The Trouble with Sinus Tachycardia

 

Sometimes recognizing sinus tachycardia can give us fits.

What? Sinus tachycardia? One of the most basic rhythms?

The discussion that follows will highlight some of the difficulties sinus tach can present at high rates. The pitfalls of using the generalized term "SVT" will also be discussed. This discussion is not meant to imply that this issue is easy to navigate. It can get very difficult, and very dicey. The consequences of misinterpreting the rhythm and missing sinus tach can have very deleterious effects for our patients.

We are all good at recognizing sinus tachycardia at rates between 100-150, but when rates exceed 150 it seems to become problematic.

Is it difficult to recognize this?

No.

How about this one?

More difficult.

 

When sinus tachycardia occurs at high rates, our ability to correctly differentiate it from other types of SVT apparently decreases. P waves start to blend into the T waves. Instead of talking about discreet stand alone P waves, we talk about "notches" and "bumps". It is all too easy to look at a rate >150 and simply call it "SVT".

 

We know what sinus tach is: a sinus rhythm at rates faster than 100 (in adults), which is a normal physiological response to compensate for the increased needs of the body. I won’t spend time listing all of the possible causes, ranging from running around the block to septic shock.

AVNRT, a type of SVT that is responsive to Adenosine, is a re-entrant tachycardia that relies on a circuit through the AV node to sustain it. Block down the AV node, and the dysrhythmia terminates. Quite a bit different from sinus tach. Different mechanisms, different treatments.

Several case studies involving the above strips and ones like it have appeared on our FB page, and the FB pages of other EMS educational sites. What we have seen is that an alarming number of folks incorrectly identify sinus tachycardia as one of the other SVTs and want to treat with Adenosine or cardioversion.

Consider this rhythm strip that appeared on our page and another educational paramedic page:

The patient was a sick adult male, hypotensive. P waves are subtle, but they are there. Due to the rate, however,  a majority of providers (hundreds!) identified this as "SVT" and wanted to immediately cardiovert. 

Here is the followup ECG taken a couple of hours later. The patient was severely dehydrated and had received a few liters of fluid:

Now that the rate has slowed, sinus tach is clearly visible.

While we are discussing this, we should be clear about our terminology. Sinus tach is one of the Supraventricular Tachycardias. "SVT" is an umbrella term that represents a group of tachydysrythmias that originate above the ventricles. They will generally be narrow tachycardias, unless aberrant conduction is present. Some of the other types of SVT are AVNRT, AVRT, A-Flutter, A-Fib, junctional tachycardias and atrial tachycardia. Not only is sinus tach one of the SVTs, it is by far the most common SVT!

One of the issues that’s come to light is the fact that “SVT” is seemingly often taught as a “dysrhythmia” itself rather than what it really is: a group of dysrhythmias. I really don’t like the term “SVT” because it implies a diagnosis, when in fact it should motivate a provider to form a list of differentials and consider the H’s and T’s.

"Could this be sinus tach? A-Flutter? AVNRT?"

Treating "SVT" as a stand alone dysrhythmia leads folks to believe there is one “treatment” for SVT, when in fact the treatment is determined by which type of SVT the patient has.

What are we even taught about SVT?

Generally speaking these days, when students are taught SVT they are taught that a narrow tachycardia faster than 150 or 160 is "SVT". Simple as that.

How do we differentiate sinus tach from SVT?

That’s easy: rate!

If the rate is over 150 (some use 160), then it is “SVT and not sinus tach” and should be given adenosine or cardioversion! Quickly!

If you were taught that, raise your hand. Wow… that’s a lot of hands!

 

While we are on the subject, where did the rate limit of 150 or 160 come from?

I have NO IDEA. There does not seem to be any research I can find that even suggests that these numbers can be used to differentiate ST from other SVTs.

In fact, I could not find any research that demonstrates that absolute rate plays any part in differentiating ST from other SVTs.

All I could find is references to the guideline used to determine the theoretical maximum sinus tachycardia in healthy people: “220 – age”.

This “formula” is a guideline at best. It intends to illustrate that very young people can have ST at very high rates, and that as we age, it should be more difficult to achieve higher rates of sinus tach.  However, we deal with really sick patients, and theoretical guidelines are not good enough to help us with this issue.

What I know is what you all know. That medics are taught that at rates above 150, you can no longer see P waves, so you have to assume it is “SVT”.

“154= SVT”

“146= ST”

Easy as pie! Whether or not P waves are visible does not seem to factor into the equation.

 

Perhaps you don’t want to accept that these teachings do not seem to be based on anything concrete, but these are the facts. Sinus tach commonly exceeds rates of 150, and P waves are often discernable. More on this in a bit.

