Understanding Shock VI: Fluid Resuscitation

So we know now that in any hemorrhagic shock, controlling the bleeding is step one, and restoring the supply of something resembling blood is step two. Should we also consider infusing some other fluids, even those that don’t help carry any oxygen?

Why would we even consider such a thing? It would make sense if “fluid” is what we’re missing, which is the case when shock is caused by something like dehydration. But in hemorrhage, we’re missing blood, not water. Still, there are a few reasons this might be worthwhile. Let’s discuss the “pro” arguments first, then come back around and talk about the “cons.”

 

The hydraulic argument

Fundamentally, the human vascular system is a hydraulic circuit.

In other words, it’s a giant circle of stretchy elastic tubes, like those long circus balloons. It’s all filled with fluid, which stretches out those tubes and pressurizes the whole system. Then a central pump pushes all the fluid in the system around in an endless loop.

One of the properties of such a system is that, without adequate internal pressure, it won’t work. It’s not that it works badly; it just fails altogether. And although pumping harder and faster can help elevate the pressure a little, and squeezing down on the tubes to make them smaller can help more, in the end if there’s not enough fluid in the system, nothing’s moving anywhere. If the heart isn’t filling with a certain amount of blood during diastole, it won’t push it forward during systole; it can’t pump out what it doesn’t take in.

So maybe there’s a certain logic for maintaining an adequate blood pressure, no matter what sort of fluid we’re actually circulating. Although pressure alone doesn’t carry oxygen, maintaining some pressure is certainly a prerequisite for carrying anything. To put it dryly, although BP isn’t everything, people with no BP are dead.

Moreover, some of the pathways in the shock cascade are, perhaps, initiated by low intravascular volume as much as by actual inadequate oxygen delivery. If we can keep the circulating volume pretty decent, maybe we can convince the body that all’s well — no need for a freak-out today.

 

The extravascular resuscitation argument

Flip back the calendar to the era of the Vietnam War, a landmark time in trauma care. Researchers like Dr. Tom Shires were experimenting on dogs.

They’d do things like drain from them a fixed volume of blood, then clamp off the bleeding and wait for a bit. Then they’d put back every drop of blood they’d removed. Most of the dogs died nonetheless, a phenomenon you and I now understand, since we’re totally experts in the self-sufficiency of the shock process.

But then they’d repeat the experiment. Only this time, rather than just giving the dogs back their blood, they’d also give them some crystalloid fluid. Just water with some stuff like electrolytes in it. This time, more of the dogs survived.

The theory explaining this goes something like so: where is most of the fluid in your body? We know that a high percentage of our bodyweight is water, but does that flow mostly in the blood? Anatomists talk about three different fluid “spaces”: the intravascular space (inside the vessels, where the blood circulates); the intracellular space (the interior of our actual cells); and the interstitial space (the “sea” of fluid permeating the tissue beds but outside the cells, bathing and nourishing them). Fluid moves between these spaces as needed, but at any given time, the majority of your body’s fluid is actually in the interstitial and intracellular (the extravascular) spaces — that is to say, not in the blood at all.

Shock causes increased permeability of the tissues and of the vascular tree, while simultaneously dropping intravascular (hydrostatic) pressure. So when the dogs entered shock, after a short while fluid began to “leak” from the interstitial and intracellular spaces back into the intravascular space. In essence, the dogs’ tissues were returning some of their retained fluid back into the bloodstream — and human tissues do this too. This shift actually increases the vascular volume, which is nice in a sense, and can be seen as a method of compensation: the body is tapping some of its reserve fluid to restore what was lost. However, it does leave the tissues dry. By infusing some saline along with the blood, Shires was helping his test subjects resuscitate both spaces. The intravascular space needed blood, but the extravascular spaces just needed fluid. (Of course, if we replace the blood, eventually the extravascular tissues will be rehydrated and the loaner fluid returned; but if we didn’t provide any extra fluid, that would once again leave the intravascular compartment a little light. Also, some of it — which leaked into neither the intravascular nor extravascular spaces, but the “third space,” areas such as the abdomen where it doesn’t belong — won’t be readily returned at all.)

Some combination of these two arguments became the foundation for a decades-long practice whereby hemorrhaging patients are given a certain amount of crystalloid (usually saline, or a modified form of saline like Lactated Ringer’s), often prior or in addition to giving blood products. In many cases this fluid is titrated to maintain a desired blood pressure, and this practice is still widespread today, especially in the prehospital world. In some cases, colloidal fluids (which contain large molecules such as proteins) are also used and have generally similar effects.

