EKG Challenge No. 14 Case Conclusion: The EKG Sign Formerly Known as Prince?

On a Sunday afternoon, an elderly gentleman is brought into the emergency department by his wife complaining of chest pain that began one hour ago.  He is diaphoretic and appears very uncomfortable.  An EKG is obtained.  The patient has no prior EKGs available.

When you first look at the EKG, you note that there appears to be an abundance of PVCs... ventricular trigeminy actually.  Given the patient's clinical appearance, you suspect an acute MI.... now to just sort out the EKG to support your clinical gestalt.

Given the prevalence of ventricular ectopy,  you begin your analysis by identifying sinus beats [although you can use PVCs as well - see these posts (1) and (2)  on Dr. Smith's ECG blog]:

Sinus beats outlined in blue.  Other beats are premature ventricular contractions (PVCs)

 If you take one sinus tracing for each lead:

Secondly, you observe that the tracing follows left bundle branch block (LBBB) morphology.  New LBBB may be considered the criteria "formerly known as" an indication for cath lab activation.

 

The 2004 ACC/AHA STEMI guidelines included new LBBB as a indication for Cath lab activation in patients presenting with symptoms suspicious for acute MI.  This was changed in the 2013, largely due to data suggesting that this was responsible for a large number of "false positive" cath lab activations [1].  Two separate studies involving patients with LBBB evaluated for suspected STEMI found an overall low prevalence of coronary lesions amenable to PCI [2,3].

In "normal" LBBB, repolarization is characterized by ST segment and T wave deviation away from the major direction of the terminal QRS waveform - also known as "appropriate discordance" [1]. Hence, in leads where the QRS is positive, the ST segment (and often the T wave) are deflected in the opposite direction and vice versa:

Appropriate discordance makes it more difficult, but not impossible, to assess for acute myocardial infarction with underlying LBBB.  In 1996, Sgarbossa and colleagues retrospectively derived and independently validated a clinical prediction rule for EKG diagnosis of acute myocardial infarction in the context of LBBB using positive biomarkers as a gold standard [4].   These three criteria are illustrated in the figure below:

Image source: ecg12lead; Table source: Sgarbossa et. al. (1996)

There are few important things to note about the Sgarbossa criteria.  First, Sgarbossa criteria only need to be met in a single lead.  Second, the three criteria are not equal in their sensitivity or specificity with respect to predict myocardial infarction and thus are awarded different points within the model.   In the initial study, concordant ST elevation was found to have a sensitivity of 73% (95% CI 64-80) and specificity of 95% (95% CI 86-96), while concordant ST segment depression had a sensitivity of only 25% (95% CI 18-34) and specficity of 96% (95% CI 91-99).   The third criteria, discordant ST segment elevation > 5 mm, has a sensitivity of 31% (95% CI 23-39) and specificity of 92% (95% CI 85-96).  Thus, the Sgarbossa criteria were specific, but not necessarily sensitive, for acute myocardial infarction as diagnosed by positive biomarkers.

Source: Sgarbossa et. al. (1996)

A meta-analysis of subsequent studies evaluating the Sgarbossa criteria was published in 2008 [5].   Based on calculated sensitivities and specificities (see below), this study recommended at the Sgarbossa score of > 3 (i.e. only concordant ST elevation anywhere  or concordant ST depression in V1, V2 or V3) physicians should treat for acute myocardial infarction.  A Sgarbossa score of 2 (i.e. meeting the discordant criteria alone) was deemed "inadequate to diagnose myocardial infarction."

Source: Reference 5

Smith et. al. (2012)  addressed the low sensitivity of the initial Sgarbossa criteria by postulating that changing the third component (excessive discordance) to a proportional rule instead of a 5 mm absolute cutoff would increase both the sensitivity and specificity of the criteria.  They defined "Abnormal, excessive discordance" as a ST/S ratio of < -0.25. 

Image Source: Smith et. al. (2012)

The authors proposed a "modified" unweighted Sgarbossa criteria:

            1. Concordant ST elevation > 1 mm in any lead
            2. ST segment depression > 1 mm in V1, V2 or V3
            3. ST/S ratio < -0.25 in any lead with > 1 mm of ST segment elevation or depression

The EKG was considered positive for ischemia if any of the above criteria were met.

Based on a data set using angiographic occlusion or troponin value > 10 ng/mL as their cutoff for "true MI", they calculated a sensitivity of 91% (95% CI 76-98) and specificity 90% (83-95) for the Modified Sgarbossa criteria.

