Mastering BLS Ventilation: Algorithms

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

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

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

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

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

Click to expand

Click here for a PDF version (recommended if printing)

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

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

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

Mastering BLS Ventilation: Supplemental Methods

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

  1. 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.
  2. 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.
  3. Expect obese, bearded, elderly, toothless, or traumatic patients to be difficult to bag.
  4. 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.

Basic two-hand seal
A slightly different version with thumbs wrapped around, resembling a "double EC"
Both methods compared

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

  1. 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.
  2. Optimal airway diameter and angles can be achieved by protracting the jaw and simultaneously elevating and extending the head into a “sniffing position.”
  3. Pediatric patients may not need additional head elevation to achieve this, or may even need padding of the back.
  4. Obese patients may need substantial head elevation.
  5. Very obese patients may need to be “ramped” to level their torso before attempting other airway maneuvers.
  6. 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

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

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

 

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

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

  1. 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.
  2. Preventing gastric inflation would be difficult even in healthy people, and is extremely difficult in the apneic and unresponsive patient.
  3. Loss of tone in unconscious patients lying supine reliably produces soft tissue airway obstruction which must be cleared.
  4. 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

The Curious Incident of the Dog in the Diagnosis

 

“Is there any point to which you would wish to draw my attention?”

“To the curious incident of the dog in the night-time.”

“The dog did nothing in the night-time.”

“That was the curious incident,” remarked Sherlock Holmes.

Sir Arthur Conan Doyle, Silver Blaze

We can learn a lot from Sherlock Holmes.

If there’s anybody who better personifies the ultimate diagnostician, I don’t know who. Sir Arthur Conan Doyle, creator of the Holmes canon, was himself a physician and purportedly based his famous detective on Dr. Joseph Bell — who, it was said, could glean a dozen esoteric facts of a patient’s background, history, and complaints from a single glance. (Holmes himself, of course, was not a medical man; that role was played by Watson, the earnest physician who carried his stethoscope wrapped inside his hat.)

Holmes didn’t diagnose illness. Instead, he diagnosed crimes. But the methods were the same, so much so that among the countless fictional characters based upon the Holmesian archetype, some have been crime-solvers (cf. Monk), yet others have been medical doctors (House is the best). Perhaps we shouldn’t model ourselves after the man, who was a single-minded addict and misanthrope, but when it comes to diagnosis — something we can’t escape in medicine — he knows whereof he speaks.

 

The diagnostic method

Holmes tells us in The Sign of Four that detection involves nothing more than three skills: observation, deduction, and knowledge. Let us consider what he means when faced with, for example, a complaint of chest pain.

Observation: we perceive a middle-aged male, alert and seated upright, rubbing at his sternum with a pained expression. His skin is slightly pale, his respiratory rate is slightly elevated, and he is hypertensive. He complains of “tight” 4/10 chest pain whenever he breathes. Upon auscultation we detect diffuse, bilateral, biphasic wheezing. We note a history of coronary artery disease, diabetes, and COPD.

Knowledge: Chest pain in adults indicates a high risk for acute coronary syndromes. Pallor, tachypnea, and hypertension are consistent with this diagnosis. Sharp, mild, pleuritic pain is not, nor is wheezing, all of which are more consistent with a primarily respiratory etiology. But we also know that MI often presents atypically, particularly in diabetics.

Deduction: Both cardiac (ACS) and respiratory (COPD exacerbation) diagnoses top our differential. An ECG and biomarkers are needed to further evolve the odds.

 

So what just happened? We observed using our medical assessment — the history, physical, and diagnostic tests — thus yielding a collection of facts and data. We took the set of background knowledge we already possessed, regarding pathophysiology, epidemiology, and hazard ratios, and used it to “fill in the blanks” and provide context to our assessment findings. Finally, we connected the dots together and used deduction to decide what we’re dealing with.

Holmes knew this method well. He might observe your tattered boots, and using knowledge he possessed of typical wear patterns in the various trades, deduce that you make your living as a longshoreman. Simplicity itself.

Why is this a useful model for diagnosis? Because it highlights the fact that these three skills are entirely distinct, though all quite essential. Observation requires skill with the physical exam, the ability to take a nuanced history, the acumen to interpret diagnostics — it’s simply the trait of being aware. (Holmes, succinctly: “Data, data, data! I can’t make bricks without clay.”) Knowledge is knowledge: it’s memorized facts, what you learn in school or from books, and it gives us the basis to understand the raw material we discover in our assessment. Finally, deduction is the mental capacity to analyze, discover patterns, weigh odds, use your imagination, and extract from the vast pool of observation and knowledge the particular pieces that are actually relevant. (Holmes: “… to recognize out of a number of facts which are incidental and which are vital.”)

 

The hidden danger

Here’s the rub: we’re almost too good at deduction. Humans are excellent at finding patterns in anything. If I leave you my tea-cup for long enough, you’ll undoubtedly find an image revealed in the leaves.

That’s good — but it’s an error. Because there’s not really any image in the tea leaves. But if you’re good at observing details, and have a strong imagination, you’ll still “deduce” many wonderful things from it. Call it apophenia: people want to connect the dots, even when there aren’t any. So we create connections that may be true, but are not always true. We develop stereotypes. Simplifications. False associations.

In medicine, we’re especially prone to this. Because we do know that the human body is interconnected, and that patterns are the rule rather than the exception. Indeed, a large part of developing experience and clinical judgment is increasing your catalog of mental connections. Crackles mean CHF. Irregular pulses mean A-fib. People with Foley catheters have UTIs. Homeless people are drunk. Toe pain is a nonsense complaint. We can’t avoid making the connections, because just like when Holmes examines your boots, those connections are essential to doing our job. But at the same time, we need to learn when to reign them in, or we enter an inescapable diagnostic tunnel after the first moments of patient contact.

It is a capital mistake to theorize before one has data. Insensibly one begins to twist facts to suit theories, instead of theories to suit facts.

A Scandal in Bohemia

What’s the secret? Knowledge.

Sure, we gather the pieces from our assessment, and we automatically start to connect them together. We can’t help that; patterns jump out at us, we’re natural pattern-finding machines. But using our knowledge, we can look past those simplistic, eye-catching patterns, because knowledge tells us something more subtle: what’s missing.

She’s all false positives. See, that’s the trouble with naturals. They don’t see what’s missing.

Lie to Me, “Moral Waiver”

Okay, Friday night, a “man down” call for a homeless guy on the sidewalk. You’re already thinking: drunk. And the initial observations confirm it: he rouses sluggishly, slurs his speech, and pushes you away as he rolls back over. But then you open the mental box that you filled with this sort of thing in your training, and you reflect: where’s the bottle? And this is a strange spot — it’s cold, wet, public and unsheltered. And come to think of it, is that a medical alert bracelet? We should probably check this guy out a little more. Maybe take his blood sugar, look for any trauma, shake him awake and ask some questions.

The initial pattern recognition is there, but you don’t have to be a slave to it, because you know what else to look for. Even if five clues say one thing, if we don’t see five others that ought to be there, that tells us something different. Pertinent negatives, they call ’em in the business.

Maybe there’s nothing else; maybe the drunk is just drunk. But we’re too smart to make that kind of assumption. Because we know that getting it right doesn’t just mean registering the hits — it means checking off the misses, too.

Holmes would expect no less.

 

 

Am I Normal? Finding the Baseline

When it comes to vital clinical skills that simply aren’t taught in EMT class, it’s hard to think of one more important, more frequently called upon, and less formally instilled than this: the ability to determine a patient’s medical baseline.

What’s that even mean? Simple enough. People call us because they have problems — specifically, new problems, or at least new complications of old problems. They don’t call us because of the stroke they had five years ago, or their existing stable angina, or because they still have dandruff. (Okay, sometimes they do, but then we ask why they really called.) So when you’re presented with the patient who has all of those things, the question is: what’s new?

Usually, of course, they tell you. “What’s going on?” “Oh, my stomach hurts.” Most days their stomach doesn’t hurt, today it does, they want to know why. Fair enough. But then you continue through your history and physical — does this hurt too? can you feel that? look here, please — and you find various other abnormalities. Are those new? If so, they may be important. If not, nobody cares. Nobody will thank you for performing a masterful assessment, stroking your beard, and announcing to the world: “I believe the patient has… cancer!” when it was diagnosed a year ago and the patient is already undergoing a planned course of treatment.

This was all much easier in the textbook. They spent quite a while teaching us what healthy people are like — their vital signs, their anatomy, their physiology — so that we’d recognize when someone deviated from that, and we could figure out why. And of course, that method works. As long as your patients are healthy. Unfortunately, healthy people don’t call 911 nearly as often as sick people. Forty years ago, maybe the majority of our patients were generally well individuals with acute problems — broken legs, allergic reactions, unexpected heart attacks — but nowadays, the bread and butter of EMS consists of treating acute exacerbations of chronic disorders, or new complications in the setting of multiple comorbidities.

So how do you figure out which irregularities are worth remarking upon, and which are unremarkable for the patient? Here are some tips.

 

1. Ask the Patient

When they’re able to help out, the patient is one of the best sources of information. Do you know how your blood pressure usually runs? Is your pulse normally a little slow? When did you get this bruise?

Patients with adequate memory and cognition are generally pretty good historians about their own bodies. Not necessarily the details — sometimes the endless litany of acronyms, tests, and diagnoses can blur together — but the personal stuff. They are intimately aware of the fact that they’re usually nauseous in the mornings, they’re told about their high BP whenever they visit the doctor, and they notice their abnormal pupil every time they look in the mirror. Patients with some cognitive impairment may be less able to help you out here, but as a rule, they should still be your first source — you should simply view their input with the appropriate amount of weight based on their perceived reliability. Of course, you should try to corroborate, and the best way is to…

 

2. Ask Someone Else

Most sick people, particularly those who aren’t 100% capable of taking care of themselves, have other people closely involved in their care. For those who live at home, these people are often family members or occasionally an aide or visiting nurse; for those living in a facility, it’s the nursing staff. (And for a patient being discharged from the hospital, it’s the doctor or nurse responsible for them.)

These people have spent ample amounts of time with the patient, so they “know” them — but moreover, they’re medically trained (or in the case of family, often have a sort of on-the-job medical familiarity of the patient’s conditions), so they know them medically. They not only have a reliably story to tell, they can often answer questions about the kind of medical signs you may be puzzled by. Oh yes, he’s got A-fib, his pulse is always like that. No, normally he’s alert and oriented, conversational, I don’t know what’s wrong with him now. Even friends or bystanders can sometimes help you out here — oh yes, Jeff has epilepsy, he takes medication for it, but he hasn’t seized like this in years.

This is the kind of information to gather before you leave a scene, because not only can it be important, you may be the only person who can obtain it. Once you show up at the hospital, if relevant history is missing from the clinical picture, the ED staff may try to make some calls and ask questions, but it’s much more difficult than if you did your job right to begin with.

This is also why it’s highly advisable, whenever time permits, to perform a reasonably full assessment prior to leaving the scene. That way when you find something striking, you can simply ask someone — is this normal? Nothing’s worse than taking an initial set of vital signs ten seconds after you start transporting, finding a blood pressure of 86/40, and wishing you’d done it five minutes earlier so you could’ve asked the nurse. (In fact, if you did this before leaving the floor on a discharge, they might just decide not to send the patient after all.)

One trick I’ve tried when I wasn’t smart enough to assess on scene is to simply call back. You’re bringing someone from a facility, and on the way, you find something funny. You’d love to know if it’s new or existing. Crack open the paperwork (or ask your dispatch) and find the phone number for the sending facility, punch it into your phone, ask for the floor or wing you took the patient from, and request the nurse who covered your patient. Then you can identify yourself and just inquire: “Hey, this dude’s got a blown pupil. Is he always like that?” This probably won’t work with most scene calls, unless you have a number for an emergency contact, but I suppose you can try to track someone down.

When nobody’s available to answer your questions, your best bet is simply to…

 

3. Consider the Context

As we often talk about, clinical decisions and diagnoses aren’t made from isolated findings. You have to look at the whole picture.

I love dialysis patients, because they’re like case studies in exercising clinical judgment. I have had regular dialysis patients who were at baseline non-verbal, marginally responsive, routinely hypo- or hypertensive, routinely tachy- or bradycardic, dyspneic, hemiparetic… pretty much anything you can imagine. Obviously if you know them you might have a better idea of their baseline, but again, with some of these people, I would not bat an eyelash to find them with a blood pressure of 80/70 on one day and 176/100 the next. Was either one an emergency? Not necessarily. It was probably something the dialysis staff and potentially their nephrologist would like to know about, but once again, it’s not helpful to anyone if you throw up your hands and announce that the person with kidney failure is sick. They know.

In any case, how do you figure out when their derangement is significant? Look elsewhere. Big problems have a big footprint. If the patient is communicative and reliable, how do they feel? Lousy? Fine? Weak, dizzy, nauseous? Pain in their chest, their head? Consider their history, look elsewhere in the body, and examine their medications. Assemble all the data you can, so that your findings are no longer a lonely, isolated result, but just one of many meaningful indicators.

To suggest that something might be important yet has no effects is to invite the question: if it’s not affecting anything, who cares? For instance, I once discharged a patient whose pulse was in the low 40s. No notation of this was found in her documentation, nor any obvious reason why she should be bradycardic. I eventually called back to her floor and her nurse confirmed that it was typical for her. But even if this hadn’t been possible, I would still have known the rest of her presentation: she was alert, oriented, mentating well, pleasantly conversational, and had a reasonable blood pressure and normal skin signs. She was experiencing no distress or acute complaints, and she was reliable enough that if she had been, she’d have been able to communicate her symptoms. So what were the chances that her bradycardia was something new, alarming, and indicative of a dangerous situation? Not very high.

The biggest challenge here is the patient with so many other comorbidities that they become difficult to clinically assess. If they can’t communicate well (or can’t communicate in your language), and at their baseline they have a wide variety of derangements, it can become difficult to wade through everything and isolate new badness from the tangle of typical badness. Use your noggin and do your best.

Finally, your fallback is always…

 

4. Get to the Right Hospital

Barring anything else, even in the most baffling of situations, most clinical mazes can be untangled if you transport the patient to their usual hospital.

By this I mean wherever they’re typically followed. It may or may not be their requested destination, although it usually is; in any case it’s where they get most of their care (often a nearby community hospital, although sometimes it may be more distant). Some providers give little consideration to these requests, preferring to push for transport to the closest facility or specialized points of entry, but this isn’t just a matter of where the patient likes the meatloaf and the nurses. If you show up with the non-communicative patient with a bizarre presentation and minimal available history, at a hospital that’s never seen them before, they are going to be just as baffled as you are. Eventually they may be able to sort most of it out, but only after substantial time and potentially invasive and unnecessary testing — not exactly the most timely and appropriate care. Remember that although one hospital can usually request records from another, it’s often a cumbersome process involving phone calls and faxed charts, and will never be as comprehensive as what the original facility has access to. (The exception may be hospitals that share an affiliation, which may use the same computer system and hence can mutually access shared records.)

Extremely complex medical histories should go to their customary hospital whenever possible. In some cases, the situation may be so unique that an outside facility won’t even want to touch it — your patient will simply be stabilized and transferred to their normal hospital. This is particularly true when there’s been a recent procedure, devices like an LVAD are in place, or the patient has a rare medical disorder; these patients really may need to be attended to by the specific physician who knows their case, and that kind of familiarity can’t be transmitted by fax.

 

Long story short, this whole process can be challenging, but managing it is one of the basic skills we need to hone if we’re working in the field. Any monkey can point to the ways that someone differs from textbook normality; it takes a discerning eye to pick out the changes that are relevant to our business of emergency medicine.

Your High Horse

What happened to kneeling?

People have problems, so they call the ambulance. We arrive and find them — mostly — seated in a chair, or lying in a bed, or perhaps down on the ground. Then we kneel beside them and introduce ourselves. We ask questions, put our hands on them, give medicines, and so on down that clinical flow you learned in school.

Here is what we don’t do: stand six feet away, look down at the patient (and maybe, maybe deign to bend over a little, with our hands on our thighs like we’re admiring a gregarious puppy), and shout in their direction. “Do you want to go to the hospital?” This is not yodeling practice. This is caregiving.

When did we stop kneeling? More and more, this practice seems to be spreading, and it’s reached the point where I can hardly remember the last time I saw one of us kneel beside a patient. Occasionally somebody will kneel to take vitals, but the provider actually speaking and interacting with the sick person still towers over them like a cop chalking off a body.

Yes, yes, I get it. Your knees are bad. I’ve been there. And your back, it’s stiff. You’re not 21 anymore, you can’t go kneeling willy-nilly. Sure.

But we’re not talking about an Olympic sport here, okay? We’re talking about kneeling, at least for a moment, in whatever manner you can successfully perform. At the very, very least, sit down on something so you’re level with the patient. Park your butt beside them on the sofa or pull up a chair.

It’s about patient comfort, because they want to feel like they’re engaging with a fellow human, not yelling up at Rapunzel’s tower. But it’s also about the dynamic it creates between you. As a novice provider, when I first read Thom Dick write about humility, I didn’t understand. But as time passed, it made more and more sense to me (something that happens suspiciously often with Thom’s stuff). Body language says something, not just to others, but to yourself.

When you kneel, you’re saying: I’m here to help. I’m here to serve you. We don’t kneel very much anymore, not in the modern Western world, but we understand instinctively why one would kneel before a king. It’s not in spite of the effort it takes you to get down there, it’s because of it: by making yourself uncomfortable, you’re demonstrating a willingness to put someone else’s needs before your own.

It’s not saying that they’re your master, and you’re not making them the boss of anything. They’re not making you kneel, which is all the difference: it’s a gift, freely given. You’re acknowledging that the patient is important. More prosaically, it’s very much like the relationship that the cashier at Wal-Mart is supposed to have with you (at least in theory). If you met him on his day off, he might cut you off in traffic, flip you the finger, and drive away cackling. But while you buy batteries, at least, it’s his job to help you out. If he’s lucky, he enjoys doing that; if he’s not, he feels forced into it because he wants to keep his paycheck. We’re in a different boat, though, because our obligation doesn’t come from a boss looking over our shoulder. It comes from the fact that we accepted a duty (perhaps sacred, perhaps mundane, but a duty either way) — that when someone calls 911 and asks for our help, we’ll come and serve them. That makes us servants, and not in a bad way.

Something different happens when you refuse to lower yourself before a patient. It tells everyone in the room, including the patient and especially including yourself, that although you’re here, and although you might perform the clinically-indicated medical treatment, you’re not putting yourself out at all. Drive-by care is all you’re willing to offer. It’s like telling the patient: “Just to be clear, we were in the area anyway, and I thought you might have some snacks.”

I have great respect for police, and we work alongside them often. But their business is very different from ours, and it highlights the dangers in conflating the role of EMS with that of public safety. The job of a caregiver is to serve. The job of a cop is to enforce. It means they have to elevate themselves — you can’t exert authority unless you’re coming from a place of some kind of superiority (legal, moral, even physical). It means they have to judge. I don’t know if they enjoy it, and I do know that it’s highly necessary. But it takes a different kind of person, or at least a different kind of thinking, to judge people than it takes to serve them. Try to imagine a cop kneeling, or helping to wipe Mrs. Smith’s bottom. Now imagine yourself wearing aviators, crossing your arms and leaning against the wall while you bark at her, and understand that it’s just as misplaced.

What’s funny is that when you accept this “lesser” role, you can find an awful lot of meaning in it, because it’s a privileged place too. The privilege isn’t something you exert over others: rather, it’s freely granted to you by the patient. When they see that you’re here to help them, they give you permission to enter their home, to touch their body, to ask them the most intimate questions. This is essential, because you need that access to do your job (and it’s why I believe that mixing EMS and law enforcement would mean a major blow to our ability to treat people). But it’s still a gift. And I think that’s worth something. Even sore knees.

A Million and One Towelplications

Yes. Towels, sir. I said towels.

What’s the big deal with towels? Well, you’ve got them around, first of all. Or you ought to. A decent stock of linen really amounts to essentially supplies for an ambulance, and yes, I maintain that even if you do use the crinkly disposable paper sheets. Blankets for sure, sheets if you use ’em, and towels. Lots of towels.

Towels are the duct tape of padding-related conundrums. If you can’t do it with a towel, it doesn’t need doing. Other than stopping bleeding, checking your oil, and (I suppose) actual cleaning, most applications involve using them as some sort of padding. But to become a towel samurai, you’ll first need to learn the three basic towel forms: Rolls, pads, and snakes. (Towel supply is a little limited at this exact hour, so I’ve substituted an old bath towel, which I’ll thank you not to abuse.)

 

The Towelbox

Pads are simply towels folded flat, into squares or rectangles of the desired size, like a napkin. Good for basic flat padding purposes — just make sure you fold intelligently to obtain the size and thickness you need (and don’t be afraid to stack multiple towels together).

 

Rolls, on the other hand, are constructed by folding long rectangular pads and then rolling them into fat, tight little cigars, like toilet paper. Great for makeshift pillows, extra-thick padding, and anything requiring bulky structure or space-filling.

 

Finally, snakes are towels unfolded to their full length and then twisted (or folded very thin) to make long noodles. You can even tie them end-to-end to make ropes. Great for “lengthwise” padding, makeshift towlines, wrapping around stuff, etc.

Got it? Good. Now, here’s a few uses for the things beyond just cleaning up your messes.

 

Padding Voids

You were taught to do this in school, and then you promptly stopped bothering. Shame on you. It takes practice to get good at it, but if you do, you can seriously reduce the physical abuse you’re inflicting on your patients by backboarding them.

Make small rolls to fill the lumbar void, and rectangular pads for thick spaces like between the legs. Blankets may be needed for particularly large areas, which is fine — blankets are just towels on steroids, after all.

Take the time to pad in a similar fashion when applying splints, particularly box-style splints, and you can substantially increase their effectiveness. Works great for scoop stretchers too. Patient with a hip fracture on the ground or in a bed? Scoop them up, and generously pad between and over their legs. Once you secure the straps there should be nowhere to move, and you’ve turned the device into a secure, large-scale lower-body splint with essentially no movement of the limb. Not bad.

 

Silencing Equipment

We talked about this before — particularly when it comes to backboards, which have a habit of banging around in their enclosures, a towel roll (or if the gap is slim, a thick pad) can be a quick fix to muffle the noise a little.

 

Head Immobilization

Most services nowadays have gone over to commercial head blocks or headbeds; the days of sandbags (or liters of saline) are sadly over. However, there are still places that use primarily towel rolls, and even if you carry commercial blocks they make a great backup — and we always need backups. Frankly, I think good towel rolls work better than most other methods, too; they compress and mold against the head, making them both comfortable and secure.

Stack together two or three large towels, folded into long rectangles, then roll them together tightly into a thick cylinder about the same length and not much thinner than a human head. Take some tape (I like 2″ cloth tape for this) and tape a couple rings to hold it together — a loop near both ends seems to yield better padding than looping the middle. Make a second roll just like it, and you’ve got headblocks! (The roll depicted is probably a little longer than necessary.)

Secure them alongside the patient’s head and tape the same as you would commercial blocks. Just make sure they’re fat enough to provide real support; a single rolled towel, for instance, never seems like enough bulk.

 

Ghetto Collars

So you sized the patient, you reached for a no-neck C-collar, and it’s too small. Oh, it’s not a matter of neck length; they are indeed neckless. Rather, it’s a question of girth. They’re just too big for the collar to reach around. And sadly, although most rigid cervical collars come in a variety of heights, there are usually no options to size for diameter (pediatric collars may be smaller, but there’s rarely any “bigger” size available). What to do?

Try a towel snake. Using a long towel (or two), twist it into a thick rope and wrap it around the patient’s neck like a scarf. Don’t choke them, but wrap it snugly; most towels seem long enough to circle a typical neck with plenty of overlap, which I leave in the front as a chin support. Slap a little tape across the overlap to more or less secure it, and there you have it — a good-faith attempt at cervical immobilization, not as effective as a rigid collar but far better than nothing. (You can always sit there holding manual immobilization too, I suppose. But remember that the collar is mostly a reminder, and the blocks and straps are doing the majority of the work to actually limit motion.)

 

We could go on forever about towels, and I don’t even know most of the tricks; this is the sort of thing you figure out gradually over the course of a long career. (Although Christopher Watford did turn us onto towel animals as popularized by Carnival Cruise Lines, and if you can master those you’ll be a big hit at parties.) Thom Dick has a stellar collection of ideas that he writes about in his columns. We’ll probably do a sequel to this eventually, but in the mean time — what are your favorite uses for towels?

Glucometry: Clinical Interpretation

Continued from Glucometry: Introduction and Glucometry: How to Do it

Implementing glucometry into your overall assessment means understanding three things: when to use it, what the results mean, and when it fails.

 

Indications

First of all, by and large the only people with derangements of their blood sugar should be diabetics. The rest of us are generally able to maintain euglycemia through our homeostatic mechanisms, except perhaps in critical illness causing organ failure and similar abnormal states. Now, if someone injected you — a non-diabetic — with a syringe of insulin, you’d become terribly hypoglycemic, since it would overwhelm your body’s ability to compensate for the loss of glucose. But nobody’s likely to do that if you’re not a diabetic, unless it’s meant for somebody else and a drug error occurs, or I suppose if they’re trying to assassinate you.

With that said, people walk around who are diabetic and don’t know it. I’ve lost track of the patients I’ve transported who presented with signs suggestive of a diabetic emergency, denied a history of diabetes, and came back with a BGL of 600. Well, my friend, I have some bad news for you. “Everybody is diabetic, even if they’re not” is my attitude. Almost a fifth of older Americans are diagnosed, and the older and sicker they are, the more common it is.

Which brings us back to: who needs a BGL?

The most correct answer is anybody with clinical indications of either hypo- or hyperglycemia. As we saw, diabetes itself is really associated with hyperglycemia, which is why the classic signs of hyperglycemia are usually used to diagnose diabetes: polyuria (excessive urination, as extra glucose is excreted by the kidneys and brings water along with it osmotically), polydipsia (excessive thirst and water consumption, to replace the fluids urinated out), and polyphagia (constant hunger, since despite all the sugar floating around it’s not reaching the cells very easily). If your patient is complaining of those, you might be the first one to discover their condition. The diagnosis doesn’t require elaborate tests and imaging; a fasting glucose over 126 BGL tested on multiple occasions, or just once in combination with clinical symptoms, or a post-prandial (after eating) glucose exceeding 200, is the definition of type II DM. (With that said, I wouldn’t go around diagnosing your patients; that’s not your job, and you’re not quite that good.)

Once the glucose gets higher than the “renal threshold” — usually around 180 in average folks — the body starts to excrete it into the urine. This can actually be detectable by chemical dip-stick, or even by odor and texture at very high levels.

When hyperglycemia becomes severe and prolonged enough, we start to worry about diabetic ketoacidosis. Although burning fat and protein is not necessarily dangerous (some popular diets actually put you into a mild ketogenic state intentionally), extensive accumulation of ketones caused by a total lack of insulin (as in type I diabetics — DKA is rarely seen in type II) creates a metabolic acidosis in the body. This is when the long-term harm of hyperglycemia becomes a short-term hazard. DKA causes altered mental status, usually elevated states of confusion and disorientation, and combative behavior isn’t uncommon. Combined with the acetone odor that sometimes presents on the patient’s breath — which can smell like alcohol — DKA patients can seem suspiciously like drunks, and treating them like drunks is a great way to go down a bad path. (A word of wisdom: not only is everybody diabetic, but drunks are definitely diabetic.) DKA also frequently presents with symptoms of dehydration, due to the osmotic water loss in the urine; nausea and vomiting; and deep, rapid Kussmaul breathing to blow off the acidic CO2.

A few situations can cause short-term hyperglycemia, including stressors of any kind (there’s even “white coat hyperglycemia,” where patients tend to produce elevated sugars at the doctor’s office), but these typically won’t produce anything like the massive levels leading to DKA.

With all of that said, you need to really build up some glucose before hyperglycemia becomes symptomatic, and even more than that before it becomes acutely dangerous and unstable. That’s why as a rule, we’re more concerned with hypoglycemia, usually due to medication administration, physical exertion, or metabolic demand exceeding what was expected. Hypoglycemia again presents as altered mental status, in this case more often an inhibited rather than an elevated state: confusion, lethargy, disorientation, inability to focus or follow commands, weakness, headache, seizures, and eventually coma and death. The fun part is that the impairments can present as focal as well as generalized deficits: unilateral weakness of the limbs or face, speech slurring, poor gait, vision abnormalities, and more. In fact, hypoglycemia is a neurological chameleon, and can look like almost anything; it’s particularly notorious for imitating strokes, and for causing (not imitating) seizures. Interestingly, kids are particularly prone to hypoglycemia due to their gigantic heads, full of glucose-hungry brain.

Despite all this, the primary manifestations of early hypoglycemia are actually not symptoms of hypoglycemia. Rather, they’re caused by catecholamines — by the body releasing stress hormones, primarily epinephrine, in a response to the emergency. (This is not an irrational move: epinephrine helps us release and retain glucose.) As a result, we often seen the same signs we’d expect in anybody with a profound sympathetic stimulus: pale and diaphoretic skin, anxiety and shakiness, tachycardia and hypertension, even dilated pupils. Wise diabetics recognize the early signs of this sympathetic response and drink some Pepsi. As levels keep dropping, these symptoms combine with the neurological effects of glucose starvation to produce a confused, sweaty, increasingly stuporous individual. If left untreated, finally the sugar drops until we’re looking at the picture of impaired and diminished consciousness caused by true hypoglycemia. So just like always, the signs of compensation are our early warning system; once the body decompensates, it’s already late in the game.

To make a long story short, anybody with altered mental status, or any kind of general systemic complaint (weakness, fatigue, anxiety, nausea, etc.) should probably get their glucose tested, whether or not they have a known history of diabetes. This is true even if you suspect another cause, such as stroke. Not only can diabetic emergencies look like anything, they can also be comorbid; it is extremely common for patients to have another problem, yet also to bring a high or low sugar along for the ride, due to the illness throwing a wrench in their normal intrinsic and extrinsic glycemic homeostatic systems.

A number of years ago, there was some limited but compelling research that suggested poorly-controlled blood glucose (meaning not severe derangements but merely small deviations from the ideal range) was associated with increased mortality among an inpatient population with a wide variety of conditions. In other words, if you were hospitalized with something like sepsis, you were more likely to end up dying if your sugar tended to float around 160 instead of 110. As a result, it become trendy to practice extremely tight and aggressive glucose management for virtually everybody; diabetic patients were being tested every few hours and ping-ponged around using medication to keep their numbers textbook-perfect. More recently a number of studies have suggested that this may be less important than was thought, and in fact that excessive paranoia leads to a lot of iatrogenic harm from accidental insulin overdoses. This battle is still being fought in the hospitals, but for our purposes a reasonable take-away would be: when managing acute illness, from sepsis to head injury to cardiac arrest, once everything else is done it’s not a bad idea to check the patient’s sugar.

 

What’s the Number Mean?

So you’ve taken a blood glucose, either by capillary finger-stick or from a venous sample. Now what?

We mentioned that the “normal” range is something like 70–140. Diabetics seeking to control their condition and not have their toes falling off in a few years usually strive for tighter control of their BGL than is needed for acute care; a sugar of 175 is a little on the high side for a routine check, but a pretty meaningless elevation for our purposes.

All things are also relative, in that a given BGL must be compared to the patient’s baseline to predict its effects. In other words, poorly-controlled diabetics who are routinely sitting at 200 may become symptomatic of hypoglycemia at relatively high levels, whereas very well-controlled diabetics who usually run lower may be able to drop very low indeed without noticing it. However, a few rules-of-thumb are useful:

Non-diabetics usually become noticeably symptomatic below a sugar of, on average, about 53. (Diabetics, particularly those who are usually poorly-controlled, are more variable — their average symptomatic threshold is more like 78.)

After a recent meal, diabetics may demonstrate hyperglycemia to various degrees depending on whether they ate a Cobb salad or an entire chocolate cake. Non-diabetics should not exceed 200 or so. A few people can exhibit hypoglycemia after meals, due to alcohol consumption, “dumping syndrome,” or some other phenomena, but far more often they’ll exhibit similar symptoms without any true hypoglycemia; some people get shaky and sick due to postprandial epinephrine release.

After an unusual period of fasting (“haven’t eaten since yesterday”), non-diabetics should still have a largely unremarkable sugar. For diabetics, it will depend mainly on how much and what type of medication they’re using.

There’s usually a gap of 10–20 mg/dL between hypoglycemia that’s noticeable to the patient (i.e. sympathetic effects) and hypoglycemia that causes cognitive impairment (i.e. neurological changes). This is their safety margin, when they’re taught to eat or drink some fast carbs; if it keeps dropping they may no longer be able to take care of themselves.

But here’s the problem: the sympathetic “warning signs” can be mediated or impaired for various reasons. For one thing, if your body has to flip that switch often, you become numbed to it, and your hypoglycemic thresholds becomes lower and lower. And many patients with various metabolic and endocrine failures simply can’t muster much of a stress response — the same reason why the elderly may not produce tachycardia and other shock signs when they become hypovolemic. Finally, drugs like beta blockers that directly block sympathetic activity can seriously obscure hypoglycemia. Grab your nearest bottle of beta blockers and read the list of adverse effects: one will be hypoglycemic unawareness, a five-dollar term that means beta blockade can make it difficult to know when your sugar drops low.

Another important consideration in evaluating glucose levels is the expected trend. For instance, a BGL of 70 in a diabetic patient might not excite anybody. However, if you’re testing her because her nurse said that she just accidentally received four times her normal insulin dose, then a BGL of 70 should be alarming, because it’s probably going to keep dropping, and she doesn’t have very far to go.

To make a long story short, the clinical effects of both hypo- and hyperglycemia can vary substantially. What to do? It’s simple: assess the patient physically, obtain a history of their oral intake, medications, and metabolic demands (such as exercise), test their sugar if there’s any possibility of glucose derangement, and compare all those data against each other. A low number in the setting of obvious clinical symptoms is bad. A low number in an asymptomatic patient, or a normal number in a patient with highly suggestive signs and symptoms, should force you to bring out your thinking cap and weigh the odds.

What about treatment? Severe hypoglycemia needs ALS or the hospital — they’ll receive IV dextrose. Severe hyperglycemia needs the hospital only, where they’ll receive carefully-dosed insulin; this is generally considered too dangerous to administer in the field (although patients may have their own), so paramedics are reduced to giving fluid boluses, which may help dilute high glucose concentrations (not a very elegant solution) and is probably needed by a patient in DKA anyway, but isn’t really a fix.

What about oral glucose, in the cute little tubes we carry? Typically these are gels containing 15g of glucose, taken orally (either swallowed or held in the mouth — against the cheek or under the tongue — until it’s absorbed). Do they work? Sure. But it’s not much sugar and it’s not very fast. I found one source that suggests 15g of oral glucose should raise the BGL by 50 mg/dL within 15 minutes of administration — but I’ve never found it to be nearly that effective. In my experience, a bump of about 10 mg/dL per tube is about the best you can hope for in the short-term. If you need more than that, go with the medics and the IV syrup.

 

Testing Errors

When is a tested capillary or venous glucose unreliable? Usually it’s your fault.

Well over 90% of BGLs that test outside the maximum error range (remember, around 15%) are due to user error. Some of the main ones:

  • Your meter requires lot coding, and you failed to do so or used strips from the wrong lot.
  • You failed to clean the skin before lancing, contaminating the sample (not to mention creating an infection risk), or you had some D50 on your glove and it got mixed in there.
  • Rather than gently wicking the sample into the strip, you “smeared” the two together with mechanical pressure, interfering with the expected reaction process.
  • You drew blood from an arm with an IV infusion of D50, TPN, or other meds distal to it. Particularly when peripheral perfusion is poor, always try to sample at a different limb from any running drips.
  • You tried to reuse a non-reusable strip (gross).

Okay, okay, so nobody’s perfect. Factors that may not be as obvious include:

  • Temperature. The test reaction is designed to function within a specific temperature range, which is broad (often around 40–104 degrees) but not limitless, so don’t use them in freezing weather, and try not to leave your equipment ungaraged without climate control when it’s very hot or cold out.
  • Altitude. Just in case you’re an Everest expedition doctor.
  • Humidity. The strips have trouble when it gets very humid.
  • Air. The reagents in the strips will actually degrade if exposed to air for sufficient periods of time, so make sure that you keep them in their tightly-sealed case, and follow their printed expiration dates.
  • Time. If you draw whole blood and leave it around (much more likely to happen in the laboratory than in the ambulance), the erythrocytes will metabolize glucose at about 5-7% per hour.

The good news is that in many of these situations, internal error-checking within the glucometer will recognize the problem, and flash an error rather than a reading. Errors messages are usually numbered and can be informative, but each manufacturer uses different codes, so read the manual if you want to know what “ER2” means. (Hint: not enough blood in the sample is by far the most common.) Many of the other problems can be caught if you regularly check the meter using a known-value test solution, which you should be doing anyway according to most drug and safety agreements. (By the way, both the test strips and those vials of solution are usually meant to expire a few months after opening — the printed date is for an unopened bottle — so if they’ve around forever it’s probably time to retire them.)

What about physiological states that can interfere with the reading? We’ve discussed a few, but briefly:

  • Hematocrit. Anemia from any cause, including cancer or blood loss, causes falsely high readings. High crit, common in neonates, causes falsely low readings.
  • PaO2. Oxygen interferes with the electrochemical redox reaction; thus high concentrations of dissolved oxygen cause falsely low readings, and low PaO2 (i.e. hypoxia) cause falsely high readings, potentially masking a true hypoglycemia.
  • pH. Primarily in meters using the glucose oxidase enzyme, alkalosis will cause falsely elevated readings, while acidosis causes falsely low readings. The acidosis of DKA can therefore cause falsely low readings, masking the profound underlying hyperglycemia, so if the clinical picture screams DKA, don’t necessarily let the glucometer tell you different.
  • Macronutrients. High levels of circulating proteins or fats can cause falsely low readings due to dilution.
  • Hypoperfusion and inadequate circulation. See our previous remarks on this, and remember that venous sources will be more accurate than capillary.

Finally, are there medications that can interfere with glucometer accuracy? There sure are. These in particularly are highly device-dependent, with the glucose oxidase-type meters most often affected. Generally, the effects are not profound, but occasionally they may be clinically relevant.

  • Ascorbic acid. Better known as Vitamin C, some people take megadoses of this stuff, thinking it’ll cure their cold or flu. Depending on the meter it can cause falsely high or low readings, usually a minimal change, but at “megadose” levels the effect can be significant.
  • Acetaminophen. Also known as Tylenol. The effect is similar to ascorbic acid, but even more modest; it should only be considered in major overdoses, and even then the difference is unlikely to break 35.
  • Dopamine. Massive doses, such as might be used for intensive inotropic support, can modestly influence glucose dehydrogenase-based meters.
  • Mannitol. High doses can elevated the measured BGL by around 35.
  • Icodextrin. This is a dialysate solution used for peritoneal dialysis (not hemodialysis — this is where they pump fluid into the abdomen, let it sit, then drain it out), mainly in patients with diabetes. It metabolizes to maltose, which can cause falsely elevated readings in certain meters. There’s at least one tragic and unfortunate case report of a patient death resulting from massive insulin overdose due to this effect, not noticed until the true BGL was obtained by laboratory analysis. If your patient undergoes peritoneal dialysis, try to find out what dialysate is used, and if that’s not possible, it may be safest to assume their sugar is lower than you’re measuring.

 

Conclusions

After all this you’re probably thinking glucometry is so convoluted and rife with pitfalls that you’re better off just eyeballing how sweet your patients are. But don’t let me turn you off! This remains one of the best assessment aids we have, because diabetic emergencies remain some of the most common, most treatable, and most easily confused disorders that we encounter. We can’t perform exploratory surgery, and we may never see prehospital CT scans, but this is a diagnostic test that’s so cheap and simple, with such real potential to affect your decisions, that it should be available everywhere. If you maintain your equipment, learn how to do it right, and keep a few basic confounders in mind, it’ll serve you well as one of your most reliable tools.