Understanding Shock X (supplement): Fluid Choices

Although it may not be immediately relevant to most of us prehospital folks, the ongoing battle for supremacy in the world of IV fluids is a fascinating topic that’s worth following. We know that blood is the good stuff, but we remain interested in concocting an artificial fluid that can replace volume and mitigate the shock response — maybe even carry oxygen or support clotting — yet remain logistically feasible for everyday use. The current contenders are:


Normal Saline (aka NS)

Probably the most common fluid used today, this is nothing more than sterile water with .9% NaCL (table salt) dissolved in it. This amount of solute more or less approximates the concentration of our body’s water, which makes normal saline “isotonic”: its tonicity is approximately equal to our cells, making its osmotic pressure very low. In other words, it’s basically the same raw liquid we already have circulating, so its volume of distribution — the amount of saline that will leave the intravascular space, once we drip it in there — is relatively low.

That doesn’t mean we don’t lose a lot, though. Once it’s had a chance to settle out, quite a bit of infused saline will end up in the interstitial space. Typically this distribution will be in the ballpark of 1:3–1:4 — in other words, if we give a liter of saline, within an hour or so only about 250–300ml will remain in the intravascular space. Sicker people (who have problems like increased capillary permeability) have even higher volumes of distribution.

The benefits of normal saline: it’s very cheap. It’s very stable, lasting approximately forever on the shelf, and has minimal storage requirements. It’s compatible with every patient and every med. It’s easy to administer (any access will do, preferably large-bore).

The downsides: it carries no oxygen, impedes clotting, promotes inflammation, produces acidosis (called a hyperchloremic acidosis, since it’s secondary to the chloride content), and generally does absolutely nothing for you except increase the intravascular volume, and it does only an okay job at that.


Lactated Ringer’s (aka Ringer’s Lactate)

This stuff is basically normal saline with some extras. Like NS, it’s isotonic, so the volume of distribution is the same. But in order to mitigate the acidosis produced by NS, it’s got lactate added. Lactate converts to sodium bicarbonate in the blood, and bicarb is a strong base, so Ringer’s essentially comes “buffered” — it should have less impact on the pH. This is good, and large volumes of this stuff have a more benign effect than large volumes of saline. (Ringer’s also includes some other electrolytes, such as potassium and calcium, bringing it closer to the composition of blood serum.)

The downsides: for many prehospital services, the main “downside” is that they don’t want to stock multiple types of fluid, so once they’ve stacked NS on the shelves they’re done. Ringer’s is not as appropriate for general use, since it’s incompatible with some medications and contraindicated in some patients. There is also an old belief that it’s incompatible with blood products — that is, if you hang a bag of PRBCs on your Ringer’s line, the calcium in the Ringer’s will stimulate the coagulation cascade (PRBCs are usually stored by adding citrate, which prevents clotting by binding up calcium) and create emboli. This is now generally understood to be false.


Hypertonic solutions

Now we get into the more interesting stuff.

Remember we agreed that normal saline and Lactated Ringer’s are isotonic? What if we use a fluid that is hypertonic? This would mean that the fluid has a higher tonicity (more dissolved stuff) than our cells. Since the golden rule of osmosis is that water moves toward the space with the higher concentration of dissolved solids, adding hypertonic fluids to the blood — and hence making the blood hypertonic — will cause fluid to move from the intracellular into the intravascular space.

Why would this be good? Well, for one thing, it yields an awesome volume of distribution. Compared to the isotonics, distribution is actually reversed; we end up with more than we put in, not less. Infusing a liter of a typical hypertonic can yield an eventual volume increase of nearly 8 liters.

Isn’t it bad to suck fluid out of our cells? It would seem like it. However, for short-term use (such as emergency trauma care), the effects of this generally seem to be benign. In fact, there is some evidence that using hypertonic solutions may attenuate the inflammatory response associated with fluid administration — perhaps just because we don’t need to give as much of it.

So far, there’s insufficient evidence for the routine use of hypertonic fluids in the civilian world. So far, the research suggests that they’re “at least” as good as the isotonics. The military is another story, though; they love this stuff, because it’s light. Whether or not they should be doing that, in order for a combat medic to dump 4 liters of saline into someone, he’d have to carry 4 liters of liquid on his back — alongside absolutely everything else he’s going to need. Much better to bring some easily-portable 250ml bags of a hypertonic. It’s like an expand-o-fluid.

There are various hypertonics out there, including high-concentration salines (such as 3.0% — call it abnormal saline if you want to be cute) and others. So far nothing’s really landed on top, although mannitol is often used to suck fluid from the brain and cause “shrinkage” during cerebral edema.



Saline is a crystalloid fluid because it’s water with small ions dissolved in it. The sodium (Na) and the chloride (Cl) are not like particles of sand, swirling around in there but too small to see — they’re fully dissolved and dissociated.

