You are called to transfer a 63 year old female from a community hospital to a large medical center.

Upon arrival at the local hospital, you are confronted with chaotic scene. You see your patient, now resting, and are told she presented with chest pressure and palpitations a couple of hours ago, was also becoming obtunded, and her family had stated she had not had any any similar episodes in the past. Her vitals are as follows:

• Pulse:   200 and irregular
• BP:   132/76
• RR:   22 regular
• Eyes:   Pearl
• Skin is cool and dry

They hand you an ECG and tell you she presented in the following rhythm:

And with the following history:

• She had sudden onset of chest pressure and palpitations, which began while she was doing some work around the house.
• Nothing changed the discomfort
• felt like "pressure" and "palpitations"
• No radiation
• she rated the pressure as a 7/10
• began one hour prior to presentation
• No allergies to medications
• She takes a "pill for blood pressure", name unknown
• Past medical history significant only for hypertension
• had a normal breakfast and lunch
• She can not recall any specific trigger for the episode

In the ED prior to your arrival, she had received the following treatments:  Lopressor, Amiodarone, Magnesium Sulfate, Heparin, Lidocaine, Morphine and Versed.

None of these treatments changed the patient's rhythm:

The patient's mentation continued to decline, and her BP started to crash. After three attempts, she was successfully cardioverted. Here is the post-conversion 12 Lead:

You transport your patient, now stable, to the medical center without incident.

So, now the key questions:

• What was the presenting rhythm and why?
• What is the post-conversion rhythm and why?
• What are the best treatment options for this rhythm?

We could not have been happier at the number of insightful comments we received on this case! Many of you caught on to our purpose for this case as we could not have picked a better borderline example!

When we last left our crew they were preparing to transport a 50 year old male who appeared acutely ill. Their first 12-Lead ECG suffered from excessive baseline wander, but appeared to have some ST-elevation present. Attempts were made at improving the quality of the tracings with little success.

Here is the initial 12-Lead ECG, this time with the computerized interpretation included:

This 12-Lead ECG shows marked baseline wander, sinus bradycardia, ST-elevation of at least 1 mm in II, aVF, and V4-V6 with ST-depression in leads aVR and V1. The monitor's algorithm believes the ST-changes are the result of Early Repolarization.

They attempted to troubleshoot the baseline wander with patient coaching, and after two more attempts they captured the following 12-Lead ECG; again with the computerized interpretation included:

This 12-Lead ECG also shows marked baseline wander, a sinus rhythm, ST-elevation of at least 1 mm in II, aVF, and V4-V6 with ST-depression in leads aVR and V1. In this tracing, just 2 minutes later, the monitor's interpretation has changed to read the ominous *** ACUTE MI SUSPECTED *** message, suggesting an inferiolateral infarct pattern.

Between these two 12-Lead ECGs we can clearly see that ST-elevation is present in leads II, aVF, and V4-V6 with ST-depression clearly visible in aVR and V1. It is difficult to tell with the baseline wander whether any PR-segment changes exist or if the J-point in aVL is depressed.

At this point our differentials should include:

• Acute inferiolateral myocardial infarction
• Pericarditis
• Early repolarization

Given our patient's recent history of strep throat, diffuse ST-elevation, concave-up T-waves, and ST-depression in aVR and V1 we should strongly consider pericarditis. The baseline wander present makes accurate evalution of the PR-segment difficult, but a case could be made for PR-elevation in aVR. Compare our tracings with the discussion to 39 year old male CC: "Sick".

However, given the presentation of typical MI symptoms and a borderline ECG (albeit without reciprocal changes), we have no conclusive means of ruling out an inferiolateral myocardial infarction. If your service area has the ability to, it would be beneficial to transmit these borderline ECGs to a receiving facility for a second opinion. Compare our tracings with the discussion to 77 year old female CC: Chest Pain.

Our crew found themselves in quite the pickle!

In these instances it is prudent to err on the side of the patient and treat this as a STEMI, which is exactly what the crew did.

Upon arrival at the PCI center the following ECG was acquired:

The ED 12-Lead shows a normal sinus rhythm without ectopy. ST-elevation of at least 1 mm exists in leads II, aVF, and V4-V6. ST-depression is present in lead aVR. The monitor's interpretation is unknown.

The ED physician concurred with the activation and the patient was sent for an emergent cardiac catheterization.

No culprit lesion was found and the crew was later informed the patient was being treated for pericarditis.

This case represents a false positive, however, it is the author's opinion that this case does not represent an inappropriate field activation due to the borderline field ECG.

Some clues on the 12-Leads that favor pericarditis include a lack of reciprocal ST-depression in aVL, a normal QTc, concave-up ST-segments, and ST-depression in aVR and V1. When available echocardiography could be utilized to look for wall motion abnormalities prior to sending this patient to the cath lab.

When designing a STEMI system to provide maximal benefit to the patient a certain false positive rate is to be expected. The system must recognize the existence of this gray area and allow for overtriage in order to be successful for both the patients and their providers.

