Tag: assessment

Get Up, Stand Up: Orthostatics

Orthostatic vital signs. Nurses think they’re a pain in the neck. Some doctors think they’re of marginal usefulness. Many providers simply think they’re a dying breed.

Like many old-school physical exam techniques, though, they’re dying only because high-tech imaging and laboratory techniques have largely replaced their role. And I don’t know about you, but my ambulance doesn’t come equipped for an ultrasound or serum electrolytes. Diagnostically, EMS lives in the Olden Days — the days of the hands-on physical, the stethoscope, the palpation and percussion, the careful and detailed history. For us, orthostatics have been and still are a valuable tool in patient assessment.

How are they performed? Orthostatic vital signs are essentially multiple sets of vitals taken from the patient in different positions. (They’re also sometimes known as the tilt test or tilt table, which is indeed another way to perform them — if you have a big, pivoting table available. Postural vitals is yet another name.) They usually include blood pressure and pulse, and are taken in two to three positions — supine (flat on the back) and standing are the most common, but a sitting position is sometimes also included, or used instead of standing. This is useful when a patient is unable to safely stand, although it’s not quite as diagnostically sensitive.

Why would we do such a dance? The main badness that orthostatics reveal is hypovolemia. With a full tank of blood, what ordinarily happens when I stand up? Gravity draws some of my blood into the lower portion of my body (mostly these big ol’ legs). This reduces perfusion to the important organs upstairs, especially my brain, so my body instantly compensates by increasing my heartrate a bit and tightening up my vasculature. No problem. However, what if my circulating volume is low — whether due to bleeding, dehydration, or even a “relative” hypovolemia (in distributive shocks such as sepsis or anaphylaxis)? In that case, when my smaller volume of blood is pulled away by gravity, my body will have a harder time compensating. If it’s not fully able to, then my blood pressure will drop systemically.

“But,” you cry, “surely this is all just extra steps. Can’t I recognize hypovolemia from basic vital signs — no matter what position you’re in?”

Well, yes and no. If it’s severe enough, then it will be readily apparent even if I’m standing on my head. But we routinely take baseline vitals on patients who are at least somewhat horizontal, and this is the ideal position to allow the body to compensate for low volume. By “challenging” the system with the use of gravity, we reveal the compensated hypovolemias… rather than only seeing the severely decompensated shock patients, who we can easily diagnose from thirty paces anyway. Like a cardiac stress test, we see more by pushing the body until it starts to fail; that’s how you discover the cracks beneath the surface.

Do we run on patients with hypovolemia? Oh, yes. External bleeding is a gimme, but how about GI bleeds? Decreased oral fluid intake? Increased urination due to diuretics? How about the day after a frat party kegger? Any of this sound familiar? It would be foolish to take the time to do this when it won’t affect patient care — such as in the obviously shocked patient — but there are times when what it reveals can be important, such as in patients who initially appear well and are considering refusing transport.

Here’s the process I’d recommend for taking orthostatics:

  1. Start with your initial, baseline set of vitals. Whatever position your patient is found in, that’s fine. Deal with your initial assessment in the usual fashion.
  2. Once you’re starting to go down a diagnostic pathway that prominently includes hypovolemic conditions in the differential, start thinking about orthostatics. If your initial vitals were taken while seated, try lying the patient flat and taking another pulse and BP. If possible, wait a minute or so between posture change and obtaining vitals; this will allow their system to “settle out” and avoid capturing aberrant numbers while they reestablish equilibrium.
  3. Ask yourself: can the patient safely stand? Even in altered or poorly-ambulatory individuals, the answer might be “yes” with your assistance, up to and including a burly firefighter supporting them from behind with a bearhug. (Caution here is advised even in basically well patients, because significant orthostatic hypotension may result in a sudden loss of consciousness upon standing. You don’t want your “positive” finding to come from a downed patient with a fresh hip fracture.) If safe to do so, stand the patient and take another pulse and BP. Again, waiting at least a minute is ideal, but if that’s not possible, don’t fret too much.
  4. For totally non-ambulatory patients, substitute sitting upright for standing. Ideally, this should be in a chair (or off the side of the stretcher) where their legs can hang, rather than a Fowler’s position with legs straight ahead.
  5. For utterly immobile patients who can’t even sit upright, or if attempting orthostatics in the truck while already transporting, you’ll need to do your best to position them with the stretcher back itself. Fully supine will be your low position, full upright Fowler’s will be your high position, and a semi-Fowler’s middle ground can be included if desired.

On interpretation: healthy, euvolemic patients can exhibit small orthostatic changes, so hypovolemia is only appreciable from a significant drop in BP or increase in heart rate. From supine to standing, a drop in the systolic blood pressure of over 20 is usually considered abnormal, as is an increase in pulse of over 30. (Changes from supine to sitting, or sitting to standing, will obviously be smaller, and therefore harder to distinguish from ordinary physiological fluctuations.) A drop in diastolic pressure of over 10 is also considered aberrant. You can remember this as the “10–20–30” rule.

Try to remember what’s going on here. As the patient shifts upright, their available volume is decreasing, for which their body attempts to compensate — in part by increasing their heart rate. It’s a truism that younger, healthier, less medicated patients are more able to compensate than older and less well individuals. So for the same volume status, you would be more likely to see an increase in pulse from the younger patient, perhaps with no change in pressure; whereas the older patient might have less pulse differential but a greater drop in pressure. (On the whole, the pulse change tends to be a more sensitive indicator than pressure, since almost everyone is able to compensate somewhat for orthostatic effects. As always, if you look for the compensation rather than the decompensation — the patch, rather than the hole it’s covering — you’ll see more red flags and find them sooner.)

Are substantial orthostatic changes definitive proof of hypovolemia? No, nothing’s certain in this world. Another possible cause is autonomic dysregulation, which essentially means that the normal compensating mechanisms (namely baroreceptors that detect the drop in pressure and stimulate vasoconstriction, chronotropy, and inotropy) fail to function properly. You do have enough juice, but your body isn’t doing its job of keeping it evenly circulating. Vasovagal syncope is one common example of this; I’ve got it myself, in fact, and hence have a habit of passing out while squatting. This sort of thing is not related to volume status, although if you combine the two the effect can be synergistic. A good history can help distinguish them: ask the patient if they have a prior history of dizziness upon standing.

Finally, pulse and pressure are not the only changes you can assess. One of the best indicators of orthostatic hypotension is simply a subjective feeling of light-headedness reported by the patient. Although sudden light-headedness upon standing can have other causes (the other big possibility is benign paroxysmal positional vertigo — although strictly speaking, BPPV tends to cause “dizziness,” which is not the same as “lightheadedness”), hypovolemia is certainly one of the most likely. So stand ’em up when it’s safe and reasonable, ask how they feel, grab the vitals if you can, and maybe even take the opportunity to see how well they walk (a nice, broad neurological test — the total inability to ambulate in a normally ambulatory patient is a very ominous sign).

Orthostatics are usually recorded on documentation by drawing little stick figures of the appropriate postures. For those who find this goofy, or are documenting on computers without “stick figure” keys, a full written description will do.

Managing STEMI Mimics in the Prehospital Environment

Here’s one for the medics in the audience, or anyone interested in the box with the squiggly lines.

ST elevation means acute MI. Or does it? Most medics understand that this isn’t always the case, but many don’t recognize how often it’s not, and looking deeper — sorting out true STEMI from the many non-MI pathologies that also produce ST-elevation — is not the easiest task.

The following is a PowerPoint presentation I produced for use in either continuing education coursework or merely as a standalone reference. The main intended audience is EMS providers at the paramedic level, but most of the information is at least somewhat relevant to all levels of care.

The topic is the recognition and management of “STEMI mimics,” to steal Tom Bouthillet‘s phrase: non-ACS conditions that nevertheless present with signs and symptoms resembling acute MI, particularly ECG changes such as ST segment elevation.

This is best taught by a knowledgeable instructor, but it’s designed to be usable as a self-contained reference for ambitious students; these are info-rich slides, not just graphical accompaniments to a lecture. It does assume a foundational paramedic-level education, as well as a basic understanding of ideas like sensitivity and specificity — a review of our tutorial may be in order. The illustrative ECGs are labeled with “answers” in the slide notes of the PowerPoint versions, although not on the PDF, so that’s probably the best version if this material is new to you.

Although fairly comprehensive, it’s intended as a practical guide for field assessment and treatment, rather than an in-depth examination of the etiology and course of care for every pathology discussed. For additional information, the sources for most of the contentious claims and data are listed on the slides; sources for the more everyday material are available by request. And remember to follow your service’s protocols and understand exactly where and how far you have flexibility to make some of these calls; in many cases, the decisions will be made for you.

There are 192 slides in the full presentation; the most common feedback is that this can make for a very dense and potentially drawn-out class. There is one natural “intermission” point for a break at about the halfway mark, between the introductory discussion on general ideas and before diving into specific and individual mimics. If desired, the course can be broken up further into multiple units or even multiple days.

Feel free to share, redistribute, or use for your own purposes; this is educational material made available without charge or obligation.

[Edit 10/28/12] This presentation was later enhanced into a narrated video lecture

The Rhythm Method


One two three — five six seven

What’s the missing number?

If you said four, congratulations. You have a basic human ability to recognize patterns — one of the best tools we have to separate us from the monkeys and sea-slugs.

One of the simplest types of pattern is a rhythm, and the simplest rhythm is a steady cadence. Ba-dump, ba-dump, ba-dump. Imagine a metronome or a drummer tapping out a fixed, continuous pace at an unchanging rhythm.

This is also one of the most basic and useful tricks you’ll ever use when taking vitals!

See, measuring vitals involves feeling, hearing, or observing a series of fairly subtle blips over a period of time. Unfortunately, interference is common in the field, and it’s a rare day when bumps in the road and bangs in the cabin don’t eat up at least one of those blips.

When taking a radial pulse, if over 15 seconds you count 18 beats, you have a pulse of 72; but if just a couple of those beats are lost due to your movement or the patient’s, suddenly it becomes 64, which is a substantial difference. This is no good; we want better reliability than that.

Rhythm is the answer. A pulse is typically a regular rhythm. So are respirations. So are the Korotkoff sounds of a blood pressure. In order to establish this rhythm, you only need to hear two consecutive beats, and appreciate exactly how far apart they are. If you can do this, then you can continue to mentally tap out that pace — hopefully, while continuing to feel, see, or hear the true beats, which will help you to maintain the right speed, but even if you miss some, you’ll still have your mental beat to count. Even if you miss most of them!

So you feel for the pulse, and you palpate the first couple beats. Then you hit a tortuous section of road that throws you around the cabin, and you’re unable to feel anything for several seconds. But you already had the rhythm in your head, so when you pick up the pulse again, you haven’t lost the count — and you’ll end up with an accurate number.

Now, in sick people these rhythms aren’t always regular. And if you observe that a pulse or respiratory cycle isn’t regular, then this system won’t be as effective — for instance, there’s not much point in trying to find the “beat” to an A-Fib pulse. But small irregularities or breaks in the rhythm are okay, as long as there’s still a regular cycle underlying it; for instance, occasional dropped (or extra) beats won’t change the basic rate.

Give it a try. If you got rhythm, vital signs will never give you trouble again.

What it Looks Like: Agonal Respirations

See also what Jugular Venous Distention, Seizures, and Cardiac Arrest and CPR look like

Education and experience are both important to making a well-rounded provider, and each of the two have distinct advantages. Perhaps the greatest advantage of experience is that it gives you the best ability to recognize situations you’d otherwise only know by description or by photograph.

Nowadays, though, with the Wonders of Modern Technology, we have some tools that can help bridge this gap. Experience is still essential — but there’s no reason that the first time you see a seizure or cyanosis should be in a situation with real stakes.

So let’s go through some of the common medical events and conditions we talk about, learn about, but may not truly know the presentation of until we encounter it.

Today, it’s:

 

Agonal Respirations

Agonal respirations are an inadequate pattern of breathing associated with extreme physiological distress, particularly periarrest states (that is, it is usually seen just prior to cardiac arrest, as well as during and for some time after). Although not always seen during arrest, it is not uncommon, and there is some evidence that it may be associated with better outcomes than arrests without agonal breathing. Whatever the case, it can easily be confused for ordinary respiration, leading to the mistaken impression that the “breathing” patient must also have a pulse; this confusion is part of why the American Heart Association no longer recommends checking for breathing as part of layperson’s CPR.

As for healthcare providers, whether we’re able to put the label of “agonal” on it or not, we should be able to recognize from the rate and depth that this is not adequate respiration to sustain oxygenation, and ventilatory assistance (as well as a check of hemodynamic status) is in order. But recognizing the specific nature of this breathing can be a very useful red flag to set your “code” wheels in motion.

