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You said you don't have many interventionalists? Seems to me like thats the likely reason. If you have say three of them, they likely take call every third night. If something like that were the case, it is quite understandable not wanting to be called in for bogus cases. A similar problem occured at one the local hospitals with stroke alerts. Nurses were calling them in from the floors without notifying the resident. After several neurologist trips into the hospital for amaurosis fugax and diabetic 3rd nerve palsy, the neurologists required that only physicians initiate the stroke alert protocol. Getting called out of bed for a real case sucks enough, let alone getting called out of bed for a bogus consult. I would imagine that it wouldnt take more than one or two screw ups to ruin things for everyone.

I would try not to think of ion channels as discretely open or closed. Better to think of it as a whole class of receptors spending a greater percentage of their time in a closed state. Sort of a lower probability of opening state. One way to force them more towards the open state is to alter the gradient of the relevant ion across the channel. Thats the idea behind giving calcium, although it seems it is not considered standard of care in the absence of a specific indication, it is theoretically possible that it would be efficacious. The mechanism of change in the relevant calcium channel permeability is allosteric change secondary to the binding of cAMP to cyclic nucleotide gated ion channels. Therefore change is dependant on the concentration of cAMP within the cell, which is affected by a number of trans acting factors (beta agonists, glucagon, and an large cadre of others). The state of these channels will therefore depend not only on the degree of depth of the adrenergic blockaide, but on a number of other factors. The point is, it's better to think of the function of proteins as a continuum rather than an on-off situation.

This sort of thing is likely to vary heavily by service. There is no need for things like antibiotics or thrombolytics in urban areas, but there very well may be in less urban areas.

You actually don't even really need to wait to get the cultures/gram stain back. Just the CSF glucose and total protein should be sufficient to justify starting antibiotics in the right clinical scenario. You'd then expect the cultures to confirm in the next day or two. Actually, that thought brings up another potential issue with prehospital antibiotics. Generally, it is considered best to collect specimens for culture prior to initiating treatment. If antibiotics are administered, the likelyhood of cultures growing will fall. This leads to diagnostic uncertainty and may commit the treating physician to completing the antibiotic course even in the face of poor clinical indications for continued therapy (for medicolegal reasons). Another thing to keep in mind is that the above mentioned penicillin family antibiotics wont cover all causes of bacterial meningitis (most...but not all). The big uncovered group would be certain strains of pneumococcus.

Two thoughts: 1. Why will pressors not work? These are soluble catacholamines infused directly into the circulation, akin to endogenous production of epinephrine by the adrenal glands. That is to say that the receptors for catecholamines are located on the end organs (like the vascular smooth muscle and heart). While the SNS may no long be able to produce catecholamines because of denervation, the tissues will still be able to respond to catecholamines, unless of course we have given him medications to block those receptors...say...to control his hypertension. Alpha or beta blockers would likely make the hypotension worse in someone like this, however, administration of a bunch of adrenergic agonists plus high endogenous production will eventually overcome this. 2. The idea that the parasympathetic NS will not function. While it is true that you are blocking the PNS, keep in mind that in this pt the PNS dosent have any function that is helpful to you. On the other hand, it can do some things to work against you, namely decrease peripheral vascular tone and slow the heart rate. I guess one other thought: Neurogenic shock should probably not be the first thing that pops into ones head in a scenario with hypotension and then cardiac arrest following a traumatic injury. While certainly possible, there are other causes that would likely deserve a higher position on your differential. Neurogenic shock is probably the most rare form of distributive shock. Further, it generally should be transient and relatively mild in terms of the degree of the hypotension owing to several means of physiologic compensation...soluble catecholamines and decreased parasympathetic output in response to hypotension. Hope this clarifies a little. All the best.

By what mechanism do you propose that atropine would make the situation worse? Atropine is a parasympatholytic. The simplified version of the pathophys is that that you have unopposed parasympathetic tone causing excessive vasodilation. Blocking the parasympathetic input, which causes smooth muscle relaxation, would likely tend to help the situation more than harm. The reality however, is that someone like this likely has very little parasympathetic output owing to the hypotension.

