OVeractiveBrain

The device was implanted on the left side. Im sure it isnt a simple "hook up electrode here" though i havent read the articles posted about the device yet. The Vagus nerve carries many afferent and efferent signals (the two most noticable are those that innervate cardiac tissue via ACh-R and those that transmit baro/chemo receptor signals from the aortic sinus/bodies to control ventilation). If the device were simply set to depolarize all nerve fibers in the nerve itself, multiple systems would go haywire. However, in terms of THIS patient, the device WAS NOT ACTIVATED YET. The fact that she needed the device leads me to believe that she had a neurotransmitter deficiency. Extrapyramidal reactions occur most frequently with dopamine antagonists. If she is on schizophrenic meds (probably dopamine antagonist) and has some problems with depression (naturally low levels of dopamine or seratonin) that need to be treated surgically (really low levels of NT) then that might cause the Extrapyramidal reactions.

So I had the same patient again today, one week later, 3 days after being discharged with aspiration pneumonia. Guess what she still has? Whoops...

Thanks, i take that as a compliment

Another case study: 28 yo caucasian female coming from home. She has an extensive psychiatric history with a number of meds, many new, that I did not recognize. She recently had a surgery that implanted a "neurlogical pacemaker" (a device that, when active, will stimulate afferents from the carotid sinus via the vagus and glossopharyngeal nerves that is supposed to increase the relative amounts of dopamine, seratonin and norepinephrine released into the brain to treat psychiatric disorders), with a sizeable incision with stitching near the left carotid artery. She went to the store at 1300 and took longer than she usually does, according to her parents, who she lives with. People started calling her "retarded" and she was so upset she returned home. She presents now at 1800 with restlessness and the inability to stop moving. Her extremities seem out of her control, making purposeless rolling and weaving motions. Despite her best efforts, she is unable to control her extremities. Finger touch / nose touch is out, though she is able to make good strong hand grasps and stand with assistance. Her speech is slightly slurred. She cant really stand up on her own, but it not that unsteady gait with CVA, its more of that "im a psych and OOPS i fell down" but im not ruling out unsteady gait. Family Hx: No cardiac, No pulmonary, No Ca, No CVA, NO IDDM, lots of psych (bipolar, shizo, depression) Social Hx:She is clean from cocaine and heroin for three years, denies any drug use. Amongst other psych meds she takes Yaz(brith control) and smokes cigarettes. Denies drug use, denies possibility of pregnancy, parents confirm compliance with medications. HEENT: Normal, no discharge, PEARL Speech: Slurred Mentation: GC:15, CAOx4 Motor: PMSx4, unstedy gait, good hand grasps and muscular tone, uncontrolled movements, though can apply force in certain directions, cannot stop movements VS: BP: 140/80 HR:112 sinus tach, 12-Lead: refused 12-lead (female, psych, im a guy, no shirt off, gave ER trouble too) RR: 16, clear equal bilaterally Skin: Warm Pink & Dry, mildly flushed in face (faired skin girl, probably gets flushed easily), afrebrile, cap refill great Sp02: 98% RA, 100% 4LPM bG: 97 Pain: None General Appearence: well kept, frustrated at the inability to stop moving, though not agitated nor anxious I checked for tract marks and searched her purse/coat while the family checked her drawers while the FD was extricating her with our stair chair. I didnt find anything, and she had this aura of pride when she said she was clean. She didnt even take anything from anyone that might have been laced with something. Given her psych and drug history I was unsure as to whether i could trust her, so i prodded a little more to no avail. (I dont want it to sound like that this was my main focus because it has gotten so much attention in the post, but it was one of my promininet differentials). To be honest, I didnt know what was going on. The slurred speech and "unsteady gait" made me nervous. Though it was unsteady becasue she was restless. With the amount of medication she is on (including schizophrenia meds) and with the new neurological pacemaker (which i never heard of) I got to thinking it might be stroke. Recent surgery in or around the carotid artery + overweight + birth control + smoking = CVA. But it didnt present like a CVA. It was like a giant dystonic reaction involving her entire body. Some research on the intarweb revealed a possible diagnosis of Tardive Diskythesia, a desire to move extremities as a result of dopamine insufficiency (seen with reglan and schizo meds*ding ding*). I went down the route of stroke, providing routine ALS and a priority I transport (lights + sirens) to the nearest facility (family wanted to go to the specialists' hospital for the next morning). I reflected after doing some research on dystonia and realized that benadryl was NO WHERE in my mindset when considering this patient. I mean, we give benadryl with reglan to reduce extrapyramidal reactions, but I just never thought that a) this is a dystonic reaction and i could give benadryl to make it stop. To be honest, i really assumed dystonic reactions were more focal (in the hands, conjucate gaze, lip smacking, cervical torticullis, eye blinking, individual muscle flexion without release, etc). This was just so general. Since I didnt know what it was and she had some risk factors for CVA, i went with CVA. But that just sounds like im filling out my treatment code box and not treating the patient. She wasnt in any distress so i wasnt terrifically worried, but we were as far out in town as you can get, so I wanted her to a physician fast. Ultimately, Im thinking psych meds + natural dopmaine insufficiency (thus the "pacemaker") --> augmented restless leg syndrome or some sort of dystonic reaction. But im interested to hear what people might be thinking along this one. Really it was just so strange that I wanted to share it; no one i talked to about it really knew what it was nor what they would do. But if anyone has any thoughts, throw em out there. All the interesting cases happen at the end of my day, so i never have a chance to follow up with the patients afterwards.

