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Archives for wide-complex-tachycardia

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77 year old female: Unresponsive – Discussion

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This is the discussion for 77 year old female: Unresponsive, if you have not read the case report we recommend you start there!

First, a hat tip to our readers who were unafraid to tackle this challenging scenario. Second, we were very impressed to see a number of readers correctly identify this challenging rhythm!

When we left off our crew was attending to an altered 77 year old female they picked up at a local skilled nursing facility. The patient's presentation seemed fairly routine for an Altered Mental Status rule-out.

However, once she was placed on the monitor her status became less clear:

We'll See What Shakes Out - Rhythm Strip

Given the fast rate and possibility for SVT, atrial fibrillation, or even ventricular tachycardia the crew needed more information.

When faced with an uncertain rhythm strip it is best to acquire more leads, and a 12-Lead is a wonderful way to do so:

We'll See What Shakes Out - 12-Lead

So what are we looking at?

  • Many readers pointed out the irregularly irregular tachycardia present in just about every lead.
  • Some readers pointed out the regular rhythm present in lead III.
  • Other readers noted the 3-Lead and 12-Lead were full of artifact.
  • Some readers gave up with cries of, "Treat the Patient! Not the Monitor!"

Ok, I can read the comments; tell me what it is!

The answer is easiest to see in the initial rhythm strip. A closer inspection reveals that when you try to line up Leads II and III, they do not even march out!

We'll See What Shakes Out - Rhythm Strip Marked Up

If we were to display a tracing of the pulse oximetry waveform, it would likely be more evident that only Lead III is providing a useful display.

So why did our patient's pulses not match with her cardiac rhythm?

And why did our patient have an irregular tachycardic rhythm in every lead but Lead III?

Both prehospital and hospital providers who routinely acquire electrocardiograms are familiar with artifact obscuring rhythm and 12-Lead interpretation. Common causes of artifact on the ECG include power line intereference, patient movement, and baseline wander. Lesser known causes of artifact on the ECG include cable failure, neurostimulators, lead placement over arterial pulse points, and electrode manipulation.

Cardiac monitors are designed with electrical filters which screen out intereference which is of a frequency that exists outside the range of physiologic parameters. Unfortunately, if the frequency of an artifact occurs at a near-physiologic rate it will be up to the provider interpreting the ECG to mentally "screen out" the interference.

In this case our patient has advanced Parkinson's disease, which is a degenerative neurological disorder affecting the central nervous system. The most visible symptom of this disease is the motor dysfunction and the characteristic tremors it produces in the periphery. As with any patient motion, it can cause artifact on the surface ECG.

If we take a closer look at Leads II and III we can see that the Parkinsonian Tremors present produced artifact at a rate of 250-300 and looked surprisingly like Atrial Fibrillation with WPW!

We'll See What Shakes Out - Lead II and Lead III

There have been multiple case reports of Parkinsonian Tremors mimicing ventricular tachycardia, ventricular fibrillation, atrial flutter, and supraventricular tachycardia. In one case, a comatose ventilated patient inappropriately received defibrillation for what appeared to be ventricular tachycardia!

When evaluating a patient with tremors it is best to place the leads in the Mason-Likar configuration, i.e. the limb leads are placed on the chest and abdomen. However, sometimes even that will not help and a switch to an anterior-posterior configuration (roughly approximating the pads position, or V4-RA and V8-LL) may be your only option to record a semi-clean tracing.

Remember, as prehospital providers it is important that we be able to explain our findings on the ECG because it may have a large impact on the patient's inhospital care.

Epilogue

Our crew was perplexed as to the discrepancy between the patient's pulse rate and that the rhythms in Leads II and III seemed, "out of sync". They contacted medical control for guidance and were advised to transport to the closest facility and to withold rate control while the patient's blood pressure was adequate.

Narcan was administered due to a persistently low SpO2 and pinpoint pupils. The remainder of the transport was unremarkable and the patient's vital signs remained relatively unchanged. A palpable pulse of 70 was weakly present at the radials while a monitored heart rate of 250-280 was given.

Upon arrival at the receiving facility the patient was noted to have converted to a normal sinus rhythm, with an RBBB and ocasional PVC's. However, during the course of her ED stay she had another "bout of tachycardia" on the monitor and was sent to the floor for observation. It is the opinion of this author that the patient's recurrent tachycardia was merely artifact, likely similar to that seen in her prehospital ECG's.

We hope you enjoyed this case as much as we did!

Posted by on August 22, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

65 year old male CC: Fall with injury – Conclusion

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This is the conclusion to 65 year old male CC: Fall with injury. You may wish to review the history and clinical presentation.

When we left off the patient was in severe heart failure with the following 12-lead ECG.

As we have mentioned before on several occasions, the most important thing when treating a patient with a tachycardia is to decide whether or not the tachycardia is causing the symptoms or the symptoms are causing the tachycardia.

In other words, you should try to rule out the possibility that it's a compensatory tachycardia. As this case clearly demonstrates, this can be very difficult! 

The crew felt that the differential diagnosis for this wide complex tachycardia (from most likely to least likely) was VT, 2:1 atrial flutter with LBBB, sinus tachycardia with LBBB, or some other SVT with aberrancy.

Due to the patient's instability, the treating paramedic felt there was little to lose and much to gain by attempting synchronized cardioversion. If the rhythm was VT or 2:1 flutter the patient's condition might improve dramatically. If it turned out to be sinus tachycardia with LBBB he'd be in the exact same position.

Attempt #1

Attempt #2

There appeared to be no change in the heart rhythm.

A report was given to online medical control and the patient was transported emergently to the hospital.

On arrival the patient was placed on BiPAP and started on a NTG drip.

Here was the 12-lead ECG on arrival.

The patient was given lopressor 5 mg slow IV push.

The conversion rhythm shows sinus rhythm at 92 bpm with left bundle branch block.

So, we now know that the patient probably had LBBB at baseline. However, without a heart rate histogram it's difficult to say whether or not this was 2:1 flutter that converted sinus rhythm or sinus tachycardia that was slowed down with the lopressor.

This is often overlooked in the emergency setting but in the inhospital setting it's very important to document the onset or termination of an arrhythmia for this very reason.

The patient's SpO2 came up above 90% and the patient became more alert and was attempting to communicate by the time EMS was done writing their report. No further information is available.

Posted by on July 2, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

65 year old male CC: Fall with injury

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Here's a very interesting case submitted by a faithful reader who wishes to remain anonymous. Some changes have been made to preserve patient confidentiality.

EMS is called to a local breakfast restaurant for a 65 year old male who fell in the parking lot. He was reported to have suffered a head injury.

On arrival the patient is found sitting in his car. He appears critically ill. Skin is pale and diaphoretic. Nail beds are blue. The patient's level of consciousness is significantly diminished. His shirt and pants are wet and it's not clear if he was incontinent of urine or spilled a drink on himself. He has audible expiratory rales without the need for a stethescope. 

The patient states that he tripped and fell. His wife states that he was "fine" prior to falling but she does not impress EMS as a good historian. When asked about his history she says, "heart." 

The head appears atraumatic with the exception of some abrasions to the face. He admits to head pain "all over" and keeps muttering "please take me to the hospital."

Due to the patient's diminished level of consciousness it is not possible to clear the cervical spine with any established criteria. However, the paramedics conclude that the patient cannot be laid flat and elect to defer spinal immobilization. The patient is placed on the gurney with the head elevated and vital signs are assessed.

  • RR: 30
  • HR: 148
  • NIBP: 150/77
  • SpO2: 58 on room air

The patient is placed on a NRB mask @ 15 LPM. The chest is exposed and no chest trauma is apparent. Breath sounds: rhonchi and rales bilaterally

The patient is given a dose of SL NTG and loaded in the back of the ambulance. At this point the patient appears peri-arrest.

