Although somewhat late out of the gate, we’ve finally put together an organized, all-inclusive site index for archived posts. Browse by topic and brief description to find what you’re looking for; we’ll make an effort to update the index regularly with new material, and it’ll be periodically reorganized as needed. Have at it!
Author: Brandon Oto
Understanding Shock VIII: Prehospital Course of Care
Now that we have a pretty good idea of how shock works, what does it all mean for our treatment in the field?
Much like cardiac arrest and some of the other “big sick” emergencies, there are really a couple essential interventions we need to execute, maybe a couple others that aren’t a bad idea, and beyond that, our main job is to ensure that we don’t kill our patient by wasting time doing anything else.
Step 1: Control the bleeding
As we emphasized ad nauseam, the number one goal with the bleeding patient is to stop the bleeding. No need to beat this to death, but just remember: if you can control the bleeding, yet don’t get much of anything else done, you’re doing absolutely fine.
Step 2: Transport to surgery
In most significant cases of hemorrhage, definitively controlling the bleeding will require surgical intervention. We don’t do surgery, but we do set the stage, which is why it’s essential for us to know what we’re doing. Get thee to a trauma center, and quickly!
Can other hospitals perform surgical intervention? Sometimes. Maybe. A world-class trauma surgeon might happen to be in the building for a conference. Maybe the operating room is between scheduled procedures and happens to be clean and available. But the point to a trauma center is that it’s guaranteed to have certain resources available, and that’s the kind of place we want to bring these patients. 9 times out of 10, if we transport them elsewhere, they’ll simply end up being transferred back out to the trauma center anyway, making the whole exercise essentially one very long transport. Can a small community hospital help stabilize the patient before surgery? Sure — but as we know, everything else is a distant second priority to bleeding control. Even transfusing blood may need to be done sparingly until the leak has been corked.
What about ALS? Do these patients need paramedics? Now, if they acutely decompensate and need airway management or other interventions you can’t provide (or have other issues like pneumothorax), then ALS-level care would be valuable. But outside of that, and even granting that to a certain extent, a medic unit is not going to stitch up the bleeding, and meeting them will certainly delay transport to surgery at least by a few minutes. True, they’ll be able to initiate IV access that can be used for blood later, but in most cases this takes mere seconds at the ED (where there’s plenty of room, good lighting, and ample personnel) — and prehospital IVs will sometimes be replaced anyway.
Step 3: Promote oxygen delivery
Okay, you shock technician, now what?
Can we talk about coagulopathy of trauma — aka the “deadly triad”?
Bleeding control is the priority, right? And bleeding control requires clotting. But there’s a set of conditions guaranteed to obstruct clotting, and three of them are almost always present during hemorrhagic shock.
One is hemodilution. When we top off our bleeding patients with non-blood fluids, as we’re so fond of doing, it dilutes both oxygen-carrying capacity (since we’re not adding red blood cells) and clotting speed (since we’re not adding platelets or clotting factors). So this one’s our fault, and can be readily avoided by simply resisting the urge to replace blood with salty water.
One is acidosis. If you’ve been paying attention, you know that acidosis tends to develop in shock due to anaerobic cellular activity, and can be further encouraged by overzealous fluid administration. Is this the end of the world? (After all, a little acidosis might even improve oxygen delivery by shifting the oxyhemoglobin dissociation curve.) Well, the trouble is that acidosis also leads to coagulopathy. According to some in vitro studies, in fact, even mild acidosis can precipitously decrease platelet aggregation, and in significant acidosis platelets won’t activate at all. Zero.
The last is hypothermia. Not only do cold patients have poor oxygen delivery and other problems, they clot poorly; low temperatures cause coagulopathy too.
Now, we can’t do much about the initial trauma. We can discourage acidosis by limiting fluid use, and ensuring that ventilations remain adequate. What about hypothermia? Do our trauma patients get cold? What would you expect when you take someone who’s bleeding, strip them naked on a cold sidewalk, pump cold saline into their veins, and chuck them into an ambulance carefully heated to your comfort?
Keep your trauma patients warm. This is not about human kindness or TLC, this is a serious and important intervention for shock. Hypothermia is great for cardiac arrest, it may be beneficial in some other scenarios, but it is not good for bleeding people.
How about supplemental oxygen? Well, I suppose so. In the patient with adequate respirations, it is doubtful that “topping off” their PaO2 will affect them appreciably; but as they begin to decompensate, they’ll need all the help they can get.
Positioning? Remember how big a deal they made about the Trendelenburg position in school — how it pulls blood from the lower extremities into the core? And ever noticed how it’s not exactly our number one emphasis in the field? Trendelenburg has little real evidence supporting it, and the bulk of what does exist suggests its effect is fairly minimal — it moves only a little blood, the effect is transient, and the body’s compensation can actually cause a paradoxical reduction in core perfusion. Mostly these studies were done in healthy people, so it’s possible that our shocky patients do get a little benefit — and one supposes that if things are dire enough to need every last cc of blood, you can give it a shot. But typically it won’t do you too many favors. (I certainly wouldn’t advise propping the patient bolt upright, though!)
Step 4: Supportive care
Supportive care means battling secondary problems as they arise. It doesn’t mean waffling over nonsense while your patient bleeds out.
If the patient’s airway is compromised, or you have legitimate reason to think that it may become compromised, then it should be managed. If they’re breathing inadequately, they’ll need assistance. Beyond that, any other care should only occur after you’ve stuck a cork in the bleeding and started rolling toward the guys with knives. Cardiac fiddling, pain management, splinting or minor bandaging — these should take place en route or simultaneous to other care, if at all. Shock kills people; is a nice sling-and-swath going to save them?
Spinal immobilization? It’s been pretty definitively shown to hurt rather than help in penetrating trauma. What about combined blunt and penetrating? There’s no evidence that it helps and some evidence that it’s harmful. We have no reason to think that tying people to boards does anything good, but we do know that wasting time here does everything bad. So if your local protocols demand immobilizing these patients, I won’t tell you otherwise — but please, at least, try and hurry.
That’s it, folks. Let’s wrap it all up next time by talking about recognizing the beast.
Key points:
- Stop the bleeding to the greatest extent possible in the field.
- Immediately and without delay transport to a facility capable of emergency surgery.
- Provide other supportive care as necessary, without delaying #1 and #2.
- Maximize oxygen delivery with supplemental O2, keeping the patient warm, and consider the Trendelenburg position.
- Minimize delays created by any and all non-essential care.
Understanding Shock VII: Negatives of Fluid Resuscitation
The last time we talked, we learned about the arguments in favor of non-blood fluid resuscitation. What are the arguments against it?
The “blow out the clots” argument
The vascular system is a pressurized circuit. Bleeding means poking an opening in this circuit, and we know that repairing this hole is our number one priority.
The body is pretty good at fixing leaks in its vasculature. But it’s not magic. It’s going to try to form a stable clot that covers and seals the hole, just like wrapping tape around a leaky pipe fitting.
What’s a good way to make this task harder? Increase the pressure inside the pipe. The faster that blood wants to rush out of the hole, the tougher it’s going to be to get a clot to stick there.
Imagine your inflatable raft has a pinhole in it, so you cover it with a piece of tape. It seals well. Then you drop a cooler of beer onto the raft, increasing the internal pressure. The tape blows off. Simple.
Many providers have therefore moved towards the practice of permissive hypotension — resuscitating only to a lower than normal blood pressure — and/or delayed resuscitation — waiting for substantial fluid replacement until bleeding has been controlled. Permissive may mean a pressure of 80, 90, or 100; it may mean giving crystalloids sparingly and only until blood becomes available; or it may mean giving nothing at all except the good stuff. Or you can take a page from the military, which says to resuscitate until a radial pulse is palpable, and the patient’s mental status is restored — then stop.
The dilution argument
There’s another reason why filling the patient with salt water might make it harder to control their bleeding.
Their body is trying to build clots at the location of injury. We want to encourage this process. In order to occur, it requires the activity of circulating platelets and clotting factors.
Mixing the patient’s blood with saline increases its volume but doesn’t increase the number of these clotting precursors. In other words, we’re diluting their blood, just like a bartender watering down your drink. There’s more volume in your cup, but there’s no more of the stuff we care about. And since the ability to form clots is closely related to the concentration of the clotting components, diluting the blood means slower clotting.
Together, these two arguments form a compelling case against the “volume for the sake of volume” theory. The patient’s ability to form clots and stop the bleeding isn’t a small thing; in a way, it’s the only thing. In fact, INR (a measure of clotting speed) has been shown to be a key predictor of whether a trauma patient will survive their injuries.
The proinflammatory argument
One of the key forces in the shock cascade is inflammation. So it seems like promoting more inflammation is the last thing we’d want.
But surprise: infusing fluids can do exactly this. It’s not entirely clear why this happens, but it’s unquestionably true; fluids encourage the inappropriate immune response and increase inflammation and tissue dysfunction. Suffice to say that this is bad.
Back in Vietnam, when aggressive fluid resuscitation really became trendy, doctors were perplexed to find many of their volume-resuscitated patients with a severe condition called “Da Nang lung” (nowadays Acute Respiratory Distress Syndrome) — wet, failing, edematous lungs with no cardiac cause. The combination of increased fluid volume plus increased inflammation means failing lungs. Or check your nearest ICU to see some abdominal compartment syndrome, where fluid fills the abdomen until the organs fail. What were you were saying about fluids being harmless?
The acidosis argument
The pH of our bodies is a hair over 7. Pick up the nearest bag of normal saline and read the label. What’s its pH?
Is it 7? No? More like between 5.0 and 6.0? Interesting. Remember that pH is a logarithmic scale, so we’re talking a difference of 10–100 here. So that nice “normal” fluid can promote significant acidosis.
Is this bad? Only if you like clotting. Acidosis is detrimental to coagulation (among other things), for reasons we’ll get into later. Clotting is good!
The what’s-the-point? argument
In the end, the most compelling argument against pouring what amounts to water into trauma patients is this: fundamentally it is not what they need. Their problem is not a lack of normal saline. “When I find a patient who’s bleeding crystalloid,” some providers are fond of saying, “I’ll give them crystalloid. But usually, the puddle on the ground is blood.”
Now, in some patients, crystalloid may indeed be what’s missing; we’ll touch upon situations like sepsis and dehydration later. But if they’re bleeding, it seems like — at best — playing with any fluid except those that can restore oxygen-carrying capacity or promote clotting is a waste of time that could be spent patching the hole and rushing toward surgery. And at worst, it may be exacerbating the problem.
For a long time, paramedics were taught to fill the hypotensive patient with fluid until their blood pressure was normal. The jury is still out on the best practices for fluid resuscitation, but there is fairly widespread agreement now that this is a bad idea. Many progressive systems have gone the route of giving no crystalloid whatsoever for hemorrhagic shock, or at least giving it very sparingly. Seeing the numbers 120/80 on the monitor seems like a good thing, but shock is not a blood pressure, raising the blood pressure is not necessarily beneficial, and we’re supposed to be making the patient feel better, not ourselves.
So, stop the bleeding, and restore the stuff that matters. Since we rarely give blood in the field, the first one is the main business of EMS. And oddly enough, it’s very much a BLS skill.
Summary:
- Increasing the blood pressure interferes with bleeding control.
- Diluting the blood discourages clotting while doing nothing for oxygen transport.
- Aggressive fluid resuscitation promotes inflammation, edema, and organ dysfunction.
- Current best practices are unclear, but likely involve a minor role for crystalloid resuscitation, in favor of bleeding control, blood products, and early surgical intervention.
Next time: mastering the field treatment of hemorrhagic shock.
Because it’s Cold Out There
http://www.youtube.com/watch?v=3pO2mdVpN20
We rarely think about it. If we did, we’d probably lose our marbles.
But it’s true.
The universe doesn’t care.
We are born, we live for a little while, and eventually, we die. In the duration, we will have hopes and fears, passions, desires, successes and defeats, joy and pain. The whole gamut is out there. And as a rule, the inexorable pull of the world is downward — into darkness, into chaos. Scientists call it entropy. We just call it life.
But it means that at any given moment, if we want to be happy — comfortable, fulfilled, free from suffering — we have to be waging a constant battle. If we ever stop paddling, we start to sink.
There’s a certain point in your youth (maybe this is the moment that you become an adult) when you realize this battle is nobody’s but your own. When you’re a child, your parents agree to fight in your ranks until you can walk and talk and drive a car. But once you step out onto the world stage, the only one wearing your colors is you. As self-centered people, we find this hard to believe; we feel like we’re important players in the grand scheme. But the truth is that although everybody else feels the same way about themselves, they certainly don’t feel the same way about you.