If we apply the Sgarbossa and Modified Sgarbossa criteria to our patient's EKG, the patient meets criteria for acute myocardial infarction.

The patient did go to the cardiac catheterization laboratory and was found to have a 100% occlusion of the mid-LAD:

Cath lab diagram demonstrating 100% occlusion of mid-LAD

So what would happen if this patient did not meet Sgarbossa criteria?  Remember Sgarbossa criteria are far from sensitive.  The modified Sgarbossa criteria significantly improve on this, but has not yet been validated in a distinct set of EKGs.  What would you do?

When this patient presented, the cardiologist was at first reticent to take him to the cath lab.  Rather than arguing technicalities on a Sunday afternoon, the attending physician, Heather Webb (@webbmd) used what I would say are some of the most important criteria in a patient who looks sick and has severe chest pain, diaphoresis and a presumed new left bundle branch block to demand that the patient go: Clinical Gestalt.

Take Home Points: Left bundle branch block makes the diagnosis of acute myocardial infarction more difficult.  The original Sgarbossa criteria developed in 1996 aimed at identifying myocardial infarction in the context of LBBB were specific but poorly sensitive.  These were improved with development of the Modified Sgarbossa criteria, which incorporated the concept for proportionality in the evaluation of ST/S discordance.  Remember that these rules do not fully account for  your pretest probability or clinical gestalt of when a patient is having an MI.  If the patient looks like they are having an MI and has a new left bundle branch block, they should probably go to the cath lab regardless.  Now for Prince's Song of the Heart...

Submitted by Maia Dorsett, PGY-4 (@maiadorsett)
Faculty Reviewed by Doug Char and Joan Noelker

Interested in reading additional resources (Thanks to @tbouthillet for sharing):
 -  ECG Medical Training  on the Modified Sgarbossa criteria
- Dr. Smith's ECG blog on Modified Sgarbossa criteria with links to additional cases
- ALiEM discussion of Modifed Sgarbossa criteria with management algorithm for new LBBB

References
1. Cai, Q., Mehta, N., Sgarbossa, E. B., Pinski, S. L., Wagner, G. S., Califf, R. M., & Barbagelata, A. (2013). The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time?. American heart journal, 166(3), 409-413.
2. Larson, D. M., Menssen, K. M., Sharkey, S. W., Duval, S., Schwartz, R. S., Harris, J., ... & Henry, T. D. (2007). “False-positive” cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. Jama, 298(23), 2754-2760.
3.Jain, S., Ting, H. T., Bell, M., Bjerke, C. M., Lennon, R. J., Gersh, B. J., ... & Prasad, A. (2011). Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. The American journal of cardiology, 107(8), 1111-1116.
4. Sgarbossa, E. B., Pinski, S. L., Barbagelata, A., Underwood, D. A., Gates, K. B., Topol, E. J., ... & Wagner, G. S. (1996). Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. New England Journal of Medicine, 334(8), 481-487.
5. Tabas, J. A., Rodriguez, R. M., Seligman, H. K., & Goldschlager, N. F. (2008). Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Annals of emergency medicine, 52(4), 329-336.
6. Smith, S. W., Dodd, K. W., Henry, T. D., Dvorak, D. M., & Pearce, L. A. (2012). Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Annals of emergency medicine, 60(6), 766-776.

EKG Challenge No. 14: Elderly gentleman BIBW (brought in by wife) ....

On a Sunday afternoon, an elderly gentleman is brought into the emergency department by his wife complaining of chest pain that began one hour ago.  He is diaphoretic and appears uncomfortable.  An EKG is obtained:

You have no prior EKGs available for comparison, but the patient denies any prior history of acute MI or CHF.  Interpret the EKG.   What do you think is going on?   What do you do next?

You can read the case conclusion here.

EKG Challenge No. 13 Case Conclusion: Sometimes The Pain Ain't From Cocaine

You are working one evening in the emergency department when you walk in to see your 4th chest pain patient of the night.  Your current patient is a 50-something year old male who's years of homelessness and cocaine abuse have made him appear older than his stated age.  He tells you that  he has been having left sided chest pain on and off for the last 3 hrs.  He received ASA and nitro x 2 in the ambulance and now feels much better.  You examine his EKG from today:

EKG #1 (day of presentation)

You then compare it to his EKG from two days ago when he came in for chronic diarrhea (and had mentioned some intermittent chest pain):

EKG #2 (EKG from two days prior to presentation)

... and compare it again with his EKG from 1 year before during an admission for chest pain in which he had a negative cardiac stress test:

EKG #3 (EKG from one year prior to presentation)

Initially, you compare his first and second EKG.  You think, "those T waves in V2 and V3 look weird, but they are unchanged from previous".  However, you note that this prior EKG was only a couple days before and you compare them with the EKG from a year before... when those strange, biphasic T waves were not present.