The fast way to find it: place your thumb on the pts olecranon (elboe). Wrap your hand around the medial aspect of the arm. The place where the tips of your fingers come down is usually right on the brachial a. You'll find it generally is located more laterally than you expect.

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I think what you will find is that Vit. B12, folate, and thiamine are the deficient vitamins in alcoholics to know. In the case of B12 owing to decreased absorption from the gut in the presence of alcohol. A normal person has a weeks of folate reserves and at least a few months of B12 reserves, so the benefit of vitamins in a non-chronic-alcoholic are questionable. However, as previously mentioned, it isnt going to hurt. The clinical manifestations of B12 deficiency (and folate deficiency because they are both involved in similar biochemistry) is typically megaloblastic anemia (anemia with big fat red cells) but can also lead to Subacute Combined Degeneration...basically a neurological condition which typically starts with balance issues due to damage to the nerves in the spinal cord that connect the cerebellum to the rest of the body. Thiamine deficiency is thought to be involved in the pathogenesis of Wernicke-Korsakoff syndrome. This is essentially a syndrome of psychosis with balance and tremor issues (cerebellar issues if you will).

Thats whats in it...but why those ingredients...random choices? Do drunks need vitamins? (which ones?). Are non-chronic alcoholics at risk of vitamin deficiency? Just trying to get some discussion going. 8)

Anyone know the reason? Is it to treat the drunkenness/hangover? or is there another reason? Any benefit to doing it in someone who is not a chronic abuser of EtOH?

Yep. That is also true. Crepitus is a term for the sensation of clicking/poping etc. You experience crepitus which leads you to the diagnosis of sub-Q emphysema, TMJ etc. crepitus (krep´itus), n a crackling sound such as that produced by the rubbing together of fragments of a fractured bone or by air moving in a tissue space. crepitus, bony, n the crackling sound noted during auscultation; also the sensation noted during palpation when the fragments of a fractured bone are rubbed together. crep·i·ta·tion (krp-tshn) n. 1. A rattling or crackling sound like that made by rubbing hair between the fingers close to the ear. 2. The sensation felt on placing the hand over the seat of a fracture when the broken ends of the bone are moved, or over tissue in which gas gangrene is present. 3. The noise produced by rubbing bone or irregular cartilage surfaces together, as in arthritis.

Wow....I was really confused there for a min. trying to think of what the heck hypercortisolism had to do with brain herniation! Now I get it.

I can contribute some memory aids: You have one heart (B1) and two lungs (B2). ABEAM = common B1 selective beta blockers Atenolol Bextaxolol Ethambutol Acebutolol Metoprolol The name ------olol, as you can see above, is pretty useful for recognizing a B-blocker. "Point and Shoot" = Parasympathetic controls errection, Sympathetic controls ejaculation. Regarding some of the things mentioned but not discussed above: 1.Nicotinic acetylcholine receptors - these are actually used quite commonly, although we often don't think of it as such. The drugs that act here are the paralytics, vecuronium for example. They cause paralysis by blocking nicotinic cholinergic receptors in the nerves that go to the muscles (which are neither sympathetic nor parasympathetic. 2. Alpha 1 blockers are actually quite common drugs, used for the indication of "BPH" Benign Prostatic Hypertrophy, basically difficulty peeing due to large prostate. This of course makes sense if you think back to "fight or flight"....no time to pee when you are fighting or running away. Flomax (tamulosin) is an example, although admittedly it is specific to a subtype of alpha receptors and should not cause a lot of orthostatic hypotension (low BP with standing up). This fact also makes terazosin (a less specific alpha blocker) a good choice for those with both hypertension and BPH. 3. It might intrest you to know that there are not only chemical differences between the parasympathetic and sympathetic systems (ie catecholamines (like epi) vs acetylcholine) but the systems are also anatomically seperate. The parasympathetic nerves come only from the cranial nerves and sacral levels of the spine; "craniosacral in origin". The sympathetic nerves only come from the thoracic and lumbar levels of the spine; "thoracolumbar in origin". Thus the parasympathetic to the heart arrives via a small nerve ( the vagus) that comes dirrectly off of the brain and travels down to the heart (and beyond...). The spinal cord is completely uninvolved. I thought of a drug that hasnt been discussed here yet: Can anyone think of an alpha agonist that can be used to treat hypertension (or withdrawl )? Seems counter-intuitive. How does that work?

