Reading Research: Diagnostics

Why do you do what you do when you do it?

Initially, we do it because we’re taught to. It comes down to us from on high, from instructors or textbooks — when you see x, do y — and we’re simply expected to learn it, memorize it, and recite it back. Then, once in the field, to follow it mechanically.

But before long, if we’re to become more than just medical Roombas, we really have to start asking Why. It’s not because we’re difficult children, or to satiate our curiosity. It’s because even at the best of times, the rules can’t address every situation. And in order to make intelligent, appropriate decisions when the circumstances aren’t clear and simple, we need to understand the underlying principles behind the rules we learn. We need to understand both the potential value and potential harm of the interventions we provide. We need to understand the meaning and importance of specific assessment findings. We need to be students of reality, and the human body, rather than of arbitrary rules.

In order to do all this, we need to be able to read research. Medical research is where these answers come from; it’s where we learn what works, and how well, and what importance to attach to the things we see. To read research, though, we need to understand the basic statistical methods they use.

Statistics is a big, big topic, and I don’t have a strong background in it, so if you really want to dive into this, take a class. The analytical and regressive methods used to crunch the data in a study are something we won’t touch here. But we do need to understand a few basic terms, because they’re central to how the results of a study are presented — in other words, if you’re looking for answers, this is the language in which they’re written. So although the idea of a post about statistics may sound as appealing as a brochure on anal ointment, bear with me; this won’t be too painful, and it’s information you can use over and over and take to your grave. Right now, let’s talk about numbers used to describe accuracy of diagnostic signs.

Sensitivity and Specificity

Take a certain test. It could be anything. A clinical finding. A laboratory test. Even a suggestive element from a patient history. Call it Test X.

Let’s say that this test is linked to a certain patient condition, Condition Y. Something bad. Something we want to find. In fact, Condition Y is the whole reason we’re looking at Test X.

What would make Test X a good test for Condition Y? Well, when the test says “You have Condition Y!”, then you should really have it. And if it says “You don’t have Condition Y!”, then indeed, you shouldn’t have it. It doesn’t have to be perfect. But it should be pretty good — otherwise, what’s the point in using the test? If it doesn’t tell us something we didn’t know before, we might as well ignore it.

When the test says “You have Condition Y,” and you really do have it, we’ll call that a true positive. When the test says, “You don’t have Condition Y,” and indeed you don’t have it, we’ll call that a true negative. Those are the findings we want; we want the test to tell us the truth, so we can base our treatments and decisions on reality.

On the other hand, when the test says, “You have Condition Y,” but you DON’T have it — in other words, an error, the test got it wrong — we call that a false positive. We thought you were positive, but whoops, you’re actually fine. And when the test says, “You don’t have Condition Y,” but it turns out that you do, we’ll call that a false negative, or a miss. The test cleared you, but it missed the badness; you actually do have the condition. These are the screw-ups.

How many true positives and true negatives does our test yield, versus how many false positives and false negatives? This determines how good our test is, how faithful to reality. The perfect test would have 100% true results, either positive or negative depending on the patient’s condition: if you have Condition Y, the test is positive, and if you don’t have Condition Y, the test is negative. There would be zero false positives or false negatives.

The worst possible test would have about 50% true and 50% false results. There would be no correlation between the test results and having the condition. In fact, it would be pointless to call this a test for Condition Y; we might as well flip a coin and call that Test X, because it would be just as useful.

Okay, so how do we determine the accuracy of a test? We take a bunch of patients, some of whom have Condition Y, and some of whom don’t, and we run them through Test X like sand through a sieve. Then we see which patients the test flagged, and see how accurate it was. (Obviously, we’ll need a way of knowing for sure who has Condition Y; this is usually done by a separate, “gold standard” test with known reliability. Correlation between Test X and the gold standard is what we’re examining here. Why not just use gold standards tests on all patients? Generally these are difficult, invasive, time-consuming, and expensive procedures — not appropriate for everyone, and certainly not of much use in the field.)

We’ll come up with a couple of figures. One is the test’s sensitivity. This describes how well our test picked up Condition Y; how alert was it, how often did it pick up what we’re looking for? If you have Condition Y, how likely is the test to say you have it? How many sick patients slipped past? If our test has 100% sensitivity, it will have zero false negatives; it will never miss, will never fail to flag a patient with Condition Y. A test with 0% sensitivity is blind; it will never notice Condition Y at all.

The other statistic is the test’s specificity. This describes how selective our test is, how cautiously it sounds its alarm. If you don’t have Condition Y, how likely is the test to say you don’t have it? Will it ever be fooled, and wrongly think that you do? A test with 100% specificity will never produce a false positive; if it shouts positive, it’s never wrong. On the other hand, a test with 0% specificity will never be right; it’s the boy who cried wolf.

Together, sensitivity and specificity describe a test’s accuracy. Intuitively, you can see how the two parameters might often work against each other; we can make a test that is extremely “paranoid,” and will catch almost everything — high sensitivity — but will also flag a great many false positives — low specificity. (Heck, we could just make a flashing red light that said “POSITIVE!” every single time, and we’d never miss anyone — of course, it’d have so many false positives that it’d be useless.) Conversely, we can make a test which is extremely judicious and selective, and when it says “positive,” we can trust that it’s probably right — high specificity — but it’ll miss a lot of true positives — low sensitivity.

Ideally, we’d like a test with high sensitivity and high specificity. But when that’s not possible, then at least we need to understand how to interpret the results.

For instance, a test with high sensitivity is very good for ruling a condition out. Because it almost always catches Condition Y, if the test says “nope, I just don’t see it here,” then that’s very trustworthy; if the patient did have it, the test probably would’ve caught it. Think SnOut: a test with good Sensitivity that comes back negative rules a condition Out.

Example: pinpoint pupils. For the patient with altered mental status, this is a very sensitive indicator of opiate use; almost everyone with a large amount of opiates in their system will present with small pupils. However, it’s not very specific, because many people will have small pupils without using narcotics (for instance, due to bright lighting). So if you don’t see pinpoint pupils, that finding rules out opiate overdose with fairly good reliability.

On the other hand, a test with high specificity is very good for ruling a condition in. Because it’s almost never wrong, if it says you do have Condition Y, you can take that to the bank. Think SpIn: a test with good Specificity that comes back positive rules a condition In. (Thanks to Medscape for these mnemonics.)

Example: a pulsating abdominal mass is an extremely specific finding in abdominal aortic aneurysm. Very few other conditions can cause such a pulsating mass, so if you find one, you can pretty reliably say that the patient has a AAA. However, many AAA patients will not have such a mass, so this is not very sensitive. But if you do find a pulsating mass, this rules AAA in fairly well.

Warning: Scary Statistics Ahead

Okay, that wasn’t so bad, was it?

Here’s where things get a little weirder. If you’re barely hanging on to the thread so far, you have permission to stop reading now.

Sensitivity and specificity are the most commonly used parameters describing the accuracy of a test. They’re properties of the test itself, so you can hang those numbers on it and they won’t change on you.

However, anyone who’s studied Bayesian statistics will understand that the true accuracy of our test is not only a factor of the test, but also depends on the prevalence of Condition Y in the population. If Condition Y is exceptionally rare in the patient group we’re looking at, then even if Test X is very specific, it will produce a large number of false positives. Conversely, if Condition Y is exceptionally common, then even if Test X is very sensitive, it will produce a large number of false negatives.

The reasons for all of this are complex. (For some additional reading, see here, and here.) But the general gist is this: if Condition Y is very unlikely to be present (either because it’s generally uncommon, such as scurvy; or because it’s an improbable diagnosis for the individual patient, such as an acute MI in an 8-year-old), then even if your test “rules it in,” it will still be unlikely. The positive test made it more likely, but it was so improbable to begin with, the odds didn’t change very much. And if Condition Y is very probable (such as a healthy heart in an asymptomatic teenager), then even if your test “rules it out,” the odds still support its presence.

What this all means is that in order to answer our real questions, we need another measure. The positive predictive value (PPV) and negative predictive value (NPV) are the answer, and really, these figures are what we’re after. The PPV answers: given a positive test result, how likely is the patient to have the condition? The NPV answers: given a negative test result, how likely is the patient to lack the condition? In other words, in a real patient, how likely is the test result to be correct?

The trouble is that PPV and NPV aren’t just characteristics of the test; as we saw above, they also depend on the prevalence of the condition, or the “pre-test probability.” What this means is that although the study you’re reading may report predictive values, they are not necessarily applicable to your patient. They’re only applicable to the patient population that was studied. Now, if your patient is similar to that population — in other words, has about the same pre-test probability of the condition as they did — then the predictive values should be correct. If not… not so much.

So do we have any more tricks? We have one more: likelihood ratios. Likelihood ratios factor out pre-test probability, producing a simple ratio that describes how much the test changed the probability. For instance, suppose we have a patient who we judge has a 10% probability of having Condition Y. We apply a test with a positive likelihood ratio of 5, and it comes up positive. What’s that mean? The math is a little bit roundabout, because we need to convert probability (a percentage of positive outcome out of all possible outcomes) into odds (a fraction of positive outcome over negative outcome): 10% is the same as 1:9 odds. 1/9 times 5 is 5/9, and if we convert that back to a percentage (positive outcome over total outcomes, or 5/14), we have the result: about 36%. The patient now has a 36% chance of having Condition Y. Conversely, suppose it came up negative, and the test had a negative likelihood ratio of .1. The post-test probability (by the same calculation) is now only around 1%.

It’s a simple device that would be far more intuitive without the odds vs. probability conversion, but suffice to say that a likelihood ratio of 1 (1:1) changes nothing, higher than 1 is a positive test (1–3 slightly so, around 5–10 is a useful test, and over 10 is highly suggestive), and less than 1 is negative (1–.5 just barely, around .5–.1 decently, and under .1 is strongly negative.) Try plugging numbers into this calculator to experiment — or drag around the sliders in the Diagnostics section at The NNT. The only bad news is that you still need to know the pre-test probability, but the good news is that you can come up with your own estimate, rather than having an inappropriate one already included in the predictive values.

How to come up with pre-test probabilities? Well, research-derived statistics do exist for various patient groups… but realistically, in the field, you will need to wing it. Taking into account the whole clinical picture, including history, physical exam, and complaints, how high-risk would you deem this patient? You don’t need to be exact, but you should be able to come up with a rough idea. Now, apply your test, and consider the results — about how likely is the condition now? If at any point, you have enough certainty (either positive or negative) to make a decision, then do it; there’s no point in tacking on endless tests if they won’t change your treatment.

Anybody still breathing? We’ll talk about odds ratios, NNT, and other intervention-related numbers another time.

[Edit 5/15/13: the follow-up post on outcome metrics is posted at Lit Whisperers, our sister blog]

People Care

This is the best book any EMT can own.

I say that as someone with a strong clinical focus, and a passion for improving and elevating the educational standards in our field. I am an avowed nerd, and drip rates, T-wave inversions, and case reviews are what keep me awake at night. Yet I consistently recommend this little “warm and fuzzy” booklet to new and experienced EMS professionals alike, and would place it before any electrocardiographic tome or trauma manual. It should be on the shelf of everybody who works on an ambulance, period.

Thom Dick is a longtime paramedic, as well as an author and speaker on the EMS circuit, and several years ago he collected many of his favorite topics into People Care: Career-Friendly Practices for Professional Caregivers. This is a paperback book of less than 100 pages, written in a personal and accessible style, and it compellingly lays out Thom’s idea of what this job is all about.

It’s not about job skills, or tips for getting through your shift, although some of these are offered. Rather, it’s really about how to understand your job — what lens you should use to view this whole EMS business. This may not seem especially important; after all, no matter what rose-tinted goggles you buckle on, you’re still going to end up bringing the same patients to the same places in the same ways (and making the same dollars for doing it). True enough. But what about you? Will you be happy doing it? Passionate? Driven? If you start out as those things, will you stay that way, or will you join the ranks of the angry, the apathetic, the disillusioned?

There are a lot of things wrong with this job. Depending on who you ask, and what their priorities are, you might get different lists. But certainly, EMS is an industry with flaws, and the men and women working to improve it should be seen as heroes. But even if things do get better, what will we do in the mean time? Hell, even after they get better, will you be happy? The goggles you wear can turn the best circumstances bad if that’s your attitude.

Thom’s work is the prescription. When we talked about Joe Delaney, I was channeling People Care; Thom’s kind of EMT is someone who views their business as helping the people who call for us, and who asks for no more than that (or less). It’s not a complicated outlook, but I think it is utterly, absolutely essential.

A lot of things are wrong with this job, but if you have the right lifeline, you can survive all of it and more. Thom’s been teaching these ideas for years now, and you might be surprised at how many of your colleagues and coworkers know him personally or have heard him speak. But if, like me, you haven’t been so fortunate, buy his book. Read it. Recommend it. Loan it out — it’s been out of print for years now. And see if it doesn’t bring some of your problems into perspective.

(I am indebted to Peter Canning for originally introducing me to this book, via his blog, Street Watch. Also of note: Steve Whitehead at The EMT Spot is an old coworker of Thom’s, and his site discusses many of these topics in a similar spirit.)

Polypharmacy in the Elderly

A tremendously valuable Educational Pearl from the wonderful UMEM mailing list, courtesy of Amal Mattu, emergency physician extraordinaire.

We already know that polypharmacy is a big issue in the elderly, but here are a few key points to keep in mind:

Adverse drug effects are responsible for 11% of ED visits in the elderly.

Almost 50% of all adverse drug effects in the elderly are accounted for by only 3 drug classes:
a. oral anticoagulant or antiplatelet agents
b. antidiabetic agents
c. agents with narrow therapeutic index (e.g. digoxin and phenytoin)

1/3 of all adverse-effect-induced ED visits are accounted for by warfarin, insulin, and digoxin.

Up to 20% of new prescriptions given to elderly ED patients represents a potential drug interaction.

The bottom line here is very simple–scrutinize that medication list and any new prescriptions in the elderly patient!

References
Samaras N, Chevalley T, Samaras D, et al. Older patients in the emergency department: a review. Ann Emerg Med 2010;56:261-269.
[Source]

The value of this is inestimable. We know that polypharmacy is a big deal, but it’s such a big deal that it can be hard to shrink down the problem enough to really consider it when an elderly patient presents themselves. Could their problem involve something on this med list that’s as long as your arm? Certainly, but where to start?

Start with the above. Over half of your problems will involve anticoagulants, antidiabetics, and easily misdosed drugs. Those are the usual suspects; they should jump out at you from the list. But we can do even better, because nearly half of those will involve one of three particular serial offenders: insulin, warfarin (aka Coumadin), and digoxin. And let’s add a fourth one: any new or recently modified prescriptions. If any of these are present in a patient with an appropriate complaint or presentation, it should be strongly considered as being part of the problem if not the actual smoking gun.

Insulin is easy, especially if you have access to finger-stick glucometry; diabetic emergencies (especially hypoglycemia), including iatrogenic ones, are so common that you might as well assume anybody with an altered mental status is diabetic — even if they aren’t. Definitive treatment is obviously oral glucose or IV dextrose, as appropriate.

Warfarin is still an extremely common anticoagulant, although a couple new alternatives are now available, and it requires close and frequent monitoring of levels in order to maintain a therapeutic dose. (The usual standard is a measure of clotting speed called INR; the test can be performed in the lab, but nowadays can also be done right at the bedside.) Various medication interactions and even dietary changes can shift this range. Overdose is associated with, no surprise, bleeding — in all forms. If necessary, supertherapeutic warfarin levels can be antagonized with Vitamin K or IV clotting factors.

Digoxin is seen less today than in yesteryear, but once upon a time everybody and their mother was on “dig,” and it’s still used with some regularity. Its most common application is for rate control of atrial fibrillation patients. Although other antiarrhythmics are now more common, dig has the peculiar magic of reducing cardiac rate while actually increasing contractility (negative chronotropic but positive inotropic effects). However, its therapeutic range is narrow and is easily shifted by pharmacological, renal, and other issues; as a result, dig toxicity is famously common. Overdose symptoms include GI problems and neurological complaints such as visual disturbances and changes in mood or energy level. It can also present prominently on the ECG, with the most classic sign being degradation of AV conduction with an increase in atrial and ventricular ectopy — for instance, slow A-fib or atrial tachycardia, a third-degree AV block, and a junctional escape with PVCs. (As a result, the atrial fibrillation patient controlled on dig may present with an unexpected “regularization” of his pulses, due to a junctional or ventricular escape taking over from the usual A-fib. This is a clue even the BLS guys can catch.) Treatment is supportive for arrhythmias and heart failure; severe cases can be managed with Digoxin Immune Fab (aka Digibind or Digifab).

Drug Families: Steroids and Antibiotics

When things go wrong
as they usually do —
Inflammation!

Inflammation

There are a lot of bad things that can happen to your body. Homeostasis, as we like to call it, is that smooth state when all your bits and pieces behave just as they ought to; and “bad things” are anything that knock this out of whack.

And what’s funny is that, no matter what that insult is, you can pretty much count on the body to respond with inflammation. Other, more specific things too, but inflammation will be there. It’s physiological duct tape: your basic, one-size-fits-all solution for any physical calamity.

Inflammation is caused by a complex blend of chemical mediators, but physically, the result is usually some combination of five classic signs.

Heat [calor]
Redness [rubor]
Swelling [tumor]
Pain [dolor]
And sometimes included, a general loss of function [functio laesa]

Try the Latin if you’re trying to impress someone at the bar.

Suppose you fall and bang your elbow, causing minor soft tissue damage. The body reacts immediately by activating a local inflammatory cascade, whereby numerous processes swing into gear. Local vasodilation occurs, bringing more blood into the area, to support faster healing; this increased bloodflow (hyperemia) produces the redness and warmth associated with injury. Vascular permeability is also increased, allowing fluid to leak into the surrounding tissue, which results in edematous swelling; this not only conveys healing factors into the damaged area, it also physically limits movement around the affected joint by “self-splinting.” Other chemical mediators increase your local sensitivity to pain, which further discourages you from movement; a decrease in the joint’s function is the result.

All of which is part of the inflammatory package. Neat!

The inflammatory cascade in soft tissue damage

Now suppose you catch a cold. Viral particles enter your mouth or nose, whether by direct contact or by inhaling them as an aerosol, and lodge somewhere in your oronasopharynx. Our response: inflammation! Your immune system recognizes the intrusion and responds with an influx of infection-fighting white blood cells, such as neutrophils and monocytes, along with the same cocktail of general inflammatory mediators (bradykinin, cytokines, etc.) that we saw with the injured elbow. The result? Swelling; excess mucus production; pain (as in sore throat); a general discomfort and sense of crumminess; and in more systemic cases, a fever to make the environment less hospitable for the virus.

It’s all the same story. When things go wrong, the body responds in various ways, but it’s almost always accompanied by some sort of inflammatory response to facilitate and assist the repairs.

Sometimes, however, this process becomes maladaptive. Whether it’s an immune response to infection or a local response to injury, short, appropriate, and effective inflammatory activity is a valuable part of our defenses — but if becomes too severe, lasts too long, or serves no purpose, then it can become part of the problem. For our bumped elbow, inflammation will promote healing, but if after a few days we find that the area is still swollen, this is no longer valuable; it’s impeding our ability to use the joint, which is what we need to do in order to circulate blood and encourage further healing. Our body’s response was excessive. So we apply ice to vasoconstrict the area, elevate the extremity, and take anti-inflammatory drugs, all to reduce that local edema and tamp down our inflammatory freak-out.

Numerous illnesses and injuries exhibit this sort of excessive, harmful inflammatory response. For example:

Traumatic brain injury is deadly because swelling within the cranium has nowhere to go, resulting in a self-feeding cycle of increased pressure and increased damage.
Sepsis occurs when an infection becomes widespread enough that it causes a system-wide inflammatory response, resulting in organ damage and vascular disruption — this cascade is self-feeding and can quickly become more harmful than the infection itself, even causing death long after the initial infection has been eradicated.
COPD and asthma are caused, in part, by inflammation of the lower airway (due to prior damage or various dysfunctions).
Shock kills early by hypoperfusion, but if that is survived, it kills later by an uncontrolled inflammatory cascade resulting from that hypoperfusion. If not managed early, this cascade can continue to spread independently of the original shock state.
The entire spectrum of autoimmune diseases is characterized by an inappropriate immune response to the body’s own tissues.
Allergic reactions, including lethal anaphylaxis, are hypersensitive immune responses to benign foreign agents like dust or foods.

To make a long story short, sometimes, inflammation sucks.

Steroids

Steroids are modern medicine’s answer. Steroids are a large class of molecule, including the anabolic steroids that “pump you up” and sex steroids like testosterone and estrogen, but what we’re interested in are glucocorticoids (sometimes called corticosteroids, which is actually a broader category, but the terms are often confused). Glucocorticoids are interesting hormones with numerous effects; as a matter of fact, they’re part of the “fight or flight” stress response we talked about before. (Put simply, catecholamines like adrenaline give you a boost to help deal with danger right now; glucocorticoids, on the other hand, give you a slightly more delayed “second wind,” so you’ll still have some juice a few hours later.) And fighting infections and healing injuries is a real waste of energy when we’re running from wild tigers. The result? Glucocorticoids inhibit the inflammatory response.

They can therefore play a role in the management of all the problems we just mentioned. Maintenance-type inhalers for asthma and COPD are often steroids. Anti-allergy nasal sprays too. Appropriate steroid use can be complex, because we must be careful not to over-inhibit our inflammatory system; for instance, although they would seem like an obvious answer to sepsis, their use for those patients is unclear and has long been controversial. Or how about using steroids to treat epiglottitis, an infectious swelling of the epiglottis that can obstruct the airway? We would expect the steroids to combat the swelling, but also to impair our ability to fight the underlying infection. So finding the balance can be difficult.

Corticosteroids can be administered locally, when a local effect is desired, such as via metered-dose inhaler for asthma. Or they can be administered globally for systemic conditions, such as by IV or oral routes for autoimmune conditions.

Antibiotics

Of course, sometimes the body is fighting for a reason.

As we’ve seen, the body responds with inflammation to a wide range of insults, but one of the most common is infection. And in the many cases of infection when our primary goal is simply to eradicate the source, pharmacological support can be beneficial.

Antibiotics are generally well-recognized as agents that kill bacteria. The terminology has become somewhat clouded nowadays, as the word “antibiotics” is sometimes used to strictly mean anti-bacterial agents, and sometimes to mean all anti-microbials, including anti-fungals and anti-virals. But the general idea of immunosupport is the same.

These agents generally work in one of two ways: either by directly killing the microbe, or by impeding its ability to replicate. They’re tuned so that they affect the bad guys without harming (not too badly anyway) our body’s own cells.

It’s therefore natural to think of antibiotic therapy as the natural opposite of steroids, and this has some truth to it. In the case of infection — which, remember, is not the only cause of inflammation — steroids do inhibit the immune response. But bear in mind that antibiotics do not, as a general rule, actually support or promote the body’s inflammatory response; rather, they work independently by attacking the infection directly along their own pathways. The result is that some pathologies (such as the contentious cases of sepsis and epiglottitis) may respond both to steroids — to manage the excessive inflammatory response — and antibiotics — to help eliminate the source infection.

Examples

Once again, remember that common drug suffixes are usually only applicable to generic drug names. Trade names tend to be unique.

Steroids

Drugs ending in -one (prednisone, hydrocortisone, clocortolone, etc.)
Drugs ending in -ide (fluocinonide, budesonide, desonide, etc.)
Drugs with pred in the name (prednisolone, loteprednol, prednicarbate, etc.)
Drugs with cort in the name (fluocortin, Cyclocort, Entocort)

Antimicrobials

Drugs beginning with ceph- or cef- are antibiotics of the cephalosporin type (cefixime, cephalexin, cefepime, etc)
Drugs ending in -illin are antibiotics of the pencillin type (penicillin, methicillin, nafcillin, etc.)
Drugs ending in -cycline are antibiotics of the tetracycline type (doxycycline, methacycline, etc.); not to be confused with the -tyline of tricyclic antidepressants.
Drugs ending in -azole are generally from a large family that can have antibiotic, anti-fungal, and anthelmintic (anti-parasitic) effects (metronidazole, fluconazole, miconazole, etc.). However, this does not include the -prazole drugs (omeprazole, pantoprazole, and others) which are actually proton pump inhibitors, with no antimicrobial effects.
Drugs ending in -floxacin are antibiotics of the quinolone type (levofloxacin, ciprofloxacin, etc.).
Drugs ending in -mycin are antibiotics of the macrolide type (azithromycin, erythromycin, etc.)
Drugs beginning with sulf- are antibiotics of the sulphonamide type (sulfamethoxazole, etc.)
Drugs ending with -adine are antivirals of the adamantane type (amantadine, rimantadine)
Drugs containing vir are generally antivirals (acyclovir, oseltamivir, ribavirin, efavirenz), including antiretrovirals for HIV treatment
Drugs ending with -vudine are antivirals (lamivudine, telbivudine, etc.)

More Drug Families: Stimulants and Depressants; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets

Drug Families: Stimulants and Depressants

There are many, many, many, many, many, many drugs.

And I think it’s noble and wise for a sharp EMT-B to learn as much as he can about as many of them as he can. General mechanism, typical routes, notable adverse effects and contraindications. The most common meds are encountered so frequently that you can’t help but become familiar with them.

But what about all the rest? (You remember those — many, many, many, etc.) Memorize them all? Maybe, but that’s a task on par with memorizing the map of London. I’ll freely admit that my own mental encyclopedia of pharmacology is weaker than it should be.

Use a reference? These are certainly handy; printed quick-books are available, as are digital versions you can access with a smartphone (Epocrates and Medscape are a couple good ones — see the Droid Medic for guidance). But we really ought to have at least a surface recognition of most drugs we come across, without having to consult an Ouija board.

Fortunately, 80-90% of the drugs you’ll encounter can be broadly categorized into a few major types. If you understand these types, and their basic physiological behavior, you’ll understand most of what’s relevant to your care; and it’s easy business to memorize which type a drug belongs to. So let’s go over some of these categories.

Some of these groups seem to fall naturally into matched opposites. So today, let’s discuss…

Stimulants and Depressants

Basically, it’s all about speeding up, or slowing down.

Most of us have heard of the “fight or flight” response, our body’s instinctive ability to step on the gas in times of need — an acute stress response that lets us climb trees, hunt mammoths, and escape from tigers. It’s the get-up-and-go state, and its physiological trigger is known to laymen as adrenaline. This is partly correct; in actuality, your body creates this high-output condition through a variety of hormonal mediators (including adrenaline, more commonly known in the US as epinephrine, but also dopamine and norepinephrine). Overall, this functionality of your autonomic nervous system is known as the sympathetic system.

Some of us have also heard of the reverse state of fight-or-flight, often called “rest and digest” (or sometimes “breed and feed”). This is the slow down, recover, repair, rebuild, and relax state; this is the brake to the sympathetic’s gas. Although slowing down is the last thing you want when escaping from sabre-toothed tigers, it’s just the ticket when you’re enjoying supper or having a snooze. This side of things is known as the parasympathetic system.

(How to keep these two straight? Try this mnemonic: the s in sympathetic is for “stress,” because this is your fight-or-flight stress response. The p in parasympathetic is for “peace,” because this is your peaceful, resting state. Thanks to Mark O’Brien for this one.)

Together, these two systems keep your body tuned like a guitar string. It’s a mistake to think that when one is active, the other is switched off; actually, they’re both active at all times, merely to different degrees. Although their combined results are directly antagonistic, they’re independent systems, which means that you can have a mixture of a little sympathetic, a lot of parasympathetic, vice versa, a lot of both, or any combination thereof.

Think of it like the hot and cold knobs on your sink. You adjust them separately, but the result is a single water temperature. A little hot and a little cold will give you warm water, but so will a lot of hot and a lot of cold. And if you want to cool it down, you can either turn up the cold, or turn down the hot. Simple.

Well, the secret is that many of the drugs we use in medicine function primarily by adjusting this balance.

A drug that turns up the sympathetic system (thus “speeding you up”) is known as a sympathomimetic. A drug that turns down the sympathetic system is known as a sympatholytic.

A drug that turns up the parasympathetic system (thus “slowing you down”) is known as a parasympathomimetic. A drug that turns down the parasympathetic system is known as a parasympatholytic.

Okay, so those are mouthfuls. But the important thing to remember is that, while they’re not identical, the result of both a sympathomimetic and a parasympatholytic will be to support your fight-or-fight responses (run from the lion!), and the result of both a parasympathomimetic and a sympatholytic will be to support your rest-and-digest behavior (take a nap!). So whichever end you approach it from, there are still only two important end results here — up and down.

Virtually the entire body is controlled by these systems. If you can keep track of how each organ system is affected when you nudge this balance one way or the other, you’ll be able to understand a great deal of how drugs do their work.

For instance, consider epinephrine itself, which we use in auto-injectors to treat severe anaphylaxis. The life-threatening effects of an allergic reaction are primarily shock, due to vascular dilation, and respiratory distress, due to bronchial constriction. Epinephrine is a sympathomimetic (okay, “mimetic” means “mimick,” and epinephrine is actually one of the body’s own sympathetic hormones, so it’s not really mimicking anything — but bear with me here). So it produces a fight or flight response. What is the sympathetic effect on the skin and peripheral vascular system? Vasoconstriction (to pull blood away from the periphery into the core). What is the sympathetic effect on the lungs? Bronchodilation (to allow for greater air exchange during exertion). So the entire cocktail of epi’s beneficial results in anaphylaxis comes from stimulating sympathetic tone.

What if I shoot some heroin? My breathing will become slower and weaker. My level of consciousness will decrease. I will become generally slowwww, because heroin (like all opiates) is fundamentally a depressant. And my pupils, pleasantly parasympathetic, will constrict — the third hallmark sign of opiate use. Who needs light when we’re relaxing?

Subtypes

Now, not all drugs from the same neck of the woods are identical, of course. The effects of the same neurotransmitters can be radically different depending on where they bind. An important distinction should be made between non-selective drugs like epinephrine, which binds with all of the primary adrenergic receptor sites (alpha-1, beta-1, and beta-2), and selective agonists like albuterol, which primarily binds only at certain receptors (beta-2 in that case). In brief:

Alpha-1 (properly styled, α₁) receptors are mainly in the blood vessels, and cause systemic vasoconstriction. Alpha-1 blockers, or antagonists, therefore cause systemic vasodilation.
Beta-1 (β₁) receptors are mainly in the heart, and increase heart rate and contractility. Beta-1 antagonists therefore slow and reduce cardiac output. (Mnemonic: you have 1 heart.)
Beta-2 (β₂) receptors are mainly in the lungs, and cause bronchodilation. Beta-2 antagonists therefore cause bronchoconstriction. (Mnemonic: you have 2 lungs.)

Naturally, none of these categories tell the whole story of a drug. (If they did, we wouldn’t need so many different ones.) Caffeine, atropine, and crystal meth are all very different drugs, even though they all fall roughly into the category of stimulants. But you can keep track of a good deal of their shared effects by understanding their common nature.

Examples

Drugs ending in -zepam (or sometimes -zolam — eg. diazepam, triazolam) are benzodiazepines, which have broad sedative effects.
Drugs ending in -alol (or -ilol, -olol — eg. atenolol, labetalol) are beta blockers, which have a sedative effect, usually localized to the heart via beta-1 antagonism.
Drugs ending in -erol (e.g. albuterol, clenbuterol) are beta-2 agonists, or bronchodilators; they are stimulants that primarily cause bronchodilation via beta-2 receptors.

Most pain killers, sedatives, and anesthetic agents are depressants.

Note: most common suffixes are only applicable to generic drug names. Trade names are usually unique.

More Drug Families: Steroids and Antibiotics; ACE Inhibitors and ARBs; Anticoagulants and Antiplatelets

Helping

“He always said if there was any way he could help someone, he would.”

Carolyn Delaney

Not too many people know about Joe Delaney anymore.

He was a running back. Played for the Kansas City Chiefs, just a couple seasons — 1981 and ’82. Played high school and college ball before that, and ran track too. He was very good.

Delaney looked like he’d make a real mark in the NFL, but his career was short, and nowadays he’s been mostly forgotten. Sure, he held some long-standing records, but who hasn’t?

His claim to fame was something different.

One day in the summer of ’83, at a park in Monroe, Louisiana, three young children waded out too far into an artificial pond, floundered, and began to drown. Delaney, nearby, heard their cries for help. Although unable to swim, he immediately dove into the water to attempt a rescue.

The situation was chaotic, stories differ, and any definitive account of the events has been lost over the years. Whatever happened, the aftermath found Delaney drowned alongside two of the children; the third had made it to safety. One of the victims had eventually been rescued, but died at the hospital; the other was recovered by divers, DOA, along with Delaney himself.

This is an EMS website, and I’m not retelling this story as a teachable moment. As public safety professionals, we instinctively turn up our lip at Delaney’s actions. “Noble, but foolish,” we quip; becoming a victim, or a martyr, is no help to anyone. Perhaps the American Red Cross tells this same story in its lifeguarding courses to illustrate the importance of safe rescue methods. I’m certainly not recommending diving into pools if you can’t swim, or running into burning buildings without protection, or jumping out of planes without a parachute. This isn’t about heroism.

I want to use Joe Delaney’s example to illustrate something else.

“People ask me, ‘How could Joe have gone in that water the way he did?’ And I answer, ‘Why, he never gave it a second thought, because helping people was a conditioned reflex to Joe Delaney.’ ” (Sports Illustrated, 1)

He was fast, and he could handle a ball, but those weren’t the kind of stories people told about this rookie running back. Instead, they talked about how he “… mowed this woman’s lawn in the dead of Louisiana summer…” “… gave this person money to get through a bad stretch…” “… turned this child away from drugs…” And how every time, he did these things without question, without hesitation. Merely out of a basic, instinctive drive to help people.

Our job as EMTs is to stabilize. Treat and transport. Provide field assessment and triage. Activate appropriate resources. It’s medicine, or it’s public safety. Or something.

There’s a lot of somethings, and I’m not sure if I can remember them all the next time the tones drop. For sure I don’t think we’re getting paid enough to do ten different jobs.

But then there’s Joe Delaney.

“He always said if there was any way he could help someone, he would.”

Just that. If there was a way — any way — that he could help another human being, he would. That was only criterion. Simplicity itself.

What if that was the attitude we adopted? What if that was the job of the EMT?

The nice thing about wanting to help is that it’s pretty simple. When that’s all you want, you don’t need much more.

Joe Delaney was known for his thriftiness, for living simply even after going pro.

“Don’t you want nothing for yourself?” Carolyn would ask Joe.

“Nah,” he’d say. “You just take care of you and the girls.” (Sports Illustrated, 2)

And it’s funny. But when you view your job as helping your patients, in any way you can, a lot of other stuff seems to fall by the wayside. Is transporting this sort of patient your business? Do you really need to fluff this pillow? I don’t know; does it help? If it does, does anything else matter?

Naturally, there are things to consider. Because typically, the way we can help is through clinical intervention, through skilled medical assessment and treatment. If we helped in another way, they’d call us something else, like “plumbers” or “dentists.” And if we’re better at our craft, we can help more. That’s why we open the books and palpate the rubber mannekins. Because we recognize that if Joe did know how to swim, more lives might have been saved that day.

But the technical aspect is a means to an end, and just one means of many.

If you ask around the base, and people are truly honest, many will admit they got into this job at least partly from a desire to help people. It’s an organic urge, and a good one, and it brings us to the table, but then the years and the worries and the details of how and why and but… start to muddy the waters, and at some point we find ourselves forgetting that basic passion. Striving towards other goals. Elevating the details. And sometimes that’s okay.

But the next time we roll up those garage doors, maybe we can think back, and remember what matters. Maybe we can take a page from Joe Delaney, and every day assert this simple promise: if there’s any way we can help someone, we will.

Lifting Things Up and Putting Them Down

It’s interesting to consider the things we do that come to symbolize our roles. Sometimes, they make sense: the pilot would not feel like a pilot if he did not fly planes, because flying planes is why his job exists. His day may consist of 99% paperwork and 1% flying, but flying is nevertheless sine qua non for piloting. At other times, the symbol is more metaphorical than real; for instance, the white lab coat has come to symbolize the physician’s trade (new graduates even receive them in elaborate ceremonies), despite the fact that a doctor’s job is not to wear coats.

Many paramedics consider endotracheal intubation to be an important part of their identity, for reasons that are unclear, but probably related to the drama, the skill, and especially the exclusivity of the act; relatively few players in the medical field are permitted to intubate, so the medic is proud of the privilege and responsibility. (Obviously, this has nothing to do with whether or not putting tubes down throats helps anybody, but that’s a topic for another day.) And in the public’s eyes, throwing a stethoscope around your neck will instantly identify you as a medical professional.

With all of that said, however, on a typical day we can do our job very well without an ET tube or a dangling scope; those are tools, but not essential tools. We do have essential tools, but they are often nothing more than boring, everyday practices, and as a result we don’t talk about them as much as we should. Know what the biggest one of all is?

Lifting

EMS is not the infantry, or even the fire service, and the level of physical fitness required to do our job is… well, let us say that most of us live up to the requirements, and no more. We rarely run anywhere and the most we’ll sweat is during a stairchair carry or the occasional chest compression. However, one physical ability is part of our job description, and that’s the ability to lift patients.

All of us do this countless times a day, whether we’re large or small, male or female, tall or short. It’s therefore tempting to say that it’s not difficult, and that even the weak can do it. The truth is, though, that a strong individual, lifting with excellent biomechanics, is simply better in this business than a weaker colleague. The difference is not always obvious, which is why both strong and weak do manage to survive in this job, but you can also “survive” in this job being barely literate or mostly blind, and nobody would doubt that those negatively impact your work. Strong people transfer patients from stretcher to bed smoothly and without bumps or drops. They can easily maneuver the unconscious patient out of the cramped, awkward corner he’s found in. And most of all, they can always, always lift and carry anyone, without requiring either extra assistance or elaborate workarounds. We all know the tiny EMT who’s otherwise a fine partner, but who needs to call for a lift assist in order to boost the stretcher when there’s anything heavier than a bird’s nest on it — and while this is often not a problem, and we may know and love that EMT, he would be a better EMT if he could lift more, and that’s simply that. More selfishly, he would also remain physically capable of doing this job as long as he cares to, no small feat in a field where back injuries are more the rule than the exception.

The good news is almost anyone can learn to lift and get stronger. In my opinion, the easiest approach to this is a simple linear strength program using barbells — and although for novices, a broad and well-rounded program is ideal, the single most important lift for the EMT is undoubtedly the deadlift.

The deadlift involves bending over, grabbing an object with your hands, and standing up. This is the exact movement that you execute when lifting a stretcher, and variations of it are used in everything from carrying the stairchair to performing a fore-and-aft lift. The primary driver of this movement is extension (straightening) of the hips using the glutes and hamstrings, and the primary static challenge is maintaining a straight and rigid spine against the load trying to round it forward, which is the job of the spinal erectors. The hips are the engine, the back is the transmission.

Extension of the knees, which is performed by the quadriceps, is generally considered a secondary driver in the deadlift, since it’s weaker than hip extension. However, performing the lift with the butt lower and torso more upright does have the advantage of keeping the spine more vertical, which makes it easier to prevent it from rounding during the lift. Although you can lift in complete safety with a very horizontal back, and the more vertical stance does limit the weight you can lift, this is generally considered a good tradeoff in EMS (where we’re not trying to lift maximal weights, so much as lift many submaximal weights in complete safety). This is why the occupational safety poster on the garage wall tells you to “lift with your knees, not with your back” (a clumsy way of saying to bend the knees more and the hips less, remaining fairly upright; you never really “lift with your back” unless you’re doing things very wrong).

The “sumo” deadlift, which uses a wider stance, more upright posture, and arms inside (rather than outside) the legs, is the closest approximation to how we typically lift a stretcher. It lets us get as close to the load as possible, which again reduces the shearing force on the spine; the conventional (non-sumo) deadlift tends to force us to lift with the load dangling out in front of us, because our knees get in the way. But no matter what, the primary challenge is to maintain a flat, rigid back, and deadlifting trains us to do this by teaching the proper posture, as well as improving our ability to hold that posture against heavy loads by taxing and strengthening the erectors.

For the purposes of this job, it is probably worth training both the sumo and conventional deadlift. My own background is primarily with the conventional, so I have some bias, but even if (like me) you primarily “pull” with conventional form, it’s worth practicing the sumo on occasion, in order to master the technique — again, when you lift stretchers and other real-life items, it’s generally more sumo than not. In sumo style, the movement of lifting a stretcher can be replicated exactly in the gym using a barbell, with the exception of the position of your palms, which are supinated (underhand, or palms forward) on a stretcher, but pronated (overhand, or palms in) with the barbell. Deadlifting heavy with a supinated grip carries some risk of shoulder strain or tearing a bicep, so it’s not worth practicing.

It’s difficult to put numbers on things, and your ability to use the right tricks and techniques in the field may let you get away with less muscular strength. But in my humble opinion, a good goal for every working EMT or paramedic should be to safely and manageably (that is, not as a back-breaking, hitching maximal lift, but something you could perform for repetitions) deadlift 200 pounds. For small females, this may be a substantial challenge that requires some training. Many moderate-sized to heavy males will be able to pull this weight with no training; those individuals should aim for 300+ pounds. 300lb is a deadlift that will allow you to handle 99% of what this job throws at you.

These are not serious weights. True strength athletes deadlift many times this (I pull around 435 myself, and am not even close to being strong), and I’m not suggesting you go down that road, although if you enjoy the training, it has many benefits. Rather, this is a readily achievable milestone, low-hanging fruit that any healthy individual who does this job should be able to work towards within a period of several months. And once strength is obtained, it’s a fairly durable adaptation; unlike some physical skills (such as cardiovascular endurance), it sticks with you even if you’re no longer training it. Once you’re there, it would be good to keep lifting at least once a week or so, but even if you do not, the daily exertions of the job should be enough to largely maintain your level of strength. This is a gift that will keep on giving, and it’s very worth setting as a goal.

Vital Signs: Blood Pressure

For other Vital Signs posts, see: Respirations and Pulse

In the grand scheme of medical skills, taking a manual blood pressure is far from difficult, but sick people and austere conditions can combine to make it another thing entirely. Obtaining a BP on an ill patient while rattling down the road is legitimately one of the most difficult psychomotor skills an EMT-Basic has to master.

Mastering it starts with stacking the odds in your favor. A good stethoscope is better than a lousy one — you don’t need a $500 cardiology model, but something with good insulation and tight-fitting earpieces can make a real difference. Of course, you’ll also want to try to take your blood pressures at times of peace: on scene, before the rig starts moving, or even shoehorned in while stopped at traffic lights.

The elbow-supported technique for finding the brachial pulse is also ideal for taking a BP; trying to hear anything when the arm is slightly flexed is a recipe for frustration. But ensure that however you arrange things, the arm is completely relaxed, because muscular tension can radically throw a measurement; this will require fully supporting the arm and sometimes reassuring the patient. “Just relax” is the line I always deliver while busily pumping the bulb.

Where to put the gauge? Wherever. I’ll usually clip it to one of the stretcher straps, but you can find a bit of blanket that it’ll nestle into, secure it to a shirt, clip it to your watchband or the edge of the cuff, or just ask the patient to hold it for you. The built-in strap on the cuff is only a good location if you’re at the patient’s right side, which is typically not where we sit while we’re transporting. There’s probably a huge market niche out there for “EMS style” cuffs with their handedness reversed… but I digress.

Although I don’t always follow all of these steps, here’s the basic approach I recommend for a routine blood pressure check:

Support the arm, ideally at a position that is horizontally level with the heart.
Palpate the antecubital fossa until you find the pulse point. Note this location.
Palpating at the radial or the AC, pump up the cuff until you lose the pulse. Note this number and deflate the cuff.
Place your scope on the AC and inflate the cuff past the previous number. Obtain your pressure in the ordinary fashion.

Starting with a palpated pressure may seem redundant, and it can be, but it has two advantages: first, it gives you a rough sense of what systolic to look for, and second, if you’re unable to auscultate a pressure, you’ll still have a palpated one to record. This is actually the officially recommended method, although it seems rarely done nowadays.

Palpated pressures are legitimate, although when they start becoming the norm it can be a sign of lazy care. The diastolic can be a valuable number, though, particularly in traumatic or cardiac cases, so remember that auscultating is still the default standard of care. And remember, particularly if you’re mixing methods, that palpated pressures often will differ from auscultated pressures (including those taken by machine), usually by 10-15 points on the low side.

What if you’re not getting anything from the arm? Well, you can try the other arm, of course. But really, the thing to remember is that you can take a blood pressure anywhere there’s a pulse, although it’s much easier when that pulse is strong and the artery proximal to it can be easily occluded. Remember that although you can palpate a pressure from any distal spot on the same artery, near or far (barring anastamoses), auscultation — which is essentially listening to the turbulence created immediately downstream of the occlusion — requires placing your scope just below the cuff, and will not be successful farther downstream. Putting the cuff (pedi cuffs when needed) on the forearm and measuring at the radial is effective; thigh cuffs work too, although the popliteal can be an evasive pulse to locate. You can even cuff the lower calf and palpate a pedal or tibial pulse, if you’re daring. Go nuts, and try to experiment before the call when you actually need it. Do make an effort, though, to use an appropriate sized cuff for the extremity; mis-sized cuffs can actually yield significantly erroneous readings. For the morbidly obese, I usually prefer to place a regular cuff on the forearm than to use a thigh cuff on the upper arm, but see what works for you.

As a final note, remember that cuffing the neck and palpating the temporal pulse is never an appropriate method of patient assessment, no matter how little blood you may suspect is reaching their brain.

On maintenance: during your morning checkout, pump some air into the cuff, close the valve and give the whole thing a squeeze to check for leaks. There’s nothing better than discovering these after you’ve wrapped it around a critical patient’s arm.

On sphygmomanometers: for obvious reasons, the resting point for the needle should be at zero. (Very cheap cuffs sometimes have a pin-stop here for the needle to rest against; this is a problem because the dial can be miscalibrated without showing it. Pin-stop gauges shouldn’t be used unless your service is seriously broke.) If you have one that needs zeroing, most cuffs can be adjusted by pulling the tubing off the dial, grasping the metal nipple with some pliers (or very strong fingers), and twisting it in either direction until the needle is zeroed. Alternately, fans of mental math can just add or subtract the false “zero” number each time they take a pressure.

And finally, on tourniquets: the immortal Dr. Scott Weingart of Emcrit has described his practice of using BP cuffs as tourniquets. You’ll hear about this from time to time, but there’s always someone who points out the damned things leak like sieves and that’s the last property you want in a tourniquet. Dr. Weingart’s solution is to pump up the cuff until bleeding is controlled (or 250mmHg, whichever is sooner), then clamp both tubes with locking hemostats. (He uses smooth ones to avoid damaging the rubber; he recommends padding with a 4×4 if you’re using a ridged hemostat.) My hemostats are all in the shop, and this may or may not fly with your agency — modifying equipment for “off-label” use is always somewhat shaky ground for us field peons — but I think it’s a splendid idea if you can swing it.

Vital Signs: Pulse

For other Vital Signs posts, see: Respirations and Blood Pressure

Ah, the almighty pulse. If I have a favorite vital sign, this is it; let me lay hands on a patient and take a pulse and my assessment is already well under way.

On the conscious patient our go-to point is the radial pulse, and like golf, mastering the radial is all in the grip. Techniques may vary here, but I always find the radial easier to palpate if you approach from the ulnar side of the arm, coming “underneath” rather than over the top of the radius. This also lets you take a pulse while easily holding onto their limb, rather than forcing you to find a place to rest it, or supporting the arm with one hand while you palpate with the other. Just grab and count, very natural. If you have no luck, you can always keep hold of their arm while using your other hand to do some searching.

The textbooks always seem to show this being done with two delicate fingers, which is silly; more fingers means more coverage, so I always use at least three. (Your little finger is kinda short, otherwise it’d be four.) Use a moderate pressure, but if you’re having trouble, try pressing both lighter and firmer, as well as moving to different spots. (While I usually wear my watch in the normal position, you’ll notice here that when taking a pulse this way, I flip it around my wrist so I can see the face.)

The main way to ensure you’re never baffled by the pulse, however, is by always being willing to look elsewhere. Some people simply won’t have a radial, and this fact may or may not have significance — it may mean they’re hypotensive, or that their arm is locally hypoperfused, but it also may be a chronic condition. Hemodialysis patients with arterio-venous fistulas in their arm are especially notorious for having peculiar or absent radial pulses, as the arteries near the fistula have been scavenged and rerouted. Make like a picky renter — go elsewhere!

Your next attempt after the radial should be the brachial. Now, in classes and textbooks I have always been taught to look for a radial in the upper arm, beneath the bicep, but I’ve never had luck with this. Rather, my target is the antecubital fossa, the same territory made popular by blood pressures and large-bore IV sticks.

Again, positioning is key here. To effectively feel this pulse, the elbow should be in full extension, but relaxed. Depending on the patient’s position, you may accomplish this by wrapping your arm around theirs and holding their elbow in your hand, but from your bench seat in the truck, an easier way to do it is to simply rest their elbow on your knee. (Either way, it’s important to support them at the elbow, because this allows gravity to force their arm into extension.) The brachial can be a real lifesaver when a radial isn’t forthcoming, and I go to it readily and often.

Logically, the next step would be a carotid pulse, but the truth is that on conscious, alert patients, this is always a little awkward; people don’t like having their neck touched. If they need it, they need it, but for the routine pulse check, I try to steer clear. The same goes for a femoral pulse, for the same reasons; there was a story at my old service of a brash young EMT who got canned for “feeling a femoral” on an inebriated coed from a campus we served.

Instead, if I can’t find a radial or brachial on either arm, I’ll often take an apical “pulse,” simply auscultating at the chest for heart sounds. This is not, strictly speaking, a pulse, insofar as it’s not counting actual perfusing beats so much as counting any cardiac noise (it therefore tells you nothing about blood pressure), but it’s a good fallback — and if you’re very suave it can even yield additional clinical information, regarding murmurs, rubs, etc.

Here are a some other tricks that can be useful:

Inflate a BP cuff and count the bounces on the sphygmomanometer needle. Although this is not an indicator of systolic or diastolic pressure, it is a legitimate way to measure a pulse.
If pulse oximetry is available, the device will usually calculate a pulse for you, and if there’s a displayed waveform you can also confirm it from that.
The aforementioned AV fistulas can be used to your advantage. Gentle palpation of visible, active fistulas should let you feel a pulsing vibration called a thrill (an indicator of healthy flow), and this is easily counted for an accurate pulse rate. (Auscultating at the fistula should reveal a buzzing sound called bruit, which can be used similarly.)
If you’re able to locate a difficult pulse point, such as a dorsalis pedis, X’ng the spot with a pen can make subsequent checks much easier.
Lowering the arm below the level of the heart can occasionally make a radial more readily palpable, especially in hypotensive situations.

Finally, when all else fails, remember your perpetual fallback: skin signs. A patient with no available pulses and no obtainable blood pressure can still give you a general sense of perfusion, both centrally and to each extremity, if you assess the color and temperature of his skin. (This is especially valuable for infants, for whom proper pulse checks can be difficult, and blood pressures even more so.) And then there’s the sidekick to this, which is capillary refill. Current teaching is that cap refill is not a meaningful sign except in the very young, because numerous chronic conditions can cause delayed refill without poor arterial pressure, and this is true; a slow cap refill in an adult shouldn’t mean much to you. However, a rapid refill is still a pretty specific sign of good perfusion, because there’s not many conditions that can fake that (with the possibly exception of distributive shocks, such as septic or anaphylactic). A quick pat-down is an ever-ready way to rapidly assess anyone’s hemodynamic status within a couple seconds.

Vital Signs: Respirations

In the eyes of many EMTs, taking vital signs is BLS bread and butter. I’m not sure if I agree, since there’s other butter I’d hate losing more, but unquestionably vitals are something we do an awful lot of and probably ought be good at. Mainly, it’s the big three: pulse, pressure, and respiratory rate (the fourth vital sign is temperature, which is not considered vital prehospitally, and the de facto fifth sign is O2 saturation, which is not always available).

But woe unto the poor freshly-anointed Basic who enters the field and discovers that taking a blood pressure off his classmate at a quiet desk has almost nothing in common with playing hunt-the-Korotkoff on an elderly PVD patient in the back of a vehicle that sounds, to the layman, almost indistinguishable from a steam locomotive. With experience, we figure it out and we get by, but I’m always interested in the tricks that people have come to rely on, and here are some of my own. Let’s start with…

Respirations

The man who said that any blind monkey can count respirations has never tried it on sick people.

The first challenge here is getting away with staring at someone’s chest without giving them the skeevs. Women may be a little more wary about this, but if you’re unsubtle enough even men may ask if you “like what you see.” One method is a classic: while taking a pulse, count your beats and then start counting respirations without looking away or dropping their wrist. It gives you an excuse to stare blankly, and the patient is rarely the wiser. Good multitaskers can even count a pulse while simultaneously counting respirations over the same interval of time, although this is a bit much for my own second-tier brain.

Alternately, you can place yourself out of the patient’s field of vision, a technique that girl-oglers will recognize. In the back of the rig, you can usually pull this off by simply moving behind the stretcher — the captain’s chair is often too far, blocking your vision unless the stretcher is very reclined, but moving to the end of the bench seat is usually far enough and more convenient anyway.

How about the shallow respirations that virtually can’t be seen? You can put a hand on their chest to feel, but this is a little weird in the conscious patient and again betrays your intentions. You’re better off maximizing your visibility. Make sure there are no piles of blankets or folds of clothing in the way, and try watching both the abdomen and the thorax, as different people breathe in different fashions. If you’re still having no luck, auscultate! Place your stethoscope and count from the lung sounds. In fact, respiratory distress patients will sometimes produce wheezes or crackles that are audible from the bedside, allowing you to get a count with the naked ear.

Some texts recommend counting for at least 30 seconds; this is accurate, but feels like a geological epoch. Unless respirations are highly irregular, I count for 15. That does mean that your results will always be a multiple of 4, but here’s a way to improve it: count partial breaths as well. If you start with the chest “up” and 15 seconds later end on a “down,” call it a half stroke — so 4.5 x 4 would mean a respiratory rate of 18. You can get even fancier with quarter-strokes but that may be a little silly unless their rate is very slow.

A final note: “ehhh, looks normal” is not a valid method for counting respirations. There are times for estimation, but one hospital-based study showed that an overwhelming number of patients were documented at triage as breathing exactly 16 times a minute. A statistical miracle! In other words, you’re not as good at eyeballing as you think; take a few seconds and do your job.

For other Vital Signs posts, see: Pulse and Blood Pressure