Key points:

  1. Bleeding control and restoring actual oxygen-carrying capacity are the main priorities in hemorrhagic shock, but there may also be value in non-blood fluid resuscitation.
  2. One argument for this is the maintenance of adequate blood pressure in order for the circulatory system to function.
  3. Another argument is the replenishment of the fluid lost from extravascular spaces.

Next episode we’ll discuss the dark side of crystalloid resuscitation.

Go to Part VII or back to Part V

Understanding Shock V: Blood Transfusion

So let’s say we’ve stopped the bleeding as best we can. Now what?

The patient is still low on blood, and we know about all the problems this will cause. So shouldn’t we try and give them some back?

Well, maybe.

It makes sense that someone who loses blood should get some blood replaced. And this is a very old concept. Once upon a time, we simply drew blood from one person and gave it to another — a process that was greatly improved when we learned how to screen and test blood for compatibility and disease. This method is still used in some settings, such as the military, which treats its entire force as a “walking blood bank.” If Pvt. Joe needs blood, they check the registries to find a match, then call up Pvt. James and have him swing by to donate a few bags.

In most other settings, however, whole blood transfusion has largely become a thing of the past. Instead, when blood is donated, it’s immediately reduced to its constituent parts. The red blood cells are pulled out and stored as packed red blood cells (PRBCs); the platelets are pulled out and stored as condensed platelet concentrate; and everything that’s left — the plasma itself, including electrolyte-rich water, clotting factors, immune factors, and other ingredients — is frozen and stored as fresh frozen plasma (FFP). One unit of blood (around a pint) yields one unit of each component. Since most patients only need one or two of these components, we can divvy them out as indicated, and the same blood supply can benefit up to three people.

So for years it’s been standard to transfuse traumatic shock patients red blood cells. As we know, the key problem of shock is inadequate oxygen delivery, and red blood cells are how we deliver oxygen. So drop in a few extra hemoglobin, perhaps top them off with a bit of fluid to keep things moving, and we should be set, right?

Maybe. But this leaves out a number of factors.

First of all, remember our prime directive. Stopping the bleeding is more important than topping off the tanks. How does our body control bleeding? Platelet aggregation and coagulation. And remember that platelets, the bricks of this process, are not reusable; if we have a lot of trauma, and we lose a lot of blood, we can easily run out of them. Does transfusing red blood cells alone provide any platelets? Nope.

So maybe we should throw in some platelets too. But wait — we know that to actually bind the platelets into a cohesive clot, we need a host of backup players, the numerous coagulation factors that live in the plasma. Does a platelet pack provide these? Nope. (Okay, platelets are usually stored in a small amount of plasma, so there’s a few, but not enough.) So maybe we should give the patient some plasma too (or even isolated concentrates of clotting factors to really supercharge the process).

The result of all this is the recent movement towards so-called 1:1:1 therapy, where trauma patients receive equal proportions of red blood cells, plasma, and platelets. In other words, they end up getting all the individual components of whole blood; we just don’t often have whole blood available, or we might give that. This is still an area of active research, and the exact ideal ratios are up for debate; the ratio of red blood cells to plasma is often either 1:1 or very close to it (1:2, 1:3, etc.), and platelets are usually given in somewhat lower quantities, but should not be neglected. The best ratio, as well as the actual quantity of blood to ultimately give, remains to be seen.

Logistics can stand in the way of some of these efforts. For instance, plasma is typically stored frozen (as FFP), and therefore needs to be thawed before use, a process that takes some time. Very large trauma centers may be able to keep a rotating supply of thawed plasma on hand for emergency use, but many facilities won’t be able to have plasma immediately available in this way. And although transfusing in the field seems tempting, the practical challenges of carrying blood products on an ambulance are daunting.

Furthermore, banked blood is not “as good” as the patient’s own blood no matter how it’s given. Even a 1:1:1 transfusion, properly typed, screened, and cross-matched, has real risks of transmitting infection or causing an adverse reaction, carries less oxygen than fresh blood, has reduced hemoglobin pliability (the little disks “stiffen,” becoming less able to squeeze down capillaries to reach the hungry cells), and reduced numbers of labile clotting factors (particularly V and VII). It carries less 2,3-DPG, its pH is lower, and due to the anticoagulants and preservatives added for storage, it’s literally larger and more dilute than the whole blood it started as. Since transfusions are generally not our problem in the field, the applicable moral here is simply that “top ’em up” is not a simple or easy answer to shock, and the only intervention that truly keeps the patient out of trouble is to stop the bleeding!

