Murder by Checklist

Reader Steve Carroll passed along this recent case report from the Annals of Emergency Medicine.

It’s behind a paywall, so let’s summarize.

What happened

A young adult male was shot three times — right lower quadrant, left flank, and proximal right thigh. Both internal and external bleeding were severe. A ~~physician bystander~~* tried to control it with direct pressure, to no avail.

With two hands and a lot of force, however (he weighed over 200 pounds), he was able to hold continuous, direct pressure to the upper abdomen, tamponading the aorta proximal to all three wounds.

Bleeding was arrested and the patient regained consciousness as long as compression was held. The bystander tried to pass the job off to another, smaller person, who was unable to provide adequate pressure.

When the scene was secured and paramedics arrived, they took over the task of aortic compression. But every time they interrupted pressure to move him to the stretcher or into the ambulance, the patient lost consciousness again. Finally en route, “it was abandoned to obtain vital signs, intravenous access, and a cervical collar.”

The result?

Within minutes, the patient again bled externally and became unresponsive. Four minutes into the 9-minute transfer, he had a pulseless electrical activity cardiac arrest, presumed a result of severe hypovolemia. Advanced cardiac life support resuscitation was initiated and continued for the remaining 5-minute transfer to the ED.

The patient did not survive.

When the cookbook goes bad

The idea of aortic compression is fascinating, but I don’t think it’s the most important lesson to this story.

Much has been said about the drawbacks of rigidly prescriptive protocol-based practice in EMS. But one could argue that our standard teachings allow for you to defer interventions like IV access if you’re caught up preventing hemorrhage. Like they say, sometimes you never get past the ABCs.

The problem here is not necessarily the protocols or the training. It’s the culture. And it’s not just us, because you see similar behavior in the hospital and in other domains.

It’s the idea that certain things just need to be done, regardless of their appropriateness for the patient. It’s the idea that certain patients come with a checklist of actions that need to be dealt with before you arrive at the ED. Doesn’t matter when. Doesn’t matter if they matter.

It’s this reasoning: “If I deliver a trauma patient without a collar, vital signs, and two large-bore IVs, the ER is going to tear me a new one.”

In other words, if you don’t get through the checklist, that’s your fault. But if the patient dies, that’s nobody’s fault.

From the outside, this doesn’t make much sense, because it has nothing to do with the patient’s pathology and what might help them. It has everything to do with the relationship between the paramedic and the ER, or the paramedic and the CQI staff, or the paramedic and the regional medical direction.

Because we work alone out there, without anybody directly overseeing our practice, the only time our actions are judged is when we drop off the patient. Which has led many of us to prioritize the appearance of “the package.” Not the care we deliver on scene or en route. Just the way things look when we arrive.

That’s why crews have idled in ED ambulance bays trying over and over to “get the tube” before unloading. That’s why we’ve had patients walk to the ambulance, climb inside, and sit down, only to be strapped down to a board.

And that’s why we’ve let people bleed to death while we record their blood pressure and needle a vein.

It’s okay to do our ritual checklist-driven dance for the routine patients, because that’s what checklists are for; all the little things that seem like a good idea when there’s time and resources to achieve them. But there’s something deeply wrong when you turn away from something critical — something lifesaving — something that actually helps — in order to achieve some bullshit that doesn’t matter one bit.

If you stop tamponading a wound to place a cervical collar, that cervical collar killed the patient. If you stop chest compressions to intubate, that tube killed the patient. If you delay transport in penetrating trauma to find an IV, that IV killed the patient.

No, let’s be honest. If you do those things, you killed the patient.

Do what actually matters for the patient in front of you. Nobody will ever criticize you for it, and if they do, they are not someone whose criticism should bother you. The only thing that should bother you is killing people while you finish your checklist.

* Correction: the bystander who intervened was not a physician, but “MD” (Matthew Douma), the lead author, who is an RN. — Editor, 7/22/14

Staying in Place: Compensation and Endpoints

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 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

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

We said before that robust management of the “A’s and B’s” requires having a wide range of options and tools available to you. At the BLS level, we don’t have many, but we do have a few. Now that we’ve explored the most important methods, let’s look at a few supplemental tricks and points to ponder.

Sellick’s Maneuver

Once again, remember our upper airway anatomy: the larynx and trachea, through which air flows to the lungs, are positioned anterior to the esophagus, through which we’d prefer air did not flow. What’s more, these twin tubes are different types of structures. The trachea is built largely of cartilaginous rings, the same semi-rigid material that makes up the wobbly front of your nose; it’s not as stiff as bone, but it holds its shape well (go ahead, give your Adam’s apple a squeeze). The esophagus, on the other hand, is a fairly soft tube made of mostly muscle, and can easily be compressed flat.

This suggests a potentially useful trick. If we press upon the front of the larynx, it will retain its shape and move posteriorly, compressing the esophagus. In other words, although you’re pushing on the airway, it’ll remain open, while the esophagus behind it narrows and flattens. It’s like squishing a cardboard toilet paper roll with a metal pipe; they’re both tubes, but one is thin and easily distensible while the other is stiff and strong.

Since one of our challenges in BVM ventilation is getting air to go down the right tube, it makes intuitive sense that flattening the esophagus (the wrong tube) will help us push air into the trachea (the right tube). If we’re not successful with that, it may at least help prevent regurgitation from coming back out from the esophagus. This is particularly important because maneuvers like the sniffing position help straighten both of those tubes, so although they do open the airway, they also tend to increase the risk of gastric inflation. Worse, overly-aggressive bagging — from a first responder, for instance — can wedge open the LES guarding the stomach, and it can remain this way after you take over. Once someone’s forced it open, even gentle ventilations can enter the stomach.

This is called Sellick’s maneuver, or simply cricoid pressure. It’s properly applied by pressing gently upon the cricoid cartilage, which is a good spot because the cartilaginous ring there creates a full circle (most of the other cartilages are C-shaped). It’s helpful during intubation, since it tends to move the glottic opening into the line of sight, but has also traditionally been used to assist with bagging.

To find the cricoid cartilage, palpate the most prominent bulge of the trachea, the “Adam’s apple” or laryngeal prominence. Move your finger downward over a small indentation (the cricothyroid ligament or membrane, where emergency cricothyrotomy would be performed) until you find another, smaller bulge. This is the cricoid cartilage.

Here’s the problem: theory aside, it often doesn’t work very well. A substantial body of evidence has shown that it often doesn’t do much to reduce gastric inflation, nor to impair regurgitation, and can even partially occlude the airway. This led the AHA to state that “. . . the routine use of cricoid pressure in adult cardiac arrest is not recommended” in the 2010 update to their BLS recommendations.

That doesn’t mean it’s useless, but it certainly suggests it shouldn’t be one of our first moves. It’ll help if we take care to do it correctly: pressure should generally be gentle (too hard and you’ll compress the semi-rigid larynx itself), straight back (it’s easy to “roll” to one side and fail to transmit the pressure to the esophagus), and applied nowhere but the cricoid cartilage. I also find that using your index and middle fingers, as in the illustration above, better facilitates this type of pressure than a thumb-and-forefinger grip. Use it as a last resort after other methods to minimize gastric inflation have failed — particularly the simplest and most effective, which is simply bagging with less force (ease the air in, don’t shoot it in) — titrate the amount of pressure to the desired effect, and in the end, don’t be surprised if it fails.

Pocket Masks

People may look at you like you’ve got six heads if you suggest it, but using a “pocket mask” is still a valid and indeed a recommended method for ventilation. Many BLS units carry the devices, which are essentially the same type of mask you see on the BVM, plus a port for supplemental O2 and a one-way or filtered valve to prevent cootie exchange. (If you don’t have such a device, you could simply detach the mask from your BVM and breathe into the hole, removing your mouth between breaths to let the patient exhale. This won’t be as effective of a barrier to infection, since there’s no one-way port, so it’s your call — but the risks are probably minor. You might even be able to increase FiO2 by leaving a cannula on the patient… or wearing one yourself.)