The cardiac monitor is attached.

A 12-lead ECG is obtained.

What would you do next?

See also:

65 year old male CC: Fall with injury – Conclusion

Posted by on June 27, 2012 • Filed under: ems-topics, patient-management, Training • Tagged: , , , , , ,

Snapshot Discussion: 32 year old Male–Chest Discomfort

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Here is the discussion for the Snapshot Case: 32 year old male–Chest Discomfort. Sorry for the delay.

If you recall, we have a young patient, a 32 year old male, with a heart rate too rapid to count. He is alert and oriented, and has a good pressure (126/70). He has been in the following rhythm for at least two hours:

 

So, what do we know about the rhythm? It is wide and fast, with a rate of 262. Since wide + fast = VT until proven otherwise, you couldn't be faulted for running it as VT.

Unfortunately as a "Snapshot Case", we don't know the outcome of this patient. However, our mission was to come up with a differential for this rhythm, so I'll share some thoughts:

  •  A-Flutter with 1:1 conduction: With rates approaching 300, it would be appropriate to consider it. I don't see any evidence of flutter waves though.
     
  •  SVT with LBBB aberration: The QRS is wide, but not that wide at 130 ms. V1 is negative, and there are monomorphic R waves in leads I and V6.   This is typical morphology for LBBB. Also, let's look at a clear QRS, from lead III:

           

           You can see that the initial downstroke of the QRS is sharp, and occurs in less than 20 ms. This as well favors SVT/LBBB over VT. If it is SVT, it could be either AVRT (WPW) or AVNRT.

  • VT: The rhythm is wide and fast, and it is possible that this is VT. The QRS is not that wide but it could still be fascicular VT (but I would have expected RBBB morphology) or RVOT VT (which would not have RBBB, but then I would expect the inferior leads to be positive not negative). It doesn't seem to meet any criteria that rule in VT (no initial R wave in aVR, concordance, etc), but that does not rule out VT. And then there is the sharp initial deflection of the QRS, instead of a slower activation. And of course the patient's age and history do not favor VT.

All in all, I think any of the above are reasonable in this case. We can't know for sure, but I lean towards SVT with LBBB aberration, probably rate related, unless he happens to have LBBB as a baseline.  You may have other thoughts, and I'd love to hear them!

As far as treating the patient, his mental status is good, his pressure is good, and he has been tolerating this rhythm for at least two hours. I think he's a good candidate for a trial of Adenosine, which might reveal the answer. If that fails, there is Amiodarone, cardioversion, or diesel as far as my protocols go. 

With no clear cut answer, I'm sure you all will have some good thoughts to add to this discussion. Sometimes, we just don't know for sure, but we still have to hone our skills of considering our differentials.

Thanks for reading, and I'm looking forward to your comments!

Posted by on May 17, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , , , , , ,

Discussion for 90 year old male CC: Chest pain– Revisited

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We are revisiting the Discussion for 90 year old male CC: Chest pain.  You may wish to review the case.

You may recall we pointed out that the VT appeared be regularly irregular, with alternating cycle lengths:

What follows is a "Guest Post" by Jason Roediger, CCT/CRAT, and Ken Grauer, M.D. (www.kg-ekgpress.com):

"The rhythm represents VT for all of the morphologic reasons discussed in your explanation. The reason for the repetitive regular irregularity of this ventricular rhythm is that the tracing represents VT with retrograde 3:2 Wenckebach Exit block out of the ventricular focus. The discharge rate of the ectopic ventricular focus is ~240/minute.

This results in a manifest ventricular rate that is about 2/3 the presumed discharge rate and reduces the manifest rate to ~160/minute. Note the characteristic Wenckebach periodicity conducting retrograde (with a 3:2 ratio) out of the ventricular focus in the laddergram below. FINAL point: in addition to the bizarre marked axis deviation, the entirely negative QRS in V6 with delayed nadir and other morphologic clues you state in support of the diagnosis of VT-WPW can be ruled out by the negative QS complexes in V4-V6 (Brugada)."

 

Many thanks to Jason and Ken for their insightful analysis. We are always learning!

 

 

 

 

Posted by on February 13, 2012 • Filed under: ems-topics, patient-management • Tagged: , , , , , ,

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

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

If you recall from the case, our crew was performing an interfacility transport of a 17 year old male with a rapid, irregular tachycardia which required cardioversion.

At the receiving facility he was diagnosed with Wolff-Parkinson-White Syndrome (WPW).  After undergoing ablation, he is expected to do just fine.

What exactly is WPW Syndrome?

In 1930, Wolff, Parkinson and White described a series of  young patients who had ECG findings of a bundle branch block pattern, short PR interval, and paroxysms of tachycardia.

In WPW Syndrome, patient's have a congenital abnormality involving the presence of abnormal conduction tissue between the atria and ventricles associated with supraventricular tachycardias. It is thought to affect about 0.1 to 3 per 1000 in the general population.

WPW is a preexcitation syndrome, where impulses are transmitted from the atria to the ventricles by way of an accessory pathway–or AP–instead of the atrioventricular conduction system.

Usually, this AP is the "Bundle of Kent", which connects the atrium directly to the ventricle. Unike the AV node, this AP transmits the impulse to the ventricle without delay, and at least a portion of the ventricular myocardium is activated before the impulse can reach the ventricles through the normal AV pathway. This is what creates the "pre"-excitation pattern:

It is this preexcitation that causes the slurred start of the QRS, known as a Delta Wave, as part of the ventricle is activated early. As this slurring occurs earlier than normal in the cardiac cycle, the PR interval will be short.   As the rest of the ventricular myocardium is activated via the normal AV conduction system, the rest of the QRS may be normal.

We can clearly see this WPW pattern on the prehospital 12 Lead of our patient:

Classic ECG findings that are associated with WPW Syndrome:

  • Presence of a short PR interval, less than 120 ms
  • A widened QRS complex with a delta wave, the slurred onset of the QRS waveform
  • Secondary ST-T wave changes

The amount of ventricular myocardium activated early by the AP will determine the size of the delta wave and the amount of PRi shortening. 

Another important consideration in WPW is that the secondary ST-T changes of pre-excitation can be confused with an MI.  As with other mimics of AMI, these changes involve a widened QRS/ST angle, i.e. ST/T wave changes opposite the direction of the QRS complex.  In fact, repolarization abnormalities are very common with WPW, and they often look like the changes associated with injury and ischemia commonly known as a pseudoinfarction pattern.

What does it mean for our patients?

While someone with WPW can remain asymptomatic for some time, the presence of an accessory pathway can result in arrhythmias. Patients may present with symptoms from mild chest discomfort, to palpitations with or without a syncopal episode, or even sudden cardiac death. As in our patient, symptoms are usually accompanied by a decreased tolerance for activity.

SVT, atrial fibrillation and atrial flutter are the most common arrhythmias associated with WPW. Because two different pathways are available a "loop" can be formed causing a reentrant tachycardia.

Depending on which direction the "loop" is traveling, there may be no part of the ventricular myocardium which is preexcited (orthodromic, 95% of cases).  However, if the direction of the loop is one in which the impulse travels first down the AP, and then back up the AV node in a retrograde fashion (antidromic), the ventricles are almost fully activated by the AP, and the QRS will be abnormally wide (5%).

Regardless of which direction the loop travels, a regular reentry tachycardia will rely on the AV node to continue.  Because of this, AV blocking maneuvers or medications can terminate the rhythm.

When a patient with preexcitation syndrome develops atrial fibrillation this is life threatening. Because of the potential for extremely fast conduction across the bypass tract, the rate may sometimes approach 300/min.

