Editor’s note: this post was eventually expanded into a cover feature in the May 2012 edition of EMS World.
There’s a concept from psychology that’s recently made the jump to the world of popular science (that misty realm ruled over by a benevolent Malcolm Gladwell; Bill Nye is his jester) known as decision fatigue.
The idea is that human beings have a limited reserve of willpower. Willpower isn’t a physical substance, something stored in a sac in your abdomen, but nevertheless it’s a real quantity. Every time you’re forced to make a decision, especially important or consequential decisions, it drains a little of this resource. Certain restorative acts, like sleep or eating, can help restore it. But if you start running low, then you start losing the ability to make weighty or difficult choices — you tend to pick the easy option, the default answer, the path of least resistance. Rather than the big picture, the long term, you start seeing only the immediate payoff. That little mental push that lets you do the right thing… well, if you spend all day pushing, by 9:00 PM you just might be out of push.
This phenomenon may ring intuitively true, but understand that it’s not horoscopes or tarot cards — this is a real behavior exhibited by all or most people. This is something you do right now, whether it’s obvious or not.
And this is very pertinent to those of us in EMS. Due to the nature of our work, we carry an unusually large burden of decisions. For the level of training and experience our job requires, we are granted a great deal of independent responsibility; in other industries, we would be working with a supervisor over our shoulder, a hands-on boss ensuring that we toe the line. Not so on the ambulance; we perform our duties on the road, alongside one partner, and typically have no direct oversight for the vast majority of our day. If you mess up badly enough, you’ll hear about it later; but to quote the luminary Peter Gibbons, “that will only make someone work just hard enough not to get fired.” We all know a few EMTs and paramedics who have learned all the hot spots, the danger zones, know exactly what they need to do (and what to avoid) in order to stay under the radar — and as long as they dance those steps, they can otherwise do, or skip doing, whatever the heck they want.
The point is, in this job you can do everything right. . . but only if you decide to.
Many of our decisions are small. When it comes down to it, even Old Man Lazybones, the 400-year-old medic who only wakes up to punch out and sometimes eat animal crackers, will generally mobilize for the cardiac arrest and the multiple stabbing. That stuff comes packaged with motivation. But what about all the little things in between? Do you change the stretcher linen between calls, or leave it? Do you sanitize that blood pressure cuff after using it on your “recent VRE” patient? Are you professional, caring, and thorough in your patient interviews, or are you starting to lapse into taxi driver mode? Do you document thoroughly, or cut a few corners? Is everything on the truck restocked for the next crew, or are you out the door? And so on, and so forth. There’s doing your very best, there’s just barely “not getting fired,” and there are many points in between, but no doubt, each time you’ll have to decide where you fall.
It’s tempting to say that what matters is simply the kind of person you are. The “good” EMT, the true professional, that guy will do the right thing. He’ll make the right choices. And the slacker, the hack, he’ll blow it off. And maybe that’s often true.
But the lesson of decision fatigue is that none of us is a saint, or an infallible machine. Every time we make one of those little decisions, every time we exert ourselves to do the right thing, we use up a little bit of our motivation. And after 8 hours, 12, 24 hours, five calls, ten calls, you’re going to start scraping the bottom of that well. The good medic will last longer, the hack won’t make it past lunchtime, but eventually, everyone starts cutting corners. Be honest with yourself, and you’ll see that it’s true. You can care, and you do care, but at some point, you’ll stop caring quite so much. In the long-term, we call it burnout, but in the short term we just call it “time to go home.”
One of the valuable observations from the research on decision fatigue is how the most successful subjects tended to cope with it. By and large, those with the best self-control didn’t survive by being the most stoic, just standing there and weathering a stream of decisions that would shake the best of us. Instead, what they did was set up their lives to minimize the drains on their self-control. They recognized that if they have to spend all day consciously choosing to do the right thing, eventually they’re going to start slacking. So whenever possible, they arrange their circumstances so that no decision needs to be made. When they grocery shop, they don’t just “buy what looks good,” because that’s a constant barrage of “cookies or carrots?” They go in with a list, and they buy what’s on the list, and that leaves no decisions to be made. And then, on the way home when they have to decide whether to yield for the slow-walking granny in the crosswalk, they aren’t already worn out from the battle of the cookies.
Good habits. Good habits will save us.
You can’t go through your shift constantly deciding to do the right thing. But you can create good habits, wherein you do the right thing automatically. This may sound like you’re creating work for yourself, but in fact it’s the opposite. “Work” is choosing to do it. Habits just happens. Waking up, brushing your teeth, driving to work, you don’t complain about having to do these, you just do ’em; they’re things you do, not things you decide to do. If every time you drop off a patient, you change the linen, then this stops being an “issue”; it’s just part of the call, part of your routine.
Setting up habits takes work, but maintaining them takes none, and you’ll quickly find that the type of EMT you are is defined by your habits as much as your decisions. Although I’m a huge proponent of good judgment, critical thinking, and wide leeway for field providers to make good decisions, the truth is that much of our work is routine. And the more of your routine you can manage by habit, the more willpower you free up for the tougher stuff. This doesn’t tie you down. It liberates you to think bigger, and aim higher.
I was never explicitly taught to write documentation in school. It fell into the “They’ll train you how they want it when you’re hired” category, and all we got was a rough idea that there were a few common formats for writing your narratives.
I’ve experimented with a few different models, including the typical SOAP, CHART, and chronological formats. I don’t want to rehash the basics of how these work, because you’ve probably either learned about them or you will. However, on a regular basis I get coworkers peering over my shoulder and commenting on my own somewhat unusual style, so I thought I’d share it for anyone looking for something new.
The biggest change in my own narratives came when I moved to a service that wrote their documentation on computers. I have poor handwriting, write slowly, and don’t enjoy it; however, I’m a fast and comfortable typist, so once we switched from pencil to keyboard my narratives improved substantially. One of the early changes I made was a conscious effort to remove 99% of the abbreviations and shorthand; when typing, it’s usually just as fast to write it out fully, and it makes everything much more readable. (If you ever think to yourself that “everyone knows what YEOIOCRIPIDRN means,” attend M&M rounds sometime and listen to a room full of fellow EMS professionals try to puzzle it out.)
The goal with my narratives is to produce an easily readable, standalone document that tells the story of the call in a similar order to how I experienced it. Because our electronic PCR software includes separate sections to record details of the physical exam, vital signs, and so forth, I’m able to omit many of the nuts and bolts. What I do mention explicitly is all unusual findings, pertinent negatives, and whatever mundane details are necessary to knit the story together. One of the risks with the free-form chronological narrative is forgetting to include this or that assessment finding, but fortunately the ePCR prompts me for these things in other screens. Typically for EMS, documentation is one-half a record of patient care and one-half covering our butts; so although I try to minimize it, I also include some amount of standard butt-covering. This should be customized to what issues your own employer happens to care about. (I had one that insisted every patient be covered with two wool blankets in the winter; so, guess what ended up in the paperwork.)
I modeled my template on the discharge notes you find in hospital charts. I always found these to be pleasantly readable and professional; particularly if you start with the ED and admission note, read the hospital course, and finally the discharge summary, you have a great top-to-bottom view of what’s going on with the patient. I write chronologically, because it keeps the story understandable and because it allows me to show the order that things occurred, which is a central part of many calls; for example, we did X treatment, but then the patient began complaining of Y, so we changed things up to Z treatment — very different from if we’d known about Y from the beginning. However, I don’t adhere zealously to the timeline if it’s not especially relevant, so I’ll often group together assessment or treatment items for efficiency; as a result it’s often not too different from a loose SOAP or CHART format.
I’ll give three examples of hypothetical calls here: one routine transfer, one typical medical emergency, and one critical trauma call. This will seem wordy, but for many unremarkable calls the majority of the narrative can be written prior to arrival, simply leaving blanks for the bits you don’t know, then filling them in and fixing anything unexpected afterwards. (It’s helpful to understand how the actual PCR will print out once it’s completed and [in our case] faxed; this lets you know how it reads, what inserts where, and so on.)
Dispatched non-emergent to Waldorf Memorial Hospital (6 West) for discharge to Mumford Rehab.
Arrived on floor and met by staff, who provide paperwork/signature/report. Patient is Mr. Jeeves, a 73 yo male with hx of COPD and CHF, who presented with chest pain and dyspnea. He was found negative on cardiac enzymes with nonspecific ECG changes, admitted for further monitoring, and eventually underwent cardiac catheterization with no acute occlusions found. He is now stable and is being discharged to short-term rehab for gait training.
He is found in bed, alert and semi-Fowler’s, fully oriented with some general confusion, and denying acute complaints. There is some peripheral pallor, and non-pitting edema of the lower extremities. Vitals unremarkable, as noted above [note: in our ePCR, the vitals screen prints out above the narrative]. A locked IV is present in his left forearm.
He is transferred to our stretcher, secured with straps x5 and rails x2, and loaded onto A56. Transport routinely with monitoring en route. No changes in status during transport.
Arrived without incident, offloaded, and brought Mr. Jeeves to his room. He is transferred into bed and left in a low position, rails up, with his call button and belongings. His care and paperwork are transferred to staff.
Dispatched emergent to apartment in Malden for abdominal pain.
Arrived on scene to find Malden FD and PD with an adult female seated, alert. She is Ms. Bergerac, a 66 yo female with hx of NIDDM, who awoke 2 hours prior with general nausea, weakness, and abdominal pain. She describes the pain as 5/10, dull and diffuse, with a gradual onset over the past several days; she states the nausea has been ongoing over the same period, with the weakness new since this morning. She states she has been taking her normal meds, but has not eaten since yesterday due to the nausea. She denies vomiting, chest pain, dyspnea, headache, or parasthesias, and states she has felt normal with no unusual events up until several days ago. She denies any falls or other trauma.
She presents as fully oriented but slightly obtunded and slow to respond, and somewhat ill in appearance. Her pupils are midsize and PERL, and her lungs are clear and equal bilaterally. Abdomen is supple and non-tender with no visible discoloration, distention or mass. She is negative for arm drift, facial droop, or speech slurring, and demonstrates equal and unremarkable CSM x4. She is tachypneic, with an irregularly irregular radial pulse; her BGL is 46.
She is given 15g of oral glucose, which she tolerates well, and is transferred to our stairchair. She is brought outside, then transferred to our stretcher, where she is secured with straps x5 and rails x2. She is loaded onto A80 and transported non-emergent to House of God Medical Center with continuing assessment en route.
Repeat vitals note a BGL of 60 and minor increase in pulse. No other changes during transport.
Arrived without incident, offloaded, and brought Ms. Bergerac into the ED. She is transferred to a bed and left with rails up. Care transferred to RN with report.
Dispatched emergent to Denmark St. and Mulvaney Rd. in Waltham for an MVA.
Arrived with Waltham FD to find two vehicles in the center of the road. A small sedan has a heavily damaged back end with 2ft of compression; a midsize SUV is behind it with a broken windshield and crushed front left wheelwell. An adult male is found ambulatory, who states he was the driver of the sedan, with no apparent injury and denying any complaints. He states that he needs no care but wants his son evaluated, a teenaged male still in the front passenger seat, who also appears well and denies complaints. The father states they were struck from behind at unknown speed while stopped at a light. Both occupants endorse restraints, and there is no gross intrusion or airbag deployment. They are left in care of FD and a second unit is requested for further care.
An adult male is found in the driver’s seat of the SUV, slumped to the right against his seatbelt. He groans to painful stimulus but does not rouse. His skin is pale and cool, respirations are slow and irregular at 8/min, and radial pulse is thready and regular at 124. Breath sounds are grossly clear and equal. Oxygen is provided at 15LPM by NRB. An open abrasion is present on his left forehead, with blood found on the left upright support. There is no other obvious external trauma. A frontal airbag is deployed. There is starring of the windshield, seemingly from the airbag, and no other interior damage. ALS is requested.
The patient is manually stabilized and a C-collar is applied; he is rapidly extricated, exposed, and fully immobilized to a long spine board. He is placed on our stretcher and secured with straps x5 and rails x2, then loaded onto A104. (A11 arrives and assumes care of the other patients; see their runsheet for further.) Transport emergently to Intergalactic Trauma Center with continuing assessment en route.
Bleeding from the head wound is minor. There is diagonal bruising of the chest consistent with seatbelt trauma, and no other major bleeding or deformity. The trachea is midline and there is no appreciable JVD. Chest rise is equal bilaterally, the ribs are stable, and the abdomen is supple and without distension. Vitals note a BP of 184/100, HR 80, and increasingly shallow respirations at 6/min. A grossly dilated right pupil is also noted to develop en route. An OPA is inserted and well-tolerated. Ventilations are assisted by BVM with mild hyperventilation at a rate of 20/min.
P4 intercepts at this time and assumes dual-medic care.
[Documentation note: See PCR 121512 for full patient demographics, billing, and ALS care en route.]
Let’s just get it out of the way. As a Basic EMT, and to a slightly lesser but still very similar extent as a Paramedic, you are typically viewed as unskilled rank-and-file. You are more like the kid flipping burgers at Burger King than a nurse or a doctor. This is a consequence of supply vs. demand, low barriers to entry in this business, and minimal labor and political representation. I don’t think it’s right, but it is the way it is.
(Note: those working for fire departments and other public services may find that this information does not apply. If that describes you, I applaud you for your good fortune. But for the thousands employed with private services, read on.)
This is a difficult and personal subject for me. I’ve been employed with several ambulance providers, and I’ve been fired from more than one. There were various reasons, but in the end, there was one overarching reason, which is that I didn’t understand how to be the kind of EMT that employers wanted. The lessons that follow may not apply everywhere, but based on my experiences with numerous companies in two different geographical areas, they are generally more true than not, and if you’re newly entering this industry in a field position, they’re worth holding close to your heart.
First, understand that, as we noted, you are not a high-value employee. In fact, you are essentially a low-wage service worker, and you are largely interchangeable with anyone who holds the same certification. Moreover, the job market is currently Bad, and even when it was better, there were people out there who would do this job for free; in other words, even though demand for your skills is still reasonable, supply is very high. Although your service needs a certain number of EMTs and/or paramedics, and although they may perform some amount of screening or testing to find the best candidates (better employers will do more of this), as a general rule there is a limitless supply of people standing behind you, all holding the same card. And your company is just as willing to pay them instead of you.
Second, your employer is in the business of making money. Just like BK needs someone to flip their burgers, ambulance companies need someone to drive and tech their ambulances, so you are a necessary part of their business model. But you are far from unique or irreplaceable. Since it’s not very difficult to hire an EMT, it’s never very difficult to fire one and hire another. So if you ever become more trouble to keep around than you’re worth, you’re inching towards termination.
Third, and most importantly, the money is in the money. A principled and respectable private service will try to drive their financial success through clinical excellence, but whether they do or not, their financial success remains the bottom line. Your Lifepaks and MDTs may or may not get upgraded, but the marketing and PR is never in question. So if by your actions, inaction, or even by association you’re ever involved with something that jeopardizes your company’s revenue stream, you’re absolutely begging them to reconsider taking their chances on a fresh hire.
So, do you want to keep this job, be it briefly or for a long career? (Whether you should be taking advice from me is a fair question, but at least you’re hearing it from experience at the wrong end of every error.) Job stability in this field depends on three skills, and you don’t need them all. Pick any two and you’ll do okay. You might even sneak by with just one. But when the day comes that you don’t have any to protect you, your days are numbered.
1. Protect the Money
You can kill patients, break equipment, curse like a sailor, and drive rigs off cliffs, but if you can avoid impacting your employer’s bottom line, you’ll probably be fine.
Billing is big. Try your hardest to help generate billable runs, because getting paid for your calls is how money is made, and consistently interfering with this will bring you the wrong sort of attention. Whatever documentation hoops they ask you to jump through, as long as they’re not unethical or detrimental to patient care, just do it.
Furthermore, your company’s continued existence is predicated on maintaining certain contracts that it holds with cities, counties, hospitals, and other facilities. These contracts give your company the right to transport some or all of their patients, and that can mean many calls and many dollars per year. If you look unprofessional to someone important, piss off a staff member, or make a clinical error that comes to the wrong person’s attention, you are making the Powers That Be at that organization wonder if they shouldn’t be handing their patients and dollars to a different ambulance company. And that is numero uno on the list of ways to lose your job. Don’t think that the facts will save you, and don’t think that they’ll be reasonable or go to bat for you, because if being able to say “the people responsible have been terminated” is good for business, then nothing else will matter.
Play the game. If you’re asked to wash the truck with a toothbrush, wear a tie and a monocle, and give all of your patients free backrubs, just do it. Play the game, or someone else will.
2. Be Liked
They never taught you this in school (and school was where you’d have found many of us just before we became EMTs), but if the right people like you, nearly anything is possible. If not…
You don’t have to be universally popular, but you should not be “that guy,” because when push comes to shove, somebody with an office and a salary is going to have to decide whether you should keep working here, and if they never liked you to begin with you’re not going to have any armor.
Here’s the big, big secret. You may think that life should be fair, or at least employment should, and if you do your job and don’t screw up too big, there’s no grounds to fire you. In other jobs, you might be right. But we just saw that you hold no sway in these parts, cowboy. Moreover, in most places you were hired under a contract that included the words “at will,” which means they can get rid of you for no reason at all. (Wholly legal? Maybe, maybe not, but most of us won’t be bringing any lawsuits, because it’s a lot of trouble and being “the dude who sued” is not great for your future employability.) So here’s the way it really works: they can terminate anyone, or they can keep anyone. It all depends on what they want to do.
If you’re well-liked by the people who have a say, then you can screw up, and it will be water under the bridge. It may be documented and recorded, or it may simply be swept aside, but nothing will come of it. On the other hand, if you’re someone they’d rather no longer worked there, then you don’t even need to screw up to find your way to the chopping block. Because the fact is, nobody is perfect; even if you think you’re a company man, in the 40+ hours you punch each week, they can find a violation here, an error there, a complaint, a concern. If you ever start getting called to the deck for driving 26 in a 25 MPH zone or parting your hair left instead of right, update your resume, because this is known as “building a paper trail.” (If you’re lucky, maybe they have no problem with you yet, and they’re just preparing a case for the future. Some places are optimistic like that.)
3. Stay Under the Radar
This is the master key of maintaining your employment. Many people lack one or both of the previous virtues, but still keep their job for 10 years because they’ve got this one down pat.
If you’re hired today, and starting tomorrow nobody ever hears your name again, then your job is safe. Your name has to cross someone’s desk before they can tie you a noose. So if you’re ever going to screw up, just make sure that it’s never in a way that draws attention.
EMS is rife with uniformed men and women who show up, clock in, work their hours, and go home. They may be interesting people or boring ones, smart or dumb, up-and-coming or cheerfully stagnant. They may be loved or hated by their coworkers. They may even give bad care, write bad documentation, and draw ire in every ED they enter. But so long as it’s never the kind of thing to make anybody complain to the supervisors, then they’ll do just fine.
On the flip side, they might be a Super EMT, aces in every category, but if their name and face are constantly attracting the eye of the bosses, then they’re at best one or two steps from seeking new employment. Because being a bother is not a good virtue if you’re not valuable.
Truth be told, if you’re wise, then you’ll probably stay off the radar even for the most harmless reasons. No attention is good attention, not even asking to change a shift or replace a shirt, and while some of that is obviously necessary it should certainly be minimized. It’s a fine, fine art you’ve mastered when you’re hired as a new medic, and five years later nobody upstairs knows you beyond a vague sense that might work there.
There you have it. The big three.
You will notice that nowhere in the above list do I include clinical competence. For a long time, I believed that if you were a good EMT, that was enough to keep you safe — and if you were an exceptional EMT, that would even make up for a few things. This couldn’t be further from the truth. Possibly in a few cases, such as if you assist with training and continuing education, your knowledge and skills can be a feather in your cap. But as a rule, nobody in charge knows or cares about how good you are. You’re just one of the many EMT-Bs or EMT-Ps from the big group of identical licenses on the payroll. So if you think that being the fastest intubator in the West will protect you from violations of the Big Three, then you are sadly mistaken.
Indeed, this is yet another reason (you know, beyond the basic moral ones) to treat your patients and facility staff with respect and compassion. By and large, they don’t know if you’re any good at medicine — the patient in particular — but they know if you were a dickhead, and dickheads are the people they call and complain about. You can nearly kill someone, but if you smile, hand them a warmed blanket, and shake their hand, they’ll go away thinking you were the nicest young man they ever met. For all the great ideas on kindness and empathy in our favorite EMS book, Thom Dick’s People Care, it’s worth noting that its subtitle is not “How to Get into Heaven,” but “Career-friendly Practices for Professional Caregivers.” Career-friendly indeed.
It may sound like I’ve become a terrible cynic, but in truth, I think I’ve just come to understand the basic realities of the field we work in. We may wish the world were different, but we may also wish for a pet unicorn and world peace; things are the way they are, and the truth is that you should be able to maintain a long and successful career, providing the most outstanding care you can offer, if you simply learn how to stay employable.
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.
Chest pain. It’s our favorite thing to ask about and maybe our favorite thing to find. Never more does EMS get its chance to shine than when diagnosing the acute MI, and chest pain is how we start down that path. In many cases, everyone from the vomiting drunk to the elderly broken hip gets asked about their chest.
But next time you throw in, “Any chest pain?”, consider this. Not only do many heart attacks fail to present with chest pain at all, even among those that do, the specific symptoms may not amount to what your patient considers “pain.”
Pain means different things to different people. What I call pain, you might call discomfort, and my girlfriend might call a funny feeling. Tightness, palpitations, burning. Trying to list it all would leave you on scene for 20 minutes with a thesaurus, but if you don’t find the right words, then the answer you get might simply be “no.” And you’ll miss the big one.
The solution is in one magic phrase:
How does your chest feel?
I learned this gem from Captain Kent Scarna of Boston EMS, and it joins the ranks of the most useful assessment tricks out there. Because despite all the ambiguity in the chest, this one pretty much captures it all. If there’s frank pain, the patient will tell you all about it. But if there’s fluttering, itching, a feeling like they just ate a canary, this invokes that too. As a diagnostic screening, it is appropriately vague. There is a time and a place for direct questions, but when it comes to chest pain, starting off open-ended is the way to go.
How does your chest feel? Fine, it feels fine. Okay then. If you’re truly concerned you can follow up to confirm — “No pain or discomfort?” — but there’s no need to break out the Webster’s. It’s sensitive but specific; it casts a wide net, but it still unpacks fully. What else could we want?
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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 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.
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.
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.