Here are a few simulated examples, performed by medical actors. They range in presentation and context.

http://www.youtube.com/watch?v=M99bRjmsC7E

Finally, here’s a treat — this is a video of a real-life cardiac arrest at a beach in Australia. Starting after the first shock, from 2:39 onward, you can see a great example of agonal breathing. The rest of the video is also a nice example of an honest code being worked in the field — not perfect, but real. (For bonus points, how could their CPR and other treatment have been improved?)

(Thanks to Dave Hiltz for inspiring today’s topic.)

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]

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:

  1. Adverse drug effects are responsible for 11% of ED visits in the elderly.
  2. 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)
  3. 1/3 of all adverse-effect-induced ED visits are accounted for by warfarin, insulin, and digoxin.
  4. 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).

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

How and Where? The Cornerstone of BLS

It’s common to observe, and not wholly off-base, that the EMT-B has only a limited toolbag at his disposal for the field treatment of his patients. There are literally only a fairly small number of interventions he is trained and permitted to perform, and most of those are for the trauma patient; for the typical medical patient, he can do very little unless they are actively trying to die. Now, it’s true that for those dying patients, he may have everything he really needs; BLS is the backbone of life support, no matter if you’re a doctor or a lay responder. Still, it’s easy to feel powerless as a Basic with the many distressed or ailing patients for whom we can do very little except transport them and set the stage for their eventual definitive care.

The first and largest clinical skill that the EMT needs to master is undoubtedly patient assessment, but if we’re talking about interventions — that is to say, actions you take that directly change the course of the patient’s care — I believe that limited or not, he has at least one very important role to play. The most important BLS intervention is decision-making.

No, we don’t push drugs or relieve pneumothoraces, but we still make decisions. These can be treatment-related, such as the decision to assist respirations or splint an extremity; they can be logistical and somewhat banal, such as how to best maneuver a stretcher into a home or where to park the ambulance. But with every single patient, we’ll repeatedly make one particular group of decisions — decisions which, at the least, will play some role in their care and eventual outcome, and at the most can determine whether they live or die. Foremost among these decisions are three:

  1. Where does this patient need transport to? What facility or point-of-entry will be most beneficial, given his presentation and suspected diagnosis? Would it be appropriate or acceptable for the patient to refuse transport?
  2. In what manner should this patient be transported? How quickly does he need to go? Is there no hurry, or does every second count? Do we need lights and sirens? Does the receiving facility staff need to be notified of special circumstances (such as trauma, stroke, or cardiac alerts)? After arriving, what information and what degree of urgency do you convey in your report?
  3. Would the patient benefit from any additional resources? You may be the only eyes and ears on scene; if fire or police are needed for safety reasons, it is your responsibility to call for them. Furthermore, would the patient benefit from ALS-level care?

It may be true that we generally can’t cure the primary cause of a patient’s complaint, and in many cases can’t even offer meaningful supportive care short of true life support. But these decisions are still central to the care the patient eventually does receive, and most of all how quickly. Of course, some decisions are made for us by our policies and protocols, and other decisions are patently obvious, but that still leaves substantial room for wisdom or foolishness.

Consider a critical trauma patient extricated from a MVC. In one case, we arrive and direct the fire department’s rescue, setting up the scene for safe and easy access. The patient is rapidly removed and assessed, loaded up, and transport is begun emergently to the level I trauma center 10 minutes beyond the closest community hospital. As we depart, we call ahead and notify the trauma team, relaying our status and ETA. En route, we are able to intercept with a paramedic crew, who hops aboard and jump-starts the patient’s care with IV access, pain management, and other measures. We quickly navigate through traffic and arrive in good time, bringing the patient directly into a trauma room, where staff are waiting and immediately assume care. The report is handed over, including several critical findings, and the patient is stabilized and rushed into surgery.

In this case, we “did” very little for the patient, in the sense of treatment. But consider if things had gone differently. We arrive on scene and bungle things, parking in the wrong spot and jamming up the access routes; it takes us many minutes to assess the situation and call for heavy rescue. The extrication is slow and belabored; when finished, we evaluate the patient incompletely, with a medical rather than a trauma approach. He is loaded and transported to the nearby community hospital, driving with the flow of traffic, and no entry notification is given. When we finally arrive, we sit in the triage line, give a minimal report to the nurse, and the patient is placed in a secluded hallway bed. We head out for our next call, never realizing that the patient sat there for many minutes until a doctor finally assessed him more closely and realized his severity, at which point he called immediately for ambulance transfer to the trauma center. The transferring unit took 10 minutes to arrive, 10 more to assume care, the transport itself took another 20, and the patient finally arrived in surgery an hour and a half after we first arrived on scene.

Although the eventual treatment might be identical, the difference in the timelines for these parallel patients could very well have a profound effect on their outcome. There is some debate currently as to whether time-to-care for many EMS patients could be far less important than we traditionally assume, but even if it is, there is no question that some subset of patients still exists for whom time is critical.

For a realistic illustration, consider the following, a true story of a call I ran:

You are dispatched BLS and non-emergent to a rehab facility for the complaint of “cellulitis.” On arrival, you take a report from a nurse, who explains that the patient has been with them for a week and has been experiencing inflammation of his arm for much of that time. He is severely demented but otherwise has a minimal medical history.

While you talk, your partner comes out of the patient’s room, informing you that she was unable to obtain his blood pressure. Curious, you head in, finding an elderly male accompanied by his wife. He is cheerfully confused, oriented to self only (baseline per his wife), but in no distress. He appears generally well.

His respirations are unremarkable, but his radial pulse cannot be felt, and he has a thready, barely palpable brachial pulse, 90 and regular. With several attempts, you are able to obtain a BP at ~84 systolic. His skin, however, is warm and slightly red — not overtly hot, but certainly not cool. (Your service does not carry thermometers.)

You speak with the nurse, who checks the chart and confirms the patient is typically normotensive, up to and including his last vitals check earlier today. You begin loading the patient onto your stretcher while you obtain a detailed history from the wife. Eventually, you learn that during his recent hospital stay, he had developed a seemingly minor infection of the arm due to an infected IV site.

Although the patient is still presenting well, your assessment is challenged by his poor cognitive baseline, and you are very concerned about the possibility of a developing sepsis. The seeming rapidity with which the patient’s blood pressure has dropped is especially troubling. You load up the patient, giving him some supplemental oxygen for good measure (pulse oximetry is not available), and obtaining further details of his history.

His requested facility is also the closest, a community hospital 5-10 minutes away, and the same hospital at which he was recently an inpatient. If an ALS intercept were available, you would attempt to meet them, as early goal-directed therapy for the treatment of sepsis has been shown to significantly improve outcomes, and some of those milestones are achievable in the field (such as fluid bolus). However, the nearest fly-car is several towns away, and an intercept would take much longer than direct transport. You elect to head straight for the emergency department. You attempt to call in an entry notification, but are unable to raise the receiving staff prior to your arrival.

Upon arriving, you wheel the patient into the busy ED. A harried nurse asks if this is the cellulitis patient (the facility had called previously), which you affirm. She tells you to put him in an overflow hallway bed. Pulling her aside, you mention that you have some concerns about the patient’s hypotension and the possibility of sepsis, painting a brief clinical picture. She has one of the techs clear out the critical care room near the entrance, and you move your patient there instead. After a detailed report to another nurse, you transfer over care, shake hands, and clear out. As you leave, the patient is in the process of having blood drawn.

This was ultimately a simple call, with neither sturm nor drang, and the prevailing emotion was an orderly calm rather than any frank emergency. But consider: supposing this patient were indeed septic (I was unable to obtain any follow-up), there is a clear correlation between time to definitive care and eventual morbidity and mortality. (The best practices of early sepsis care are still evolving, but most would agree that the condition should be treated as a time-critical life threat just like stroke or acute MI.) The fact that the patient seemed to be in minimal distress or extremis does not entail that he was not at a critical juncture. If he had been treated as a simple cellulitis patient going in for evaluation and non-urgent care, he would have — at best — languished in a hallway bed until eventually funneling through the facility’s triage process and being stepped-up to a higher acuity of care.

This, to me, is the central clinical skill of the EMT, on top of basic life support and trauma care, and of course patient assessment. Skilled assessment with the knowledge of pathophysiology and best practices to understand the meaning of your findings is the first half of the puzzle, and making the appropriate decisions to streamline the patient’s continuity of care is the second. This is something that can and should happen with every single patient, and it’s the most basic of BLS tools.