OVeractiveBrain

Hello all: I have recently run into a complicated problem in Labor and Delivery, which I am sure will come up again in my career in medicine. Thes setup: 20G in the left forearm with a dual port hub (one for the fluid line one for instant access to medications). The fluid line then flows back to a three way device. From there, two lines are connected, in one, a 1000cc NS bag, which is turned off. The other line is to a 500cc NS bag we were to bolus into a patient. The problem: When we opened the line wide open, nothing ran. At first, the nurse failed to remove the plastic lock that had pinched off the line. Fixed that. Still wont run. What we checked: THe line flushed well, a 10cc bolus injected through the medication port flushed well, no disruptions, skin raises, etc. Basically, the line is patent. All the blocks are wide open. That is, the roller-wheel was wide open, all blocks were open, no kinks, or pinches. The infusion bag was closed to allow the bolus to flow in. OPening the infusion bag caused the fluid to back up in the bolus bag. Changed the heights of the infusion and the bolus bag to level, above and below one another. When we put positive pressure on teh bag (the bolus bag), it flowed well, dripping at what I expected a wide open line to do. Opening the infusion bag at this point caused fluid to flow back into the infusion chamber. What im thinking: Either we misused the three-way, and only one of the lines should have been running, or there was some serious back pressure from the veins. Granted she was a pregnant woman in contractions, but her pressure was 118/52 at a HR of 72. In addition, contracting muscles serve only to push fluid towards the heart, not back against the flow. No, there was no BP cuff on that arm, nor was there ever any blood backing up into the line. I ask this question because i want to know other solutions. We ended using a pressure bag (like the ones hospitals use for heparin infusions in MI transports) around trhe bolus in order to get the fluid to flow. I dont have these, nor do i know of any in any service in my area. Should the occasion arise in teh field i would like to have a better solution other than "just squeeze the bag" as I might have other things to do at the same time. - OVeractiveBrain

TheOtherPhil hit it right on the head [bONK] Dale Dubin's Book is simple, with excellent pictographic memory aids. I suggest starting there. ITs strict wrote memorization with little explanation. You will be able to say "look at that, that is X." Nuances and pathophysiology is lost in Dubin's book, but is the material is covered well beyond the need-be of a paramedic. Garcia's book, and accompanying website, is excellent. There, the nuances (such as all criteria for differentiating RBBB or what subtle changes in P-wave morphology means) and detail are exquisite. Rapid Interpretation of EKGs seems to be favored by paramedic instructors, but I did not like the material itself. I found most of my class lost in the information, and only those who had read Dubin's book or had done 12-leads previously able to comprehend and keep up. Its good for Rate Rhythm Quality of a 3-lead (probably why its chosen for Paramedic CLasses) but its instruction on the 12-lead is subpar. -OveractiveBrain

Get out while you still can -OveractiveBrain

Correct me if I'm wrong here (perhaps we are both right...), but I thought Bicarb was used in TCA OD in order to retard + prevent metabolism of the injested drug? This is the reason why Bicarb should only be given to TCA OD if the injestion was recent. Ingested TCA that has already been metabolised wont be affected by Bicarb, if I am remembering correctly?

