EKG challenge

EKG Challenge No. 15: Too Much Ibuprofen?

Paramedics bring in a 29 year old male with a history of depression and alcohol abuse for a reported ibuprofen ingestion of unknown quantity as a suicide attempt.  The patient initially was somnolent and admitted to alcohol use, but while being transported suddenly had a generalized tonic-clonic seizure.  Paramedics quickly administer IV diazepam for the resolution of seizure activity, and he is post-ictal on arrival to the ED.  Blood pressure is 98/60 with an irregularly irregular heart rate of 62 on the monitor.  He has no history of seizures or cardiac disease in his records.  His 12-lead EKG shows this:  

How would you describe the EKG?  Can you make a diagnosis from this EKG?  What would you do next? 

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.