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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: , , , , , , , , , , , ,

63 Year Old Male: “Dental Pain” — Discussion

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This is the discussion to "63 year old male: "Dental Pain". You may wish to review the case.

For starters, i think we all agree that the patient, with his signs and symptoms, needs to be transported. We have all had patients like this who don't want to go, even though we know they should. Patients say they don't want to go for different reasons… some want to use us as a "litmus test", gauging their need to go by our reaction. Others don't want to put us through the trouble. Some are afraid of not coming home, and some, just plain don't want to go. We have to do everything possible to convince them to go, and as we know, sometimes that requires quite a bit of persistence!

Now, about that 12 lead:

There is sinus rhythm, with a rate of about 80 and a normal PRI. The QRS is wide (124ms). There is Right Bundle Branch Block, with an rsR' in V1, and s waves in I and V6. 

Do we see any other abnormalities on the 12 lead? RBBB should have T waves appropriately discordant to the terminal portion of the QRS. There should be no ST elevation in the right precordials…  in fact, you might expect a slight bit of ST depression in V1 and V2 opposite the QRS. For the most part though, the ST segments are not deviated as they are in LBBB, which makes it possible to assess ST segments normally. Let's take a look in V1 and V2:

There is a slight amount of ST elevation in V1. This is not normal. V2 has concordant T waves, without ST elevation, which is also concerning.

Is this an anterior STEMI? Not so fast… let's see what the rest of the 12 lead shows:

There is ST elevation in aVR (about 2mm)  and slight ST elevation in V1, with ST depression in leads I,II,III,aVF and V3-V6. This constellation of "global" ST depression with ST elevation in aVR and V1 is typical for subendocardial ischemia. Could it be posterior STEMI? Not likely in this case. The anterior ST depression of posterior STEMI is usually maximal in V2-V4, and that is not the case here. It looks different as well. It helps me to visualize the direction of the ST segments. Think about where the ST depression is: inferior and lateral. What would be reciprocal to inferior and lateral depression? Rightward and superior ST elevation, which is exactly what we see here. This is what it looks like on the hexaxial reference system:

 

We see the direction of ST depression (blue arrows) and the reciprocal ST elevation (red arrows).  You can't have a STEMI in aVR, so you can see this is just opposite the diffuse ST depression. In the precordial leads, the lateral ST depression is opposed by the slight ST elevation in V1. This would not be considered a  STEMI.

This pattern of diffuse subendocardial ischemia could be due to a left main lesion, proximal LAD lesion, or 3 vessel disease. We can not tell from the ECG. People rarely survive long with a left main occlusion, which makes that unlikely (unless there was much collateral circulation). The most common issue is left main ACS, which is not a STEMI equivalent.

In the field, we treat this patient for ACS with our standard meds… For some agencies that carry Clopidogrel, probably not a good med for this patient in case he needs CABG. At the hospital, he won't get thrombolytics because it is not STEMI. Most likely he will be medically managed, with PCI to follow if medical management doesn't work, or his symptoms worsen.

Unfortunately, we don't have an outcome for this patient, but he crew was able to convince him to be transported.

For more information on subendocardial ischemia, read this great post by Dr. Smith.

Posted by on April 20, 2012 • Filed under: ems-topics, patient-management, training-development • Tagged: , , , , , , ,

81 year old female CC: Chest Pain – Conclusion

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This is the conclusion to 81 year old female CC: Chest Pain.

Due to a significant language barrier, we were unable to obtain a useful medical history. Yet this case highlights the importance of a good scene assessment to gain additional information of clinical importance.

First, let's examine the patient's 12-Lead ECG.

We have a bradycardic, wide complex rhythm with no visible P-waves. It is also unremarkable for ischemia or infarction. Given the rate, we have a few possibilities:

  • Junctional rhythm with RBBB
  • Idioventricular rhythm

In the field, the distinction between these two possibilities is entirely academic. Our treatment modality relies instead on our patient's presentation.

As our patient is asymptomatic, of interest in this case is one of our patient's medications.

Digoxin is commonly prescribed for atrial fibrillation and atrial flutter. It works by increasing the refractory period of the AV node, effectivily slowing AV nodal conduction and the ventricular rate. It follows naturally that digitalis toxicity commonly includes bradyarrhythmias and AV nodal blocks. 

A second look at the 12-Lead ECG shows fibrillatory waves in V1 and V2, consistent with underlying atrial fibrillation. Likely our patient is suffering from digitalis toxicity with atrial fibrillation, a 3rd degree AV block, and an idioventricular escape rhythm. Other high risk differentials include myocardial infarction and hyperkalemia.

The paramedics on this call began with a working diagnosis of digitalis toxicity, performing serial 12-Leads enroute to identify ischemic changes. They started an IV, applied combo-pads to the patient, and closely monitored the patient until they arrived at the receiving facility.

At the receiving facility, blood labs were drawn and the patient's digoxin levels returned at 3.0 ng/mL, which is above the normal therapuetic range of 0.8-2.0 ng/mL. The patient's troponin levels remained below 0.4 ng/mL.