Nobody cares about your problems like you do. Not even remotely close. They’re busy with their own battles, which are just as burdensome to them as yours to you. So we learn that if we want to solve our problems, change our circumstances, or just keep from backsliding in the constant undertow of life, we’re on our own. The tools we bring to the table are the only ones available, and our to-do list has only our name at the top. There is no oversight, unless we have strong religious views; no referee ensures that the dice land fair; and if the game proves too difficult, we don’t get to quit and try another.
Isn’t this horrible?
Of course it’s horrible. What could be more horrible than to be utterly alone in an uncaring universe?
So we try to build ties. From the little twirling piece of driftwood we’re clinging to, we throw out ropes to the other flotsam and jetsam. We bring them close and tie knots in the hope of building a raft that can stay afloat during the next storm. Maybe this way, we think, if I capsize, someone will pull me back in.
This is hard work, though. Because our own problems are bad enough, and to tie ourself to someone else means we’re taking on some of theirs, too. It means when they get hit, it’s our job to try and keep them afloat. That’s a lot of responsibility, and our plate was already full to begin with. (Everybody’s plate is full, no matter how big it may look from the outside.) So at the best, we only make a few really strong ties.
Oh, we might have a lot of weak ones. Folks we know, and who will occasionally drift by to exchange favors or chat. Maybe a group that we’ll cruise with for a while. But make no mistake: they might be floating alongside us, but they haven’t tied any knots in that rope. If you start to founder, the best you can hope for is a little sympathy as they sail on ahead, and maybe toss you a spare life preserver. It’s not their problem.
The ones who really throw in their lot with you — who say that in thick or thin, in sickness or health, they’ll be at your side, fighting to keep you afloat — they’re few and far between. Maybe a little family, one or two close friends. A significant other. That’s all.
What do you think happens when you get older?
If you have the good fortune to live to a very old age, then a lot of things will change. Life is not going to suddenly become easy; if anything, it will become harder. And where are those ties you’ve built?
Dead. Moved away. No longer capable of anything more than clinging to life.
The luckiest among us will make it to the very last pages of life with our partners-in-crime still at our side. The spouse of fifty years, the close and loving family, the lifelong friend. But for most of us, these lifelines are lost over the years, one by one. And eventually, we may have nobody. Nobody to fight for us, to love us, or even to note our passing.
The next time you transport the 80-year-old man with dementia, who never seems happy and complains about everything —
The next time you’re called to the home of the little old lady with toe pain, whose husband died recently after a lifetime spent together —
The next time you pick up the same homeless man from under the bridge, drunk once again —
Try to imagine what it would be like to be truly alone.
Nobody to lean on. Nobody to throw you a rope when you start to founder. Most of all, nobody who gives a damn you exist. Imagine what it would be like to know that you could walk into the sea tomorrow and nobody would even know you’d died — let alone that you’d lived.
We can’t be everything for these people. But one day, hopefully not soon, you might just find that you’ve become one of them. So do what you can, knowing that nobody else is likely to. Knowing that, even when it has little effect, the difference between having somebody to fire a few shots for you, and having nobody — can be all the difference in the world.
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:
- 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.
- One argument for this is the maintenance of adequate blood pressure in order for the circulatory system to function.
- Another argument is the replenishment of the fluid lost from extravascular spaces.
Next episode we’ll discuss the dark side of crystalloid resuscitation.
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!
In brief:
- Blood transfusion is an important step in treating traumatic shock, secondary only to controlling the source of hemorrhage.
- Modern “component” blood banking allows for the administration of almost any ratio of red blood cells, plasma, and platelets.
- 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.
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:
- The prime directive in correcting shock is reversing the original cause; this takes precedence over any other treatment.
- In trauma, this means stopping the bleeding; that usually means surgery, and before that, direct pressure or tourniquets.
- Achieving this control is absolutely essential and absolutely time-critical.
Understanding Shock III: Pathophysiology
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:
- The processes of shock are multiple and self-reinforcing.
- Inflammation plays a major role.
- Multi-organ dysfunction and failure also plays a major role.
Next time: so what do we do about it?
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:
- Shock is characterized by inadequate oxygen delivery to the cells.
- This is typically caused by inadequate bloodflow to the tissues.
- 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.
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