Sorry ive been away for so long. So some info i may have left out in the original post, that Ill reiterate that led down the path of Pulmonary Edema. For Pulmonary Edema Why I jumped to CHF: -That percolating sound upon spontaneous respiration of 'im full of fluid' heard without a scope as you walk up to her. It was only really after the intervention that i was curious as to whether i had made the right decision (left cleared, right didnt) * -Relatively fast onset (basically overnight) -afebrile contributing factors: -pt improvement (easier to breathe, better color, less sluggish, though still pretty lethargic) after lasix -no "cardiac hx" but she does have HTN -(retrospective) improvement in lung sounds (particular left) in the semi fowlers position, and increased pulse ox post intervention Against Pulmonary Edema, why i second guessed: -Predisposing condition -Normal ECG (no rotation, no ACS, no hypertrophy, nothing cardiac on the monitor nor 12-lead to suggest a cause of CHF) -No Hx indicative of CHF, Hx of pneumonia *ERDoc's comment about right side having higher incidence of pn To some of the other comments: -She wasnt dehydrated nor septic; oral mucosa was wet, there was no tenting of skin, and she was afebrile. I wasnt really concerned about electrolytes at that point either, as her pressure was fine and she had been normal and functioning until that day. -CPAP would have been great, but the closest thing ive got is manual PEEP (a BVM with some positive pressure on release). I had considered it when I first got to her, since she was unresponsive with spontaneous respirations. Once we managed to extricate her (all the while on 15LPM NRB) she came around a bit. Since i had other things I had to manage (and i was traveling down the route of CHF, question of pn) i decided not to dedicate my time to convincing her it would be worth while for me to force air into her lungs. -I really would have liked to give NTG. Again, all we have is the spray, and her neurologic disorder cause her to be unable to lift the tongue and open her mouth. Something to do with a change of meds for pain in her face. Yes, i could have ripped open her mouth and sprayed it in prior to giving the lasix, but since the dose of lasix was so low and I had access (we have to have access prior to NTG admin) i went for what was easier for me. -I wasnt going to take a conservative approach either. Some one found with a GCS of about 9 who improves with 02 but was still sluggish with poor presentation with a transport time of about 20 minutes or longer warrants some intervention. I guess Im really not describing her presentation well enough to justify my actions. Also, I wrote the initial post with the tone of "crap, did I do somethign wrong" instead of "this is what i did but that stupid nurse thought i was wrong," so im not suprised people are finding out of favor with my intervention. My saving grace is the paramedic in back with me agreed, so Im not all worried, just interested in what people have to say. In any case, im sure this will initiate a new barrage of posts, but I appreciate the feedback, harsh or not. But dont worry, you cant insult me. And if you did, id just report you to an admin. Just Kidding. No Im Not. Yes I am. Kidding. The real point of the post, what I was tryign to get to, was not "whether i did the right thing" but more along the line of "have you had aspiration pneumonia present as a possible CHF" and "can some one without any cardiac findings at a paramedic level be suffering from edema."