The patient was diagnosed with acute digitalis toxicity and admitted for observation. The patient was scheduled for a pacemaker implantation and lost to follow-up by the EMS agency.

Posted by on September 13, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , ,

68 year old male CC: Chest Pain – Conclusion

7 comments

This is the conclusion to 68 year old male CC: Chest Pain.

When we last left off, our patient was sitting outside a convenience store with a sensation of, "somebody punching me in the chest".

Our patient had a fast, irregular pulse, and we had acquired a rhythm strip and a 12-Lead ECG.

The rhythm strip shows a grossly irregular, narrow complex tachycardia with a rate between 120 and 160. The R-R intervals and TP segments are constantly changing as well. This is atrial fibrillation with a rapid ventricular response, also known as uncontrolled atrial fibrillation.

When dealing with AF and RVR it is important to determine if this is an acute onset or rather chronic atrial fibrillation exacerbated by some underlying problem. As our patient is a poor historian, this is difficult to say.

"Healthy as a horse," he exclaims. Let's evaluate that statement in the context of his 12-Lead ECG (with the computerized interpretation added).

Quick Thinking - Initial 12-Lead with Interpretation

As most readers correctly noted, we have atrial fibrillation with a Right Bundle Branch Block and a rapid ventricular response. An interesting finding is the apparently narrow QRSd in the limb leads due to the frank ST-depression. This highlights the importance of seeing the problem from more than one lead!

Also, most spotted the ST-elevation in leads aVL, aVR, and V1 (in red) accompanied by otherwise global ST-depression (in blue). This is suggestive of severe 3-vessel disease or even Left Main Coronary Artery occlusion! However, given we have a tachycardia present, we need to consider our differentials:

  • Acute onset of AF with RVR: ECG changes suggestive of demand ischemia with concomitant coronary artery disease
  • Chronic AF exacerbation: ECG changes suggestive of evolving myocardial infarction
  • Digitalis toxicity: "scooped" ST segments

While digoxin is a common drug taken by patients with chronic atrial fibrillation, digitalis toxicity is most often accompanied by bradycardia and AV-blocks. Junctional tachycardia is another common finding. A rare and bizarre finding was covered recently on Dr. Smith's ECG Blog: bidirectional ventricular tachycardia. However, digitalis toxicity is not known to cause ST-elevation in aVR and V1, and so it does not fit our clinical picture.

At this point, the paramedics were left to choose between acute paroxysmal AF and chronic AF. They elected to transport the patient to a PCI-capable center and treated the patient enroute with an IV fluid bolus and nitroglycerin for the chest pain. They contacted medical control for orders and were asked to monitor the patient as long as he remained stable.

Without knowing the patient's prior history of atrial fibrillation it is difficult to suggest a specific method of treatment in the field, especially while the patient remains stable. Paroxysmal atrial fibrillation responds well to cardioversion or calcium channel blockers. Whereas chronic atrial fibrillation often requires a correction of the underlying problem. Regardless, preparations should be made for cardioversion should the patient's condition worsen.

Upon arrival at the ED the patient's records were found, along with prior ECG's, which showed no history of atrial fibrillation but an extensive cardiac history including CAD.

During his initial assessment in the ED the patient became hypotensive and was cardioverted at 100 J with a return of a normal sinus rhythm and adequate blood pressure. Troponin levels remained below 0.4 ng/mL.

The patient remained stable through observation and was discharged home with a diagnosis of acute paroxysmal atrial fibrillation.

Posted by on September 9, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

64 year old male CC: Indigestion – Discussion

11 comments

This is the discussion to 64 year old male CC: Indigestion.

If you recall, we had a stubborn gentleman complaining of indigestion with a significant cardiac history. Considering the symptoms kept our patient awake, are highly suggestive of a coronary event, and we have uncompensated hypotension, we should have a keen interest on any ECG findings.

The rhythm appears to be regular, sinus in origin, rate of ~70 bpm, without ectopy. There is a fixed PR-interval of 0.2 s and a 1:1 association of P-waves to QRS complexes. The QRS is wide at 0.18 s, likely due to a bundle branch block. Normal sinus rhythm with a bundle branch block.

Evaluating the QRS complex in V1, we see it is wide and V1-positive confirming our suspicion of a bundle branch block. However, given the changes in leads I and V6, it is not a classic Right Bundle Branch Block. Instead we have a non-specific intraventricular conduction defect, or IVCD. A right axis deviation is present.

Looking at the contiugous lead groups:

  • Inferior: pathologic Q-waves present, isoelectric ST-segments, non-specific T-wave abnormalities
  • Septal: baseline wander, minimal ST-depression in V1-V2 (potentially attributed to the baseline)
  • Anterior: pathologic Q-wave in V4, isoelectric ST-segments, non-specific ST-T-wave abnormalities
  • Lateral: pathologic Q-wave in V5-V6, isoelectric ST-segments, non-specific ST-T-wave abnormalities
  • High-Lateral: unremarkable outside of underlying conduction defect
  • aVR: unremarkable outside of underlying conduction defect

Pathologic Q-waves in the inferiolateral lead groups are consistent with our patient's history of multiple prior MI's, however, without a prior ECG it is tough to determine if these are not from a recent myocardial infarction.