Another thing to keep in mind as you pursue your education is that at some schools there are different levels of certain classes. If you are going to take a class, you should make sure you are taking it at a level which allows you to use it as a pre-requisite for medical/PA/BSN etc school in the future (some schools, esp if smaller only offer one level). For example, at my alma mater, there are at least two different levels of chemistry, and 3 levels of physics. People here can easily be trapped in that the lower level chemistry is sufficient for the BSN, but will not be recognized by most medical school admission depts as meeting the prerequisites. Thus a nurse who had no intention of pursuing medical school but who developed it after graduation would have to do another year long chemistry course to meet the pre-reqs. I'm sure different universities have different ways of denoting these classes, here the first level of most science courses is labeled "XXXX for non-science majors" and will not be counted as fulfilling the prereqs by most medical schools (the reason for the designation is that here they also do not fulfill the req for a degree in a science such as bio, chem, physics, biochem, etc). So if you're going to spend the time, effort and $$ taking a class, its best to be sure that it fulfills the pre-reqs for anything you are even slightly thinking about doing in the future, as it may save you quite a bit of greif repeating a course that is largely similar to one you've already taken. Also, I highly reccomend www.studentdoctor.net and the forums there for anyone considering medical school (there are also PA and nursing sub-forums).

If you're interested in knowing why the oral dose must be much higher, google "first pass effect".

You could reasonably expect JVD in someone with a large PE causing right sided heart failure. However, I would expect that a OE that large would quickly result in death secondary to hypoxia.

Most of the body's Ca is albumin bound. When you increase the pH you suddenly increase the ability of albumin to bind Ca and thus the fraction of the total Ca that is ionized drops (bound Ca is by definition not ionized). So total Ca would remain unchanged but ionized calcium ("iCal") would be decreased. Apparently the cost of an iCal relative to a total Ca is what keeps the total Ca measurement in existence, as iCal is much more physiologically relevant.

I suppose you also have to consider that the course is designed for many different types of providers. Even some of the pharmacists here have to take it. I took it during my second year of medical school and the things I needed taught were probably rather different than a nurse or medic or pharmacist. For example, I knew my pharmacology pretty well, but if you would have asked me what vial of lidocaine looked like or how to get it into a patient, I wouldn't have had the faintest idea.

Yes. The effect of nitroglycerin is largely due to its capacity to dilate the body's large vein ("compliance vessels"). This causes decreased venous return to the heart and thus decreased myocardial oxyen demand. If coronary vasodilation plays any role at all, it is small. This makes sense as one would expect ischemic coronary arteries to already be maximally dilated by their own production of vasodilatory metabolites (CO2, adenosine). In fact, in this system, one might even expect nitrates to cause dilation of vessels proximal to the blocked vessel, causing decreased flow to the ischemic area (the cardiac steal phenomenon).

The FAA has the authority to put in place "temporary flight restrictions", I doubt the emergency management agency does, however. This is what the FAA does over football games, fireworks displays, missle launches etc. I dont know a whole lot about it, not being a pilot, but i'd bet you could get the FDA to put up a TFR in an emergency unless there is some FAR rule against it.

Actually you are correct in principle, just not using "afferent" and "efferent" correctly. That is that you are correct in that in the original reply "dendrites" synapsing on the heart is technically not the correct terminology. To be a dendrite, a process has to carry information toward the nerve cell body. I believe there is an additional complication in that these vagal efferents are preganglionic parasympathetic. Thus they should have to synapse on a post-ganglionic parasympathetic cell on the end organ (heart in this case) then a short post ganglionic fiber would synapse with the effector cell (in this case a cardiac muscle cell....but, I would hesitate to call it a NMJ because it is muscarinic).