From the Trauma Professional’s Blog at http://regionstraumapro.com/

 

In brief:

  1. Blood transfusion is an important step in treating traumatic shock, secondary only to controlling the source of hemorrhage.
  2. Modern “component” blood banking allows for the administration of almost any ratio of red blood cells, plasma, and platelets.
  3. Transfusing primarily red blood cells is the traditional approach, but a movement has recently developed toward more balanced ratios.

Next time: the legacy of crystalloids.

Go to Part VI or back to Part IV

Understanding Shock IV: Bleeding Control

 

The first, the last, and always the most important answer to the shock progression is to fix the underlying cause.

To illustrate the principles, let’s focus for the moment on traumatic shock caused by hemorrhage — you were injured, began to bleed, and now you’ve got less intravascular blood. What should we do about that? Stop the bleeding? Give you more blood?

If you’re caught in a sudden rainstorm, should your first reaction be toweling yourself off, or getting under shelter?

Both will be needed, but one will be futile without the other.

Shock caused by bleeding is cured by stopping the bleeding. The body will try to do this on its own, but definitively, in significant trauma, this is almost always accomplished through surgery. Trauma is a surgical disease; its medicine is an operating room, sutures, and cautery.

Prior to that, just about anything we can do to stop or slow the bleeding is worth doing. Direct pressure on an injury is often very effective. Pressure slows the flow of blood and promotes the clotting process (by creating stasis and degranulating platelets). It most often fails when it can’t be properly applied — such as when the bleeding is internal, as with a lacerated abdominal organ.

Tourniquets for extremity injuries are perhaps the most definitive pre-surgical intervention of all, and despite years of demonization they have been shown to be generally effective in most cases, with relatively minor risks. More discussion of tourniquets will come another day.

To contrast, consider the counter-example of septic shock. The initial insult there is an infection. How do we treat infection? Antibiotics. Early antibiotic therapy is so important for the sepsis patient that the time from hospital arrival to administration of antibiotics is recorded, and measured in minutes.

The takeaway:

  1. The prime directive in correcting shock is reversing the original cause; this takes precedence over any other treatment.
  2. In trauma, this means stopping the bleeding; that usually means surgery, and before that, direct pressure or tourniquets.
  3. Achieving this control is absolutely essential and absolutely time-critical.

Go to Part V or back to Part III

Understanding Shock III: Pathophysiology

An example of the shock cascade
Another model
Yet another model

 

The common thread that defines the shock process is inflammation.

As we know, inflammation is the body’s response to damage. When things go wrong, when trouble calls, we ring the bell for inflammation to make it right. Often this serves us well, but like any militia, if left unchecked it can be worse than the problem it came to fix.

The many twists and turns of the pathology of shock are still not fully understood, but here are some of the important stepping stones along the way:

Shock occurs, and many of the body’s systems are left without adequate oxygen. Although oxygen supplies our primary method of generating energy — the aerobic metabolism — we do have secondary systems in place that can produce energy without oxygen, the anaerobic cycles. In the setting of shock, these take over.

But they’re not great. They provide far less energy than aerobic metabolism, and they produce by-products that accumulate in the body. Among other things, this includes the accumulation of hydrogen ions, creating a widespread acidosis. Think about running sprints or lifting heavy weights; think about that burning feeling, and the eventual failure of your muscles. Operating in an anearobic mode causes trouble and is shortlived at best.

Sooner or later, this isn’t enough to keep things working, and cells begin to accumulate toxic products and eventually shut down. They’re not quite dead yet; they’re hurting, but they can still recover. Like a business that shuts its doors in the off-season, there simply isn’t enough inflow for them to operate right now.

The trouble is, we need those cells. They make up the tissues that form the heart, the brain, the lungs, the kidneys, the liver, and so forth. When the cells close up shop, the organs begin to fail. When organs fail, they cease to provide their essential functions. Let’s consider just one, the heart.

The heart pumps blood. When it loses its effectiveness, it pumps less blood. This means less circulation of oxygen, which means hypoxia is exacerbated. Look at that — we just magnified the problem. If the shock gets worse, is that going to help the heart pump any better? Dream on. The vicious cycle accelerates further.

As hypoxic damage to the cells progresses, the body responds with widespread inflammation to repair it. The trouble is, there’s no real hope of repairing anything without restoring the oxygen supply — but that never stopped Old Man Inflammation. One of his brute-force tactics is to increase capillary permeability, the “tightness” of tissues; everything becomes more susceptible to leakage. The fluid that runs throughout your body begins to ooze everywhere. Generalized edema occurs. In some cases, this is just gross; look at the bloated extremities of the recently dead for an example. But what happens when there’s edema and inflammation of the vital organs? They fail. Fluid in the lungs impairs respiration. Fluid in the brain causes increased intracranial pressure. Another blind response of the inflammatory system is apoptosis, where hypoxic cells — sensing that they’re done for — trigger self-destruct mechanisms and tear themselves apart. Unfortunately, you need those cells.

