ERDoc

Not true. Admitted a guy to the CCU with stable VTach. We tried to chemically and electriclally convert him in the ER. He ended up on I believe a procainamide and amiodarone drip in the CCU. He ended up being transferred to another facility to have an ablation of an accessory pathway 3 days later. Never decompensated and only complained of intermittent palpitations. 403, without much detail, it sounds like you might have gotten a bad role of the dice, but again that is hard to say. VTach that is stable can become unstable.

I'm not making an arguement for or against them in the ambulance. It should help you in your assessment, but not be the end of your assessment. They do have real use in the hospital.

No I don't. Shoot me a PM. I'll be aorund.

Yup, increased RBC production and hyperventillation and increased cardiac output among others.

I think it has two names. It is either called the Jets or the Giants.

Dwayne, when you go to altitude there is less O2 in the air, so there will not be as much in the blood. You will initially see a low pulse ox. After a few days, the body will compensate (in most cases) and the pulse ox will return to normal. There is much more going on physiologically, but this is a simple explanation. The partial pressure of atmospheric oxygen is half at the base camp on Everest of what it is at sea level. Emedicine probably has a good article on altitude sickness that might help answer some of your questions.

This is wrong in so many ways. If you have let your pt's oxygen level fall so low that they are cyanotic, you have failed them. Pulse ox is also helpful to know how serious the cyanosis really is. If you have a hemoconcentrated pt (ie smoker, COPD etc) they will become cyanotic at a much higher sat than an anemic person will. In order to become cyanotic you need to have 5grams/dl of deoxygenated hemoglobin. In a person with anemia with a hgb of 6, you would need to drop your oxygenated hgb to 1g/dL before you would be cyanotic. This equates with a pulse ox of 16 before they become cyanotic. You had better well know that they are in trouble before they get a sat of 16%. Don't speak for what goes on in hospitals before you have actually managed pts in one. Pulse ox is standard of care. It is used to make clinical judgements all of the time, including in acute care settings. Research your facts before you blindly post.

The neuron without a dendrite is the pseudounipolar neuron. It has two axons with one bringing the signal in and the other bringing it out. They are usually found in the dorsal root ganglion with one axon going to the CNS and the other going to the periphery. Here is a post with some good pictures for those interested http://faculty.washington.edu/chudler/cells.html

I like the term elevated lactate better. Now, hexa... is fear of the number 666. accomodation (in reguards to pupils) In an earlier post, someone asked about LGL, there is also another definition besides what was given

The higher cert is not going to be blamed for everything, at least where I came from. The only thing that the guy in the back will be blamed for is making an inappropriate decision to go L&S. It is up to the driver to use due reguard. The drive has sole responsibility for how he/she handles the driving. I wasn't saying that the driver was making the decision to use or not use L&S, but I can see from my post where I may have made it sound like I was saying that. Sorry about the confusion. I actually just reread the original post and can see where this one could justify L&S. You have a BLS crew with a person that is weak and dizzy. For all you know as a BLS provider, this person may be on the verge of going into Vfib or some other rhythm not compatible with seeing tomorrow. Even in the ER the little old ladies that are weak and dizzy scare the hell out of me and I have all sorts of good stuff to check them with. If I haven't said it before, this partner is a tool.

Your partner is a tool. He is a prime example of why EMS lacks respect and few recognise it as a profession. He sounds like the kind of person that would hopefully be weeded out if more education was required. There are very few calls which actually need lights and sirens. Weak and dizzy, not likely to need it, depending on vitals (even then L&S may be overkill). Most codes DO NOT need L&S. Traumas are one of the few calls that I can think of that would justify L&S, although it is hard to make true generalizations as each case is different.Obviously the law varies from area to area, but overall it is up to the guy in charge to determine if the call should be run with or without L&S. If is decided that L&S are needed, then it is up to the driver, and him/her alone to make the best decision on how to do that safely. Long story short (too late) your partner is a tool.

Welcome Dr. Bledsoe. It is truly an honor to have you here. I was wondering if in your travels you have found there to be a difference in the accident rates between nongovernmental and governmental HEMS. In the system that I started off with, the helicopter program was run by the county police and was staffed with two pilots/POs and a flight medic from the university hospital. Safety was of prime importance. Just curious if you have found this to make a difference.

It also depends on what their definition of critical is and what they are using it for.

Out of curiosity, were they given orders to do the c-section? This may help with our discussion about pericardiocentesis. This could set presidence.

Perimortem means around the time of death. Generally it applies to the time of injury to the time of death or shortly thereafter (usually the mother is not pronounced until the fetus is out). There are not very many cases so it is hard to do a good study. It is also hard to get approval for a prospective study. Most of the info comes from retrospective chart review.

Incorrect. Neurons are either afferent or efferent. If they carry information to the CNS they are considered afferent and if they take information from the CNS to the periphery they are efferent. The signals enter the neuron through the dendrite (at least in those neurons that have them) and they travel down the neuron to the the axons which form the synapse with whatever they synapse on. Your use of the terms afferent and efferent are incorrect. 10 points for anyone that can say which neurons do not have dendrites.

What sort of pulse increase and BP decrease does everyone use as their cut off to say if someone is orthostatic or not? What research backs your values?

Dust, here's a little blurb from emedicine with some info on the statistics: Providing reliable estimates of maternal and neonatal outcome from this rare and catastrophic event is virtually impossible. The American literature primarily contains case reports and very small series. The United Kingdom previously included some data in the Confidential Enquiry into Maternal Deaths, but, as the name suggests, the registry applied only to cesarean deliveries in which the mother did not survive. Also, this database was dissolved on March 31, 2003. When active, the Confidential Enquiry into Maternal Deaths noted that from 1994-1996, 13 deliveries occurred that were classified as either postmortem or perimortem. Of these, only 2 babies were born alive, and one of them died shortly thereafter. The registry strongly supports the concept of rapid choice for delivery because the outcomes in the group labeled "perimortem" (patient moribund or undergoing cardiopulmonary resuscitation) were significantly better than those in the group labeled "postmortem" (patient thought to have already expired) (Whitten, 2000). In 10 years, 40 perimortem deliveries were registered, of which 25resulted in neurologically intact surviving infants (62.5%). Here's link to the full article http://www.emedicine.com/med/topic3398.htm

Dust, you can probably find what you are looking for here. I've heard that they suck the best: www.bunnyranch.net :twisted:

You do have all of the equipment that you need. All you need is a needle and a syringe, the bigger the better. If you have an effusion, especially a chronic one that is causing tamponade it is going to be fairly large and difficult to miss. I drained 120cc out of a pt similar to this one and she still had a moderate effusion when the cardiology guys finally showed up (I think I may have made it a scenario here too). Traumatic tamponade will not be as large because the pericardium does not have time to accomodate the additional fluid. You can get tamponade from as little as 50cc and even less in an acute tamponade. As for it being out of your scope of practice, can't argue that one. Would you do it if the doc on the phone walked you through it? What if it was your medical control and not just the recieving hospital that was directing you to do so?

Dwayne, I think the problem that you are having is seperating the electrical from the mechanical. They are related, but not the same. What the EKG shows you is what is happening electrically. The QRS is the depolarization. This usually causes the heart muscle to contract. The T wave is repolarization, which does nothing to the heart mechanically. Systole is the contraction of the heart, which is usually caused by depolarization. Diastole is the relaxation of the heart muscle, not caused by any electrical phenomenon. Repolarization is just the electrolytes that were mixed up during depolarization resetting themselves. I said "usually" previously because as others have said, you can have electrical activity without muscular activity (PEA or EMD). You will see a normal looking EKG (depolarization and repolarization) but there will be no mechanical activity (no systole or diastole, aka asystole).

Just to clean up things a bit. Acetylcholine (Ach) is released by the presynaptic neuron into the synaptic cleft. Once in the cleft the Ach binds with Ach receptors on the post-synaptic target (the SA node in this case). Acetylcholinesterase is the enzyme that breaks down Ach once it is released from the presynaptic neuron. This limits the action of the Ach. Atropine competes with the Ach to bind with the postsynaptic receptors. The difference is that atropine does not cause any postsynaptic events. It does not actually do anything to the Ach. In organophosphate(OP) poisoning, the OP binds with the Acetylcholinesterase, preventing it from breaking down Ach. This allows the Ach to exert its affects without being inhibited. Atropine is used so that the Ach cannot bind to the postsynaptic receptor in OP poisoning.

ACLS dictates treating any of the causes of PEA, so why wouldn't you do a centesis?

I have thought about it on many occasions, but I'm not sure if it is the right thing to do. :wink:

I find a firm but loving backhand to the occiput does the trick. If you hit just the right spot you can jar the English speaking part of their brain. I also reserve one for the medics who bring in said pt without having a full report.