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.

 

Colloids

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

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.

The “Big Picture” Diagnosis

Our topic for today: diagnosis using a broad constellation of indicators, not a single red flag.

To mix things up, rather than read about it, let’s talk about it.

Here’s the quote I mentioned, from TOTWTYTR at the CCC blog.

Eight Tips on Ambulance Wrangling

One of these days, we’ll have to do a comprehensive post on care and feeding of the multi-wheeled chariot we call the “waaambulance.” For the time being, however, here are a few morsels that most people don’t figure out until they’ve been in the business for a few months at least. These apply mainly to any Type II (van) or Type III (van cab with box module) ambulance based on the Ford chassis, although they may have some application to other vehicles as well.

  1. If you turn the ignition key too far, it may get stuck slightly past the “on” position, in which case most of your vehicle electronics (FM radio, air conditioning, etc.) will not work. It’s not broken; just turn it backwards slightly.
  2. In a similar vein, you may occasionally find that after switching off the power, your key is trapped in the ignition. Give the gearshift a wriggle while turning and pulling at the key. Jiggle the steering wheel too.
  3. Lock yourself out? For shame. On many Type II (van) units, there’s an easy solution: unscrew your antenna (either the FM antenna or a stout two-way) and head to the back doors. The leftmost of the two lights above the license plate should be easily removable, and you can poke the antenna up into the gap and use it as a probe to “lift” the base of the locking post. Then open the sucker up and unlock the rest using the electronic switch (or just climb through to the cab). Of course, your service may also have installed an emergency unlock button somewhere hidden, but you should hopefully know about that…
  4. The knob that you pull to activate the headlights has another function. If you twist it while it’s in the “on” position, it will adjust the brightness of your dashboard console (including the LCD radio display and the lights behind the dials); give this a try if your radio seems inexplicably dim. And if you turn it all the way to the left (it will click), it’ll usually activate the overhead light.
  5. If you have a digital odometer, there should be a button beside it that cycles through your tripometers and resets them. If the ignition is off and you need to retrieve the odometer mileage for paperwork, you don’t need to turn the key; just press this button and the display will light.
  6. If you have a “momentary” switch that disables the backup alarm (rather than one that can be switched off permanently), you can hold it down while shifting into reverse (you may have to shift left-handed) in order to avoid any beeping; this is a nice courtesy to avoid deafening your partner if they’re back there spotting you. Otherwise you’ll usually let out at least one beep before you can hit the switch. Once you’ve shifted you can let it go.
  7. The newer gasoline vans have a third “cigarette lighter” charging port located inside the glove compartment.
  8. Diesel vehicles can safely be fueled while the engine is running. There’s no need to shut down and kill the AC and everything else. I would not, however, try starting the engine while fueling it.

Pulse Oximetry: Application

The final part of a series on oximetry: start with Respiration and Hemoglobin and Pulse Oximetry: Basics

Pulse oximetry is not always available in EMS — depending on level of care, scope of practice in your area, and how your service chooses to equip you — but when it is, it’s a valuable tool in your diagnostic toolbox. Just like we discussed before, and just like any other piece of the patient assessment, using it properly requires understanding how it works and when it doesn’t.

 

Clinical context: When a sat is not a sat

Simply put, oximetry is the vital sign of oxygenation. It is the direct measurement of the oxygen in your bloodstream. It does not quite measure the oxygen that is actually available to your cells, but it gets close.

First, remember that actual oxygen delivery requires not just adequate hemoglobin saturation, but also enough total hemoglobin, moving around at an adequate rate. In hypovolemia, such as the shocky trauma patient, or in anemia, you might see a high SpO2 — which may be entirely accurate — but this doesn’t necessarily mean that the organs are not hypoxic. After all, you could have nothing but a single lonely hemoglobin floating around, and if it had four oxygen bound to it, you would technically have a sat of 100%. But that won’t keep anyone alive. Evaluating perfusion is a separate matter from evaluating oxygenation.

Second, remember our discussion of the oxyhemoglobin dissociation curve. The fact that you have oxygen bound to your hemoglobin doesn’t mean that it’s actually being delivered to your cells. That is, you can be hypoxic — inadequate cellular oxygenation of your organs — without being hypoxemic — inadequate oxygen present in the blood. Oximetry will only reveal hypoxemia.

Two of the strongest confounders here are cyanide and carbon monoxide (CO) poisoning. The main effect of cyanide is to impair the normal cellular aerobic cycle, preventing the utilization of oxygen; since it has no effect on your lungs or hemoglobin, the result is a normal saturation, yet profound hypoxia, since none of the bound oxygen can actually be used. Carbon monoxide, on the other hand, involves a twofer; it binds to hemoglobin in the place of oxygen, creating a monster called carboxyhemoglobin. CO has far more affinity for carboxyhemoglobin than oxygen does, so it’s hard to dislodge, and you therefore lose 1/4 of your available binding sites in the affected hemoglobin. But it doesn’t stop there. Carboxyhemoglobin also has a higher affinity for oxygen. This creates a leftward shift in the oxyhemoglobin dissociation curve — the oxygen that actually does bind finds itself “stuck,” and these well-saturated boats happily sail past increasingly hypoxic tissues without ever unloading their O2.

Consider the oximetric findings in these patients. The cyanide patient will have unimpaired blood oxygenation, so (unless he has already succumbed to respiratory failure due to the effects), a normal sat will be seen; however, hypoxia will be clinically apparent, particularly as ischemia of the heart and brain. Carbon monoxide, on the other hand, will reveal a normal or elevated (100%) sat which is partially accurate — some of that is true oxygen — and partially baloney, since CO looks the same to the oximeter as O2. But this is moot, because neither the bound CO nor the bound O2 is available to the cells. Oximeters do exist that can detect the presence of carboxyhemoglobin, known as CO-oximeters, but they are expensive and uncommon, and there is some question as to their accuracy. Your best helper here is in the patient history: both CO and cyanide are produced by fires, or any combustion in enclosed spaces (such as stoves or heaters), cyanide being released by the combustion of many plastics. You should be very wary of normal sats in any patient coming from a house fire or similar circumstances.

(Both cyanide and CO poisoning are known for causing bright red skin. In both cases oxygen is not being removed from hemoglobin, so arterial blood remains pink and well-saturated. Carboxyhemoglobin itself is also an unusually bright red. This skin, a late sign, is usually seen in dead or near-dead patients.)

Third, consider that although oximetry is an excellent measure of oxygenation, this is not the same as assessing respiratory status. It’s a little like measuring the blood pressure: although it’s a very important number, BP is an end product of numerous other compensatory mechanisms, and a normal pressure doesn’t mean that there aren’t challenges being placed on it — merely that they’re challenges you’re currently able to compensate for. Perhaps you’re satting 98%, but only by breathing 40 times a minute, and you’re fatiguing fast. Perhaps you’re satting 94%, but your airway is closing quickly and in a few minutes you won’t be breathing at all. These are clinical findings that may not be revealed in SpO2 until it’s too late.

Fourth: oximetry measures oxygenation, but not ventilation. When you breathe in, you inhale oxygen; when you breathe out, you exhale carbon dioxide. Although we use the term ventilation to describe the overall process of breathing, formally in the respiratory world it refers to the removal of carbon dioxide. Is oxygenation the more important of these two functions? Certainly; it will kill you much faster. But hypercapnia (high CO2) caused by inadequate ventilation is also a problem, and pulse oximetry does not measure it. (Capnography is the vital sign of ventilation, but that’s a topic for another day.) Now, insofar as oxygenation is primarily determined by respiratory adequacy (rate, volume, and quality of breathing), and respiration both oxygenates and ventilates, oximetry can be a good indirect measurement of ventilation; if you’re oxygenating well, you’re probably ventilating well too. This remains true if breathing is assisted via BVM, CPAP, or other device. But this is not true if supplemental oxygen is applied. Increasing the fraction of inspired oxygen (FiO2) improves oxygenation without affecting ventilation; on 100% oxygen I might be breathing 8 times a minute, oxygenating well, but ventilating inadequately.

Finally, it’s worth remembering that once you reach 100% saturation, PaO2 may no longer correlate directly with SpO2. If you reach 100% saturation at a PaO2 of 80, we could keep increasing the available oxygen until you hit a PaO2 of 500, but your sat will still read 100%. So without taking a blood gas, we don’t know whether that sat of 100% is incredibly robust, or is very close to desatting. (That’s not to say that a higher PaO2 is necessarily better; recent research continues to suggest that hyperoxygenation is harmful in many conditions. Not knowing the true PaO2 can be problematic in either direction.)

 

Hardware failure: When a sat is not anything

In what clinical circumstances does oximetry tend to fail? The primary one is when there isn’t sufficient arterial flow to produce a strong signal. This can be systemic, such as hypovolemia — or cardiac arrest — or it can be local, such as in PVD. (The shocked patient has both problems, being both hypovolemic and peripherally vasoconstricted.) Feel the extremity you’re applying the sensor to; if it’s warm, your chances of an accurate reading are good. The best confirmation here is to watch the waveform; a clear, accurate waveform is a very good indicator that you have a strong signal.

Tremors from shivering, Parkinsonism, or fever-induced rigors can also produce artifact on the oximeter. Some patients also just don’t like the probe on their finger. Try holding it in place, keeping the sensor tightly against the skin and the digit motionless. If there’s no luck, try another site. Any finger will work, or any toe, or an earlobe. (Some devices don’t require “sandwiching” the tissue, and can be stuck to the forehead or other proximal site, but these are uncommon in outpatient settings.)

There are a few other situations that can interfere with normal readings. In most cases, nail polish is not a problem, but dark colors do decrease the transmittance, so some shades have been reported to produce falsely low readings in the presence of already low sats or poor perfusion — as always, check your waveform for adequate signal strength. Very bright fluorescent lights have been reported to create strange numbers, and ambient infrared light — such as the heat lamps found in neonatal isolettes — can certainly create spurious readings. A few other medical oddities fall into this category as well, including intravenous dyes like methylene blue, and methemoglobinemia, which produces false sats trending towards 85%.

Is oximetry a replacement for a clinical assessment of respiration, including rate, rhythm, subjective difficulty, breath sounds, skin, and relevant history? Absolutely not. But since none of those actually provide a quantified assessment of oxygenation, they are also no replacement for oximetry. It is a valuable addition to any diagnostic suite, particularly to help in monitoring a patient over time, as well as for detecting depressed respirations before they become clinically obvious — especially in the clinically opaque patient, such as the comatose. When it’s unavailable in the field, we readily do without it. But when it’s available, it’s worth using, and anything worth using is worth understanding.