wrmedic82

Just incase you are thinking about going the fire route. Just a word of advice. I would start with a 911 EMS service first and gain as much experience and knowledge as possible as a medic. Get a couple hundred calls under your belt, then make the transition. You will benefit alot more by doing this as your focus will be on EMS vs EMS/Fire which may make somethings obscure or it may not. But thats just my opinion. I know some great firefighters who practice medicine very well, and are very knowledgeable. Im still working my way there through EMTP school hopefully to be done at the end of this year. This is just my opinion.

As far as pay goes. More pay is great. However I hate to say it but most the money to be made is in fire departments. They seem to be the go-getters when it comes to grants and other means of funding.

I never understood how someone could forget to fill in history, allergies, medications, signatures and the like. Either there's something written in the box (even if it's the UNK box marked) or not. Don't providers at least do a once over look at their PCR before turning it in?

Now laziness I can understand. Solution: Until we become professionals with a professional work ethic, I say companies start paying their employees minimum wage with differentials based on doing their job. Let's see how many people "forget" to get a signature when a dollar or two and hour depends on doing paperwork properly.

I fully agree with you. I tend to write a book when I chart. But you would be surprised

I will pass on the hug thing however you can send that pizza to 551 E. Berry St, FT Worth, TX 76110

Back in the day when I used to volunteer we used Motorola Minator 4 pagers which were tone activated, and allowed dispatch to talk directly to all volunteers via the radio. It would give an annoying chirp so you couldnt ignore it if your tone was sounded. It worked great for our purposes however we didnt run very many calls (maybe 400 a year). Where I work now we do that in a day (the EMS organization not me personally) so it wouldnt be ideal. Check what your communication centers capabilities are before cutting the check.

5

Our system uses 1 toughbook per truck. We utilize Visinet for routing, tracking, and to gain information from dispatch about each call we run. For documentation we have Lifenet ePCR from physiocontrol. (same guys that make Lifepak)

Pros Visinet: Gives a quicker idea of the location of a call vs using a Mapsco Map. You can track your own movements for more precise routing (depending on who is navigating its not completely idiot proof) You can have it talk you to the call like a personal GPS.

Cons Visinet: Keeping a connection sometimes is a pain in the @%&

Pros Lifenet: Ensures that all pertinent info (demographics, MOI, NOI, ect) is entered to keep from accidental omission of information. The chart will not allow you to finalize a chart unless information that is deemed by the software as critical items are filled in. (example: signatures, demographics, meds, allergies, PHx ect.) Also you can set it up to fax the chart from your truck provided you truck has a built in gateway.

Cons Lifenet: It crashes daily and may make you want to throw your toughbook every now and then.

Drinking water to dilute a smaller amount gives you a little better of a chance but not by much. It's so caustic that it erodes tissue pretty quickly, which is why it's so catastrophic when you drink a large amount.

Bleach is a much safer attention drink...

How sad. Too bad the guy didn't stop to think...

Wendy

CO EMT-B

I don't know I would try to dilute with water. Reason being a lot of your corrosives are water reactive. With any chemical I would contact poison control before any interventions are started. I have some data from one program(s) I use on HAZMAT scenes. This maybe useful.

Reactivity Documentation

CAUSTIC SODA, SOLUTION LYE

mixed with

WATER

Summary

[C] Exothermic reaction. May generate heat and/or cause pressurization.

[D3] Combination liberates gaseous products, at least one of which is toxic. May cause pressurization.

[D5] Combination liberates combustion-enhancing gas (e.g., oxygen). May cause pressurization.

[D6] Exothermic, generation of toxic and corrosive fumes.

[D7] Generation of corrosive liquid.

May produce the following gases:

Corrosive Fumes

Ammonia

Oxygen

Details

CAUSTIC SODA, SOLUTION

Belongs to the following reactive group(s):

Bases

Water is a reactive group.

Reactivity Predictions (for each pair of reactive groups)

Bases mixed with

Water

Hazard Predictions

[C] Exothermic reaction. May generate heat and/or cause pressurization.

[D3] Combination liberates gaseous products, at least one of which is toxic. May cause pressurization.

[D5] Combination liberates combustion-enhancing gas (e.g., oxygen). May cause pressurization.

[D6] Exothermic, generation of toxic and corrosive fumes.

[D7] Generation of corrosive liquid.

Potential Gas Byproducts

Ammonia (NH3)

Oxygen (O2)

Corrosive Fumes (CorrosiveFumes)

Acetaldehyde Ammonia resinifies (oxidizes, hardens and turns yellow or brown) on long exposure to air. The compound is very soluble in water. It reacts exothermically with water to evolve gaseous ammonia. [Hawley].