• What are your thoughts on the conclusion to this case?
• How many attempts at acquiring a clean tracing should be made?
• If your system allows Paramedic activation of STEMI, are you provided constructive feedback?

It's around 05:00 when the tones go off at your fire station for a medical response at a large apartment complex.

You leave the bunkhouse with the engine crew and check enroute. Dispatch relays you are headed to a 50 year old male with chest pain.

Upon your arrival to a first floor unit, you find the door unlocked and the patient sitting in a chair in his living room. He appears anxious, is pale and is holding his chest. The engine crew begins obtaining vital signs and places the patient on the cardiac monitor.

The patient tells you he was awoken from sleep with "some really bad pressure". He'd had the same pain, "come and go yesterday," and that he saw his doctor and was diagnosed with "strep throat".

When you ask about any other history he says he only has high blood pressure and high cholesterol, but denies taking any medications at all. 

• Pulse: 56, strong and regular
• BP: 136/94
• Resps: 22, labored
• SpO2: 96%
• Skin: pale, clammy

The patient is placed on a nasal cannula at 4 L/min.

You perform a focused assessment of the patient's chest pain:

• Onset: yesterday
• Provocation/palliation: nothing makes it better or worse, not reproducible upon palpation
• Quality: "Pressure"
• Radiation: localized retrosternal, does not move
• Severity: 8 of 10
• Timing: "went away 8 hours ago, woke me up so I called 911."

One of the firefighters hands you the 3-Lead as your partner is placing the electrodes on for a 12-Lead.

The patient denies any medication allergies and is handed 324 mg of chewable aspirin. Your partner hands you the 12-Lead.

Due to the wandering baseline you ask your partner to work on a cleaner tracing. The patient is instructed to breath slowly and to stay still. After the second attempt your partner hands you the following 12-Lead.

The patient states he feels very nauseous.

You're 10 minutes from the nearest hospital, 15 minutes from the nearest PCI center, and your patient has been to them both.

• What do you think is wrong with the patient?
• Is the recent diagnosis of "strep throat" important?
• Should this patient go to the PCI center or to the community hospital?
• How would you continue treating this patient?

Well, they're in the news again for all the wrong reasons.

Image credit: Fox 5 News

Click HERE for video.

Once again, owner "Doctor" Jon Basso is full of shit.

"The gentleman could barely talk…He was sweating, suffering. Anyone with an ounce of compassion would've felt for him…I actually felt horrible for the gentleman because the tourists were taking photos of him as if it were some type of stunt. Even with our own morbid sense of humor, we would never pull a stunt like that."

If you believe that one I've got some swamp land in Florida you might be interested in. He's loving this publicity.

Don't get me wrong. I like naughty nurses as much as the next guy.

Photo credit: Outhouse Rag

Maybe even more! 

But the Heart Attack Grill makes light of the death and suffering associated with cardiovascular disease.

Don't encourage them by visiting their establishment.

See also:

Diner suffers cardiac arrest while eating a Triple Bypass Burger in restaurant called the Heart Attack Grill

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!

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

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

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

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

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

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

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

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

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

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

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

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

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!

You are called to the local ER to transfer a 17 year old male to a large metro hospital for evaluation. Your patient  presented to the local ER with chest pain and palpitations following mild exertion. He was alert and oriented, and other than his elevated heart rate, his vitals were within normal limits.  Upon presentation to the ER:

• O:   Discomfort began during exertion
• P:   Exertion makes it worse
• Q:   Dull pain, substernal
• R:   non-radiating
• S:   3/10
• T:   about 20 minutes prior to ER arrival

• S:   Chest pain/palpitations
• A:   NKDA
• M:   N/A
• P:   No previous medical hx
• L:   Unknown
• E:   Mild exercise

As far as vitals go, all i can tell you is that they were within "normal limits" with the exception of heart rate. The patient is given trials of adenosine, lidocaine, digoxin, and cardizem, without successful conversion. In fact staff noted that the rhythm seemed to "speed up a bit" after the adenosine. He is put on an Amiodarone drip, which slows the rhythm a bit.  They then elected to cardiovert, and after three attempts he converted to a sinus rhythm.  Here is one of the rhythm strips and a 12 lead they acquired:

At the time you make contact, the patient has no complaints and is still in sinus rhythm. You apply your cardiac monitor and acquire your own rhythm strip and 12 lead:

Your trip to the metro hospital is uneventful, and he remained stable in your care.

What do you think is going on with this patient?

What is your interpretation of the ECGs?

Is there anything further you want to do for this patient?

This is the conclusion to 64 year old female CC: Trouble Breathing.

When we left off our crew was attending to an elderly female patient in respiratory extremis. Pulmonary edema was present and their initial 12-Lead was concerning.

