AZCEP

If you don't know what's in "the box", how can you know when you are thinking outside of it? Ask the questions, think through the problem, make yourself better. More providers need to have the same desire to do these simple things. Eventually, you will be able to dynamite "the box" through your ability to...wait for it...THINK[/font:fbd3f7b356].

Okay, I've got to get in on this silliness.

For a brief moment, it is possible for the muscle to be contracting and the myocyte to be repolarizing. The cell uses the calcium ion to initiate the contraction. Because it moves after the sodium, it will be a bit later to leave the cell allowing relaxation. Keep in mind that most biologic processes are occurring at the same time. It is very difficult to say that one process ends and another begins in black and white. It would make things simpler, but look for the gray.

The contraction won't necessarily last from the beginning of depolarization to the end of repolarization. Depolarization (QRS complex) initiates the contraction, but it has to happen prior to the start of systole. Repolarization is started when the electrolyte balance determines that they need to move back to the starting point. As the amount of sodium and potassium reach their diffusion thresholds, they will move to balance. The calcium and magnesium that follow, cause the contraction to end and relaxation(diastole) to begin.

The question of how does the atropine have an effect, has been answered. It works to counteract the ACh at the muscarinic receptor site. The connection of the vagus nerve in the atrial/junctional tissue is the dendrite. The synapse is the space between the dendrite and the effector organ/tissue. In this case the SA/AV nodal tissue. Atropine does not work directly on the vagus nerve. Insert "what happens in vagus, stays in vagus" here. The atropine is working on the muscarinic receptor site, where the ACh is taking effect. Similar to how Narcan competes with opioids at specific narcotic receptors. The blood is providing a mechanism for the drug to be circulated to the receptor sites. It will not have a direct effect on the vagus nerve. For illustration purposes only: Some patients with seizure disorders have a device implanted that will stimulate the vagus nerve prior to a seizure. This action increases the activity of the parasympathetic nervous system, slowing the generation of impulses in the CNS. These patients will still respond to atropine, because the drug is going to blunt some of the actions of the PNS. The patient that has had a heart transplant, on the other hand, won't respond well, if at all, to atropine because the vagus nerve no longer has direct effects on the heart. Atropine can work on the other organ systems that the vagus nerve innervates above the level of the transection. Is that a better answer?

The vagus nerve (Cranial nerve X) directly innervates the right atria, near the SA node, and the AV junction. The connection that you speak of would be the dendrite. The nerve itself transmits it's message with acetylcholine (ACh) to the given tissue that it comes into contact with. The trouble with using atropine for the high grade AV block is due to the loss of conduction through the AV node more than ACh's effect on the atria. When the vagus nerve is stimulated, conduction through the AV node slows down. This accounts for the effectiveness of most vagal maneuvers on reentry tachycardias. Atropine works through a counteraction of the ACh. It basically blocks the release of the neurotransmitter from the dendrite into the synapse. Less ACh released, less cholinergic effect (S-L-U-D-G-E) from the muscarinic receptors that atropine works on. ACh is contained fairly well within the synapses. Should a cholinergic agent make it into the blood stream, the effects will be much longer acting. Check the organophosphates, for example. Neurotransmitters don't have a half-life that allows them to be directly dangerous to the functional level of the cells. Problems arise when the neurotransmitters stimulate the release of other hormones that will last longer. The short answer, Atropine counteracts cholinergic effects on the muscarinic receptor site.

Actually, not bad Dust. Consider for a moment the action potential that is created by the movement of the electrolytes. Since you have Dubin's book, you should be able to find a picture to follow along. Phase 0-1: Sodium and potassium are moving quickly in/out of the cell, rapidly changing the membrane potential. At the end of phase 1, the QRS is formed showing ventricular depolarization. The electrical event ends. Phase 2: Calcium moves into the myocardial cell facilitating contraction of the muscle. Notice that phase 2 begins at, or shortly after, the peak of the QRS complex. As Dust mentioned, the electrical stimulus moves through the myocardium to initiate the mechanical contraction. If the muscle can accept the stimuli, you get contraction, and movement of the blood. If the muscle can't contract, you get an electrical event without any blood movement--PEA. Phases 3-4: Primarily deal with the electrolytes returning to the resting state. Sodium/potassium return to their original locations, calcium slowly exits the cell, and the sodium/potassium pump returns the the cell to it's resting membrane potential of roughly -90 mV.

I would recommend looking at www.capnography.com for the expected waveforms You will be able to make a real-time determination on the ventilatory status of the patient. You will also be able to determine if the specific treatment you are using is making a difference, or the patient is not responding to it. Good point. I didn't write that comment too clearly, now did I? :roll: A good assessment is possible without it, but to determine how effective treatment is a continuous trend of ventilations is very useful. Many times it is very difficult to elicit audible breath sounds, and capnography adds to the ability to make good clinical decisions. We should all be able to base initial treatment on the patient presentation, but more information is useful for the decision making process.

We have it, and yes it can change the treatment that is provided. Intubated cardiac arrest, for example. If the patient has minimal CO2 detected following 2 minutes of compressions, there is less likelihood that they will be resuscitated. Consideration to terminate can be made much earlier, regardless of the rhythm that is found. Reactive airway disorders: you can gauge the effectiveness of the treatment you are providing based on the waveform. If the patient is unable to adequately ventilate the distal airways, you will see a change in the waveform and the numerical value when the treatment you are using starts to work. COPD: Because of the pathophysiology of the disease, the waveform is different from normal to start. When treatment is effective the wave will "normalize". In any of these situations, you will alter your treatment plan based on the information that you receive. Your assessment and the information from the capnography should work together to tell you how effective you are treating the patient. Capnography alone can't tell you, and neither can a good assessment.

It sounds like you did the right thing by not letting age and appearance to cloud your judgement. The fact she is relatively young tends to put providers off their guard for ACS, but it can still happen. Is it common in the young and healthy? No, but if they have a cardiovascular system, it can still occur. Were there any other leads on the 12 lead that showed notched P-waves? Typically, the right atrial enlargement will have an abnormally tall P-wave without a notch, while the left atrial enlargement will produce a wider than normal, notched P-wave. If there are other signs of a cardiac event, perhaps there is something in the history that was overlooked. You might not have had the chance to go deep enough to find it, and it might not be there anyway. I do agree with Shane that the presentation could very well be a response to a seasonal infection. It would be good to follow up on this one, just to find out what actually happened.

God Bless those that are unable to be where they want to for the holidays.

Just as performing the procedure has to be justifiable to the "reasonable man", so would refusing to do it. Inappropriate orders are given all the time, and following clarification, are either withdrawn or reaffirmed. D50 or bicarb down the ETT, for example. Yes, I've received them, and no, I did not follow the given order. Too often we get caught in the trap of thinking that we have to do what we are told. When it is obviously wrong, we have to be smart enough to realize it.

The descriptor wasn't added. Similar to the 0-10 scale for pain. 1 being your average healthy adult human, SICK being, well, death warmed over. Better?

Way to answer your own question. +15 for realizing the futility of chasing an arbitrary system of approval. Happy now?

I've always thought that FORD backwards was DROF, but I've been wrong before. I can appreciate the problem with convincing someone of your findings, but the opportunity to use the procedure doesn't present too often to keep fresh on it. With the degree of difficulty that some have with securing an airway, do we really want to allow them to go to this extreme? The educational system could do a better job of providing the education to do so, but the procedural skill would still fade.

Some of the looks that we get upon delivery of these patients are pretty comical, but the situation itself is a long way from funny. Shocking, maybe. Confusing, occasionally. Frustrating, frequently. Never funny.

Perhaps it is a matter of diluting the procedural skills, but the infrequent use of this procedure was the reason it was taken out of our local scope roughly 15 years ago. If I'm in the ER, with some back up help, and the same degree of direction I'd give it a shot. Until that happens, I wouldn't feel comfortable doing it prehospital. I might consider it, but I'd be a ways from pulling the needle out to do it. Even in house, this procedure isn't done with any great regularity locally. So I'd opt out of this one, and for the record, no open chest cardiac massage either.

845 lbs with 8 people, a chainsaw and a flat bed auto wrecker.

OOOOOHHHHHH!!!! Doc, you tricky so and so. I'd have to say no to the pericardiocentesis. Yes, it would buy some time. Yes, it is probably fairly simple to do. Having not actually seen one--and as an aside, seeing a few that have gone very bad--I wouldn't feel comfortable stepping that far over the proverbial line.

A couple problems with this blanket statement: 1. Many places allow BLS providers to either assist the patient with their own, or administer medications. ASA, NTG, albuterol, Epi pens, some even allow glucagon. With your comment, you've effectively hamstrung any credibility you might have had. A quick search of this very site would have told you so. 2. IV's are also allowed by many places to be initiated by BLS providers. You are correct that "some states" require the intermediate as the minimum, but just as many will allow basics to establish vascular access on their own.

There are scarce few things that have to be done in a time sensitive manner in medicine. Airway clearance, needle decompression, maybe manual defib, but few others. The EMT pushed a schedule II narcotic, with an ALS provider available. The ALS provider falsified the patient care report. Perhaps FFEMT4100 could explain how administration of this medication is of immediate benefit to the survivability of this particular patient. Seems I must have missed that day of pharmacology. The ALS provider sounds to have been doing BLS things, while he allowed his BLS partner to do an ALS procedure that could have, and probably should have, waited. Then he falsified his documentation to cover his/their a$$es. Comedy of errors.

Perhaps thinking critically isn't a popular activity for prehospital providers, but when it is used correctly it is very useful. Rid makes a good point regarding the actual lack of a national "scope of practice". Many locations are operating with the understanding that DOT/NHTSA have a set of rules for what is allowed. Unfortunately, they don't. The DOT curriculum from '99 is the closest you get. I can't count the number of times that I've thought and done things that many wouldn't consider. Just a few examples: --Lidocaine for pre-intubation. At the time, unheard of locally. --Magnesium for refractory bronchospasm. Again, not in protocol, and eyebrows raised during review. --Epinephrine infusion during cardiac arrest. Amazing what a little math can do for you. --Benadryl for pain relief/sedation. Maybe it just looked like they were itching. --Overdrive paced Torsade at 165/minute. Luckily, the pacer was able to capture it. There's probably more, but that should be plenty for now. Until the patients that want my help decide that they will follow the protocols that are in place, I don't feel a particular need to give them the ability to decide every step that I will follow. Some providers need the structure that protocols provide, some don't. Patients don't want to follow the rules that I do, why should I force treatment on them that I'm reasonably sure isn't going to work?

Give it some time gents. "Super weed" has been extremely popular for us. Sedative effects of the THC, and usually a stimulant effect from PCP/Ketamine/formaldehyde/whatever the h#&& else they decide to dip it in. We've even had some marijuana/Robitussin combinations recently.

If they are able to separate family from the situation, absolutely allow them to help. Particularly if you have no one else to do so.

That is great video. Thanks Rid.