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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

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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?

24 year old male: “Anxiety Attack”

23 comments

This great case comes from a long time reader who wishes to remain anonymous. As always, details have been changed to protect patient and provider privacy.

You're dispatched on an ALS quick response vehicle by law enforcement requesting EMS to check up on a subject. Dispatch notes indicate officers were called reference a domestic disturbance and have two subjects in custody. A BLS ambulance just around the corner from the call checks on scene and requests ALS continue.

You're directed into a small apartment by an officer and find the BLS crew obtaining vitals from a young man, who appears pale, seated on a couch, uncuffed. The officer says, "he started complaining of chest pain and his hands tingling after we arrested him, might be an anxiety attack. He and his girlfriend really got into it."

You check in with the BLS crew who are obtaining his vitals and introduce yourself to the patient. He looks up at you and simply states, "It's SVT."

One of the crew looks up and nods his head while giving the vitals:

  • Pulse: too fast to count
  • BP: 118/64
  • Resps: 18, unlabored
  • SpO2: 94% r/a, cap refill normal
  • JVD: moderately elevated

A quick assessment is made:

  • Signs and Symptoms: Palpitations and SOB
  • Allergies: None
  • Medications: None
  • PMHx: "I've had SVT a lot, like twice already this month."
  • Last In's and Out's: Dinner
  • Events: verbal altercation with girlfriend

During your exam the BLS crew has placed the patient on the monitor for you:

Happens All the Time Man - Initial Rhythm Strip

As it prints out, you tell one of the officers that he's definitely a patient and will be going with you to the hospital.

A 12-Lead is acquired:

Happens All the Time Man - Initial 12-Lead

  • Is this patient actually in SVT?
  • What is your treatment plan?
  • What sort of medical problems could this patient have?

57 year old male: Chest Discomfort – Conclusion

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This is the conclusion to 57 year old male: Chest Discomfort. We suggest you read the backstory first!

We're now in the back of the ambulance with our stubborn 57 year old male with a rapid heart rate. He looks unwell, but is otherwise hemodynamically stable. Our partner is working on a line.

Let's review the initial rhythm and 12-Lead ECG:

Round and Round He Goes - Initial Rhythm

The rhythm strip shows a narrow complex tachycardia at approximately 150 bpm. Atrial activity is not visible and may be buried in the T-waves. Our differentials include: sinus tachycardia, supraventricular tachycardia (e.g. AV Nodal Reentry Tachycardia and orthodromic AV Reciprocating Tachycardia), 2:1 atrial flutter, and junctional tachycardia.

Round and Round He Goes - Initial 12-Lead

The 12-Lead also shows a narrow complex tachycardia at approximately 150 bpm. Atrial activity is vaguely appreciable in the T-waves of V1 and III. The list of differentials remains unchanged, however, given the continued regularity sinus tachycardia seems less likely.

The paramedic who sent this case in elected to treat the patient with adenosine to convert or unmask the underlying rhythm.

Round and Round He Goes - 6mg Adenosine Bolus

The post-adenosine rhythm strip shows clear flutter activity in leads II and aVF, however, the paramedic admits they did not initially notice the F-waves. The rhythm then devolved into an irregularly irregular rhythm and a strip was printed.

Round and Round He Goes - After first Adenosine

While there is some baseline wander present, given the previous ECG, it seems very likely that this is atrial flutter with a variable response. However, the rhythm quickly accelerated to its original rate of 150 bpm.

As the treating paramedic did not appreciate atrial flutter, they administered a second dose of adenosine.

Round and Round He Goes - 12mg Adenosine Bolus

Atrial flutter is readily appreciable in Leads II and aVF, and as before the rhythm accelerated to its original rate.

Round and Round He Goes - After second Adenosine

The treating paramedic recognized atrial flutter and contacted medical control asking for orders for Cardizem.

Orders were received for 10 mg Cardizem slow IV push, which resulted in some reduction in rate but without conversion to a sinus rhythm.

Round and Round He Goes - After 10mg Cardizem Bolus

The patient was transported to a local hospital where he was placed on a Cardizem drip, resulting in conversion to a sinus rhythm after a few hours. A follow-up with a cardiologist was scheduled and the patient was discharged home without sequelae.

Any time you are faced with a regular rhythm at around 150 bpm, remember that the most common atrial rate in atrial flutter is 300 bpm and the most common conduction is 2:1.

57 year old male: Chest Discomfort

70 comments

The following is a great case from Mordy E, and as always some details have been changed to protect patient privacy.

You and your partner are refueling your ambulance at a gas station when a woman walks up and asks if you could, "come check out my husband."

As you walk over to their car she states that, "he's had chest pain for almost 5 hours now and didn't want me to call 911."

Your patient is standing, pumping gasoline, and appears unwell and diaphoretic. He seems reluctant to accept care at first, but you encourage him to let you check him out and he admits to chest discomfort.

He sits down in the passenger seat and lets you evaluate him.

  • Onset: 5 hours ago
  • Provocation/Palliation: nothing makes it better or worse
  • Quality: "pressure"
  • Radiation: "to my jaw"
  • Severity: "it isn't that bad"
  • Timing: constant

Your partner puts the monitor on the back seat and places electrodes while you get a set of vitals.

  • Pulse: 150, weak at the radials
  • BP: 102/68
  • Resps: 22, unlabored, clear bilaterally
  • SpO2: 94% r/a

As the initial rhythm strip prints and your partner places electrodes for a 12-Lead, you get a quick medical history.

  • PMHx: hypertension, hyperlipidemia, palpitations
  • Meds: "some pressure medication"
  • Allergies: seasonal allergies, NKDA
  • Last In's/Out's: breakfast
  • Events: sudden onset of chest discomfort which woke him up this morning

Your partner hands you the rhythm strip and leaves to grab the stretcher as the 12-Lead prints.

Round and Round He Goes - Initial Rhythm

You tear off the 12-Lead and the patient asks, "well, is something wrong with my heart?"

Round and Round He Goes - Initial 12-Lead

Your partner places the stretcher in front of the patient and says, "yessir, your heart is going too fast. Let's get you on our cot and into the back of our office so we can do something about that."

As you wheel the patient to the unit, your partner asks:

  • What is our patient's rhythm?
  • What did the 12-Lead show?
  • How should we treat this patient?

77 year old female: Unresponsive

66 comments

This is a great case sent in my a reader who wishes to remain anonymous. We hope you find it as intriguing as we did!

After clearing up from a routine interfacility transfer, you're dispatched for a 77 year old female who is unresponsive at a local extended care facility. A BLS engine crew is enroute as well and has a few minute lead on your unit.

As you're arriving the engine crew hails you on a tac channel and relays that the patient is unresponsive, but breathing and they have put her on a NRB and are checking her blood glucose level.

You're directed to the room where the engine crew is completing their assessment of the patient. The facility staff states the patient was alert and oriented at 0600 when they did their rounds. However, when they came back at 0900 to give the patient breakfast and her morning medications they found her unresponsive.

Apparently, EMS is called frequently for this patient becoming unresponsive, although she does not know why. She hands you the patient's paperwork as the captain from the engine gives you the patient's vitals:

  • GCS: 8 (E2 M2 V4)
  • Pulse: 60, weak at the radials
  • BP: 118/56
  • RR: 16, clear bilateral lung sounds
  • SpO2: 82% on room air, 94% on a non-rebreather
  • BGL: 102 mg/dL (5.6 mmol/L)

As your partner helps the engine crew move the patient to your stretcher you read over her paperwork:

  • PMHxhypertension, osteoarthritis, renal cysts, urosepsis, advanced parkinson's disease, history of UTIs, dementia, history of plueral effusion, COPD
  • Medshydrocodone, sorbitol, ferrous sulfate, dulcolak, prednisone, albuterol, ativan, heparin, aspirin, colace, sinemet, synthroid, tylenol, furosemide, potassium chloride, aricept, multi-vitamin, claritin, lactulose
  • Allergiescipro, septra, florinef, bactrim, levaquin, zoloft, gentamicin

A quick physical exam reveals moaning to painful stimuli, pinpoint pupils, whole body tremors, a foley catheter with adequate output amber in color. The remainder of the exam is unremarkable.

In the back of the unit you place the patient on nasal capnography while your partner places the patient on the monitor:

We'll See What Shakes Out - Rhythm Strip

At this point your partner grabs the 12-Lead cable and begins placing electrodes while you acquire an IV.

We'll See What Shakes Out - 12-Lead

You're 10 minutes from a local hospital, and 15 minutes from a cardiac center.

  • What is our patient's rhythm?
  • What does the patient's 12-Lead show?
  • What are your treatment priorities?

Leave your answers below!

Looking for the conclusion? 77 year old female: Unresponsive – Discussion.

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?

52 year old male CC: Seizure

33 comments

You're working a QRV on a busy weekend, when you get dispatched for a "man down". No transport units are initially available, but a BLS crew from a neighboring town are on their way.

Upon your arrival an officer on scene directs you inside to a man he says, "looks like he had a seizure".

Your patient, a 52 year old male, is seated on the ground with a family member holding a cold washrag to his forehead. He is responsive to verbal stimulus, but isn't making any sense.

His wife introduces herself and fills you in on the story. Apparently, they were watching TV when he suddenly went unresponsive and began, "shaking all over". She also says that he has never had a seizure before and usually is never sick. When you ask about alcohol or drug usage she becomes evasive.

You introduce yourself to the patient and feel for a pulse at the radial. His skin is hot and moist and his radial feels quite fast. He's slowly coming around and smells of cigarrette smoke.

  • Pulse: 180 bpm
  • BP: 112/64
  • RR: 26
  • SpO2: 92% r/a
  • Lungs: clear and equal bilaterally
  • Temp: 99.9 F tympanic
  • BGL: 188 mg/dL

The wife states the patient takes something for his cholesterol and hypertension. You attach your monitor and see a narrow complex rhythm at 180 bpm.

The patient is now answering questions appropriately, but with some hesitation. He denies that he's had seizures before and denies taking any drugs.

The BLS crew arrives as you acquire the following 12-Lead:

Cherchez le P - Initial 12-Lead

  • What is the patient's rhythm?
  • Is the patient's condition related to the rhythm?
  • What is your course of treatment?

Discussion for 17 year old male CC: Chest pain and palpitations – WPW Part II

13 comments

This is Part II of the discussion for 17 year old male CC: Chest pain and palpitations. You may wish to review Part I of the discussion.

As we covered in Part I, our patient was experiencing the life threatening combination of Wolff-Parkinson-White (WPW) and atrial fibrillation.

The EMS 12-Lead Blog team broke this conclusion up into two parts due to the importance of understanding this particular dysrhythmia. The patient survived in spite of the treatment provided, however, with the proper education both in-hospital and pre-hospital providers can rapidly identify and appropriately treat WPW and atrial fibrillation!

We also discussed that the danger in this arrhythmia is that the AV node no longer provides an effective "speedbump" for the barrage of atrial impulses. Any treatments which further slow or block the AV node without also slowing or blocking the accessory pathway will likely be lethal.

Thankfully, there are some key findings in WPW and AF which pre-hospital providers can use to identify this arrhythmia:

  • Bizarre, constantly changing morphologies due to varying preexcitation

     
  • If the rate meets or exceeds 300 bpm, or less than or equal to one large box, an accessory pathway must exist
  • If the rate exceeds 260 bpm, you can be confident an accessory pathway exists
  • If the rate exceeds 220 bpm, you need to be suspicious of an accessory pathway

Remember, slowing down the AV node in patients with uncontrolled atrial foci–such as atrial fibrillation or flutter–can be lethal! Stick with cardioversion or procainamide. The following, striking 12-Lead is from  a 59 year old female with palpitations (from the amazing Harvard WaveMaven case files):

Once you've seen it, you can't forget it!

However, as noted in Part I, not every patient with an accessory pathway will present with atrial fibrillation. Often they will present with a regular supraventricular tachycardia with either a narrow or a wide complex.

In the case of a regular, wide complex rhythm without discernable atrial activity treat as per ventricular tachycardia. However, it bears repeating that at rates exceeding 220 bpm an accessory pathway may be present, so avoid lidocaine and amiodarone and favor procainamide or cardioversion.

In the case of a regular, narrow complex rhythm treat as per SVT. Some of these patients may be very young, however, this should not keep you from treating them if they are unstable.

Adenosine is safe and effecacious for the treatment of SVT in children. However, vagal maneuvers can be particularly successful. With infants you can place an ice pack on the bridge of their nose to stimulate a vagal response. In older children ask them to blow through a small syringe or straw.

  • Accessory pathways, like WPW, can cause conduction rates to exceed 250 bpm and sometimes exceed 300 bpm
  • Without the speed limits imposed by the AV node, accessory pathways which receive no innervation to control them may allow lethal arrhythmias with the drugs
  • Cardioversion is a safe and effective treatment for unstable or potentially unstable tachyarrythmias such as WPW and atrial fibrillation

68 year old male CC: Chest Pain

17 comments

Here is a great case submitted by a faithful reader who wishes to remain anonymous. As usual, details have been altered to ensure patient and provider confidentiality.

Hurricane Irene has kept your night shift wet, windy, and you've bounced from one stranded motorist call to another. Dispatch chimes in and puts you out on a chest pain call, 68 year old male at a convenience store, no other information.

You arrive to a neighborhood grocery store and see a small crowd in the doorway. An older gentleman is seated on the ground, in no apparent distress.

You introduce yourself and ask what is going on while your partner acquires vitals.

  • Onset: 45 minutes ago he awoke with some chest pain, but went to the store anyways for supplies
  • Provocation: nothing makes the pain better or worse
  • Quality: "it's like somebody keeps punching my chest"
  • Radiation: he localizes the pain to the left side of his chest
  • Severity: increased to an 8 of 10, "sometimes I can't catch my breath"
  • Timing: constant

Your partner turns and gives you his vitals:

  • Skin: cool, dry
  • HR: 130, irregular but strong radials
  • RR: 26, yet unlabored, too windy to hear lung sounds
  • BP: 138/86
  • SpO2: 95% on room air
  • Temp: 36.9 °C
  • BGL: 195 mg/dL (10.8 mmol/L)

Your patient reports a general "cardiac" history and is unable to remember what medications he is on, stating only that they, "are numerous."

With some help from the bystanders you assist the patient to your stretcher and move him to your unit to get out of the elements. Your partner places him on the cardiac monitor while you place him on a nasal cannula and listen to his lung sounds.

You note that his lung sounds are clear and equal bilaterally as your partner hands you the initial 3-Lead. Your patient denies any history of arrhythmias and says at his last checkup he was, "healthy as a horse."

A 12-Lead ECG is acquired.

With Irene still pummeling the Eastern seaboard, it will be at least a 20 minute ride to the closest facility, 30 minutes to the closest PCI capable center. Your partner asks if you'd like him to request a driver.

What is your patient's rhythm and what treatments should your patient receive?

What does the 12-Lead ECG show?

Does the patient need a PCI capable facility, why or why not?

Narrow complex tachycardias – Part III

15 comments

Documenting the heart’s response to adenosine

Let’s look at some different cases where adenosine was used. Rather than give you all the details about the age, gender, chief complaint, and vital signs, I’m just going to show you the rhythm strips.

Right now I’m only concerned with how the heart behaves during the administration adenosine.

The PRINT button is your friend!

Case #1

These strips were given to me by the same paramedic who did such a wonderful job in Part II. For some reason, with this patient, he didn’t bother obtaining a 12-lead ECG prior to giving the adenosine.

He did, however, remember to press the PRINT button prior to giving the drug.

The following five rhythm strips are continuous.


Case #2

I pulled these strips from the archives of the LP12. The paramedic in charge of the call suddenly remembered to hit the PRINT button after he gave the adenosine.

Better late than never!


There was reportedly no change in the heart rhythm after the adenosine. The paramedic in charge stated that the post-adenosine heart rhythm looked identical to the initial rhythm.

Case #3

The paramedics in this case actually did capture 12-lead ECGs of the pre and post-adenosine heart rhythms. However, I’m only going to post the strips of the initial rhythm and the heart’s behavior during the administration of the drug.

Case #4

I pulled this case from the archives of the LP12. The treating paramedic did not capture a 12-lead ECG. He also didn’t push the PRINT button until the several seconds after the administration of adenosine.


So what do you think?

Take a look at these cases and ask yourself some questions.

How are they the same?

How are they different?

Assuming that the patient was symptomatic but hemodynamically stable, was adenosine indicated?

Does the behavior of the heart during the administration of adenosine give you any information as to the mechanism of the tachycardia?

Based on what you see, would you give adenosine again?

Would you switch to another drug?

Look carefully!

Looking forward to hearing your comments.

If you have rhythm strips laying around that were taken during the administration of adenosine, please scan them and email them to me at ems12lead@gmail.com.

I’m also interesting in any and all rhythm strips of attempted transcutaneous pacing (TCP)!

See also:

Narrow complex tachycardias – Part I

Narrow complex tachycardias – Part II

Narrow complex tachycardias – Part III

Narrow complex tachycardias – Part I

18 comments

I've come to dislike the term "SVT" (supraventricular tachycardia).

In the first place, it's not an arrhythmia. It's an umbrella term that covers a group of arrhythmias which require the AV node for their maintenance.

Most importantly, it includes sinus tachycardia!

For some reason, this is a difficult concept for many clinicians to grasp, partly because of myths passed on from generation to generation.

For example, my least favorite of all.

"If the rate is 150 or greater, it's SVT."

Does it mean that junctional tachycardia at a rate of 149 is not SVT? Does that mean that sinus tachycardia can't be 151? 161? 171? 

As Ray Fowler, M.D. often reminds us, the maximum sinus rate (give or take a few %) is 220 minus age.

I think the term "SVT" is less helpful than the term "narrow complex tachycardia" for figuring out a differential diagnosis.

Why?

Because at first glance, you won't always know it's SVT, but you should be able to figure out whether or not a tachycardia has narrow QRS complexes.

Regardless, there's no point in wasting precious time and energy making this more difficult than it needs to be.

A tachycardia is a heart rate equal to or greater than 100. A supraventricular rhythm originates above the ventricles. A narrow QRS rhythm has a QRS duration < 120 ms.

From the AHA ECC 2005 Guidelines, Part 7.3: Management of Symptomatic Bradycardia and Tachycardia:

Narrow–QRS-complex (SVT) tachycardias (QRS duration < 0.12 s) in order of frequency

  • Sinus tachycardia
  • Atrial fibrillation
  • Atrial flutter
  • AV nodal reentry
  • Accessory pathway–mediated tachycardia
  • Atrial tachycardia (ectopic and reentrant)
  • Multifocal atrial tachycardia (MAT)
  • Junctional tachycardia

In other words:

Sinus tachcyardia is, by far, the most common form of SVT!

This is important because the first arrhythmia you should consider when faced with a narrow complex tachycardia (or SVT) is sinus tachycardia!

And what antiarrhythmic do we use for sinus tachycardia?

All together now!

NONE!

We consider the Hs and Ts (as we should for any arrhythmia before reaching into the drug box) and we treat the underlying cause.

Let me give you an example.

An 18 year old female calls 9-1-1 and complains of palpitations.

EMS responds to the scene and finds her lying on the floor with absent radial pulses and a pressure of 80/40.

However, she's conscious, alert, and oriented to person, place and time.

The cardiac monitor is attached.


The paramedic in charge of the call diagnosed the heart rhythm as SVT.

An IV was started, and the patient received adenosine 6/12/12.

It didn't resolve the arrhythmia.

Why?

Because had they asked, the patient had an elective abortion earlier that day.

She had vaginal bleeding and soaked through at least 8 maxipads.

In light of this new information, what is the heart rhythm?

How about sinus tachcyardia?

How about appropriate and compensatory sinus tachycardia?

So what was the patient's problem? If you don't know, it's on this list and it starts with an H.


Do you see why it's important to include sinus tachycardia in the differential diagnosis for tachycardias?

Failure to consider sinus tachycardia can have serious consequences and put the patient at risk for iatrogenic harm.

See also:

Narrow complex tachycardias – Part I

Narrow complex tachycardias – Part II

Narrow complex tachycardias – Part III