Tag: cardiology

Advanced CPR Techniques for Basic Providers

Handstand CPR

 

So you’re an EMT operating at the BLS level, and you understand that when it comes to cardiac arrest, you’re the man. Sure, you’ll call for the medics if you get there first, but the stuff that’s really important — compressions and defibrillation — well, that’s right in your wheelhouse.

But it may seem a little simple. Simple is beautiful, but maybe you’re wondering what else you can do to really master the art of resuscitation, especially when you’re out there on your own. Take it up a notch, if you will. And a lot of the cool stuff that’s being tried in the big world, such as pit-crew choreography and various supportive devices, are only available if your service makes a large-scale decision to adopt them. What can you do as an individual provider to absolutely ensure your peri-dead patients have the best chance of survival?

Here are some ideas.

 

Don’t Stop Compressions, at All, Ever — Seriously, Just Don’t

Hopefully at this point you don’t need to be convinced that stopping compressions is a bad thing. It truly is. The mountain of evidence is unequivocal: any time spent not-compressing kills people; each interruption in compressions kills people; pausing after compressions before defibrillating kills people; pausing after defibrillating and before resuming compressions also probably kills people; and so forth.

The trouble is that, despite this knowledge, we still stop all the goddamned time. There’s a lot going on during a code, and a lot of things you might want to pause for. But let’s go through a few and see if we really have to stop:

 

Stop for Pad Application?

As soon as you found the patient, you began compressions, right? As long as they weren’t wearing a honking seal-skin anorak, you can do that just fine over a shirt, blouse, or other light garment. (Hint: anoraks and similar loose outerwear can often just be pulled off the arms overhead, like removing a T-shirt.) Bam, in you went.

Now your partner needs to apply AED pads, though. Should you stop what you’re doing? Heavens, no. Let him work around you if he needs. He can unzip, rip, cut around your hands, tug the fabric out from under them as pressure lifts between compressions, and clear as much of the chest as he needs. Then he can simply apply the pads. No interruptions, no problem.

In some cases, a CPR-feedback device will be present, either combined with the pads as a one-piece unit, or as a separate “puck.” Either way this usually needs to go between hands and chest, but you should be able to slip it under there with (at most) a brief hiccup in the rhythm

 

Stop for Rhythm Analysis?

Unfortunately, if you’re using an AED (rather than a manual monitor like the medics are toting), you will need to stop compressing and come off the chest in order for the device to analyze the rhythm. Otherwise, the electrical motion artifact produced will confuse the computer. So as soon as the device tells you to stop compressions for analysis, clear the body — but don’t go far (in fact, I would simply hover), and as soon as it’s finished, get back on there.

You may need to stop for manual rhythm analysis as well, but some monitors have a filter that can allow the medics to “read through” compression artifact.

 

Stop while Charging?

So the AED finished analyzing and advised a shock; now it’s charging. Can you compress during this period? Yes. Both common sense (it won’t shock unless someone pushes the button, so… don’t push the button) and at least one study (albeit for manual, not automated defibrillators) have shown this to be safe. There are some AEDs that will get confused if you compress during this time, so know your gear. [Edit: per our “para-engineer” friend Christopher Watford, the Philips FR2+, FRx, and FR3 AED models, plus the Zoll AEDPlus and AED Pro, may complain and possibly halt if you try to compress while charging or shocking. Lifepak AEDs should be mostly okay. Chris and David Baumrind — two of the conspirators behind EMS 12-Lead — wrote a feature for JEMS discussing the behavior of various AEDs if you attempt these maneuvers. Required reading!]

Once the device has charged and is ready to shock, clear everybody except the compressor, ensure that they’re clear, and coordinate between the compressor and button-pressor. Something like, “I’m going to count to three, and when I say three, I’m going to come off and you’re going to press shock, okay? One — two — [come obviously clear] and shock — aaand back on.” The actual defibrillatory shock takes a fraction of a second, and the device will verbally announce once it’s delivered, so you can get back on the chest almost immediately after pressing “shock.” There is no residual “charge,” it doesn’t “take a while” to deliver, it’s a quick blip, so you’ll only need to clear the chest for a moment — no more.

 

Stop while Shocking?

As a matter of fact, do we need to clear the chest to shock at all, or can we keep our hands down, compressing continuously while the electrons flow?

Instinctively, most of us say “No thanks!” However, a little logic suggests the risk may be low. Electricity follows the path of least resistance, and if pads are properly placed and well-adhered to the chest, this path should always be through the patient’s chest. The alternate path up into your hands is much longer, and will only exist at all if you have a connection to the ground, which (if present at all) will probably run through fabric and other insulators. Since almost all AEDs now are biphasic — these use less current than the old monophasic devices — and since pretty much everybody wears rubber gloves while they compress, risk is probably quite small.

The evidence supports this somewhat. Consider these studies: Lloyd, Neumann, Sullivan (supports multiple-gloving in my view), Yu, and Kerber.

This idea has been gradually gaining traction, and some folks have already started doing it routinely, mostly of their own volition. Salt Lake City Fire has even been experimenting with making it a standard option during all resuscitations. For the most part, the worst adverse effect reported seems to be a tingling sensation, particularly if there’s a tear in your gloves. It’s reasonable to ensure that you’re wearing intact gloves, especially over prolonged efforts (multiple shocks may break down the material), and probably wise to double- (or triple-) glove. If there’s a feedback device between your hands and the chest the risk is even lower (or you could lay something like a rubberized blanket over the chest to totally insulate yourself, as in the Yu study).

Now, everybody has a story about a guy who knows a guy whose ex-partner’s bartender was touching a patient during defibrillation, got blown across the room and set on fire, and now can’t pronounce vowels. For the most part, this seems to be purely legend. The trouble is that there isn’t sufficient evidence yet proving it’s safe to make this an official practice on a top-down level; but that doesn’t mean you can’t make the decision for yourself.

If you have an arrhythmia (especially with an ICD or pacemaker), or another legitimate reason to be concerned about your own heart, it’s probably reasonable to pass. For everybody else, to paraphrase Dr. Youngquist of SLC Fire, this practice is probably safe for providers — if not yet for administrators. So you might not see this in your protocols for a little while, but I’ll bet it doesn’t say not to do it, either. The decision is yours.

(There is a possibility that some AEDs, particularly those with feedback technology, may detect the ongoing compressions and refuse to deliver a shock. Again, see above for more info.)

 

 

Stop for Ventilations?

Until you get some kind of tube into the patient’s airway, you’re going to have a hard time bagging any air in unless you pause compressions first. One option would be to simply skip it and perform continuous compressions, which is very reasonable, especially early in the code, or really whenever in doubt. But if you do pause to ventilate, take as little time as possible — pause, breathe goes in, exhale, second breath, and then immediately back into compressions (no need to wait for the second exhalation).

 

Go Faster — and Probably Harder

The currently recommended rate for chest compressions is “at least 100 per minute.” In other words, that’s not a target, that’s a minimum. Can you go too fast? Probably, but it’s hard, and it’s much easier to go too slow.

There’s an accumulating body of evidence, however, that points toward a more exact rate — right around 120/minute. Up to that number, more people survive if you push faster; above that number, fewer survive. It’s not for-sure yet, but in this business, not much is totally sure.

Since it fits the official “over 100” recommendation anyway, I now use 120 as my target rate, and I think you should too. It does mean that your old go-to songs for musical pacing, such as Stayin’ Alive (or perhaps Another One Bites the Dust) won’t work anymore, since those are matched to 100/minute beats. But 120/minute is simply twice per second, and most people can approximate that pretty well, or you can find a faster song (try this app for suggestions).

With that done, are you pushing hard enough? The recommendations are at least two inches deep in adults, so you should at least be hitting that. (It’s deeper than you think.) But as much as some people are willing to go wild on the rate, few people ever seem to challenge the depth. Unless you are an 800-lb gorilla and the patient a 70-lb granny, you are unlikely to cause meaningful damage, and there is a direct link between depth of compressions and cardiac output. Try to really aim for the mattress, and whatever depth you’re hitting, even if you think it’s pretty good, go a little deeper.

 

The Knuckle Hinge

Does it matter how you hold your hands against the chest? Maybe.

What really matters is that you provide good compressions, but hand position can affect that. What you should do is find a CPR mannequin and experiment until you figure out what works best for you. But while you’re experimenting, here’s something to try.

Most people lay one palm over the back of their other hand, and either interlace their fingers (as the AHA videos usually depict) or don’t (I don’t, since I find it somewhat awkward, but since it forces your arms to externally rotate, it can help encourage providers to lock their elbows). Either way, as you meet the chest, you’ll be making contact with the heel of a palm and one set of knuckles.

“Glue” these knuckles to the chest; they don’t move, so once you’ve found your position, you’re locked-in. But each time you compress, do allow your palm to lift off the chest, “hinging” at the knuckles as they remain in contact. Don’t come up very far — just enough that you could slip a sheet of paper between palm and chest — but get a little daylight in there.

What’s the point? One of the more common errors when otherwise high-quality compressions are performed is a failure to allow the chest to fully recoil. You can go deep, but if you don’t come all the way up at the top, you’re still not producing the largest possible stroke. What’s more, unlike poor depth, this isn’t always obvious by looking at the chest (either to you or to others), so the safest method to ensure full recoil is to actually lift off the chest. If you remove your hands completely, though, you tend to lose your place, and your hands can “wander” until you’re pushing on the patient’s feet or your partner’s face. The knuckle hinge allows the best of both worlds.

 

Assign a Monitor

Isn’t this tiring? Now you’re pumping away crazy deep, twice a second, full recoil, and not stopping for almost anything.

Even if you’re an Olympic decathlete, this will start to wear you out fairly quickly. You’re full of adrenaline, and you’re a rockstar lifesaver, so you won’t say anything, and perhaps you won’t even notice; you’ll keep plugging away. But before long, you won’t be pushing quite as hard or deep, or quite as fast, or maybe you’ll start leaning on the chest instead of recoiling all the way. I promise you will; many studies have shown this; and what’s more, you’ll probably still think you’re doing good work.

No problem. As long as we have adequate manpower (and in most places, there are plenty of people on scene at a code), simply assign one person to monitor the quality of compressions. If it’s you, your sole job is to sit somewhere with your head close to the action, staring at the up-and-down, and ensuring it follows all the criteria we’ve discussed. If it needs to be faster, you tell them to speed up until they’re on pace. If it needs to be deeper, tell them. If they ever pause for any unnecessary reason, yell at them like an Italian grandmother until they start back up. And once it’s clear that they’re fatiguing, you make them swap out, and ensure that the swap happens with minimal delay. The AHA recommends switching every two minutes, but use a smart approach; some compressors will last less, some more, and if you reach a mandatory pause (for rhythm analysis, say), you might as well change even if the current person has some juice left.

Depending on resources, they may be swapping with you, or there may be enough people sitting around that you can have a rotating pool of dedicated compressors. You can maintain the same person as monitor (the easiest method, if you can spare them), or just have each on-deck compressor act as monitor.

Useful tools for the monitor include a watch with chronograph, but even better would be a metronome. That way you can set up an audible pace (120/minute, remember) that any monkey can follow. A few services do carry actual digital metronomes, but if not, most smartphones have metronome apps available. (Find and download it now, not in the patient’s living room.) You can also throw an MP3 from an appropriately-paced song onto your phone, if nobody minds running a code to a soundtrack (probably not ideal when there’s an audience). The monitor person can keep track of other times as well, such as the ventilatory rate once an advanced airway is placed, total duration of the code, times of medication administration, and so forth. A pad of paper or strip of tape down the leg are helpful.

An electronic feedback device is a helpful adjunct to this role, and if resources are limited can replace it, but it’s not quite the same. If it is available, tracking the automatic feedback (and ensuring the compressor obeys) is the monitor’s job.

Whether or not a monitor is assigned, everybody performing compressions (really everybody at the scene) should understand that it’s still their responsibility to ensure quality. This is particularly important when it comes to eliminating interruptions, because even if there’s somebody to yell at the compressor when he stops, if he’s stopping all the time that’s still a lot of pauses. An effort should be made when assigning a compressor (who isn’t you), such as a first responder or bystander, to make them understand that they “own” their compressions, and it’s their responsibility to do ’em right and stop for nothing. The monitor’s job? Just to keep them honest.

 

Ask Why

Cardiac arrest happens for a reason, and even though it’s the most time-sensitive, treat-the-ABCs syndrome that exists, there are still times when you’ll never fix the problem without understanding the cause.

In a perfect world, you’d show up, compress, apply AED, shock, get a pulse, the patient sits up and hugs you, you transport and all’s well. In a realistic world (depending on your area), usually ALS shows up at some point and things take a more technical direction. But if you’re working the arrest for more than a couple minutes, have adequate manpower, but are still BLS-only, then your extra providers shouldn’t be sitting around twiddling their thumbs; they should be gathering information, planning the next step, and preparing for transport.

Ideally, one person is running the code. Either that person or somebody competent he delegates to should communicate with family or bystanders, examine available records, dig through the meds, whatever — try to determine both the history of the present event, and a reasonably-complete past medical history and medication list. Partly, this is for later management; the medics or the ED may need it. But it’s for you, too, because it may suggest your course of care.

Without an ECG, you haven’t got much to tell you what’s happening, except that the patient’s got no pulse. (Auscultating the chest may indicate whether a regular heart rhythm is present which is simply not perfusing — PEA, or if you’re a magician you may be able to “hear” V-tach — but you have to stop compressions to appreciate much.) You’re unlikely to be able to magically predict whether you’re dealing with V-fib versus torsades versus asystole. But you may be able to guess that certain correctable causes are present.

For instance, was the patient complaining of classic MI symptoms (crushing chest pain, nausea and vomiting, dyspnea) for twenty minutes before he finally became unresponsive? And he’s had two heart attacks before, with several stents placed? It’s a fair bet that he’s had another, which caused this arrest, and you may not have much luck getting him back until that artery can be opened back up. You can and should still work him initially on scene, but your mental goal should be delivering him to a PCI-capable hospital, so while you do your thing, stay on that track. If you get a few “no shock advised” messages with no pulse, or perhaps shock once or twice but he remains severely unstable, try to get him packaged as you continue your awesome compressions, notify the hospital of the situation and your suspicions, and get him over there. Try for ALS, who can perform a 12-lead ECG, which will facilitate this process (and your protocol may not permit you to divert to a more-distant PCI hospital otherwise).

Do you have reason to suspect hypovolemia as the cause of arrest? Is there obvious external bleeding… or is there a rigid and distended abdomen, perhaps with a story of abdominal pain or blunt trauma? In that case, you can push or shock all you want; you’re not going to refill an empty pump. Maybe chest trauma with a potential tension pneumothorax or cardiac tamponade? Transport ASAP to a trauma center (and perhaps ALS, since they can decompress a pneumo and give some volume if appropriate).

Is this a hemodialysis patient who missed two sessions, has been lethargic and sick-appearing, poorly-tolerating exercise, and finally fell asleep and didn’t wake up? Suspect hyperkalemia, a true “ALS-curable” condition, so if medics are available, work it until they arrive. If they’re on the dark side of the moon, transport with the best compressions you can manage.

Is the patient a known diabetic, taking insulin, and a story consistent with hypoglycemia? Check that sugar if you can, and if it’s something perverse like 7 mg/dl, get them to either ALS or an ER — both can administer intravenous sugar.

Could it be a hypoxic arrest? All arrests are hypoxic after a few minutes — dead people don’t breathe — which is why it’s usually reasonable to breathe for them (although far from a top priority). But if you walk in to find a post-drowning victim, or a hysterical mother saying her child choked and now has no pulse, you may have a cardiac arrest whose underlying cause is nothing more than hypoxia: their heart didn’t get enough oxygen, so eventually it gave up too. They still need compressions, and may need to be shocked, but most of all they need oxygen, so opening the airway and bagging in high-concentration O2 is a top priority. (Compare this against the post-MI patient above, who doesn’t need any oxygen at all until you have enough hands to provide it without delaying compressions and AED use, and even then doesn’t need much.)

Possible pulmonary embolism? Poisoning? Commotio cordis? The list goes on. The point is, if you have the resources to take a moment, gather some information, step back, and think, you can often do a pretty good job of guessing what brought you here, even without the benefits of the ECG. In some areas, your policies and protocols will dictate pretty clearly what decisions you can make, and it may not matter much. But flip through that rulebook now, because often times people assume it says more than it does (for instance, “closest appropriate facility” is more common than “closest facility”). When in doubt, you can always call medical control and make your case.

(As a general point of safety: continuing CPR while packaging and transporting emergently is difficult at best, and both unsafe and low-quality at worst. This should factor into your decision-making, as should the specific obstacles presented by extrication, and the potential availability of a mechanical compression device, which can make the process substantially easier.)

Just don’t ever try to argue that only ALS is allowed to think.

BLS is all yours, and cardiac arrest remains a fundamentally BLS problem. Own it.

Staying in Place: Compensation and Endpoints

Red queen running

 

Man’s leaning against a wall. He doesn’t move for hours. Just stands there not moving. Finally, someone says, “You been here all day — don’t you have anything to do?”

“I’m doing it,” he answers.

“Doing what?”

“Holding up the wall.”

 

And who’s to say he’s not? Maybe he’s working as hard as he can to make sure that wall doesn’t fall down.

In this situation, the man is a compensating mechanism. He is struggling to prevent changes in the wall; keeping that wall upright is an endpoint he cares to maintain, to sustain, to keep intact.

How do we know that the wall isn’t holding up the man? Because we don’t care about the man. Whether he leans or falls doesn’t matter much to anybody. But it would be a terrible thing if the wall collapsed. So we’ll let the man lean or shift in order to prop up the wall when it starts to totter — we’ll use him, adjust him, to compensate for any wall-changes. That’s why he’s there.

If the wall gets weak enough or tilts too far, though, he won’t be able to keep it up. He’ll try, but he’s not infinitely strong, and then maybe the wall begins to tilt or collapses completely. Since we know that under normal circumstances, he’s doing his best to prevent this, if we walk in and see that the wall is tilting, that is not a good sign. It may mean that despite his best efforts, the man has exhausted his strength and is no longer able to resist further wall-changes; or it may mean that, for some reason, the man isn’t doing his job properly. Either way, any further tilting will be unopposed, and will probably happen rapidly and uncontrollably.

 

Compensators and endpoints

This same dynamic plays out within the human body. As we know, living organisms seek to maintain a certain homeostatic equilibrium. We put our vital metabolic processes in motion and we don’t want them to halt or change, despite any insults or fluctuations imposed upon us by our surrounding environment. So our bodies struggle to keep all of our complex systems at an even keel, using a diverse and powerful array of knobs, dials, and other regulatory tools. Not too hot or too cool, not too acid or too basic, not too fast or too slow. Just right.

The kicker is this, however. Some of our physical parameters are more important than others. In other words, while some parameters have room to adjust, others aren’t negotiable, can’t change much, without derailing our basic ability to function and survive. Things like blood pressure (or at least tissue perfusion, for which blood pressure is a pretty good surrogate measure) are essential to life; your pressure can fluctuate a little, but if it drops too low, you are unquestionably going to suffer organ damage and then die. And yet there are many insults that could potentially lower our blood pressure if we let them: if we bleed a little, or pee a little, or don’t drink enough water, or sweat, or even just stand up instead of sitting down. How do we preserve this vital parameter despite such influences?

By compensating, of course. Our body gladly modulates certain processes in order to preserve other, more important parameters. So in order to maintain blood pressure, perhaps we accelerate our heartrate. In an ideal world, it might be nice if the heart were thumping along at — let’s say — a mellow 80 beats per minute. It’ll use little less energy and less oxygen than if it were beating faster. But it’s really important to keep our blood pressure up, and speeding up the heart can increase the pressure, so we gladly make that trade and induce tachycardia. (Many of these compensatory systems are linked to the sympathetic nervous system, our body’s standard “all hands on deck” response to stress and crisis.)

So imagine we find a patient who’s bleeding and notice that he’s tachycardic, with a normal blood pressure. This suggests a compensated shock; the body is using tachycardia to maintain that normal pressure we see; although his volume is lower than usual, the critical endpoint of adequate blood pressure is still intact.

But what if instead, we found him tachycardic and hypotensive? Well, that’s not good. We see that the body is trying to compensate, but we also see that the important endpoint — blood pressure — is falling nonetheless. The body would never intentionally allow that; BP is too important. So we recognize this as decompensated shock. The hypovolemia has progressed so far, and volume is now so low, that he can’t make up the difference anymore — the compensatory slack has run out — and any further decreases in volume will probably lead to an immediate and unopposed drop in pressure. There’s nothing more the body can do on its own; it’s out of rope.

The skilled clinician — or “homeostatic technician” as Jeff Guy says — uses this predictable progression to understand what’s happening in almost any crisis. Because primary insults are initially covered up by compensatory mechanisms, they may not be immediately apparent, and the earliest and most detectable signs of physical insult are usually nothing more than the footprints of the answering compensation. Thus, when when we encounter those, we know to suspect the underlying problem even if it’s not obvious yet. It’s like seeing brakelights flash from cars on the road ahead; even if you can’t see an obstacle yet, you know people are slowing down for something.

Obvious signs of decompensation usually show up late. Once the primary, underlying problem is revealed by failure of the corrective mechanisms, it’s often progressed so far that it’s too late to address. If you wait to brake until you can see the wreck itself, you might not be able to stop in time.

 

Two signposts for decompensation

There are two great ways to recognize which signs and symptoms connote decompensation.

The first is to understand which physical parameters are endpoints — which functions the body tries to preserve at all costs. These processes are only compromised as a last resort, so if you see them deteriorate, things are in the end-game; the body doesn’t intentionally sacrifice these for the benefit of anything else.

The second clue is more subtle. In this case, you observe a compensatory mechanism (not an endpoint), but find that it’s no longer successfully compensating — it’s failing, and starting to unwind and scale back, rather than doing its job. The changes in the compensatory system are inappropriate, resulting in less of what we need, not more. This happens when our systems are so damaged that they can’t even fix problems and pursue homeostasis anymore; our infrastructure, maintenance, and repair systems are breaking down. Consider this: we saw how tachycardia could be compensatory, but could bradycardia ever be beneficial in shock? Probably not. So if we found a shocked patient with bradycardia (and likely hypotension, the failing endpoint), we should be very alarmed indeed. There’s nothing helpful, compensatory, or beneficial about bradycardia in the setting of shock, so we recognize that the body would never go there on purpose. It’ll only happen when the machinery itself is falling apart.

Consider, for instance, Cushing’s Triad, the collection of signs often encountered after severe traumatic brain injury, when intracranial pressure has increased enough to squeeze the brain out from the skull like toothpaste. The triad includes hypertension, bradycardia, and irregular or slow respirations. What’s interesting is that, while all are a result of increased ICP, one of these is compensatory, while the others are merely the result of damage. Hypertension is the body’s compensatory attempt to force blood into the brain despite the elevated pressure in the skull. But bradycardia and bradypnea simply result from pressure upon the regulatory centers of the brain tasked with maintaining breathing and heart-rate. That’s why hypertension may be seen earlier, while the other two signs won’t usually manifest until the brain is actively herniating. One signals compensation, the other two decompensation.

Of course, there can be other reasons why compensatory mechanisms might fail, or at least exhibit lackluster performance. Some medications or other aspects of a medical history (potentially unrelated to the current complaint) might throw a wrench in the system. For instance, beta blockers (such as metoprolol and other -olol drugs) limit heart-rate as part of their basic mechanism, so patients with beta blockade often have trouble mustering compensatory tachycardia during shock states. That doesn’t mean they’re any less shocked; in fact, it means they’re more susceptible to hypotension, and that you must be especially on the lookout, because you won’t see one of the red flags (a rapid heart-rate) you might usually expect. Elderly patients with many comorbidities are generally not able to muster up effective compensation for anything, so they can deteriorate quickly, and without much fanfare. Ironically, healthy pediatric patients are the opposite: since they’re so “springy” and smoothly functioning, they compensate very well, with few changes in observable endpoints, until suddenly running out of slack and crashing hard because they’re already so far from shore.

Here are a few important compensatory signs, breakdowns of compensatory systems, and vital physical endpoints:

 

Appropriate signs of compensation

  • Tachycardia — increases cardiac output
  • Vasoconstriction (cool, pale skin) — raises blood pressure
  • Diaphoresis (sweatiness) — decreases temperature when necessary, but is often just a side effect of sympathetic stimulation
  • Tachypnea — increases oxygenation, CO2 blowoff, and cardiac preload
  • Fever — part of the immune system’s response to infection
  • Shivering — warms a hypothermic body

Inappropriate changes in compensatory mechanisms

  • Bradycardia — reduces cardiac output, rarely useful in illness; as a chronic finding may be the result of high levels of cardiovascular fitness (in healthy young patients) or medications (in sick old patients); but acutely, it is an ominous finding
  • Bradypnea — reduces oxygenation, CO2 blowoff, and cardiac preload
  • Hypothermia (or normothermia when a fever is expected) — suggests a failure of temperature regulation

Inviolable endpoints

  • Blood pressure — can elevate in stress states, but should not drop below resting levels
  • Mental status — except in the presence of a drug or similar agent directly affecting cognition, maintaining appropriate alertness and mentation are always a top priority for the body
  • Blood glucose — kept at normal levels in almost all situations, except when the regulatory systems fail, as in diabetes mellitus
  • pH — most of the cellular machinery fall apart if significant acidosis or alkalosis occurs
  • Low O2 saturation or cyanosis — although oxygen saturation can dip briefly without harm, and in some patients (particularly those with COPD, or long-time smokers) it may run low at baseline, a significant acute drop — or the clinical equivalent, which is frank cyanosis — is always inappropriate.

Managing STEMI Mimics in the Prehospital Environment: Video Lecture

A while ago we shared a PowerPoint presentation, Managing STEMI Mimics in the Prehospital Environment. This diverges somewhat from our prime directive around here by focusing on an ALS topic (ECG interpretation), but for the medics, it’s a topic that I think is important.

It’s also dense and difficult, in this case amounting to a 190+ slide presentation. In an attempt to unpack things a little, and to further explore our recent forays into multimedia content, we’ve got ahead and created a narrated slideshow walking through this subject.

This is still tough material, but as an overview it should be fairly approachable. The trick, of course, is to follow it up by viewing a large volume of pertinent ECGs to get some practice in applying the concepts. See our Links page for some great sources for practice strips, or visit the old standby, EMS 12-Lead — probably the best source on the internet for ECG education.

It’s broken into three parts, with total time of about 1:45. Treat it like a continuing education lecture, take your time if needed, and feel free to print the slides themselves for review. (Unfortunately, the lecture does assume at least a baseline ALS-level knowledge base, so if you’re just getting started with electrocardiography you may want to start elsewhere.) For any questions, throw ’em out here!

Part 1 (43:26):

Part 2 (34:06):

Part 3 (26:57):

Understanding Shock IX: Assessment and Recognition

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

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

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

 

Early or Insignificant

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

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

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

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

 

Compensated Shock

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

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

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

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

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

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

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

 

Decompensated Shock

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

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

 

Alternative Forms of Shock

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

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

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

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

 

In sum, remember these general points:

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

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

 

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

Understanding Shock III: Pathophysiology

An example of the shock cascade
Another model
Yet another model

 

The common thread that defines the shock process is inflammation.

As we know, inflammation is the body’s response to damage. When things go wrong, when trouble calls, we ring the bell for inflammation to make it right. Often this serves us well, but like any militia, if left unchecked it can be worse than the problem it came to fix.

The many twists and turns of the pathology of shock are still not fully understood, but here are some of the important stepping stones along the way:

Shock occurs, and many of the body’s systems are left without adequate oxygen. Although oxygen supplies our primary method of generating energy — the aerobic metabolism — we do have secondary systems in place that can produce energy without oxygen, the anaerobic cycles. In the setting of shock, these take over.

But they’re not great. They provide far less energy than aerobic metabolism, and they produce by-products that accumulate in the body. Among other things, this includes the accumulation of hydrogen ions, creating a widespread acidosis. Think about running sprints or lifting heavy weights; think about that burning feeling, and the eventual failure of your muscles. Operating in an anearobic mode causes trouble and is shortlived at best.

Sooner or later, this isn’t enough to keep things working, and cells begin to accumulate toxic products and eventually shut down. They’re not quite dead yet; they’re hurting, but they can still recover. Like a business that shuts its doors in the off-season, there simply isn’t enough inflow for them to operate right now.

The trouble is, we need those cells. They make up the tissues that form the heart, the brain, the lungs, the kidneys, the liver, and so forth. When the cells close up shop, the organs begin to fail. When organs fail, they cease to provide their essential functions. Let’s consider just one, the heart.

The heart pumps blood. When it loses its effectiveness, it pumps less blood. This means less circulation of oxygen, which means hypoxia is exacerbated. Look at that — we just magnified the problem. If the shock gets worse, is that going to help the heart pump any better? Dream on. The vicious cycle accelerates further.

As hypoxic damage to the cells progresses, the body responds with widespread inflammation to repair it. The trouble is, there’s no real hope of repairing anything without restoring the oxygen supply — but that never stopped Old Man Inflammation. One of his brute-force tactics is to increase capillary permeability, the “tightness” of tissues; everything becomes more susceptible to leakage. The fluid that runs throughout your body begins to ooze everywhere. Generalized edema occurs. In some cases, this is just gross; look at the bloated extremities of the recently dead for an example. But what happens when there’s edema and inflammation of the vital organs? They fail. Fluid in the lungs impairs respiration. Fluid in the brain causes increased intracranial pressure. Another blind response of the inflammatory system is apoptosis, where hypoxic cells — sensing that they’re done for — trigger self-destruct mechanisms and tear themselves apart. Unfortunately, you need those cells.

And hey, what about that acidosis? Our cells (including the ligand-receptor complexes that trigger our sympathetic processes) are designed to function at a specific pH. Placing them in an acidotic environment impairs their function. Combo attack!

But what about our compensatory systems? When our body sees shock, it does things like vasoconstricting, increasing heart rate and contractility, and attempting to maximize the availability of oxygen. That’s great when it works. But when things progress, it’s not so great. Vasoconstriction can choke off the organs, giving them even less oxygenated blood. Tachycardia increases the heart’s demand for oxygen.

And oh, by the way, none of this is adds much to the body’s ability to combat the original cause of the shock, whether that was traumatic injury, a septic infection, or something else.

Key points:

  1. The processes of shock are multiple and self-reinforcing.
  2. Inflammation plays a major role.
  3. Multi-organ dysfunction and failure also plays a major role.

Next time: so what do we do about it?

Go to Part IV or back to Part II

CPR for Dummies: How to Save a Life

One of the peculiarities of EMS education — and as a byproduct, of EMS practice and culture — is that we spend the majority of our time focusing on the minority of our calls. Think about it: your textbook has pages and pages devoted to ruptured aortic aneurysms, placentas previa, and mid-femur fractures — and when’s the last time you saw one of those? But scarcely a paragraph is given to the routine transfer, the drunk asleep on the sidewalk, or the MVC with minimal injuries. Call it an inverted pyramid: the most important stuff is low-volume, the most common stuff is pretty easy.

Whatever. The point is, at the very apex of this pyramid is the cardiac arrest. In its purest form, cardiac arrest is exactly why EMS exists. It couldn’t be higher stakes — as a disease, it’s absolutely certain to be life-threatening — and it’s terribly time sensitive, but the potential exists for a total cure if everything goes well.

Unfortunately, like many low-probability calls, we don’t get a great deal of experience with these — even less if your shift isn’t dedicated to emergencies. And when we don’t get much experience with something, that’s when training needs to fill in the gaps.

CPR and BLS resuscitation can seem like a confusing topic, especially given the frequent and seemingly arbitrary changes to the guidelines. The truth is, though, that it’s only gotten simpler and simpler — and you don’t need to follow the research (read: be a giant nerd like me) in order to know exactly what to do. Here’s the short, stripped-down, painless rules for how to save a life.

 

Push and Zap

Basically, after around sixty years of research on resuscitation, there are only two things that we know for sure help people survive cardiac arrest: chest compressions and defibrillation.

Literally, just those two things. Oh, there’s other stuff — ventilation, drugs, devices — that seem to help briefly, but so far nothing else has been proven to get someone’s heart beating again and let them walk out of the hospital with a working brain. Now, some of those other things do seem like pretty good ideas, and in many cases we started doing them before we knew if they’d really help or not, so we’re still doing them because people are used to it; it’s part of our training, and it’ll take some extra-compelling evidence to make us actually stop doing that stuff. But still, the story so far: chest compressions and defibrillation definitely help people survive, and that’s it.

What this means is that they should be your number one priority. If your patient is in cardiac arrest, that’s what they need. Other stuff? It may or may not be helpful; if you have the chance, or the personnel, and it doesn’t interfere with chest compressions and defibrillation, then you could go ahead and do it. It might help. But delaying or stopping the big two for that other stuff is like making a thirsty man wait for a drink of water while you comb his hair.

 

Early, Hard, Fast, Uninterrupted, and Full Recoil

Okay, so, chest compressions. Easy enough. Anyone can do ’em, all you need is your hands, just jump in there and push.

However, that’s not quite the whole story: the quality of compressions matters a great deal. We are literally pumping blood here; we are creating mechanical pressure to replace the squeezing of the heart. Just like you can wriggle a bicycle pump ineffectually without making much progress on inflating your tires, so too can you make goofy movements on someone’s chest without providing much perfusion. Even at its best, CPR only provides weak circulation compared to a real heartbeat; if you give poor CPR that’s even worse.

So here are the key components:

  • Early: Compressions should be initiated as soon as possible after arrest. That means, if I go down now, ideally you’ll start pushing on my chest as soon as I hit the ground. Typically that’s not possible, but mere seconds really do matter here; the longer there’s no circulation, the more tissue is endangered (all tissue, but particularly the vulnerable heart and brain), and the less likely that defibrillation will be successful — or if it is, the more likely there will be permanent complications.
  • Hard: Good chest compressions are a violent, aggressive act. We now recommend a depth of at least 2 inches in adults, which if you examine a mannequin (or fellow human) is remarkably deep. (Yes, “at least” means that going deeper is fine; compressions that are “too deep” are rarely seen in real life.) This isn’t a gentle cardiac massage, it’s not the mellow bouncing you usually see in movies, it’s a deep, powerful, oscillating thrust. It should tire you out, which is why we recommend changing personnel frequently; even when you think you’re still doing well after a few minutes, you’re probably not.
  • Fast: The recommended rate is now “at least” 100 compressions per minute. Since nobody knows what this means without a metronome, I highly recommend “musical pacing,” or using the beat of a well-known song to learn the rate. Stayin’ Alive by the Bee Gees is the classic; I like Queen’s Another One Bites the Dust myself. Again, 100 is an “at least” rate, so faster is better than slower. Admittedly, if you go extremely fast the heart won’t have time to fill between squeezes, but most “ludicrous speed!” CPR tends to have poor depth, and self-regulates anyway once you get tired.
  • Uninterrupted: Just like it’s essential to begin compressions as soon as possible, it’s equally essential to stop them for nothing. It’s not just that every moment you spend off the chest is “dead time” in which no blood is circulating; it’s worse than that. Chest compressions need to generate some “momentum” in order to create enough pressure to perfuse the heart; several consecutive compressions are needed before you’re really moving much blood at all. If you keep stopping — and studies show that everyone stops far more than they realize, to fiddle with one thing or another — you’re wasting those gains as soon as you’ve achieved them. Maximizing this “compression fraction” should be a primary goal; once you get on that chest, don’t stop for anything else unless it’s literally more important than circulating blood.
  • Full recoil: Among otherwise skilled rescuers, one of the most common errors is failing to allow for full recoil of the chest. In other words, you press down deeply, but rather than releasing fully, you start the next compression before you’ve come all the way up. This shortens the stroke of the pump just as much as if you were giving shallow compressions, and for several complex reasons (in particular the loss of preload) can reduce circulation in other ways too. We do this one particularly when we start to get tired, and begin to leaaaan forward to rest on the chest.

Defibrillation

It’s really as simple as this: once the heart’s entered fibrillation (or to a lesser extent a pulseless V-tach), the only plausible way to fix it is with electricity. These people are not going to “come to”; they are not going to have a Baywatch moment where they cough out water and wake up, even if you give them great CPR. They have an intractable problem, and the cure for it is an electric shock. Defibrillation is life-saving.

For most of us, this means using an AED, the automated devices you see everywhere from airports to ambulances. The reason they’re everywhere is because their use is time-sensitive, and if you drop dead ten miles from the nearest one, it might as well be ten light-years. No matter where you are, compressions must be performed to buy you time, and a defibrillator must be found to shock you back. If both don’t happen quickly, you will probably stay dead forever.

There are argument about some of the technical aspects of defibrillation, such as pad placement and waveform, but so far none of these details have proven to be very important. What is important is that you shock early, and get ready to shock without interfering with those compressions. Whenever possible, while one person gives compressions, someone else should clear off the chest by cutting or pulling the shirt from under the compressor’s hands, place the pads around them, and start the AED’s cycle. For many models of AED, there will be a period of several seconds while it walks you through voice prompts (telling you to stay calm, call for help, etc; these devices are designed to be usable by laypersons with no training), which should be ignored while you continue your CPR.

Once the AED tells that it’s analyzing the rhythm, you will need to stop compressions; this is the computer’s opportunity to decide whether the patient can be shocked or not, and interfering with this will just delay the process. If it doesn’t advise a shock, get back on the chest; you may have better luck later. If it does advise a shock, get back on the chest anyway! It’ll need to charge first, which may take quite a few seconds, and remember — every second matters. (Just make sure the whole team’s on the same page here, so that nobody pushes “Shock” until you’re clear.)

As soon as the AED announces that it’s ready to shock, everyone should be ready: cleared from the patient and prepared to shock. In a coordinated fashion, the compressor should clear the chest, the shock should be delivered, and he should immediately resume compressions with a pause of only a second or two. Rinse, lather, repeat.

When do you stop this process? When someone much smarter than you says to stop; or when the patient demonstrates clear signs of life (such as movement, breathing, or improved skin signs — or for the medics, a spike in end-tidal CO2). Don’t keep stopping to palpate pulses and otherwise fiddle with the patient. Like a soufflé or a Schroedinger’s cat, you must have faith in the process here, because checking on the process will assuredly cause it to fail.

 

It Ain’t Rocket Science

People, there are other details to this process, which is why they make us take CPR classes and carry the little cards around. And in 2015, there might be some new ideas on how we can do it best. Research continues apace in the countless EMS systems around the world that are experimenting with different technologies, techniques, and methods to improve survival. That’s how we’ve come from 1–2% survival rates to the 50%+ that a few cities now enjoy. It’s slow going, but it’s going.

But the best methods won’t matter if you don’t use them, and a lot of effort has been given to make our current methods truly simple. You literally can’t go wrong if you give great compressions and defibrillate as soon as possible. You can certainly go wrong if you forget that those are the two most important, life-saving measures — but you’d never forget that, would you?

Push and zap, folks. It’s so easy, an EMT can do it.

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.

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!

Significant JVD
A different, much larger view of the same (click to enlarge)
Click through for a good discussion of JVD assessment
Some more subtle JVD
The basic method of measuring JVD
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

Some Things to Say (part 2)

 

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?

More things to say in part 3

Managing STEMI Mimics in the Prehospital Environment

Here’s one for the medics in the audience, or anyone interested in the box with the squiggly lines.

ST elevation means acute MI. Or does it? Most medics understand that this isn’t always the case, but many don’t recognize how often it’s not, and looking deeper — sorting out true STEMI from the many non-MI pathologies that also produce ST-elevation — is not the easiest task.

The following is a PowerPoint presentation I produced for use in either continuing education coursework or merely as a standalone reference. The main intended audience is EMS providers at the paramedic level, but most of the information is at least somewhat relevant to all levels of care.

The topic is the recognition and management of “STEMI mimics,” to steal Tom Bouthillet‘s phrase: non-ACS conditions that nevertheless present with signs and symptoms resembling acute MI, particularly ECG changes such as ST segment elevation.

This is best taught by a knowledgeable instructor, but it’s designed to be usable as a self-contained reference for ambitious students; these are info-rich slides, not just graphical accompaniments to a lecture. It does assume a foundational paramedic-level education, as well as a basic understanding of ideas like sensitivity and specificity — a review of our tutorial may be in order. The illustrative ECGs are labeled with “answers” in the slide notes of the PowerPoint versions, although not on the PDF, so that’s probably the best version if this material is new to you.

Although fairly comprehensive, it’s intended as a practical guide for field assessment and treatment, rather than an in-depth examination of the etiology and course of care for every pathology discussed. For additional information, the sources for most of the contentious claims and data are listed on the slides; sources for the more everyday material are available by request. And remember to follow your service’s protocols and understand exactly where and how far you have flexibility to make some of these calls; in many cases, the decisions will be made for you.

There are 192 slides in the full presentation; the most common feedback is that this can make for a very dense and potentially drawn-out class. There is one natural “intermission” point for a break at about the halfway mark, between the introductory discussion on general ideas and before diving into specific and individual mimics. If desired, the course can be broken up further into multiple units or even multiple days.

Feel free to share, redistribute, or use for your own purposes; this is educational material made available without charge or obligation.

[Edit 10/28/12] This presentation was later enhanced into a narrated video lecture