I had an interesting case today: 50 yo female with history of MS and pneumonia in January. She is a caucasian female coming from home, where she is wheel chair bound, and has VNA (visiting nurse) assistance. She is normally concious alert and oriented, able to speak and move upper extremities (MS has paralyzed her legs) without much complaint at all. Last night, the VNA noticed that she had some difficulty speaking. It was not slurred speech, its just that she couldnt get the words out right to make a whole sentence. This is most likely from a change in MS medication in order to stop the pain in her face (i imagine some medication that focuses on injured nerves of the face, deadening sensation and also the ability to speak). Now heres where we are now. This morning the patient is unresponsive, found in her wheelchair, with rapid labored respirations. After some 02 she opens her eyes spontaneously and is able to communicate through head nods that "she aint good." Right now she is GCS:15, but sluggish, unable to speak, but making obvious attempts at communication. PMS present where they should be, PEARL. Lung sounds are wet (lets just go with crackles) without wheeze, has a global sound with diminished bases, and you can hear a gurgling sound as she breaths (even before when she was unresponsive). Shes a little pale, bu ther numbers are WNL, SpO2 98 on 15LPM NRB.. Right off the bat im thinking CHF. She is unable to lift her tongue to the roof of her mouth (either through communication, nerve damage or the fact that she is hypoxic) so NTG is out, we dont have CPAP nor PEEP, so thats out too. I could have tried using a BVM as a PEEP, but i went for more benign treatment since at this point she was awake and aware. I gave her 40mg of Lasix, dropped her pressure from 132/p to 114/p, right side clear, left side still junky, all throughout. ED Nurse says "Aspiration Pneumonia" no doubt. Ok, that was long, but heres the question: Was it CHF or pneumonia? The presentation I saw sounded like pulmonary edema. Lasix diuresed her well and cleared the right the side, but the LEFT side still had full-on fluid sounds. 12-Lead revealed no ACS, no LVH nor axis deviation, she has no cardiac history other than HTN and she takes no diuertic nor rate control medication. You would think, if a person were in pulmonary edema, there would be a problem that led to it. For example, ventricular failure, rate for filling time, an infarct, a hx of, something. This woman had no history and overnight she flashes to full up. She sleeps laying down, one or two pillows, and its not because of diff breathing, its because of pain in her neck. AFTER the lasix, it sounded wet, yet I had a unilateral rales, still without wheezing. There was nothing to indicate a reason for pulmonary edema, and, while the lasix helped her, it certainly did not fix the problem (transport time of about 20 minutes). I myself was unsure whether to go down the route of pneumonia or pulmonary edema. I chose Pulmonary Edema, and the ER nurse hinted that i was wrong for doing so. Talking to my partner who said a pulmonologist onc told him that a paramedic in the field will be unable to differentiate a pneumonia from edema due to resonance and a generally untrained ear. While early pneumonia may be localized and audible in one field, the chances are slim. Now i think thats crap, because pneumonia should sound different, but its still something I consider. So is it pneumonia or CHF? Have you ever had a patient in pulmonary edema with no predisposing factors, and that did not worsen over time but just shot up almost over night? Have you had an aspiration pneumonia (or any pneumonia) that presented like CHF? I suppose a great way to find out would have been to look at her chest xray, but since I dont have access to such things, Im just going to assume I was right in what I did. Overactive

I think what he may have been talking about is the new tool called the Boogie (check the spelling, im not sure). When an LMA is inserted you can bag quite well. LMAs are an easier to device to use than endotracheal tube (i.e. you just ram it in their mouth without a laryngoscope, lifting anything or seeing anything) and, on top of it, its really hard not to get it in right. The Boogie is a long thin flexible instrument, similar to a guide wire (ET tube "stilette") but thicker. By passing it throught the LMA (and into the trachea), remove the LMA, then just slide the tube (while visualizing or not) over the boogie into the trachea, remove boogie and bag. Now, this is technically not intubating WHILE ventilating, but that process takes about 10 seconds and its guaranteed, opposed to "difficult airways", failures, and general paramedic incompetence. Its the closest thing to "Intubate While Ventilating" i can think of, without performing a cricothyrotomy while BVMing (and you should not do this if you are able to bag). If you think about it, its oftly hard to put a large metal blade AND a plastic tube into some one's mouth while there is a large plastic mask that seals their mouth and nose attached to a rubber inflated bag as big as there head. Overactive

Unrelated to the patient, but particularly of interest your question about why Beta blockers: In my EMS system our protocols are designed towards rate control, not rhythm conversion. In our tachycardia protocol (including rapid afib) if the patient is ALREADY on beta blockers, we are to give Lopressor 5mg q 5min max 15mg (all we carry) IVP until the rate is controlled. Only if they are not already on BEta Blockers should we look towards cardizem or verapamil (sometimes we have both, sometimes just cardizem, why Im not so sure) to control the rate. Our dosages are the 10mg prefilled birsto-jets and not the 0.25mg/kg followed by 5-15mg / hr recommended by ACLS. Our system has two major level I teaching hospitals within 5 minutes of one another, and never a transport time more than 20 minutes, so the goal is to control rate, rather than convert rhythm. I, too, was taken aback by the protocol for Beta Blockers rather than Cardizem, but eh, whatcha gonna do? We obviously treat underlying causes first, but if there is a tachydisrhythmia, do as above.

