Archives for September 2011

Job Stability in EMS

Let’s just get it out of the way. As a Basic EMT, and to a slightly lesser but still very similar extent as a Paramedic, you are typically viewed as unskilled rank-and-file. You are more like the kid flipping burgers at Burger King than a nurse or a doctor. This is a consequence of supply vs. demand, low barriers to entry in this business, and minimal labor and political representation. I don’t think it’s right, but it is the way it is.

(Note: those working for fire departments and other public services may find that this information does not apply. If that describes you, I applaud you for your good fortune. But for the thousands employed with private services, read on.)

This is a difficult and personal subject for me. The start of my career was a rocky one; there were various factors, but in the end, the one overarching reason was that I didn’t understand how to be the kind of EMT that employers wanted. The lessons that follow may not apply everywhere, but based on my experiences with numerous companies in two different geographical areas, they are generally more true than not, and if you’re newly entering this industry in a field position, they’re worth holding close to your heart.

First, understand that, as we noted, you are not a high-value employee. In fact, you are essentially a low-wage service worker, and you are largely interchangeable with anyone who holds the same certification. Moreover, the job market is currently Bad, and even when it was better, there were people out there who would do this job for free; in other words, even though demand for your skills is still reasonable, supply is very high. Although your service needs a certain number of EMTs and/or paramedics, and although they may perform some amount of screening or testing to find the best candidates (better employers will do more of this), as a general rule there is a limitless supply of people standing behind you, all holding the same card. And your company is just as willing to pay them instead of you.

Second, your employer is in the business of making money. Just like BK needs someone to flip their burgers, ambulance companies need someone to drive and tech their ambulances, so you are a necessary part of their business model. But you are far from unique or irreplaceable. Since it’s not very difficult to hire an EMT, it’s never very difficult to fire one and hire another. So if you ever become more trouble to keep around than you’re worth, you’re inching towards termination.

Third, and most importantly, the money is in the money. A principled and respectable private service will try to drive their financial success through clinical excellence, but whether they do or not, their financial success remains the bottom line. Your Lifepaks and MDTs may or may not get upgraded, but the marketing and PR is never in question. So if by your actions, inaction, or even by association you’re ever involved with something that jeopardizes your company’s revenue stream, you’re absolutely begging them to reconsider taking their chances on a fresh hire.

So, do you want to keep this job, be it briefly or for a long career? (Whether you should be taking advice from me is a fair question, but at least you’re hearing it from experience at the wrong end of every error.) Job stability in this field depends on three skills, and you don’t need them all. Pick any two and you’ll do okay. You might even sneak by with just one. But when the day comes that you don’t have any to protect you, your days are numbered.


1. Protect the Money

You can kill patients, break equipment, curse like a sailor, and drive rigs off cliffs, but if you can avoid impacting your employer’s bottom line, you’ll probably be fine.

Billing is big. Try your hardest to help generate billable runs, because getting paid for your calls is how money is made, and consistently interfering with this will bring you the wrong sort of attention. Whatever documentation hoops they ask you to jump through, as long as they’re not unethical or detrimental to patient care, just do it.

Furthermore, your company’s continued existence is predicated on maintaining certain contracts that it holds with cities, counties, hospitals, and other facilities. These contracts give your company the right to transport some or all of their patients, and that can mean many calls and many dollars per year. If you look unprofessional to someone important, piss off a staff member, or make a clinical error that comes to the wrong person’s attention, you are making the Powers That Be at that organization wonder if they shouldn’t be handing their patients and dollars to a different ambulance company. And that is numero uno on the list of ways to lose your job. Don’t think that the facts will save you, and don’t think that they’ll be reasonable or go to bat for you, because if being able to say “the people responsible have been terminated” is good for business, then nothing else will matter.

Play the game. If you’re asked to wash the truck with a toothbrush, wear a tie and a monocle, and give all of your patients free backrubs, just do it. Play the game, or someone else will.


2. Be Liked

They never taught you this in school (and school was where you’d have found many of us just before we became EMTs), but if the right people like you, nearly anything is possible. If not…

You don’t have to be universally popular, but you should not be “that guy,” because when push comes to shove, somebody with an office and a salary is going to have to decide whether you should keep working here, and if they never liked you to begin with you’re not going to have any armor.

Here’s the big, big secret. You may think that life should be fair, or at least employment should, and if you do your job and don’t screw up too big, there’s no grounds to fire you. In other jobs, you might be right. But we just saw that you hold no sway in these parts, cowboy. Moreover, in most places you were hired under a contract that included the words “at will,” which means they can get rid of you for no reason at all. (Wholly legal? Maybe, maybe not, but most of us won’t be bringing any lawsuits, because it’s a lot of trouble and being “the dude who sued” is not great for your future employability.) So here’s the way it really works: they can terminate anyone, or they can keep anyone. It all depends on what they want to do.

If you’re well-liked by the people who have a say, then you can screw up, and it will be water under the bridge. It may be documented and recorded, or it may simply be swept aside, but nothing will come of it. On the other hand, if you’re someone they’d rather no longer worked there, then you don’t even need to screw up to find your way to the chopping block. Because the fact is, nobody is perfect; even if you think you’re a company man, in the 40+ hours you punch each week, they can find a violation here, an error there, a complaint, a concern. If you ever start getting called to the deck for driving 26 in a 25 MPH zone or parting your hair left instead of right, update your resume, because this is known as “building a paper trail.” (If you’re lucky, maybe they have no problem with you yet, and they’re just preparing a case for the future. Some places are optimistic like that.)


3. Stay Under the Radar

This is the master key of maintaining your employment. Many people lack one or both of the previous virtues, but still keep their job for 10 years because they’ve got this one down pat.

If you’re hired today, and starting tomorrow nobody ever hears your name again, then your job is safe. Your name has to cross someone’s desk before they can tie you a noose. So if you’re ever going to screw up, just make sure that it’s never in a way that draws attention.

EMS is rife with uniformed men and women who show up, clock in, work their hours, and go home. They may be interesting people or boring ones, smart or dumb, up-and-coming or cheerfully stagnant. They may be loved or hated by their coworkers. They may even give bad care, write bad documentation, and draw ire in every ED they enter. But so long as it’s never the kind of thing to make anybody complain to the supervisors, then they’ll do just fine.

On the flip side, they might be a Super EMT, aces in every category, but if their name and face are constantly attracting the eye of the bosses, then they’re at best one or two steps from seeking new employment. Because being a bother is not a good virtue if you’re not valuable.

Truth be told, if you’re wise, then you’ll probably stay off the radar even for the most harmless reasons. No attention is good attention, not even asking to change a shift or replace a shirt, and while some of that is obviously necessary it should certainly be minimized. It’s a fine, fine art you’ve mastered when you’re hired as a new medic, and five years later nobody upstairs knows you beyond a vague sense that might work there.


There you have it. The big three.

You will notice that nowhere in the above list do I include clinical competence. For a long time, I believed that if you were a good EMT, that was enough to keep you safe — and if you were an exceptional EMT, that would even make up for a few things. This couldn’t be further from the truth. Possibly in a few cases, such as if you assist with training and continuing education, your knowledge and skills can be a feather in your cap. But as a rule, nobody in charge knows or cares about how good you are. You’re just one of the many EMT-Bs or EMT-Ps from the big group of identical licenses on the payroll. So if you think that being the fastest intubator in the West will protect you from violations of the Big Three, then you are sadly mistaken.

Indeed, this is yet another reason (you know, beyond the basic moral ones) to treat your patients and facility staff with respect and compassion. By and large, they don’t know if you’re any good at medicine — the patient in particular — but they know if you were a dickhead, and dickheads are the people they call and complain about. You can nearly kill someone, but if you smile, hand them a warmed blanket, and shake their hand, they’ll go away thinking you were the nicest young man they ever met. For all the great ideas on kindness and empathy in our favorite EMS book, Thom Dick’s People Care, it’s worth noting that its subtitle is not “How to Get into Heaven,” but “Career-friendly Practices for Professional Caregivers.” Career-friendly indeed.

It may sound like I’ve become a terrible cynic, but in truth, I think I’ve just come to understand the basic realities of the field we work in. We may wish the world were different, but we may also wish for a pet unicorn and world peace; things are the way they are, and the truth is that you should be able to maintain a long and successful career, providing the most outstanding care you can offer, if you simply learn how to stay employable.

Drug Families: Anticoagulants and Antiplatelets

One of the most common drugs we encounter in the field are various forms of anticoagulant and antiplatelet medications. These are relevant to our care both in their therapeutic role as well as in their adverse reactions and potential for harm.

Unfortunately, coagulation is a miserably complex process, and it has to be understood at least generally in order to understand these drugs. In the hope of making this less confusing, rather than throw a wall of text at you, the worker gnomes at EMS Basics have put together an illustrated video. View this, then read on — the drugs won’t make any sense if you don’t start with the physiology.

This form of teaching is a new frontier here, so any input or feedback is welcome. Due to both personal and technical failings, it didn’t turn out exactly how I’d hoped, but hopefully things will continue to improve in the future.


Now that we understand the process, we should talk about the drugs.

There are two major categories here: anticoagulants and antiplatelets. Antiplatelet drugs inhibit the initial step of platelet aggregation and adhesion, where they collect at the wound site in activated form and create a loose plug. Anticoagulants have no effect on this, but instead interfere with the production of fibrin, and therefore prevent a solid clot from growing.

As a general rule, the anticoagulants are rather more clinically significant, as far as their effects on bleeding.



First off, to be clear: tPA (tissue plasminogen activator) is not an anticoagulant of any shade. It is a thrombolytic; it attacks and degrades existing clots, dissolving their fibrin bonds. It has no role as a protective agent, and would be far too hazardous in such a role anyway; even its emergency use for acute events like ischemic stroke always requires careful weighing of benefit vs. risk — because the risks are significant.

With that said, there are two main anticoagulants we see frequently in the field.


Warfarin (Coumadin)

Coumadin is an old drug with an interesting backstory; one of its original uses was for rat poison. It’s given orally.

Nowadays, it’s mainly used for chronic anticoagulation of patients at high risk for embolic events. For instance, if you’re in atrial fibrillation at baseline, the blood in your atria isn’t being pumped downstream effectively, and tends to pool. We saw that brisk movement of the blood is one of the main ways we prevent clotting; A-fib is therefore a risk factor for hazardous clots. So when possible, these patients are covered by Coumadin or similar drugs.

The mechanism is interesting. Recall that for the activation of several factors, primarily in the extrinsic and common pathways (including thrombin and Xa), Vitamin K needs to be present. (For some factors, Vitamin K is also needed for the initial production of their inactive forms.) The process looks like this: in order for the factors to be activated, a second background process must also occur, where Vitamin K is changed into a form called Vitamin K epoxide. Once this is done, Vitamin K epoxide can be cycled back into Vitamin K, allowing it to be reused again for the next activation.

Coumadin prevents this second step. It allows the inital activation and conversion, but it blocks Vitamin K epoxide from being recycled to Vitamin K. So over time, as you use up available Vitamin K, it doesn’t get replaced, and you end up with less and less of it available. Less available Vitamin K means less activation of thrombin and its precursors, which means less fibrin, which means less clotting.

Obviously this process takes time. Since Coumadin has no effect on the active factors already present, if we start you on Coumadin today, it won’t have any effect for several days. We need to wait for currently circulating factors to degrade. So for newly anticoagulated patients, a more fast-acting drug is usually used to cover this loading period; heparin is common.

Other than its widespread use, warfarin is also famous for frequent misdosing. It has a narrow therapeutic index, where it’s very easy to give too much or too little, and depending on diet and other drugs, the appropriate dose can change daily. It therefore requires regular monitoring of the patient’s actual anticoagulation, which is done through a test called the prothrombin time (PT). This is a lab test that measures clotting time with an emphasis on the extrinsic and common pathways, and gives a result in seconds. Due to different PT tests available, a standardized result has been devised called the INR (or International Normalized Ratio). This is essentially a ratio of your clotting time over the standard clotting time; a normal result is therefore close to 1.0. Obviously, anticoagulated patients should have a longer clotting time, so 2.0–3.0 is more typical. Much higher than this puts one at high risk of bleeding — into the GI tract, into the lungs, into the nose and mouth, and if trauma occurs, the chance of significant bleeding is magnified. A too-low INR, of course, simply removes the benefits of protective anticoagulation.

In the event of overdoses that need reversal, patients can receive supplemental Vitamin K, as well as plasma (or concentrates) to replace the missing factors directly.



Heparin is another old drug. It’s actually a biological substance naturally present in the blood, one of the body’s own anticoagulants, and when extracted for pharmacological use it’s derived from sources like pig intestines. Lovely. You can’t take it orally, so as a rule it’s given by IV.

Compared to warfarin, heparin has a more direct mechanism. Recall that one of the antagonistic factors that works to deactivate thrombin (as well as a few other factors) is antithrombin. Heparin, when taken in therapeutic doses, multiplies the effects of antithrombin by several thousand times. It therefore deactivates far more factors, which are then unable to produce fibrin. Thrombin and factor Xa are two of the factors most affected.

You can already imagine that heparin will probably work much faster than Coumadin. Aside from being given intravenously, it’s not simply stopping the influx of new Vitamin K and waiting for the old factors to degrade; it’s actually going in and deactivating them directly. In fact, heparin takes effect within half an hour or so. However, its half-life is short, so it’s often given as a continuous drip. Obviously, its usage is typically for acute events, such as acute coronary syndromes, or the bridging to Coumadin we mentioned.

However, there is another version of heparin that’s available. To briefly describe the chemical structure of heparin, it’s a polysaccharide, or a repeating chain. When we cook this stuff from pig parts, we end up with a collection of heparin chains in widely varying lengths. The problem is that only chains of a relatively long length will deactivate thrombin. So depending on the actual size of our heparin molecules, unaltered heparin — known as unfractionated heparin — can be fairly unpredictable in its effectiveness as an anticoagulant.

Even very short chains, however, will deactivate factor Xa, and since Xa is a necessary precursor for thrombin, this has the same effect. So if we can produce an artificial product that only includes short heparin chains, then it will mostly affect Xa rather than thrombin, and its effects will be more predictable. This is called low molecular weight heparin, and it has several advantages. It’s easier to manage, it requires less close monitoring, and it has a longer half-life. In fact, it can be given once a day by subcutaneous injection; for instance, post-operative patients can be taught to inject themselves and sent home with the ability to manage their own anticoagulation. Most of these LMWHs end in -arin: enoxaparin (Lovenox), dalteparin (Fragmin), and tinzaparin (Innohep) are common. Fondaparinux (Arixtra) is also used; although technically not a LMWH, it’s very similar in all respects.

Heparin can be monitored by testing the partial thromboplastin time (PTT), which focuses on the intrinsic and common pathways. LWMH can, if necessary, be monitored by testing levels of factor Xa. Overdose leads to bleeding complications, and in a few cases heparin can induce a disorder called heparin-induced thrombocytopenia (HIT), causing a paradoxically elevated chance of clotting. Super-therapeutic levels can be reversed by protamine sulfate, which binds to heparin and prevents its utilization.


Dabigatran (Pradaxa)

A few brief words on this relatively new drug, only made available over the past year or so.

Dabigatran is an anticoagulant from a wholly different class known as direct thrombin inhibitors. Unlike the somewhat roundabout pathways of warfarin and heparin, these drugs inhibit thrombin directly, and may therefore be somewhat more predictable and easily managed.

In the case of dabigatran, it’s being marketed as a replacement for Coumadin. Although supposedly just as effective for chronic anticoagulation, its claim to fame is that it requires no monitoring of INR, which would be a huge burden lifted from patients and caregivers.

Still very new, it remains to be seen how widely it will be adopted. The main concerns about it are: 1. Cost, and 2. Reversal. Unlike warfarin, which in the case of hazardous events (the proverbial bonk-to-the-head with an epidural bleed) can be readily reversed by Vitamin K and fresh frozen plasma, there is no easy or clear method of reversing dabigatran. Some ideas are out there, but clinical experience remains scarce at this point. In any case, this drug isn’t too common yet, but you may start to see it more often.





Aspirin is probably in your medicine cabinet somewhere. It has widespread uses from analgesia to antipyretic effects, but also plays a role in platelet adhesion. It’s taken orally, although IV aspirin does exist, and is used both for chronic risk-reduction and acute treatment of coronary syndromes. This stuff is good enough that nearly everybody you know with wrinkles on their face probably takes it every day.

As platelets are activated and degranulate, one of the chemicals they release is thromboxane A2. It has several effects, including vasoconstriction of the immediate area and stimulating further platelet activation. However, it also promotes platelet adhesion by a pretty neat mechanism.

Remember fibrinogen? The inactive precursor of fibrin? Unlike some of the other inactive factors, this one has its own chance to be the star of the show. Fibrinogen can form a bond between activated platelets, attaching at their glycoprotein IIB/IIIA receptors and creating a link. This isn’t anywhere near as strong as a fibrin bond, but it’s enough to make platelets stick together and clump. Thromboxane activates glycoprotein IIB/IIIA receptors and allows the formation of these fibrinogen bridges.

Aspirin inhibits thromboxane release. Fewer fibrinogen bonds are formed, and less platelets adhere. Coagulation itself proceeds unimpeded, but there are fewer platelets in the clot to be married by fibrin.

Due to the widespread effects of aspirin, overdose is a complex subject. Altered mental status, neurological and cardiovascular signs, sensory disturbances (blurred vision or ringing of the ears), and GI problems are all possible. However, there are typically no obvious bleeding abnormalities. Treatment of acute toxicity can include attempts to limit the dosage (such as gastric lavage and activated charcoal), bicarb, supportive care, and if necessary hemodialysis.


Glycoprotein IIB/IIIA inhibitors

This mouthful of a name is another class of drugs from the antiplatelet family. They’re typically not used chronically like aspirin; one reason is because they’re given intravenously, with oral forms rarely seen. (Another reason is because they’re simply stronger drugs). We see these most often used during and after known coronary “events,” such as a STEMI, NSTEMI, or a coronary catheterization, at which times they can help prevent reocclusions.

Their mechanism is similar to aspirin. As we saw, fibrinogen binding to glycoprotein IIB/IIIA receptors helps bind together platelets and allows them to adhere and aggregate. GBIIB/IIIA inhibitors block these receptors by competitive binding, and hence prevent the fibrinogen bonds.

We rarely see these in the field, but common ones include: abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Adverse effects mainly involve bleeding.



Although there are a few drugs in this class, by far the most common is clopidogrel (Plavix). Think of these as an alternative, somewhat more powerful aspirin; they work similarly, have similar effects, and are used for similar purposes. Like aspirin, some people use it chronically and it can be given in acute events as well. It can “stack” with aspirin for a synergistic effect, or be used in its place for those who cannot tolerate aspirin.

Once again, the mechanism will sound familiar. One of the pathways that activates glycoprotein IIB/IIIA receptors requires the binding of adenosine diphosphate, or ADP. (ADP is more famous as the product of ATP once energy is released, but it has its fingers in a lot of cellular pies.) The thienopyridines block ADP binding and hence discourage platelet aggregation. Prasugrel (Effient) is another drug in this class.

Adverse effects generally involve bleeding diatheses.

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; ACE Inhibitors and ARBs