Differentiating Syncope: A Few Pearls

Syncope. To a fresh-faced student, it’s a snappy word for fainting. To someone with experience, it’s a heavy sigh, because we take a lot of calls for “syncope” and most of them are no big deal. But to a veteran provider, syncope is a deep, dark diagnostic hole—because syncope can be caused by countless different disorders, and although some are benign, a few of them are deadly.

Comprehensive diagnosis and treatment of syncope deserves its own dedicated series, and one of these days we’ll try and work through it from A to Z. Every etiology is unique and has its own distinct pathophysiology, presentation, and treatment considerations. Syncope sucks.

But for now, we’ll just talk about a few take-home pearls that can pay dividends in the everyday management of your next syncope call. We don’t support simplistic rules of thumb ’round these parts, but sometimes 95% of the work can be done by 5% of the know-how, and that’s just fine.

Here are a few dead-simple roadsigns to help guide you through the most common and most important causes of syncope.

Did they pass out and fall, or did they fall and then pass out?

Syncope means that somebody passed out and fell down. It doesn’t mean that they fell down and then lost consciousness. If they tripped on an oil can, fell over and smacked their head on a rock, they may have blacked out, but there’s no mystery there—it’s a simple trauma call.

So, our first step should be to take the raw he passed out and sift it into a more precise description. One problem is that people who lose consciousness often have a poor or unreliable memory of those events, so they may not always be helpful; this is why it’s nice to have witnesses who can tell the story. Of course, witnesses aren’t always reliable either.

Okay, so what do they remember?

To the extent that the patient remembers it, how do they describe the event?

A prodrome is an early, sometimes subtle set of symptoms that warn of a problem developing. Prodromes are our friend, because although they can be very brief or non-obvious, when present they can help indicate what happened. So, ask! It’s the O in OPQRST, and it’s the E in SAMPLE, so it’s the beginning and end of our patient history—no excuses!

Vasovagal syncope is one of the most common causes of syncope, involving a transient drop in blood pressure, and vasovagal syncope is usually preceded by a prodrome. If you’ve never had the experience of standing up too fast and getting briefly faint, here’s the gist: you become light-headed, your vision blurs or darkens, you feel weak, you may stumble, and finally you go down. There may also be broad neurological symptoms, such as visual disturbances (“seeing spots”), strange sensations, shaking, and more. (Basically, your brain isn’t getting enough oxygen, so odd stuff happens.)

How about seizures? Many seizures are preceded by a prodrome known as an “aura,” which can manifest as various unusual neurological abnormalities; read more in our piece on seizures. Did the patient truly lose consciousness, or do they claim that they remained somewhat aware? In a simple partial seizure, the patient will remain aware of their surroundings (although these often don’t cause a “syncopal” collapse); in most others they will experience a gap in consciousness.

Syncope caused by cardiac arrhythmias, such as a run of V-tach or a Stokes-Adams attack, will sometimes be preceded by a palpable sensation of weakness, or palpitations (“fluttering”) in the chest. However, in many cases there will be no warning whatsoever.

What did the witnesses see?

It’s one thing to hear about a prodrome from the patient, but you may get a different story from the bystanders.

What did they see before he went down? Did he become absent, demonstrate tics or tonic immobility, perhaps complain of an aura? Did he demonstrate obvious clonic jerking of the muscles or urinary incontinence? If he’s acting normally now, was there a period after the event where he demonstrated sluggish activity or unusual behavior, consistent with a post-ictal period? These are all suggestive of a seizure.

Were his eyes open or closed for the duration? Closed is typical of classic syncope, such as a vagal event; open is more appropriate for a seizure. If open, were they rolled back? This also suggests seizure.

Did the patient say, do, or complain of anything before or after the event, which he may no longer recall? Dizziness, headache, chest pain?

Did he stumble, lean against something, or seem to become dizzy? After he went down, did he regain consciousness almost immediately? These are suggestive of vasovagal; once a horizontal position is reached, perfusion to the brain is restored and the problem resolves. If he remained unconscious for a prolonged period while prone—or his initial episode occurred while already seated or reclined—this is highly unusual for vasovagal.

Was he walking and moving normally, in no distress, when he suddenly collapsed like a marionette with its strings cut, hitting the ground with no attempt to protect himself? This is strongly suggestive of a cardiac event and these patients should be considered high-risk for sudden death.

Is there a suggestive history or surrounding circumstances?

Sometimes, the chain of events or the patient’s medical history may suggest an etiology.

Is there a known history of a seizure disorder like epilepsy? How about diabetes? (Take a blood sugar if you’re capable of it; in my book, everybody with an altered mental status is diabetic.) Do they have often pass out or become light-headed?

Have they been eating and drinking as normal? Have they had the flu, and been unable to keep down fluids for the past two days? Were they partying all night? Vomiting? Are they a marathon runner who collapsed in 110 degree weather? Dehydration is a common cause of syncope, particularly in the young, healthy population.

Is there a known condition which may have neurological or metabolic involvement? Cancer with metastases to the brain? A recent infection? A congenital heart condition, such as Long QT, hypertrophic cardiomyopathy, or Brugada? For that matter, are they currently drunk or using drugs? If they take psychotropic or other medications, are they compliant with these, or could there have been an under- or over-dose?

Has there been any recent trauma, such as a fall, motor vehicle collision, or assault with injury?

Have there been repeated lapses in and out of consciousness, rather than a single event? This is an ominous sign suggesting a significant problem.