In any event, It is in this region of rates, between 150 and 200, where sinus tach is often mistakenly called “SVT”, and the risk of inappropriate treatment rises. Don’t believe it?

Before you can say “SINUS TACH”, I could show hundreds upon hundreds of comments left by medics stating that a rhythm “could not be sinus tach because the rate is over 150”.  And these comments were made by the medics who are motivated enough to visit educational sites and participate. 

The result of this is that too many medics are not correctly trained to deal with this issue. Sinus tach is unrecognized. The P waves are ignored, and the rhythm is labeled “SVT”, and the patient is in danger of suffering in more than one way:

For staters, they may receive an inappropriate treatment. A sick patient in sinus tach does not need to go through trials of adenosine, or even worse, cardioversion.  In addition to the discomfort, those treatments won’t work. Sinus tach is not a reentrant rhythm that relies on the AV node for its perpetuation, so adenosine or cardioversion won’t resolve the arrhythmia.

One of the most overlooked consequences of mistreating this rhythm is the fact that these patients are not getting the treatment they really need. These patients need lots of fluids. If medics are giving drugs and electricity, they certainly are not administering large boluses of NS.

It is easy to imagine how difficult the choice may seem. The sick patient in sinus tach will look shocky. He may have palpitations or chest pain, and may be altered. In other words, it will be very tempting to attribute the patient presentation to rate problem, even though the rate is compensating for their underlying medical issue.

Without a sound understanding of what sinus tachycardia really is, and what rate ranges are reasonable, it becomes much more difficult to make the right choice.

 

Probably right about now, some of you will want to blame ACLS for all of this. Consider the 2010 “Adult Tachycardia (with pulse)” algorithm [1]:

 

 

Box 1 states: “Heart rate typically greater than or equal to 150 if tachyarrhythmia”. 

What does that mean? What it seems to mean to a great many people is that a rate greater than 150 is "SVT".

If the patient appears unstable, we are performing synchronized cardioversion by box 4. There is no mention of sinus tach anywhere on this algorithm.

I’ll admit, I think that algorithm could be better. I think there should be a box that gets you out of that algorithm if sinus tach is recognized, similar to what appears on the ACLS Pediatric Tachycardia algorithm [2]:

 

 

Here, if the tachycardia is narrow, you are directed to one of two boxes which require you to assess for the presence of sinus tachycardia. I believe that a box like this in the adult algorithm would help clear up a lot of confusion.

In defense of the AHA, however, the simplified algorithm is based on the assumption that students have read the ACLS Provider Manual, on which the algorithm is based.

The following appears in the “Foundational Facts: Understanding Sinus Tachycardia” box on page 125:

           “Sinus tachycardia is caused by external influences on the heart, such as fever, anemia, hypotension, blood loss, or exercise. These are systemic conditions, not cardiac conditions. Sinus tachycardia is a regular rhythm, although the rate may be slowed by vagal maneuvers. Cardioversion is contraindicated.” [3]

Clearly, on page 125 of the ACLS Provider Manual, sinus tachycardia has been excluded from the adult tachycardia algorithm. It is a shame that fact is not reflected on the algorithm itself, because evidently a very large number of ACLS students do not read the manual and may incorrectly assume that rate is the determining factor.

 

I know some of you are thinking, “is this much to do about nothing? Is sinus tachycardia at rates above 150 as rare as an isolated posterior STEMI?"

We put this issue to the test. We brought in two well known electrophysiologists, Dr.’s John Mandrola and Mark Perrin, to shed light on this issue and share their perspectives with us. Readers of our blog will recognize them as past contributors and experts in their field.

I asked Dr. Mandrola about the utility of the “220-age” formula, and here is what he had to say:

           “The old formula 220- age equals the max heart rate represents only an estimate. It can vary by up to 10-15%. That's a lot. Normally a 30 year-old would have a max of 190. But with the variation, ST could be as high as 200. I see tons of patients for 'tachycardia', that's supposedly abnormal. Often its just ST. The short answer is that human heart rates vary quite a bit–at the high and low end.”

I then asked him what we really want to know: how common is ST at rates above 150:

          “The sinus node is highly innervated with both sympathetic and para-sympathetic neurons. Adrenaline can easily push the sinus rate above 150. Stress, anxiety, fever, dehydration, drugs, heat, and many other things can do this.  

            If a patient has upright p-waves and the diagnosis is ST and is unstable, it's not because of a primary electrical disturbance. ST is a sign not a primary arrhythmia. Patients with ST should be resuscitated, but not with shocks, with fluids, oxygen and rest perhaps and comfort perhaps.”

 

I asked Dr. Perrin for his thoughts about using a rate of 150 as a cut-off between sinus tach and other types of SVT and he had this to say:

            “Thinking that ST has an upper limit of 150-160 is kind of crazy. The septic, those in congestive cardiac failure, people with pulmonary emboli, hemorrhaging patients, etc, etc… all of these could hit heart rates of 190-200 or higher.

                 It is an easy diagnosis to make as well – because the P will always be present. Perhaps if the rate is > 200 it may disappear into the T wave a little. The only real differential is atrial tachycardia/flutter, and this is pretty unlikely to destabilize a patient.”

We discussed the issue medics are having in the field with inappropriate treatments of sinus tachycardia. I asked if he had any first hand experiences with it:

           "In fact, I have found, anecdotally, that paramedics are quick to shock patients. I have misgivings about this, especially for narrow-complex rhythms. We live in a city. ERs are close by. Why shock so quickly? There's some data that shocks harm the heart.”

My sincere thanks to Dr.’s Mandrola and Perrin for their contributions. As always, peer sourcing is great way to gain additional insight and expertise.

Hopefully this discussion has been educational for those who thought that 150 was any kind of limit for sinus tachycardia. The fact of the matter is that sinus tach at rates between 150- 200 not only exists, but is not uncommon. We need to be better at assessing for sinus tachycardia, because it is the most common SVT. We need to make sure we are doing right by our patients, giving them what they need and keeping them our of harm's way.

We also need to be better educators and providers.

Some will say, "we are teaching to the Registry", or "we are teaching to ACLS".  

They will say, "in the real world, they will know what to do".

From what I have seen, it doesn't work like that. Providers fall back on what they were taught, which often happens to be incorrect.

It begs the question, why are we teaching something we know is not correct? That can't be good for anyone.

For those who didn't know this information before, you know it now. Let's see if we can change the way we educate and provide care in this area.

It seems to be a deeply rooted problem, ingrained in decades of education. Time for a change. I don’t know if the issue has been raised before, but we are raising it now. 

As always, I look forward to your comments!

 

_

Footnotes:

[1],[3]-  Advanced Cardiovascular Life Support Provider Manual

                  2011, American Heart Association

[2]             Pediatric Advanced Life Support Provider Manual

                  2011, American Heart Association

 

29 Comments

  • Lungs says:

    Preach it!  I love that you are hitting this hard.  It needs to be a sustained campaign blasting the dogma about SVT and the "rules" for "diagnosing" it.  It continues to be a pet peeve of mine.  Thanks for making an effort to educate.

  • Cardio says:

    I just took ACLS and had a problem during testing b/c my moderator put "SVT" on the monitor but I treated it as sinus tachy b/c there were discernable p waves before each QRS…I'm glad more emphasis is being placed on this b/c I was apparently the only one in my class that caught it. 
    We also had a case where our pt was going down hill and had a HR of >160 my medic was getting ready to push adenosine but someone pointed out that there were discernable p waves. during the post call to medical control they told him that he was wrong and he should have pushed it b/c according to the HR "it is SVT" and this is our medical control that was arguing this!!! Obviously everyone needs a lesson on SVT vs sinus tachy

  • Brooks Walsh says:

    David -
    Excellant review! You have presented a very clear description of the issue, and this shoud be mandatory reading for every paramedic student. None of this is controversial medicine, and ought to be common sense.
    I wish we could move past this issue, and start arguing about the truely difficult topics; e.g. at what heart rate do you shock atrial fibrillation? Now, that is a sticky issue…

  • David Baumrind says:

    Thank you Brooks!

    It just so happens that shocking a-fib is next on my list of issues to tackle!

    We have to make some headway here first though lol!

  • Bravo! This is a topic that needed to be addressed. Can not tell you how many medics I've seen in the 150 = "SVT" mindset….
    Fantastic review.

  • Shawn Gilliam says:

    Great write up! I spent some significant time teaching ACLS to Nurses, Doctors and Paramedics around Florida. I was shocked at how much 'poor' information is out there. This was a pet peeve of mine and stressed that we need to treat the patient not the monitor! So many say it but cannot put that into practice. The quality of education could improve in all arenas. I had a Doctor start to provide 'rules' to distinguish 3rd degree heart block in my class and one of the rules was it always had wide complexes… I had to pull him to the side and remind/ educate him on the potential for the A/V node to become the pacer with a faster narrow complex. The rule of SVT by mere heart rate was an issue that I addressed in every class; however, one of my 'tests' was a patient with high heart rate due to illness and most would go right into the ALS treatment algorithm. Keep up the great work.

  • Many important points are made in this Commentary by David. I'll restate some of them with addition of another perspective – especially since I am one of those who looks at SVT rate as ONE of the many factors I consider when contemplating the diagnosis.

    - As per David – SVT (= supraventricular tachycardia) is not a "diagnosis". It is instead a designation of a group of arrhythmias in which the impulse arises at or above the AV node. This includes not only "regular" SVTs – but also irregular ones such as AFib, MAT, sinus tach with PACs. It also not only includes narrow complex SVTs – but supraventricular tachycardias in which the QRS is wide due to either preexisting bundle branch block or aberration. It is potentially a big group.

    - Everything becomes easy for those rhythm strips in which clear sinus P waves are seen to be both present and upright with normal PR interval in lead II. Things are not so easy when nice, upright sinus P waves are not present – or they may be present, but you are not sure – or you see something that looks like atrial activity, but can't be sure what kind of atrial activity it is (flutter waves, ATach, or sinus P waves after all). And it certainly is not easy when the QRS is wide due to preexisting BBB (bundle branch block), in which case it doesn't take that fast of a rate to hide P waves …. (the QT as well as the QRS tends to increase with preexisting BBB).

    - 12 Leads are Better than One. Except for those cases in which atrial activity is very clearly defined – the diagnosis of SVT is often precarious from a single lead. The faster the rate – the more this statement becomes true. It is easy to get fooled. Most patients in SVT are stable. More leads are better than one to be more certain of the diagnosis.

    - You will NOT always know for sure IF a rhythm is sinus tach or not. Most of the time – you will probably know – or probably have a good hunch – but you will NOT always know. Sometimes, even doing 12 leads won't answer those questions. Clearly such patients shouldn't be cardioverted. If we are dealing with supraventricular = narrow complex tachycardias – emergent cardioversion is rarely (at most) needed. While most definitely NOT advocating for use of Adenosine to treat sinus tachycardia – I would simply make the point that on occasion it may not necessarily be wrong to give Adenosine for an undifferentiated regular SVT in which there is need to know and you are uncertain of the diagnosis. I'm less inclined to want to give Adenosine if I think an SVT is likely to be sinus tach – but there are times despite authoring scores of books on this subject that I just don't know at the scene that a particular SVT is definitely not sinus tach ….

    - I take full responsibility for being one of those who have promoted consideration of rate as a diagnostic aid in the differentiation of various supraventricular tachycardias. I have always stressed that rate is just ONE of many factors used in the decision-making process – and there are NO absolutes. In my 30 years of doing and teaching stress testing in the office – I saw hundreds of patients with sinus tach at rates over 160/minute. BUT – in the "horizontal patient" (ie, a patient who presents to you for care, and who has not just run a 100 yard dash) – the finding of a regular SVT at a rate >170/minute in an ADULT should make you think that sinus tach is less likely. This does not mean impossible – but it does mean statistically less likely.

    - If confronted with a reguar SVT at a rate of ≥150/minute in an adult – and you don't see sinus P waves – then I submit that the differential diagnosis will be one of 3 entities in >90% of cases (unless you are an EP cardiologist who is routinely referred the most problematic of arrhythmias). This differential is: i) Sinus Tach; ii) PSVT (AVNRT); or iii) AFlutter. Rate IS helpful – because IF the rate is ~150/minute you ought to be strongly considering untreated AFlutter as a possibility. Of course – ANY of the above 3 entities could be present when the rate is ~140-160/minute – but think of AFlutter until you've done enough leads and follow-up to rule it out. AND – when the regular SVT without clearly identifiable sinus P waves has a rate of >170-180/minute – the chances become much greater that neither AFlutter nor Sinus Tach is the diagnosis. To me – this statistical likelihood IS helpful as ONE of the factor I use when contemplating the differential diagnosis of a problematic SVT.

    - The above said – YES, it still IS possible for Sinus Tach in a "horizontal adut" patient to be 180/minute. One of the KEY ways to recognize that such a rapid SVT rhythm is sinus tach is by moment-to-moment monitoring. Unlike PSVT – it is likely that the rate of Sinus Tach will vary some, especially IF you are able to institute some effective treatment for whatever was causing the Sinus Tach. Another BIG clue is the clinical History. Are we dealing with an extremely ill septic patient who is hypovolemic and has always been in sinus tach, and over recent hours/minutes shows progressive gradual increase in rate now to 180/minute in which sinus P waves are no longer visible – OR – are we dealing with a patient who was totally well and very suddenly develops the onset of tachycardia that now shows a regular SVT @ 180/minute without P waves. HISTORY is critical – including past history, perusal of the chart, review of prior tele tracings.

    - So GREAT points made by David in this post. I simply wanted to offer the perspective of one who has been at the bedside by a number of patients in whom I DID NOT KNOW which of the above 3 SVT rhythms I was dealing with (sinus tach; aflutter; psvt) for many, many minutes. As to what to do – Sometimes – "Ya just gotta be there". It is rare that such patients need electricity – and if sinus tach is a likely diagnosis, then electricity is clearly contraindicated. 12-leads are sometimes much more revealing than one. At times a vagal maneuver may be revealing (including on occasion "chemical valsalva" with adenosine) – but often a tincture of time assessing the clinical situation and treating underlying conditions will confirm the diagnosis be it sinus tach or other rhythm. At other times – it may become apparent that the SVT is flutter/psvt/atach – in which case rate-slowing antiarrhythmics may be in order.
     

  • Adam Pernice says:

    This is a GREAT article!!!! I didnt finish reading this, but I plan on it. I am definitely going to spread the word and article….

  • concerned paramedic says:

    Thank you, Dr. Grauer, for giving us a little “two for the price of one.”

    This was a wonderful article. Good patient assessment, along with the true comprehension of the rhythms taught, should guide our treatment modality. Unfortunately we are taught to pass tests and not treat patients.

  • David Baumrind says:

    Ken,

    Thank you as usual for your thorough additions to this post.  Of course, you raise several valid points, probably deserving of a followup post to this sometime.

    I kept this post on a more basic level, attempting to return to the "horse before the cart". While you consider rate as a factor in your analysis, it is based on assessment and a list of differentials for you to consider.

    The point of this post is to highlight the fact the opposite occurs too often. Instead of forming a thoughtful list of differentials to consider, rate is used to "make" the diagnosis, which i am sure you would not advocate.

    I think it is really an educational rather than analytical issue at this point. 

    Thank you for the analysis… I will follow up on this again!

     

    -David

  • Thank you David for your follow-up comment. We BOTH agree that rate should NOT be used to "make" a definitive diagnosis. That said – I still DO think that regardless of the level of the provider – awareness that IF a regular SVT not showing definite sinus P waves (clearly upright in lead II with an appropriate PR interval) has a rate in excess of 170/minute in an adult – that statistically this clearly favors PSVT (AVNRT) as the diagnosis. In no way is Sinus Tach "ruled out" by an SVT rhythm at this rate – but it clearly becomes far less likely.
    THANKS again for your receptivity to my viewpoint. Since I am one of those who has both verbally and in print openly advocated for consideration of rate in the SVT differential diagnostic process for many years – I felt a STRONG need to respond to your column. That said – I do understand  where you are coming from.

  • Floyd says:

    The cardiologist who commented in the article said there is some evidence that shocks harm the heart. I have heard there is evidence that it does no harm. Does anyone know where the data is on this?

  • maddog medic says:

    I have been guilty of perpetuating this oversimplification in my ACLS teaching. As a paramedic, though, I've not "practiced what I preached."

    Let me explain: I teach ACLS to mostly nurses and non-EMS physicians. I often use heart rate as a strong diagnostic indicator in narrow-complex tachycardias. Though I also stress that they should look for other diagnostic clues for underlying cause to guide their decision about whether it's SVT or not, often I've been guilty of using "SVT" as a diagnosis and not a classification of rhythms. Keep in mind that many of my students are not very experienced in cardiac assessment and treatment, don't speak English as a primary language and work in environments where they are only called on to diagnose these rhythms in their ACLS refresher courses.

    Thank you for helping me get my mind straight as to how I should be teaching this.

    I don't, however, do this in my practice. I work in the desert in the Middle East. Most of my patients who have rhythms over 150bpm are usually suffering from things like dehydration or traumatic blood loss. In the 3.5 years I've been here, I've cardioverted someone once, electrically and successfully. All the rest of my patients have either responded to fluid challenges, Vasalva's maneuver or died.

    I didn't cardiovert those dehydrated and volume depleted patients because my diagnostic brain, without my willful control, was already painting a full picture of the patient and headed down a completely different treatment pathway without even considering "Edison" or "Medicine" for a rapid heart rate.

    Here's the thing: I'm an experienced provider who is curious about these sorts of things and make decisions (I like to think) based on the entirety of the patient presentation. How do we convey this sort of global, diagnostic thinking and decision making to our students? If I'm making the same teaching mistake that's been going on for so long, then it begs the question of how do we stop teaching the wrong thing to our students or how do we start teaching the right thing?
    I am extremely grateful for the intelligent, vociferous and gregarious men and women in medicine who take time an effort to share their thinking on these matters. You 'da best!
    –maddog

  • shaun says:

    well said, this just take us back to basics and clinical decision making and move away from treating the machine and consider the patient in front of us. you make me go back to the ACLS book
    well done kep it up and keep us on track.

  • Not trying to sound ignorant, but I will be starting medic school soon, and am wondering if I am reading this right.  ST is differentiated from SVT by the prescence of P waves?  I am one that has always heard SVT is SVT regardless.  It's little tidbits of info like this that keep me coming back to your page. 

  • David Baumrind says:

    Dieseltherapist,

    Good luck in Medic school! For the most part, the presence of P waves suggests sinus tachycardia (or atrial tach), but not AVNRT (what most people are referring to when they think of "SVT"). SVT is actually not a rhythm itself, but an umbrella of rhythms that originate above the ventricles. Just remember, in medic school, you might not learn it that way. I would suggest reading many of the great comments left on this thread.

    -David

     

  • David Baumrind says:

    Shaun,

    Thanks for the comment. While I agree that clinical decision making is the cornerstone of what we do, I caution you not to fall into the trap of "treat the patient not the monitor".

    In fact, for the most part the rhythm analysis and appropriate treatment of the patient can not be accomplished without correct interpretation of the rhythm  off "the machine". 

    The basics are treating the patient, but also using the machine to correctly interpret what is going on. There is no taking away that piece!

    Thanks,

    David

  • Good article, I mostly agree with what you say. I'll get what I don't agree with out of the way early, then add other comments,

    These patients need lots of fluids.

    Not always, actually not often. The most common cause of Sinus Tachycardia I saw during my career was respiratory distress. One of the doctors you consulted in your post mentioned it briefly. Patients with CHF or even severe Asthma can reach rates of up to 170. I've found that treating the respiratory causes is beneficial. One of the key differentiators I use is BP. If a patient has a HR of 150+ and a good BP, I think CHF or other respiratory disease.
    Now to the comments.
    I won't let the AHA off the hook so easily as do you. I think the "anything greater than 150 is SVT" myth comes from them. I also thing that calling a rhythm "SVT" comes from them. If we just teach students to refer to anything with a rate of 150 or more as "SVT" how can we expect them to understand treatment options.
    They should put that differentiation into the handbook and the algorhythms. Most students don't read the textbook because the AHA has made the book unreadable.
    I think what we (as an industry) teach paramedics and even doctors about SVT blinds them to looking for P waves if the rate is greater than 150. If they don't look for P waves, they aren't going to see them. I've seen experienced attending physicians at renowned teaching hospitals make that same mistake.
    When I teach ACLS, one of my frequently failed, excuse me, retested, stations involves a patient with a heart rate of 160, repiratory rate of 40, BP of 210/120, and unclear breath sounds. Most students either start out treating that as Asthma or an SVT of some sort. Those who do, kill their patients.
    Again, good post and you point out a significant hole in how we teach new paramedics. Not to mention in how some not so new paramedics (and physicians) treat really ill patients.

  • David Baumrind says:

    TOTW:

    Thank you for your insightful comments.

    You are absolutely right about ST and respiratory distress caused by asthma or CHF… Those patients don't need fluids. In my mind, those conditions would be more easily differentiated by most providers than severe dehydration or sepsis (of course, I could be wrong in that assumption).

    As for letting anyone off the hook, I can't necessarily disagree with you. I chose to focus on the "what do we do now" vs. the origin of the myth.

    Thanks again for sharing your thoughts!

    -David

  • Joshua Roberts says:

    The sad thing is… as educators, you are almost forced into teaching it so the information "fits" what NREMT and ACLS preach, simply to pass.  You can also present "real word, real practice" to the students, but I've found that it often makes the water muddier for them.  I hate the practice of teaching to pass a flawed exam, because this is why our public schools are failing.  One solution would be to have a quality "after school" training program before the new medics hit the street.

  • David Baumrind says:

    Joshua,

    If your two points are that we can't teach "real world, real practice" to the students because it "muddies the water", and that we need an "after school" training program to teach what they should learn in the first place, we are in big trouble!

    Students will treat "real patients" in the "real world", so if we don't teach for that, just what are we doing anyway?

    Thanks for the comments!

  • Dr. Michael M says:

    I see many posts here but…a couple of things.

    SA node normally fires at the rate of 100-160 BPM (Normal), AV node slows it down to 100-80BPM. This delay is necessary so a single impulse from the SA node will depolarize Atria then giving time to ventricles to fill, the same impulse will depolarize Ventricles. However, before ventricles contract, the same impulse is further slowed down by Bundle of His to Purkinje fibers, so that the normal HR is 60-100BPM. This is a difference from AV to Bundle of His and bundle branches.

    Sinus – means normal
    Sinus Tachycardia – means HR 100-160 BPM at rest (many causes Ex. sympathetic over stimulation or blood loss). Normal because there is one P wave to each QRS 1:1 (normal)

    SVT – there are few in this group mentioned in some posts…This is NOT a normal heart’s response to stress. You will see multiple P waves before each QRS

    I hope this clarifies as to the difference between Sinus Tachycardia and SVT

    • Christopher Watford says:

      Dr. Michael,

      Your comment confuses the terms and mechanisms at play.

      When talking about the sinoatrial nodal rate, people are most commonly referring to the range of possible rates. The normal intrinsic sinoatrial nodal rate excludes all autonomic influence, and is somewhere between 90 to 110 bpm. This range is relatively fixed throughout the process of aging. If you include autonomic influence, we find that the parasympathetic tone plays the strongest role in the basal sinoatrial rate which changes as patients age. During exercise sympathetic tone plays the strongest role in the sinoatrial rate.

      When talking about conduction, however, the AV node introduces a delay in the conduction of the wavefront. Conduction through the AV node does not actually slow down the depolarization rate of the sinoatrial node. You are correct that this delay encourages appropriate atrioventricular coordination.

      Furthermore, conduction through the Bundle of His is not slowed at all and very rapidly continues into the bundle branch system and the Purkinje fibres which terminate in the working myocardium. Conduction in the Purkinje system is as fast as 4 meters per second, roughly 8 times faster than AV nodal conduction.

      In short, the normal heart rate primarily depends on autonomic influence not on the speed of conduction.

      Sinus tachycardia simply means a sinoatrial rhythm with a rate above the reference range, which is roughly >90 bpm (traditional teaching uses 100 bpm as the cutoff to make calculation via ECG paper easy).

      Likewise, sinus bradycardia simply means a sinoatrial rhythm with a rate below the reference range, which is roughly <50 bpm (again, traditional teaching uses 60 bpm as the cutoff to make calculation via ECG paper easy).

      Lastly, SVT is not a rhythm. This cannot be stressed enough. Supraventricular tachycardia is any tachycardia which utilizes atrial or atrioventricular nodal tissue for the maintenance of the rhythm.

      • David Baumrind says:

        Thank you for your clarifying comments Christopher! I’m fairly certain I couldn’t have said it better myself.

        • Dr. Michael M says:

          Christopher

          I apologize if I came across as condescending. You are all very smart, I respect and applaud all of you for your career choice.

          My intent was to make this post short and “sweet” while answering the question about the difference between Sinus Tachycardia and SVT. I find that health professionals often have a difficulty in differentiating between those two terms.

          I did not introduce the concept of conductivity. Perhaps it’s my fault but my reference to “slows down” was meant to indicate inherent automaticity within heart’s electrical conduction system. Ex. in a complete AV block the ventricles will still contract due to automatic foci in Bundle of His, where atria and ventricles will contract independently. This was simply my attempt to explain the 60 BPM low normal reference number, below which SA nor AV node may be in control of “pacemaking”.

          Obviously, when I said “slows it” down I did not refer to the actual slowing down of SA node by AV node but the electrical impulse or “wavefront”.
          Again, it’s probably my fault in desire to make this post short, I was not clear enough.

          Christopher, you are absolutely correct in all of your statements including that the parasympathetic system is dominant. However, what changes with age is the ability of the sympathetic system to influence cardiac tissue. During an exercise (sympathetic increase) a young individual will be able to increase HR to much higher levels than an older person. Accordingly, you will notice that elderly patients at rest will have lower HR than younger patients. It’s the excitability exerted by sympathetic system that decreases with age and not due to the “change” or increase in parasympathetic activity.
          Hence, the reference range I provided for the SA node of 100-160BPM includes infants.

          I think that you are all very knowledgeable about this topic. However, let me point out that when we think about the heart we really mean ventricles. Atria just forces extra 20-25% of blood to the ventricles during diastole. It also happens that the SA node, as the name implies, is located in atria. I find that sometimes we are confused by all these terms: Tachycardia, Ventricular tachycardia, Supra ventricular tachycardia, Sinus tachycardia etc.

          - Tachycardia – simply means that (heart) ventricles are contracting at the rate greater than 100 BPM at rest being the key word.
          Some may ask where does this number come from and why is it normal? Is it normal to have 172 HR at the gym?
          How come all 4 chambers do not contract at the same time?
          To answer these questions, we all know and have to remember that:
          Depolarization = Contraction = Systole
          This is the premise and principle of discovery of ECG to trace cardiac muscle contraction based on electrical activity in the heart that can be picked up and represented on ECG paper. This electrical activity is typically generated by the primary “pacemaker” or Sinoatrial node, which typically fires an elec. impulse at the rate above 100 BPM but can be stimulated by the sympathetic system to a much higher rate depending on age and activity (even 180 in a young athlete). This is also the upper elc. automatic capability of the AV node foci. What this means is that even in the absence of the SA node activity the AV node will pick up pacing activity and the ventricles will still contract. So this is the reason for the 100 BPM.
          Typically, the SA node will fire at the level higher than 100 to a normal of 160 in infants at rest. Hence it will maintain the pacing function, generating an electric impulse delayed by AV node to adult average HR of 76-82 BPM to allow time for ventricles to fill with blood during diastole. This is the reason why an elec. impulse from SA node does not depolarize or cause contraction of all four chambers at the same time.
          Consequently the same is true for Bradycardia or HR below 60 BPM due to automaticity of Bundle of His foci (60-40) and Purkinje fibers (40-20). What this means is that above 60 BPM all is good because pacing still comes from SA or AV node.

  • Susan M says:

    Great article! As with anything in EMS, the rules are not hard and fast. I was having a discussion with an ED doc recently and she wanted to reinforce to EMS that VTAC needs to be FAST to give Amiodarone. If you give Amiodarone to a slow VTAC (below 120) you can put the patient into asystole. Black and white rules help us pass exams, but after school is done, we need to educate ourselves on these topics so we really learn clinical decision making! Thanks for the article.

  • kyle says:

    Just adding to the comments here. When I started ems my cardiology was weak. It’s gone from weak, to being the one co workers go to with questions. Ken, I understand your point, but I do come from the other side on this. I was a medic that was taught “unstable > 150 cardiovert”. and I wasn’t alone. Cardiology isn’t the only thing taught in a paramedic program, and they range from 6 months to 14. ( I was fortunate and had a 14 month class). There is a mountain of information to process and digest, and then many of us find ourselves suddenly the only acls provider on a scene not long after graduation.

    I don’t think the point of this article is to dissuade consideration of rate, I don’t think any of us will take it that way either. I think the point is to refute what we were taught.

    “treat the patient not the monitor” I HATE that phrase. It’s used by medics all over the country to justify lack of ability to interpret an EKG. I like “Treat the patient AND the monitor”. Long before I ever put a monitor on a patient (I say long, I mean a minute or so) I have my differentials all lined up. I’m using the monitor to rule in / out possibilities. EMS education needs to move to a “gather your clinical impression, see if the monitor supports your suspicions.”

    We have a few weeks to learn 12 leads, and how to treat the conditions various rhythms imply. Simple rules like “shock unstable > 150″ allow you to save more lives than you will take. It’s a hard truth, but that’s how medics are taught. If you want to learn how to save MORE lives, that’s up to you.

    This article I believe is saying, that this particular gambit is unnecessary, as it wouldn’t take that much effort to restructure it to “shock unstable > 150 when you can’t see a p wave and don’t think it’s sepsis or something”

    It doesn’t seem like alot more to learn…. But when you’re learning 100 other things that week, it can be.

  • Tom G says:

    Great article, great comments! Before I started medschool I worked as EMS as well – and I have to admit I’ve never been taught this topic in a way so clear and comprehensive! Thank you!

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EMS 12-Lead

Cardiac Rhythm Analysis, 12-Lead ECG Interpretation, Resuscitation

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Comments
Kevin
44 year old male CC: Palpitations
Why on earth would you risk VF, by giving Adenosine to rule out rhythms.. This is dangerous, and foolish. There might be a slight chance that this is WPW.. You might as well just give him Cardizem, they are both AV nodal blockers... I don't know why the AHA even added this stupid idea..
2014-10-22 13:31:06
Vince DiGiulio
The 360 Degree Heart – Part II
It is standard practice in electrocardiography to label the first 90 degrees counter-clockwise from "zero" that way. When you see a patient with "left axis deviation" you'll see that their measured QRS axis is somewhere between -30 and -90 degrees. Imagine if you saw someone with a mean QRS axis at 5 degrees. Now imagine…
2014-10-21 14:00:37
Bryan
The 360 Degree Heart – Part II
I don't understand why (-)III and aVL are be labeled -60 and -30 degrees instead of 300 and 330 degrees?
2014-10-21 13:43:29
The 360 Degree Heart – Part II | EMS 12 Lead
The 360 Degree Heart – Part I
[…] first post in our “360 Degree Heart” series attempted to visualize how the different frontal plane […]
2014-10-21 12:50:56
Eric Strong
Axis Determination – Part VI
This is a great discussion of axis determination. One minor suggestion: I think it's potentially misleading to refer to an axis between 0 and -30 as "physiologic left axis deviation", since "axis devitation" implies deviation from normal, and axes between 0 and -30 are perfectly normal, (depending on age and body habitus). It may be…
2014-10-05 17:09:00

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