Staying in Place: Compensation and Endpoints

Red queen running


Man’s leaning against a wall. He doesn’t move for hours. Just stands there not moving. Finally, someone says, “You been here all day — don’t you have anything to do?”

“I’m doing it,” he answers.

“Doing what?”

“Holding up the wall.”


And who’s to say he’s not? Maybe he’s working as hard as he can to make sure that wall doesn’t fall down.

In this situation, the man is a compensating mechanism. He is struggling to prevent changes in the wall; keeping that wall upright is an endpoint he cares to maintain, to sustain, to keep intact.

How do we know that the wall isn’t holding up the man? Because we don’t care about the man. Whether he leans or falls doesn’t matter much to anybody. But it would be a terrible thing if the wall collapsed. So we’ll let the man lean or shift in order to prop up the wall when it starts to totter — we’ll use him, adjust him, to compensate for any wall-changes. That’s why he’s there.

If the wall gets weak enough or tilts too far, though, he won’t be able to keep it up. He’ll try, but he’s not infinitely strong, and then maybe the wall begins to tilt or collapses completely. Since we know that under normal circumstances, he’s doing his best to prevent this, if we walk in and see that the wall is tilting, that is not a good sign. It may mean that despite his best efforts, the man has exhausted his strength and is no longer able to resist further wall-changes; or it may mean that, for some reason, the man isn’t doing his job properly. Either way, any further tilting will be unopposed, and will probably happen rapidly and uncontrollably.


Compensators and endpoints

This same dynamic plays out within the human body. As we know, living organisms seek to maintain a certain homeostatic equilibrium. We put our vital metabolic processes in motion and we don’t want them to halt or change, despite any insults or fluctuations imposed upon us by our surrounding environment. So our bodies struggle to keep all of our complex systems at an even keel, using a diverse and powerful array of knobs, dials, and other regulatory tools. Not too hot or too cool, not too acid or too basic, not too fast or too slow. Just right.

The kicker is this, however. Some of our physical parameters are more important than others. In other words, while some parameters have room to adjust, others aren’t negotiable, can’t change much, without derailing our basic ability to function and survive. Things like blood pressure (or at least tissue perfusion, for which blood pressure is a pretty good surrogate measure) are essential to life; your pressure can fluctuate a little, but if it drops too low, you are unquestionably going to suffer organ damage and then die. And yet there are many insults that could potentially lower our blood pressure if we let them: if we bleed a little, or pee a little, or don’t drink enough water, or sweat, or even just stand up instead of sitting down. How do we preserve this vital parameter despite such influences?

By compensating, of course. Our body gladly modulates certain processes in order to preserve other, more important parameters. So in order to maintain blood pressure, perhaps we accelerate our heartrate. In an ideal world, it might be nice if the heart were thumping along at — let’s say — a mellow 80 beats per minute. It’ll use little less energy and less oxygen than if it were beating faster. But it’s really important to keep our blood pressure up, and speeding up the heart can increase the pressure, so we gladly make that trade and induce tachycardia. (Many of these compensatory systems are linked to the sympathetic nervous system, our body’s standard “all hands on deck” response to stress and crisis.)

So imagine we find a patient who’s bleeding and notice that he’s tachycardic, with a normal blood pressure. This suggests a compensated shock; the body is using tachycardia to maintain that normal pressure we see; although his volume is lower than usual, the critical endpoint of adequate blood pressure is still intact.

But what if instead, we found him tachycardic and hypotensive? Well, that’s not good. We see that the body is trying to compensate, but we also see that the important endpoint — blood pressure — is falling nonetheless. The body would never intentionally allow that; BP is too important. So we recognize this as decompensated shock. The hypovolemia has progressed so far, and volume is now so low, that he can’t make up the difference anymore — the compensatory slack has run out — and any further decreases in volume will probably lead to an immediate and unopposed drop in pressure. There’s nothing more the body can do on its own; it’s out of rope.

The skilled clinician — or “homeostatic technician” as Jeff Guy says — uses this predictable progression to understand what’s happening in almost any crisis. Because primary insults are initially covered up by compensatory mechanisms, they may not be immediately apparent, and the earliest and most detectable signs of physical insult are usually nothing more than the footprints of the answering compensation. Thus, when when we encounter those, we know to suspect the underlying problem even if it’s not obvious yet. It’s like seeing brakelights flash from cars on the road ahead; even if you can’t see an obstacle yet, you know people are slowing down for something.

Obvious signs of decompensation usually show up late. Once the primary, underlying problem is revealed by failure of the corrective mechanisms, it’s often progressed so far that it’s too late to address. If you wait to brake until you can see the wreck itself, you might not be able to stop in time.


Two signposts for decompensation

There are two great ways to recognize which signs and symptoms connote decompensation.

The first is to understand which physical parameters are endpoints — which functions the body tries to preserve at all costs. These processes are only compromised as a last resort, so if you see them deteriorate, things are in the end-game; the body doesn’t intentionally sacrifice these for the benefit of anything else.

The second clue is more subtle. In this case, you observe a compensatory mechanism (not an endpoint), but find that it’s no longer successfully compensating — it’s failing, and starting to unwind and scale back, rather than doing its job. The changes in the compensatory system are inappropriate, resulting in less of what we need, not more. This happens when our systems are so damaged that they can’t even fix problems and pursue homeostasis anymore; our infrastructure, maintenance, and repair systems are breaking down. Consider this: we saw how tachycardia could be compensatory, but could bradycardia ever be beneficial in shock? Probably not. So if we found a shocked patient with bradycardia (and likely hypotension, the failing endpoint), we should be very alarmed indeed. There’s nothing helpful, compensatory, or beneficial about bradycardia in the setting of shock, so we recognize that the body would never go there on purpose. It’ll only happen when the machinery itself is falling apart.

Consider, for instance, Cushing’s Triad, the collection of signs often encountered after severe traumatic brain injury, when intracranial pressure has increased enough to squeeze the brain out from the skull like toothpaste. The triad includes hypertension, bradycardia, and irregular or slow respirations. What’s interesting is that, while all are a result of increased ICP, one of these is compensatory, while the others are merely the result of damage. Hypertension is the body’s compensatory attempt to force blood into the brain despite the elevated pressure in the skull. But bradycardia and bradypnea simply result from pressure upon the regulatory centers of the brain tasked with maintaining breathing and heart-rate. That’s why hypertension may be seen earlier, while the other two signs won’t usually manifest until the brain is actively herniating. One signals compensation, the other two decompensation.

Of course, there can be other reasons why compensatory mechanisms might fail, or at least exhibit lackluster performance. Some medications or other aspects of a medical history (potentially unrelated to the current complaint) might throw a wrench in the system. For instance, beta blockers (such as metoprolol and other -olol drugs) limit heart-rate as part of their basic mechanism, so patients with beta blockade often have trouble mustering compensatory tachycardia during shock states. That doesn’t mean they’re any less shocked; in fact, it means they’re more susceptible to hypotension, and that you must be especially on the lookout, because you won’t see one of the red flags (a rapid heart-rate) you might usually expect. Elderly patients with many comorbidities are generally not able to muster up effective compensation for anything, so they can deteriorate quickly, and without much fanfare. Ironically, healthy pediatric patients are the opposite: since they’re so “springy” and smoothly functioning, they compensate very well, with few changes in observable endpoints, until suddenly running out of slack and crashing hard because they’re already so far from shore.

Here are a few important compensatory signs, breakdowns of compensatory systems, and vital physical endpoints:


Appropriate signs of compensation

  • Tachycardia — increases cardiac output
  • Vasoconstriction (cool, pale skin) — raises blood pressure
  • Diaphoresis (sweatiness) — decreases temperature when necessary, but is often just a side effect of sympathetic stimulation
  • Tachypnea — increases oxygenation, CO2 blowoff, and cardiac preload
  • Fever — part of the immune system’s response to infection
  • Shivering — warms a hypothermic body

Inappropriate changes in compensatory mechanisms

  • Bradycardia — reduces cardiac output, rarely useful in illness; as a chronic finding may be the result of high levels of cardiovascular fitness (in healthy young patients) or medications (in sick old patients); but acutely, it is an ominous finding
  • Bradypnea — reduces oxygenation, CO2 blowoff, and cardiac preload
  • Hypothermia (or normothermia when a fever is expected) — suggests a failure of temperature regulation

Inviolable endpoints

  • Blood pressure — can elevate in stress states, but should not drop below resting levels
  • Mental status — except in the presence of a drug or similar agent directly affecting cognition, maintaining appropriate alertness and mentation are always a top priority for the body
  • Blood glucose — kept at normal levels in almost all situations, except when the regulatory systems fail, as in diabetes mellitus
  • pH — most of the cellular machinery fall apart if significant acidosis or alkalosis occurs
  • Low O2 saturation or cyanosis — although oxygen saturation can dip briefly without harm, and in some patients (particularly those with COPD, or long-time smokers) it may run low at baseline, a significant acute drop — or the clinical equivalent, which is frank cyanosis — is always inappropriate.

Mastering BLS Ventilation: Algorithms

Continued from Mastering BLS Ventilation: Introduction, then Mastering BLS Ventilation: Hardware, then Mastering BLS Ventilation: Core Techniques, and finally Mastering BLS Ventilation: Supplemental Methods

Over the past few weeks, we’ve explored a large number of BLS tools for maintaining a patent airway and pushing oxygen through it. This is good, because the only reliable way to address this dilemma is by having a large toolbox. Nobody can oxygenate every patient with just one trick, no matter how skilled they are.

But a box of tools isn’t an approach to the airway, no matter how big it is. It’s just a box. You need more than that — you need a plan. If I toss you an apneic person, what are you going to do? What if that fails? What’s plan B? And plan C? Then what happens?

The only way to answer these questions is by creating your own scheme, a roadmap to fall back upon. I can’t give it to you, because I don’t know your variables. I don’t know your specific skillsets, what you’re comfortable with, what you’ve practiced and in what situations, versus what you’ve never done in your life. I don’t know what your local protocols are, and what equipment you have available (including extra toys like supraglottic airways or Narcan/naloxone), your typical transport times, or the general availability of ALS. I don’t know what type of patients you usually encounter, how many personnel you have on hand to manage them, and what sort of extrications are involved.

But you know those things. Roll it all into a ball so you understand your resources and challenges, consider the various tools we’ve discussed, and make a plan.

Click to expand

Click here for a PDF version (recommended if printing)

Here’s an example I concocted. This is a flowchart patterned after the airway algorithms commonly used in the ED or the ICU, and it incorporates most of the ideas we’ve talked about. It assumes certain things, so I’m not putting it forward as something to follow religiously. Rather, it’s meant as an example: this is the type of thinking you need to be doing. You probably won’t take the time to chart it out, but you should at least be thinking about it now, because figuring it out on scene with the sick person is too late. Mentally walk through what you’d do at each juncture, imagining yourself treating a real patient in your real ambulance using your real gear. Think about your responses to each dilemma, and if you discover you’re unsure about any details, seek out additional training or practice to patch those holes; for instance, spending some time with a (high quality) mannequin and a BVM can be beneficial. Even just a few minutes playing with the BVM (try bagging yourself until you really understand how the pressures and airflows work), the non-rebreather, your various airways, and so forth can help develop familiarity with little-used tools, so you truly understand how all the valves function, how to size and adjust everything, even where it can be found in your bags. This is particularly important if you rarely use these tools, because infrequent or not, you still need to exhibit mastery when the time comes.

Questions, comments, or remarks on our proposed model are welcome.

Thanks for sticking with us through this exploration of the art and science of BLS ventilation.

Mastering BLS Ventilation: Supplemental Methods





Sellick’s Maneuver









Pocket Masks





Mouth to Mouth




Just options, folks. Airways need options.


Jaw Thrusts





Risk Factors for Difficult BVM Ventilation


Patients who are often challenging to bag include:



The End-Expiratory Pop








Key Points



Continued at Mastering BLS Ventilation: Algorithms

Mastering BLS Ventilation: Core Techniques




Hand Technique

How do you hold a BVM to the patient’s face?



In theory.






Basic two-hand seal


Both methods compared




The Sniffing Position





Image courtesy of





Image courtesy of



Image courtesy of



Key Points

  4. Obese patients may need substantial head elevation.




Mastering BLS Ventilation: Hardware



Continued from Mastering BLS Ventilation: Introduction

The basic tool of BLS oxygenation is the bag-valve-mask, aka the bag-mask (as the AHA calls it), aka the Ambu-Bag (as most in-hospital staff call it, after one of the popular manufacturers), aka the self-inflating resuscitator. We’ll talk about techniques for optimizing for BVM success later. For the moment, let’s discuss some of the other auxiliary aids available. As we do, remember our main challenges: if we don’t minimize the resistance to airflow into the trachea, we’ll be prone to inflating the stomach instead of the lungs. And if we don’t minimize obstructions higher in the pharynx, we won’t be able to introduce any air at all.


Nasopharyngeal and Oropharyngeal airways

The NPA (or nasal trumpet) and OPA are the mainstays of BLS airway adjuncts. Essentially, they’re just curved pieces of plastic or rubber, designed to be inserted into the upper airway to prevent soft tissue from collapsing and obstructing the lumen.

When I first learned about these, it was just after hearing about the head-tilt chin-lift and jaw thrust, which were purportedly enough to open any self-obstructing airway. Why did we need these tools? “This way,” my instructor advised, “you don’t have to sit there holding their airway open.”

Well, yes and no.

The standard theory behind these devices is this: in a supine, unconscious patient, the tongue (and other soft tissue) wants to collapse into the pharynx. If we can jam something in the way, it will essentially “splint” open the passage — stick a foot in the door — much as if we were holding tissue back with a tongue depressor. Positioning the head and neck in such a way that it widens the relevant gaps would accomplish the same thing.

Under this thinking, we have several redundant tools to accomplish the same purpose. Whether we open the airway by tilting their head and lifting their jaw, or by sticking an OPA in the mouth, or by sticking an NPA in the nose, the result is the same.

But this doesn’t quite reflect reality. Sometimes it will, but in many patients with difficult airways, it’s not so simple to maintain a patent passage for airflow. In an obese patient with challenging upper airway anatomy, the amount of soft tissue standing in your way may be profound, and it can obstruct the lumen in multiple places. Additionally, tone may be so lacking that it easily “molds” around anything you stick in there.

In other words, if you place a BLS airway, the only breathable passage you’re really guaranteed is the lumen enclosed by the device itself: the central hole or grooves. And that’s not very much room. Our goal isn’t to create a tiny breathing tube, it’s to maximize the amount of usable airway — we’d like to be able to ventilate through as large a diameter as possible. That means using everything we can.

So proper positioning is helpful. So is an OPA. And perhaps an NPA. Or two.

In fact, if at all possible, it’s always worth trying to insert multiple airways. This is typically not taught to EMTs (since textbooks subscribe to the the “splinting” rather than the “protected lumen” theory), but it’s widely practiced in the ED and by experienced paramedics. If you’re having any difficulty at all bagging, shoot for an OPA with bilateral NPAs; filling all the available holes with patent airways is always a good idea.



Remember what you’re actually doing with each airway. With an NPA, you’re separating the soft palate from the superior and posterior nasopharynx, and if it’s properly sized, it should be long enough to create a passage through the laryngopharynx, nearly to the epiglottis. (If it’s too long, it can stimulate the gag reflex, or jam into the vallecula or epiglottis, actually obstructing the larynx; if it’s too short, it may not protect the laryngopharnyx, or even may not fully span the nasopharynx, allowing the soft palate to shut.) With an OPA, you’re separating the lips, depressing the tongue to prevent it from obstructing the oral cavity, and more importantly protecting the laryngopharynx in the same way the NPA does — keeping the tongue or other anterior structures clear.

So if you only insert an NPA, the nose is your only guaranteed airway. If the mouth itself is shut — and we typically squeeze it shut when we bag using the “EC clamp” technique — nothing will flow through the oropharynx. Conversely, if we only insert an OPA, there is no guarantee that the nasopharynx will remain patent, particularly where the soft palate wants to meet the posterior pharynx.

So use both, because we want it all.


