine users can have thrombotic events, just like everyone else, and at young ages. It's generally a bad idea to dismiss cocaine-associated ST elevation as "just vasospasm". They should go to cath like everyone else.

'zilla

Agree 100%. I guess it's one of those cases where a presumptive diagnosis is made based on likelihood and you have to go with the numbers until proven otherwise. In that sense should be treated as standard MI if the S+S are there.

I noticed an earlier respondent advocated benzo's and CCB's if cocaine induced MI is the culprit. Would any one have used beta blockers for rate control in this scenario?

Stay safe,

Curse

Various backyard pharmaceuticals can have numerous effects on the ECG. Really depends on the actual substance taken. Sometimes it is not the active that causes the problem but rather the other substances it has been “cut” with. Perhaps the most prevalent example I have seen of this is with GHB overdoses that presented with peaked T waves on the ECG. It was not the GHB that caused this change however it was due to the potassium that the GHB had been mixed with to derive the finished product.

In this particular case you presented it sounds classical for a possible case of cocaine induced MI - if of course an illegal drug was being considered as the cause. History is a big determinant here and I note your pt denied illegal drugs. Guess the drug screen is the only way to tell if they’re lying or not. Happy to elaborate further on cocaine induced MI if necessary however I am unfortunately short on time. I’m sure Mr Google can provide some answers here for any interested parties though. Hope this helps.

Stay safe,

Curse

I have found that sux is a great drug for pain, my pain from listening to the patient scream, just give it to em, intubate em and they won't be screaming anymore.

Make sure you give versed and some pain relief before you paralyze them.

The last two sentences above are said with sarcasm dripping

Hilarious :wink:

And no need for the discalimer. I'm sure we have all felt like that at some stage. After all who needs physical restraints when you have sux!!!!

Stay safe,

Curse :evil:

We use two pneumonics in our service. DIVINE for contraindications and SADMC for cautions. DIVINE stands for Decompression(complications with nitrogen narcosis as nitrous oxide is N2O2), Inhalation(people with inhalation injuries need as much O2 as possible because the nature of their injuries has already compromised the bodies ability to perform gas exchange), Ventilation (you must be able to ventilate the space to prevent the gas from affecting the provider), Inability to comply (entonox is self administered so the patient must be able to comply with directions, Nitro in the last 5 minutes (N2O2 has a mild vasodialatory effect on it's own which will have an additive effect to that of Nitro), Embolus (primarily concerned about a PE). N2O2 is heavier than air so it will collect in dead spaces. This also precludes it from use in conjunction with any chest wall trauma.

Cautions using SADMC are: Shock (N2O2 has a mild vasodialatory effect. Not really a help with a patient in shock. Shock also affects a patients ability to comply). Abdominal distention (vasodialatory effect, N2O2's propensity to collect in dead spaces). Depressant substances (N2O2 is a CNS depressant which means it could have a greater effect on someone who is already CNS depressed). Maxillo-Facial injuries (Affects a patients ability to use the delivery device. N2O2 collecting in dead spaces). COPD patients (These patients already have a compromised respiratory system).

GREAT answer!!!!

Pneumonics are your friend.

Another one I have heard apply to entonox in order to remember some common CI's is CHUNDER

C - Chest injuries (usually also think abdo here for the same reason)

H - Head injuries / Heat (pertaining to fire)

U - Unconscioussness / Under zero degrees celcius

N - Nutters (psych pts - politically incorrect I know, but it's not MY pneumonic)

D - Diving (within previous 48 hrs)

E - Early age (Too young to self administer)

R - Refuses

And should be used with caution in pt's vomiting - hence CHUNDER

Stay safe,

Curse :evil:

Anyone ever performed or been witness to a venous cutdown in the field?

Stay safe,

Curse :evil:

Wish we had Nitrous Oxide. but oh well. its on the approved drug list for the state.

I wouldn't be too keen for it. I often find it more of a hinderance than a help. It is big and bulky and I anecdotally don't find the efficacy particularly good. In fact we are currently in the process of phasing it out of service. There are also certain clinical conditions that preclude its use - particularly in trauma. Actually there's a good question!!!

Outline when you would not give entonox and also state the reasons why.

Stay safe,

Curse :evil:

It is a reference to the newer AHA guidelines that recommend one shock followed by two minutes of CPR. I suspect the original post was referencing situations back when "stacked shocks" were common practice.

Take care,

chbare.

Interesting!!!!! Perhaps we have differing recommendations.

In Australia, the Australian Resuscitation Council (ARC), still recommends an initial 3 stacked shock strategy in cases where the arrest (VF/VT) is witnessed by the rescuer and a defibrillator is immediately available. Please see page six on the following link;

http://www.resus.org.au/policy/guidelines/...py_for_aals.htm

It would be interesting to establish whether the ARC recommendations and the AHA standards conflict on this particular topic. And if so debate the possible reasons for this discrepancy. If someone could provide a link to the AHA guidelines I would be appreciative.

Stay safe,

Curse :evil:

You're going to stay outside for 6 minutes? :?

Why would this take 6 minutes?

Stay safe,

Curse :evil:

Isn't the gist of that formula kinda of a priori knowledge?

To be entirely honest I'm not sure what you really mean by this. Don't get me wrong I understand the words, but just dont really understand what your overall feelings on this theory are. As such, I would appreciate if you could provide more info here.

Stay safe,

Curse :evil:

how about the hagen formula

The larger the catheter the more fluid that can go thru the cath into the body.

a 22 ga will give x amount while a 14ga will give a lot more.

I'm not sure of the actual formula numbers.

Hagen-Poiseuille equation

GOLD star to Ruffems!!!! Well done. :hello1:

The application of this equation can get pretty advanced. However when you nut it all out it is basically saying the shorter and fatter a tube, or IVC, is - the greater the flow. So basically, in trauma don't insert a LONG THIN central line. Insert a SHORT FAT 14G IVC

Stay safe,

Curse :evil:

Sure, grammar and spelling are not the focus of this thread. Simply pointing out that those who wish to slam others for spelling or grammar errors should first examine their own writing carefully. Presentation is everything, and a misspelled word can be so distracting that one can literally become completely sidetracked from an argument that is otherwise well constructed and thought out.

Wendy

CO EMT-B

On that note could you please explain what a RAPPOR is? (Read below from another thread)

Unfortunately, expressing that SI is not a valid mechanism or a good mechanism may alienate your rappor with your patient and not do anyone any good... but at the same time, you can't say "good, sure, cut your wrists instead of taking that overdose" because it's positively reinforcing a behavior that is less negative than the alternative but surely still a negative.

Touche!!!

Anyway this is boring me now and I am happy to move on. None of us can spell , myself included. So let's engage in our illiterate debates on here with true typo freedom and get back to the clinical issues at hand.

Stay safe,

Curse :evil: