Hurry Up and Wait

So you chuck the ill patient onto the stretcher, throw some straps over him, bang him into the ambulance. Your partner, the stunt driver known only as “Maverick,” spins you out onto the throughway and mashes on the Faster pedal until it stops going down. The radio is playing “Go, Speed Racer!” as you slam through traffic, taking corners at 45, the straights at 70, and sounding more sirens than they have names for. (Maverick, bless his heart, has subscribed to the two-footed school of driving, where the gas stays floored and corners are managed by tapping the brake with the left foot.)

Mere seconds later, having covered twenty miles, fractured your spine twice, and pounded every piece of unsecured equipment to powder, your rig squeals into the ER on a cloud of blue smoke, drifting sideways into the ambulance bay like a riced-out Honda. Maverick leaps out, throws open the rear doors, and . . .

. . . then stands there scratching his ass for five minutes while you disconnect wires, find a place to perch the monitor, swap over the oxygen to a portable tank, and make sure everything’s clear to pull out the stretcher.

Really?

With critical patients — particularly those receiving ALS care — more time can be saved by setting up the patient for transfer prior to arrival than can be saved by driving dangerously. If you’re truly in a “load and go” situation, remember that the clock doesn’t stop just because you crossed the finish line at the parking lot. Whatever the patient needs (surgery, pharmacological care, invasive measures), presumably it wasn’t to wait outside the hospital while you fiddle with things. If seconds really matter, then you should be able to throw open the doors as soon as you stop moving and wheel the patient straight out and into the ED. “But I’m busy with patient care,” you say? Well, if there aren’t enough hands, then decide whether whatever you’re doing is more important than the time you’d save. But if it is, then stop acting like you’re in such a hurry.

The equivalent of this on your initial response would be pulling your boots on and getting out the chute faster, rather than trying to make up the time on the road. But that’s a topic for another day.

Pulse Oximetry: Application

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

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

Clinical context: When a sat is not a sat

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

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

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

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

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

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

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

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

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

Hardware failure: When a sat is not anything

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

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

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

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

Pulse Oximetry: Basics

Just tuning in? Start with Respiration and Hemoglobin, or continue to Pulse Oximetry: Application

Once upon a time, the only way to measure SaO2 was to draw a sample of arterial blood and send it down to the lab for a rapid analysis of gaseous contents — an arterial blood gas (ABG), or something similar. This result is definitive, but it takes time, and in some patients by the time you get back your ABG, its results are already long outdated. The invention of a reliable, non-invasive, real-time (or nearly so) method of monitoring arterial oxygen saturation is one of the major advances in patient assessment from the past fifty years.

Oximetry relies on a simple principle: oxygenated blood looks different from deoxygenated blood. We all know this is true. If you cut yourself and bleed from an artery — oxygenated blood — it will appear bright red. Venous blood — deoxygenated — is much darker.

We can take advantage of this. We place a sensor over a piece of your body that is perfused with blood, yet thin enough to shine light through — a finger, a toe, maybe an earlobe. Two lights shine against one side, and two sensors detect this light from the other side. One light is of a wavelength (infared at around 800–1000nm) that is mainly absorbed by oxygenated blood; the other is of a wavelength (visible red at 600–750nm) that is mainly absorbed by deoxygenated blood. By comparing how much of each light reaches the other side, we can determine how much oxygenated vs. deoxygenated blood is present.

The big turning point in this technology came when “oximetry” turned into “pulse oximetry.” See, the trouble with this shining-light trick is that there are a lot of things between light and sensor other than arterial blood — skin, muscle, venous blood, fat, sweat, nail polish, and other things, and all of these might have differing opacity depending on the patient and the sensor location. But what we can do is monitor the amount of light absorbed during systole — while the heart is pumping blood — and monitor the amount absorbed during diastole — while the heart is relaxed — and compare them. The only difference between these values should be the difference caused by the pulsation of arterial blood (since your skin, muscle, venous blood, etc. are not changing between heartbeats), so if we subtract the two, the result should be an absorption reading from SaO2 only. Cool!

Most oximeters give you a few different pieces of information when they’re applied. The most important is the SaO2, a percentage between 0% and 100% describing how saturated the hemoglobin are with oxygen. (Typically, in most cases we refer to this number as SpO2, which is simply SaO2 as determined by pulse oximetry. This can be helpful by reminding us that oximeters aren’t perfect, and aren’t necessarily giving us a direct look at the blood contents, but for most purposes they are interchangeable terms.) But due to the pulse detection we just described, most oximeters will also display a fairly reliable heart rate for you.

Small handheld oximeters stop there. But larger models, such as the multi-purpose patient monitors used by medics and at hospital bedsides, will also display a waveform. This is a graphical display of the pulsatile flow, with time plotted on the horizontal axis and strength of the detected pulse on the vertical. With a strong, regular pulse, this waveform should be clear and regular, usually with peaked, jagged, or saw-tooth waves. Very small irregular waves, or a waveform with a great deal of artifact, is an indicator that the oximeter is getting a weak signal, and the calculated SpO2 (as well as the calculated pulse) may not be accurate. This waveform can also be used as a kind of “ghetto Doppler,” to help look for the presence of any pulsatile flow in extremities where pulses are not readily palpable. (To be technical, this waveform is known as a photoplethysmograph, or “pleth” for short, and potentially has other applications too– but we’ll leave it alone for now.)

Most modern oximeters, properly functioning and calibrated, have an accuracy between 1% and 2% — call it 1.5% on average. However, their accuracy falls as the saturation falls, and it is generally felt that at saturations below 70% or so, the oximeter ceases to provide reliable readings. Since sats below 90% or so correspond to the “steep” portion of the oxyhemoglobin dissociation curve, where small PaO2 changes might correspond to large changes in SpO2 — in other words, an alarming change in oxygenation status — the fact that your oximeter is losing accuracy in the ranges where you most rely on it is something to keep in mind if using oximetry for continuous monitoring.

The lag time between a change in respiratory conditions (such as increasing supplemental O2 or changing the ventilatory rate) and fully registering this change on the oximeter is usually around 1 minute. And at any given time, the displayed SpO2 is a value calculated by averaging the signal over several seconds, so any near-instantaneous changes should be considered false readings.

Keep reading for our next installment, when we discuss the clinical application of oximetry, and understanding false readings.

Respiration and Hemoglobin

We brought up pulse oximetry several weeks ago, and it seems like a topic worth exploring in detail. What’s this device all about, and how should we be using it?

In order to get there, though, we should really start with some basics of pulmonology and respiration. Don’t worry — we’ll get to the good stuff soon enough.

Oxygen transport physiology

The cells of the human body use oxygen molecules (two oxygen atoms forming an O2) as a vital component of their basic metabolism. Most can survive briefly without oxygen, but not for long and not well.

Delivering oxygen to the cells is a process that starts in the lungs. Oxygen in the ambient air is inhaled into the thin-walled sacs called aveoli, where they easily diffuse across the membrane wall into tiny capillaries filled with blood. (At the same time, carbon dioxide [CO2] is diffusing in the other direction, from the blood out into the alveoli, to be exhaled out as waste.) This oxygen “dissolves” into the blood in the same way that fizzy CO2 is dissolved in a can of Pepsi.

The concentration of oxygen present in arterial blood is a concentration called PaO2, and is directly related to the concentration of oxygen inhaled into the alveoli. (This is referred to as PO2, or the partial pressure of oxygen.) In other words, the more oxygen you breathe in, the more will cross over into the blood. Breathing faster and breathing higher concentrations of oxygen will both achieve this.

Just like in the Pepsi, the amount of oxygen your blood can dissolve is limited by the PO2 of the gas surrounding it. The trouble is that amount of oxygen you breathe in can only produce a very low PaO2 — nowhere near enough bloodborne oxygen to sustain human life. (The kinds of life that can survive on dissolved oxygen alone are the lumpy ones that just kind of roll around from place to place.) So animals like humans have developed a method of carrying far more oxygen in their blood than the fluid itself can absorb. We call it hemoglobin.

Hemoglobin are little iron-based proteins. We have zillions of them in our blood, and they like to cluster into donut-shaped discs called red blood cells (or erythrocytes).

Each hemoglobin has four binding sites where oxygen molecules like to attach. Each site can bind one oxygen, and only one. Four oxygens per hemoglobin is maximum occupancy.

So the process goes like this: We breathe oxygen into our lungs. It disperses across the thin membranes of the alveoli, entering the capillaries, where it dissolves into the bloodstream. This dissolved oxygen is then bound by circulating hemoglobin, like a fleet of buses. These drift downstream until they arrive at the tissue beds — muscle, skin, heart, liver, brain, anything and everything — where the process happens in reverse. The hemoglobin unload their oxygen, which diffuses across the cell walls, and is taken up by the cellular machinery for conversion into energy by aerobic metabolism.

Later, after the aerobic cycle has used up the oxygen, the waste fuel that comes from the other end will be carbon dioxide. This will diffuse back into the blood, where some is bound by hemoglobin, but the majority remains in solution (either unchanged or in the form of sodium bicarbonate); it returns to the lungs, reenters the alveoli, and is exhaled. The cycle is complete.

Oxygen delivery

This whole process is obviously critical. The delivery of oxygen from the lungs to the tissue beds requires adequate function of the lungs, of the blood itself, and of the surrounding environment that allows for oxygen binding and unloading.

In the lungs, this process can be compromised in numerous ways. As we saw, oxygen must enter the alveoli and blood must circulate through the alveolar walls in order for transfer to occur. These two processes are referred to as V (for ventilation) and Q (for perfusion). Inadequacy of either one is called a V/Q mismatch. For instance, obstructive lung diseases tend to decrease the total alveolar membrane available to oxygen — blood is still circulating there, but the gas can’t reach it. This is a failure of V (or shunt). A pulmonary embolism, on the other hand, blocks bloodflow to part of the lungs — you still breathe oxygen into those areas, but no blood is present to receive it. This is a failure of Q (or deadspace). (Obviously, someone who isn’t breathing at all will be inadequately oxygenated in a much simpler way.)

In the blood itself, other problems can occur. First, understand that the total amount of oxygen delivered to your body is not only determined by how much is bound to the hemoglobin, but also by how many hemoglobin are available. A low blood volume — such as in hypovolemia — will compromise this. A normal blood volume, but low hemoglobin count — as in anemia — will also compromise this. An adequate volume and hemoglobin count, but inadequate circulation — low blood pressure and poor cardiac output — will result in a “traffic jam,” with plenty of buses and plenty of passengers, but not enough movement from Point A to Point B.

There can also be problems with either the binding or unloading of oxygen.

The oxyhemoglobin dissociation curve

Adequate oxygen delivery depends on the hemoglobin binding, transporting, and ultimately unloading O2 molecules. As we saw, although oxygen does dissolve into the plasma itself, it is not nearly enough to sustain life; we need those hemoglobin working properly to act as ferries.

Each hemoglobin can bind zero oxygens, one, two, three, or four. How many it binds is directly related to how much oxygen is dissolved in the blood; the more oxygen in solution (PaO2), the more will bind onto hemoglobin (SaO2). If 50% of our total binding sites were occupied by oxygen (for instance, if all of our hemoglobin had two bound oxygen each), we would say our arterial blood is 50% “saturated” — an SaO2 of 50%.

If we graph the PaO2 on one axis, against the SaO2 on the other, we get a line called the oxyhemoglobin dissociation curve. This describes what pressure of oxygen we need to achieve in the blood in order to reach a given saturation of hemoglobin.

Interestingly, this line will not be straight, but rather an S-shaped (or “sigmoid) curve. The reason is that although more oxygen means more binding, not all binding is the same. It takes a fair amount of pressure to bind the first oxygen, but once it’s bound, the affinity of that hemoglobin to bind is substantially increased. It now wants to bind more. Once it binds its second oxygen, its affinity is increased even more; it now takes very little additional PaO2 to bind at the third site. After the third, however, a certain amount of “overcrowding” comes into play, and the fourth binding site has a lower affinity than the third. The curve flattens back out.

Here’s the trick. This curve is not set in stone. It is determined by a number of physiological parameters, which can shift the line to the left or right.

Movement of the line to the right means that for a given PaO2, you will achieve less saturation. The affinity of hemoglobin for oxygen is low; it “doesn’t want” to bind, so you must reach a higher pressure of dissolved oxygen before it will attach to the hemoglobin. On the other hand, since it doesn’t want to be there in the first place, it will very readily unload at the tissue beds. Oxygen is hard to bind but easy to deliver. Factors that shift the curve to the right include: warmer temperatures; acidosis; and high 2,3-DPG (an “unload more oxygen” signaling molecule produced in hypoxic conditions, like COPD, CHF, airway obstructions, and high altitudes). These are all conditions seen in metabolically active states like exercise, where we need more oxygen down in the trenches.

Movement of the line to the left means that for a given PaO2, you will get more saturation. The affinity of hemoglobin for oxygen is high; it binds very readily, so little oxygen needs to be present before it will find a binding site. However, since the affinity between hemoglobin and oxygen is so strong, it will not want to unload into the tissues. It’s easy to bind but hard to deliver. Factors that shift the curve to the left include: cold temperatures; alkalosis; and low 2,3-DPG (of which inappropriately low levels are often seen in sepsis and iron deficiency).

Which do we want? Generally, moving the curve to the right is preferable in critical illness. Although it seems like a problem that we need to get more oxygen onboard, in reality this is usually possible with active medical intervention: we have supplemental oxygen, assisted ventilations, and at the end of the day can always just help someone do more breathing. However, what we can’t do is help them unload oxygen at their vital organs. For someone in a high-demand state, such as the shocked trauma patient, we want to maximize the delivery of oxygen to their body; the last thing we want is plump, well-saturated hemoglobin that refuse to unload their cargo where it’s needed.

Still awake? Tune in next time to hear about how oximetry works and what it should mean to you.

Keep reading with Pulse Oximetry: Basics and Pulse Oximetry: Application

Pediatric Infectious Airway Emergencies

Most of us in EMS are pretty good with the typical adult respiratory illnesses — your asthmas, your COPDs, your CHF exacerbations. Maybe the occasional pneumonia. But upper airway illnesses can be harder to keep straight, and two of them are known for occurring especially in pediatrics.

Croup

Croup is an infectious disease, usually caused by viral infection of the upper airway. Once upon a time, it was typically caused by diptheria; with the widespread adoption of diptheria vaccination in the US, this has become rare, and the most common cause is now the parainfluenza virus.

Croup is typically seen in children from 6 months to 6 years of age; approximately 15% of all children will contract it at some point.

Its characteristic finding is a coarse, barking, “seal-like” cough. High-pitched stridor is also often present, as is hoarseness of voice, and dyspnea at late stages. All are caused by narrowing of the upper airway due to inflammation from the infection.

This inflammation is normally at the level of the trachea, possibly stretching down into the large bronchi and up into the larynx, but below the level of the glottis.

The onset is usually gradual, lasting from several days to two weeks. Often, there will be fever or coryzal (cold-type) symptoms, such as congestion or headache. A sudden onset is uncommon; usually there will be a day or two of cold symptoms prior to the onset of cough or hoarseness. The upper airway symptoms are often worse at night. (Occasionally, croup may have a spasmodic cause, sometimes triggered by an allergic reaction [akin to asthma]; in these cases coryzal symptoms are rarely present.)

The main differential here should be croup vs. epiglottitis vs. an aspirated foreign body or anaphylaxis. In most cases, these last can be ruled out by a thorough history. As for epiglottitis, it can best be revealed by the severity of symptoms. In almost all cases, croup does not cause significant airway obstruction leading to major dyspnea or hypoxia. A poor general impression (“big sick”), diminished responsiveness, or respiratory failure should point you towards epiglottitis instead. Drooling is not normal. Death is possible but very rare.

Other signs and symptoms are as typical for respiratory difficult in children, including tachypnea, tachycardia, hypotonia (weak or flaccid muscle tone in the exhausted child), chest retractions, and potentially low O2 saturation. In severe cases, as respirations become shallow and weak, stridor and coughing may not be audible.

Treatment is generally supportive. Keep the child comfortable and reassured, if possible with their mother or other caretaker — panic will increase their oxygen demand and may increase stridor. Provide supplemental oxygen as tolerated; blow-by may be most appropriate. Nebulized racemic epinephrine is appropriate field care for significant cases, and most will receive steroids in the hospital. Steam or humidified oxygen is an old standby, and is anecdotally popular, but research suggests it has no benefit.

Epiglottitis

Epiglottitis is similar in presentation to croup. Its cause is also infectious, but bacterial instead of viral, and historically the microbial agent was almost always hemophilus influenza type B, a bacterium unrelated to the flu except by name. Effective HIB vaccine became widespread in in the late 1980s; as a result, epiglottitis in the US today is actually more common in adults than in vaccinated children. When it does occur in pediatrics, it is typically between the ages of 3 and 7.

Like croup, epiglottitis is a narrowing of the upper airway. However, it occurs higher, above the glottis, and primarily involving the epiglottis and surrounding tissue. Due to inflammation of this flap at the gate of the airway, a sore throat and difficulty swallowing are almost always present. Fever, stridor, and hoarseness of voice are common, as is a muffled speaking voice and tenderness of the larynx, which may present as severe pain provoked by even gentle external palpation. Typically in children there are no other prodromal symptoms such as congestion; adults often do experience coryzal symptoms.

The chief distinction between epiglottitis and croup is the severity. Although far less common, epiglottitis should be considered an acute emergency, and the narrowing of the airway can lead to significant or total obstruction and resultant respiratory failure. The classical late clinical presentation is the young child found in a “sniffing” position, tripodding or sitting upright, with audible stridor (or quiet respirations as failure approaches), drooling and close to exhaustion. (Drooling results from the inability to easily swallow.) Symptoms can be insidious in onset, but usually progress very rapidly. Mortality in adults with epiglottitis is around 7%, although less than 1% in children.

Treatment may involve supplemental oxygen, but maintaining a patent airway should be your main concern. Intubation may be necessary, sometimes suddenly, so prepare for a difficult airway even if the situation seems relatively controlled. Cricothyrotomy is appropriate as a last resort. Direct manipulation can provoke further inflammation, so the use of basic airways (OPA/NPA) is unhelpful and unwise. Although laryngoscopy can help confirm the diagnosis of epiglottitis (the epiglottis and arytenoids will be cherry red and swollen), it can also provoke spasm and further inflammation, so it is discouraged in the field unless immediate and unhesitating intubation is intended.

Albuterol is not indicated, and epinephrine has no benefit. In-hospital care includes antibiotics to clear the infection, and possibly the use of steroids to manage swelling.

Acceptable Risk

Following up on our previous post where we discussed patient refusals, it behooves us to say a few things about risk.

The culture of “everyone goes to the ED” is not writ in stone, and in some places, efforts are underway to expand it into a more sophisticated system. For instance, some patients might be transported directly to detox programs, homeless shelters, urgent care facilities, or psych treatment. Some, of course, don’t need to be transported at all, and can stay home, perhaps with instructions to follow up with their PCP. A few areas are experimenting with, or at least moving towards, the concept of an “Advanced Practice Paramedic” or “Advanced Paramedic Practitioner” who could sensibly and intelligently perform this assessment and triage, determining whether patients need immediate definitive care, or (in essence) “clearing” them of acute high-risk pathologies. Ideas like this may prove central to solving the many problems of healthcare in general and EMS in particular, such as ED overcrowding and the inefficient use of available resources.

However, just like the issue of patient refusals, to even discuss the possibility of such a system requires a fundamental shift in our thinking. At the moment, the approach is, “Try to recognize and treat Sick People — but if you don’t, that’s okay, because they’ll recognize them at the hospital.” Obviously, this practice is based firmly on the presumption that most or all of our patients do end up being evaluated in a full-fledged emergency department. Even the very notion that a patient can refuse to be transported ends up as a grudging allowance — we reluctantly acknowledge that we can’t actually kidnap people, but we still make them jump through hoops to make it entirely clear that we wanted them to go all along.

What if we started to accept that some of these patients don’t need an emergency room? Realistically, and retrospectively, it’s obvious that many of them don’t. Other destinations are more appropriate, and in some cases, no transport at all is necessary. But in order to make decisions like that, we need to be able to accept the assessment, clinical decision-making, and risk stratification of our field providers.

It goes without saying that instituting such a practice would require additional training, and providers (such as this mythical APP) practicing at a higher level than our current EMTs and medics. But it’s bigger than that. We have to be willing to let go of the safety net of everyone filtering through the ED. We have to be willing to accept the field workup as final — or at least, good enough that no further evaluation is immediately needed.

Closely wedded with the prehospital culture that treats patient refusals as bogeymen is the in-hospital culture that says every patient needs a comprehensive workup to rule out every possible killer. It doesn’t matter if the odds are 1,000,000 to 1 that the problem is benign rather than a massive MI or hidden PE; that 1/1,000,000 chance of missing the Badness is still unacceptable, so the patient gets the works.

We have the mindset that any miss is one miss too many.

This costs a lot of money. It puts patients through a lot of hell. But most of all, if we’re going to imagine a world where not every patient ends up even going to the emergency department, we have to accept a world where the ones who don’t will not receive that exhaustive workup.

Certainly, this triage process be handled sensibly, and conservatively, because we’re here to help people, not let them die at reasonable rates. So where do we draw the line? Is one miss in a thousand acceptable? One in a million? One in a billion?

We can draw the line wherever we want, but no matter where, there’s going to be a qualitative difference between a reasonable risk and “we did everything.” Because eventually, we’re going to miss one. A well-trained and conscientious clinician is going to assess a patient in their home, and appropriately conclude that their complaint is not dangerous, and that patient is going to die.

Because it happens — because flukes are inevitable. If we throw the kitchen sink at them, and we still lose, then at least we can hold ourselves blameless. But if we take a more reasonable approach, then we have to accept in advance that occasionally, the chips will fall against us. And that has to be okay.

The prevailing belief today is that anytime something goes wrong, something was done wrong. Adverse outcomes are an indicator of error, either an individual error or a flaw in policy or protocol. If I follow our procedures to the letter, and a patient slips through the cracks, it means we need to change the procedure.

Can we get to the point where we understand that if a situation is correctly evaluated, and the risks are correctly balanced, and we simply happen to get unlucky, that the decision was still right? Where we can stop spending ever-increasing amounts of time and money in the pursuit of ever-more-infinitesimal risk?

I don’t know. But if we can’t, then we’re never going to be able to solve some of these problems. Because perfection doesn’t exist, and chasing it is a good way to get very tired.

But it’s Just a Broken Nail!

One of the most common topics of debate in this business is something that should be simple. When is it okay for a patient to refuse transport to the hospital?

On the face of it this is a strange dilemma. When is it “okay”? What does that even mean? When is it okay to have Milano cookies and a bottle of Scotch for dinner? I don’t know. Leave me alone.

The chain of reasoning goes something like this. People call 911 because they have problems, and they don’t know how bad those problems are. By and large, we — the EMTs and paramedics on the ambulance — don’t know either. We don’t have the training or the tools to truly rule out major problems. So the only safe thing is to take the patient to the hospital. There, tall men with white coats, eight years of medical training, large expensive machines, and extensive liability insurance can decide if the patient is dying or not.

Okay. In some ways, that makes sense.

In other ways, it’s absurd. We all experience symptoms or incur injuries from time to time, and for the most part, we do not feel the need to visit the hospital to rule out deadly causes. Although it’s always a remote possibility that something is horribly wrong, in most cases it’s extremely unlikely, and it’s senseless to make an emergency out of every ache or sniffle. As we recently discussed, although it is possible to be very sick without looking like it, it is uncommon. If I woke up today with a minor headache, I wouldn’t want to spend hours of my time and hundreds of dollars at the emergency room “just in case.” So why does that suddenly become a reasonable course of action just because an EMS crew is standing in front of me?

There’s one good answer to this, which is that normally, I wouldn’t call 911 for a headache. So if there’s an ambulance here, it already means that for some reason, I had some special concern about this episode. Perhaps it was unusually bad, or prolonged, or I have medical history which makes me worried about what a headache might entail. Alternately, perhaps a friend or family member called on my behalf, but even then, presumably it’s because they had some reason to be worried.

This is all true. People who call for an ambulance are self-selected to be a higher-risk group than the general population. The headache patient who does dial 911 is more likely to be sick than the headache patient who doesn’t.

However, this isn’t always the case, and even when it is, it isn’t always significant. Some patients, or friends and family of patients, have a very low threshold for concern. Sometimes people misinterpret warning signs. Sometimes things just happen. Consider the hundreds of calls we take each year for minor MVCs. Someone dents their fender in traffic, a concerned passerby calls 911, and we show up to evaluate the occupants. There are no noteworthy injuries, and it wasn’t even the people involved who called for us. Is there a chance they have head bleeds, spinal fractures, pulmonary contusions? There’s always a chance. But do they need to go to the hospital? Or, put another way: they didn’t plan on going to the hospital before we arrived. We performed our medical assessment and found nothing alarming. Does the simple fact that we’re here mean there’s any better reason for them to go to the hospital than before we arrived?

Obviously, the answer is no. But we still tend to default to transporting them.

A cynic might suggest that this is because in most areas, ambulance providers can only bill for transports, not for refusals. In fairness, I don’t think this is usually the main reason.

A bigger reason is liability. There is a real concern on the part of providers, and on the part of the services employing us, that anytime we fail to transport a patient to definitive care, we might be “missing” something bad. As a result, they might later sue us for missing this. Would they have a case? Maybe, maybe not; it would depend on whether we followed the standard of care, and whether we implied to them that we “knew” they were okay with any greater certainty than we truly had. That’s the underlying issue, after all. It’s up to the patient whether they want to go, but we are medical professionals, with impressive uniforms and stethoscopes around our necks, and patients are therefore inclined to think that we know things they don’t. They’re inclined to do what we recommend. But even if we think they’re okay, we don’t know they’re okay, so our “recommendation” is usually to see the doctor, because that’s the only truly “safe” choice from our point of view.

Fair enough. But there’s a small problem with this. We’re lying.

Or at least deceiving. We are trained to assess patients, look for abnormalities, and identify findings that point to the possibility of injury or pathology. If we perform this task, and find nothing alarming or even suspicious, we are going to be thinking, “they’re probably okay. I’m not worried.” Why, then, do we turn to the patient and say, “You should really go to the hospital. I’m worried.”? One major national ambulance company has a policy that you should never ask, “Do you want to go to the hospital?” as it implies a choice — but instead, “Which hospital do you want to go to?” Railroading at its finest.

Certainly, it would be just as misleading to tell a patient, “You’re definitely okay.” We don’t know that, because as we already agreed, we lack the training and resources to diagnose anything for sure. But we do have enough tools to make medical decisions, which we do all the time — what’s the best transport destination? which medication is indicated? — and here, too, we can make an analysis of the risk factors. It’s not the same analysis that would be made by a team of doctors with a hospital at their backs, but as long as we don’t pretend that it is, that shouldn’t be a problem.

Think of it this way. If you were in the patient’s situation, would you want to go to the hospital?

Bear in mind that this isn’t a small thing. Depending on your circumstances, this may involve missing work (even losing a job), arrangements needing to be made for babysitting, housesitting, or pet care, cars retrieved, plans cancelled, and oh yes — a bill ranging from a few dollars to many thousands. Can’t pay that? Now your credit is on the line. You can also look forward to hours of sitting on a series of stretchers, wheelchairs, and beds, while busy people wearing scrubs stick sharp things into your flesh, capture your bodily excreta in plastic cups, and ask you an endless series of the same questions over and over and over. You will miss sleep, get behind on projects or errands, and in the end you will have to find a way to get yourself home and clean up from all this chaos. Possibly with a new infection that you picked up in the waiting room.

If we are responsible, we should view transportation to the hospital as a medical intervention in the same category as medications, invasive procedures, and diagnostic tests. It has certain indications and benefits, but also certain risks and harms associated with it, and we should consider both sides in balance before making a recommendation on the best choice. Certainly, that decision will have to be made by the patient, not by us, because it’s the patient who is undergoing these risks and benefits, so it’s they who get to decide how to weigh them. But they also don’t have the medical understanding of the situation that we do. So that’s our job: to transmit to them what we’ve found in our assessment of their complaint. The risk factors, the positive or negative findings on their physical, any alarming vital signs, and the salient features of their history. In many cases, this process is why they called us — because although they’re experiencing something abnormal, they don’t know if they should be worried or not. We won’t have all the answers, but we can give them more information than they had before, and they can use that information to better inform their decision on whether to seek further care. (Remember, this might include scheduling an appointment with their PCP, visiting an urgent care clinic, getting a ride to the ED or driving themselves, and of course the old “wait-and-see” approach. Even when more care is needed, the ambulance isn’t the only answer.)

For the reasons of liability, and policy, and the general fear-mongering attitude that has swept over the healthcare industry in recent years, this is a very difficult line to walk, and in many cases to preserve your job and license you may need to err on the side of “encouraging” a patient to be transported. However, I find it ethically troubling when we mindlessly push everyone towards the ED, no matter what common sense or their medical situation tell us. When we visit someone with a complaint that we’d ignore in ourselves, our partner, or our mother, and convince them to climb into the ambulance anyway, whose best interest are we looking out for?

Are we hurting the patient to help ourselves?

Are we okay with that?

The Art of the Transfer (part 3)

Continued from part 2…

There’s another benefit of patient transfers beyond the merely educational. You get to meet the people.

Oh, you meet people on emergencies. Depending on the nature. Dead people don’t talk much. (You get a look at their houses, maybe.) And really sick people, well, you’re pretty focused on the medical stuff then. Patch this, pump that, push the magic potion. When did it start? Have you felt this way before? What Russ Reina calls the business of being a “flesh mechanic.”

But on a routine transfer, and to a lesser extent on the non-emergent “emergencies” (when you have little to do and no hurry to do it), you get to actually chat with the human being upon your stretcher. Imagine that! They don’t just have a name and date of birth — they have a trade, a family, a history, a life.

Everyone has a story. Some of them are more interesting than others on the surface, such as the retired spy or the film star, but everyone has a story, and they’re all worth hearing, if you care.

Most of these people are old. If you’re not old, you may think this means they have less to say to you, but really, it’s the opposite. You’re 25 and they’re 90; all of the problems you’ve got, all the changes in the world you think are new, every dilemma you’ve ever faced, they’ve seen it and heard it and done it. They’ve been alive for several of you. Do you think people live that long without knowing their way around?

I once heard it suggested that you don’t really grow any wiser as you age, because although you learn from your mistakes, there are still an infinite number of future mistakes to be made. You never “run out” of new errors.

Perhaps that’s true. But even if the 90-year-old benefits little from his wisdom, that doesn’t mean you can’t borrow some of it. And even if his experiences or decisions differ from yours, they were just as important to him as yours are to you, and you can bet the stories are worth hearing.

Where else can you meet such a range of people? And not just meet, but find yourself forced into spending one-on-one time with them? If you’re a misanthrope, this is not a good career for you. Multiple times a day you’ll be placed in a small box with a stranger for a period lasting minutes to hours. It’s like speed dating.

But if you like people — enjoy meeting them, appreciate their company, take pleasure in their lives — then there’s no better job to have.

Drug Families: ACE Inhibitors and ARBs

Understanding the renin-angiotensin-aldosterone system is like following one of those dotted-line Family Circus cartoons — not just long and tortuous, but seemingly designed just to be obnoxious.

Here’s the basic idea. The RAAS is the basic system your body uses to control blood pressure, as well as related values like fluid volume and sodium levels. The most important thing to understand is that the activation of this system causes an increase in blood pressure. Following the trail:

First, renin is released by the kidneys. Renin attacks circulating angiotensinogen, turning it into angiotensin I. Angiotensin I is attacked by circulating angiotensin converting enzyme (or ACE), which turns it into angiotensin II. Angiotensin II has various effects, one of which is to stimulate the release of aldosterone.

Whew.

But this isn’t as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin I’s main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.

Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production — more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.

To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the system simply upregulates itself to maintain your blood pressure using the remaining volume. (Unlike the sympathetic and parasympathetic systems, which also play a major role in regulating blood pressure, regulation via the RAAS is captained mainly at the kidneys, where low pressure and throughput induces increased renin production.)

Cool? Cool.

Okay, so the role of ACE, or angiotensin-converting enzyme, was to transform the useless angiotensin I into the powerful angiotensin II. What do you think a drug called an ACE inhibitor would do? Indeed: it inhibits the activity of ACE, thus reducing the production of angiotensin II, which then causes reduced production of aldosterone and vasopressin.

Less angiotensin II means less vasoconstriction; the systemic circulation opens up, reducing blood pressure. Less aldosterone means less fluid is retained at the kidneys, so urine output is increased, reducing circulating volume, and again, reducing blood pressure. Handy!

A secondary role of ACE is to degrade, or break down, bradykinin. Bradykinin is basically just another vasodilator. If ACE is inhibited, then less bradykinin will be broken down, hence more bradykinin will be available. The result is more vasodilation — once again, reducing blood pressure.

Readers who can recognize patterns will probably have deduced that ACE inhibitors are used primarily to reduce blood pressure. Obviously, this includes the typical patient with primary hypertension that needs to be managed to reduce long-term morbidity. But it also means other things:

Reduced afterload — the resistance the heart has to push against when it pumps blood — means less work for the heart. This is beneficial for patients with heart failure, whose hearts aren’t pumping very well to begin with; or with coronary artery disease, whose hearts need to manage their workload to match the oxygen they’re able to bring in. It reduces “remodelling,” where the heart and the arteries thicken and change shape to better pump hypertensive volumes, with harmful results. And it reduces the damage following myocardial infarction.
Reduced preload — the amount of blood that passively fills the heart during diastole — — also means less work for the heart. Greater preload causes greater filling and hence greater contraction, which all means more work, more oxygen demand, and more remodelling. In heart failure, where the heart is unable to fully expel its contents, reduced preload also means less “extra” fluid to back up into the lungs and circulation, and therefore less edema.
Better renal function. This is a desirable effect in patients with various forms of kidney disease.

Angiotensin receptor blockers (ARBs) are a closely related family of drugs. Instead of interfering with the conversion of angiotensin I to angiotensin II, they simply prevent angiotensin II from binding with its receptors. The effects are therefore largely the same: vasodilation; reduced aldosterone production, with corresponding greater urine output; and reduction in hypertension with less work for the heart.

The main difference between ACE inhibitors and ARBs goes back to bradykinin. If you remember, ACE plays two roles: converting angiotensin I to angiotensin II, and degrading bradykinin, a vasodilator. Since ARBs have no effect on ACE, bradykinin is broken down normally. This may result in slightly less vasodilation, but it also reduces the side effects of elevated bradykinin, which can include edema and a nasty cough. ARBs are most often used in patients who can’t tolerate ACE inhibitors.

Overdose on ACE inhibitors is generally unremarkable. The main effect is hypotension, but it is rarely severe.

Examples

Generic names of ACE inhibitors and ARBs are very, very easy. Trade names are harder, but do have some common elements.

ACE inhibitors

Drugs ending in -pril are invariably ACE inhibitors (enalapril, ramipril, captopril, lisinopril, etc.)
Drugs ending in -ace are often trade names of ACE inhibitors (Altace, Tritace)
Drugs ending in -tec are often trade names of ACE inhibitors (Vasotec, Renitec, Novatec)

ARBs

Drugs ending in -sartan are invariably ARBs (losartan, valsartan, candesartan, etc.)

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; Anticoagulants and Antiplatelets

Treat the Patient?

We’re taking a short break from our series on transfers to discuss a recent post on the EMT-Medical Student blog. One of the issues he brought up is the old saw, “Treat the patient, not the machine.” Rogue Medic struck on this as well.

What do people mean when they say this? They mean that if you attach a diagnostic tool like a pulse oximeter, and it gives you a result that is at odds with the rest of your assessment, then it is probably wrong, and you should not base your decisions on it. It can be broadened to the BLS level, including findings like vital signs, by saying: “Treat the patient, not the number.”

And it’s essentially true. In fact, something I frequently harp on is that diagnosis must always be based on a broad constellation of consistent findings, not on any one red flag. We like red flags, we want red flags, because they’re easy, but it never works that way. The body is an interdependent system, and if a pathology is present, then it almost always has multiple effects detectable in multiple places.

This idea can be looked at differently by asking another question: is it possible to be severely, acutely sick without showing it? I don’t mean long-term problems like cancer; you can’t look at someone and detect that. But if someone’s dying in front of you, of a proximate cause like hypoxia, is it always obvious based on their presentation?

Generally the answer is yes. That’s why it’s wrongheaded to look at a healthy patient with pink skin, normal respiratory rate, calmly denying shortness of breath, but with a low oxygen saturation, and say, “Oh no — he’s hypoxic!” If your oximeter says 72%, what’s more likely — that the number is wrong, or that the patient is somehow hypoxic without any other evidence of it?

Call this the phenomenon of the Hidden Killer. Is it common? Is it real?

It is not common. But it is real. And that’s what’s not recognized when people say, “Treat the patient…”

Why do we take 12-lead ECGs on chest pain patients? Because a clinical assessment alone cannot reliably detect ST elevation, which (simplifying the issue!) is diagnostic for a heart attack.

Why do we take CT scans of blunt head injury patients? Because a clinical assessment alone cannot reliably detect intracranial hemorrhage.

Why do we perform abdominal ultrasounds in multi-system trauma patients? Because a clinical assessment alone cannot reliably detect abdominal bleeding.

Now, some critics will say that all of these will indeed present with obvious, frank clinical findings. The major STEMI patient will eventually enter cardiogenic shock. The head bleed will become comatose and present with Cushing’s Triad and herniation. The abdominal hemorrhage will have guarding, distension, and eventually outright shock.

All true enough. But we’d like to find them earlier than that. It’s true that severe and late pathologies are usually obvious, but our job is to find them when they can still be treated, not after their effects are permanent or lethal. Heck, we could also just provide no medical care and wait until everyone died to make a diagnosis, which would extremely easy to assess, but a little pointless. It is rare that big problems do not have a big assessment footprint, but “small” problems can still be a big deal.

Consider the much-maligned pulse ox. Surely it does not replace a full assessment. But when used appropriately and its role understood, it provides valuable information. A drop from 99% to 94% saturation may not be clinically obvious, but it is potentially significant and surely worth knowing about. What about the patient who is non-verbal at his baseline? Is he going to complain if he drops from 95% to 87%? Will it be frankly obvious from his skin and breathing? Maybe, maybe not. (How about if he’s on a mechanical ventilator at a fixed rate?) If not obvious, does that mean it’s no big deal?

Is the pulse ox always correct? No. But like all things except magic, it’s wrong in predictable ways, ways that can be accounted for, and when it is wrong, that can tell you something too. It requires adequate peripheral circulation, and poor perfusion will make it read low. How is the patient’s distal perfusion? Pink and warm? Good capillary refill? Then you’re probably okay. Carbon monoxide poisoning will make the sat read high. Has the patient been in enclosed spaces with heaters or open flames? Working around engines? Is there any potential source of CO in their history? If not, you’re probably okay. Alternately, does their sat read unusually high compared to their clinical presentation? You might then consider carbon monoxide — something you might not have otherwise have known without the oximeter. It didn’t give you a correct number, but by knowing how and when it fails, it gave us a useful answer.

Here’s a recent example. I picked up a patient with a blood pressure of 54/4. That is a ridiculous blood pressure; arguably, nobody should have it, on the theory that a pressure that low should be pretty close to unobtainable. But, there it was. We diverted to the nearest hospital and I was subsequently chewed out by the receiving nurse.

Do I think that patient truly had a central arterial pressure of 54/4? Nah. Although she wasn’t doing well, her skin was better than that, and although she was altered and combative, she wasn’t comatose. However, her pressure was undoubtedly low, and just how low? If I don’t go with this number, then I’ve got no guidance. The clinical picture was clouded. I couldn’t ask if she knew what day it was; I couldn’t ask what her complaints were; she was non-verbal. She was tachycardic and hypoxic and diaphoretic; she was certainly sick. So, treat the patient, or treat the number? The number may not have been right, but it was concerning enough that it couldn’t be ignored without an assessment that otherwise screamed “no problems here!”, which was not what we had.

Treat the patient? We always treat the patient. A hands-on physical and history is a vital, vital tool for assessment, but other tools are also useful. Some people lament the downfall of the traditional clinical assessment, from the days when doctors with fingers like pianists made diagnoses from findings like Ewart’s sign, and it is shame, but the reason that the high-tech tools like imaging and labs have become de rigueur is that they work well — they diagnose many problems with a speed, sensitivity, and reliability that is not otherwise possible. Nobody would ever say, “Treat the patient, not the unstable cervical spine fracture,” because we recognize that’s the sort of thing you may not otherwise notice until it’s too late. That’s why we spend big bucks on CT scanners.

It all matters. It’s all useful. We should neither cast aside our individual numbers nor ignore the bigger picture. Data is something that, like money and sex, you can never have too much of.