The potential ST-depression in the septal leads may be reciprocal changes in the setting of a posterior MI. The patient's skin condition made acquisition difficult, but coupled with the patient's signs and symptoms it would be prudent to explore this possibility. Attempts could be made at the acquisition of a posterior view.

The interventricular conduction defect present may be an acute finding or it may be a baseline finding. Given the QRSd is around 0.18 s there is a non-trivial defect present. Without access to the patient's prior ECG's we are unable to determine its significance.

While examination of the 12-Lead ECG for this patient did not yield any acute findings, in conjunction with our patient assessment we have enough to form a differential diagnosis:

  • Acute myocardial infarction
  • Recent myocardial infarction
  • Congestive heart failure
  • Pulmonary embolism (albiet less likely due to symptoms)

However, any differential diagnosis for this patient is rendered moot by his stubborn desire to refuse transport!

The paramedics on this call rolled up their sleeves and got to work convincing this gentleman that his signs and symptoms were anything but normal. He begrudingly sat on the stretcher and consented to transport.

They placed him on O2 by nasal cannula, obtained IV access, administered a fluid bolus, and transmitted the 12-Lead ECG to a local STEMI receiving center. His blood pressure improved enough with fluid administration to allow nitroglycerin, which the patient said improved his discomfort.

Transmission of the patient's ECG was key in this case as the receiving facility determined acute changes were present.

The patient was taken directly to the cath lab where a 90% occlusion of the LAD, just proximal to a previous stent, was found. The lesion was ballooned and stented, and the patient was admitted to the CCU for recovery.

Some additional questions for discussion:

  • Why was this patient's hypotension uncompensated?
  • Are there any differentials we missed?
  • Why was indigestion left off the list of differentials?
Posted by on July 1, 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: , , , , , , , , , , , , , , ,

An unusual case of right bundle branch block – Discussion

10 comments

Here is the conclusion to an unusual case of right bundle branch block.

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

This 12-lead ECG shows acute anterior STEMI in the presence of right bundle branch block, but you really need a trained eye to see it.

We talk a lot about the “rule of appropriate T-wave discordance” with bundle branch blocks. What makes this case difficult is the fact that the T-waves are appropriately discordant.

However, the J-points are concordant in leads V1-V4!

If you look carefully you will see that the point at which the QRS complex turns into the ST-segment (the J-point or “junction” point) is elevated above the isoelectric line.

That’s abnormal for right bundle branch block. In fact, if the J-point isn’t isoelectric in the right precordial leads it should be slightly depressed (in the same direction as the T-waves).

Lead V4 looks the most abnormal.

If you’re still having doubts, consider that Q-waves are present in leads V1-V4.

That’s what Tomas Garcia, M.D. means when he says to “consider the company” that any ECG abnormality keeps.

Finally, let’s look at leads III and aVF.

We are forced to assume that these are reciprocal changes. Once again, it’s the sum of all these abnormalities that is significant. They are more than the sum of their parts.

This patient was in fact diagnosed with an acute anteroseptal ST-elevation myocardial infarction.

See also:

An unusual case of left bundle branch block

An unusual case of left bundle branch block – Discussion

Posted by on February 9, 2011 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,

An unusual case of right bundle branch block

18 comments

Here’s a case submitted by Captain Jack Sparrow from the UK Ambulance Forum.

I’m presenting it here with minor modifications.

Turns out Mark Glencorse isn’t the only clever Brit! We Yankees can learn a lot from the way they do things across the pond.

EMS is called to the residence of a 69 year old male with a chief complaint of chest pain.

Onset: Gradual while driving
Provoke: Nothing makes the pain better or worse
Quality: Describes pain as pressure
Radiate: The pain does not radiate
Severity: 3/10
Time: Similar episode over the weekend while gardening

Past medical history: CVA x 13 years ago, AF
Past surgical history: None
Allergies: No know drug or environmental allergies
Medications: Warfarin, digoxin, others

On arrival the patient is found sitting in a chair.

Skin is pink, warm, and moist.

He appears ill.

Vital signs

RR: 16 regular
Pulse: 130 irregular
NIBP: 137/102
GCS: 15
BGL (BM): 146 (8.1)
SpO2: 99 on RA

Breath sounds: clear bilaterally with normal air entry

No obvious trauma or anything else out of the norm.

The cardiac monitor is attached.

A 12-lead ECG is captured.

What’s wrong with this patient?

See also:

An unusual case of right bundle branch block – Discussion

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

Update to 74 year old male CC: Chest pain

10 comments

Here are the serial prehospital 12-lead ECGs for 74 year old male CC: Chest pain

Angiograms and cath report to follow.

Pay close attention to the right precordial leads (V1-V3).

Consider the following graphic.

The most important changes occur between 16:41:26 and 16:50:30.

Just for fun, here it is “flipped”.

See also:

Cath report for 74 year old male CC: Chest pain (with angiograms)

Posted by on April 26, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , ,

63 year old male with sudden onset shortness of breath

26 comments

This is an interesting case submitted by Tom Bernesser who is a paramedic from North Carolina.

I got to know Tom through the EKG Challenge forum at the EMS Village where he always posted fascinating case studies.

Here’s the story.

63 year old male presents with acute onset of dyspnea.

He reported 4 previous MI’s with similar presenation, only dyspnea – no pain or discomort as was the case on this morning.

Past medical history:

NIDDM, HTN, MI, CHF, CVA and is bed-confined for the most part. He’s also fairly obese.

Vital signs:

BP of 146/90
HR 104
RR 24
SpO2: 87 on RA, 100 on O2 via NRB mask @ 15 LPM

BGL: 141 mg/dL.

He did have diminished lung sounds bilaterally, maybe some rales in the bases but was able to speak in full sentences.

He also had some pedal edema, but wasn’t taking any diuretics.

He’s at a Skilled Nursing Facility (SNF) but of course there is no old EKG on site for comparison.

Another note, he did have occasional bouts of multifocal PVC’s probably about 10-15/min.

Here is the 12-lead ECG.

Here is the computerized interpretive statement.

As you can see, it’s giving the >>>> ACUTE MI <<<< message.

Would you activate the cardiac cath lab?

Why or why not?

Posted by on March 1, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , ,

50 year old male CC: Respiratory distress, chest pain

37 comments

EMS is dispatched to a 50 year old male in respiratory distress. En route, dispatch advises that the chief complaint is actually chest pain.

On arrival, the patient is found lying supine on the floor just inside the front door to his house. He is cold to the touch and pale but his skin is not diaphoretic. He denies falling and the head is atraumatic.

He appears to be mildly short of breath and admits that he is having chest pain.

Onset: 3-4 hours ago while walking
Provoke: Nothing makes the pain better or worse
Quality: He is unable to describe the pain (some language barrier)
Radiate: The pain radiates down both arms
Severity: The patient gives the pain a 10/10
Time: The patient does not admit to any prior episodes, although he does state the he was recently diagnosed with anxiety and is scheduled for a “cardiac exam”

He denies nausea or vomiting.

Vital signs:

Resp: 24
Pulse: 70
BP: 80/60
SpO2: 92 on RA

Breath sounds: slight rales bilaterally

A 12-lead ECG is captured.

The patient and his family request to be transported to the local (non-PCI) community hospital.

What is your impression?

What should the treating paramedic do next?

*** UPDATE ***

The treating paramedic was very concerned about the 12-lead ECG. Even though it technically did not meet the criteria for a STEMI Alert in his system, he persuaded the patient to request transport to the PCI-hospital across town.

It was his intent to capture a 12-lead ECG with posterior leads V7-V9 once the patient was loaded in back of the ambulance.

He didn’t get the opportunity because the patient went into ventricular fibrillation.

A precordial thump was delivered with no success (don’t pretend like you wouldn’t have enjoyed it).

Chest compressions were initiated while the monitor was charged. A shock was delivered at 150 J and chest comrpessions were immediately resumed.

Approximately 1 minute later the patient regained consciousness. He remained in sinus rhythm for the remainder of the transport.

An additional 12-lead ECG was obtained post-arrest.

Does this change things for anyone?

*** UPDATE ***

Here’s the exciting conclusion to the case!

The patient was taken straight to the cardiac cath lab at the receiving PCI-hospital (apparently the cardiac arrest got their attention).

The angiogram revealed a total (or near-total) occlusion of the left main coronary artery (limiting flow to both the left anterior descending LAD and circumflex LCX arteries).

The lesion could not be stented.

A balloon pump was placed and the patient was prepped for CABG.

Posted by on January 8, 2010 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , ,

Right bundle branch block – Part III

11 comments

Let’s take another look at the ECG from Part II.


I asked you to look carefully at this ECG, and then using the concept of appropriate T-wave discordance, see if anything bothers you.

Does anything stand out?

How about lead V4?


Here you can see the terminal deflection (blue arrow) is positive, and so is the T-wave (inappropriate T-wave concordance). There is also at least 1 mm of ST segment elevation. That’s definitely abnormal!

Now let’s look in the inferior leads. They all look abnormal, but I’m going to use lead aVF as the example.


The terminal deflection is negative (blue arrow) and the T wave is also negative (inappropriately concordant T-wave). The inferior leads are reciprocal to the anterior leads. Could this represent reciprocal changes? Absolutely!

It is sometimes said that reciprocal changes are of no value in the presence of bundle branch blocks. That’s not entirely true! You just have to interpret them within the context of appropriate T-wave discordance.

In other words, in the presence of bundle branch block, if the terminal deflection of the QRS complex is negative in lead III and positive in lead aVL, then you will have pseudo reciprocal changes (positive in lead III and negative in lead aVL). This is a normal finding in left bundle branch block, for example.

If, however, the terminal deflection of the QRS complex is negative in lead III (as in this ECG) and the same lead is showing inappropriately concordant ST-segment depression or T-wave inversion, then it’s probably not a pseudo reciprocal change. Why? Because it’s opposite the expected pattern.