Are there frank clinical signs that suggest a diagnosis?

This is less likely to be useful than the history, but it can help rule in or rule out major, acute emergencies.

Cardiac abnormalities may manifest with irregular pulses, and active decompensation may be revealed in the blood pressure. Whenever possible these patients should receive ECG monitoring, including a 12-lead. Orthostatic vital signs can be considered if vagal, orthostatic, or hypovolemic etiologies are suggested.

All syncope patients, including suspected seizures, should get a neurological workup, particularly a Cincinatti Stroke Scale.

Respiratory adequacy, including pulse oximetry where available, should be assessed.

Evaluate the abdomen for signs of hemorrhage, and inquire about blood in the stool or emesis as well.

Ensuring Appropriate Triage

It’s no secret that I’m a strong believer in patient advocacy, and that I feel one of the most important roles for EMS is to ensure that patients get directed to the right destination with the right priority and resources. Bob Sullivan at EMS Patient Perspective recently gave a post that hits on all of these points, discussing how to ensure that “undertriaged” patients don’t fall through the cracks at the ED. These details on how to work the system are some of the most valuable things we learn with experience, and to a large degree they’re what allow the ten-year veteran to help patients in ways the novice can’t. Give it a read!

What it Looks Like: Jugular Vein Distention

See also what Agonal Respirations, Seizures, and Cardiac Arrest and CPR look like

Jugular vein distention or JVD (alternately JVP — jugular vein pressure or jugular vein pulsation) is right up there among the most mentioned but least described clinical phenomena in EMS. If you tried to count how many times it occurs in your textbook, you’d run out of fingers, but many of us graduate without ever seeing so much as a picture of it, never mind developing the acumen to reliably recognize it in an emergency.

JVD is simply the visible “bulging” of the external jugular veins on either side of the neck. These are large veins that drain blood from the head and return it directly to the heart. Since they’re located near the surface, they provide a reasonably good measure of systemic venous pressure.

JVD is elevated any time venous return is greater than the heart’s ability to pump the blood back out. Remember that we’re not talking about the vessels that plug into the left heart; that involves the pulmonary arteries and veins, which are not visible in the neck. (Instead, the best indicator of pulmonary hypertension is audible fluid in the lungs.) Rather, we’re talking about the systemic vasculature, which drains into the right ventricle via the right atrium. When veins aren’t getting emptied, we look downstream to discover what portion of the pump is failing. JVD is therefore caused by right heart failure. (Of course, the most common cause of right heart failure is left heart failure, so that doesn’t mean it’s an isolated event.) If JVD isn’t the heart’s fault, then we look to fluid levels. Too much circulating volume will lead to bulging veins for obvious reasons; the flexible tubes are simply extra full.

Although it’s probably most often seen, and most diagnostic, in volume-overloaded CHF patients, the main reason JVD is harped upon in EMS is because it’s a useful sign of several acute emergencies. Mainly, these are obstructive cardiac conditions, where some sort of pressure is impeding the heart’s ability to expand, and immediate care to relieve the pressure is needed in order to prevent incurable deadness. Much like the bladder, the heart is just a supple bag of squishy muscle, and although muscle is very good at squeezing, it has no ability to actively expand. The heart therefore fills only with whatever blood passively flows into it, and if it’s being externally squeezed by pressure in the chest, it can’t fill very much.

Tension pneumothorax is perhaps the most common cause, where air leaks from the lungs into the chest cavity with no way to escape; as the pressure in the chest increases, it bears down on the heart. Associated symptoms are respiratory difficulty, decreased breath sounds on the affected side, and hypotension. Pneumothorax can be readily corrected by paramedics using needle decompression.

Cardiac tamponade is another cause, where fluid leaks from the heart into the pericardium, an inflexible sac that surrounds it (this leakage is called a pericardial effusion), eventually filling the available space and compressing the myocardium. Associated symptoms are hypotension and muffled heart sounds (these plus JVD are known as Beck’s triad). Tamponade cannot be treated in the field, but an emergency department can perform a pericardiocentesis, where a needle is inserted through the pericardium. (For the medics out there, electrical alternans on the monitor is also supportive of tamponade.)

A rather less common syndrome that can produce similar obstructive effects is severe constrictive pericarditis, inflammation of the pericardium usually caused by infection.

JVD is not an all-or-nothing finding — the amount of distention visible at the neck will depend on the degree of venous pressure. Gravity wants to pull blood back down, so the more venous pressure, the higher on the neck distention will climb; profound JVD reaches many inches up the neck, slight JVD will only cover a few centimeters. The pressure can actually be quantified by measuring the vertical height of the highest point of distention (measured from the heart itself, using the angle of Louis as a landmark), but this is probably more detail than is needed in the field. Suffice to say that distention reaching more than 2-4cm of vertical distance (as opposed to the distance on the neck) above the chest is usually considered pathological, and less than 1-2cm can be considered suggestive of hypovolemia.

If it changes with respiration, JVD should rise during expiration and fall with inspiration. Breathing in involves using your diaphragm to create “suction” in the chest, reducing pressure and allowing greater venous return — draining the jugulars. A paradoxical rise in JVD during inspiration (think: up when the chest goes up) is known as Kussmaul’s sign (not to be confused with Kussmaul respirations, which is a pattern of breathing), and is particularly suggestive of obstructive pathologies.

JVD can be difficult to appreciate in all but the most significant cases. It helps to turn the patient’s head away and illuminate the area with angled backlighting, which creates a “shadow” effect. Jugular pulsation should not be confused with a visibly bounding carotid pulse. To distinguish them, remember that although jugular veins may visibly pulsate, their rhythm is generally complex, with multiple pulsations for each single heartbeat (you can feel the carotid to compare the two). The jugular “pulse” will also never be palpable; the distention can be easily occluded by the fingers and will feel like nothing.

Strictly speaking, the internal jugular is usually considered more diagnostically useful than the external jugular, but it’s far harder to examine, so the latter is often used. For various reasons, many people also find the right jugular more useful than the left, although in an ambulance it’s harder to examine.

Most often, JVD is examined in an inclined or semi-Fowler’s position of 30-45 degrees. If the patient is supine, a total lack of visible JVD is actually pathological and indicative of low volume; in this position the jugular veins are usually well-filled. (Think: flat veins in a flat patient is bad.) JVD when the head is elevated is more to our interest.

Some examples of visible JVD follow, plus some examination tips. It is recommended that you start checking this on your healthy patients now, so you’ll know what it looks like before you try to make a diagnostic call using its presence. And until you do, stop documenting “no JVD” on your assessments!

A different, much larger view of the same (click to enlarge)

Click through for a good discussion of JVD assessment

A nicely thick and squiggly external jugular

Here’s a student making her external jugular “pop” by heavily bearing down, aka the Valsalva maneuver. This markedly increases thoracic pressure, increasing venous backup; it’s an exaggeration of the effect seen during normal exhalation.

Another example of someone inducing JVD by a Valsalva

http://www.youtube.com/watch?v=FlhQGqdEfg8

Here’s a great video demonstrating the appearance of JVD, how to measure it, and testing the abdominojugular reflex (formerly known as the hepatojugular), which involves pressing down on the abdomen to raise thoracic pressure.

A brief clip of jugular venous pulsation, visible mainly toward the suprasternal notch.

http://www.youtube.com/watch?v=sOpn6_r7Wo4

Live from Prospect St: The Reluctant Tumble (conclusion)

Previously part 1 and part 2

Being reluctant to force Joe into an undesired ambulance ride, the crew contacted their supervisor. He arrived, evaluated the patient, agreed with their conclusions, and called Dr. Scrubs to discuss the matter. He was unable to dissuade the doctor from his decision.

The crew and supervisor approached Joe together and informed him of the circumstances; although all parties agreed that he should rightly be able to refuse transport, they felt they had been overruled by a higher authority, and if he would not come voluntarily they would be forced to compel him. Under this duress, Joe finally agreed to be transported, loudly and vocally protesting.

He was taken to his preferred hospital and care was handed off to staff with a full description of the situation. Less than 30 minutes later, another crew was sent back to the hospital to return Joe home; the attending ED physician had deemed his involuntary hold to be invalid and inappropriate, and refused to hold him against his will. No further evaluation was performed.

The encounter was documented extensively and quality improvement measures involving EMS and the base physician are expected.

Discussion

This case was not medically complicated, but it involved some difficult issues of consent and risk. Let’s look at the medicine and then at the wrinkles.

Medical Considerations

We were dispatched for a chief complaint of a fall — a very common mechanism of injury. When evaluating the fall, what should our main concerns be?

First, we should examine the mechanism itself. How far was the fall? In this case, as it often is, the fall was from a standing height, and from a standstill (i.e. not propelled while running, stumbling while breakdancing, etc.). This is often seen as the dividing line for significant versus non-significant falls; in many areas, falls from standing height or greater are considered an indication for spinal immobilization. (Other areas say greater than standing height; 3x standing height or more; or other numbers.) The elderly in particular are considered at higher risk for spinal injury, due to weakened bones and tighter ligamentous connections between vertebrae.

Typically, a blow to the head with loss of consciousness is also considered high risk for spinal injury. This is under the assumption that a blow with enough force to cause LOC may also have enough force to damage the spine. These considerations are all valid, but should only be seen as some of the many factors involved in stratifying risk; they must be considered alongside other elements like the physical assessment. In some systems, you may be forced to immobilize based on mechanism without other considerations. In others, you may be allowed to rule out immobilization based on certain findings, most of which Joe has; for instance, he denies neck or back pain or tenderness, denies peripheral parasthesias (numbness or tingling) or weakness, ambulated well, turns his head, and has no confounding factors like a distracting injury or altered mental status. In any case, the post-fall presentation was so benign that risk seemed low, and given the patient’s overall reluctance it is highly unlikely that he would have consented to a collar and board.

The use of warfarin (trade name Coumadin), on the other hand, does significantly increase the risk of intracranial hemorrhage (ICH), especially after blunt trauma to the head. Although again, Joe’s assessment was very reassuring — normal vitals, no complaints, and a baseline neurological status — it is very possible for ICH to have a delayed onset of presentation. The best example of this is the subdural hematoma, where cases of moderate severity sometimes take hours or days to develop, due to the venous rather than arterial source of bleeding. This delay is particularly common in the elderly, where (possibly due to shrinking of the gray matter, which leaves additional room for blood to collect before pressure begins compressing the brain) a classic scenario is the fall with a blow to the head, no complaints for hours afterward, and then sudden deterioration. Some sources state that 60% of geriatric fall patients who experience LOC from a blow to the head will eventually die as a result. Since in this case, we were delayed on scene for quite some time, there would be value in ongoing and repeated assessments of symptoms, neurological status, and vital signs while we waited around.

The patient’s pupils were unusual in appearance, which can be an indicator of brain herniation; however, this syndrome typically presents with one very large and round pupil. An irregularly shaped pupil as we saw here is more indicative of a structural defect, the most common of which is probably cataract surgery, which can leave the pupil off-round.

An incomplete medical history is common in scene calls involving the elderly. However, many do carry med lists, and in most cases you can reconstruct the majority of the patient’s diagnoses based on their medications. In this case, we found digoxin (or digitalis), which is almost always used to control atrial fibrillation; this is consistent with the patient’s irregular pulse, and with the warfarin, which helps prevent A-fib induced clots. Metformin (Glucophage) is an antidiabetic that helps control glucose levels. Citalopram (Celexa) is a common antidepressant of the SSRI type. Advair (fluticasone and salmeterol) is a preventative asthma/COPD inhaler combining a steroid with a long-acting beta agonist; it is used regularly to minimize flare-ups and is not a rescue inhaler. Omeprazole (Prilosec) is used for gastroesophageal reflux disease (GERD), aka heartburn. Ibuprofen is a non-steroidal anti-inflammatory (NSAID) used for pain relief and reduction of inflammation.

As VinceD noted in the comments, one essential question in any fall — and indeed in almost any traumatic event — is what caused it. Here we have a somewhat vague account which suggests a mechanical fall, i.e. tripping or loss of balance; this is not necessarily benign, as a history of repeated mechanical falls suggests deteriorating coordination or strength, but it is usually not indicative of an acute medical problem. However, many elderly patients (and some of the younger ones, too) will attribute any fall to tripping, so this claim should be taken with a grain of salt. It helps to have a witness to the event, as we do here, although witnesses are not always reliable either. In any case, what we want to know is: what happened just before the fall? Was the patient simply walking and tripped on a rug? Did he have seizure-like activity? Was he standing normally when he suddenly lost muscle tone and collapsed? Did he complain of feeling faint or dizzy? Was he exerting himself or straining on the toilet? Things happen for a reason.

Ethical and Legal Considerations

The bigger question is whether it’s okay for Joe to refuse transportation.

This is an odd question, because ordinarily we assume that people are free to go where they want, and calling 911 (or having it called for them) does not surrender this right. However, there is an attitude among those with a duty to act, such as healthcare providers and public safety officers, that individuals who are not cognitively able to understand their situation and make decisions in their best interest need to be protected from their own impaired judgment. This is equivalent to taking your friend’s keys so he won’t drive drunk, under the assumption that he wouldn’t want to drive drunk were he making sensible decisions. The legal term is implied consent, the same principle by which we transport children, drunks, and unconscious people.

How do we know if somebody is unable to make their own decisions? There is not an obvious line. For many providers, their rule of thumb is the old “A&Ox4”: if someone knows who they are, where they are, when it is, and what’s going on, then they are alert and oriented and capable of making decisions. Of course, this is only one piece of the mental puzzle. Social workers, psychiatrists, and other specialists have a full battery of tests that can help further reveal cognitive capacity. Can you perform these in the field? It’s probably more than you’re likely to do, although you might perform something simple like the MMSE. But some basic questions that highlight the patient’s judgment can help supplement your routine assessment — questions like, “Suppose you were at the mall when you started to smell smoke and heard the fire alarm. What would you do?” where any rational response is acceptable.

It’s important for the patient to be able to demonstrate that they understand what’s going on. Even someone with ordinary mental competence — unless they’re a fellow knowledgable healthcare professional — needs to be informed (to the best ability of the provider) of the possible risks and consequences of refusing care. In this case, it would involve giving them some description of the above possibilities (spinal fracture, head bleed, etc.), and ideally having the patient then relate them back to you, demonstrating good comprehension of those facts. The base physician’s view that Joe hadn’t fully demonstrated this understanding was a key part of his decision that he needed to be transported against his will.

Other important points are to ensure that the patient knows that refusal doesn’t preclude future care (“if you change your mind, you can always call back”); and that the ability of the providers to evaluate the patient on scene is at best limited. Any implication that you know what’s really happening to the patient or can definitively rule in or rule out any medical problem is unwise and legally risky. In fact, even suggesting possibilities or probabilities can be problematic if you’re wrong; on the other hand, failing to do so can leave them uninformed, so this can be a Catch 22. Your best bet is to outline some basic possibilities, carefully inform them of the limits of your training and resources, and be smart enough that you generally know what you’re talking about in the first place.

One complication in this case is the presence of someone who claims to be Joe’s health care proxy. A proxy (closely linked to the idea of a durable power of attorney) is a person whom, while of sound mind, you designate to make decisions for you if at a later time you are not of sound mind. Crucially, if you are still capable of decision-making, a proxy does not have the ability to override you; their role is to act on your behalf when you cannot. In other words, the decision of Joe’s proxy is only relevant if we do find (or in some areas, if an authority such as a judge has decided) that he’s incompetent to refuse or consent to treatment; thus, her presence does not necessarily alter the basic dilemma.

In this case, the physician’s attitude was that the problem was primarily medical: does the patient need emergency department evaluation to rule out dangerous processes? Medically, he does. However, the first question actually needs to be: Is the patient capable of evaluating risk and making decisions in his own best interest? If he is, then he is technically “allowed” to decide whatever he wants. Even a clearly dying man can refuse medical care based on religious views, personal preference, or any reason whatsoever (although barring a proxy or advanced directive, once he’s unconscious he can usually be treated under implied consent). This is different from the person who actively tries to take his own life; for philosophical reasons we view this as different from passively allowing oneself to die for lack of medical treatment. We prevent people from committing suicide but allow them to refuse medical care.

Realistically, although this fundamental right does not change, it’s fair to consider the surrounding medical circumstances to help decide how pressing and high-risk the matter is. In this case the doctor clearly felt that the risk was so high that it required going to extraordinary lengths, including overruling the patient’s own decisions and potentially even harming him, to ensure that a dangerous situation wasn’t “missed” — in short, that the ends justified the means. Dr. House is famous for this approach.

Legally, in most areas EMS providers are seen as operating under the bailiwick and legal authority of their medical director, and online medical control is an extension of this authority. In other words, within reason we are bound by the orders of medical control. The details of this relationship vary, and are not always fully explored. For an example, consider this true story from 1997 in New Jersey:

A North Bergen dual-medic crew is dispatched to a pregnant, full term female in cardiac arrest. Downtime is unknown, and they work the code for a number of minutes without response. Determining that the mother is likely unsalvageable, and concerned for the health of the fetus, they contact medical control. After a “joint decision” the base physician verbally talks them through performing an emergency C-section on scene. They deliver and successfully resuscitate the fetus, and both patients are transported. The mother is declared dead soon afterwards, but the infant lives for a number of days before dying in the hospital. In the aftermath, the paramedics are cited for violating their scope of practice, and their licenses to practice are revoked in the state of New Jersey. The physician is forced to undergo remediation training to maintain his medical control privileges.

Is the moral that acting in the patient’s best interest is not always a defense against liability? Maybe. Is the moral that medical control cannot authorize you to perform otherwise illegal acts? Maybe. Is the moral that we should protect ourselves before the patient? I don’t know about that, but it’s something to think about. In this case, the course for Joe that seems most ethical to me — allowing the patient to make his own decisions — also lets us avoid potential liability for battering and kidnapping. However, it does force us to refuse a direct order from medical control. Invoking our supervisor gives us a bigger boat either way, and would be a big help to protect us from trouble coming from our employer, one of the most likely sources. It’s also true that, while we may have believed that Joe was competent, he is at least somewhat diminished, so we’re less than completely confident. Nobody wants to put themselves on the line by taking a stand, only to be proven wrong.

Fortunately in this case we were able to avoid getting violent at all, but it was a near thing. If it did prove necessary, it should have been done with ample manpower and many hands; in some areas chemical sedation by paramedics may also be authorized. And I would certainly not recommend acting without the doctor’s signature on a legal document.

With everything viewed in retrospect, the situation would have been much more easily resolved had the doctor not been involved in the process. At the same time, however, if a simple refusal had been accepted, and CQI later went over the call — especially if Joe experienced a bad outcome — the crew would have been in a difficult place.

No matter what, such a situation is highly unusual, flush with liability, and should be thoroughly documented in all respects.

Live from Prospect St: The Reluctant Tumble (part 2)

You kneel beside Joe and ask, “So, would you like to go to the hospital?”

“No!” he vociferously replies — a theme that will be repeated often over the next few minutes.

You explain the risks — that given his anticoagulation (Coumadin), and given that he struck his head and seemingly lost consciousness, there is a non-trivial possibility of bleeding into or around his brain. That although he feels well now, it’s not impossible for such a problem to develop insidiously and not manifest with symptoms until it’s too late. That you can take him to the hospital of his choice, in total comfort, he can receive some quick tests, and if nothing is wrong he’ll be back home before he knows it.

Joe wants to hear none of this. He just came out of the hospital, enjoyed it not at all, and that was just the latest episode in a long series of hospitalizations. “They ruined my hip” on one occasion, he opines, and he’s already been fooled before by “home before he knows it.” No sir; he’s not going anywhere.

You try, your partner tries, the neighbors try, the proxy tries. No way, no how.

Well, okay. But this is not the sort of incident to just brush aside, and you’re well aware of the risk inherent to patients refusing transport, particularly in a risky circumstances like this. So you pick up your phone and hit your hotkey for medical control.

“Needletown Hospital; this is Dr. Scrubs. How can I help you?”

“Hi doc, this is Maverick from Poketown BLS 48. We’re on scene with a high risk refusal.”

You fill him in with the story. He asks a couple questions, then requests to speak with Joe, and finally talks to the proxy for a few minutes. When the phone gets back to you, Dr. Scrubs informs you that he really thinks Joe needs to go.

Well, okay. You dive back in, bolstered with a physician’s opinion, and attempt to get Joe on board the hospital train. He’s not having it. The whole entourage keeps hammering away at him, but he’s simply not budging.

You call back Dr. Scrubs, bringing him up to speed. “We’re making no headway here. He just doesn’t want to go.”

He asks to speak to Joe, and the sounds of his best MD magic come wafting over the speaker, but Joe just has less and less polite things to say, until finally he comes out with, “You’ll have to handcuff me before I’m going anywhere! And just go ahead and try it!” He hangs up on the doctor.

You call back. “I gotta tell you, doc, I don’t see us convincing this guy. If you tell me that we must take him, then I’ll take him, but I think we’d have to do violence to him and start a battle royale here. Is that what you want?”

Dr. Scrubs replies, “Well, I think he needs to be seen, and it sounds like his proxy does too. I’d like to hear your opinion.”

You pause, then carefully say, “I do not think that it would be inappropriate to leave him, although obviously it would be preferable if he came in. I don’t know that I’d make the same decision, but I might, and I don’t see the situation as so high-risk as to justify anything really extreme.”

“Head injury, on Coumadin, loss of consciousness, you don’t think he needs to be seen?”

“We obviously can’t clear him here. But he’s stone normal by our assessment from every angle, and he’s not going to be left alone.”

“Well, I don’t think that’s a great idea. And he wasn’t really able to logically explain to me the risks of his decision. Anyway, his proxy agrees, so I’m not sure if I see the problem.”

“Doc, the problem is that although he does have someone here who says she’s his health care proxy, by our assessment he is at this time totally oriented, competent, and exercising sound judgment. So I’m not really comfortable kidnapping him, unless you want to sign a Section [your state’s involuntary mental health process, for those who are a danger to themselves or others].”

“Sure, I’ll do that. I can fax it to your dispatch and to the receiving hospital.”

“So you want us to tackle him?”

“Do what you have to do.”

You hang up the phone and look around. Police have left the scene, but could be easily recalled. Joe sits before you, a 79-year-old in fair condition, but no Evander Holyfield.

What do you do?

What are the legal considerations?

What are the ethical considerations?

Live from Prospect St: The Reluctant Tumble

It’s 9:00PM on a Wednesday, and you’re the tech on A48, a dual-EMT, transporting BLS ambulance. You are the 911 coverage for Poketown, a midsize urban area; ALS is available for intercept as needed. You carry fingerstick glucometry, activated charcoal, glucose, aspirin, and epinephrine.

You are just starting to yawn when a tone hums from the radio, and a voice declaims:

“Ambulance 8, take the response to 91 Eastbrook Rd. That’s priority 1 to 9-1 Eastbrook Road in Poketown, apartment 710, for the fall.”

You acknowledge, flip your lights on, and head that way. This is an apartment block in the middle of town that you know well.

You arrive to find Poketown Fire and Police already on scene. You load your bags into the stretcher, plus a backboard, and head into the elevators, which are so small you have to fold the cot to fit inside; you wonder how you’re going to fit the patient if you end up boarding them.

You arrive at the apartment to find an elderly man sitting in his wheelchair, accompanied by neighbors and friends, including a young woman who describes herself as his healthcare proxy. He greets you cheerfully, telling you that he’s Joe, 79 years old. He was walking around the apartment with his walker when he brushed against the refrigerator and fell backwards; his proxy tried to catch him but failed, and he hit the ground. He denies falling, then denies hitting his head, saying he landed on his butt, then finally agrees that he hit his butt then his head; his proxy, however, tells you he fell straight back like a board and struck the posterior of his head on the ground. She says his eyes rolled back for a few seconds and he seemed unconscious, after which he quickly came around and moved himself to his chair. She was alarmed and called 911 immediately after; the fall was about 15 minutes ago.

He presents as fluidly conversational, friendly, and fully oriented. He is slightly hard of hearing, speaks in a loud voice, and doesn’t always understand your questions the first time around, but he’s generally “with it” and remembers the full chain of events that led him here. He jokes around with you and the firefighters and offers to marry you to one of his daughters, who has “lots of money.” You tell him you wouldn’t know what to do with it.

Physically, he seems well, with no notable trauma. There is a small lump on his occiput which may or may not be baseline (hey, heads have funny shapes), but he denies any pain or tenderness there. He also denies pain or tenderness of the neck or back, and in fact denies everything, saying he’s just fine. A “lifeline” bracelet is present on his right wrist. His vitals show:

Skin: Slightly cool in the feet, some ecchymosis throughout, otherwise dry and unremarkable.
Pulse: Weak, slightly irregularly irregular radial pulses at 78
BP: 110/70
RR: 16 and unlabored
BGL: 124

Your physical exam notes no other gross trauma. His left pupil is large and abnormal in shape; he states that he has bilateral cataracts. His right pupil is round, slightly small, and somewhat reactive. His eyes track in all directions with no major nystagmus. His lungs are clear bilaterally. He demonstrates equal CSM in all extremities, and no facial droop, arm drift, or speech slurring. A full neuro exam notes no deficits. He denies chest pain, dyspnea, nausea/vomiting, general weakness or dizziness, peripheral weakness or parasthesias (numbness/tingling), or any other complaints. During your exam, he actually gets up and ambulates back and forth across the room with his walker, moving slowly but well with no major gait disturbances.

While you talk, your partner is examining the medication list provided by his proxy. It includes:

Digoxin
Metformin
Citalopam
Advair
Omeprazole
Coumadin
Ibuprofen

His full medical history is otherwise not readily available. He does state that he was just released from the hospital two days ago, after a 5-day stay for diverticulitis. He is allergic to morphine.

What is your general impression of this patient’s priority?
What do you think is going on? What are you worried could be going on?
What is your next step?

Drug Families: Anticoagulants and Antiplatelets

One of the most common drugs we encounter in the field are various forms of anticoagulant and antiplatelet medications. These are relevant to our care both in their therapeutic role as well as in their adverse reactions and potential for harm.

Unfortunately, coagulation is a miserably complex process, and it has to be understood at least generally in order to understand these drugs. In the hope of making this less confusing, rather than throw a wall of text at you, the worker gnomes at EMS Basics have put together an illustrated video. View this, then read on — the drugs won’t make any sense if you don’t start with the physiology.

This form of teaching is a new frontier here, so any input or feedback is welcome. Due to both personal and technical failings, it didn’t turn out exactly how I’d hoped, but hopefully things will continue to improve in the future.

Now that we understand the process, we should talk about the drugs.

There are two major categories here: anticoagulants and antiplatelets. Antiplatelet drugs inhibit the initial step of platelet aggregation and adhesion, where they collect at the wound site in activated form and create a loose plug. Anticoagulants have no effect on this, but instead interfere with the production of fibrin, and therefore prevent a solid clot from growing.

As a general rule, the anticoagulants are rather more clinically significant, as far as their effects on bleeding.

Anticoagulants

First off, to be clear: tPA (tissue plasminogen activator) is not an anticoagulant of any shade. It is a thrombolytic; it attacks and degrades existing clots, dissolving their fibrin bonds. It has no role as a protective agent, and would be far too hazardous in such a role anyway; even its emergency use for acute events like ischemic stroke always requires careful weighing of benefit vs. risk — because the risks are significant.

With that said, there are two main anticoagulants we see frequently in the field.

Warfarin (Coumadin)

Coumadin is an old drug with an interesting backstory; one of its original uses was for rat poison. It’s given orally.

Nowadays, it’s mainly used for chronic anticoagulation of patients at high risk for embolic events. For instance, if you’re in atrial fibrillation at baseline, the blood in your atria isn’t being pumped downstream effectively, and tends to pool. We saw that brisk movement of the blood is one of the main ways we prevent clotting; A-fib is therefore a risk factor for hazardous clots. So when possible, these patients are covered by Coumadin or similar drugs.

The mechanism is interesting. Recall that for the activation of several factors, primarily in the extrinsic and common pathways (including thrombin and Xa), Vitamin K needs to be present. (For some factors, Vitamin K is also needed for the initial production of their inactive forms.) The process looks like this: in order for the factors to be activated, a second background process must also occur, where Vitamin K is changed into a form called Vitamin K epoxide. Once this is done, Vitamin K epoxide can be cycled back into Vitamin K, allowing it to be reused again for the next activation.

Coumadin prevents this second step. It allows the inital activation and conversion, but it blocks Vitamin K epoxide from being recycled to Vitamin K. So over time, as you use up available Vitamin K, it doesn’t get replaced, and you end up with less and less of it available. Less available Vitamin K means less activation of thrombin and its precursors, which means less fibrin, which means less clotting.

Obviously this process takes time. Since Coumadin has no effect on the active factors already present, if we start you on Coumadin today, it won’t have any effect for several days. We need to wait for currently circulating factors to degrade. So for newly anticoagulated patients, a more fast-acting drug is usually used to cover this loading period; heparin is common.

Other than its widespread use, warfarin is also famous for frequent misdosing. It has a narrow therapeutic index, where it’s very easy to give too much or too little, and depending on diet and other drugs, the appropriate dose can change daily. It therefore requires regular monitoring of the patient’s actual anticoagulation, which is done through a test called the prothrombin time (PT). This is a lab test that measures clotting time with an emphasis on the extrinsic and common pathways, and gives a result in seconds. Due to different PT tests available, a standardized result has been devised called the INR (or International Normalized Ratio). This is essentially a ratio of your clotting time over the standard clotting time; a normal result is therefore close to 1.0. Obviously, anticoagulated patients should have a longer clotting time, so 2.0–3.0 is more typical. Much higher than this puts one at high risk of bleeding — into the GI tract, into the lungs, into the nose and mouth, and if trauma occurs, the chance of significant bleeding is magnified. A too-low INR, of course, simply removes the benefits of protective anticoagulation.

In the event of overdoses that need reversal, patients can receive supplemental Vitamin K, as well as plasma (or concentrates) to replace the missing factors directly.

Heparin

Heparin is another old drug. It’s actually a biological substance naturally present in the blood, one of the body’s own anticoagulants, and when extracted for pharmacological use it’s derived from sources like pig intestines. Lovely. You can’t take it orally, so as a rule it’s given by IV.

Compared to warfarin, heparin has a more direct mechanism. Recall that one of the antagonistic factors that works to deactivate thrombin (as well as a few other factors) is antithrombin. Heparin, when taken in therapeutic doses, multiplies the effects of antithrombin by several thousand times. It therefore deactivates far more factors, which are then unable to produce fibrin. Thrombin and factor Xa are two of the factors most affected.

You can already imagine that heparin will probably work much faster than Coumadin. Aside from being given intravenously, it’s not simply stopping the influx of new Vitamin K and waiting for the old factors to degrade; it’s actually going in and deactivating them directly. In fact, heparin takes effect within half an hour or so. However, its half-life is short, so it’s often given as a continuous drip. Obviously, its usage is typically for acute events, such as acute coronary syndromes, or the bridging to Coumadin we mentioned.

However, there is another version of heparin that’s available. To briefly describe the chemical structure of heparin, it’s a polysaccharide, or a repeating chain. When we cook this stuff from pig parts, we end up with a collection of heparin chains in widely varying lengths. The problem is that only chains of a relatively long length will deactivate thrombin. So depending on the actual size of our heparin molecules, unaltered heparin — known as unfractionated heparin — can be fairly unpredictable in its effectiveness as an anticoagulant.

Even very short chains, however, will deactivate factor Xa, and since Xa is a necessary precursor for thrombin, this has the same effect. So if we can produce an artificial product that only includes short heparin chains, then it will mostly affect Xa rather than thrombin, and its effects will be more predictable. This is called low molecular weight heparin, and it has several advantages. It’s easier to manage, it requires less close monitoring, and it has a longer half-life. In fact, it can be given once a day by subcutaneous injection; for instance, post-operative patients can be taught to inject themselves and sent home with the ability to manage their own anticoagulation. Most of these LMWHs end in -arin: enoxaparin (Lovenox), dalteparin (Fragmin), and tinzaparin (Innohep) are common. Fondaparinux (Arixtra) is also used; although technically not a LMWH, it’s very similar in all respects.

Heparin can be monitored by testing the partial thromboplastin time (PTT), which focuses on the intrinsic and common pathways. LWMH can, if necessary, be monitored by testing levels of factor Xa. Overdose leads to bleeding complications, and in a few cases heparin can induce a disorder called heparin-induced thrombocytopenia (HIT), causing a paradoxically elevated chance of clotting. Super-therapeutic levels can be reversed by protamine sulfate, which binds to heparin and prevents its utilization.

Dabigatran (Pradaxa)

A few brief words on this relatively new drug, only made available over the past year or so.

Dabigatran is an anticoagulant from a wholly different class known as direct thrombin inhibitors. Unlike the somewhat roundabout pathways of warfarin and heparin, these drugs inhibit thrombin directly, and may therefore be somewhat more predictable and easily managed.

In the case of dabigatran, it’s being marketed as a replacement for Coumadin. Although supposedly just as effective for chronic anticoagulation, its claim to fame is that it requires no monitoring of INR, which would be a huge burden lifted from patients and caregivers.

Still very new, it remains to be seen how widely it will be adopted. The main concerns about it are: 1. Cost, and 2. Reversal. Unlike warfarin, which in the case of hazardous events (the proverbial bonk-to-the-head with an epidural bleed) can be readily reversed by Vitamin K and fresh frozen plasma, there is no easy or clear method of reversing dabigatran. Some ideas are out there, but clinical experience remains scarce at this point. In any case, this drug isn’t too common yet, but you may start to see it more often.

Antiplatelets

Aspirin

Aspirin is probably in your medicine cabinet somewhere. It has widespread uses from analgesia to antipyretic effects, but also plays a role in platelet adhesion. It’s taken orally, although IV aspirin does exist, and is used both for chronic risk-reduction and acute treatment of coronary syndromes. This stuff is good enough that nearly everybody you know with wrinkles on their face probably takes it every day.

As platelets are activated and degranulate, one of the chemicals they release is thromboxane A2. It has several effects, including vasoconstriction of the immediate area and stimulating further platelet activation. However, it also promotes platelet adhesion by a pretty neat mechanism.

Remember fibrinogen? The inactive precursor of fibrin? Unlike some of the other inactive factors, this one has its own chance to be the star of the show. Fibrinogen can form a bond between activated platelets, attaching at their glycoprotein IIB/IIIA receptors and creating a link. This isn’t anywhere near as strong as a fibrin bond, but it’s enough to make platelets stick together and clump. Thromboxane activates glycoprotein IIB/IIIA receptors and allows the formation of these fibrinogen bridges.

Aspirin inhibits thromboxane release. Fewer fibrinogen bonds are formed, and less platelets adhere. Coagulation itself proceeds unimpeded, but there are fewer platelets in the clot to be married by fibrin.

Due to the widespread effects of aspirin, overdose is a complex subject. Altered mental status, neurological and cardiovascular signs, sensory disturbances (blurred vision or ringing of the ears), and GI problems are all possible. However, there are typically no obvious bleeding abnormalities. Treatment of acute toxicity can include attempts to limit the dosage (such as gastric lavage and activated charcoal), bicarb, supportive care, and if necessary hemodialysis.

Glycoprotein IIB/IIIA inhibitors

This mouthful of a name is another class of drugs from the antiplatelet family. They’re typically not used chronically like aspirin; one reason is because they’re given intravenously, with oral forms rarely seen. (Another reason is because they’re simply stronger drugs). We see these most often used during and after known coronary “events,” such as a STEMI, NSTEMI, or a coronary catheterization, at which times they can help prevent reocclusions.

Their mechanism is similar to aspirin. As we saw, fibrinogen binding to glycoprotein IIB/IIIA receptors helps bind together platelets and allows them to adhere and aggregate. GBIIB/IIIA inhibitors block these receptors by competitive binding, and hence prevent the fibrinogen bonds.

We rarely see these in the field, but common ones include: abciximab (ReoPro), eptifibatide (Integrilin), and tirofiban (Aggrastat). Adverse effects mainly involve bleeding.

Thienopyridines

Although there are a few drugs in this class, by far the most common is clopidogrel (Plavix). Think of these as an alternative, somewhat more powerful aspirin; they work similarly, have similar effects, and are used for similar purposes. Like aspirin, some people use it chronically and it can be given in acute events as well. It can “stack” with aspirin for a synergistic effect, or be used in its place for those who cannot tolerate aspirin.

Once again, the mechanism will sound familiar. One of the pathways that activates glycoprotein IIB/IIIA receptors requires the binding of adenosine diphosphate, or ADP. (ADP is more famous as the product of ATP once energy is released, but it has its fingers in a lot of cellular pies.) The thienopyridines block ADP binding and hence discourage platelet aggregation. Prasugrel (Effient) is another drug in this class.

Adverse effects generally involve bleeding diatheses.

More Drug Families: Stimulants and Depressants; Steroids and Antibiotics; ACE Inhibitors and ARBs

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