Lithium Amide is flammable and reacts with water or moist air to generate a dangerous amount of heat [Chem Reviews 12:61. 1933]. Lithium amide reacts vigorously with water to generate gaseous NH3. In experiments at Argonne National Laboratory, in which it was mixed with water and stirred at room conditions, about 23 percent of the theoretical yield of NH3 evolved as a gas in the first 0.6 minutes [brown, D. F., et al. (2000) Development of the Table of Initial Isolation and Protective Action Distances for the 2000 Emergency Response Guidebook, ANL-DIS-00-1, Argonne National Laboratory, Argonne IL].

Magnesium Diamide may spontaneously ignite upon exposure to air. Soluble in water. Reacts violently with water to form caustic ammonia/ammonium hydroxide and heat.

Potassium Peroxide reacts exothermically with water (or moisture in the air) to give oxygen and a caustic solution, potassium hydroxide [NFPA 491M] .

Sodium Methylate ignites in moist air [Wischmeyer 1966]. The compound with moist air, autoignition is possible; strong reducing agent; reacts with light metals forming H2 gas, with fire and explosion hazards; reacts violently with water to form methanol and sodium hydroxide, and with acids, causing hazard of methanol ignition [Handling Chemicals Safely 1980 p. 850].

Sodium Superoxide reacts with moisture and carbon dioxide in the air. Reacts vigorously with water to give oxygen and sodium hydroxide.

wrmedic82,

I'm sorry, but you'll have to elaborate more on your question? Aside from being vague, it is poorly worded; I did not understand your line of thought. Thank you.

ok on a spigmomanometer the numbers are only even. My question is how did they get 115/75 being optimal when both numbers are odd. I thought I was clear when I asked..my bad

I hope you attach that literature to your ACR otherwise your going to be out of luck in court. A dozen slick lawyers asking you how you know what the patients normal limits are, and you say we saw XYZ literature, they say well where is it? You = screwed.

When a patient tells you their norm, provided they know their norm, its something to keep in hindsight. You always treat the patient based on chief complaint, and clinical presentation. A patient may have their normal BP and still be dehydrated if that is their clinical presentation, or it may be elevated in some circumstances. Common sense wont hurt much either (unless common sense lies to you frequently) . Another thing to consider is protocols. In our system if someone has a systolic below 90,according to hypotension protocols they get a initial 250ml fluid bolus, then give 20cc/kg (standard) to maintain a systolic at or above 90.

In recent years there has been a continuing reconsideration of what is deemed a normal blood pressure (BP) reading. While most experts believe that 120/80 is an optimal BP reading, current research suggests that 115/75 is the new optimal.

nd then determine their normal BP. Hospital healthcare practitioners do that.

Just curious and don't take this as sarcasm but when did BP have odd numbers vs even numbers.

I am not much for monitors as Ive seen them be drastically off too many times. funny case and point was watching the monitors BP cuff take a pressure while not being attached to the patient or anyone for that matter. I am sure routine calibration would fix that. I just like sticking to old reliable spigmomanometer and stethoscope

I guess you can call vital signs WNL if you compare them to what is written in literature. However like others have said vital signs are relative to the patient. Its not a bad idea to ask the patient what thier norms are.

No. If a person has a Pulmonary Emboli, they will be tachcypneic with a measured low PaCO2 and not have an abundance of O2.

You also do not know their carrying capacity for O2 such as Hb, CO exposure and MetHb from some nitrates.

No, not necesssarily. You do not kow the PaCO2/PetCO2 gradient.

There are several causes for a low ETCO2. Air entrainment by tachypnea will dilute the ETCO2 measurement.

Deadspace ventilation, low tidal volume ventilation, hypovolemia, hypothermia, lung parenchymal destruction and low cardiac output will give a low ETCO2. Of course you can always have the issue with poor equipment maintance and failure to calibrate.

This is often the mistake some who don't understand V/Q mismatching will make on CCT when they try to "normalize" the PaCO2 of a ventilator patient by just looking at the ETCO2. Thus, the rec'g hospital ends up with a very acidotic patient.

A DKA and some sepsis (or whatever metabolic acidosis) patients can get their PaCO2 into the single digits and still be very acidotic.

This I definitely agree with. I will do a thorough assessment for organic problems of the patient before I write them off as anxiety and it is doubtful if I will even assume it then until all lab data is in. We have had many young people with new onset diabetes and their body will not let them slow down. One should consider an organic cause quickly during the initial examine and move on with further assessment to find the organic cause.

With a patient with a PE, wouldn't the SpO2 be low?? Case and point I'm going to make is I had a patient who was later confirmed to have 4 PE's have a SpO2 of 64 and ETCO2 56. As far as the other stuff there is nothing for us to determine PaO2, PaCO2, ect. So how does that effect our treatment. And yes a patient in DKA can have ETCO2 in the single digits due to tachypnea, but lets say the proverbial paramedic not thinking tries to get the patient to slow respirations. If he is successful in doing so then ETCO2 would significantly rise. Again I go back to patient assessment prior to treatment. If you have access to recent lab work...awesome. This is often not the case. So me personally I would see how the patient presents (i.e anxiety, DKA, sepsis) and go from there. That is where we definitely agree.

When we hyperventilate, we breathe rapidly. We breathe so fast we can't get full tidal volume into our lungs. We breathe in a small out of o2 and retain more CO2, thus making us more acidiotic. Having more co2 and less o2 in your system being circulated, will lead to cyanosis, which is a lack of oxygen.

I hate to disagree with you there bud, but you actually blow off all your CO2 and have an over abundance of O2 when a person hyperventilates. That is why you will see when you place the person on SpO2 and ETCO2 monitors that the person's SpO2 will be 100% and their ETCO2 will be 19 or lower.Thus making the patient alkalotic, not acidotic. Its again important to evaluate the patient, because if they are hyperventilating secondary acidosis( Example DKA ), we do not want to coach the patient into slowing their respiration.

Worst comes to worst, the person passes out, and resumes normal breathing. Or they continue to breath fast to compensate.

Report it....Its every individuals responsibility to maintain their own cert. If the guy is not responsible about keeping his cert up, what else is he not being responsible about ? Besides most states will allow credit for online CE's, as well as count card classes for CE credit. So he has no excuses other than not doing it. Hell soon ACLS will be online with no need to take a formal class. (sad but true).

Introduction

In recent years, more studies have demonstrated the importance of lead aVR during the analysis of the 12-lead electrocardiogram (ECG) in patients with acute coronary syndrome (ACS). These studies have indicated that lead aVR is a strong predictor of left main coronary artery (LMCA) occlusion when used in isolation[1] or in conjunction with other leads.[2] Studies have indicated that the presence of simultaneous ST-segment elevation (STE) in leads aVR + aVL[3] or the presence of STE in aVR that exceeds the amount of STE in lead V1[4,5] is highly specific for LMCA occlusion in patients with ACS. Other studies have discussed STE in lead aVR in less specific terms, simply citing that this finding is indicative of either LMCA occlusion or left anterior artery occlusion,[6,7] or indicative of either LMCA occlusion or triple-vessel disease.[8] The magnitude of STE in lead aVR that is considered significant is inconsistent among these articles; some articles have evaluated any STE in aVR, whereas others have focused on STE greater than 1 mm. This difference may account for the varying specificities for LMCA involvement. Regardless, the literature continues to show with increasing consistency that STE in lead aVR in patients with ACS is associated with more ominous coronary occlusions. Patients with LMCA occlusions, left anterior artery occlusions, or triple-vessel occlusions have a worse prognosis, requiring more aggressive immediate therapy and often bypass surgery. Emergency physicians who find ECG predictors of any of these 3 conditions in their patients with ACS (whether ST-segment elevation myocardial infarction [sTEMI] or non-STE ACS) would be prudent to mobilize resources for rapid invasive therapy. Additionally, because many of these patients will require coronary artery bypass grafting, it certainly seems advisable to withhold clopidogrel.[4] Below is a summary of one more study that adds to the literature indicating that STE in lead aVR predicts more pronounced coronary occlusions and a worse prognosis.

Admission ST-Segment Elevation in Lead aVR as the Factor Improving Complex Risk Stratification in Acute Coronary Syndromes

Szymanski FM, Grabowski M, Filipiak KJ, Karpinski G, Opolski G

Am J Emerg Med. 2008;26:408-412

Summary

Szymanski and colleagues evaluated the association of STE in lead aVR with mortality. The investigators assessed 205 consecutive patients with non-STEMI ACS for STE in lead aVR of at least 0.5 mm. Patients were divided into 3 risk groups on the basis of their Thrombolysis in Myocardial Infarction (TIMI) risk score,[9] a validated ACS scoring system that is used to gauge 14-day risk for adverse outcome in patients admitted with ACS. Low-risk patients had 0-2 points; intermediate-risk patients had 3-4 points; and high-risk patients had 5-7 points on the TIMI scale. STE in lead aVR was found in 114 patients. The researchers found that the presence of STE in aVR was a strong and independent predictor of 30-day mortality (odds ratio, 7.8). During this 30-day period, 18 patients (8.8%) died. Of those who died, 16 of 18 (88.9%) had STE in aVR vs 98 of 187 (52.4%) of the survivors who had STE in aVR. Mortality also increased with the severity of STE in aVR. Mortality was 2 of 91 (2.2%) for patients without STE in aVR, 8 of 74 (10.8%) for patients with STE of 0.5 mm, 4 of 29 (13.8%) for patients with STE of 1 mm, 2 of 9 (22.2%) for patients with STE of 1.5-2.5 mm, and 2 of 4 (50%) for patients with STE of ≥ 3 mm. The increases in mortality were statistically significant.

Viewpoint

When considering the TIMI risk stratification scores, the researchers discovered that patients with STE in aVR, when compared with patients without STE in aVR, had higher death rates in the low-risk (18.5% vs 0%) and intermediate-risk groups (15.5% vs 2.6%). The study authors concluded that STE in lead aVR in patients with ACS was a good predictor of short-term mortality and could be used synergistically with TIMI scores for early stratification of risk. The takeaway point is simple: When patients with ACS, including non-STE ACS, demonstrate STE in lead aVR, the aggressiveness of early management must be increased. These patients have more complex coronary lesions and will likely benefit from earlier invasive therapy.

Abstract

This study aimed to analyze the prognostic value of the presence of ST elevation in lead aVR [aVR(+)] in initial standard electrocardiogram (ECG) performed on admission in combination with clinical variables and Thrombolysis in Myocardial Infarction (TIMI) risk score for unstable angina/non-ST-elevation myocardial infarction (UA/NSTEMI). In 205 consecutive patients with UA/NSTEMI, we retrospectively evaluated admission ECG for aVR(+) of more than 0.5 mm. With the use of multivariate analysis, admission aVR(+) was found to be a strong and independent predictor of 30-day mortality. Mortality also increased with the severity of aVR(+): 2.2%, 10.8%, 13.8%, 22.2%, 50% (P value for trend <.0001). In prespecified low-risk groups by clinical factors, those with aVR(+) had higher death rates than those without aVR(+): 16.1% vs 2.2% (P = .04), 13.9% vs 1.1% (P = .001), 12.4% vs 1.1% (P = .002), 9.6% vs 1.2% (P = .02), and 6.7% vs 0% (P = .05) for patients with negative troponin, heart rate of 110 beats per minute or less, systolic blood pressure greater than 90 mm Hg, Killip I class on admission, and age 70 years or younger, respectively. Patients with aVR(+) compared to patients without aVR(+) had higher death rates in the low- and intermediate-risk groups by TIMI risk score. Our findings suggest that aVR(+) has significant prognostic value in patients with UA/NSTEMI and may provide an additional prognostic value to the conventional cardiovascular risk factor, particularly in patients in the low-risk and intermediate-risk groups.

Must WHOLE HEARTEDLY DISAGREE .... this is ABSOLUTLEY NOT IN Billy Bobs Protocols !

Correction : Into your BEER CAN :>)

sheesh AK !

YES!!!!!!!

There is no evidence to support the practice so I wouldn't be wasting my time on this useless assessment if I were you. We can never truly become a profession that practices evidence based medicine if people keep doing things that they think are right or things that they do because "that's the way it's always been done."

you talk about evidence based medicine and yet there is not a shred of documented proof that ACLS drugs have better outcomes, or even work at all in patients in cardiac arrests. Don't get me wrong Im not advocating against giving vasopressin, epi, or atropine. But I find your comment somewhat hypocritical.

Some things to look at

http://content.nejm.org/cgi/content/extract/340/22/1763

http://www.annals.org/cgi/content/full/129/6/501

http://www.ncbi.nlm.nih.gov/pubmed/7023292

http://www.eboncall.org/CATs/81.html

http://www.ncbi.nlm.nih.gov/pubmed/15642869

However I did dig up a couple articles about checking for pulses being ineffective. To each their own. Im not against checking pulses during CPR nor do I think that stopping to check for a pulse during CPR really has a true negative outcome. Thats my story and Im sticking to it.

http://emcrit.org/1-resus/007-adult.resus.htm

http://www.merck.com/mmpe/sec06/ch064/ch064d.html

This is our protocol

Eclampsia

1. Magnesium Sulfate infusion 2 Grams no faster than 1Gram/min. Mix 4cc of 50% Magnesium

Sulfate and 100cc Normal Saline in a Volutrol (60 gtts set) and infuse wide open rate. May repeat once

if seizure is still present. Monitor patellar reflexes for Magnesium toxicity and discontinue if they

appear.

a. Bend the patient’s leg to a 90° angle and tap on the patellar reflex. If the patient’s reflex

causes the leg to continually bounce, discontinue the Magnesium Sulfate infusion.

