AZCEP

Most times, that is what learning is. Figuring out that you know what you know. Even more often, understanding that you know how to apply what you know is more difficult.

The recommendation is as follows: --If a patient presents with bilateral dilated pupils, ventilate at 5/min greater than normal for the age. (child-20+5=25, infant-30+5=35) Continue this until the pupils constrict, then ventilate at normal ranges for the age. --If a patient presents with asymmetrical pupillary size, ventilate as above until symmetry returns, then return to normal rates. Seems that we are telling people it is okay to hyperventilate as long as you pay close attention to the pupils. :roll: This may work in an operating theater where there are enough people to dedicate someone to this function. Everywhere else will end up with hyperventilated, hypocapneic, brain herniations.

Honestly, if we are going to use them, we need to understand how the device works. Yet another problem to be solved through education. For lower extremity fractures and unstable pelvic fx, there is nothing better. Aside from a full body vacuum splint, which few agencies can afford to part with. Like every patient we need to manage, think the problem through and manage accordingly. Occasionally, you will find that the navel-down air splint (MAST/PASG) is the best tool for the job.

emt322632 Let's think about what Albuterol does. Hmmmm...bronchodilates? Yes, but what else, more simplified. Hmmmm...stimulates beta 2 receptors? Right, and that will cause what to happen, not just in the bronchi? Hmmmmm...smooth muscle relaxant? Bingo! Now, where is there smooth muscle that will be responsive to beta stimulation? And how will those areas respond to the relaxation? Focusing a minute on the vasculature, which vessels will be most affected by beta stimulated smooth muscle relaxation? Arterioles... right-o! Now with this reduction in afterload, what will happen to cardiac output? We would expect it to....increase, right again. With the increase in cardiac output, what will happen to preload, or the volume of blood left in the left ventricle when it is done contracting? We should expect it to increase as well, due in part to our not increasing the venous capacity. This blood has to go somewhere, right? So, now that we have increased preload, momentarily, how will the heart respond? See how easy this is?! The heart will not be able to compensate for the increased volume for a short period, and the CHF will?...get worse. The patient becomes more short of breath, blood pressure increases from sympathetic influences, heart rate increases, the sick heart gets sicker. Luckily this doesn't happen to every patient that Albuterol is given to with CHF as the problem. When you do this the first time, and your pucker factor rockets off the chart, you won't do it again. :shock:

Thank you Rid! Finally, someone remembering that the first effect to be seen from Lasix is vasodilation. Reduce preload, give the fluid in the lungs someplace to go, improve the situation. The chest film isn't going to be much help in telling pulmonary edema from pneumonia or effusion, and God help you if you can't breathe and you are waiting for the lab to tell you what treatment you should receive. Also consider, Dopamine and Lasix are used together to improve hemodynamics fairly commonly. Using fluid boluses with Lasix can also help this situation, not as dramatically as with Dopamine, but the effect would be along the same lines. As an aside, there must be a dozen or so separate threads on CHF at the same time. Is this really this big of a problem?

Two of the easiest are the hepatojugular reflex and the Valsalva maneuver. The Valsalva will give you a response when you are taking a blood pressure. Have the patient bear down, or exhale against a closed glottis, the blood pressure will drop, then when they stop, their blood pressure should overshoot where it was to begin with. If CHF is present, the blood pressure won't be able to make the big jump past the original. The hepatojugular reflex is a piece of cake to assess. Have the patient recline to about 45 degrees on the gurney, if they are able. Find the liver, palpate with moderate pressure, and watch the jugular veins. When they jump out at you, this is a positive.

Sweet video Rid!

Move to LSB, more for ease of moving the patient than for immobilization. BLS adjuncts, and bag-mask-ventilation as we move to the ambulance. Ambient temperature of environment? Any idea how long he has been there? ETOH? Evidence of drug use? Pupillary response? BGL? VS/ECG/EtCO2/SpO2? Bilateral IVs are a bit much, one would be good for now. 12.5 gm of Dextrose, reassess BGL, consider more definitive airway. Transport by ground.

Nasal intubations are won/lost by inadequate equipment more often than not. If you are going to do these regularly, invest in the Endotrol tube and the BAAM whistle. Nothing available will make it easier to successfully place a nasal tube. "Conscious" is a bit of a misnomer. If they are conscious, they won't tolerate the oral attempt too well. Unless they make their living swallowing swords, or other, ahem, items. Even with moderate sedation, oral attempts trigger a sleepy patient to come up swinging.

Christ Punisher! Why did you have to bring that whole mess up?

Yep, I should have read the scenario a bit closer. You listed it right there. My "Uh-oh" flag would be raised using Cardizem with a blood pressure that low, but I guess it worked out. Flood these patients with benzo's and wait for the street corner pharaceutics to wear off.

Why no BZD? Other than the Versed for induction, seems they missed it. A blood glucose might have been a good idea as well. Might consider some IV fluids while we are doing things.

Whit, You may know about glucagon, but you still have a long way to go before you can say you know enough about it. Fact of the matter is there is a difference between glucose, glycogen, and glucagon. To add one more, dextrose is different from glucose. If you want to discuss a topic intelligently, use the terminology correctly.

ERDoc, The main issue that I have with a BLS provider using glucagon is based in the description that was given by whit. Apparently they are not being taught what all of glucagon's actions are. For an instructor to stand back and tell his EMT class that there are no side effects, and that, regardless of the underlying situation, the hypoglycemic patient should be given this drug is dangerous. I gave the description that I did because I have been on the receiving end of a glucagon injection several times. Yes it was given safely, but the fact remains it would have been a good idea to have some idea what my heart rate and blood pressure were doing as follow up. Obviously there are better, and safer ways to increase the BGL. Give EMT's all the drugs in the world, just give them the amount of education that they need to use them safely. Not too much to ask, is it?

The next time this happens, in your most innocent, unknowing EMT posture, ask this tool of a paramedic how long does it take to knock out a patient's hypoxic drive? The response will be priceless, I promise. You did right. If the patient can't breathe, then they get oxygen. Only one relative contraindication to oxygen administration, and I'm betting this patient wasn't inhaling paraquat so they get it also. Keep in mind this idiot paramedic was an idiot before he became a medic, so it wasn't the paramedic part that made him act the way he did.

Whit, You need to re-read the response that was given by ERDoc. He stated that the hypoglycemia was bad, and that glucagon is not the method of choice to correct the problem. Yes, hypoglycemia is bad. However, there has been no evidence that transporting a hypoglycemic patient with signs of neurologic involvement without vascular access for IV dextrose administration is deleterious to the patient's condition in the short amount of time that most EMS agencies operate under. Have you had an opportunity to research this drug's actions on your own? We have been more than willing to assist you in educating yourself, and you don't seem to be able to take the hint. READ the description that I provided for you. It will help you understand that glucagon IS NOT GLUCOSE.

Understand the difference in the level of information you are after. Find yourself a good A & P/Pathophysiology course/book/program and make sure you understand it. This is the make/break of many paramedic students.

And still no response to come. Makes it seem that he became scared when presented with actual facts. Yes whit72, I am calling you out. You are willing to bash those you don't know with your opinions. Respond to my post of facts about this drug that you think you should be able to administer. I am ready for any response you can give. 8)

I would hold off on the epi for now, but definitely have it ready. Due to the patient taking a beta blocker, there is a possibility the epi would have a blunted effect, right? The glucagon might help this situation. Reassess, lung sounds and keep a close eye on the oropharynx for signs of edema.

Know your job, and let me worry about mine. I really don't need a pop quiz on patient management every time I run a call with you, but thank you for the aggravation.

I certainly hope whit72 is reading this Angioedema? Stridor? If so, epi 0.3 mg IM and get the glucagon out

Medical history and medication list? Oxygen, IV, Benadryl, ECG, with Epi warming up Might also consider a Combi-vent SVN, and steroid of choice

I guess lucky for her, she still was able to resume normal cardiac activity following the standstill, eh? I don't think I'd like to watch that for very long.

It would be nice to see the strip, but it sounds like PSVT. Rapid onset and termination. Symptoms during episode with some resolution when the rate slows down. Mid-late 20's is a pretty common time for this to be found. The discomfort he described sounds like an ischemic event due to the rate. The sick just keep getting younger and younger.

The initial ABG is a bit odd. Mild alkalosis with respiratory compensation, and a RR of 12-14? Did the family say anything about an anti-depressant? I'd agree with punting. A vent rate of 14 should not have altered the ABG all that much.