I’d also like to point out that leads V2 and V3 look really strange in this ECG. Why? Because there’s a merging together of the S-wave and T-wave (sometimes seen in severe hyperkalemia). This is a really ugly T-wave abnormality, especially since we would normally expect a terminal R wave in lead V2 with right bundle branch block.

Something’s going on here!

Let’s look at some serial ECGs. This one was taken just 4 minutes later.


Now what do you see?

*** Update 07/13/09 ***

Here’s the final ECG in the series, recorded as the ambulance arrived at the hospital.


Quite a difference! Once again, it’s easy to see the value of serial ECGs.

Let’s take a look at lead V2 and see how it changed from the first ECG to the last.


The problem (or perhaps the challenge) is that this final piece of the puzzle wasn’t present until arrival at the hospital. Fortunately, it was one of 17 PCI hospitals in the State of South Carolina!

This is why paramedics need to be able to interpret a 12 lead ECG at a high level. Every Patient Counts! We need to make sure that STEMI patients are delivered to the right hospital!

QRS confounders like right and left bundle branch block can make the ECG diagnosis of STEMI more difficult, but these are the patients who receive the most benefit from reperfusion therapy, and prompt, expertly performed primary PCI is the preferred strategy!

We shouldn’t delay a high risk patient’s care because we can’t read their ECG. Unfortunately, it happens every day all over the country.

That’s assuming the EMS system has 12 lead ECG monitors in the first place.

See also:

Right bundle branch block – Part I

Right bundle branch block – Part II

Right bundle branch block – Part III

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

Right bundle branch block – Part II

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Once you’ve identified a RBBB on the 12 lead ECG, the next thing you want to do is determine whether or not you’re dealing with a normal RBBB or an abnormal RBBB (or new RBBB).

You may remember this graph from my previous post: Who benefits the most from reperfusion therapy?


It shows that patients with “new BBB” receive the most benefit in terms of lives saved per 1000 treated with fibrinolytics (based on the FTT Collaborate Group). We often here it claimed that patients with “new LBBB” receive the highest benefit from prompt reperfusion therapy, but it’s worth pointing out that the FTT Collaborative Group did not distinguish between LBBB and RBBB.

Generally speaking, RBBB does not mimic or obscure the ECG diagnosis of acute STEMI the way LBBB does. However, sometimes it can (remember the update to Funky Trouble-Looking RBBB with AMI).

So how do we know what’s “normal” for right bundle branch block? We use the concept of “appropriate T wave discordance”. This concept usually comes up in the context of discussing LBBB, but it’s also useful for RBBB (and paced rhythms, ventricular rhythms, non-specific IVCD, and so on).

For RBBB, the concept is that when the terminal deflection of the QRS complex is positive, the T wave should be negative. Likewise, when the terminal deflection is negative, the T wave should be positive.

You may recall this graph from my previous post: Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria – Part II.


The blue and red arrows show the expected relationship between the terminal deflection and the T wave with RBBB.

Remember, the terminal deflection is the last deflection in the QRS complex.

Consider the following case.

EMS is contacted for a 77 year old male complaining of chest pain. On arrival, you find the patient lying supine on the couch. He is ashen in color and diaphoretic with absent radial pulses. He responds sluggishly but appropriately and states that he is having severe sub-sternal chest pain.

His shirt is cut off and the combo-pads are applied, revealing the following heart rhythm.


It appears to be sinus rhythm with wide QRS complexes and occasional PVCs.

A 12 lead ECG is captured.


Using the concept of “appropriate T wave discordance” is there anything about this ECG that bothers you?

See also:

Right bundle branch block – Part I

Right bundle branch block – Part II

Right bundle branch block – Part III

Posted by on July 10, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

Right bundle branch block – Part I

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How do you identify RBBB on the 12 lead ECG?

Forget about turn signals and bunny ears!

All you need for the ECG diagnosis of RBBB are the following:

  • A supraventricular rhythm
  • QRS duration equal or greater than 120 ms (0.12 s)
  • Terminal R wave in lead V1
  • S wave in lead I

It’s that easy!

Let’s look at an example.


What’s the rhythm?

Borderline sinus bradycardia with 1°AVB and occasional PACs.

Is that a supraventricular rhythm? Yes!

Let’s move on.

Is the QRS duration equal to or greater than 120 ms (o.12 s)?

In other words, are the QRS complexes “wide”?

Be careful! It’s easy to fixate on the tight R wave and discount the S wave with RBBB. If this was a tachycardia at a rate of 150, it might appear to be a narrow complex tachycardia, when in fact, it would be a wide complex tachycardia!

The QRS duration is > 120 ms. Just barely, but it’s like being pregnant. It either is or it isn’t!

So we have a supraventricular rhythm with wide QRS complexes. This process is important because one of the most important and basic rules of electrocardiography is:

Wide complex rhythms are ventricular until proven otherwise!

Once you have determined that a supraventricular rhythm is wide, you can examine QRS moprhology to figure out what kind of intraventricular conduction delay is present.

Let’s look at the 12 lead ECG.


Is there a terminal R wave in lead V1?

Yes!

What do we mean by “terminal R wave”?


The last wave of a QRS complex is the terminal wave, or terminal deflection. If a QRS complex ends in an R wave, then it has a terminal R wave. It can also be said that the terminal deflection is positive.

I would call the QRS complex in this 12 lead ECG an rsR’ complex. Compare it to the rsR’ complex in this PowerPoint slide.

It’s important to think in terms of the terminal deflection (or terminal R wave) in lead V1 with RBBB because the QRS morphology can be quite variable!

Consider these examples.


All of these QRS complexes are different. Most are positively deflected but some are negatively deflected. Most start with an R wave, but a few start with a Q wave. However, they all share one important feature.

They all have a terminal R wave!

Why?

Ask yourself a question. If the right bundle branch is blocked, which ventricle depolarizes first?

The left ventricle!

So which ventricle depolarizes last?

The right ventricle!

What is the only precordial lead on the right side of the chest?

Lead V1!

A terminal R wave in lead V1 represents late right ventricular depolarization.

The terminal S wave in lead I represents the same thing, because the positive electrode for lead I is on the left shoulder. So, late left-to-right ventricular depolarization moves away from the positive electrode for lead I and toward the positive electrode for lead V1.

Remember when I said that the first step was to establish that you were dealing with a supraventricular rhythm?

The QRS complex in the top row, far right, was cropped from a run of VT (lead MCL-1 which is a surrogate for lead V1). The QRS complex in the bottom row, far right, was also taken from a run of VT.

So, you have a supraventricular rhythm, with wide QRS complexes, and a terminal R wave in lead V1. You’re 99% of the way toward calling this a RBBB.

All we have to do now is search lead I for a terminal S wave.

Does lead I show a terminal S wave?

Yes!

ECG diagnosis: Borderline sinus bradycardia with 1°AVB and RBBB, occasional PACs.

See also:

Right bundle branch block – Part I

Right bundle branch block – Part II

Right bundle branch block – Part III

Posted by on June 19, 2009 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , ,

Identifying STEMI in the presence of LBBB – Sgarbossa’s Criteria – Part II

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In Part I, we discussed Sgarbossa’s Criteria for identifying AMI in the presence of LBBB. We also talked about the “rule of appropriate T wave discordance” for bundle branch blocks and other forms of abnormal depolarization (like ventricular rhythms or paced rhythms).

You will recall that I drew a distinction between a QRS complex’s main deflection and its terminal deflection, even though they are one in the same for LBBB. I explained that it’s helpful to think in terms of the terminal deflection, because then you can apply the “rule of appropriate T wave discordance” to RBBB as well as LBBB.

And so you can!

Let’s look at an ECG.

This is from one of my “old” 12 lead ECG classes. In those days, I cropped the computer measurements and interpretive statements because I didn’t want the students to “cheat”. Nowadays, whether it’s EMS or firefighting, I’ve come to believe in reality-based training. In real life, for good or bad, you get an interpretive statement.

But, this ECG is a good example of an important concept.

So let’s look at this ECG. It’s a sinus rhythm. It has a normal axis. We know that for several reasons.

The QRS complex is smallest in lead aVL, so the perpendicular lead on the hexaxial reference system is lead II. Lead I is almost equiphasic so the perpendicular lead is aVF. The value of lead II is 60 degrees and the value of lead aVF is 90 degrees, so the frontal plane axis is somewhere between 60 and 90 degrees.

Or, to do it the “easy” way, lead I and lead aVF are both positively deflected, so we know we’re in the left inferior quadrant.

Or, because leads I, II, and III are all positive, so we know the axis is normal.

It really doesn’t matter what method you use. I use all three for every ECG.

The QRS duration is wide. When supraventricular rhythms are wide, we look at lead V1 to see if it shows RBBB or LBBB morphology. This ECG shows a terminal R wave in lead V1, which is RBBB morphology. Next we check lead I and look for a terminal S wave. We find one!

This is a simple RBBB.

You will notice that in many leads, the T wave is deflected the same direction as the QRS complex (II, III, aVR, aVF, V2, V3, V4, V5, and V6). In other leads, the T wave is deflected opposite the main deflection of the QRS complex (aVL, V1). I did not list lead I because the QRS complex is close to equiphasic.

So, how should these T waves be deflected?

The answer is, they should be deflected opposite the terminal deflection of the QRS complex, and so they are!

Look at the following image.

As you can see, when the terminal deflection of the QRS complex is negative, the T wave is positive. When the terminal deflection is positive, the T wave is negative. In other words, even if the main deflection of the QRS complex is positive, as long as the terminal deflection (or last deflection) is negative, the T wave is positive.

That’s why I’m encouraging you to always think in terms of the terminal deflection, even though for LBBB, the terminal deflection is also the main deflection.

There is method to this madness!

Although not part of Sgarbossa’s Criteria, the “rule of appropriate T wave discordance” can help you pick up on AMI in the setting of RBBB (or bifascicular block) because an inappropriately concordant ST segment and/or T wave can tip you off that something is wrong!

For example, this case from Dr. Smith’s ECG blog.

In the last lesson, we introduced Sgarbossa’s Criteria. Let’s take a look at a graphic that shows exactly what we’re looking for.

The first example shows > 1 mm of concordant ST segment elevation (and a concordant T wave). Both are abnormal for LBBB.

The second example shows > 5 mm of discordant ST segment elevation and a discordant T wave. Discordant ST segment elevation > 5 mm is abnormal for LBBB (with one very important caveat) but a discordant T wave is normal for LBBB!

In the last example, there is concordant ST segment depression in the right precordial leads, which is abnormal for LBBB, but a discordant T wave, which is normal for LBBB.

If you have a patient with signs and symptoms consistent with ACS and the ECG shows LBBB with concordant ST segment elevation, then chances are excellent that you are dealing with a STEMI.

Likewise, if you have a patient with signs and symptoms consistent with ACS and the ECG shows LBBB with concordant ST segment depression, especially in the right precordial leads, then chances are excellent that you are dealing with a STEMI.

The original criteria didn’t take into account the depth of the S wave, and as we know from other STE-mimics like LVH, the deeper the S wave, the higher the ST segment elevation. So a blanket statement that 5 mm of discordant ST segment elevation indicates acute STEMI in the setting of LBBB is not helpful in those situations where the S wave is > 50 mm deep like the example below.

Stephen Smith, M.D. of Dr. Smith’s ECG Blog has suggested that a more sensitive and specific marker is discordant ST-elevation > 0.2 the depth of the S wave (ST/QRS ratio).

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part I

80 year old male CC: Chest pain

Excessive discordance as a marker of acute STEMI in LBBB

80 year old male CC: Chest pain – Conclusion

“New” LBBB – What’s the big deal?

Sgarbossa’s Criteria – New Graphic

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)

Posted by on December 15, 2008 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , , , , , ,

Identifying STEMI in the presence of LBBB – Sgarbossa’s Criteria – Part I

18 comments

There has been a lot of discussion lately about identifying AMI in the presence of LBBB (see Dr. Bearemy’s “My Emergency Medicine Blog” here and a recent thread on the EKG Club). I’ve also been receiving a lot of emails offlist, so I think a full discussion is in order.

In my recent post Who benefits the most from reperfusion therapy? I posted a graph that demonstrates how patients with new bundle branch block benefit the most from reperfusion therapy.

*** Important Update ***

Recent evidence suggests that new (meaning previously undetected) LBBB patients do not “rule-in” for AMI at any greater rate than any other group of patients! That’s why it’s so important for health care practitioners to understand Sgarbossa’s criteria! Those are the patients who need immediate reperfusion therapy in the cardiac cath lab!

*** End Update ***

The problem is that in many prehospital 12 lead programs (and regional STEMI systems), patients with LBBB or a QRS duration > 0.12 sec (120 ms) are excluded! In other words, patients with wide QRS are taken to the local community hospital without interventional capability. Or, the cath lab is not activated while EMS is still in the field.

Why would you exclude the very patients who stand to benefit the most from prompt, expertly performed PCI at a cardiac center?

Simple.

It’s too difficult to figure out whether or not the BBB is new! The ECG diagnosis of STEMI can be difficult in the setting of BBB.

In False Positive Cardiac Cath Lab Activations I reviewed Larson, Menssen, Sharkey et all, False-Positive” Cardiac Catheterization Laboratory Activation Among Patients With Suspected ST-Segment Elevation Myocardial Infarction, JAMA 2007;298(23):2754-2760.

I quoted:

Patients with new or presumably new left bundle-branch block had an inordinately high prevalence of false positive catheterization laboratory activation (almost half did not have a culprit artery). Patients with a previous myocardial infarction or previous coronary bypass surgery had a significantly higher prevalence of no culprit artery, likely because of abnormal baseline ECG results.

This is obviously a big problem, and subjecting all patients with LBBB and signs and symptoms of ACS to an emergent cath or the risks associated with thrombolytic therapy is not the answer, as some authors have suggested.

If only there was some kind of algorithm that could help distinguish between patients with LBBB and acute STEMI from patients with LBBB who are not experiencing acute STEMI.

But there is such an algorithm! It’s been around for over 10 years!

The GUSTO investigators Sgarbossa et al., Electrocardiographic Diagnosis of Evolving Acute Myocardial Infarction in the Presence of Left Bundle-Branch Block. N Eng J Med 1996; 334(8):481-487 published an algorithm which has come to be known as “Sgarbossa’s Criteria”.

The criteria seems complicated but it’s really not. Like anything else, it’s a tool. A very important tool for a critical subset of patients.

The original paper contains a flow chart from which the patient receives a score. I’m not going to publish the flow chart, because it’s not something you need to memorize.

Here is the criteria. A patient is presumed to be experiencing an evolving AMI if any of the following are present.

