THE_DITCH_DOCTOR

Ever stop and think why we are certified and received such low pay?

Personally I'd like to see a four year degree be the baseline for EMT-Paramedic, with expanded scope practice, but this is unlikely to happen because of the vast majority of EMS agencies being only interested in keeping us as technicians who are easy to churn out in relatively large numbers. A 2-year degree is a good start, but not ideal. As for the real "education" beginning on the street, well.....sort of. You begin to learn the exceptions to the rules and you learn the "tricks of the trade" but that is training- not education. Training is concerned with the how and the when of something, and most people excel at this manner of thing. True education is learning and knowing how and when to question the why of something. You don't pick that up in the street with most EMS services.

But of course you have to look at the flip side of the coin- you're going to attract the people who "can't find anything better to do" (read as 'weren't smart enough to get into college'), not to mention attracting a very large number of immature adrenaline junkies, even more than we wind up with now. Yes, you might attract a few new excellent medics and even a greater number of decent medics- but no matter how much you speak of the reality of EMS, you are still going to increase, by a far greater factor, the number of glory seekers, attention whores, and Randy Rescue wannabes that you wind up with. Instead of attracting the younger versions of Buddha and Ridryder, you're going to attract more people along the lines of IcyHot and LittleFireCracker. We already do a piss poor job of weeding out these people from volunteer agencies as it is, so why go and increase the numbers even further? Let me use this website as an example- we had a very good group until that JEMS advertisement ran. Since then the number of members has taken off at a very accelerated rate, and I think increasing the number of good productive members is a great thing. But the trouble becomes that when raise the awareness of something, especially something perceived as being "cool" or "exciting" by a good portion of the general public, then you are going to attract a lot of less than desirable individuals- the a--holes, the fruitcakes, the egocentric wannabes, the people who live out where the buses don't run and the phones don't have 911. The question is this- is the cost in having to put up with the 10 or 15 people as annoying and obtuse as IcyHot, worth gaining one person who is eager and willing to learn (for example CVFD_EMT). In the online world, it maybe fine to have this balance, but in the real world I think it would be a dangerous balance.

Food? Where? When? Something about EMS? Huh? What?

It's in the planning stages, and the plan is to involve one of the professors from the medical school (the psychology professor (since placebo effect and psychological dependence are both psychological conditions) is simply aiding in putting together the psychological testing part of the study. As for the specifics of the study, I'm not going to get into them here due to the specifics not having been set up completely yet, but suffice to say that all standards for testing will be followed and remember that placebos are part of nearly any pharmacology study. This is not going to be an EMS study- it will take place in an academic medical center after approval by the facility's institutional review board.

I think a lot of it is psychological combined with air trapping (almost like a supped up version of hyperventilation). I've seen excellent results from using CPAP in patients with severe exacerbations, but the idea we are working on is that a lot of "attacks" are simply panic attacks- ever notice how some COPD'ers freak out over very minor things (such as if you try to take their inhaler from them). Like I said it's just a personal theory that I would like to see tested, but I think they feel better simply because we are doing something that they have been told will make them better.

The potential issue isn't the lack of potency of the albuterol, but rather the pathophysiology of COPD- the problem isn't always bronchospasm. Often it is just simply a problem with air trapping due to a loss of the elastic recoil of the lungs and a loss of surface area due to alveolar destruction, or that the tenuous balance is upset by an infection or something else going wrong- not a bronchospastic event. Basically you can give them all the bronchodilators in the world and it won't make one bit of difference in a lot of cases. You see subjective improvements in many stable COPD'ers following treatments (they tell you they feel better or even great after the treatment), but you often don't see objective evidence (increased peak flows or significant changes in breath sounds for example) to support that.

Sorry, it will remain an ALS level skill

I am putting together a clinical study (with the assistance of a psychology professor at my school) to assess the possibility of the placebo effect playing a major role in the relief experienced following treatment with bronchodilators (most notably albuterol). My theory is that it's most often due to a placebo effect because there is often not audible wheezing in these patients, rather the breath sounds are just diminished to varying degrees and no change is seen in peak flow measurements done in conjunction with the nebs. Basically it's my theory that the people feel better simply because we are doing something, not because we are actually doing anything that changes something from a physiologic standpoint. What does everyone think?

Well, you're nothing if not inventive in your analogies Buddha.

You mean how much would the peripheral veins constrict in relation to the dilation of "vital" areas? Right?

Probably at least another 3 weeks. Sorry.....

I'm still working on it. Remember this isn't going to be a simple 100 question, fill in the answer or multiple choice test like a lot of you are used to. There are going to be two steps to this exam (you have to pass the first one (covering basic clinical sciences and pathophysiology) with an 80% to be able to take the second test (one presenting clinical scenarios and requiring you to make decisions about courses of treatment). Seeing as I work full time and go to school it will take me quite a bit of time to write this exam and get it submitted. Trust me, I will get it to everyone just as soon as I can.

OK....a few points 1. NOT all COPD'ers have a functional hypoxic drive. It takes prolonged (and I'm talking weeks) of markedly elevated PaCO2 levels before the CO2 receptors that normally help adjust ventilation rates become insensitive and this normally only occurs in end stage patients. The rule to keep in mind is that you should use the lowest possible FiO2 necessary to maintain adequate tissue oxygenation- but this applies to ALL patients, not just COPD'ers. 2. CO2 levels are not primarily dependent upon oxygen levels. CO2 is most rapidly changed through ventilation. You can put a person upon 100% O2 and if they maintain a normal minute ventilation (around 5 liters of air per minute), most people's CO2 levels will not decrease that much (because they are still producing the same amount of O2 every minute, but it's not being exhaled at a greater rate). 3. Oxygen levels (on SpO2 for instance) are not adequate measures of appropriate ventilation. The one thing I see a great deal of confusion among EMT's and paramedics is the differences between oxygenation and ventilation. These two mechanisms are intertwined but separate and the adequacy of each is determined through different measures. Oxygenation is the absorption, delivery and use of oxygen by the tissues. It is effectively assessed either through SpO2 or by the PaO2 reading on a blood gas. It can be affected by derangements in ventilation (hypoventilation has a greater effect than hyperventilation), by changes in oxygen binding levels (example: the greater affinity of hemoglobin for carbon monoxide decreases blood oxygen levels by decreasing the amount of hemoglobin free to bind with O2), or by impairment of tissue utilization of O2 (example: the mechanism of cyanide toxicity is impairment of an enzyme necessary for the use of O2 in cellular metabolism), and a few others. Oxygenation is basically the result of adequate ventilation combined with adequate perfusion if the pulmonary capillary beds....it gets pretty complicated but suffice to say that indicators of sufficient oxygenation do not also imply sufficient ventilation. Ventilation is the physical movement of air in and out of the lungs, and is best reflected by CO2 levels (ETCO2 is a rough approximation of the PaCO2 level we obtain in hospital when we do blood gases). Impairment of ventilation can be due to: Physical hindrance of lung expansion (tension pneumothorax, skeletal misalignment (scoliosis for example), skeletal trauma (rib fractures, etc)) Changes in pulmonary compliance (a measure of how easily the lungs expand- increased compliance (as occurs in COPD) means the lungs expand more easily (but also tend to not recoil as much upon exhalation leading to more air trapping), where as decreased compliance means that lungs tend to be "stiffer" and take more force to expand ("hard to bag") and the best example of this is acute respiratory distress syndrome (ARDS) or severe sarcoidosis. Airway obstruction Decrease in drive to breathe (head injury, narcotics OD, etc), Etc. Any questions, please let me know......

No, it's all a matter of mask seal, minute ventilation and a myriad other issues. According to most textbooks, a nasal cannula SHOULD deliver approximately: 1- 24% 2L- 28% 3L- 32% 4L- 36% 5L- 40% 6L- 44% Now what they fail to mention is that these are: a. Rough estimates b. based upon healthy volunteers with normal RR, minute ventilation and tidal volumes c. based upon people with no nasal anatomical malformations (septal deviations, etc), no obstruction to flow (stuffy nose being an example) The following factors affect FiO2 in a low flow system (such as a nasal cannula) Increase FiO2 Higher O2 input (increase O2 flow) Closed mouth breathing/pt not talking Low inspiratory flow (slow inhalations) Low tidal volume Slow respiratory rate Low minute ventilation High I:E ratio (longer inhalation than exhalation) Decreases FiO2 Lower O2 input (decrease O2 flow) Mouth open breathing/pt talking Higher inspiratory flow (rapid inhalation) Larger tidal volume Higher minute ventilation Fast respiratory rate Short inspiratory time High I:E ratio (Taken from Table 34-4, Page 748, Egan's Fundamentals of Respiratory Care) Basically the point is that most O2 delivery systems (with notable exceptions being correct ventilation with a BVM, or via a CPAP mask, or via an ET tube) do not approach high concentrations- or even reliably produce the stated FiO2's at the level of the alveoli.

OK....time for respiratory physiology 101: Normal PaCO2 (and ETCO2 which correlates with PaCO2) is 35-45 mm Hg (you don't want to go below 30 in a head trauma or stroke victim (i.e. someone with signs of increased ICP or other intracranial pathology) for the very reason discussed in the article, but this guy is taking it a bit too far (although the author of the article is partly to blame). Normally a NRB at 15 L/min will deliver a fraction of inspired O2 (FiO2) of ~60-80%. The exact amount depends on how well the mask fits the face and the also varies with the patient's minute ventilation- at excessively high minute ventilations tend to get lower FiO2 while on masks because they will entrain outside air in an effort to pull in as much air as they need (remember an adult male is capable of moving >120 liters of air per minute at maximal effort under extreme circumstances). 100% by NRB is a pipe dream in 99.9% of cases. As a reminder, you can get a rough idea of the FiO2 by using the following formula: FiO2 = 0.21 + (4 x Oxygen flow rate in LPM) FYI 0.21 is 21% (the amount of O2 in our atmosphere)

No, I don't get reimbursed. Sometimes though I have had ambulance crews (mainly people I am friends with), let me restock from the ambulance (seeing as I am taking what they would have used on the patient anyhow ) but this is the exception rather than the rule. You just learn to eat the cost of the supplies for the most part if you choose to carry your own kit.

Can do... Breakdown of the scores by MD's (there are a couple on here) Respiratory therapists (it would be unfair to count my scores under the EMT-I section as it would skew the results one way or the other) Registered Nurse/EMT-P EMT-Paramedics EMT-Intermediates EMT-Basics First Responders Wannabes Any other categories?

I think you are far more knowledgeable than you let yourself believe Richard. I've told you that before. Just have faith in yourself and you will do fine.

Sorry, I've been busy and haven't had much time to work on it lately. It's slowly coming along but it will be a while before it gets posted. Sorry for the delay.

At the request of CO, here's a new poll thread. Why did you get into EMS?

Still more reasons I don't like the LP12: http://www.medicscape.com/modules.php?op=m...icle&sid=33

MRL's SUCK. Period. I've heard good things about the new Phillips defibs though.

Zolls are better hands down. I actually turned down a job because they were using LP12's. :x

If they are impaired to the same level, then I would do something- probably make them go home and sleep it off.