Many readers correctly noted the normal sinus rhythm, a 1° AV Block, and a wide QRS. Other readers pointed out the apparent Left Bundle Branch Block due to a negative QS complex in V1. Only a few readers picked up on the abnormal presentation of the LBBB: lead I has an rS complex and there is right axis deviation! Right axis deviation is a very uncommon finding in LBBB [1].

Just as it is important to know what a normal 12-Lead looks like, we also need to know what our abnormal 12-Leads should normally look like. In the case of LBBB, we expect V1 to be negative and leads I/V6 to have broad, monomorphic R-waves.

We also expect the T-waves to be discordant with the dominant deflection of the QRS. A picture is worth a thousand words in this case:

In our case we have three troubling findings:

1. An rS complex in Lead I with Right Axis Deviation, which is very uncommon in LBBB.
2. Concordant ST-segments in leads V5 and V6.
3. Excessive ST-segement elevation in leads V2 through V4.

Many readers stated that a Left Bundle Branch Block is a STEMI mimic and precludes an activation of a STEMI alert until an old 12-Lead is used in comparison. However, criteria exists to diagnose a STEMI in the face of a LBBB or Paced rhythm.

Additionally, this patient's 12-Lead does not show a normal LBBB, but rather a non-specific intraventricular conduction defect or IVCD. Dr. Garcia would encourage, "considering the company it keeps," [2] which includes acute myocardial infarction!

Sgarbossa's criteria (and its modifications) for diagnosing STEMI in the face of LBBB or a Paced Rhythm has been covered in depth before so we'll only cover the positive criteria found on our 12-Lead:

1. Is there ST-segment elevation ≥1 mm that is concordant with the QRS complex? Yes.

   

2. Is there ST-segment depression ≥1 mm in leads V1, V2, or V3? No.
    
3. Is there ST-segment elevation ≥5 mm, or ≥20% the depth of the S-wave, that is discordant with the QRS complex? Yes.

   

With 2 of the 3 criteria met (only 1 is required), we can be very confident that we're looking at a STEMI. Additionally, any concordant ST-elevation present should always suggest a STEMI.

The paramedic in this case recognized the concordant ST-elevation and the abnormal LBBB, called in a STEMI alert, and transported the patient to the PCI capable center. The patient improved significantly on the non-rebreather and CPAP was not necessary. Prior to arrival a second 12-Lead ECG was acquired:

Enroute the patient proved to be difficult for IV access, and received external jugular access in the ED. Labs were drawn while they waited for the cath lab team to arrive.

In the cath lab a 100% occlusion of the LAD was found and corrected with stenting.

For QA purposes an old ECG was retrieved after the call to compare to the field ECG:

Given this prior ECG, the new LBBB alone would likely cause a STEMI activation. However, in the absence of our more definitive changes this is a very weak criteria for activation [3].

Even without the prior ECG, we have an abnormal LBBB (most likely IVCD due to a peri-infarction block) with concordant ST-elevation and a patient presenting with signs of actue left sided heart failure: all of which point to an acute myocardial infarction!

This case highlights the importance of knowing what abnormal should normally look like and understanding that not every patient fits the protocol. We hope you enjoyed this case as much as we did, so be sure to continue the discussion below.

1. Childers R, et al. Left bundle branch block and right axis deviation: a report of 36 cases. J Electrocardiol, 2000; 33 Suppl:93-102. [PubMed]
2. The Art of Interpretation Series. http://www.12leadecg.com/
3. Jain S, et al. Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. Am J Cardiol, 2011; 107(8):1111-6. [PubMed]

It's late into your shift when the tones go off for breathing problems at a local extended care facility. Enroute you're advised it is a 64 year old female with a "low O2 sat," and to, "use the main entrance."

As you arrive a staff member is waiting for you at the door and directs you to a familiar room. The patient, a larger woman well known to your unit, is noticably anxious and struggling to breathe even on a nasal cannula.

The staff informs you she's not been feeling well all day, and only recently developed shortness of breath. Your partner places the patient on a non-rebreather at 15 L/min and grabs a quick set of vitals.

A quick look at the patient reveales pale skin, circumoral cyanosis, pink frothy sputum, and a respiratory rate in excess of 30. She has a long cardiac history, and is often transported by your service. Your partner relays her vitals:

• Pulse: 120 bpm, weak radials
• B/P: 110/74
• SaO2: 78% on 2 L/min via NC
• Resps: 36, shallow
• BGL: 224 mg/dL

Auscultation of her lungs reveals rales in all fields.

Your partner asks if you'd like to put her on the monitor and you reply, "let's get moving and get it in the truck."

Once in the back of the truck you begin attaching the monitor, while your partner prepares CPAP. Her oxygen saturations have improved to 89% and her pulse and respirations have decreased noticably on the non-rebreather.

The rhythm strip is obscured due to patient movement, however, the 12-Lead prints out without issue.

You're 20 minutes from a PCI capable center and 5 minutes from a community hospital where the patient's physician often has her transported.

What does this 12-Lead ECG show?

What interventions does this patient need?

Do you need anymore information to make the appropriate treatment and transport decision?