In this case scenario, I don't know if I can truly fault the firefighters. If I was dispatched on the same call, with no indication of a potential for violence from dispatch. All you know is that its a medical call on a elderly. Not expecting to be met by a group of teenagers who want to start trouble. I might have done the same thing and made scene. Its easy to say Ah Ha fire just had a wake up call. And they may have. But we all do it. And do we stage on every call? HELL NO WE DON'T!!!!

I will say a couple things en light of this article. 1. extra emphasis on scene size up. Its easy to size up the patient. But what about the surroundings? If you were on scene in stead of fire ( because they are notorious for bullet proof t-shirts and bunker gear) faced with the same scenario, and saw a group of possibly angry teens walking into your general direction, would you step out of the vehicle? God I hope not, but this happens more often than its published in the media.

The second thing I would like to emphasize is don't be afraid to back out. Its kinda common sense if the scene is not safe to stage until PD secures the scene. I don't feel the need to beat that further into the ground, not saying its not important. It is not abandonment if your safety is compromised due to bystanders, family members, etc. Ask any experienced incident commander, and they will tell you that the scene is dynamic and always changing. If the scene becomes unsafe for you and your partner there is no shame in backing out for your safety. I'm not sure how much time fire had before they realized "holy crap we are on the receiving end of a beating." But lets say they had 60 seconds before they got jumped. If they saw it coming or if you saw it coming wouldnt you do something to protect yourself by getting out of the situation??

Ask yourself, if you were dispatched P3 Sick Person 123 Anyplace Dr, Anyplace, TX USA 12345 75/f conscious, breathing, CC ABD pain. Would you stage???

And yes I pulled that call out of random because this is common call we all run on. Would you stage based on this information alone?

I will treat them, massage them, do everything I can to make those darling ff feel better and up to doing their job again. no matter how long it takes, or what it takes..............I'm there!

Got something brown on your nose there bub

Here is a link that supports what Im talking about.

http://lowfatcooking.about.com/od/healthan...onstickpans.htm

Was the bottom of the pot/pan coated with teflon???

I know it sounds crazy. I read in a studyway back when ( sorry this is the fireman in me coming out) that a pot/pan coated with teflon left on a heating element with nothing cooking inside the pot/pan the teflon begins to form a colorless, odor less gas that can cause asphyxiation. I will have to re-research to recall the actual form of gas created. So its possible that the reason for AMS is hypoxia. Of course I havent read the vitals so Im not saying that this is what it is. However just throwing out a possibility.

I would have to say

1. PPE

2. Oxygen

3. BVM

4. Monitor / Defib

5. Manual BP cuff

6. Stethoscope

Congratulations on your new bundle of joy.

Greetings. First time poster here. My name is Dave, and I live in the SF Bay Area. I recently took the EMT-B course, passed the NREMT and have all state/local certifications.

I have applied with a local AMR location that has a primary 911 service contract with the county. Very large metropolitan area, suburban and urban environments. Needless to say, the jobs are quite competitive, especially for EMT-B's.

I have made it through the first two parts - written test and interview. The interview was probably the biggest hurdle. All that remains is a skills test. I didn't receive a lot of details about this, so I am assuming the usual Basic skills will be tested - CPR/BMV/C-collar/O2 admin. etc.

Can anyone who as been through the AMR process and taken their skills test fill me in on any details? I have had zero real-life experience, and the only time I have had to use these skills were the brief moments in class.

This is the last part, I've come a long way and I don't want to blow it here. Any help greatly appreciated!

Just remember the basic's. Start with personal safety, and the ABC's. Correct any problems that you come across that involve the ABC's. and go from there. Everything else will come with time and experience.

Including the ever-popular injecting your own hand instead of the patient.

Ok I gotta hear about this

granted your 3 inches taller but your wee wee is 3 inches shorter

i wish i had all the knowledge the world can offer

wish granted but now your stuck with a partner who is a dyslexic agnostic paranoid schizophrenic who thinks the dog is out to get them.

I wish for more a lottery jackpot win