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The Trouble with Sinus Tachycardia

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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

 

24 year old male: “Anxiety Attack” – Conclusion

11 comments

This is the conclusion to our case 24 year old male: "Anxiety Attack". Be sure to read Part I before the conclusion!

When we left off, our providers were on scene with a young man, in custody, who was pale and had a radial pulse too fast to count. A narrow complex tachycardia was present on the monitor to which our patient helpfully pointed out, "it's SVT".

Let's find out if our patient is right!

Happens All the Time Man - Initial Rhythm Strip

The initial rhythm strip shows a regular, narrow complex tachycardia at approximately 200 bpm. Differentials include SVT (e.g. AV Nodal Reentrant Tachycardia and Orthodromic AV ReciprocatingTachycardia), atrial tachycardia, atrial flutter, and atrial fibrillation. However, given the rate, it would seem unlikely to be flutter, and given the near dead-on regularity it excludes atrial fibrillation.

Happens All the Time Man - Initial 12-Lead

The 12-Lead ECG confirms much of what we saw in the initial rhythm strip. We have a regular, narrow complex rhythm at 200 bpm. Retrograde P-waves are appreciable in leads II, III, aVF, and V1. These P-waves are often termed pseudo-S or pseudo-R' waves, and are most commonly seen in AVNRT. However, ST-elevation in aVR during SVT is a sign of orthodromic AVRT.

Regardless of mechanism, it is safe to say that our patient was right! He is currently experiencing SVT.

The treating paramedic also came to this conclusion and began treatment by lying the patient down and attempting vagal maneuvers. The patient was coached to bear down and then to blow through an empty 10 cc syringe, both without effect:

Happens All the Time Man - Vagal Attempt

An 18 gauge IV was established in the left antecubital fossa. 6 mg of adenosine was then administered rapid IV push followed by a 20 cc normal saline bolus flush. The following was captured:

Happens All the Time Man - Adenosine

This rhythm strip shows an interruption in the AV nodal reentry circuit with a conversion to a sinus tachycardia.

A repeat 12-Lead was obtained by the crew:

Happens All the Time Man - Post-conversion 12-Lead

The post-conversion 12-Lead shows a sinus rhythm without delta waves, epsilon waves, or acute ST/T-wave changes. The computerized interpretation notes a short PR interval of 98 ms, however, this author reads the PRi as normal at ~120ms. If an accessory pathway is present, conduction is concealed on the patient's baseline 12-Lead.

The patient was transported by the crew without incident and was lost to follow-up by EMS. However, this case shows that sometimes our patients will know exactly what is wrong, which underscores the importance of obtaining a good history.

  • What conditions could this patient have which caused his SVT?
  • What treatments may this patient receive if he continues to suffer from SVT?

52 year old male CC: Seizure – Discussion

10 comments

This is the discussion for 52 year old male CC: Seizure. Be sure to check out the backstory!

We had lots of great comments for this case, and as always many of you were right on target.

Let's take a look at the initial 12-Lead:

Cherchez le P - Initial 12-Lead

We have a narrow complex tachycardia at 180 bpm, with some very subtle P-waves best seen in the lateral precordials. Given the patient's age, it is difficult to say whether or not this rhythm is sinus in origin or some other tachyarrhythmia.

Dr. Marriott's advice when you don't see obvious P-waves is to,

Cherchez le P on let T!

In case you don't speak French, this means to search for the P-wave on the T-wave. So I've marked up the initial 12-Lead to help highlight the atrial activity:

Cherchez le P - Initial 12-Lead - Marked Up

The P-waves in the limb leads, especially lead II, are bizarrely tented and give rise to what looks to be a large T-wave.

In this case the paramedics were not certain as to the etiology of the tachycardia. They established an IV, administered a fluid bolus, and attempted vagal maneuvers; all of which resulted in no change in the rate or the rhythm. They then administered 6mg of adenosine via rapid IV push and witnessed a "conversion" to the following 12-Lead:

Cherchez le P - Final 12-Lead

At this point the patient's initial rhythm becomes obvious. P-waves are now clearly distinct from the T-waves. They have retained their bizarrely tented appearance and the PR interval appears to be unchanged.

Cherchez le P - Final 12-Lead - Marked Up

Given these findings it is likely this patient was experiencing an inappropriate sinus tachycardia.

As many of you noted, the situation surrounding this patient's seizure seemed suspect. While the patient adamantly denied any drug use, the ED suspected a stimulant was behind the patient's seizure and tachycardia. However, the patient became lost to follow-up and the cause of his tachycardia remains unknown.

  • Given a narrow complex tachycardia of unknown origin, do you feel it is appropriate to try an adenosine bolus?
  • Would this patient have benefited from a benzodiazepine?

83 year old male CC: “Cardiac patient in distress” – Conclusion

7 comments

This is the conclusion to 83 year old male CC: "Cardiac patient in distress". You may wish to check out the previous post for details about the patient's clinical presentation.

Let's take another look at the 12-lead ECG.

This ECG shows a regular narrow complex tachycardia at a rate of 170.

Could it be sinus tachycardia? One of the "rules of thumb" for the maximum sinus rate is 220 minus age. This patient is 83 years old. 220 – 83 = 137. Granted, this is just a rule of thumb so I'm sure expections exist but 170 is a good distance from 137.

I agree with some commenters that atrial fibrillation can appear regular at very fast heart rates. However, a trained eye can still pick up on some irregularity with rates < 200. You can also use calipers or fold the ECG paper in half and line up the R-waves to verify that the rhythm is regular.

In this case the rhythm is clearly regular which rules out atrial fibrillation but not 2:1 atrial flutter.

In lead V1 we can see atrial complexes (inverted or "retrograde" P-waves) after the QRS complex. We're narrowing in on the mechanism of this tachycardia. If we play the odds there's a good chance this is AV nodal reentrant tachycardia (AVNRT). However, it could still be 2:1 atrial flutter or the less common (but not uncommon) orthodromic AVRT.

You will recall that the paramedics documented "cannon waves" that corresponded to the heart rhythm. Some of you asked, "What are cannon waves?" Cannon waves are pulsations that are visible in the external jugular veins when the right atrium contracts against a closed AV valve. 

Normally atrial systole is an end-diastolic event (the so-called "atrial kick"). When the P-waves follow the QRS complexes the pressure generated by ventricular systole have already forced the AV valves shut. Hence, the atria contract against closed AV valves and back pressure creates a visible "wave" or pulsation that is transmitted back up the superior vena-cava and to the external jugular veins.

Here's an example to give you an idea although this patient's external jugular veins are severely distended and the heart rate is much slower. For the current case study the patient's cannon waves were fast, regular and visible just above the clavicle on the right side.

Does determining the exact mechanism of the tachycardia matter in the field? No, because that's not possible. We don't have an EP lab. However, we can carefully document the arrhythmia before and after treatment on those occasions where the patient is not critically unstable! 

The first thing the treating paramedics did was put this patient in a supine position and place him on oxygen which perked him up a little bit. Remember, BLS before ALS. I am aware of the controversy associated with placing a patient in Trendelenberg. However, I think we can all agree that lying flat is better than sitting or standing when you're hypotensive! 

Vagal maneuvers were attempted (the patient was asked to "bear down" and blow into an empty syringe) with no effect to the tachycardia. An IV was started but unfortunately the only good peripheral access was a 20 G IV in the back of the left hand.

Many (perhaps most) lf you recommended synchronized cardioversion for this patient. I have no quarrel with that. However, I do know that it's easier to say than do when you have a conscious, talking patient in the back of the ambulance. It also helps if you carry the right drugs and don't have to play "mother may I" with online medical control.

In this case paramedics pushed the PRINT button and gave 6 mg of adenosine followed by a 5 ml "flush" of 0.9% NS. It took more than 30 seconds to have an effect (Clinical tip: always follow adenosine with a minimum of a 20 ml flush) but here's what happened. The next four strips are continuous.

With the conversion to sinus rhythm the patient felt much better.

Vital signs were re-assessed.

  • RR: 18
  • Pulse: 100
  • NIBP: 138/81
  • SpO2: 100

A post-conversion 12-lead ECG was captured.

The patient was transported to the hospital in a position of comfort.

No further information is available.