OPAs are more widely used, but it’s a shame to neglect the NPA. The advantage, of course, is that patients with an intact gag reflex can still tolerate an NPA, whereas the OPA may stimulate vomiting. It’s unwise to use the “try and see” approach with the OPA, because there’s nothing quite like copious emesis to make a difficult airway more difficult. Kyle David Bates teaches the helpful tip of inspecting for saliva and secretions collecting in the mouth; if there are none, the patient likely has an intact gag reflex. If they are present, an OPA is probably safe. But suction is always worth keeping on-hand and prepared.

It’s taught that NPAs are contraindicated in patients with significant facial or cranial trauma, on the theory that you may pass the device through a basal skull fracture right into the brain. This is probably a negligible risk; the entire concept seems to be based on two (yes, that’s the number before three) case reports in the literature. If your suspicion is quite high (blood from the nose with a positive halo test, for instance), you may want to steer clear, but with a truly difficult airway, remember that oxygenation is more important than an extremely remote risk of poking the patient’s noodle.

NPA placement can be facilitated by ensuring you lubricate the device first (water-based jelly should be available, although traditionally the patient’s saliva can be used as a last resort), aiming “in” (posteriorly) rather than “up” (superiorly), and lifting the nose to facilitate this angle. Also, remember that each nasal fossa has erectile tissue which takes turns engorging and partially obstructing airflow (allowing cyclical “resting” of the mucosa), so at any given time, one nare will likely allow easier NPA passage than the other; if you’re having difficulty, just switch sides. (Stripping part of this tissue away from the concha will occasionally cause post-insertion bleeding, but it’s rarely significant.)

As for the OPA, we usually teach insertion with the tip pointing up, followed by a 180-degree rotation once it’s fully inserted. Just remember that it’s also acceptable and sometimes easier to insert it tip-down while holding back the tongue with a tongue depressor or finger.

Another somewhat prosaic benefit to the OPA is that it may help provide structure to edentulous [toothless] patients when you’re trying to bag them, although simply leaving dentures in place can also work.


Apneic Oxygenation

You may not think that the lowly nasal cannula and non-rebreather mask really qualify as useful airway tools in an apneic patient. But oh, you would be wrong.

Pop quiz: is it possible to oxygenate the blood without actively moving any air? In other words, can you breathe without breathing?

You might say no. But why not? Gas exchange in the alveoli is not an active process; you’re not forcing the O2 molecules across the membrane by any chemical or muscular exertion. They simply diffuse passively, like gin dispersing into your tonic. All you’re doing when you breathe (either spontaneously or via positive-pressure ventilation) is providing a fresh supply of air to ensure that the concentration of oxygen in the alveoli remains higher than the concentration in the blood (thus allowing diffusion to occur). If we can keep the alveolar oxygen levels high without breathing, that’s just fine.

Suppose, for instance, that we place the apneic patient on a nasal cannula at relatively high flow. This should fill the pharynx with near-100% O2. Even without breathing, gas exchange is occurring in the alveoli; oxygen is diffusing across the membrane into the blood where it binds hemoglobin, and carbon dioxide is diffusing the opposite direction. Far less CO2 is moving out than oxygen is moving in, however (due to differences in solubility and hemoglobin affinity), so there’s actually a net “loss” of gas. This creates some “suction” or a partial vacuum in the alveoli, which will draw in whatever gas is waiting in the upper airway to fill it. Since we’ve flushed that space with pure O2, oxygen will move down that gradient, enter the alveoli, and continue diffusing into the blood, creating a continuous flow. Using this method, patients have been demonstrated to maintain reasonable sats for ridiculously long periods (up to 100 minutes in ideal circumstances).

This is a technique called apneic oxygenation. Although referred to by different names, it’s not new (among other things, it’s a traditional component of most brain-death evaluations), but it’s recently been getting more publicity. In particular, Scott Weingart of EMcrit and Richard Levitan recently published a paper comprehensively describing its use in difficult intubations. They advise placing a cannula at 15 L/min in order to suffuse the pharynx with near-100% O2, and this recommendation has some support in the literature. (Interestingly, whether the patient has their mouth open or closed may not matter.) We’re usually taught that nasal cannulae shouldn’t be used at flows this high, since it’ll dry and irritate the mucosa of the nose, and this is true; however, for short periods in critical patients, a dry nose is not the foremost concern.

How could this be useful for our purposes? Our main challenge with the BVM is ensuring that positive pressure goes where we want it to. This is obviously essential. But if bagging is initially challenging, could we potentially buy time? As long as the airway down to the glottis is open to flow, at least partially, it takes no skill at all to place a cannula (probably already present) and run up the flow to 15 L/min. Even if we’re totally unable to ventilate effectively, this will help keep the patient oxygenated and saturated while we work on a more definitive solution.

A couple of caveats: first, there must actually be a somewhat patent (if not totally secure) airway for this to work. If upper airway structures (or even a foreign body) have totally occluded the nasopharynx or laryngopharynx, no oxygen will reach the trachea. Second, this is a short-term temporizing measure only, because although it may help oxygenate, it will not help to “ventilate,” meaning to remove waste carbon dioxide; as discussed, CO2 is much less capable of passively diffusing without actual tidal movement to clear the alveolar space. Sustained apnea will therefore lead to continually increasing hypercapnia. Finally, this is really intended for patients with largely normal V/Q ratios; it will probably be of limited use for patients with significant shunt (e.g. bronchoconstriction, pulmonary edema, etc.) or dead space (e.g. pulmonary embolism). In other words, it’s of little help to your respiratory patients, whose problem is that their lungs aren’t working properly; if they’re moving air at all, they’re most likely suffusing their alveoli with high-concentration O2, it’s just that they’re just unable to exchange it. They need something like CPAP to help recruit more usable alveoli. Apneic oxygenation is for patients with working lungs who merely aren’t breathing spontaneously or adequately protecting their airway.

Can’t you just use a mask for this? Eh. Studies suggest that O2 from a non-rebreather tends to remain outside the face (in the bag and mask itself) unless the patient actually breathes, since it’s easier for the gas to simply overflow from the exhalation ports than to penetrate their airway; this is distinguished from the cannula, which actually shoots pressurized oxygen directly into the nasopharynx.

However, when it comes to patients who do still have some spontaneous respirations, a non-rebreather can certainly be useful, and here’s a way to supercharge it. Contrary to popular belief, you’re not actually delivering 100% oxygen with a typical mask at 15 L/min — more like 60–70% in most cases. This is due both to the poor seal it generally forms with the face and to the fact that at least one external port is usually left open to room air, so that if the oxygen supply is interrupted or becomes inadequate the patient won’t be suffocated. However, you can get closer to 100% FiO2 by simply cranking up the flow. Once you hit around 30–60 L/min, enough surplus oxygen is overflowing through the mask that the patient should be breathing nearly pure O2. Your portable oxygen tank probably won’t allow a flow this high (and it’d quickly run empty if it did), but most wall- or ambulance-mounted regulators should, although it may be near their maximum flood. Just crank the regulator up to 15 and keep turning until it won’t turn anymore; the indicator won’t change, but the flow will keep increasing. (Although I won’t be the one to recommend it due to the [likely overstated] safety concerns, you could probably also get good results by taping over any valveless ports in the mask, and holding it tightly sealed to their face — or better yet, letting them hold it.)

It may seem convenient, incidentally, to simply press a BVM against their face. Although this may — may — produce an effective seal, it provides poor O2 flow for spontaneous respirations; often times patient-initiated breaths simply bypass the reservoir and draw room air.


Key Points

  1. When it comes to BLS airway adjuncts, the more the better. Two NPAs and an OPA is ideal.
  2. NPAs are generally safe; the risk of penetrating the cranial vault is probably negligible.
  3. Don’t go poking around with the OPA in already-difficult airways; make an effort to determine whether a gag reflex is present before stimulating it.
  4. If an open airway to the lungs exists, but ventilations are difficult, a nasal cannula at 15 L/min is an excellent way to provide apneic oxygenation as a temporizing measure to maintain saturation.
  5. The only “high-flow” oxygen device on your ambulance for a spontaneously-breathing patient is a non-rebreather with flow of 30+ L/min.

A general reminder: although we are cavalier with failing to include in-line or footnoted citations, these are all evidence-based recommendations, and readers are encouraged to inquire for the literature behind anything that seems surprising or dubious.


Continued at Mastering BLS Ventilation: Core Techniques, then Mastering BLS Ventilation: Supplemental Methods, and finally Mastering BLS Ventilation: Algorithms