When intravenous medications were first being pushed, no one cannulated anything. When heroin uesers shoot up, they dont cannulate. Of course you COULD do direct injections into a vein. But as AZCEP said, with an actual cannulation you have additional access should repeat medications be required, you can run a line to dilute and apply forward pressure, etc. I have a tough time believing that you could get a syringe needle into a vein and not blow out the other side but you cant get a 24G catheter to slide in. Granted the length of the needle might be different, but if youre choosing your site well enough, it shouldnt matter. If a patient's veins are so fragile that a soft tipped catheter causes them to blow, chances are the pressure from your pushing the medication will cause it to blow too.

A resident mentioned that there is an acute antidote for acute cocaine toxicity (being SOB, CP, N/V, elevated heart rate). I didn't quite believe them, but just because I haven't heard of something doesn't mean it doesnt exist. The only thing I could find is dynorphin, which new studies show might prevent the pleasurable, and dangerous, effects of cocaine. The study was more aimed at preventing addiction and not-so-acute effects. So...anyone heard of a legitimate treatment for acute cocaine toxicity? I know we can treat some of the symptoms or use what tools we have to maintain stability. Thats not what Im asking. Anyone who has any knowledge or potent links to an antidote (even a treatment) for a cocaine OD, it would be much appreciated.

There has been a lot of chatter in my area about advanced directives and living wills. DNR transfers / papers / bracelets are pretty standard: If in cardio-pulmonary arrest, do not resuscitate. The problem becomes when the conditions of cardio AND pulmonary arrest is not present. If they have stopped breathing, a DNR does not preclude the use of intubation to maintain ventilations, nor does it preclude intravenous access and administration of medications. To address this, at least as I know it in CT where I just came from, there are further advanced directives that are not simply DNRs. They are used to indicate food stuffs, whether a feeding tube should be placed or whether intubation or IV access should be initiated. This gets a little hairy as these papers supposedly represent the patient's wishes and should carry as much strength as a DNR. However, I have heard and seen providers disregard these forms, stating that if they are going to put in an OPA and bag, they might as well intubate as well (since this will avoid aspiration or poor patient outcomes). Other problems that arise are when families' decisions to not lay in accordance with the directives. I am under the impression that if there is an MDs (APRN, PA, whoever has authority) signature on the form, then we should obey it. However, when it comes to certain protocols, I am hesitant. I do agree that if they want a patient resuscitated with an OPA, I should be allowed to resuscitate with a tube. I guess I can get around that by NOT intubating, but by combi-tubing instead, but Id rather have some concept of what should be done and what should not. So I sometimes find myself torn between following the directives or delivering the maximum of my care. On one hand, I want to cover my ass by doing everything Im allowed. On another hand, I want to do the best for my patients as I can. On a third hand I want to respect the wishes of the patient and their families. On a final fourth, Id rather not increase the cost of healthcare by admitting a patient to be sustained with meds and respirators that does not want to be sustained at all. Ethical, Moral and Economically torn. The questions I pose to this community are these. (1) Are there these advanced directives that attempt to dictate your care in your area (2) What is the official (company, department, med control) rulings on these in the prehospital setting? (3) What are YOUR own feelings on these in your services.