  1. ST segment elevation = or > 1 mm that is concordant with the QRS complex.
  2. ST segment depression = or > 1 mm in leads V1, V2, or V3.
  3. ST segment elevation = or > 5 mm that is discordant with the QRS complex.

It is the last criterion that has caused the most controversy and requires qualification.

However, before we address the third criterion, we have to dispose of a common misunderstanding.

What do we mean by concordant and discordant? The short answer is, concordant means “the same direction” and discordant means “the opposite direction”.

The rule of appropriate T wave discordance

In the presence of abnormal ventricular depolarization (left bundle branch block, right bundle branch block, paced rhythm, ventricular rhythms) the T wave should be deflected opposite the terminal deflection of the QRS complex (appropriate T wave discordance).

What is the terminal deflection?

The terminal deflection is the last deflection, or wave, of a QRS complex.

Please take the time to learn this! It is extremely important!

Take a look at the following image.

You will notice that each of these QRS complexes is labeled according to the waves are present. If the wave is large, it gets a capital letter. If the wave is comparatively small, it gets a lowercase letter.

I could talk about this image for a long time, but for now, I just want you to notice that an Rs complex is positively deflected while an rS complex is negatively deflected, even though both of them contain only an R and an S wave. But the terminal deflection of each is negative, because they both end in an S wave!

Why is this important?

When teaching Sgarbossa’s Criteria, students always get confused as to whether or not the ST segments and T waves should be deflected opposite the main deflection of the QRS complex or opposite the terminal deflection.

Well, guess what?

With LBBB, the terminal deflection is the main deflection!

So why are we splitting hairs?

Because if you learn to think in terms of the terminal deflection, you can use the rule of appropriate T wave discordance for RBBB, too!

Let’s start by looking at a patient with a normal LBBB.

I have no idea why the GE-Marquette 12SL interpretive algorithm is giving the “data quality prohibits interpretation” message for this ECG. There’s a little bit of artifact in the inferior leads, but it’s not that bad!

This is a normal looking LBBB. We know the frontal plane axis is around 0 degrees, because the QRS complex is isoelectric in lead aVF. Therefore, the perpendicular lead in the hexaxial reference system is lead I. Since lead I is positively deflected, we can place the frontal plane axis at 0 degrees. A physiological left axis deviation (0 to -30) is normal for left bundle branch block.

To put it another way, a negative QRS complex in lead III is normal for LBBB, but it should be upright and monomorphic in lead I.

Now, let’s look at the QRS complexes and the T waves.

You will notice that in every lead, the T wave is deflected opposite the QRS complex! This is “appropriate T wave discordance” in the presence of left bundle branch block.

To help illustrate this point, consider the following graphic.

The blue arrow shows the direction of the terminal deflection of the QRS complex (which is also the main deflection in the setting of LBBB). The red arrows shows the direction of the ST segment and the T wave.

This is what we mean by “appropriate T wave (and ST segment) discordance” with LBBB. Note that with RBBB, the T wave should be discordant, but the ST segment should remain isoelectric. This is why RBBB is usually not listed as a STE-mimic.

With LBBB, there is also a discordant shift of the ST segment, which is why it’s one of the most common STE-mimics! ST segment elevation in the right precordial leads (V1-V3) is a normal finding for LBBB!

In Part II, we’ll look at the “rule of appropriate T wave discordance” as it applies to RBBB and talk more about Sgarbossa’s Criteria.

See also:

Identifying AMI in the presence of LBBB – Sgarbossa’s Criteria Part II

80 year old male CC: Chest pain

Excessive discordance as a marker of acute STEMI in LBBB

80 year old male CC: Chest pain – Conclusion

“New” LBBB – What’s the big deal?

Sgarbossa’s Criteria – New Graphic

Discordant ST-segment elevation in LBBB or paced rhythm

Found on the Lifenet Receiving Station (LBBB with concordant ST-depression in leads V3 and V4)

62 year old male CC: Chest pain (LBBB with ST-elevation > 0.2 the QRS complex)

58 year old female CC: Chest pain

58 year old female CC: Chest pain – Conclusion (meets all 3 of Sgarbossa’s criteria)

Posted by on December 13, 2008 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , , , , , , , , , , , ,

82 year old male CC: Chest pain

9 comments

Here's an interesting case I pulled off the LIFENET Receiving Station.

Update: ECGs were retrieved from the archives of the LP12 for better data quality.

82 year old male complaining of chest pain.

PMH: HTN, including pulmonary hypertension

Meds: Unknown antihypertensives, ASA

Vital signs:

Resp: 20
Pulse: 60
BP: 120/73
SpO2: 96 on RA

Breath sounds: clear

Skin is cool, pale, and diaphoretic. The patient admits to mild dyspnea. He also admits to slight nausea but he has not vomited. He describes his pain as pressure and 6/10 in severity.

The cardiac monitor is attached.

A 12 lead ECG is captured.

What is your interpretation of this ECG?

Update: Here is the 12 lead ECG obtained on arrival at the ED.

Do you see why serial 12 lead ECGs are important?

Posted by on November 29, 2008 • Filed under: ems-topics, patient-management • Tagged: , , , , , , , , , , , , , ,