Opiate receptors in the brain respond to naturally occuring opiods (opiates) and synthetic opiods (the difference between opiod and opiate is often overlooked and is commonly inconsequential). There are three types of opiod receptors in the brain, that produce different effects in different ways. Mu-Receptors are located in the Spinal Trigeminal Nucleus, Caudate and Geniculate Nuclei, the Thalamus and The spinal cord. These are responsible for the primary effects we see with the administration of opiods - analgesia, euphoria, respiratory depression, nausea, GI inhibition and miosis (pupillary constriction). Kappa-Receptors produce modest forms of analgesia dysphoria, miosis and repiratory depression when activated on their own and are found in the basal ganglia, nucleus accumbens, hypothalamus, spinal cord and periphery. These can be seen as "adjunct receptors" to the Mu Delta Receptors are poorly understood and are located in the limbic system Morphine strongly binds to Mu receptors and partially to kappa receptors, but not to delta receptors. Demerol strongly binds to Mu receptors but NOT kappa receptors. Fentanyl and Methadone are in the same class of binding affinity for Mu receptors as Demerol. Talwin is a mixed agonist / antagonist that binds only to Kappa receptors, and not to Mu receptors. These differences are largely in part due to their gross differences in chemical structure. That being said, morphine is the most likely of the three to demonstrate side effects, especially miosis and is nearest to most naturally produced opiates in the body. Heroin is a simple chemical transformation of morphine. This is why we see miosis most commonly with morphine administration. All this being noted, Demerol WILL produce pupillary constriction, given a sufficient dose. Its effects on membrane dryness or GI tract mobility may be more potent than its effects on the pupils, but it will cause pupillary constriction. The key thing to remember is that the administration of an opiod doesnt magically effect the brain, nor are all opiods equal in chemical structure, solubility or explicit binding affinity. This is why we will more likely see miosis with fentanyl or methadone than with demerol. But liek demerol, it takes a fairly sufficient dosage of methadone to cause miosis and respiratory depression. Keep in mind demerol is only 1/50th as potent an analgesic as morphine. Talwin is an agonist/antagonist. It binds and activates opiod receptors, but then prevents them from being reactivated. Given its antagonist properties, we should not see signs of opiod overdose with talwin, unless an extremely high dosage is used. IN SHORT: The differences in chemical structure contribute to alterations in solubility, binding affinty and receptor options for binding. This in turn results in different presentations between opiods. Some induce pupillary constriction more than GI immobility, while others produce mucous drying over nausea. The point is, that given a sufficient amount of any opiod both miosis and respiratory depression (the things we medics really look at for in diagnosing an opiod overdose) can be produced. It helps to have a lab and urine analysis handy to make real hard-cased diagnoses. -OveractiveBrain

People find it easier to be repetitive, and the mL volume comes up a bit off if you draw up 125mg. Thusly ~60gtts /min in the set up i gave it pretty good. If youre concerned at all, and the first fraction is a little more than 1/2, drop it to 52gtts/ min which is really not going to matter, since your gtts/min are never precise preceise, in the area of 50-60gtts/min is appropriate. If youhad a pump you could do it directly irrelevant of the concentration. However, it is difficult to choose arbitrary (such as 125 over 150) dosage amounts as the packaging comes preset mLs. Its easier for peopel to understand how to draw up the 150 (since they JUST gave it) and a drop count thats off by 10% really isnt that bad, as youre eyeballign the drip rate anyway. -Overactive

Always get a twelve lead, and make it count. The 12 lead is invaluable and takes only about 30 seconds - a minute to get. YOur partner can be setting them up while you do everything else. My viewpoint is that if you are an ALS crew, and youre going to the hospital with ALS established, your patient warrants a 12lead. That would be any Diff Breather, any Fatigure, any AMS, CP, or whatever else have you. Performing an appropriate 12 lead would have tipped you off to the MI. Ive taken 12 leads of guys in Vtach at 220-240 and had no difficulty reading the 12-lead, so rate should not be a deterrent. Usually, it is electrode placement, moving ambulance or electrcal disturbance ("No Cell Phones Allowed"). The 12-lead would have also fixed the SVT vs Physiologic Tachycardia. If it were a reentrant rhythm, P waves would be absent, regardless of the rate. If you were going to go after rate, it should have been a bit sooner, thouh I can see waiting until he goes over 150 and shows some signs of instability before trying to treat it. WIthout any slowing of the rhythm with 6mg, I would be concerned with, and hesitant to give any more. The fact that he was having problems for the past several nights does seem to indicate something along teh lines of CHF. However, for him to code on you right then and there is a bit rare for a 60 yo CHFer without any real difficulty breathing. Pneumonia was where I was going as well, and PE seems pretty attractive given the painful inspiration. Then again, an MI has that same sign. Im pretty sure he had a silent MI that CAUSED the Pulmonary Edema, not the edema that caused the MI or the code. Whats worse is the guy had a language barrier, so getting a good history is rough as it is. You have to go with more of the signs and symptoms than the story. Bottom line, DO A 12 LEAD EVERY PATIENT EVERY TIME -OveractiveBrain

The gentleman was placed on a crapload of LR. His potassium level was probably through the roof. Potassium controls the inward hyperpolarizing current in cardiac as well as skeletal muscle. This means, at high levels of K, the inward hyperpolarizing current dominates the open potassium channels. This manifests itself in profound bradycardia, increased irritability (especially after 5 hrs of administration and an already apparent MI). Hyper K can also be noticed by a flat P wave and Heightened T waves. If it were not HyperK the fact that he had potassium administered at all with crushing chest pain was a mistake. By the time you found him he was probably so badly infarcted it as too late. Remember that the heart will respond to infarct first by increasing heart rate to compensate for the lack of 02, then wear itself out faster. If you caught this guy in the latest stages of an evolving MI, the tissue was so badly necrossed that no matter how much electricity you put across him, there would not be enough live tissue to contract. Atropine and TCP are the recommended therapies, but if the prison put a CP pain on ringers and told to wait it out, they sentenced him to death right then and there. Even with an increaed fluid challenge and all the medications you have, again, the heart was so badly damaged that it was too late. IN response to above comment about atropine use: If the patient is bradycardia as a RESULT of an MI, hes dead. Hes in the final stages of the MI and you can watch him die. If the MI is the result of bradycardia, you an save that person with atropine and TCP. Without an excellent history, the only way to tell the two apart is to give them the atropine. Should it make the MI worse, then you havent lost much, PCI or fibrinolytics are still indicated, and hes still circling the drain (just as he was before). If you make teh MI better, you save him. Most protocols are pretty straight forward when it comes to hypotensive bradycardia = Atropine and TCP, unless a high degree block is noted, in which case TCP is the best choice. Note that Atropine can cause rapid atrial rate, while the AV conduction system may overload and fail to conduct (or conduct less frequently than at the atrially bradycardic pacer). Other electrolyte imbalances or sugar can be ruled out. His sugar was in the 100s, hypocalcemia results in often spastic muscle contractions prior to electrical conduction problems. Hyper K can be seen on the ECG as above. Hyponatremia should not be expected unless their was profound weight loss, diarhea or vomitting. If he were on any meds that slowed the heart, you probably should have known about them and treated them accordingly (Glucagon for B-blocker, Calcium Gluconate / Chloride for Ca++ channel blockers) That being said, pad placement or user error is most often the problem when it comes to electricity and monitors. However, given this patient, I would be confident in saying that you more than likely did everything right, this guy was a gonner before you even got there. -OveractiveBrain

Amiodarone should be used when the focus of disrythmia cannot be established, when there is sufficient time (10 minute push) and when there is not significant hypotension. Amiodarone is given for any tachycardia, narrow or wide and given 150mg IVP over 10 minutes backed up by an infusion. Some protocols say 1.0mg/min for 6hrs then 0.5mg/min for 12, others just say 0.5mg/min. A simple way of making it is taking your 150mg dose (which is approximately 125mg) in 250mL in a 60 gtts set running at ~60gtts/min Math: 250cc x 0.5mg x 60gtts = 60gtts/min (250/125 = 2, 2 * 0.5 = 1 both fractions multiply out to 1) 125mg 1.0min cc Amiodarone is given in Vfib/Pulseless Vtach arrest by administering 300mg IVP. Amiodarone DOES NOT HAVE the side effect of lidocaine (seizures) and is safer to use in the acute setting. Though it may cause more profound hypotension than lido, and therefore should be used with caution in patients with less than 100 systolic (i know hard numbers are often misleading), its incidence of adverse side effects is less. Much talk of amiodarone's problematic toxicity comes from its chronic use and the toxicity comes from its preparation, not the drug itself (though may). Therefore, if the patient is stable enough to sit around for 10 minutes (i.e. is throwing up runs of PVCs opposed to a full on VTach at 220, and yes, i know to assess my patient fully) give them Amio. Otherwise, give them lido. It really comes down to your own preference and the stability of the patient. Amio is a great drug to make the problem go away. If they are stable and mildly symptomatic (palpitations, mild dyspnea, sweats, no AMS, no N/V, no CP) then Amio is the way to go. If they are starting to crap out on you, but cardioversion is not indicated (high hr, dropping BP, mentation still established, again still no CP) then go for Lido. When the patient finally starts to die (i.e. AMS, CP, N/V, Syncope, Pulselessness) light that sucker up. Recommended 200J biphasic or 360J monophasic Ventricular, 100J monophasic atrial (for your PSVTs which amio can also help with). -Overactive

Ill wrong forum you Fizzy. Baaaaaaaaah! Didnt realize there was an ALS forum (thus the ranking Newbie). Good to hear that were right and that THE INSTRUCTOR, who is supposedly imparting his vast wisdom upon us is wrong. Hope he doesnt read these forums.

I would suggest, when posting in an attempt to justify your credibility and some how 'reverse the coin' of the old addage that nursing homes often provide insufficient care, that you at least attempt to sound intellectual. The series of incomplete sentences and elipses can be quite painful to read, forcing us to deduce that it was EMS personnel that neglected to bring in the Oxygen for a diff breather. On the other hand, since your story is incoherent as it is (as some one pointed out TEN (10) L/min 02 NC is far above the range of use for a NC which is 1-6L/min, magically improving saturation numbers) perhaps the ems personnel were incorrectly informed of the patient's needs. Telling the dispatcher "shes usualy on oxygen, she has her own tank, which ive turned up" can be relayed to the crew as "Oxygen delivery already established." Granted, it is good practice to come in more prepared than not, but I would not be so quick to jump on EMS as you are, especially when your rant, and seemingly your care, is full of holes. -Overactive

In a recent debate over whether an ST elevation was considered significant or not a nit-picky argument over the definitions of some words came out. The scenario: There is marked ST elevation in the precordial leads V1-V3. In a lecture and in most course manuals, v1 and v2 are rigidly defined as "SEPTAL" while V3 and V4 are defined as "ANTERIOR." In order to be a significant finding and suspect of Myocardial Infarction, there must be "st elevation in two or more anatomically contiguous leads." The argument: My argument is that despite the convenient summary chart in ACLS which defines V1/V2 as septal and V3/V4 as anterior, the electrode placement is such that there is a continuous picture of the heart, beginning from the right side of the septal wall in V1 down to a lateral/inferior view of the left ventricle in V6. That being said, V2 and V3 should be considered anatomically contiguous. In fact, the muscles of the heart have no true boundaries "Septal" "Anterior" or "Inferior", those are arbitrary definitions of general space used by clinicians to describe and anticipate the location of arterial blockage. IN this particular scenario, I suggested that an occlusion of the diagonal branch of the Left Anterior Descending coronary artery could lead to an infarction of mainly the septal wall but also part of the anterior wall. Thusly, from a technical standpoint, v1-v3 are anatomically contiguous and are all technically significant, and would lead a clinician to suspect a blockage more proximal to the aorta given the expanse of the area infarcted. The counter argument, which the instructor reinforced (and I believe incorrectly) was that since the chart defines V1/V2 as contiguous, V3/V4 as contiguous but NOT V2/V3, and therefore there is some aberrant recording in lead V3 and only a septal infarction is suspected. While this argument would not change prehospital care, it might lead to a misdiagnosing of the anatomy, and why I have taken such pains to determine a true answer. It is possible that the septal wall be fed by the right coronary artery. If we assume that the ST elevation is insignificant, and that it is only a septal wall MI, it is possible to incorrectly assume a right coronary artery occlusion, whereas we would be more likely to be correct assuming a left coronary artery blockage from V1-V3 significance. The question I pose is, and from strictly a technical definition standpoint: are precordial leads contiguous with one another, V1 --> V6 as we go across the chest. Thanks to all those who reply. -Overactive