I am under the assumption that if we have the capacity to allow the patient's autonomy to deny cardioversion, they are most likely not symptomatic enough to indicate cardioversion. This was one of the points I tried to stress in my reply post (about 10 ago). IF you are going to cardiovert in the prehospital setting, there better be one hell of a good reason. Otherwise, try something else; we have the options to do so. Since in THIS particular case the patient was altered and, instead of repeating all the symptoms again, "circling the drain" cardioversion is indicated and should be given. That being said, I agree with ERDoc that you can both maintain a calm environment and control a situation in an ambulance. The only difference should be the number of people you have to help (obviously in a serious case you can always have more hands in an ER where you can be limited to just yourself and maybe your partner in prehospital care). However, I do not see the use of cardioversion when indicated "against a patient's decision" as a removal of their autonomy. If they are not of a competent mind (AMS being one of the strongest indicators for compromised circulation and the need for cardioversion) it should be up to the provider to decide. I think in every post I make i say that "it depends." If the family is against it, and the patient is, and your partner and the police officer behind you, ok, maybe you dont. But in most cases the decision is not so clear and we must use our judgement. But Ill say it again, if cardioversion is indicated in the prehospital setting, the patients condition is probably such as NAME so eloquently described: so altered that they cannot decide themselves. Even if it were not as extreme as "eyes rolled back in their head" some one who has been cardioverted without sedation in the past certainly has a conditioned response to fear and pain when they hear cardioversion, and may be able to express "i dont want to be hurt" but it will come out more like "no." So, if altered, light em up. If not altered, though severely symptomatic, a judgment call is necessary. I would say to have the pads on ready to shock, but dont, since they are mentating well, and treat with other medications. not in response to cardioversion but just in general treatment plans, I am not a fan of ASKING permission when giving a therapy, especially in the acute setting. I always say what Im going to do, what it is for and what might happen, but I pitch in a way that says "im going to do this, so if you dont want me to, you better say so now cause here it comes" and its done. Personally, Id rather not give a med or perform a therapy other than saline if I dont have to. So if Im giving one, the patient needs it, so theyre going to get it. Obviously this is my own practice and highly circumstantial, but I would rather inform and give rather than wait for permission. I dont want anyone to think I go around giving patients treatments without their consent, I just get it by explaining how much they need it; selling a definite one-sided pitch, implying their is no other option. On a final note about DNRs (which i saw a ways back) there is definitely some controversy over how much a patient can or cannot allow based on predetermined decisions and a living will. in fact, Im going to start a thread of the same subject right now.

Three more things: (1) Burn yourself. Take away the burning object. You still hurt don't you? More to the point. Lift weights. When you stop lifting, you still are sore. You are sore the next day too. When muscle is fatigued or damage, the pain will continue even after the insult is removed. (2) Nitroglycerin is a relatively mild coronary vasodilator. Its primary action is venous dilation leading to a reduced venous return, reducing frank-starling forces reducing how hard the heart has to work. As more blood fills the chamber the harder and more forcefully the muscle contracts (and therefore uses more oxygen of which it is already starved). So with advanced stages of ACS, the heart muscle has already suffered the insult and reducing the venous return cannot eliminate the damage nor the pain. At early stages (NSTEMI and angina) the minor coronary dilation and major reduction in venous return spares the tissue greater insult. This is the equivalent of lifting light weights for a little soreness. Nitro acts as a spotter. (3) Coronary Steal. While the main effect of nitroglycerin (and NOT all nitrates) is to reduce venou return, it does have some effect on coronary vasodilation. This also contributes to alleviating pain from angina or NSTEMI. As venous return is reduced and coronary arteries expand, both collateral circulation and direct flow through the occluded artery are increased. So, by reducing the work load on the heart and improving coronary flow the pain is relieved. In advanced stages of ACS coronary dilation has already occurred, most likely to the max. As a vessel becomes occluded and the tissue distal to the occlusion becomes starved for oxygen chemical signals (primarily C02) induce vasodilation of the vessels supplying the tissue. Arteries can dilate, but they are limited in dilation. If a vessel is totally occluded or has been for some time, the maximum dilation can already be reached. This patient is most definitely STEMI, probably Q wave. As you give nitro to this patient you reduce venous return which helps them (yay!). However, the minor coronary dilation that occurs occurs NOT in the occluded vessel (which is dilated already as a result of hypercabnia [high c02] or hypoxia) but in coronary vessels near to it. Those vessels WERE constricted to provide increased flow to deficient tissues and are now dilated, so blood flow that could potentially go to the starved tissue is "stolen" (thus the term cardiac steal) to healthy perfused tissue. Again, not really a problem with Nitroglycerin, but is the purpose of some nitrates. Also, obviously, if there is 100% occlusion they are screwed anyway. Keeping with the lame analogy, this is like lifting more than you can, calling a spotter to help, and having him push down against you.

It always depends, right? But if they need cardioversion, they get "this is going to hurt" while the machine is going :DODODODODODODODODODO: If they hate me for it, too bad. As the placard mounted on my medic instructor reads, "this wont hurt me a bit." Alternatively, have them looking at your PARTNER while you shock, that way they'll hunt HIM down after they gets out of the ER. I haven't ever sedated, nor have seen another provider sedate, nor really even heard of fellow providers sedate prior to cardioversion in the prehopsital or ER setting. The scenarios I have heard of it being done is the non-emergency setting, like with the cardiologist after a sustained stable vtach or in an ICU. I know AHA recommends sedation prior to cardioversion, but if they are bad enough to require cardioversion prehospitally (with all the risks of embolism etc for this patient) then they get a whole lot of electricity. If they are stable enough for you to suppress their respiratory drive and wait for the effects of a benzo, you probably could try other meds first. A bit of anecdotal evidence from an ER: We had a patient who was in a sustained ventricular tachycardia, diaphoretic but pink, no ALS, slightly out of breath. As medication was going in his mental status changed from alert to a little out of it. The GCS fell to about 13. The doctor pushed us out of the way, jumped to the lifepack and discharged. Granted he was a little skittish and probably could have not pushed us out of the way en route to the paddles, but the point is if they're bad enough to need it, just give it.