How do we recognize it?

Atrial fibrillation and WPW is an irregularly irregular tachycardia, with wide and bizarre complexes of differing morphologies, and an R-R interval that can be 250 ms or less. 

As in our patient's ECG above, some impulses are transmitted through the the AP and some through the AV node, hence the varying morphogies. If we knock out the AV node with antiarrhythmics, all that will be left is the accessory pathway, which will gladly conduct the rapid impulses of the atria directly through to the ventricles.

Without the protective phsyiologic blocking of the AV node, the result may be ventricular fibrillation! Adenosine, beta blockers, and calcium channel blockers are all absolutely contraindicated. 

The best treatment for an unstable patient with atrial fibrillation and WPW is electrical cardioversion.

Once identified and appropriately treated, WPW is associated with an excellent prognosis. For more information about WPW Syndrome, click here.

Stay tuned for Part II of this conclusion where we delve further into this important syndrome!

Posted by on February 6, 2012 • Filed under: ems-topics, patient-management, training-development • Tagged: , , , , , , ,

Discussion for 90 year old male cc: chest pain

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I hope you all had happy holidays!

Here is the discussion for 90 year old male cc: chest pain.  You may wish to go back and review the case.

So, let's get into the case!  There are the usual questions we need to answer as we try to determine the rhythm.  Is the rhythm wide or narrow? Regular or irregular? Is there atrial activity?

It is also important to note that there were a couple confounding factors.  The data quality was not great, which is never helpful. The crew tried to get a better tracing, and this was the best they could get.  As a side note, refer back to this post where Tom Bouthillet outlines his approach to achieving a high level of data quality in his tracings. Sometimes, there is nothing we can do to improve the data quality on a particular patient.  But it is important to make excellent data quality a priority.

Another factor in this case was that a couple of leads, notably V2, looked unusual and narrow, and could throw off someone's interpretation.

So, back to our initial 12 lead:

It is a wide complex tachycardia, at a rate of about 150, which appears at first blush to be regular.  Our differentials include:

  • VT
  • Sinus tach with aberrancy
  • SVT with aberrancy

As far as the wide complexes go, there are no real signs of atrial activity, although as some pointed out, in lead V2, there appears to be something resembling an atrial wave preceding a narrow QRS.  Let's talk about that piece, because many of you put a lot of stock in V2 looking narrow.

We should remember that when considering whether the rhythm is narrow or wide, we look at the widest complex we can find and use that for our measurement, not the narrowest. Why? Because from time to time, part of the QRS in a particular lead may be isolectric, and make the QRS appear narrow when in fact it is not.  Consider the following:

If we draw a line connecting the beginning of the QRS complexes in these leads, we can see that what appears to be a narrow QRS and possible P wave in lead V2 is actually part of the wide QRS as measured against the other leads! If you use this method on lead III, you will also find that what appeared to some as an inverted P wave, is actually part of the QRS as well. This is precisely why we use the widest complex to determine QRS duration and not a narrow one.

What was also confounding was that the rhythm did not look regular, but regularly irregular. If you look closely at the 12 lead and the rhythm strip, you will see that there are two alternating cycle lengths, a short R-R followed by a longer R-R at 340 ms and 380 ms respectively.  Thanks to Christopher Watford for the following graphic illustration:

While the default for a regular WCT is to assume VT unless proven otherwise, I have to admit that this ECG left me feeling uncertain, because of the irregularity. We have to be extremely concerned about an irregularly irregular WCT, such as A-Fib with WPW, but this rhythm is not irregularly irregular so that is off the table.

Because this ECG seemed somewhat unusual to me, I took the liberty of asking Stephen Smith, M.D., of Dr. Smith's ECG Blog to take a look at it.  He also ran it by his associate, renowned ECG Master K. Wang, M.D. for analysis:

From Dr. Smith:

"I believe this to be VT.  Much VT does not have concordance, and aVR has a wide, monophasic initial R-wave".

Although as yet unvalidated, Dr. Smith prefers Sasaki's criteria for VT, and you can find a great post on his blog that deals with Sasaki's criteria here.  As to the alternating cycle lengths, he had this to say: 

"If there were some consistent variation in the QRS morphology, I would say that there is something else going on.  But there is no such consistent difference between QRSs after 340 ms vs 380 ms…So I would just have to say that it is VT with grouped beating, although I admit that is strange."

From Dr. K. Wang:

"I agree it is VT. As you know, if either of the initial or the last part of the QRS is isoelectric in a given lead, the QRS can be narrower than what it actually is in that lead (it can never be wider than what it actually is).  Judging from the other leads taken simultaneously, that is what happened.  Also look at lead III. There seems to be a negative P wave in front of each narrow QRS, but again, judging from other leads taken simultaneously, what appears to be a negative P wave is already within the wide QRS of other leads and it is part of the QRS, not a P wave. That is what i think."

My sincere thanks to these two ECG greats for their contributions to this case.  

One more caveat with regards to using criteria for VT which you have heard early and often on this site:  While it is ok to use the criteria to rule in VT, the failure of the criteria to rule in VT does not rule out VT!!!  VT can look like almost anything, so don't fall into the trap thinking that if it doesn't meet "criteria", or a certain morphology, it can't be VT.  It most certainly can.

Now that we have settled on VT, how do we treat this patient? Where will we transport him? Well, if you believe that the VT is the primary problem, and that the patient does not need PCI, it certainly seems reasonable to go to the closest facility ten minutes away rather than the PCI facility.  

As for the patient, he is alert and oriented, has a pressure of 130/90, but has substernal "chest pressure".  Is this patient stable? Do we treat with antiarrhythmics? Cardiovert? Or do nothing?

While you can say that under ACLS guidelines, the chest pressure makes this patient unstable, However, I do think there is a difference between "chest pressure" and "crushing chest pain."  From the presentation the patient was ambulatory, in "no obvious distress", apparently tolerating the VT.  I think it would be fair to say the patient is stable enough to not need immediate cardioversion in the field.

If we decide the patient does not need to be immediately cardioverted, antiarrhythmics become the other choice.  His pressure is good, and the risk of giving amiodarone or another antiarrhythmic is that we cause the very hypotension and instability that we are trying to avoid.  I think it is reasonable prepare for deterioration, but at the same time monitor closely and hold off on treatments that could be detrimental to the patient until ED arrival.

To me, this is another case that illustrates the difference between decisions we learn in class and decisions we have to make in real life.  Patients do not read our text books or attend ACLS.  They present in that grey-not-so-sure zone where their stability is delicately balanced against what we do and what we decide not to do.

In this case, the crew was unable to gain IV access. They applied the pads as a precautionary measure, and transported the patient to the ED without further incident. After arrival at the ED, IV access was secured.  The patient was treated with a trial of antiarrhythmics, then successfully cardioverted.

Thoughts and comments?

Posted by on January 3, 2012 • Filed under: ems-health-safety, ems-topics, patient-management, Training, training-development • Tagged: , , , , , ,

90 year old female CC: Seizure – Conclusion

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This is the conclusion to 90 year old female CC: Seizure. Be sure to start there first!

When we left off, we had completed our initial assessment of a 90 year old patient who, based on bystander accounts, had a seizure. She is pale, cold to the touch, and feels lethargic.

During our assessment she had an increase in her pulse rate and a 12-Lead ECG was obtained:

This is a wide complex tachycardia at a rate of about 200. Our differentials include ventricular tachycardia, SVT with aberrancy, and preexcited wide complex tachycardia from Wolff-Parkinson-White. Regardless, all wide complex tachycardias should be treated as V-Tach until proven otherwise!

When I first saw this ECG, I found the computerized interpretation very interesting because it is almost 100% incorrect.

A quick look at the measured rate shows the cardiac monitor's interpretation cannot be trusted. Using the big block method, the rate is between 150 and 300 bpm, and when calculated is around 206 bpm.

Additionally, the cardiac monitor believes the rhythm to be atrial fibrillation with a rapid ventricular response. However, as many of our astute readers noted, this is clearly ventricular tachycardia. 

An initial R-wave in aVR is over 98% specific for ventricular tachycardia1!

Based on Patrick J. Lynch's medical illustration; Creative Commons Attribution 2.5 License 2006

If we look at lead aVR, we see the ventricles are depolarizing towards this lead. Clearly this cannot be a supraventricular rhythm such as atrial fibrillation or SVT. In those cases the initial axis will nearly always point away from aVR.

The paramedics in this case correctly diagnosed ventricular tachycardia as well, and began their treatment in the field.

They initially administered 100 mg of lidocaine, however, it had no effect.

Next they elected to use synchronized cardioversion and premedicated the patient with 20 mg of etomidate.

A synchronized shock of 100 J was administered, while the patient was sedated, with a return of a sinus rhythm. A post-conversion 12-Lead was obtained:

This 12-Lead ECG shows a sinus rhythm with a 1st degree AV block and PVCs. There does not appear to be evidence of a STEMI, electrolyte disturbances, or pre-excitation from WPW.

The patient was packaged and had an unremarkable transport to a nearby hospital. The patient was admitted for observation and discharged without incident.

This case highlights a few key points:

  1. The computerized interpretation is no substitute for a human's interpretation.
  2. Wide complex tachycardias should be treated as ventricular tachycardia in the field.
  3. An initial R-wave in aVR is diagnostic of ventricular tachycardia.

What are your thoughts on the case?

[1] Vereckei A, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm; 2008 (5): 89-98.

Posted by on November 14, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

90 year old female CC: Seizure

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This interesting case is thanks to Dana from Redmond Medic One, we hope you enjoy it as much as we did!

You're dispatched with a nearby engine company to an assisted living facility for a 90 year old female who has had a seizure. Dispatch notes indicate the patient is alert at this time.

You're by the officer off the engine outside, who leads you in to the dining area. You see an awake elderly female, seated in a chair, being assessed by the engine company. Her husband states she had a seizure which, "lasted maybe 10-15 seconds, her arms and legs were jerking the entire time."

While your partner gets a report from the firefighters, you introduce yourself and ask the patient how she feels.

"Well, I felt ok earlier. Never had this happen before."

  • PMHx: COPD, diabetes, "heart attack", CABG, dementia, "mass in my lung"
  • Allergies: NKDA
  • Medications: Coumadin, "nebulizer"
  • Last ins/outs: was eating dinner when this happened
  • Events: sudden onset, tonic/clonic activity, no apparent post-ictal period

Your partner relays the initial vitals:

  • Skin: pale, cold, dry
  • Pulse: 123, irregular
  • BP: 94/64
  • Resps: 24, unlabored
  • SaO2: 96% on 3 L/min via NC
  • BGL: 188 mg/dL (10.4 mmol/L)
  • Temp: 99.7° F tympanic

As the monitor is turned on it begins chiming. Electrodes are quickly added for a 12-Lead.

When asked about the rapid heart rate, her husband states, "she's had a fast heart before when she takes her nebs, but never this fast."

One of the firefighters obtains a repeat set of vitals:

  • Pulse: 200, weak radials
  • BP: 92/68
  • Resps: 16
  • SaO2: 98% on 3 L/min via NC

You're less than 10 minutes from 2 hospitals, including a PCI capable facility.

Your patient states dryly, "I feel pretty tired."

What is your interpretation of the rhythm and do you agree with the monitor's interpretation?

Is this a load and go situation?

What do you do next?

Posted by on November 7, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , ,

Discussion to 60 year old male CC: “I don’t feel well”

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This is the discussion for 60 year old male CC: "I don't feel well".

Go back and familiarize yourself with the history and clinical presentation because it's important to the case (as it always is).

Here is the rhythm strip and 12-lead ECG that was presented.

You may recall from my series on ineffective or inappropriate ICD shocks rhythm analysis for patients with an implantable cardioverter-defibrillator can be challenging.

That's because patients with sick hearts often suffer from both atrial fibrillation and bundle branch blocks which predisposes them to "wide and fast" rhythms.

If you've taken nothing else away from the EMS 12-Lead blog I hope you've taken away the message that "wide and fast" is VT until proven otherwise! 

Granted, irregular wide and fast rhythms are a special case. In the first place you avoid adenosine according to the 2010 AHA ECC Guidelines. That's because atrial fibrillation is unlikely to respond to adenosine, not to mention that giving adenosine to a patient with WPW and atrial fibrillation can precipitate VF.

So let's look at the differential diagnosis of the wide complex tachycaria.

Could it be VT?

Sure. It's rare for VT to be irregular but it's certainly not impossible. We need to remember that the patient has received an ICD so one assumes the patient is at high risk for malignant ventricular arrhythmias. "But the axis is normal!" you might say. Yes, but as I've mentioned so many times before, it's an EMS myth that VT always shows an extreme axis deviation. In fact, LBBB in lead V1 with a normal frontal plane axis is normal for VT orignating in the right ventricular outflow tract.

Could it be AF with LBBB and RVR?

Yes. This is entirely possible. Quite often irregular wide complex tachycardias turn out to be AF with RBBB, LBBB, or nonspecific IVCD. It's a bit unusual but certainly not impossible for LBBB to show a normal frontal plane axis.

So, if it could be either VT or "SVT" (a term I don't care for) with aberrancy (or preexisting bundle branch block) then how should we treat the patient? Should we treat the patient at all?

When faced with a situation like this I think it's far more important to "risk stratify" the tachycardia rather than "diagnose" it. In other words, remember the first rule of medicine: "Do No Harm!"

Above all else, avoid IV medications that could kill the patient if it turns out to be VT.

So why isn't the ICD shocking? Because the rate isn't fast enough. It's not unusual at all for patients with an ICD to present with a wide complex tachycardia below the rate limit that initiates cardioversion or defibrillation.

So what else happened in this case?

En route to the hospital an additional 12-lead ECG was captured and several more rhythm strips.

This 12-lead ECG reveals an important problem with prehospital 12-lead ECGs. They often crop the S-wave, especially in the right precordial leads (V1-V3) which can makes it impossible to compare the ST-segments to the depth of the S-waves (rule of proportionality).

The patient was delivered to the emergency department where the following 12-lead ECG was taken.

Now we can see the depth of the S-waves in leads V1-V3 and there's a problem (beyond the fact that the precordial leads have been placed differently on the patient's chest).

If this is a left bundle branch block then excessively discordant ST-elevation is present in leads V2 and V3 which indicates acute STEMI.

So what was the outcome?

All we know for certain is that the patient received successful synchronized cardioversion in the emergency department. The paramedic who submitted the case was told by the RN in the emergency department that the QRS complexes were narrow after the cardioversion (which would support a ventricular origin). However, we don't have a post-cardioversion 12-lead ECG to confirm.

We also don't know whether or not the patient ruled-in for AMI. But I certainly wouldn't be surprised! 

Posted by on June 24, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,

60 year old male CC: “I don’t feel well”

55 comments

Here's an interesting case from an faithful reader who wishes to remain anonymous. Some changes have been made to help preserve patient confidentiality.

This is a 60 year old male, who activated EMS for not feeling well.

The call came in from a home way out in the county, and although it was dispatched as a low acuity sick call, the responding unit ran emergency traffic to the home.

On arrival, a BLS fire unit was on scene, triaging the patient green.

Report from the firefighter EMT was as follows: Patient contacted EMS for slight shortness of breath, we have him on 15 liters O2 NRB mask, he just had a pacemaker put in three days ago.

Patient is alert and oriented x4,

VS as follows:

  • BP-180/90
  • RR-28
  • O2 sat- 98% on non rebreather (RA sat was 92%)
  • Pulse- around 100

Patient contact reveals the patient sitting upright in his recliner, speaking in full sentences.

He states that she is absolutely not going to the hospital no matter what!

On further questioning, patient says he has been feeling a “funny feeling” in addition to a little shortness of breath for the past hour.

  • Onset of one hour
  • Exertion makes it worse  
  • Severity is a 2/10 
  • Was walking to the restroom when the funny feeling started 

It feels like its getting better as long as he stays still. He hasn’t taken any of his meds today.

Questioning of family members reveals that he received multiple prescriptions but hasn’t had them filled yet. He has been off all of his meds since he left the hospital two days ago.

They are unsure of all of the medications but know that they included:

  • Coumadin
  • Amiodarone
  • Lasix 

Patient has no drug allergies.

Hx of:

  • Diabetes
  • HTN
  • CAD
  • A-fib
  • Pacemaker/ICD placed three days ago

Ate a big meal last night

Bilateral breath sounds are clear and slightly diminished.

EMS crew convinces patient to go to the local hospital 20 minutes away just to get checked out.

Patient finally agrees but is adamant about walking to the truck or else he is not going.

During the trip to the truck, patient begins to experience severe dyspnea and says that he needs to sit down.

The patient sits down on the cot for transport to the unit. Audible rales are heard when the patient begins complaining of the severe dyspnea.

In the truck, patient is attached to the cardiac monitor and a 12 lead is performed.

What is the differential diagnosis for this heart rhythm?

What do you think is going on?

How would you treat this patient?

See also:

Discussion to 60 year old male CC: "I don't feel well"

Posted by on June 14, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

74 year old female CC: Chest pain – Conclusion

29 comments

This is the conclusion to 74 year old female CC: Chest pain.

As usual I enjoyed reading the comments! My goal is to get you guys thinking and it’s nice to see you discuss “stable versus unstable”, the need for sedation, and the importance of considering the Hs and Ts!

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

This is an unstable wide complex tachycardia which we must presume to be ventricular tachycardia.

We presume it is ventricular tachycardia because that is our default ECG diagnosis for “wide and fast” rhythms.

The fact that she has a history of MI makes VT all the more likely.

We need to avoid the temptation to over-think heart rhythms like this! As much as 12-lead ECGs have advanced the EMS profession, this is one small area where we have taken a step backward, IMHO.

Before 12-lead ECGs a “wide and fast” rhythm like the one you see above was VT. Now you can’t turn around without someone labeling a clear-cut case of VT as “SVT with aberrancy.”

However, in this case (hopefully) the debate is irrelevant because the patient is unstable.

Why?

Because the patient is experiencing chest pain, radial pulses are absent, the patient looks “shocky” and the level of consciousness is diminished.

Immediate synchronized cardioversion is indicated. That’s exactly what this crew decided to do.

About a minute later the rhythm started to stabilize.

What should the crew do next?

If you said, “Obtain a 12-lead ECG!” move to the head of the class!

Now we have some insight as to why this patient was in VT!

Vital signs are re-assessed.

RR: 20
Pulse: 86
BP: 138/92
SpO2: 100 with O2 via NRB @ 15 LPM

If this was your patient what would you do next?

Posted by on April 25, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

74 year old female CC: Chest pain

51 comments

Here’s another great case from Michael M.

EMS is called to the residence of a 74 year old female with a chief complaint of chest pain.

On arrival the patient is found lying on her side in bed. She is conscious but lethargic and it’s clear she has vomited.

Skin is cool, pale and diaphoretic. She looks very ill.

The spouse states that he “thinks it’s her heart.”

Past medical history: MI x 3 years ago with stents, HTN, high cholesterol
Meds: ASA, atenolol, simvastatin, spironolactone

Vital signs are assessed.

RR: 24 shallow
Pulse: radial absent, carotid very rapid
NIBP: unable to auscultate
SpO2 does not register

The cardiac monitor is attached.

Is there anything else you’d like to know about this patient?

What is your interpretation of the ECG?

How would you treat her and why?

See also:

74 year old female CC: Chest pain – Conclusion

Posted by on April 22, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , ,

78 year old male CC: Dizziness – Conclusion

18 comments

Many apologies for the delay, your author worked a 48 over the weekend and was unable to get time to type up this article!

This is the conclusion to 78 year old male CC: Dizziness.

There were so many great comments on this case, including some great discussion on classifying wide complex tachycardias!

All Hallows' Eve - Initial Strip

The first rhythm strip clearly shows a wide complex tachycardia. An important point to note is the rate is well above the predictive maximal sinus rate for our patient’s age. This rules out sinus tachycardia with a bundle branch block. At this point, providers may ask themselves if this is Ventricular Tachycardia or SVT with aberrancy.

If we take a look at the 12-Lead ECG, we can look for signs which rule-in Ventricular Tachycardia.

All Hallows' Eve - Initial 12-Lead ECG

We have a QRS duration of ≥140 ms, amplitude of R > R’ in V1, a non-specific IVCD, and an R wave in aVR; all of these point to Ventricular Tachycardia. Additionally, the patient has a significant cardiac history. Some readers noted the normal axis and what potentially are P- or F-waves. I would offer that these points are moot: from this ECG alone we cannot rule-out Ventricular Tachycardia.

Wide and fast is Ventricular Tachycardia until proven otherwise.

Besides, our patient is unstable and needs immediate synchronized cardioversion.

Which is just what the crew did! Given the potential for atrial flutter, the initial cardioversion setting was 50 J. With no conversion they increased the energy to 100 J.

All Hallows' Eve - Synchronized Cardioversion at 100 J

No change was noted. A supervisor on scene mixed up 150 mg of amiodarone and began a 10 minute infusion. After no change with two cardioversions, the decision was made to move the patient to the unit.

In the back of the truck a sudden change of responsiveness was noted. The energy setting was increased to 150 J.

All Hallows' Eve - Synchronized Cardioversion at 150 J

At 150 J the cardioversion was successful!

All Hallows' Eve - Post-cardioversion

A ghost made off with the final 12-Lead; true story.

The post-cardioversion 12-Lead showed diffuse ischemia and the patient ended up receiving an Automatic Implantable Cardioverter-Defibrillator. Great job by the responding crew!

UPDATED 12 APRIL 2011

Jeremy asked how the QRSd was measured in this case. Usually I try and find the earliest onset and match that with the latest end in a grouping of leads, then use the largest value to map each grouping. The following image may help illustrate this point.

All Hallows' Eve - QRSd Marked Up

I first saw this visualization on Dr. Smith’s ECG Blog, where he uses it for more than just determining the QRS duration in “Cardiac Arrest, Wide Complex, Is it STEMI?” and “Wide Complex Tachycardia; It’s really sinus, RBBB + LAFB, and massive ST elevation”.

See Also:
Differential diagnosis of wide complex tachycardias – Part I
Differential diagnosis of wide complex tachycardias – Part II
Differential diagnosis of wide complex tachycardias – Part III
Differential diagnosis of wide complex tachycardias – Part IV
Differential diagnosis of wide complex tachycardias – Part V
Differential diagnosis of wide complex tachycardias – Part VI

Posted by on April 11, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , ,

78 year old male CC: Dizziness

49 comments

Hot on the heels of the last case is another great case study, this one is from a reader named Baby Medic. I hope you enjoy it!

It is a busy Halloween night, when you and your EMT partner are dispatched to an outlying address in your service area for a 78 year old male complaining of dizziness.

After navigating a mess of rural farm roads, you arrive at a small house off a long dirt driveway. Out front you are met by the patient’s wife, who frantically directs you inside and down to the basement. There you find your patient, a noticeably larger man, sitting in a recliner with one hand on his chest. As your partner kneels down to obtain vitals, you ask him what is going on.

Onset: Chest pain started about 15 minutes ago, while watching TV
Provocation/Palliation: Nothing makes it better or worse
Quality: “Something is pushing on my chest”
Radiation: The pain is only localized retrosternal
Severity: 10 of 10
Timing: The pain is constant

Your partner briefly interrupts to say he cannot find a radial pulse. You continue with your history.

Allergies: NKDA
Medications: He can’t remember (you send his wife to find them)
Past Medical History: Extensive cardiac history, including CABG, HTN, and he was recently discharged from the hospital after carotid artery surgery
Last Ins/Outs: Normal dinner
Events: “Sitting in my chair, watching TV, got real dizzy and then the pain started.”

Your partner anxiously relays the patient’s vitals while he attaches the cardiac monitor.

Pulse: Could not palpate a radial pulse
BP: 82/54
RR: 24, labored; lungs clear and equal bilaterally
SaO2: Beeps and displays E34

A physical exam reveals no JVD, a soft, non-tender obese abdomen, and good pulse/sensory/motor in all extremities. The only remarkable feature is dusky, cool, diaphoretic skin.

An alarm sounds on the cardiac monitor as the initial rhythm strip is printed.

All Hallows' Eve - Initial Strip

Your partner acquires a 12-Lead ECG while you interpret the rhythm strip.

All Hallows' Eve - Initial 12-Lead ECG

What rhythm is present? Does the 12-Lead ECG help with your interpretation?

You’re 20 minutes from the nearest hospital and 45 minutes from a PCI capable facility. How would you treat this patient?

See Also:
78 year old male CC: Dizziness – Conclusion

Posted by on April 7, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,

Not So Fast!

2 comments

The January 2011 EMS 12-Lead column has been posted at EMS1.com.

Not So Fast!

Enjoy!

Posted by on January 6, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , ,

41 year old female CC: Chest pain

40 comments

Here’s a case submitted by Bob Sullivan from New Castle County EMS.

EMS is called to the residence of a 41 year old female with chest pain.

Onset: Sudden while sweeping the floor
Provoke: Nothing makes the pain better or worse
Quality: Tightness
Radiate: The pain does not radiate
Severity: 8/10
Time: 20 minutes prior to EMS arrival

Past medical history: MI, Pacemaker/ICD
Medications: amiodarone

Vital signs:

RR: 22
Pulse: Very rapid
BP: 150/80
SpO2: Not registering

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is placed on O2 via NRB @ 15 LPM and IV access is established.

What do you think the paramedics should do next?

*** UPDATE ***

Paramedics give 150 mg amiodarone over 10 minutes via piggyback infusion.

The patient’s BP drops to 90/48 and the patient’s clinical status is observed to deteriorate.

Synchronized cardioversion is performed.

The rhythm is now narrow complex but extremely fast and unstable.

The ICD delivers a shock and the patient is observed to be in VF.

After waiting a few seconds (to see what the ICD is going to do) paramedics shock the VF.

The rhythm starts to stabilize and the patient’s BP comes up to 142/74.

Are you ready to drop this patient off at the emergency department?

Posted by on December 13, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,

12 year old male CC: Palpitations

42 comments

Here’s a case submitted by Bob Sullivan, NREMT-P from New Castle County EMS in Wilmington, DE.

The case occurred six years ago so certain details are missing. However, there is more than enough here to discuss the most relevant points about the case.

The patient was a 12 year old male whose only complaint was palpitations.

The patient’s pulse was extremely rapid. However, he appeared to be perfusing adequately and the blood pressure was stable.

A 12-lead ECG was captured.

And another.

Online Medical Control was contacted and the treating paramedic was advised to watch the patient’s blood pressure and cardiovert if the patient became unstable.

The patient converted after the ambulance went over a bump. Unfortunately, a post-conversion 12-lead ECG was not recorded.

At the time, Mr. Sullivan was a new paramedic. He states that his co-workers felt that he should have given adenosine, since a 12 year old “could not be in VT.” He also mentions that he’s gotten different interpretations from each doctor he’s shown it to.

The case has been bothering him ever since.

What do you think is the best field treatment for a patient like this?

What do you think of Online Medical Control’s advice?

What do you think is wrong with this patient?

Posted by on March 15, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

68 year old male CC: Chest Pain

44 comments

Here’s another great case submitted by Robert Bees.

EMS is called in the very early morning to a 68 year old male complaining of chest pain and shortness of breath.

On arrival, the patient is anxious and appears acutely ill. He is oriented to person, place, and time.

Skin is cool, pale, and diaphoretic.

The patient feels light-headed and admits to nausea but has not vomited.

Onset: While sleeping
Provoke: Nothing makes the pain better or worse
Quality: Poorly localized heavy pressure
Radiate: The pain does not radiate to the arms, back, neck or jaw
Severity: 8/10
Time: Patient states he occasionally “feels bad” but “not like this”

Past medical history: MI with stents x 2 years ago.

Medications: ASA, Lipitor, Tenormin, NTG

Patient states he took NTG x 1 prior to EMS arrival which made him “feel worse”

Vital signs:

Resp: 22 shallow
Pulse: 140
BP: 88/54
SpO2: 92 on RA

Breath sounds: rales – patient becomes very light-headed sitting up

The cardiac monitor is attached.

A 12-lead ECG is captured.

What now?

Posted by on February 21, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

77 year old male CC: Palpitations

36 comments

EMS is called to the residence of a 77 year old male complaining of palpitations.

Upon arrival, paramedics find the patient lying in bed. He is awake but lethargic. He is oriented to person, place, and time.

The patient’s skin is cool, pale, and diaphoretic.

He admits to chest discomfort and mild shortness of breath. Breath sounds are clear bilaterally.

Past medical history is significant for HTN and CABGx3 (a year and a half ago).

Medications: unavailable

Vital signs are assessed.

RR: 22 and shallow
Pulse: Too rapid to count
BP: 88/68
SpO2: Does not register

The cardiac monitor is attached.


A 12-lead ECG is captured.


What is your assessment of this ECG?

How would you treat this patient?

*** UPDATE ***

The patient was transported to the emergency department where he immediately received synchronized cardioversion.


Here is the post-cardioversion 12-lead ECG.

Posted by on December 13, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,

Update to: 78 yom CC: “Chest heaviness”

7 comments

Lots of interesting comments on this case.

Here is the update.

I opted to treat this patient as a presumed monomorphic ventricular tachycardia which is hemodynamically stable. I placed an 18 ga catheter in his left AC at a TKO rate. At approximately 1005 I administered 130mg (1.5mg/kg) of Lidocaine slow IV push which had no effect. At approximately 1010 the patient started vomiting profusely in a projectile fashion. He complained that he now hurt everywhere and he had a headache. At this point we decided to move to the truck even more rapidly than we already were. Enroute I gave him a second dose of Lidocaine this time 65mg (0.75mg/kg) with again no effect at approximately 1015.

At 1017 we arrived in the ER driveway and as my partner was placing the vehicle in park the patient went semi-conscious with a GCS of 9 (E3 V2 M4) and an absent radial pulse. We rapidly unloaded him to the already pre-alerted and waiting ER team. Within several minutes they successfully cardioverted the patient after one shock with a resultant bradycardic sinus arrythmia from 48-56 for a HR. He was subsequently transferred without incident to the regional tertiary care centre for ICD insertion.

Here are the serial ECGs that were captured en route to the hospital.


This case was handled very well, in my opinion. If you’ve read my tutorial on the differential diagnosis of wide complex tachycardias, then you know I believe that wide complex rhythms should be considered ventricular until proven otherwise!

I might not have given a second dose of lidocaine if the patient started projectile vomiting after the first dose, but it’s impossible to know the proximate cause.

Here are some recent comments on the case left by a reader named Billy.

Although VT should be the default diagnosis for a wide complex tachycardia, what sort of criteria do you suggest be used other than QRS morphology?

What sort of criteria to determine that a wide QRS rhythm is supraventricular? That’s an interesting question. Personally, I would require an old ECG for comparison, irregularity to suggest atrial fibrillation, the appearance of flutter waves, or a spontaneous slowing of the heart rate that reveals the rhythm to be sinus tachycardia.

What do you mean by VA conduction not being able to be differentiated from AV conduction? Are you saying that VT can produce retrograde conduction to the atria, resulting in a P wave after the QRS complex originating from the ventricles?

That’s exactly what I’m saying!

Also, I didn’t mean to say that because there appears to be a bifascicular block that makes it SVT. I was wondering why you thought that was unlikely in the first place for this patient, which would suggest VT.

Not to beat a dead horse, but “wide and fast” suggested VT prior to identifying the QRS morphology. VT can mimic virtually all intraventricular conduction defects! I thought RBBB/LPFB was unlikely because the RBBB morphology was atypical in lead V1 (with serial ECGs it became more typical). “Wide and fast” meant VT before we learned how to identify RBBB, LBBB, and bifascicular blocks. Unfortunately, many paramedics seem to throw that right out the window once they learn how to recognize these patterns! It’s very dangerous thinking.

I am interested to how akroeze ended up treating this patient. Regardless, I think amiodorone would be a good choice. Correct me if I’m wrong, but I believe amiodorone works on many mechanisms, including Ca, K and Na channel blocking, as well as beta blocking, which makes it effective on both VT and SVT’s. In these types of situations where a wide complex tachycardia might be SVT amiodorone should treat the arrhythmia no matter where the pacemaker is, making it a safe choice, whereas cardizem would be a better choice in narrow complex SVT’s since its Ca channel blocking is more pronounced.

I agree with that! Amiodarone would have been a perfectly acceptable antiarrhythmic to try in this scenario. In the absence of amiodarone, lidocaine was a viable option.

I would also like to present a “chicken vs. egg” question: What if this is in fact an MI? If you use the 220-age rule then this patient’s maximum heart rate is 142. With the heart rate being 180 I think it’s pretty clear this patient’s problem is an arrhythmia and not an MI (though we might see an MI once the arrhythmia is corrected). Suppose the patient was a bit younger and the heart rate is borderline at about 140 or so, with the same morphology in all leads. I think you can make an argument for inferior ST depression with elevation in the lateral leads. So, do you treat the tachycardia, or for ACS?

Tachycardia in the setting of acute STEMI is bad. For sinus tachycardia you treat the underlying cause. I’ve seen several cases of sinus tachycardia and acute STEMI mimicking a wide complex tachycardia, so you’re wise to consider it. It’s also not unheard of for STEMI patients to experience VT, so you could easily see an acute injury pattern coexistent with VT. All I can tell you is that no one said our job was going to be easy! Sometimes the best thing we can do for our patients is recognize our own limitations.

Posted by on October 23, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,

78 yom CC: “Chest heaviness”

32 comments

Here’s an interesting case submitted by Alex Kroeze. He is currently taking a sabbatical from blogging but was kind enough to share this interesting case with me.

Here is the story in Alex’s own words.

78 year old male with a history of MI with cardiac arrest around 1975 as well as diabetes (metformin) and fairly well controlled hypertension. He had no history of dysrhythmia as best as I could determine. This gentleman had a sudden onset at rest at approximately 0900 this day of 2/10 chest heaviness with no radiation/provoke/palliate and it is constant in nature. When he told his wife, she felt his pulse and noted it to be extremely rapid. She wanted to call EMS immediately however he was resistant to this; eventually she decided to call us anyway even though he still didn’t want to.

On arrival he appears in no acute distress. He is calm with no shortness of breath, nausea, or other stated complaints beyond the heaviness. His lungs are clear apices to bases. He has a noticeably variable ‘loudness’ to the S1 heart tone. His apical heart rate is measured to be 180 beats per minute and he has a good strong radial pulse. No Cannon A waves noted on quick inspection. He is placed on the stretcher and oxygen is applied while vital signs and ECG are acquired (see attached files).


I think that’s enough for starters.

What is your interpretation of the ECGs?

Treatment plan?

Posted by on October 17, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

44 year old male CC: Palpitations

25 comments

Here is an absolutely fascinating case submitted by G.W. Lyster (who credits the case to J.C. Neetz).

It's a patient who presented with a wide complex tachycardia who ended up receiving the kitchen sink!

Here are the basics.

44 YOM C/O "palpitations". Denies CP, SOB, N/V, dizziness, weakness. Pt in NAD.

Meds include Coreg, et al. (poor historian on meds) No allergies. Hx MI 8 days ago with stent, MI 5 years ago with "rapid heart rate".

P228, R20, SaO2 98, BP 160/102, BS 116, Skin WPD

Here is the initial rhythm:

Here are the 12 lead ECGs:

During the course of treatment, the patient was shocked at 100, 200, 300, and 360 Joules.

Here's an example:

After the unsuccessful shocks, the patient received lidocaine, adenosine, and procainamide! This particular service does not carry amiodarone.

Here is the code summary.

At the emergency department, the patient converted post-amiodarone.

Here is the patient's disposition:

Supervisor was able to obtain the following:

ICU Dx with recurrent arrythmia. No further episodes. They decided he had a non-acute MI (unknown age). He will get a consult to determine if there is a conduction issue (re-entry rythym). The Cardiologist thought he may have a WPW, but he will need the follow up with a specialist in regards to further exploration of the conduction pathways.

Posted by on September 2, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part VI

7 comments

Let’s take a look at a couple of rhythms you never want to see on the monitor.

First, from ABC of clinical electrocardiography – Broad complex tachycardia Part II, BMJ 2002; 324:776-779:


This is an irregular and polymorphic wide complex tachycardia that appears to show a streamer effect, or “turning of the points.”

Is it Torsades de Pointes?

The answer is, it’s impossible to tell from this rhythm strip!

Why?

Because the key distinction between polymorphic VT and Torsades de Pointes (which is a form of polymorphic VT) is that Torsades de Pointes will have a prolonged QT interval in the underlying rhythm!

This rhythm strip doesn’t show the underlying rhythm, so it’s impossible to diagnose as Torsades de Pointes, unless you can derive something useful from the history that would make you reach for the magnesium sulfate instead of the amiodarone (or defibrillator).

Since a normal QT interval varies with heart rate, what we’re really talking about is a prolonged QTc interval (the small ‘c’ stands for ‘corrected’ and normalizes the QT interval for the heart rate).

Most of the books I’ve read suggest that a QTc > 460 ms is prolonged and > 500 ms is clinically significant.

Dr. Wes has an interesting case of Torsades de Pointes here.

There are some very interesting YouTube videos that show Torsades de Pointes here and here.

Here’s another from ABC of clinical electrocardiography – Junctional tachycardias, BMJ 2002; 324:662-665:

This is an irregular and slightly polymorphic wide complex tachycardia. It’s also very fast! Anytime a tachycardia approaches 250 beats/min., you should be very suspicious of an accessory pathway (or Wolff-Parkinson-White Syndrome).

What else makes this rhythm different from the first? All of the “points” of the QRS complexes are pointing the same direction (in this case down). Familiarize yourself with this rhythm! These patients are rare, but they’re out there!

If you have atrial fibrillation on the monitor, and the shortest R-R interval is 6 small blocks or less, then you should treat it like WPW, and stay away from antiarrhythmics!

Atrial fibrillation in the presence of WPW is a very dangerous rhythm, and one of those occasions where you can kill your patient by selecting the wrong medication. The only safe drug for AF/WPW may be procainamide.

Consider this interesting transcript from Amal Mattu M.D.’s December 2008 podcast at EMedHome.com (thanks for the tip, Maciek!):

Another concern that you need to be aware of is, if you have a patient who has AF with WPW, stay away from amiodarone. Even now, AHA continues to list amiodarone as a viable option, but it’s not a viable option. In fact, the only published reports on using amiodarone in rapid AF and WPW have indicated that amiodarone is associated with adverse outcomes. There’s a handful of case reports of patients that had rapid AF and WPW. They got amiodarone and they decompensated. There are, to my knowledge – and I’ve looked through the literature in detail multiple times – and I have yet to find even a single case report or a single case series or a published study saying, “I had a patient with rapid AF and WPW, I gave him amiodarone, and they did well.” Not a single publication that I can find. The only publications on that particular scenario that have ever been published in the literature are “patient did worse” so my recommendation and a handful of other peoples’ recommendations also; “Stay away from amiodarone if you’re taking care of a patient with rapid AF and WPW.”

Remember the first rule of medicine!

If your patient is hemodynamically stable, then transport the patient to the emergency department for cardioversion. It’s probably the safest option.

You can see an example of what I’m talking about here and here.

Do you noticed any similarities between these two case studies? Look carefully!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 16, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , ,

Differential diagnosis of wide complex tachycardias – Part V

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Let’s switch gears a little bit and discuss irregular or polymorphic wide complex tachycardias.

First I need to tell you a story.

A few years ago I was teaching ACLS to a group of mostly nurses at the local community hospital. I volunteered to teach Bradycardias, Tachycardias, and the Hypotension/Shock/Acute Pulmonary Edema algorithm.

At first the education coordinator was thrilled! Apparently not many ACLS instructors feel comfortable teaching the Hypotension/Shock/Acute Pulmonary Edema alogrithm.

Keep in mind, I was following along with the AHA ACLS PowerPoint slide set. I wasn’t freelancing. I was explaining and elaborating, but I wasn’t introducing material that is outside the scope of the ACLS objectives.

I arrived at Irregular (or Polymorphic) Wide Complex Tachycardias.

I had just written on the board the differential diagnosis, which included:

  • Atrial fibrillation/flutter or (multifocal atrial tachycardia) with bundle branch block
  • Polymorphic VT
  • Torsades de Pointes
  • Atrial fibrillation with Wolff-Parkinson-White Syndrome (WPW)

When suddenly, the education coordinator yelled out from the side of the room, “You’re scaring the hell out of them!”

I was struck dumb!

I didn’t know what to say. I looked back at the screen, and I looked at the dry erase board where I had just written the differential diagnosis, and then I looked back at the education coordinator, shrugged my shoulders, and said, “What do you want me to do?”

To be honest, this wasn’t the first run-in I had had with this particular education coordinator.

A couple of years prior, I was a student in one of her ACLS classes. She handed out a cardiac rhythm strip test. I identified one of the heart rhythms on the test as 2:1 atrial tachycardia. She marked it wrong. When I asked about it, she said the correct answer was sinus tachycardia with 2°AVB and 2:1 conduction.

I laughed and said, “Is the atrial rate > 100?”

She said yes.

“And you agree there is 2:1 conduction?”

She agreed that there was.

“So you acknowledge that 2:1 atrial tachycardia is technically correct?”

She gave me look of utter contempt, leaned forward, and said quietly, “What do you think you are? A cardiologist?”

I’m not entirely sure this person likes firefighters. Let’s just say she used to be married to one, and leave it at that.

All of this to say, the differential diagnosis of irregular (or polymorhpic) wide complex tachycardias is a very neglected subject, both in paramedic school, and in ACLS class! But you have to know the differential diagnosis to select the correct treatment modality!

You can kill a patient who presents with an irregular (or polymorphic) wide complex tachycardia if you select the wrong drug!

That should “scare the hell out of you” far more than the differential diagnosis written out on a dry erase board.

Let’s start with atrial fibrillation.

Atrial fibrillation with intraventricular conduction defect (including right and left bundle branch block) can be considered a VT mimic at high rates, because the higher the heart rate, the more difficult it is to pick up on the irregularity that is normally the hallmark of atrial fibrillation!

In training (using the heart rhythm simulator) I sometimes give paramedics a scenario like this:

89 year old female contacts 9-1-1 complaining of chest pain and shortness of breath

On arrival, respirations are 36 and labored

Skin is pale and diaphoretic

Begin your assessment!

When they attach the monitor, they see atrial fibrillation with a nonspecific intraventricular conduction defect at a rate of 160.

I take that back. What they see when they attach the monitor is a wide complex tachycardia.

This example from Wide Complex Tachycardia: ECG Differential Diagnosis. Am J Emerg Med 1999; 17:376-381 should give you an idea what it looked like when printed out (which is different from how it looks on the monitor).


When they assess the BP (if they assess the BP) it comes back 160/110.

When they asses breath sounds (if they assess breath sounds) I say “wheezes with a poor tidal volume”.

When they assess the SpO2 (if they assess the SpO2) I say “72″.

Can you guess what’s wrong with this patient?

If you said “heart failure” move to the head of the class!

You would be frightened amazed to know how many paramedics immediately lie the patient flat and prepare her for immediate synchronized cardioversion!

In the debriefing that follows, when I ask why the decision was made to start shocking the patient, the ones that have clear rationale will say, “Because she was in unstable VT!” or “Because she was in unstable AF with RVR”.

When I asked what made the patient unstable, they will say, “the chest pain!” Some will say “the shortness of breath!”

Others will want to say the BP, but then they realize they never assessed it.

There’s a fine line between symptomatic and hemodynamically unstable.

For any patient who presents with a tachycardia, one of the most important and difficult questions you have to answer is:

Is the tachycardia causing the signs and symptoms, or are the signs and symptoms causing the tachycardia?

To put it another way:

Is this some type of compensatory tachycardia?

For the heart failure patient, atrial fibrillation and bundle branch block are extremely common. Have you ever seen acute, decompensated heart failure patient that did not present with tachycardia?

This is just my opinion, but I would try oxygen (CPAP if possible) and nitroglycerin before lying a heart failure patient flat and proceeding directly to synchronized cardioversion.

The next question you need to answer is:

Does the risk/benefit analysis favor treating this tachycardia in the field?

Choose wisely!

If you read the AHA ECC 2005 guidelines, you will see this statement featured prominently in the irregular (or polymorphic) wide complex tachycardia section.

“We recommend a 12-lead ECG and expert consultation if the patient is stable.”

Was the patient in this example “stable”? No!

Was the instability cased by the atrial fibrillation and rapid ventricular response?

In my opinion, no.

The BP of 160/110 gives you “room to play” so to speak. Nitroglycerin is a potent vasodilator. Why not give it, along with supplemental oxygen, and take some preload off the heart?

The heart rate will probably come down on its own when the SpO2 is back > 90.

You can always simultaneously prepare for cardioversion!

See also:

Differential diagnosis of wide complex tachycardias – Part I

Differential diagnosis of wide complex tachycardias – Part II

Differential diagnosis of wide complex tachycardias – Part III

Differential diagnosis of wide complex tachycardias – Part IV

Differential diagnosis of wide complex tachycardias – Part V

Differential diagnosis of wide complex tachycardias – Part VI

Posted by on January 12, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , ,