chbare

Many paint products contain a chemical known as toluene. Exposure could cause the said signs and symptoms. We should look at removing clothing and consider irrigation of the skin and eyes. In addition, high flow oxygen along with vascular access and continuous monitoring is indicated. Take care, chbare.

Possibility of pregnancy? Possible PE? Allergies, Past Hx, Vital signs? JVD? What was she doing prior to this incident (HPI?) Take care, chbare.

Hope this helps: Normal RA pressure is around 8 or less. No surprise this is roughly equal to CVP. Once we go into the ventricle, the dynamics change, and we have both systolic and diastolic influences: Normal RV systolic = 15-30, while RV diastolic = 8 or less. No surprise that this is consistent with RA pressure. In fact RV end diastolic and RA pressure should be nearly equal since this is where we get ventricular filling from. Then, the RV contracts, the tricuspid closes, and hopefully blood is ejected through the pulmonary valve. Take care, chbare.

We use a vac mattress on long transports and flights over here. What an incredible tool IMHO. Take care, chbare.

The three questions below would most likely belong in the neurological section of the quiz. Let me know if this is the type of question that you had in mind. 1) You respond to a small ER to transfer a 50-year-old male with a closed head injury to a tertiary care center. The patient is intubated, sedated, paralyzed, and on a mechanical ventilator. His vital signs are: 150/100 P-52 regular SPo2-100%. The ER Nurse reports the following radiographic findings as noted by CT scan: “The patient has a large lense shaped hematoma under the calvarium of the left temple. The Falx Cerbri is shifted to the right and compression of the ventricles is also noted.” Which of the following answers is most correct? A: You should suspect a ruptured aneurism and massive sub-arachnoid hematoma. B: You should suspect an epidural hematoma with rupture of the middle meningeal artery. C: You should suspect an epidural hematoma with rupture of the Cerbri artery. D: You should suspect diffuse axonal insult (DAI) injury based on the CT findings. 2) You respond to the scene of a drive by shooting. Police report a 19-year-old male was hit in the head by a single gunshot round. They believe the patient was hit by a 40 caliber full metal jacket round fired from a Glock 22 handgun at a range of approximately 10 yards. First responder crews have initiated care and have placed an LMA (laryngeal mask airway). The patient is unresponsive and apneic. The first responder crews have been ventilating the patient at a rate of 28 times a minute. You verify proper LMA placement with objective and subjective findings. Upon initiating waveform capnography, you note an end tidal Co2 of 17. Which of the following answers is most correct? A: You suspect the patient was hit by a bullet traveling less than 2,500 feet per second and you suspect metabolic acidosis causing the end tidal CO2 findings. B: You suspect the patient was hit by a bullet traveling approximately 3000 feet per second and you suspect the poor seal of the LMA is causing gastric inflation. C: You suspect the bullet hit the breathing center of the brain causing underlying metabolic and respiratory complications. D: You suspect the patient was hit by a bullet traveling less than 2,800 feet per minute and you suspect possible impaired cerebral perfusion relating to vasoconstriction. 3) You are called to transport an elderly patient who is status post closed head injury from the hospital back to an assisted care facility. The patient has past history of congestive heart failure CHF and is currently receiving furosemide. Upon examination the patient’s nurse tells you; “in spite of fluid restriction the patient had 4 liters of urine output last night.” What answer is most correct? A: You suspect diabetes insipidus. B: You suspect syndrome of inappropriate anti-diuretic hormone. C: you suspect Addison’s disease. D: You suspect an over dose of furosemide. Take care, chbare.

Welcome mate! From Oz eh? We just lost a medic from Oz. Had been in Afghanistan for two years and had many connections. However, he wants to focus on his EMS career and push toward obtaining intensive/critical care paramedic credentials? As I understand, he is currently registered as an advanced care paramedic? Forgive my ignorance. Anyway, welcome and I also look foreword to new blood bringing additional thoughts and discussion into the city. Take care, chbare.

Let me see if I understand correctly? You are looking for questions that are better suited for BLS providers? The questions I had in mind dive into some fairly complex subjects. Nothing out of left field; however, I definitely have a taste for going beyond, "we give NTG for chest pain" level of understanding. Obviously, the answers to these questions will most likely not be found in an EMT-B textbook. I do not want to present questions that would be considered inappropriate or incompatible with your ideas. Take care, chbare.

Diclofenac and Tramadol administered via parenteral routes are drugs of the year over here. I agree that Toradol has great properties; however, the side effect and caution profile for this med is substantial. Like most NSAID's GI complications are going to be a concern and the effects on the renal system must also be considered. I would not be a big advocate of using Pontocaine in the field. The safety profile does not justify using it IMHO. Especially due to the fact that our ability to treat and recognize ophthalmic conditions is quite limited. Take care, chbare.

Additional information. These links are to some of the tentative educational drafts and standards. http://www.nemses.org/draftstandards.html http://www.nemses.org/draft_standards/detail.cfm Take care, chbare.

I have a few ideas for great questions. They are based more on the physiological changes of disease and intervention however. Take care, chbare.

Really interesting that in one paragraph people take offense to the notion that people accept deaths, while in the next they point out that 28 dead is not bad considering the total number of flights. WTF :? Take care, chbare.

Congrats! Great news! Take care, chbare.

http://www.telegraph.co.uk/news/newstopics...-dying-man.html :shock: Take care, chbare.

Organophosphates are a large and rather diverse group of substances that are chemically related; however, organophosphate poisoning refers to the cholinergic syndrome associated with exposure to specific organophosphate agents. http://emedicine.medscape.com/article/167726-overview Take care, chbare.

I agree with Mediccjh. Get your patient and get out. First on scene, sucks to be you. In addition, there will always be some incident that will throw you for a loop. Prior to heading over to the sand box, I was working a rotor shift and had one of those calls of a lifetime. We received a call for a helicopter crash of all things. Honestly, I initially thought we were going on another training mission, as this was at a military range, and we had been doing "training missions" to help prepare soldiers training for OCONUS deployments to work around an aircraft. However, range control indicated this was in fact an actual call. When we got closer to the scene, another helicopter was flying a high recon pattern around a rugged canyon and we received report from the pilot. Immediately, the gravity of the situation sank in. We had to land over 100 meters from the crash site, then scramble up the canyon to reach the site. Amazingly, both pilots involved survived, the scene was safe, and we had the foresight to call for another helicopter en-rout to the scene. I took one patient, and my partner took another. We performed primary surveys, identified obvious injuries, gathered history, placed IV's, and gave pain medications. When the other helicopter arrived, we had the crew package and take the patient who we thought had the most serious injuries, then we packaged and flew the other patient. Never had an experience like that. Just like you, I felt like I had my ass handed to me. However, it sounds like you did a good job. Take care, chbare.

Good question when you look at this from a BLS standpoint. Provided the patients airway is patent, their not in obvious respiratory distress, and adequately ventilating and oxygenating, I would let them be. Even with the tachypnea, I would simply support and watch for any problems. Kussmauls respirations are typically rapid and deep allowing for gas exchange versus other patterns that are so shallow the patient is essentially exchanging dead space. Obviously, shallow rapid respirations (low minute volume), airway compromise, or an exhausted patient may require more aggressive interventions. This is going to be a judgment call; however, I would steer away from taking over a DKA patients respirations. I think Doc was looking at this from the point of having to intubate a DKA patient due to some type of airway compromise. In that case, we will need to be very careful about how we manage these patients. The RT's are going to play a critical role in managing the intubated DKA patient. As they can set the ventilator up to support and assist these patients with their breathing pattern. Because we are talking about a compensatory respiratory pattern, we must understand that "wiping out" the said pattern can be met with disastrous consequences. I am sure more than a few well meaning providers have tubed a DKA patient and thought they were doing the right thing when they corrected the patient's end tidal Co2 to a "normal' number, while in reality, they destroyed the patients ability to effectively compensate for the metabolic acidosis. Take care, chbare.

No worries, I suspect things are still in their infancy in any event. I am not sure what to make of it; however, it does not appear that any significant improvements in education will be mandated, other than transition training. The whole I/99's transitioning into the paramedic role without any clinical requirements is rather...interesting. Take care, chbare.

Strong work. Good call on the Mobitz I. This is not an unexpected conduction disturbance considering the location of the infarct. The said treatment is exactly what I did. Sometimes "benign neglect" or "babysitting" is the prudent way. The patient is "stable" at the moment, so why mess with things? Monitor and anticipate acute changes, absolutely; however, aggressive interventions may not be in the patient's best interest. Sometimes the enemy of good is better. That was one of the big points of my scenario. Always step back and really think about your interventions. Is the most aggressive intervention always the prudent route to take? This is why I emphasized the novice provider. It is easy to want to push and infuse all those cool drugs and interventions you have swimming around in your head from school; however, understanding the time and place to use these interventions is the true art and science behind our practice. Additionally, I wanted people to think about coronary anatomy and cardiac physiology and review the basics of fibrinolytics. I hope people liked this scenario. Again, I took a chance moving away from the typical chbare zebra scenario. Hopefully it paid off. On a side note; the exact scenario, patient demographics, and perhaps gender may have been changed a bit. I do not want AK calling BS on me because his boys most likely took care of the patient in question before I arrived. Take care, chbare.

I understand there will be a push for the implementation of these new changes in the next year or so. Just wanted to see people's thoughts on this change. In addition, I would like to see if anybody has up to date information regarding requirements, courses, and testing. From what I understand, the process is still in it's infancy. This actually does effect me as I am currently working under a contract that requires me to maintain current NREMT-I credentials. This will eventually transition into A-EMT as I understand. So, I may need to ensure I maintain NREMT credentials. Link to a fairly current article: http://www.the-iaa.org/aux/2008/Brown%20Sc...%20Practice.pdf Take care, chbare.

I think with the big push to identify RVI in patients who experience inferior wall MI, many people do not really understand what is going on and simply think that preload reducing agents are contraindicated with all inferior wall MI patients. This is in fact not the case at all, and one of the points of my scenario. We need to treat every patient differently and use our knowledge of anatomy, physiology, and pharmacology to guide our treatment. RVI is only present around 30% of the time with inferior wall MI. However, can people still have problems with blood pressure with inferior wall MI without RVI? Yes. Can people with anterior/lateral changes on the XII lead experience a right ventricular infarct? Yes, if they do not have "normal" coronary artery anatomy. so, again, we need to be flexible and look at all of these "chest pain protocols" as more of a general framework or guideline. however, we will need to take all of this into consideration when considering implementing or steering away from a specific modality. I am not telling you to ignore your guidelines; however, I hope we realize critical thinking is required to provide proper care. Again, much of this goes back to having a solid foundation of education to fall back on. Something I was told a while back continues to stick with me to this day: "people never rise to the occasion, they fall back to the level of their education and experience." What are your thoughts about using morphine on this patient? Better yet, allow me to give you the last bit of information for this scenario: An hour into the flight to Dubai, the patient settles into this rhythm: The vitals remain "stable" in the 102/66 range and the patient remains free of any complaints. What are you going to do with the rhythm? What is the rhythm? What are you going to do with the patient? Take care, chbare.

Take a look at the prior posts, the patient's lungs are clear and remained clear following the initial bolus. Let us talk about dopamine? Are vasopressors a good think to automatically jump into when considering the MI patient? What will dopamine do to myocardial oxygen demand? In addition, consider the location of this MI. Are fluids in fact a better route given what we know about RVI and alteration in preload? No worries about bladder control. Always consider the risks and benefits of your treatments. We can always place a foley, use a bed pan, or improvise. With that, what about placing a foley in the patient? Would this be a wise choice considering the medications we have given? What about "wet" sounds? Is this an absolute contraindication for a fluid challenge? No problems with learning. This is the purpose of the scenario. Take care, chbare.

I will tell you what happened: The patient was given fibrinolytic therapy in the form of TNKase as no specific contraindications were identified in the history. What things must we monitor following fibrinolytic therapy? The patient was not paced; however, the patient developed an episode of bradycardia and near syncope. Atropine was given without any noticeable change in the heart rate. However, the bradycardia was transient and the patient developed the following shortly after fibrinolytics were given: What do you think? Take care, chbare.

Take care, chbare.

Good call: The patient initially presented in a complete heart block. Subsequent XII leads and rhythm strips did a little better job of demonstrating this. The patient was initially anxious as you may remember from a prior post. The "PVC's" are in fact artifact from movement. V4R was positive. Posterior wall changes were identified as well. Does the patient's clinical condition and ECG changes support the diagnosis of inferior/posterior wall MI with RVI? Specifically, the AV block, low blood pressure, near syncope, and reported low heart rates. Is this all typical of this kind of MI. If so, why? Would atropine be incredibly effective for a third degree heart block? Would you go straight to pacing the patient in her current condition? From what I gather, people would be comfortable with fibrinolytic therapy if available? Take care, chbare.

Lets review the basics of coronary artery anatomy, assuming "normal" anatomy: You essentially start with two arteries. The right coronary artery (RCA) and the left coronary artery (LCA). What area of the heart is typically supplied by the RCA? What about the LCA? Now, work your way down. What are the main branches off of the RCA? What structures are supplied by these branches? What are the main branches of the LCA? What structures are supplied by these branches? Specifically, we have identified changes in II, III, & AVF. As stated, this signifies inferior wall involvement. With the knowledge gained by researching the questions above, what are we potentially dealing with? Does the patient's clinical picture fit with what we see on the XII lead? Let us also talk about nitrates? We generally say these work by reducing preload. Is reducing preload a potential problem with the inferior wall MI patient. What did the fluid bolus do to our preload? However, are preload reducing agents absolutely contraindicated with every inferior wall MI? Looking at the posterior wall is never a bad idea. What other areas not covered by a standard XII lead ECG would you want to look at, considering the location of this possible STEMI? You are on the right track regarding the complaints of pain. What have we done by increasing blood pressure? It relates somewhat to the preload question above. In addition, look closely at the XII lead. Look carefully at lead III. You do not have much to go on; however, focus on identifying P waves. Take care, chbare.