Colloids are different. A colloid is a large molecule, something too big to easily cross cellular membranes. These don’t dissolve in the same way; they’re more like ice cubes rattling around in your glass. Blood itself is a colloid, since it contains big molecules like red blood cells.

“If blood is colloidal,” the wags say, “why not try giving colloidal fluids?” Well, all right then.

One big benefit of this would be the volume of distribution. Since the colloidal solids can’t easily escape across the membranes, they remain in the intravascular space and hence keep the oncotic pressure high.

But they’re usually expensive. And tend to be more complicated (in indications and contraindications) than crystalloids. And can be more finicky to store. And for the most part, have been shown to be no better than crystalloids. Oh well.


Artificial oxygen-carrying colloids

Well, here’s a neat idea. Maybe an arbitrary colloid isn’t much good, but can we make one that mimics blood — can we come up with a fluid that actually binds and carries oxygen in the same sort of way as our red blood cells? If we could create such a thing, and if it were broadly compatible and not too expensive and had a reasonable shelf-life, it would be the next best thing to using blood and a major breakthrough.

We have created such things, either wholly artificial or derived from purified (usually cadaverous) blood samples. You can store them for ages, although they’re not particularly cheap, being new, on-patent drugs. So far they all seem to have little to no benefit in outcome — and often an increased rate of complications like heart attacks. Hmm. The search continues. (The trick may be to come up with something that shares more of blood’s qualities, such as positive-feedback binding, and maybe even some clotting goodness. We’ll see.)


Hypotonic fluids 

Like half-normal saline! Good stuff, right? Wait, no. That would have a god-awful volume of distribution. Excellent, you’re paying attention.


Blood Products

You really were paying attention! Full circle we come. Although blood is not all things to everybody, and has its own negatives and caveats, at the present date if you lose blood the best replacement is blood. Of some kind.

Of what kind remains a bit of a mystery. Men in white coats continue to play with different mixtures of red cells, and plasma, and platelets, and even various concentrates and precipitates of specific clotting factors. One of the latest miracle additions is tranexamic acid, which antagonizes natural thrombolytics (remember plasmin?) and seems to reduce bleeding. There are also cool devices, used mainly during surgery, that “salvage” your own lost blood, rinse it off, and give it right back to you, which obviously simplifies some things.

Of note is an approach to transfusion developed by the anaesthesiologists at Shock Trauma in Baltimore. They like to give PRBCs and plasma until you reach a reasonably permissive pressure. Then they bolus some opiate goodness (fentanyl is nicely controllable). This puts a brake in the patient’s compensatory catecholamine response — their clamped-down veins and arteries relax a little. Which drops the pressure again. So they give some more fluid. Which raises the pressure again. Then they give more fentanyl. Repeat repeat repeat. The end result? A well-resuscitated patient — with a nice pressure — but with a relaxed, normal vasculature — and a normal volume. It’s not hard to fill up a severely compensating patient; their pipes are tiny. But it’s also not as good as filling them up to a normal perfusing volume. Neat idea. (Plus, pain management or sedation for surgery is no problem with that much fentanyl on board!)

Best of all, of course, is simply not to lose the blood to begin with. Tourniquets have really made a resurgence, and many feel that at this date, nobody with reasonably timely medical care should ever die from an extremity injury — not if you can slap a tourniquet somewhere proximal and cinch it down until the bleeding stops. The military has led the way with this, as with the use of hemostatic agents — powders you sprinkle on (or, nowadays, often come pre-embedded in a dressing) which help chemically promote clotting when combined with direct pressure.


Okay, so where does all of this leave us?

We’re not sure. Despite decades of research into this topic, best practices remain uncertain. But the following are probably true:

  1. Extremes are probably to be avoided. Too much or too little of anything is rarely good.
  2. If there is any benefit for non-oxygen-bearing, non-clotting fluids in hemorrhagic resuscitation, it is likely limited to a supplemental or temporizing role.
  3. Further evidence may or may not demonstrate a benefit from hypertonic solutions.
  4. A really usable “instead of blood” fluid remains the holy grail, and is not yet available.

and most of all…

  1. There are significant negatives associated with any fluid administration, so in order to produce real improvements in survival, any benefit must be substantial enough to outweigh this basic harm.

Thanks to everyone who stayed with us through this lengthy chat about shock! I want to give particular thanks to Dr. Jeffrey Guy, whose teachings were instrumental in forming the core of my own material.


Back to Part IX

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.


  1. Increasing the blood pressure interferes with bleeding control.
  2. Diluting the blood discourages clotting while doing nothing for oxygen transport.
  3. Aggressive fluid resuscitation promotes inflammation, edema, and organ dysfunction.
  4. 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.


Go to Part VIII or back to Part VI

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

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.


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.