And hey, what about that acidosis? Our cells (including the ligand-receptor complexes that trigger our sympathetic processes) are designed to function at a specific pH. Placing them in an acidotic environment impairs their function. Combo attack!

But what about our compensatory systems? When our body sees shock, it does things like vasoconstricting, increasing heart rate and contractility, and attempting to maximize the availability of oxygen. That’s great when it works. But when things progress, it’s not so great. Vasoconstriction can choke off the organs, giving them even less oxygenated blood. Tachycardia increases the heart’s demand for oxygen.

And oh, by the way, none of this is adds much to the body’s ability to combat the original cause of the shock, whether that was traumatic injury, a septic infection, or something else.

Key points:

  1. The processes of shock are multiple and self-reinforcing.
  2. Inflammation plays a major role.
  3. Multi-organ dysfunction and failure also plays a major role.

Next time: so what do we do about it?

Go to Part IV or back to Part II

Understanding Shock II: What the What?

. . . the rude unhinging of the machinery of life.

Samuel Gross

 

When we say shock, what do we mean?

First, to be clear, we’re not talking about “shock” as in “I’m shocked by all this,” or as in “shell shock,” or as in “tasers give an electric shock.” Shock is a formal medical term with a specific meaning.

Here’s the simple definition: shock is what happens when your body runs low on oxygen.

Your entire body, from the top of your horns to the bottom of your hooves, is made of cells. Your cells do various things to keep you alive. In order to do those things, they need a supply of oxygen. Just like your car runs on gasoline or your computer draws electricity, if your cells don’t have oxygen, they don’t work. Essentially, every death, no matter what started the trouble, is caused in the end by insufficient oxygen delivered to the cells.

Without oxygen, eventually your cells die, and then, so do you. However, before that happens, you enter shock.

Mind you that we’re not talking about localized tissue hypoxia. If you tie a tourniquet around your arm, your hand will run out of oxygen and have problems. If a clot blocks an artery in your brain, parts of your noodle will die. These are problems, but they aren’t shock. Shock is a generalized situation; shock happens when hypoxia is widespread and systemic.

Why would such a thing happen? Usually, it happens because there isn’t enough blood flowing to supply oxygen to your organs. Blood is the expressway for oxygen delivery; without enough blood moving at the right speed to all the nooks and crannies of your body, the oxygen won’t get there, and your cells will start to lose their little minds. Blood plays a lot of roles, but this is by far the most important. So although hypoxia is the problem, inadequate perfusion is typically the cause, and we often talk about blood supply as a shorthand for talking about oxygen delivery. There are different types of shock with different underlying causes, but this is the common element that unites them.

Everyone on board so far? If you made it past page 2 of your EMT textbook, you probably knew all of this. But there’s a twist coming, and it’s important. To illustrate it, consider this parable.

You’re shot in the belly, and you bleed out a large portion of your blood onto the ground. We bring you to the hospital, where surgeons repair every inch of damage; you are made as good as new. We replace every drop of blood you’ve lost. At this point, your tissues are repaired, your blood supply is restored, and you’re alive.

But a week later, you die in the ICU.

Why?

The key to understanding shock is this:

Shock is caused by inadequate perfusion, but shock is far more than that.

Say what?

Okay, put another way: no matter what causes the shock, shock leads to more shock.

 

The shock cascade

When cells become hypoxic, what happens next?

What happens is that they start to do their jobs badly, and this leads to all sorts of systemic problems. When the organs stop working properly, it leads to worsening shock and decreased perfusion, which in turn worsens the original hypoxia, which causes further dysfunction. This process feeds itself.

Dr. Jeff Guy uses this metaphor: suppose you drop a lit match in a dry forest. At this moment, what is the problem? Simple: a burning match. Correcting the problem is equally simple: extinguish it.

But then, the match catches some leaves, and the leaves ignite some dry twigs, and there’s a small fire. What’s the problem? Well, now it’s a little fire going. We can correct it, but we’ll need some blankets or water or well-placed dirt.

What about two minutes from now? The flame has grown, and now it’s a bonfire. We can put it out, but it’ll take some real effort, and it’s going to leave damage.

What about an hour from now? The entire forest is ablaze. The only hope of stopping it will be a massive effort by helicopters and tanker trucks, and even then, most of the trees are probably a lost cause. Maybe we won’t be able to beat a fire that size no matter what we do.

Question: even if we can find that original match in the forest fire, will putting it out extinguish the blaze?

Of course not. The fire has spread.

Shock is a forest fire. The initial hypoperfusion is one thing, and we should try and correct it. But if we don’t, and it starts to cause damage, then that process will start to run away on its own. It will start to cascade, and expand, and feed itself; a new monster is born. Once this has happened, guess what?

We can completely fix the initial hypoperfusion, and still lose the patient.

This happens all the time. Shock occurs, for whatever reason, and we recognize and treat it. But we got there too late. The fire spread. We extinguished the match, but we couldn’t put out the blaze before the damage was too profound to survive. The complications of shock affect nearly every organ system, disrupt nearly every physiological parameter, and undermine the very homeostatic mechanisms that exist to help “fight the fire.” Once this process gets past a certain point, there’s no beating it; the essential fabric of the body is corrupted, and its ability to repair and maintain itself is destroyed. Days or weeks later, despite our best medical care, the patient dies from general, widespread complications. “The operation was successful,” as the surgeons say, “but the patient died.”

That doesn’t mean that we shouldn’t try to fix the initial shock state. That means we should try to fix it immediately.  It means it’s a time-critical, every-second-counts priority — because it’s not the kind of thing we can handle at the last minute. If we don’t nip it in the bud, we’ll go down paths that we can’t come back from.

So, the lessons for today:

  1. Shock is characterized by inadequate oxygen delivery to the cells.
  2. This is typically caused by inadequate bloodflow to the tissues.
  3. Once initiated, shock involves numerous pathological processes that range far beyond the initial hypoxic injury. These complications can persist long after the underlying trigger is corrected.

Next time: a deeper look into some of the “unhingings” that characterize the evolution of shock.

Go to Part III or back to Part I

Understanding Shock: Introduction

Ladies and gentlemen, it is time to crack the door to a vast and terrible realm.

It won’t be a short journey, and it won’t be an easy one. But it is our destiny.

What am I talking about? I’m talking about shock, of course.

Prehospital providers don’t understand shock. That’s understandable — because shock is complicated. It’s as complicated as disease processes get.

But we need to understand it. Shock is quite literally in our blood. Since the very birth of EMS, reducing the harm associated with shock states has been one of our main reasons for existing. It kills many, it debilitates many more, it spares no age, race, or gender, and its physical effects are exhaustively widespread. Yet when properly managed, many of those patients can be saved.

We should all be experts. To work in EMS is to be, among other things, a shock technician. This is our wheelhouse.

So, although it will take more than a few posts to walk through the different facets of this Very Big Topic, let’s talk about shock.

Sharpen your pencils, gird your loins, and stand by for further.

Understanding Shock II: What the What?

Understanding Shock III: Pathophysiology

Understanding Shock IV: Bleeding Control

Understanding Shock V: Blood Transfusion

Understanding Shock VI: Fluid Resuscitation

Understanding Shock VII: Negatives of Fluid Resuscitation

Understanding Shock VIII: Prehospital Course of Care

Understanding Shock IX: Assessment and Recognition

Understanding Shock X (supplement): Fluid Choices

Unique, Just Like Everyone Else

A few years back, a video of a lecture by Carnegie Mellon professor Randy Pausch made the YouTube rounds, becoming enormously popular; you’ve probably seen it. He later wrote a book discussing and unpacking many of the points he brought up in the lecture. If you haven’t watched or read them, I highly recommend both.

In any case, in the book Pausch describes the birth of his first child, how a complicated birth (a placental abruption) forced him to rush his wife to the Magee-Womens Hospital at the University of Pittsburgh Medical Center, and how his newborn child was brought into their neonatal ICU. He writes,

At Magee, they did a wonderful job of simultaneously communicating two dissonant things. In so many words, they told parents that 1) Your child is special and we understand that his medical needs are unique, and 2) Don’t worry, we’ve had a million babies like yours come through here. (91–92)

This is an elegant account of the demeanor we should all be trying to strike with the families of patients, and indeed with our patients themselves.

Many beginning providers, understandably unsure, will approach each patient like an antique porcelain vase: precious, delicate, and prone to breakage. This is the right attitude as far as priorities — we should take our care seriously — but that doubt is communicated in our body language and tone, and it’s not what sick and scared people want to hear. Imagine being the patient whose doctor says, “Man, look at that! I’ve never seen anything like that! Can we publish you?” or “Okay, I’m not going to lie, I’ve never done this in my life. But I did stay at a Holiday Inn Express last night…”

On the other hand, it can be very few moons indeed until you’re a “veteran” in the worst sense of the word, dragging your technically skilled but burned-out husk from patient to patient, seeing nothing but a stack of paperwork and a routine litany of tests and treatments. Her? Oh, just another abominal pain. Yawn. Her name? Search me. Is it lunchtime yet?

See, people want to be treated like people, and people are unique, precious (at least in their own eyes), scared, and need to be engaged with on the same human level as when you say “thank you” to your barista or read a bedtime story to your son. But people are also machines, and the trick to fixing broken machines is to fix a lot of them, and treat them all the same. We need to be able to reconcile these paired, antagonistic traits, because otherwise we can’t do what they called us to do. It’s not a matter of nailing one goal but missing the other: you miss both. You can’t reassure anyone if you don’t competently address their actual problem, and you can’t practice sound medicine if you don’t engage with patients as people.

That’s the trick that the obstetrics and neonatal teams at Magee pulled off, and it’s all the more important for us, who have to approach patients without the comforting backdrop (that is, comforting to them and to us) of a bright beeping hospital. It’s the trick of quiet confidence, of demonstrating without words that you know exactly what you’re doing, that you bring tremendous skill and experience to the table — but that those tools are being brought to bear for your patient, for the scared individual you’re kneeling beside. The “all the kings horses” response by fire and EMS, the loud and alarming transport to the hospital, the wires and tubes and countless gloved hands — it’s overwhelming and frightening if you’re thrown into it as an unknown environment, but if you understand that it’s all being done for you, then it’s comforting. It’s like calling for help and getting the Wolf. That’s exactly what you wanted in your time of need.

You may not want to date a cocky lawyer. But he’s the one you’d want at trial.

Oldest Trick in the Book

 

I’ve never been to nursing school. But I like to imagine it goes something like this:

On the first day, you walk into class, surrounded by other bright-eyed, eager young students ready to learn the art and science of nursing. Textbooks weigh down your bag, and your pencils are sharp and ready.

Before you stands your instructor, an impressive-looking MSN whose carriage suggests many, many nights spent awake amidst the cool blue lights and quiet beeps of a MICU. As you watch, she strides to the whiteboard and writes in block letters:

Lesson One: The ID Flip

Lesson two is eye-rolling.

Most hospitals, just like most ambulance services, require that clinical staff wear an ID badge at all time. This identifies them by name and role (nurse, doctor, PA, etc.), and often gives them access to secure areas as well.

Long ago, some canny soul discovered that when patients know your name, they can complain about you. If they decide that they don’t like you, whether justified or not, they can call people — like your boss — and unleash angry, entitled, and very personalized tirades about “Sarah Roberts, that mean witch who told me to shut up and stop smoking heroin.”

“Well,” we figure; “if they don’t know our name, they can’t complain.” So although the powers-that-be did insist that badges be worn, we started hanging them in odd places, like from our belt, or inside a pocket. Or covering them with stickers and other things. But the best of all answer of all was elegantly geometric, made especially easy by free-spinning retractable ID clips: simply twist the card so it faces your chest, and the only thing visible is whatever text happens to be printed on the back. Technically, you’re still wearing the thing, and if the boss notices you can just say “whoops, it got twisted,” but nobody can actually read your name, and, ninja-like, you can move through the ward unseen, a bescrubbed ghost.

The nurses have turned this into an art-form, and in some places it’s like finding a four-leafed clover to see an RN with a visible ID (usually I figure they’re new there). But we’ve become awfully fond of this in EMS as well.

People, I realize that the world’s a rough place, that patients can be impossible to please, and that even the best of us need to take steps to ensure we still have a job tomorrow. I do understand this. But there’s a certain point where you have to stop digging trenches, and realize that if you’re giving great care, following procedure, behaving professionally, and generally toeing the line, then you should be willing to stand behind your work. If you’re employed at the kind of place that’s willing to take any complaint as reason to show you the door, I assure you that no amount of ID-flipping will save you. Your days are numbered. Of course, even a good service will eventually start clearing their throat and looking at you pointedly if your personnel file begins to grow particularly fat, but at that point, maybe you really should consider managing your douche coefficient.

Besides, this should all be moot, because when you meet your patient you’re introducing yourself by name anyway. Because that’s just common courtesy when you greet people. And patients are people. Right?

Strive to do the kind of work that allows you the confidence to stand behind it. When someone points at you with forehead veins a-pulsing and demands to know your name so your supervisor can “hear about it,” tell them and tell them proudly. Sometimes, doing the right thing won’t be a defense against trouble — but you can be sure that playing “who, me?” will run out of rope even sooner than that.

Clip your ID somewhere obvious — mine goes on my shoulder — where patients and staff alike can easily see it, and know what to call you and what role you’ll be playing in this show. When I see somebody with a visible ID, I take this as a good sign about their responsibility and willingness to own their work. And those are qualities we need in EMS.

CPR for Dummies: How to Save a Life

One of the peculiarities of EMS education — and as a byproduct, of EMS practice and culture — is that we spend the majority of our time focusing on the minority of our calls. Think about it: your textbook has pages and pages devoted to ruptured aortic aneurysms, placentas previa, and mid-femur fractures — and when’s the last time you saw one of those? But scarcely a paragraph is given to the routine transfer, the drunk asleep on the sidewalk, or the MVC with minimal injuries. Call it an inverted pyramid: the most important stuff is low-volume, the most common stuff is pretty easy.

Whatever. The point is, at the very apex of this pyramid is the cardiac arrest. In its purest form, cardiac arrest is exactly why EMS exists. It couldn’t be higher stakes — as a disease, it’s absolutely certain to be life-threatening — and it’s terribly time sensitive, but the potential exists for a total cure if everything goes well.

Unfortunately, like many low-probability calls, we don’t get a great deal of experience with these — even less if your shift isn’t dedicated to emergencies. And when we don’t get much experience with something, that’s when training needs to fill in the gaps.

CPR and BLS resuscitation can seem like a confusing topic, especially given the frequent and seemingly arbitrary changes to the guidelines. The truth is, though, that it’s only gotten simpler and simpler — and you don’t need to follow the research (read: be a giant nerd like me) in order to know exactly what to do. Here’s the short, stripped-down, painless rules for how to save a life.

 

Push and Zap

Basically, after around sixty years of research on resuscitation, there are only two things that we know for sure help people survive cardiac arrest: chest compressions and defibrillation.

Literally, just those two things. Oh, there’s other stuff — ventilation, drugs, devices — that seem to help briefly, but so far nothing else has been proven to get someone’s heart beating again and let them walk out of the hospital with a working brain. Now, some of those other things do seem like pretty good ideas, and in many cases we started doing them before we knew if they’d really help or not, so we’re still doing them because people are used to it; it’s part of our training, and it’ll take some extra-compelling evidence to make us actually stop doing that stuff. But still, the story so far: chest compressions and defibrillation definitely help people survive, and that’s it.

What this means is that they should be your number one priority. If your patient is in cardiac arrest, that’s what they need. Other stuff? It may or may not be helpful; if you have the chance, or the personnel, and it doesn’t interfere with chest compressions and defibrillation, then you could go ahead and do it. It might help. But delaying or stopping the big two for that other stuff is like making a thirsty man wait for a drink of water while you comb his hair.

 

Early, Hard, Fast, Uninterrupted, and Full Recoil

Okay, so, chest compressions. Easy enough. Anyone can do ’em, all you need is your hands, just jump in there and push.

However, that’s not quite the whole story: the quality of compressions matters a great deal. We are literally pumping blood here; we are creating mechanical pressure to replace the squeezing of the heart. Just like you can wriggle a bicycle pump ineffectually without making much progress on inflating your tires, so too can you make goofy movements on someone’s chest without providing much perfusion. Even at its best, CPR only provides weak circulation compared to a real heartbeat; if you give poor CPR that’s even worse.

So here are the key components:

  • Early: Compressions should be initiated as soon as possible after arrest. That means, if I go down now, ideally you’ll start pushing on my chest as soon as I hit the ground. Typically that’s not possible, but mere seconds really do matter here; the longer there’s no circulation, the more tissue is endangered (all tissue, but particularly the vulnerable heart and brain), and the less likely that defibrillation will be successful — or if it is, the more likely there will be permanent complications.
  • Hard: Good chest compressions are a violent, aggressive act. We now recommend a depth of at least 2 inches in adults, which if you examine a mannequin (or fellow human) is remarkably deep. (Yes, “at least” means that going deeper is fine; compressions that are “too deep” are rarely seen in real life.) This isn’t a gentle cardiac massage, it’s not the mellow bouncing you usually see in movies, it’s a deep, powerful, oscillating thrust. It should tire you out, which is why we recommend changing personnel frequently; even when you think you’re still doing well after a few minutes, you’re probably not.
  • Fast: The recommended rate is now “at least” 100 compressions per minute. Since nobody knows what this means without a metronome, I highly recommend “musical pacing,” or using the beat of a well-known song to learn the rate. Stayin’ Alive by the Bee Gees is the classic; I like Queen’s Another One Bites the Dust myself. Again, 100 is an “at least” rate, so faster is better than slower. Admittedly, if you go extremely fast the heart won’t have time to fill between squeezes, but most “ludicrous speed!” CPR tends to have poor depth, and self-regulates anyway once you get tired.
  • Uninterrupted: Just like it’s essential to begin compressions as soon as possible, it’s equally essential to stop them for nothing. It’s not just that every moment you spend off the chest is “dead time” in which no blood is circulating; it’s worse than that. Chest compressions need to generate some “momentum” in order to create enough pressure to perfuse the heart; several consecutive compressions are needed before you’re really moving much blood at all. If you keep stopping — and studies show that everyone stops far more than they realize, to fiddle with one thing or another — you’re wasting those gains as soon as you’ve achieved them. Maximizing this “compression fraction” should be a primary goal; once you get on that chest, don’t stop for anything else unless it’s literally more important than circulating blood.
  • Full recoil: Among otherwise skilled rescuers, one of the most common errors is failing to allow for full recoil of the chest. In other words, you press down deeply, but rather than releasing fully, you start the next compression before you’ve come all the way up. This shortens the stroke of the pump just as much as if you were giving shallow compressions, and for several complex reasons (in particular the loss of preload) can reduce circulation in other ways too. We do this one particularly when we start to get tired, and begin to leaaaan forward to rest on the chest.

Defibrillation

It’s really as simple as this: once the heart’s entered fibrillation (or to a lesser extent a pulseless V-tach), the only plausible way to fix it is with electricity. These people are not going to “come to”; they are not going to have a Baywatch moment where they cough out water and wake up, even if you give them great CPR. They have an intractable problem, and the cure for it is an electric shock. Defibrillation is life-saving.

For most of us, this means using an AED, the automated devices you see everywhere from airports to ambulances. The reason they’re everywhere is because their use is time-sensitive, and if you drop dead ten miles from the nearest one, it might as well be ten light-years. No matter where you are, compressions must be performed to buy you time, and a defibrillator must be found to shock you back. If both don’t happen quickly, you will probably stay dead forever.

There are argument about some of the technical aspects of defibrillation, such as pad placement and waveform, but so far none of these details have proven to be very important. What is important is that you shock early, and get ready to shock without interfering with those compressions. Whenever possible, while one person gives compressions, someone else should clear off the chest by cutting or pulling the shirt from under the compressor’s hands, place the pads around them, and start the AED’s cycle. For many models of AED, there will be a period of several seconds while it walks you through voice prompts (telling you to stay calm, call for help, etc; these devices are designed to be usable by laypersons with no training), which should be ignored while you continue your CPR.

Once the AED tells that it’s analyzing the rhythm, you will need to stop compressions; this is the computer’s opportunity to decide whether the patient can be shocked or not, and interfering with this will just delay the process. If it doesn’t advise a shock, get back on the chest; you may have better luck later. If it does advise a shock, get back on the chest anyway! It’ll need to charge first, which may take quite a few seconds, and remember — every second matters. (Just make sure the whole team’s on the same page here, so that nobody pushes “Shock” until you’re clear.)

As soon as the AED announces that it’s ready to shock, everyone should be ready: cleared from the patient and prepared to shock. In a coordinated fashion, the compressor should clear the chest, the shock should be delivered, and he should immediately resume compressions with a pause of only a second or two. Rinse, lather, repeat.

When do you stop this process? When someone much smarter than you says to stop; or when the patient demonstrates clear signs of life (such as movement, breathing, or improved skin signs — or for the medics, a spike in end-tidal CO2). Don’t keep stopping to palpate pulses and otherwise fiddle with the patient. Like a soufflé or a Schroedinger’s cat, you must have faith in the process here, because checking on the process will assuredly cause it to fail.

 

It Ain’t Rocket Science

People, there are other details to this process, which is why they make us take CPR classes and carry the little cards around. And in 2015, there might be some new ideas on how we can do it best. Research continues apace in the countless EMS systems around the world that are experimenting with different technologies, techniques, and methods to improve survival. That’s how we’ve come from 1–2% survival rates to the 50%+ that a few cities now enjoy. It’s slow going, but it’s going.

But the best methods won’t matter if you don’t use them, and a lot of effort has been given to make our current methods truly simple. You literally can’t go wrong if you give great compressions and defibrillate as soon as possible. You can certainly go wrong if you forget that those are the two most important, life-saving measures — but you’d never forget that, would you?

Push and zap, folks. It’s so easy, an EMT can do it.