The advantages of this method are numerous. First of all, because you have two hands available to hold the mask, you’ll rarely have difficulty making a seal. Second, it’s extremely easy to titrate the volume and pressure of the breaths you give; unlike with the BVM, where you’re brusquely squeezing a rubber sac, with the pocket mask you’re using your pulmonary apparatus (your lungs) to assist the patient’s pulmonary apparatus, and it’s very easy to maintain tight control over the variables. Simply breathe in normally (not a deep breath) and exhale into the mask with gentle force, stopping when you see the chest rise. You should be able to do this with almost infinitely gentle pressure, making gastric inflation very unlikely.

The disadvantages: you can’t provide 100% oxygen, although if you attach the tubing and crank up a high flow, you can probably provide ample FiO2 for anybody without significant V/Q problems. But the bigger problem is the “ick” factor. Although research has shown that the risk of contracting an infectious disease during mouth-to-mask ventilation is very small, many providers still aren’t comfortable getting that close, preferring to literally stay at arm’s length. But remember: if you’re unable to effectively ventilate an apneic patient and you’ve exhausted all other options, this is a life-or-death situation, and ickiness should not be a key concern.

Mouth to Mouth

What if even the pocket mask fails, or for some reason you have no equipment of any kind available?

There’s always direct mouth-to-mouth ventilation. Nobody will fault you for opting out of this, because of the aforementioned ick factor and the theoretical chance of disease transmission, although again, research has suggested the risk is small. But if all else fails, it should be considered an option, and whether you’ll attempt it is solely up to you. Sheet-type barrier devices, which some people carry on their keychains, may reduce either ick factor or real risk, although you’re probably unlikely to find one around unless you carry your own. Remember that you’ll need to pinch or otherwise seal the nose; if your hands are busy maintaining an airway, you may be able to accomplish this by pressing your cheek against the nares.

If the mouth is obstructed or otherwise non-patent, mouth-to-nose ventilation is a viable alternative; simply ensure their mouth is shut and breathe into the nares. If a stoma is present in the neck, mouth-to-stoma or mask-to-stoma (an infant-size mask may yield the best seal) ventilation can be an option, although depending on how it’s constructed you may need to seal both the nose and mouth to make it work.

Just options, folks. Airways need options.

Jaw Thrusts

Along with manipulating the head, we know that shifting the jaw forward is essential for opening the upper airway. In fact, when we walked the Halls of the Student EMT, the wise men told us that for patients in spinal immobilization, it’s all we’re allowed to do. (A little later they usually said “. . . however, a patent airway takes priority over spinal precautions,” but most of us had already dozed off at that point.)

In any case, translating the jaw forward as far as possible, no matter how you do it, can open the airway substantially.

Along with the classic jaw thrust, there’s another method that’s rarely seen anymore. It’s real easy: with one hand, grab their mandible by the chin and lower teeth and pull up. It works. Could you get bitten? Yes. You also can’t bag them while you’re holding their jaw in your hand like Hamlet. So it’s more of a first aid tactic, but it’s very idiot-proof, so it’s nice to know about. You can see it working in this video.

Risk Factors for Difficult BVM Ventilation

It’s one thing to have a wide range of options for dealing with difficult-to-bag patients, but it’s also helpful to know before you dive in when a patient is likely to become difficult. It can help inform your decisions about priorities and flow of care, as well as the need for ALS and transport destinations.

Patients who are often challenging to bag include:

The obese. Ample soft tissue tends to occlude the upper airway (this is why they often suffer from sleep apnea), adipose tissue bears down on their chest and diaphragm, and they’re generally difficult to position how you’d like. Ramp them and get a good sniffing position ahead of time (don’t try to dynamically head-tilt them while you apply the mask — situate them beforehand, so all you’ll need to do while you bag is maintain the jaw thrust), use airway adjuncts liberally, and plan ahead — don’t ever assume it’ll go smoothly, or you’ll find yourself in over your head without backup plans.
Bearded patients. Thick beards and other facial hair make obtaining a mask seal difficult. It can help if you smear it down with some water-based lubricant (such as your NPA lube), but it can also make a mess of everything until you’re slip-sliding away like Paul Simon. You could also shave them a bit if you have a razor (with your AED gear, for instance), although they probably won’t thank you later unless it’s quite necessary.
Sleep apnea. If you happen to know (via history) that the patient suffers from sleep apnea — or to a lesser extent, even that they snore at night — this indicates an existing predisposition toward upper airway occlusion when their level of consciousness is mildly depressed, so you can expect it to be that much worse when they’re entirely comatose.
The elderly. Everything is harder with old people, including bag-mask ventilation, for numerous reasons.
Anyone with a difficult-to-protract mandible. You probably won’t know this by looking, but if you go to initially address the airway and find that you’re unable to lift the jaw until the lower teeth are at least aligned with the upper teeth (preferably until they’re anterior), you’re probably going to have a hard time, and will need to compensate by achieving optimal extension and a sniffing position.
Anyone with gross trauma to the face or neck, which may create airway occlusion, hinder your ability to make a mask seal, or generate substantial blood and other fluids requiring aggressive suctioning.
Edentulous (toothless) patients. Aside from the fact that they’re usually elderly, patients without teeth have minimal structure to the oral cavity, giving you little to press against with the mask and obtain a seal. If dentures are present, it will help to leave them in; if not, make sure to place an OPA, which provides a little support at least. Make an effort to outwardly “spread” the air-filled skirt of the mask before applying it, which helps ensure that its maximum surface area remains in contact rather than curled uselessly underneath. Also consider this alternate mask placement, which may be more successful: the mask is shifted upward, so the lower edge meets the lower lip directly.

The End-Expiratory Pop

This is an interesting, unusual, and advanced technique which I’ve only ever seen advocated by the Department of Critical Care at the University of Pittsburgh. Briefly, it consists of the following: you bag with a two-person technique if at all possible, ensuring an excellent seal (which is mandatory) and letting you focus solely on the bag. You inflate as normal, release the bag and let the patient exhale, and then near the end of the expiratory phase, you “catch” them with a small squeeze to the bag, preventing their lungs from fully deflating. This may not seem possible, because there’s a valve present that allows exhaled air to vent, but that valve’s position is determined by the relative pressures on each side, so if you insufflate gas at a higher pressure than the patient’s exhaled gas, it’ll open in rather than out. This creates a sealed, temporarily closed system supported by the pressure you’ve created in the bag. If you don’t believe it, try bagging with the mask sealed against a table, or even upon your own face using clean gear.

View an example of the technique in this video clip, from :25 to :55. Here they’re simulating assisting with spontaneous respirations, probably one of the best applications for this method.

This yields two advantages: first, it gives you an excellent “feel” for pulmonary compliance. With a leak-free seal and balanced inspiration/expiration, compliance should remain consistent. If the resistance you feel suddenly decreases, you most likely have a leak. If it increases, you likely have either an obstruction or are “breath stacking,” failing to fully allow for expiration before beginning the next breath. With practice you can develop an excellent tactile sense of the bag-lung interface… as long as your mask seal remains flawless.

Second, and more profoundly, this actually creates positive end-expiratory pressure, or PEEP. In other words, you’re maintaining positive pressure in the lungs even after exhalation, where the alveoli ordinarily might collapse. By never quite “touching ground,” pressure-wise, you keep alveoli partially distended and portions of the bronchial tree “splinted” open that otherwise might have collapsed, particularly in disorders like COPD or CHF. This is the same principle used by CPAP or BiPAP devices, and it’s a wonderful boon that’s often the only way to effectively oxygenate patients with significant atelactasis (collapsed alveoli) and shunt (portions of the lungs that air is unable to reach). If you have a patent airway and are introducing adequate amounts of 100% oxygen, yet the patient remains hypoxic (according to skin signs or pulse oximetry), it’s almost certainly because of a V/Q mismatch like this, and that situation cannot be solved without PEEP or radically more aggressive measures.

The reason this trick is so cool is because it’s probably the only way to apply PEEP at the BLS level, since in most areas we do not carry CPAP devices, or even PEEP valves for the BVM. It’s theoretically possible to tape over or otherwise partially occlude the exhalation port of the BVM, narrowing the space for expiration and therefore providing some back-pressure, but this is totally unmeasurable, not easily titrated, and interferes with the entire phase of expiration. Although trickier, the “Pittsburgh PEEP pop” is better.

Why squeeze at the end of expiration? If you squeeze earlier, you’ll interfere with exhalation of gas, which needs to happen if we’re going to adequately blow off CO2 and avoid “stacking” breaths. If you squeeze later, you missed your chance to prevent a “zero pressure” state in the lungs, so you’re starting from zero again.

Key Points

Sellick’s maneuver (i.e. cricoid pressure) can be helpful for reducing gastric inflation, but is often ineffective or even counterproductive. Use it as a last resort, applying only gentle and direct pressure, and if it’s not working, stop.
Mouth-to-mask, mouth-to-mouth, mouth-to-nose, or mouth-to-stoma can all be effective backups to BVM ventilation, particularly when unable to achieve a mask seal or unable to ventilate without inflating the stomach.
Expect obese, bearded, elderly, toothless, or traumatic patients to be difficult to bag.
A small amount of PEEP can be created with a normal BVM using a small end-expiratory squeeze; this also helps confirm the ongoing integrity of the mask seal.

Next time we’ll give a method for combining all of these concepts into a cohesive approach to the BLS airway.

Continued at Mastering BLS Ventilation: Algorithms

Mastering BLS Ventilation: Core Techniques

Continued from Mastering BLS Ventilation: Introduction and Mastering BLS Ventilation: Hardware

Now that we understand the goals and the basic tools, let’s talk about the most important techniques for optimizing airway management and providing BLS ventilation to apneic patients.

Hand Technique

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

As a rule, we’re taught something called the “EC clamp.” It looks like this:

In theory, this lets us press the mask against the patient’s face (using the “C” of our thumb and forefinger) while pulling the jaw forward (using the “E” of our other fingers behind the mandible), and still leaves one hand free to squeeze the bag.

In theory.

In reality, this is tricky at best. Partly it’s because we’re trying to seal the edges of a circle by pressing on only one side, which usually results in a leak from the other side. Partly it’s because pulling the jaw forward like this — a highly necessary action — takes a fair amount of force, and we’re in a poor position to grip from. It also doesn’t help that, if no OPA is present, this method usually squeezes the mouth shut, leaving only the nasal passage for an airway.

One useful tip: positioning the bag directly opposite your EC hand and pulling it downward can help seal off the most common point for leaks.

Does the EC technique work? It can work. And it’s fast and versatile to apply, so it’s a reasonable place to start. However, if you find that it’s not working, don’t be too surprised. You would be wise to practice the hell out of it on mannequins (or ideally in an OR or similar setting), but not everyone has that opportunity. What’s the alternative?

Use two hands. The inelegant nature of the EC clamp has been widely recognized for years, despite the fact that many of us in emergency medicine pretend otherwise. In fact, if you flip open your EMT textbook or the handouts from your last CPR class, you will notice that one-person BVM use is strongly discouraged. (In my Limmer textbook, it’s last in preference after the two-person BVM and even the pocket mask.) In the field, this is ignored, because we adopt the attitude that any EMT should be able to sit at the patient’s head and “handle the airway” without help. But that doesn’t change the fact that it’s a crummy technique, and many of the patients who are “bagged” this way only survive because they didn’t need much help to begin with.

What does work reliably is placing both hands on the mask, thumbs toward the feet and fingers behind the jaw. This way you have a hand on both sides and can easily obtain a seal (and if there is a leak it’s readily located), while also providing a strong bilateral grip to protract the jaw. You can sustain this position for a long time, and as a bonus, it tends to open rather than close the mouth.

A slightly different version with thumbs wrapped around, resembling a "double EC"

The downside is that it doesn’t leave a hand to squeeze with. Ideally, another rescuer should squeeze the bag. This lets you focus on maintaining the airway while they focus on bagging slowly, gently, and at an appropriate rate. (But remind them to stop squeezing when they see chest rise; with two hands it’s tempting to try and empty the whole bag, which is far in excess of what’s necessary if you have a good seal.) It can even help to separate the mask from the bag entirely, position it perfectly on the face, clamp down your grip, and then allow the bag to be attached and ventilation begun; this ensures everything is where it ought to be. On scene you often have enough personnel for this; in the back of the ambulance you may or may not. Can you still execute this method alone?

You can, and I highly recommend that you work out the logistics now, with your own unique body type and equipment. For patients in a bed or a high stretcher, you can often stand behind the head, hold the seal with your hands, and squeeze the bag with your elbow against your side. In the patient compartment, you can sit in the tech seat and squeeze the bag against one leg with your elbow, or between your knees if you’re an experienced Thighmaster. A supine patient on the ground can be the trickiest position; you may be able to squeeze the bag against a leg or something similar, but often your best bet will simply be to recruit help. (Again, please experiment with this now, so you’re not improvising while a patient turns blue.) Just remember that using two people to bag isn’t a failure, and has no impact on your sexual adequacy; it’s a legitimate method which is supported by literature and explicitly recommended by the experts we’re supposed to be listening to.

The Sniffing Position

We understand now that successful BLS airway management means maximizing the passable upper airway and minimizing obstructions. Bringing the jaw forward will always be helpful, by pulling the tongue and other anterior structures away from the posterior pharyngeal wall. Now let’s look a little closer at the position of the head itself.

We’re taught to rotate the head back in the head-tilt chin-lift maneuver. Why do we do this? In essence, because it helps align the oral and nasal passages with the pharynx.

In other words, in a neutral position there’s an angle that approaches 90 degrees between the oral cavity (through which air initially passes — or the nasal cavity, which is nearly parallel) and the pharynx (the initial portion of the passage down into the lungs). Such a sharp angle increases the resistance to air and increases the likelihood of occlusion. By rotating the head backwards along the atlanto-occipital joint — i.e. where the skull meets the spine — we can straighten out this corner. We can’t make it completely straight, because the head doesn’t rotate that far (if it did you’d be able to directly face the sky without leaning), but we can improve the angle substantially.

The trouble is that when we do this, we change another angle too. The angle between the pharynx and the trachea tends to sharpen in the vicinity of the larynx as we tilt the head backward. Since the pharynx follows the alignment of the upper neck and lower head, and the trachea follows the alignment of the lower neck and thorax — with the larynx and glottis smack in the middle — there’s an additional angle here that should be straightened as much as possible.

Image courtesy of http://tinyurl.com/c6logld

The good news is that with a supine patient lying on a flat surface, such as a bed or stretcher, simply rotating the head back will partially accomplish this. That’s because our occiput — the back of the skull — is somewhat bulbous and protruding, and when you tilt the head back, it rolls over this rounded prominence, elevating the head. Thus, a standard head tilt produces a small amount of neck-to-thorax flexion, which helps improve the angle at the larynx.

Many patients benefit from greater head movement, however. What we’re trying to do is shift the head forward — anteriorly — while maintaining (not increasing or decreasing) atlanto-occipital extension. In combination, this creates what’s known as the sniffing position, as it resembles someone ostentatiously “sniffing the air.” (“Leading with the chin” may be a more intuitive description.) It’s widely taught as the optimal position for intubation, but it can also reduce resistance to BVM ventilation; you may even encounter patients with perilaryngeal swelling (particularly epiglottitis) who assume this position intuitively to maintain their narrowing airway.

To establish the sniffing position, you need to pad behind the head. It’s sensible to treat each patient somewhat individually, but a good starting point is to elevate the head until the ear (that is, the canal or meatus) is horizontally aligned with, or slightly in front of, the notch of the clavicles. This is often only a few inches (average is ~7cm) beyond the elevation you’ll get from the occiput against the bed alone, but you’ll certainly need to put something back there. Pillows are usually too soft unless you fold them gratuitously, but a folded towel or blanket can work well, or really anything flat.

A few special cases are worth mentioning. First, children. Kids are notorious for having enormous heads compared to their bodies, and the frequent result is that after rotating the cranium, you’ll have created all the anterior movement you need. In fact, it’s possible you’ll need to pad the back and upper shoulders in order to avoid hyperflexion of the neck.

Image courtesy of http://www.narenthorn.or.th/node/77?page=0%2C2

Now consider obese patients. Their general airway challenges make them great candidates for this technique, but because they have extra adipose tissue on their back — which elevates their torso relative to their head — they have the opposite problem as kids: you may need to provide substantially more padding behind the head in order to achieve ear-sternal alignment.

Interestingly, though, in very big patients you may encounter a different situation. Because relatively more adipose tissue collects in the lower back and hips than in the upper back and shoulders, while supine, the morbidly obese patient may actually be “upside down”; their torso is angled uphill, resulting in their head and chest being crunched together even while lying “flat.” To achieve anything like reasonable airway positions, you’ll need to first correct this by elevating (really just leveling) their upper back. This is called ramping, and may require a substantial amount of linen, although you might be able to get part of the way there by raising the back of the stretcher a little (thus preferentially elevating their upper back, since most people slip down a fair amount). Once you’ve achieved body normality, you can create your sniffing position, aligning ear to clavicles in the usual fashion.

Image courtesy of http://bariatrictimes.com/2012/02/16/airway-management-in-bariatric-surgery-a-challenge-for-anesthesiologists/

Truth be told, there are advantages to sitting up almost any respiratory patient. It reduces the chance of airway occlusion from soft tissues, helps blood and secretions drain, reduces impedance on the chest wall, and prevents the abdominal viscera from compressing the diaphragm. The only reason we don’t manage everyone this way is because it’s hard to do much with a patient sitting high or semi-Fowler’s, such as bagging them or airway insertion. But for the patient who’s still breathing spontaneously, the simplest airway intervention is simply to keep them upright or perhaps in the lateral recovery position.

Key Points

The two-hand BVM technique is preferable to the EC technique whenever possible, and it’s far easier to perform with a second person to assist.
Optimal airway diameter and angles can be achieved by protracting the jaw and simultaneously elevating and extending the head into a “sniffing position.”
Pediatric patients may not need additional head elevation to achieve this, or may even need padding of the back.
Obese patients may need substantial head elevation.
Very obese patients may need to be “ramped” to level their torso before attempting other airway maneuvers.
When more aggressive management is not needed, an upright or lateral supine position provides the simplest protection of the airway.

Tune in next time for a few extra tricks to increase our airway options, and a comprehensive approach for bringing it all together.

Continued at Mastering BLS Ventilation: Supplemental Methods and finally Mastering BLS Ventilation: Algorithms

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

When it comes to BLS airway adjuncts, the more the better. Two NPAs and an OPA is ideal.
NPAs are generally safe; the risk of penetrating the cranial vault is probably negligible.
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.
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.
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

Mastering BLS Ventilation: Introduction

Sometimes, patients can’t breathe. When that happens, we need to breathe for them.

Simple enough. This is life support at its most fundamental, and many of the interventions classified as “BLS” are found here — techniques and devices for artificially supporting the body’s airway and breathing.

And it doesn’t seem so hard. When they taught it in class, it only took a day or two, and a few pages in the textbook encompassed the subject. How to size an OPA, how to hold the BVM, something about jaw thrusts, and you’re through. Spend a few minutes playing with a mannequin and now you’re an expert.

In the real world, though, this is not child’s play. Managing the airway of a sick, apneic patient is, at best, a high priority; at worst, it’s an unqualified catastrophe. Case reports and horror stories of airways gone wrong can be found under every roof: the failed intubation, the disastrous cricothyrotomy, the foreign body obstruction that couldn’t be cleared. These are emergencies because as we all know, without an airway, you cannot survive. It’s simple stuff.

And then there’s the BVM — aka the bag-valve-mask or “Ambubag.” Ask a room full of novice EMTs and they’ll all agree it’s about as straightforward as tying your shoes: slap it on, squeeze, any idiot could do it. But ask the senior medic in the corner, and he may paint a grimmer picture. Jeff Guy has described it as a more difficult skill than endotracheal intubation, yet one of the hot topics today in prehospital medicine is whether paramedics should remove intubation from their scope of practice because it’s too hard. But nobody’s going to take away the BVM. It’s irreplaceable; it’s the first and last line, the means of ventilation that any patient starts with, and the fallback if your next move fails. The only problem is that doing it well, and for really tough patients, doing it at all, is a purely skill-based exercise. It’s the Jedi’s lightsaber: simple, versatile, but designed for an expert.

The point is that establishing a patent airway in a sick person who can’t do it themselves, and ventilating them using that airway, is such an important task that it generally mandates a large toolbox. Airways are often managed via complex flowcharts or algorithms, where one method can yield to another if it fails, and then to another and another. Countless different devices and methods are available, so that even when obstacles are present, any moron can stumble onto something that works before the patient crashes altogether.

And then there’s us. The Basic EMT stands at the bottom of the spectrum in terms of training, yet is expected to oxygenate any patient using nothing but the meager BLS jump-kit. He has the BVM, a couple of basic airways, masks, cannulas, suction, positioning — and beyond that, just his wits and skills. And as for those, he probably spent little to no time actually practicing them in class, and may perform them only rarely in the field.

This won’t do. When it comes to psychomotor skills, these are the most essential, because we don’t have a Plan B. If BLS techniques fail, our only recourse is to sprint for the hospital or ALS, and hope nobody dies along the way.

So let’s talk about all the principles and tricks of creating a BLS airway and ventilating with the BVM. First, we’ll need to understand why it’s hard.

Basic Physiology

Ordinarily, we suck at breathing.

I mean we literally suck. We drop the diaphragm and widen the ribs, expanding the area inside our chest. This expands the lungs, forcing them to suck air into the only opening available — through the mouth and nose, down the pharynx, through the trachea, and into the bronchial tree.

That’s assuming that the airway is open, of course.

Now, what if I whack you over the head, and your body loses the ability to spontaneously breathe? We’ll want to breathe for you. Can we pull down your diaphragm and expand your chest? Not very easily, unless we stick a plunger on your sternum, or put you in an iron lung. Instead, we reverse this process: rather than creating negative pressure inside the chest, we force positive pressure in from the outside. Rather than sucking, we blow.

Blowing is a little tricky, though. One of the main problems is that there’s more than one place for air to go. Consider the pharynx, the working area of your upper airway. We can get there via two paths: the oropharynx (via the mouth and over the tongue), or the nasopharynx (via the nostrils), but they arrive at the same place, the laryngopharynx (or hypopharynx). What happens next?

If we peered into your hypopharyngeal space, we would see that two openings emerge below. One leads to a tube which lies posterior (toward your back): your esophagus, which conveys cheeseburgers and beer into your stomach. One leads to a tube which lies anterior (toward your front): your trachea, which brings air into the lungs for gas exchange. Remember these relative positions — the trachea is in front, and you can palpate it at the neck (the “Adam’s apple” is part of it). The esophagus lies behind this, and is not usually externally palpable.

Given that food and air both enter via the pharynx, how do we ensure that cheeseburgers ends up in the esophagus and air ends up in the trachea? Well, the gatehouse to the trachea is the larynx (the “voicebox,” where vocalization occurs), and the opening to this chamber is called the glottis. The glottis is normally open, but when you swallow, a couple of drape-like vestibular folds and a little flap, the epiglottis, are pulled in to cover the larynx. The result is that food is forced into the esophagus.

What about the other direction? The esophagus is formed from rings of muscles called esophageal sphincters, which help “milk” food downward when you swallow. The bottommost ring is the lower esophageal sphincter, which opens during swallowing, but otherwise is mostly constricted, sealing off the esophagus from the stomach itself. This prevents air from passing down and gastric contents from coming up (something we know as heartburn).

To summarize, as you sit here reading this, your esophagus is clamped off by your lower esophageal sphincter, and your trachea is open, allowing you to breathe. But if you take a bite of your coffee-cake, your epiglottis and vestibular folds will block off your airway, your esophageal sphincter will open, and the food bolus will be directed into your stomach.

Down the wrong pipe

The trouble with blowing instead of sucking is that we have no way of aiming where we blow.

I know what you’re thinking. If we force air down the pharynx, the esophageal sphincter should block off the stomach, ensuring that it flows into the larynx and down the trachea. Right?

Here’s the problem. Even ordinarily, your esophageal sphincter only clamps down with a small amount of force — say around 30 cmH2O (centimeters of water, a unit of pressure). This is plenty to prevent air from flowing in during regular respiration. But if air were to be pushed in with greater than 30 cmH2O of force, it will squeeze past the sphincter and enter the stomach. And if we clamp a BVM over your face and squish the bag, we can easily exceed that much pressure.

It gets worse. In order for the esophageal sphincter to work even that well, it requires muscular tone (constant stimulation), just like your postural muscles need tone to keep you from falling over. What happens when you’re unconscious? Sphincter tone decreases. So in the people we’ll actually be bagging, opening pressure may be 20–25 cmH2O or even less. Thus it’s even easier for positive pressure ventilations to force their way into the stomach.

The result? When squeezing the BVM, air often enters the stomach along with (or instead of) entering the lungs. Not only is this pointless, it makes it even harder to inflate the lungs (a bigger abdomen creates pressure on the diaphragm), decreases cardiac preload, and increases the risk of vomiting — which will further obstruct the airway.

The easiest solution is to put a tube into the trachea and seal it off — i.e. endotracheal intubation (or variations on that theme, such as a blind airway). Then we can blow air directly into the lungs without any chance that it’ll enter the wrong pipe. Unfortunately, those are tools we often lack as BLS providers.

Angles and Tissues

All of those structures we’ve been describing? They’re soft.

Soft and squishy. And it’s not just the esophageal sphincter that loses tone when you become unconscious.

In ordinary circumstances, the airway is a supple but structured arrangement of tissues that maintains its form. This is important, because there’s not very much space in there. So in the unresponsive patient, it’s no surprise that some of those tissues might collapse together, blocking off the lumen between them. (Check out this fluoroscopic video.)

The tongue is the worst. Tongues are basically big blobby muscles, attached at only one end, and if you remove all firming tone, they just flop wherever gravity takes them. So put an unconscious person supine, and gravity pulls the tongue back into the pharynx, blocking all airflow.

Or the larynx and supralaryngeal tissues run into the posterior pharyngeal wall. Or the soft palate does. Either way, anterior structures end up touching posterior structures, leaving no room in between. Our airway involves a tight 90 degree turn, and this is not a design that remains open without active maintenance. So if we want to breathe for these people, we need to find a way to unblock everything. (Like the jaw thrust — check out this airway cam.)

Mask Madness

Trying to push air into someone’s lungs by holding a mask over their face is like trying to blow up a tire by… well, holding a mask over the valve.

I teach CPR, and I can count on one hand the number of times I’ve handed the BVM to somebody and watched them achieve chest rise on the mannequin the first time. Heck, I demo the things and I don’t always pull it off.

Effectively sealing an air-filled plastic mask to someone’s face and then squeezing the bag is a task meant for more hands than any human possesses. Doing it on somebody who’s dying is exponentially more difficult. Add in the fact that they’re probably obese, toothless, vomiting, crumpled in a corner or bouncing around an ambulance, and enshrouded in a thick ZZ Top beard. Now try to get it all done without losing your cool or breaking your proper ventilatory rate. Having fun yet?

Key points

BLS ventilation using basic airways, positioning, and the BVM is a difficult, complex, and undertrained skillset for the EMT-B. Yet since we often lack rescue devices or alternate ventilation methods, it is critical that we learn to master it.
Preventing gastric inflation would be difficult even in healthy people, and is extremely difficult in the apneic and unresponsive patient.
Loss of tone in unconscious patients lying supine reliably produces soft tissue airway obstruction which must be cleared.
Obtaining a proper mask seal is a necessary prerequisite for BVM use, but is often difficult or impossible for a single rescuer.

Tune in next time to see some solutions to these challenges.

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

Understanding Shock IX: Assessment and Recognition

To wrap up our story on shock, let’s discuss how to recognize it.

We all have some idea what shock looks like. Like many pathologies, its loudest early markers are actually indirect — we’ll often recognize the body’s reactions to shock rather than the shock itself.

Although there are a few ways to classify the stages of shock, let’s just use three categories here.

Early or Insignificant

Shock that is very early or minimal in effect may have no particular manifestations. One situation where significant or late shock may also be “hidden” is in the elderly patient, or anyone with significant comorbidities; if their body’s ability to mobilize its compensatory mechanisms is poor, then the red flags won’t be as obvious. This doesn’t mean the shock isn’t as bad; in fact, it means that it’s worse, because their body can’t do as much to mitigate it.

The way to recognize shock at this stage is from the history. If we see an obvious bullet hole in the patient’s chest, and three liters of blood pooling on the ground beside him, then it doesn’t matter how the patient presents otherwise; we’re going to assume that shock is a concern. Blood volume is proportional to bodyweight, but for a typical adult, a fair rule of thumb is to assume about 5-7 liters of total volume. (Not sure what a liter looks like? The bags of saline the medics usually carry are a liter; so are those Nalgene water bottles many people drink from. “Party size” soda bottles are two liters.) Losing more than a liter or two rapidly is difficult to compensate for.

Remember, of course, that blood can also be lost internally, and aside from the occasional pelvic fracture or hemothorax, the best environment for this is the abdomen. Always examine and palpate the abdomen of the trauma patient, looking for rigidity, tenderness, or distention. Remember also that the GI tract is a great place to lose blood; be sure to ask your medical patients about blood or “coffee grounds” (old blood) in the vomit or stool.

Fluid enters and leaves the body continuously, and any disruption in this should be recognized. If a patient complains “I haven’t been able to eat or drink anything in two days,” they’re telling you that they haven’t taken in any fluid for 48 hours. If they tell you they’ve been vomiting or experiencing profuse diarrhea, that’s fluid leaving their body in significant volumes. What about the man who just ran a marathon and sweated out a gallon? Did he drink a gallon to replace it?

Compensated Shock

Significant shock will result in the body attempting to compensate for the low blood volume. Much of this work is done by the sympathetic system, and there are two primary effects: vasoconstriction and cardiac stimulation.

By constricting the blood vessels, we can maintain a reasonable blood pressure and adequate flow even with a smaller circulating volume. We normally vasoconstrict in the periphery — particularly the outer extremities and skin — “stealing” blood from those less-important tissues and retaining it in the vital core. This causes pallor (paleness) and coolness of the external skin. The sympathetic stimulation may also cause diaphoresis (sweating), which is not compensatory, but simply a side effect of the adrenergic release.

The heart also kicks into overdrive, trying to keep the remaining volume moving faster to make up for the loss. It beats faster (chronotropy) and harder (inotropy), resulting in tachycardia. Note that patients who use beta blockers (such as metoprolol) may not be able to muster much, if any, compensatory tachycardia.

A narrowing pulse pressure (the difference between the systolic and diastolic numbers) may be noted; since the diastolic reflects baseline pressure and the systolic reflects the added pressure created by the pumping of the heart, a narrow pulse pressure suggests that cardiac output is diminishing (due to loss of preload), and that more and more of the pressure we’re seeing is simply produced by shrinking the vasculature.

Tachypnea (rapid respirations) are also typically seen. In some cases, this may be due to emotional excitement, and there is also a longstanding belief that it reflects the body’s attempts to “blow off” carbon dioxide and reduce the acidosis created by anaerobic metabolism. (Interestingly, lactate — a byproduct of anaerobic metabolism — can be measured by lab tests, and is also a sign of shock, particularly useful in sepsis.) Additionally, it ensures that all remaining blood has the greatest possible oxygenation. However, it is also plausible that this tachypnea serves to assist the circulatory system: by creating negative pressure in the thorax (the “suction” you make in your chest whenever you inhale) and positive pressure in the abdomen (due to the diaphragm dropping down), you “milk” the vena cava upward during inspiration, improving venous return to the heart and allowing greater cardiac output. This “bellows” effect helps the heart fill more and expel more with each beat.

The more functional the patient’s body is — such as the young, strong, healthy victim — the more effective these compensatory systems will be. Hence the old truism that pediatric patients “fall off a cliff” — they may look great even up through quite profound levels of shock, due to their excellent ability to compensate, then when they finally run out of room they’re already so far in the hole that they become rapidly unhinged. It’s great that these people can compensate well, but it does mean we need to have a high index of suspicion, looking closely for signs of compensation (such as tachycardia) rather than outright signs of shock — because by the time the latter appears, it may be very late indeed.

Patients in compensated shock may become orthostatic; their bodies are capable of perfusing well in more horizontal postures, but when gravity pulls their remaining blood away from the core, this added challenge makes the hypovolemia noticeable. Less acute shock due to causes like dehydration may result in dry skin (particularly the mucus membranes; try examining the inside of the lower eyelid) with poor turgor (pinch a “tent” out of their skin and release it; does it snap back quickly or sluggishly?), and potentially with complaints of thirst. Urine output will usually be minimal. Generally, the more gradually the hypovolemia sets in, the more gradually it can be safely corrected; it’s the sudden, acute losses from causes like bleeding that we’re most worried about.

Decompensated Shock

As shock continues, compensatory systems will struggle harder and harder to maintain perfusion and pressure. Eventually they will fail; further vasoconstriction will reduce rather than improve organ perfusion, beating the heart faster will expel less rather than more blood, and the blood pressure will start to drop.

The hallmark of this stage of shock is the normal functioning of the body beginning to fail. The measured blood pressure will decrease and eventually become unobtainable. Pulses will weaken until they cannot be palpated. As perfusion to the brain decreases, the patient’s mental status will deteriorate. Heart rate and respirations, previously rapid, will begin to slow as the body loses the ability to drive them; like a government office that can’t pay its workers, the regulatory systems that should be fighting the problem begin to shutter their own operations. As the heart continues to “brady down,” eventually it may lose coherence (ventricular fibrillation), or keep stoically trying to contract until the last, but lose all effective output due to the lack of available blood (PEA). Cardiac arrest ensues, with dismal chances for resuscitation.

Alternative Forms of Shock

Although we have focused so far on hypovolemic shock, particularly of traumatic etiology, there are other possibilities. A wide range of shock types exist, but speaking broadly, there are only two other categories important to us: distributive, and cardiogenic/obstructive.

Distributive shocks include anaphylactic, septic, and neurogenic. The essential difference here is that rather than any loss of fluid, the vasculature has simply expanded. Rather than squeezing down on the blood volume to maintain an appropriate pressure, the veins and arteries have gone “slack,” and control of the circulating volume has been lost; it’s simply puddled, like standing water in a sewer pipe. (Depending on the type of shock there may also be some true fluid losses due to edema and third-spacing.) Imagine tying your shoes: in order to stay securely on your feet, the laces need to be pulled snugly (not too tight, not too loose). If the knot comes undone and the laces lose their tension, the shoe will likely slip right off. Your foot hasn’t gotten smaller, but the shoe needs to be hugging it properly to stay in place, and it’s no longer doing its job.

The hallmark of distributive shock is hyperemic (flush or highly perfused) rather than constricted peripheral circulation. The visible skin is warm (or hot) and pink (or red), and the patient may be profoundly orthostatic. Septic shock is associated with infection; anaphylactic with an allergic trigger; and neurogenic with an injury to the spinal cord.

Cardiogenic and obstructive shocks are a different story. In this case, there’s nothing wrong with the circulating volume, or with the vasculature it flows within; instead, there’s a problem with the pump. Cardiogenic shock typically refers to situations like a post-MI heart that’s no longer pumping effectively. Obstructive shock refers to the special cases of pericardial tamponade, massive pulmonary embolism, or tension pneumothorax: physical forces are preventing the heart from expanding or blood from entering it, and hence (despite an otherwise functional myocardium) it’s unable to pump anything out. In either case, we can expect a clinical picture generally similar to hypovolemic shock, but likely with cardiac irregularities — such as ischemic changes or loss of QRS amplitude on the ECG, irregularity or slowing of the pulse, or changes in heart tone (such as muffling) upon auscultation. Pulsus paradoxus (a drop in blood pressure — usually detected by the strength of the palpable pulses — during the inspiratory phase of breathing), electrical alternans (alternating QRS amplitudes on the ECG), and jugular vein distention also may be present in the case of tamponade or severe tension pneumothorax.

In sum, remember these general points:

The history and clinical context should be enough to make you suspect shock even without other signs or symptoms.
The faster the onset, the more urgent the situation; acute shock needs acute care.
Look both for signs of compensation (such as tachycardia) and for signs of decompensation (such as falling blood pressure). However, remember that due to confounding factors (such as particularly effective or ineffective compensatory ability, or pharmacological beta blockade), any or all of these may be absent.
Distributive shocks are mainly characterized by well-perfused peripheral skin; cardiogenic/obstructive shocks are characterized by cardiac irregularities.

Interested parties can stay tuned for a brief appendix discussing fluid choices for resuscitation — otherwise, this journey through shock is finally finished!

Go to Part X (appendix) or back to Part VIII

Thoughts from WMEMS

This past weekend, I was able to attend the Western Massachusetts EMS Conference alongside such luminaries as Scott Kier and Kyle David Bates (of the extraordinary Pedi-U podcast). We sat through two days of outstanding lectures on various EMS-related topics, and walked away with some ideas and information I haven’t found anywhere else. Here are just a few of the unique pearls from the conference. Thanks to everyone for the great time!

Kyle David Bates on Mechanism of Injury

In an MVC, ejected (that is, fully ejected) victims have a 1/3 chance of a cervical spine fracture.
They also have around 25 times higher chance of mortality than an equivalent non-ejected patient.
Is “another death in the same vehicle” a legitimate concern when considering mechanism? Yes, but make sure that death wasn’t from an localized cause—for instance, a girder in the face, or they had a heart attack before they crashed.
How about “intrusion”? Over twelve inches into the patient compartment where your patient is found (meaning, visible from inside—not from the outside, which includes the buffer space of the walls), not including areas like the hood, trunk, etc. Alternately, over 18 inches into the patient compartment in areas where your patient is not found—for instance, the rear seating area, when you’re treating the solo driver.
“Distracting injuries” can mean painful injuries that distract the patient, but also gross stuff that distracts the provider. Consider a head-to-toe on virtually everyone, even when the funky arm fracture is drawing your attention.
Many “trauma” patients are no longer being treated with surgery anyway, so sending everything to the trauma centers overloads them for no reason.
One more reason why the sternal rub is not a great diagnostic: if they do clutch at their chest in response, is that localizing—or an abnormal, decorticate flexion response? Different GCS scores, but you can’t tell.
Are extremity injuries significant mechanisms? Penetrating injury proximal to the elbows or knees should be considered threatening to the torso, so yes. Pelvic fractures? For sure. (“How much blood can you lose into your pelvis? All of it!”)
With the automobile safety technology available today, you can crash fast, turn your car into a paperweight, but walk away unharmed. We no longer care about “high-speed,” only “high-risk,” which has many factors (see the Rogue Medic’s recent post on this).
Auto vs. pedestrians: kids get upper body injuries; adults get lateral trauma as we turn and try to get out of the way. Both can get run over.
Motorcycles. Harley-type riders seem to have more head injuries: they get hit by cars, due to low profile and dark clothing, and they wear partial helmets. Sports bikes get more extremity injuries: they wear good protection, are higher visibility, but they ride fast and run into things, breaking any and every bone they have.
Rollovers: no longer trauma criteria. You can roll and do great if you’re restrained. Number of rolls, final position, even roof intrusion have no correlation to injury severity.
Extrication time >20 minutes: no longer trauma criteria. Sometimes it just takes a while due to weather, access, etc, and newer vehicles are supposed to crumple more anyway.
Are burns trauma criteria? No. If they need specialized care, it’s a burn center, but this is not that time-sensitive—more a long-term management thing—so someone with burns and trauma should go to the trauma center instead, can be transferred later for burn care.
Helicopter transport: costs can range from $2,000 to $20,000 depending on distance, and insurers are refusing to pay many of these bills due to lack of necessity. Also consider the possibility of everyone dying in a fiery crash. Weigh cost vs. benefit.

Kyle David Bates on Shortness of Breath

Anxiety is caused by hypoxia; the cure for this is supplemental oxygen.
Sleepiness is caused by hypercapnia; the cure for this is bagging.
OPA or NPA? Testing the gag reflex may create a bigger airway problem (vomit). Better yet, check the mouth for pooled saliva; if present, there is no gag, use an OPA. If absent, they have a gag and are managing their own secretions, use an NPA.
Respiratory distress means there’s a problem, but they’re compensating (compensatory signs like tachypnea).
Respiratory failure means they’re decompensating (hypoxic/hypercarbic signs like altered mental status, cyanosis, falling sats)
Respiratory arrest means they’re not breathing.
Normal inspiration:expiration cycle about 1:2. Obstructive pulmonary problems impede expiration first, because that’s the passive process—it’s easier to inhale past obstructions because it’s an active process. So asthmatics have ratios like 1:4 or 1:5, they’re using active exhalation, and using auto-PEEP maneuvers. (Pursed lips in adults, grunting in kids.)
In adults, look for retractions intercostal (between the ribs) and sternal notch (between the clavicles); in kids, look substernal (below the ribs).
40% of patients hospitalized with asthma have a pneumothorax! (Not necessarily clinically significant, though.)
Pulsus paradoxus/paradoxical pulses are a useful early sign of significant pulmonary dysfunction.
90% of asthma attacks linked with an allergic reaction; however, rhinovirus (the common cold) may now be a contender. Others include: exercise (not sure why; maybe the temperature differential), active menstruation (asthma very common in young post-pubescent women—maybe the hormones), psychological (stress, panic), aspirin use.
Kids compensate great, so cyanosis (a decompensation sign) in kids is very late and very bad.
Risk-stratify these patients, because high risk patients can decompensate fast even if they look okay now. Previous hospitalizations? ICU admits? Intubations?
Cough asthma: no dyspnea, just dry coughing. It happens.
Smokers: measured in pack-years. 1 pack a day for 20 years is 20 pack-years, 2 packs a day for 5 years is 10 pack-years; 30–35 pack-years is where we start to see bad dysfunction.
Best place to check skin? Under the lower eyelid—lift it and check the mucus membranes. Dry for dehydration, pale for shock, blue for cyanosis, the whole gamut.
Ascites is a sign of fluid overload; try the fluid wave test. (Scroll down to “Examining for a fluid wave” here.)
Nebulized ipratropium/Atrovent: its role is mainly to reduce mucus and secretions (cf. atropine). Tachycardia etc. is not a contraindication, because it’s not absorbed systemically; it remains in the lungs.
Give nebs by hand-held mask or T-piece instead of strapping it to their face; that way you have a warning of deterioration when they can no longer hold it to their face.
Bronchodilators may not work great in beta-blocked patients.
Steroids take hours to have an effect, but the earlier they’re given the better the outcomes; give ’em if you have ’em.
If they need RSI, ketamine is nice because it also bronchodilates.
“Facilitated intubation” (i.e. snow ’em with a ton of benzos/narcs)? Be careful, because if you don’t get that tube, it’ll take forever to wear off; these aren’t short-duration drugs.

Kyle David Bates on Pediatrics

Use the Pediatric Assessment Triangle! Appearance, Work of Breathing, Circulation.
Appearance: General activity level and impression. Muscle tone, interactivity and engagement, look/gaze, crying. Appropriate appearance depends on age. Indicates a CNS/metabolic problem. (Make sure to check their sugar.)
Work of Breathing: Flaring, retractions, audible sounds, positioning. Remember they’re belly breathers.
Circulation: mostly skin. Cyanosis (bad), pallor, mottling (pallor + patchy cyanosis), marbling (in newborns—bright red skin with visible blood vessels, maybe some white areas—this is normal). Check cap refill on bottom of foot in little kids.
Shock in kids is most often from dehydration.
Airway: crying is a great sign. Remember to pad under the shoulders when lying flat, their huge heads can tip them forward and block the airway. Avoid NPAs in infants. In very small kids, breath sounds can transmit, so you may hear upper sounds in the chest or chest sounds in the trachea.
Under 2 months: peripheral cyanosis is normal, central cyanosis is bad. Limited behavior, often won’t visually track. Ask parents if their behavior is normal. Ask about obstetric history, it’s still relevant. They have no immune system really, so any infection (temp over 100.4) is a serious emergency.
2–6 months: social smile, will track visually, recognize mom, strong cry and can roll/sit with support. May still be okay with strangers, but try to keep them with parents; if parents like you, they’ll like you
6–12 months: stranger anxiety (unless they’re raised very communally). Very mobile and explore with their mouth, so always think about foreign body airway obstructions, especially up the nose, especially for dyspnea with sudden onset. Separation anxiety, so keep with parent. Offer distractions (toys, etc.). Do exam from toe to head so they get used to you before you reach their face.
1–3 yrs (toddlers, “terrible 2s”): mobile, curious, opinionated, ego-centric, can’t abstractly connect cause-and-effect but learn from experience. Keep with the parents, distract them, assess painful part last (or everything you touch afterwards will hurt). May talk a lot or not much, it’s all normal, but they always understand more than they let on, so be careful what you say.
3–5 yrs (preschool): magical thinkers, misconceptions (“silly” ideas like if they leak too much they’ll run out of blood), many fears (death/darkness/mutilation/aloneness), short attention span. Explain things in simple terms, relate to them (any cartoons or toys in the house you recognize?), use toys, involve them (here hold this, which arm should I use, etc). Don’t ever negotiate, just tell them what to do; praise them often; never ridicule.
6–12 yrs (school aged): talkative, mobile, may not get cause and effect, want reassurance, involvement, praise. Live in present, may not think about danger or risk. Peer involvement. Speak directly to them, anticipate questions (will this hurt? am I going to die?), give simple explanations, don’t ever lie, respect privacy. If you need to do something painful (IVs, etc.) don’t tell them until just before, or they’ll dwell on it. Head-to-toe okay.
13–18 (adolescents): regress when hurt or sick—act like big toddlers. Can understand and theoretically have common sense, but still take risks. Peer support. Speak directly, give concrete explanations, respect privacy, have patience.
Under 21 usually considered “pediatric.”
Degree of fever temp not associated with severity. No actual danger to brain until 106–107 degrees F or so.

Dr. Lisa Patterson on Trauma and Field Triage

RR <20 in infants is trauma center criteria since this is the one easily-measurable vital sign for them.
Crushed/degloved/mangled extremities: although not life-threatening, still worth the divert, because usually needs multi-specialty care (plastic surgery, orthopedics, hand specialists, etc.) to maximize function.
Calling in “altered mental status” or “unresponsive” is not super helpful—give a GCS or otherwise specify what you mean, there’s a big range here.
Trauma activations here are typically three tiers: category 1 (life threat), category 2 (no immediate emergency, but some concern or suspicion due to mechanism or presentation), consult (no concern on initial presentation, but later decision to admit, trauma paged down to consult).
Activation may alert/standby numerous parties including radiology, OR, pharm, blood bank, lab, ICU, respiratory, anesthesiology, social workers, etc. Not a small thing.

Sean Dorr on OEMS investigations

[This is Massachusetts-specific information; local providers can contact me directly if they want to hear about some of this material.— ed.]

Ginnie Teed on Organ and Tissue Donation

Donation is hugely hugely valuable and lifesaving, but there’s not nearly enough. About 60-70% of Americans are registered donors, around 100 million people, but only 1% end up as usable donors and we need far more. Low rates aren’t from consent, they’re from the logistics of getting viable candidates.
Uniform Anatomical Gift Act (UAGA) is federal regulation providing basic requirements for process; states use this standard to form their own systems. Registered donors must be recognized and organ procurement agencies are required to advocate for them even against wishes of family, etc. Driver’s license “opt-in” now considered legal consent in some but not all states.
National Organ Transplant Act establishes the rules of the registry, blinds the entire process, prevents manipulation or line-jumping; the database is centralized and controlled; you can’t legally buy or otherwise get around the system. Manipulation is taken very very seriously and massively investigated, because it’s not only unethical, the pall it casts over the process makes others decide not to donate—the result is many lives lost.
Referrals (i.e. calling procurement organization to say, “we have a potential donor”) come from hospitals, nursing homes, clinics, whomever. This process is exempt from HIPAA.
Tissues tested more heavily than organs, because if an infection is carried through transplanted (i.e. nonliving) tissue, it’s almost impossible to eradicate.
Organs used: vital organs. Heart, lungs, kidneys and livers (most common), pancreas, sometimes small bowel. Max 9 organs per donor.
Tissues used: not living, usually good for about 24 hours after death. Bones (not marrow, which is living), although we try to not obviously mutilate people (for their family’s sake), skin (hugely beneficial), corneas, vessels, heart valves, pericardium, connective tissue (for orthopedic repairs).
Three ways to declare death: neurological (no brain activity; body only alive due to our mechanical support; recovery team responds to site and performs planned recovery); cardiac death (heart stops; not planned); planned extubation/cardiac death (patient is mechanically supported, determination made that there is no possibility to survive on their own; vent is pulled, if heart stops within 59 minutes they can take some organs; usually just the durable liver and kidneys unless bypass is available).
Live organs can only be taken from perfused patients. Someone “dead” (i.e. no pulses) can be a tissue donor but not an organ donor unless you get ROSC. No point in continuing CPR to “maintain the organs” if there’s no possibility of getting return of circulation.
EMS documentation absolutely critical for determining donor eligibility. Need to know downtime in arrests, how much CPR, any ROSC no matter how brief, events/mechanism leading to arrest. There are hard limits on fluid/blood/colloids received, so they must know how much fluid you gave (reasonable estimate is fine). Must document all needlesticks, number and location; if they find any holes that aren’t accounted for they’ll have to assume they’re a drug user or that additional lines were started and extra liters given. If you don’t want to document something at least tell the receiving staff.
If blood is drawn, label must be placed so that expiration date of tube is still readable (FDA requirement).
Every donor can save up to 200 people; failure to document can kill just as many.

UMass Memorial LifeFlight on Air Ambulance Transport

Consider: how do you want the helicopter used? Need their higher level of care? Rapid transport to trauma center? Transport multiple patients in an MCI to more distant hospitals to reduce burden on closest facilities? Can even split the crew to provide higher level of care for multiple ground ambulances.
Many services simply will not fly into a hazmat situation.
Best makeshift landing zones are schools—big open areas, everyone knows where it is.
Wires are a major hazard, make sure to warn pilot—you can see them but he can’t.
Need about 100 x 100 ft for an LZ, or 35–40 big-ish strides per side. Secure the area against bystanders.
Hazards to clear, alert the pilot to, or just pick another spot: poles, antennas, trees, bushes, livestock, stumps, holes, rocks, logs, mile markers, debris. Tall grass can hide hazards. Close all vehicle doors, put your chinstraps on, secure loose items. Don’t stare at the bird landing, turn your back and watch for hazards.
Bad surfaces are dust, dirt, snow, ice, hay. Snow should ideally be very fluffy or very packed. If they land and get iced they may not be able to take off again. Don’t wash down a dusty LZ unless pilot requests it. Paved areas are simplest and best. Large clear roadways can land multiple choppers in a row.
Lighting options: orange traffic cone at each corner, with a handlight placed in each at nighttime. Or, flashing ministrobe at each corner. Or, vehicle headlights crossing the LZ. Don’t shine anything up at the helo, don’t mark with loose material, don’t use flares.
Designate one person as LZ Command (not the IC). Nobody else communicates with the helicopter. Your portable radio probably won’t reach them; use the mobile in the truck. If there’s any hazard on final approach, say one word—”STOP”—and pilot will abort.
Most crashes are pilot error, and most pilot error is due to fatigue. There should be hour limits for a pilot, and this is a valid reason to refuse to fly.

Detective John LeClair, EMT-P, on Opiates and Prescription Pills

Heroin is still big, but pills are a huge player now too. You get an easy prescription from a walk-in clinic or ED, pay maybe a couple bucks with Medicare/Medicaid, and can not only sell them for easy cash but can crush and snort/shoot it for the same effect as heroin. Then if money or access runs low, you end up on heroin anyway to chase that high.
Oxycontin/oxycodone best selling narcotic in the nation ten years ago, but now on the wane. You scrape off the time-release coating, crush it and snort or chew it. “Hillybilly heroin,” “blue,” “oxycotton,” “kicker,” etc. Street price about $1/mg (40mg, 80mg, 160mg common), so many turned to crime. In Aug 2010, manufacturer (Purdue) added a “geling” agent which turns it to gel when it contacts water, making it difficult to snort. Try to snort this Oxycontin OP and it turns into a ball in your nose. Some people are sticking straws/tubes up in there to try and get it deeper and deeper, so airway obstructions are happening.
Percocet: oxy plus acetaminophen. For years the most common analgesic for sports injuries, so common among youth. Kids shared ’em, put out bowls of them at parties, girls prostituted themselves for pills. Taken with alcohol the APAP/Tylenol kills your liver. “Littles,” “little babies,” “little dogs.”
Opana/oxymorphone: getting popular after Oxy OP started ruining everyone’s fun. Same idea but you can still snort it. Twice as strong, and costs twice as much ($2/mg)
How to grind? Take a hose clamp, cut it, straighten it, tape it down, run the pill across the holes to grind it. Or use a Pedi-Egg, which collects the powder for you. The finer, the better high.
Heroin: snort, “skin pop” (subcutaneous), mainline. Must be pretty pure to snort, which it now tends to be, so popularity grew (people were afraid of needles due to HIV). However now some HIV/Hep is spreading through bloody noses and sharing straws anyway.
Smack, horse, china white, chiva, junk, H, tar, black, fix, dope, brown, dog, food, negra, nod, white horse, stuff. Dealers have their own “brand names.”
Heroin addicts are creatures of habit; get high same place, same way. Any change in their routine (e.g. different location) can get them amped up, changing their sensitivity and leading to OD even with their usual dose. Consider this if you find an OD somewhere like a car or alley.
“Cotton fever”: they pluck out wads of cotton from cigarette filters and drop it in the heroin to help filter it. Sometimes when they draw out the liquid they get a bit of cotton, and when they shoot it they get a sort of phlebitis/infection/sepsis.

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.