Whenever you see T wave abnormalities in a patient with possible unstable angina, you need consider an electrocardiographic syndrome of critical LAD stenosis that was first described by Hein Wellens and colleagues in 1982 and thus is referred to as Wellen's Syndrome. 

Wellens' Syndrome is a clinical-electrocardiographic syndrome with the following criteria [1,2]:
 - Prior history of chest pain - i.e. the patient is now chest pain free
- Little or no cardiac enzyme elevation
- No pathologic precordial Q waves
- Little or no ST-segment elevation
-  Symmetric or deeply inverted T waves in leads V2 and V3 (and occasionally the other precordial leads as well) OR  biphasic T wave in leads V2 and V3

As noted above, Wellens' syndrome has variable electrocardiographic presentations.  It comes in one of two forms:  symmetric, deep T wave inversions (75% of cases) or biphasic T waves (25% of cases) [2,3].  These T wave inversions are notable for their steep angle of descent and depth.  While changes in V2, V3 are typical, T-wave abnormalities may also be present in the other precordial leads (V1, V4, V5, V6) as well.  Wellens' syndrome is dynamic, which is one of the features that distinguishes it from more benign causes of precordial T wave inversion such as LVH with strain.  Dr. Steve Smith's ECG blog has this post on distinguishing benign T wave inversion from Wellens' syndrome.

Figure 1 from the original paper describing Wellens' syndrome (Ref 3).  Note the two patterns of precordial T wave abnormalities.

Wellens' syndrome was first identified by a retrospective study of patients presenting with unstable angina [3].  This study found a strong correlation between one of two distinct patterns of T wave abnormalities in V2 and V3 and high risk for progression to large anterior wall myocardial infarction.  This association was re-confirmed with a follow-up prospective study of 204 patients admitted to their hospital between 1980-1985 with unstable angina and findings of Wellens' syndrome on the EKG.  180 of these patients underwent cardiac catheterization.  All had evidence of LAD lesions,  29% of which were proximal to the first septal perforator.  In general, patients who had medical management vs. angioplasty were more likely to die of sudden cardiac death  (8/30 for medical management vs. 3/115) [4].

Given the high risk of progression to left anterior wall myocardial infarction and death, patients with Wellens' syndrome should NOT undergo a cardiac stress test. [2]  They should go cardiac catheterization sooner rather than later (probably from the ED in ideal circumstances) as they are extremely high risk for progression to anterior STEMI:

Figure 2 from the original paper demonstrating progression from Wellens' to STEMI (and death).

After intervention and with time, ninety percent of patients with Wellens' syndrome will regain a normal ST-T segment [4].  While an exact time period for resolution of EKG changes was not specified in Wellens' paper,  ST-T wave abnormalities were more likely to persist in patients who continued to have chest pain, undergo medical therapy, or had extensive collateral circulation on cardiac catheterization suggesting longer term and more permanent cardiac injury.

So what happened with our patient?  After his second presentation with unstable angina and biphasic T waves, the emergency physician diagnosed him with Wellens' syndrome and admitted him to the Cardiology service where he was taken for cardiac catheterization and underwent stenting of a 90% lesion in his proximal LAD.  While his hospital discharge summary announced that "it was felt that his chest pain was still most likely to costochondritis or cocaine use",  the change in T wave morphology on his post-cath EKG suggests otherwise:

Clinical Take Home: Proper risk stratification and correct disposition of patients presenting with possible acute coronary syndrome is a common and difficult problem faced by pre-hospital personnel and emergency physicians. While anterior T wave abnormalities can have a wide differential diagnosis with both benign and concerning causes  [including but not limited to persistent juvenile T wave inversion, pulmonary embolism, ongoing cardiac ischemia and neurocardiogenic injury], in a now pain free patient with symptoms of unstable angina a critical LAD stenosis with high risk for progression to large anterior wall MI must be considered.  These patients should undergo cardiac catheterization sooner rather than later as they are at very high risk for progression to massive acute anterior wall myocardial infarction.  Do not under any circumstances send them for a stress test, as this may trigger massive MI and cardiac arrest.  Finally, be a patient advocate.  Although coronary vasospasm from cocaine use can cause a pseudo-Wellens' syndrome, this is a diagnosis of exclusion. Just because a patient uses drugs does not mean that he/she does not have underlying coronary artery disease. 

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by Brent Ruoff
Thank you to Julianne Dean and Chris Palmer for the cases (and patient advocacy)

References:
[1]Tandy, T. K., Bottomy, D. P., & Lewis, J. G. (1999). Wellens’ syndrome. Annals of emergency medicine, 33(3), 347-351.
[2]Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens' syndrome. The American journal of emergency medicine, 20(7), 638-643.
[3] de Zwann, C., Bar F.W., Wellens, H.J. (1982). Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction." American heart journal, 103(4), 730-736.
[4] de Zwaan, C., Bär, F. W., Janssen, J. H., Cheriex, E. C., Dassen, W. R., Brugada, P., ... & Wellens, H. J. (1989). Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. American heart journal, 117(3), 657-665.

EKG Challenge No. 13: "I feel much better now"

You are working one evening in the emergency department when you walk in to see your 4th chest pain patient of the night.  Your current patient is a 50-something year old male who's years of homelessness and cocaine abuse have made him appear older than his stated age.  He tells you that he he has been having left sided chest pain on and off for the last 3 hrs.  He received ASA and nitro x 2 in the ambulance and now feels much better.  You examine his EKG from today:

EKG #1 (day of presentation)

You then compare it to his EKG from two days ago when he came in for chronic diarrhea and chest pain, but was chest pain free at the time:

EKG #2 (EKG from two days prior to presentation)

... and compare it again with his EKG from 1 year before during an admission for chest pain in which he had a negative cardiac stress test:

EKG #3 (EKG from one year prior to presentation)

  

What is your differential?  What is your management and dispo plan? 

Read the Case Conclusion here.

EKG Challenge No. 12 Case Conclusion: Because We're Only Human

You are working as the "triage physician" in a busy city emergency department when a 34 yo female presents with chest pain.   The pain is retrosternal and burning in nature and has been persistent for 3 hrs.  It is associated with some nausea, but no shortness of breath or diaphoresis.  You order a GI cocktail and get an EKG:

You systematically review the EKG.  The heart rate is normal. There is a p wave before every QRS complex, but the p-wave axis is abnormal (negative in lead II).   There is now an extreme rightward axis as the QRS is negative in leads I, II and avF.  As you analyze the ST segments for evidence of ischemia, there appears to be T wave inversions in the inferior distribution of II, III, and avF.  You start considering the differential of ectopic atrial rhythm, right axis deviation, and T wave inversions including PE or ischemia but stop yourself.  You think  "did someone switch the leads?"  You take a brief look at aVR and see that the P, QRS and T waves are positive, making you even more suspicious.

You ask for a repeat EKG to be performed:

The repeat is a completely normal EKG,  confirming your "EKG diagnosis":  Limb lead reversal, specifically Right Arm-Left Leg Lead Reversal.

To think through how this limb lead reversal causes the changes seen in the original EKG, you have to go back to Eintoven's triangle made up of three bipolar leads ( I, II and III) and three augmented unipolar leads (avR, avL and aVF) (Figure below).  The right leg lead serves as the ground.   A lead reads as "positive" when the direction of the electrical impulse the same as the direction of the vector.  In a normal EKG with a normal axis,  the QRS is positive lead I, II and avF because they are directed towards the left side of the heart. aVR is almost always negative because it is directed opposite the cardiac apex.

Lead I                    Difference between LA and RA electrodes
Lead II                   Difference between RA and LL electrodes
Lead III                  Difference between LA and LL electrodes   

Lead aVR            RA - (LA + LL)/2
Lead aVL            LA - (LL + RA)/2                 
Lead aVF            LL - (RA + LA)/2

Right Arm/Left Leg (RA/LL) limb lead reversal is essentially a 180˚ flip of Eintoven's triangle which results in the following changes:
          1. aVR and aVL switch places
          2. lead I becomes an inverted lead III
              lead III becomes an inverted lead I
              lead II is an inversion of itself

Take a moment to compare the two EKGs above, and see that this is what has happened. 

It can mimic left anterior fascicular block and inferior infarction pattern, but can be suspected based on a positive P, QRS and T wave in lead aVR and extreme right axis deviation.
  
Limb lead reversals are important to recognize in that they can mimic pathology including myocardial infarction, ectopic atrial rhythms,  and conditions characterized by diffuse low voltage (pericardial effusion or pulmonary disease)[1]. You want to be able to catch them because you do not want to make critical clinical decisions based on misinformation. There are case reports of changes in patient management that occurred based on incorrectly acquired EKGs  that mimicked a pseudoinfarction or junctional rhythm pattern, including thrombolytic therapy in a patient with a baseline abnormal EKG and limb lead reversal [2,3].

Fortunately, other than the sense that "that EKG just don't look right!",  there are typical patterns that can clue you in that a limb lead reversal may be present.  

General clues that there may be a lead reversal (limb or precordial) include [4]: 

Limb leads:
1. Abnormal P axis with positive P wave in avR and/or negative P waves in lead I and/or lead II
2. Very low amplitude in the lead I, II, or III
3. Concordant negative QRS and T waves in the leads I, II, III and/or aVF

Precordial leads:
Abnormal R wave progression in leads V1 to V6, especially when the R wave amplitude increases after an initial decrease in the precedent leads.

The above features can be highlighted by reviewing the typical lead reversal patterns [3,5].  Note images below are all from the same "patient" whose EKGs are featured above.

1. Arm electrode (LA/RA) limb lead reversal: This reversal is the most common limb lead reversal.  The tell-tale sign is an inverted p wave, QRS complex, and T wave in lead I.  In the absence of dextrocardia, this is pathognomonic of arm electrode reversal.  Remember, as general rule I and V6 point the same direction and should look the same on the EKG.  aVR and aVF have switched places, so they both look grossly abnormal as well.  An example:

Left Arm - Right Arm Limb lead reversal

In a Right Arm-Left Arm lead reversal:
                  1. Lead I will be a complete inversion of itself
                  2. Lead II and Lead III will switch places
                  3. Lead aVL and aVR will switch places

If you notice, both lead reversals involving the right arm lead to an abnormal appearance of lead aVR.  One more instance where lead aVR, which is often ignored by emergency physicans and cardiologists alike, can be very useful [6]  

2. Left Arm/Left Leg (LA/LL) limb lead reversal:  This is a more subtle limb lead reversal.  You can pick up on it by the fact that the p wave is larger in lead I than lead II.

As Eintoven's triangle is flipped 180˚ around the axis formed by aVR, the following happens to the EKG:
        1. Lead I and II switch places (hence the p wave larger in I than II)
        2. Lead III becomes an inversion of itself
        3. Leads aVL and aVF switch places

3. Right Arm/Right Leg (RA/RL) limb lead reversal: The key to picking up this reversal is an isoelectric recording in lead II.

Right Arm/Right Leg Limb Lead Reversal

This "flat-lining" of lead II happens because the right leg (ground) lead - which the electrocardiographic processor recognizes as having no potential difference from the left leg - into the right arm position.  Since lead II is the difference between the Right arm and Left leg, this comes out as a flatline.  aVR and aVF are also switched, resulting in uncharacteristically positive QRS in aVR.

 4. Left Arm/Right Leg (LA/RL) limb lead reversal: The key to picking up this reversal is an isoelectric recording in lead III.  The "flat-lining" occurs for the same reason above, except that this time there is no perceived difference between the right arm and the right leg.

Left Arm/Right Leg Limb lead reversal

5. Right Leg/Left Leg limb lead reversal usually leads to an EKG that is indistinguishable from normal.

6. Precordial Leads: Alterations  in placement of the precordial leads results in abnormal R wave progression pattern and can mimic posterior or anterolateral myocardial infarction.

Precordial leads altered to the following pattern: V6V5V4V3V1V2

Peberdy et. al. [1]  published an excellent summary of expected EKG changes:

 For more review, Life in the Fast Lane has a great explanation of Eintoven's triangle in limb lead reversals.

Take Home Points:  When evaluating EKGs, be on the lookout for the EKG findings suggesting limb lead reversals as these can mimic pathology include acute MI, abnormal atrial rhythms, and conditions causing low voltage.  Clues to finding these are abnormal P wave axis, extreme axis deviation, concordant negative QRS and T waves in the leads I, II, III and/or aVF.  When in doubt, repeat the EKG.

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by Joan Noelker and Doug Char

References:
1. Peberdy, M. A., & Ornato, J. P. (1993). Recognition of electrocardiographic lead misplacements. The American journal of emergency medicine, 11(4), 403-405.
2. Chanarin, N., Caplin, J., & Peacock, A. (1990). “Pseudo reinfarction”: a consequence of electrocardiogram lead transposition following myocardial infarction. Clinical cardiology, 13(9), 668-669.
3. Guijarro-Morales, A., Gil-Extremera, B., & Maldonado-Martín, A. (1991). ECG diagnostic errors due to improper connection of the right arm and leg cables. International journal of cardiology, 30(2), 233-235.
4. Rudiger, A., Hellermann, J. P., Mukherjee, R., Follath, F., & Turina, J. (2007). Electrocardiographic artifacts due to electrode misplacement and their frequency in different clinical settings. The American journal of emergency medicine, 25(2), 174-178.
5. Harrigan, R. A., Chan, T. C., & Brady, W. J. (2012). Electrocardiographic electrode misplacement, misconnection, and artifact. The Journal of emergency medicine, 43(6), 1038-1044.
6. Pahlm, U. S., Pahlm, O., & Wagner, G. S. (1996). The standard 11-lead ECG: neglect of lead aVR in the classical limb lead display. Journal of electrocardiology, 29, 270-274.

EKG Challenge No. 12: Once Upon a Time in Triage

You are working as the "triage physician" in a busy city emergency department when a 34 yo female presents with chest pain.   The pain is retrosternal and burning in nature and has been persistent for 3 hrs.  It is associated with some nausea, but no shortness of breath or diaphoresis.  You order a GI cocktail and get an EKG:

 What is your differential diagnosis?  What would you do next?
 Read the case conclusion here

EKG Challenge No. 11 Case Conclusion: It's Wide! It's Fast! It's a Wide Complex Tachycardia!

You are working one evening in the emergency department when a 60-something year old female is slotted for a room.  Her chief complaint?  "Fever, weakness, vomiting".    Seeing that her triage heart rate was 157, you leave your granola bar where it is and immediately walk into the room to assess her.  You see an elderly-appearing female in moderate respiratory distress.  Her temperature is 38.2,  blood pressure is 125/87, RR is 32, oxygen saturation is 93% on 5L NC.  She has a history of a bone-marrow transplant and is chronically immunosuppressed. She endorses poor PO intake and several episodes of emesis over the last few days.  She says that she came in today when she developed some shortness of breath as well.  She denies any chest pain or palpitations.  On exam, her mucous membranes are dry, her abdomen non-tender, and her breath sounds are decreased in the right base.  You are a bit disturbed by the looks of her rhythm strip on the monitor so you get a 12-lead EKG:

The EKG above features a regular tachycardia (rate of 162) with a QRS complex duration of > 120 ms with LBBB morphology.  This leads you to an initial EKG diagnosis of a regular wide complex tachycardia, which has the following differential [1,2,3]:  

Originates in the ventricle:

            1. Ventricular tachycardia

Originates above the ventricle, but has abnormal ventricular conduction:

            2. Supraventricular tachycardia (AVRNT) with delayed ventricular conduction 

            3. Atrial flutter with 2:1 block and delayed ventricular conduction

            4. Sinus tachycardia with delayed ventricular conduction 

Delayed ventricular conduction can be due to a pre-existing bundle branch block, a toxicologic insult leading to QRS widening (such as Na-channel blockade), electrolyte abnormality (such as hyperkalemia), or aberrancy.  Aberrancy refers to the situation in which one bundle branch is ready to conduct another beat, but the other has not had time to fully repolarize and occurs in the setting of tachycardias in which there is a very short interval between electrical impulses.

So how and why does one differentiate between these three scenarios?  Since we are emergency providers in the business of saving lives, the important consideration at each step of working through an EKG differential is considering  how making the "EKG diagnosis" will alter patient management.   

Since the management of sinus tachycardia is to treat the underlying cause (and not electricity or anti-arrythmmics), the first step of working through the differential is differentiate Sinus tachycardia with abnormal conduction from SVT with aberrancy and Vtach by asking

                                                   

                                                    Are there sinus p-waves?  

We underline the term sinus here because with SVT and Vtach you can get retrograde or abnormal p-waves.   To remind everyone, p-waves need to meet the following criteria for the rhythm to be considered sinus:

                                  - a p-wave in front of every QRS

                                  - Normal p wave axis:  upright in I, II; inverted in aVR; biphasic in V1.

 

If you can find a prior EKG for the patient with the same bundle branch block morphology, this lends further evidence to your cause.

If it is sinus tachycardia, then identify and treat the underlying cause.  If it is not sinus tachycardia, then you are left with two possibilities:  SVT with aberrancy or Vtach.  

The important thing here to realize is that if you treat SVT with aberrancy like Vtach (with electricity or amiodarone and admission) then you have caused no harm.  If you treat Vtach like SVT with aberrancy, then you have vastly under-estimated your patient's mortality and may do harm.  Adenosine can be given if a regular ventricular tachycardia is in the differential, but it does not reliably distinguish between SVT with aberrancy and Ventricular tachycardia, as there are a subset of Ventricular tachycardias (especially in young patients) that are adenosine sensitive [4].  If a patient with a wide complex tachycardia converts with adenosine, do not send them home (unless they have a previous EKG demonstrating a pre-existing bundle branch block with the exact same morphology).

Many algorithms have been developed to differentiate between these two conditions [5,6,7].  For those of you who are interested, more detailed descriptions of these algorithms are included at the very end of this post. 

The truth of the matter is that when there are more than five algorithms (and there are!) to differentiate between two conditions, it is likely that none of them are good enough to use in a life and death situation such as this one.  Indeed, one recent study by Szelenyi et. al. compared the "real life" sensitivity of two different recently developed algorithms (RWPT in II and Vereckei's avR algorithm) when applied by cardiologists, internists and emergency physicians [8].  Both algorithms were insufficiently sensitive for Ventricular tachycardia in this real life application:

 

Similarly, another study published by Kastrzebski et. al. found that the performance of multiple algorithms, including those cited above, was sub-par for real life use:

Image source: Reference 8

Therefore, if you are an "EP" as in Emergency Provider rather than Electrophysiologist, you should probably subscribe to the Mattu algorithm for management of wide complex tachycardias which he presented in this episode of the ECG case of the week:

  

           

Getting back to our case, you apply the Mattu algorithm to your patient.

Step 1:  Is the rhythm sinus?

You examine the EKG and find upright p-waves in lead II:

After 1 liter of fluid her heart rate comes down and you can see this even more clearly:

                       Your EKG diagnosis? sinus tachycardia with LBBB.

                       Your emergency department management?  Treat the underlying cause.

Given that this is an immunosuppressed patient with fever and tachycardia,  you have high suspicion for sepsis.   Blood and urine cultures sent.  A CXR reveals an underlying right-sided pneumonia.

The patient is started on broad spectrum antibiotics and ultimately does well.   Score: EP 1, Sepsis 0.

Take home Points: Wide complex tachycardias have an important differential diagnosis.  Start by determining if the rhythm is sinus, because this requires treating the underlying cause such as sepsis, PE, dehydration or pain.  If the rhythm is not sinus, assume its ventricular tachycardia because even if you had the time, no algorithm is sensitive or specific enough to rule out Vtach.  Electricity helps both and should be used in the unstable patient.  Remember, it's safer in the long run to assume it's T-rex and not a Tweety bird: 

Submitted by Maia Dorsett (@maiadorsett), PGY-3

Faculty reviewed by  Douglas Char

 

References:

[1]Goldberger, Z. D., Rho, R. W., & Page, R. L. (2008). Approach to the diagnosis and initial management of the stable adult patient with a wide complex tachycardia. The American journal of cardiology, 101(10), 1456-1466.

[2]Brady, W. J., & Skiles, J. (1999). Wide QRS complex tachycardia: ECG differential diagnosis. The American journal of emergency medicine, 17(4), 376-381.

[3]Hollowell, H., Mattu, A., Perron, A. D., Holstege, C., & Brady, W. J. (2005). Wide-complex tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with aberrant conduction. The American journal of emergency medicine, 23(7), 876-889.

[4]Brugada, P., Brugada, J., Mont, L., Smeets, J. L. R. M., & Andries, E. W. (1991). A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation, 83(5), 1649-1659.

[5] Pava, L. F., Perafán, P., Badiel, M., Arango, J. J., Mont, L., Morillo, C. A., & Brugada, J. (2010). R-wave peak time at DII: a new criterion for differentiating between wide complex QRS tachycardias. Heart Rhythm, 7(7), 922-926.

[6]Vereckei, A., Duray, G., Szénási, G., Altemose, G. T., & Miller, J. M. (2008). New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm, 5(1), 89-98.

[7]Szelényi, Zsuzsanna, et al. "Comparison of the “Real‐life” Diagnostic Value of Two Recently 

 Published Electrocardiogram Methods for the Differential Diagnosis of Wide QRS Complex Tachycardias." Academic Emergency Medicine 20.11 (2013): 1121-1130.

[8] Jastrzebski, M., Kukla, P., Czarnecka, D., & Kawecka-Jaszcz, K. (2012). Comparison of five electrocardiographic methods for differentiation of wide QRS-complex tachycardias. Europace, 14(8), 1165-1171.

Still up for a little more learning? Here is a summary of three of the algorithms for distinguishing SVT with aberrancy vs. Vtach.  Below is a summary of three of them as well as links to additional resources.

i. The Brugada algorithm:  One of the most well-known criteria for differentiating SVT with aberrancy vs Vtach.  It comprises a series of four questions.  If the answer to any question is "Yes" then the diagnosis is Ventricular tachycardia [5].

Brugada algorithm; Figure 1 from Reference 5.

You can link to the PV Card from ALiEM for the Brugada criteria here.

ii. R-wave to peak time at DII: This algorithm (also from Brugada) was published in 2010 as an attempt to develop simpler criteria utilizing only one lead [6].  It was developed using an EP study as a gold standard.  The basic premise is that if the R wave to peak time (duration from the onset of QRS depolarization onset until the first change of polarity) is > 50 ms in lead II, the diagnosis is Vtach.  The authors reported a sensitivity and specificity for Vtach of 0.93 and 0.99, respectively.

RWPT in lead II measurement.  Figures 5 & 6 from Reference 6.

One thing that you can see from their example (above) is that measuring RWPT really is not that straightforward.  And practically speaking, a sensitivity of 93% really is not good enough.  You can read more about this method at ALiEM here.

iii. Vereckei's algorithm for lead aVR, published in 2008, uses lead aVR to differentiate from Vtach vs. SVT with aberrancy:

The last step of this algorithm, Step 4, requires a calculated comparison of the distance traveled during the initial and concluding impulses of the QRS complex:

In the initial study, they reported a 96.5% sensitivity for the diagnosis of Ventricular tachycardia.

EKG Challenge No. 11 - Mmmm.... That looks sort of fast...

You are working one evening in the emergency department when a 60-something year old female is slotted for a room.  Her chief complaint?  "Fever, weakness, vomiting".    Seeing that her triage heart rate was 157, you leave your granola bar where it is and immediately walk into the room to assess her.  You see an elderly-appearing female in moderate respiratory distress.  Her temperature is 38.2,  blood pressure is 125/87, RR is 32, oxygen saturation is 93% on 5L NC.  She has a history of a bone-marrow transplant and is chronically immunosuppressed. She endorses poor PO intake and several episodes of emesis over the last few days.  She says that she came in today when she developed some shortness of breath as well.  She denies any chest pain or palpitations.  On exam, her mucous membranes are dry, her abdomen non-tender, and her breath sounds are decreased in the right base.  You are a bit disturbed by the looks of her rhythm strip on the monitor so you get a 12-lead EKG:

Interpret the EKG.  What is your differential?  What would you do next?  

See the case conclusion here. 

EKG Challenge No. 10 Case Conclusion: Heartbreaker

You are working in the emergency department when you get a pre-arrival for "abdominal pain, hypotensive".  You follow EMS into the room when they arrive and are confronted with an elderly female who appears very pale and quite sick.  Per the paramedics and the patient,  she has had upper abdominal pain, nausea and weakness for the last two days.  Her initial blood pressure is 80/60 with a heart rate of 112, and you start working her up for all the badness that causes hypotension and abdominal pain in the elderly.  Everyone gets cracking on some IV access,  and you head for the ultrasound to help you better evaluate the cause of this patient's hypotension.  You start with the cardiac views of your RUSH exam, and see this:

 

Given these findings, you order an EKG:

On review of the EKG you note ST elevation that is most prominent in V2 and V3 (although it can also be seen in I, II, V4, V5) without significant reciprocal ST depression:

Given the apical akinesis and ST elevation in the precordial leads, the patient is sent for an emergent cardiac catheterization, which identifies no coronary artery disease.  

Normal Coronary arteries

                                        
The cardiologist notes apical akinesis of the patient's left ventricle, which during systole resembles a Japanese pot for catching an octopus.   He diagnoses the patient with Takatsubo's Cardiomyopathy.

EKG Challenge No. 10: This one looks sick ...

You are working in the department when you get a pre-arrival for "abdominal pain".  You follow EMS into the room and are confronted with a middle-aged to elderly female who appears very pale and quite sick.  As she is placed on the monitor, you speak with her and she endorses some diffuse abdominal pain and nausea for the last two days.  Her initial blood pressure is 80/60 with a heart rate of 112, and you start working her up for all the badness that causes hypotension and abdominal pain in the elderly.  Everyone gets cracking on some IV access,  and you head for the ultrasound to help you better evaluate the cause of this patient's hypotension.  You start with the cardiac views of your RUSH exam, and see this:

 Given these findings, you order an EKG:

What is your differential?  What do you do next?  Please leave your comments.  Click here to read the case conclusion.

Thank you to Dr. Chris Holthaus for the echo video.