EKG Challenge No. 16: Time to Shock or Block?

EKG Challenge No. 16: Time to Shock or Block?

A 76 year-old male with a history of severe ischemic cardiomyopathy with an ejection fraction of 15%, atrial fibrillation on coumadin, coronary artery disease, and chronic kidney disease is brought in by paramedics from a skilled nursing facility with confusion, somnolence, and vomiting. Per EMS report, the patient has been vomiting for two or three days.


On arrival, the patient’s blood pressure is 128/78 with a heart rate of 130 and oxygen saturation of 99% on room air. On exam, he is oriented to self only. He is slightly agitated but following commands. He has some mild garbled speech and is moving all extremities well. He denies chest pain, dyspnea, or abdominal pain. His extremities are well perfused with intact peripheral pulses and preserved capillary refill. A full set of labs are drawn and pending. A head CT is performed and shows an intracranial hemorrhage and small subarachnoid hemorrhage.

 

A routine 12-lead EKG is performed:

Based on this EKG and the patient’s medical history, what are your diagnostic considerations? What should you do next to address the findings on the EKG?

Check back next week for the case conclusion and teaching points!

EKG Challenge No. 15 Case Conclusion: 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:  

The EKG machine read this as "Sinus bradycardia with 1st degree A-V block with premature supraventricular complexes, right bundle branch block, left anterior fascicular block, left ventricular hypertrophy with QRS widening and repolarization abnormality."  Great.  But this makes no sense--an ibuprofen overdose doesn't cause EKG changes like this.  SOMETHING is missing in the history!

Most concerning on this EKG are the intraventricular conduction delay (widened QRS) and the prominent R' in aVR, which should raise your suspicion for sodium channel blockade.  It was discovered later by family that there was an empty 100 tablet bottle of 50 mg diphenhydramine tablets at the house that was full just a few days prior.  

Diphenhydramine is a commonly available drug used for allergic reactions, colds, and as a sleep aid.  With mild overdoses, diphenhydramine will cause sedation and anti-cholinergic effects (dry mucous membranes, hot flushed skin, mydriasis, urinary retention, tachycardia).  Higher doses can result in central nervous system toxicity, including agitation, delirium, seizures and even coma.  Large overdoses of diphenhydramine can also cause significant sodium-channel blockade similar to class 1a anti-arrhythmics [1], which lead to the above EKG findings.  This can be seen in tricyclic antidepressant overdoses also, as there is a similar mechanism of sodium channel blockade, and includes QRS prolongation (QRS > 100 ms) and prominent terminal R waves in aVR (R' > 3 mm) [2].

EKG in a patient with a tricyclic antidepressant overdose.  The QRS duration here was 122 ms.  Note the tall R' in aVR, which is more subtle than the diphenhydramine overdose EKG above.   

 

So what to do if you come across this overdose patient with severe, life-threatening diphenhydramine overdose?  In addition to stabilizing airway, breathing, and circulation, your next step should be administering sodium bicarbonate IV, which should help narrow the QRS and ward off ventricular dysrhythmias and seizures.  Serial EKGs should be checked after sodium bicarbonate infusion (e.g. 2  mEq/kg or 150 mEq of sodium bicarbonate), and if the QRS still is > 100 ms then sodium bicarbonate should be repeated.  If the EKG remains unchanged, the use of IV lipid emulsion therapy is an option supported by a few case studies [1,3].  Consultation with a medical toxicologist or poison control center should be sought for cases with severe toxicity.   

 

Patient Follow Up

In the ED, the patient was treated with sodium bicarbonate but unfortunately and quickly had worsening hypotension refractory to pressors and went into cardiac arrest.  Despite a prolonged resuscitation, the patient ultimately did not survive.  

 

Summary

  • Never trust your overdose patients and rule out other potential ingestions with an EKG, acetaminophen level, and salicylate levels. 
  • Classic signs of sodium channel toxicity (diphenhydramine, tricyclic antidepressants, anti-arrhythmic overdoses) include
    • QRS prolongation > 100 ms
    • Tall R' wave in aVR
  • Treat sodium channel toxicity with sodium bicarbonate and consider IV lipid emulsion therapy in refractory cases 

 

Submitted by Phil Chan (@PhilChanEM), PGY-3

Faculty reviewed by David Liss (@dave_liss), Toxicology Fellow

 

References 

1) West J Emerg Med. 2014;15(7):855–858.

2) Ann Emerg Med. 2015;66:363-367.

3) Clin Tox. 2010;48:945-948

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.