Keep in mind every body that this is coming from a primary care center. They dont have a hospital backing behind them, nor the resources that we are used to hearing about. Not trying to sway one way or another, just an info bit

yet another Amio vs Lido! Get ready to be assailed! The short of it is that Amiodarone is more effective (not so proven) than lidocaine without the nasty side effect of seizures (very proven). The problem with Amio is that it is a slow infusion and requires the patient to be very stable, with worsening hypotension prior to correcting the rhythm. When it comes down to it, right now the choice is provider preference. The one clinical decision maker should be how hypotensive they are prior to choosing. The more stable, the more you should lean to amiodarone, the less stable, the more you should lean towards lidocaine, until they arrest, then it doesnt matter again. To be honest though, how much longer does it take to hang a bag of saline and inject amio into the bag than it does to hang a bag of saline and inject lidocaine IV? Its just about the same time-wise. Its just that administration of Amio guarentees hospital admission (since the half-life is so long), where as lidocaine runs the risk of seizure. until more research is done ACLS says take your pick! P.S. Amio is way more expensive than lido as a drug, and the hopsital admission can go upwards of 300,000 dollars (society)

I am currently volunteering at a free clinic in San Francisco and came across an interesting case. A 44yo African American Male with no Hx came in to examine lab values and have a 12-lead following a routine checkup. On the previous checkup a physician noticed bradycardia with irregular beats. He began to be seen at this clinic after a car vs bicycle MVA for which he was seen and released at an ED with follow up care here. Today, on his twelve lead, I (being the only ACLS certified provider besides our medical director who is "certified") noticed there was ST segment elevation in V3-V6, 3-4 mm in each lead, with reciprocal changes in II and III, no Qs (sorry, we dont have a scanner here to post the 12lead). His vitals at rest were 58 regular, 128/85, 12 clear, PEARL (assessment is limited since im technically supposed to be operating only as a medical assisstant and NOT as a paramedic). There looks like what COULD be bunny ears in III in one of the 3 serial 12 leads i did, though there is no indication of a BBB in V1 (no wide QRS, no sR / QR waves, etc). The p wave is biphasic in V1, and all QRSs are narrow. He is completely asymptomatic. My conclusion was that it must be a preexisting bundle branch, probably physicologic from previous conditions. However, if I were a paramedic and was called for ANY complaint, I feel as though i would work this guy up as a cardiac patient (ASA definitely, Nitro x 1 BP permiting probably, morphine probably not). Given that he was coming in for a cardiac checkup (hardly anyone gets a 12lead) and it was abnormal (though the 12 year old machine read "normal sinus rhythm) I thought he should have been sent to the hospital immediately. The MD disagreed, and thought that he could go for a cardiac consult. So I understand why she made the decision she did. It may or may not be ACS and since hes asymptomatic its probably not acute. However, I was just looking for some input as to what people would have done or what their thoughts are for this case. I mean, she didnt even order additional 12-leads (besides the three I did, back to back by about 2 minutes).

Im not really sure where the complexity comes in. The patient is is awake, alert, and in respiratory distress = high flow 02 (fixing hypoxemia) The patient is in a narrow complex irregular tachycardia over 200 with a history of Afib. The patient is in a severely symptomatic, most-would-consider unstable narrow complex tachycardia with respiratory (and circulatory) compromise (not the depressed BP and cyanosis). High flow 02 + cardioversion is straight out of ACLS. How can you as a provider discern whether or not this is respiratory or cardiac. Obviously no one wishes to be a see A do B medic, but Im having a tough time discerning other possible differentials. (1) Worsening dyspnea over two days (like when some one goes into rapid afib and begins to get weaker and less able to support their own respirations) (2) Hx of Afib with a narrow complex irregular heart rate (3) Monstrous pedal edema indicative of insufficient filling time (4) Cyanosis that shows this person is circling the drain. COULD these signs and symptoms be part of a CHF / COPD? Of course, they add to one another. But is it more likely that an increased heart rate to an already old, feeble heart is adding to edema both peripherally and centrally? Filling time is lessened significantly to a failed heart with probable small ejection fraction. Again a cardiac problem causing a respiratory problem. Adressing the patient's CHF but ignoring the incredibly fast rate (keep in mind that physiologic responses to hypoxia put a heart rate ~220-age, and should be regular) will not aid their situation. But by looking at this patient, their history, and their compromised state, how could you deny this person cardioversion? What if their distress IS cardiac and you give the albuterol. Their lungs open up and their heart explodes, leaving them in a Vtach arrythmia that you caused. What if their condition IS respiratory and you cardiovert them while oxygenating and getting your cpap ready? Either they return to a rapid heart rate in a compensatory fashion to their hypoxia and you then go down secondary routes of fixing it (cpap, intubation). I know that A comes before C, but not when C looks like the problem. Clinical decisions are always made based on multiple factors (including distance to hospital) but the risk of circulatory and respiratory failure by not cardioverting far outweigh the risk of possible emboli formation by cardioverting. If some one is THAT symptomatic with a heart rate that fast, why would some one deny cardioversion? The concept of preoxygenating a heart to have it responsive to cardioversion / defibrillation is valid only for a hypoxic heart. If this person has a pulse, and is perfusing distally, we can assume, at this time, the heart is perfused well enough to respond to electricity. The condition they are in however will not allow them to be there for long. Allowing them to maintain a heart rate that has such a high metabolic demand while suffering from respiratory distress can only lead to deterioration. To compound the potential cardiac dysrhythmia with Beta agonists seems folly to me. In a patient with significant, multiple, compounding history one cannot possibly hope to have such an eagle eye as to say, "definitely respiratory." I must say in a clinch decision making time, Occam's razor wins: the simplest answer is the right one. It seems to me that most people would think cardiac here, especially reading the posts. Only after the fact, once we've been "zinged" by the "right answer" do people argue for the respiratory first. Simply put: forget protocol HR > 150. Cause or effect, Presentation and history, benefit vs risk. You cant know whether the egg or the chicken came first (though probably the egg since most ancient creatures laid eggs, such as fish, before the chicken).

Dendrites carry afferent signals to teh soma most often, axons carry efferent signals from the soma to targets. UNless the vagus nerve has some reverse conduction, action potentials targeting efferents (the SA and AV node primarily in terms of our discussion) are carried along AXONS not DENDRITES. Just an FYI aside. OveractiveBrain

Pt is a 21 yo african american female who was out at a company party at a sports center (an oversized gym) playing indoor soccer with coworkers. While playing, for about 15 minutes, she felt faint, developed chest pain (described as sharp stabbing pain in the center of her chest, radiating to the back), heart rate remained tachycardiac at 120 and regular, per the trainer, and EMS was called. When we arrived she was resting comfortably in a chair, without CP, without SOB, without N/V without dizziness. Her heart rate was in the 120s, sinus tach on the monitor, BP 130/80, PEARL, lung sounds clear though she had a non-productive cough that started since the event, 12-lead non-diagnostic with a notched p-wave in V1 indicative or right sided atrial enlargement, PMS x4, GCS: 15, CAOx4, without JVD without tracheal deviation and without any signs or event of trauma, sp02 100% on room air, blood sugar: 110. She was a fit looking young woman, though she did report that she does not exercise often, despite her fit appearance. She has no history, no allergies, and takes birth control, had her last period 2 weeks ago, sees her doctor regularly, and works for a local area hospital as a registration assistant. We treated her as though she were an ACS patient, establishing an IV, keeping her on the monitor, 12-leads, 02, and ASA. Other medications were withheld due to the absence of pain, ST-segment changes, or Q waves. there are a number of potential differentials here. (1)She possibly had an Acute Coronary Event. (2)She has had some sort of AAA or aortic dissection (pain radiating from chest to back, higher risk from HTN and african-american) though she was nonorthostatic and did not have pulses paradoxsis. (3) Athletic Asthma induced respiratory acidosis which the heart responded by increasing flow to accommodate (the cough). I know that ACS can present in a variety of ways. This seems to be a case of a 21 year old exertional angina without any family or social history that would predispose her to the condition (no family history of PVD, cardiomyopathies or vascular events; no history of her own at all, though she has regular doctors visits). I was worried about a potential embolus from her birth control, though no st-segment changes were noted and she was pain free upon resting. I did not get a chance to follow up with this patient, as the hospital we went to was over an hour away from my house (another medic internship call). This sounds an oftly alot like an exertional angina, despite the lack of any predisposing factors. At the very end of the all she said that she felt a throat pain before, upon exertion. this time she felt both the throat and the chest pain. This leads me to believe the event was coronary even more (repeated exertional angina). I post this only because this is a young woman who should definitely NOT be having a coronary event, though seems to be. Did we miss something in our assessment? Have i not thought of a potential differential diagnosis that adequately addresses all our findings? Treating her as an ACS patient I feel is absolutely the right thing to do, given our findings, but is there a piece of information we missed or some disease process we did not think about?

The scenario is quite simple. An officer was pursuing a perp down a dark side of a building at full sprint, jumped 3 stairs, landed in gravel and rolled. He ended about 10 yards from the stairs. We found him propped up on his arm, sitting, his left leg rotated inward with Left leg pain. PMS is present in all extremities, no neck head or back pain. To keep the report simple, assume this is an isolated injury and that the patient is completely stable. The Volley crew on scene reported that he had proximal femoral pain. At this point I was thinking dislocation (he weighed about 100kg and had on about 10kilos of gear and armor) and agreed with the volley's decision to board him, thus immobilizing the joint above and below. The Medic preceptor decided that was unnecessary and used a scoop to transfer him to the stretcher without immobilization. As the assessment continued it was determined that the pain was not proximal, but mid-shaft. Rotation inward and mid shaft pain (without crepitus) and grossly swollen is indicative of femoral fracture. Now, PHTLS i believe would have us traction-splint the femur and secure to a long board. Perhaps the long board is unnecessary. If it were a dislocation, I believe the long board would be indicated. In the end, everything seemed to work out - the patient was seated in a position of comfort, received morphine for pain management, and he had no complaints. He received an activated trauma by triage which was downgraded by the trauma physician. I had no followup with this patient, though he seemed to be doing well (besides his leg being swollen to three times the size of his other). The question i leave open for you is: what would your trauma protocols say to do? how would you immobilize this patient? is it ok to NOT immobilize an isolated injury if the patient is able to tolerate the pain as is? This is important for I have heard similar stories (a geriatric hip dislocation standing from the toilet, slunking back to a seated position) coming under reprimand for a failure to secure the patient to a long board. However, once the trauma docs saw the patient they denied the request for a c-collar or board (coming from the nurses, who assumed it was indeed a full trauma). So a different call (though frighteningly similar) received reprimand from no-boarding and another it seemed to be the right conclusion. I must admit I am confused, and am open to response.

As some of you (Fiznat) might have guessed, my preceptor that told me of this is Shane. After being unable to find mention of it i doubted it was true. I should have had faith! Though, I must admit, hearing that there might be a contraindication to 02 (other than what i hope is that rare condition in the intensive care setting) sounded a little fishy. Im glad we managed to figure out what the deal was.

As some of you (Fiznat) might have guessed, my preceptor that told me of this is Shane. After being unable to find mention of it i doubted it was true. I should have had faith! Though, I must admit, hearing that there might be a contraindication to 02 (other than what i hope is that rare condition in the intensive care setting) sounded a little fishy. Im glad we managed to figure out what the deal was. Im definitely going to take a look at the web sources you put up, Shane, im very interested in the mechanism in particular. -Overactive

A medic preceptor today told me there is one contraindication for oxygen. It was a quite often used street drug that is no longer in fashion. It sounded something like periquot (like aliqout, but peri) though we couldnt find anything about it on the internet. I was wondering if anyone had any legitimate reasonings behind this so call-ed contraindication to high flow 02. No, Hypoxic drive is still not a contraindication for high flow 02 in teh acute setting. This is supposedly the ONLY contradindication for high flow 02 and that is an overdose on this medication. Wondering what it is and what the mecahnism could possibly be OveractiveBrain

The suggestion about volume size might explain it. THere is more pressure on a column of water 1000mL tall (however tall a 1000mL bag is) over a 500mL bag. The frustrating thing is why wouldnt the fluid just flow into the vein. Since veins are capacitors, youd thing any excess pressure would be distributed into teh vein, not up the bag applying its own pressure. However, that was not something I had thought about. The real trouble Im having with that explanation is purelu that if you have a 1000 bag running for fluids and attach a 250 bag with drug in it, you can run both, either piggy-backed or attached at a 3-way (a 3-way that allows flow from all directions) which I myself have done. This was just an irritating problem I havent seen, and i appreciate everyone's input -OveractiveBrain