Core EKG: Don’t stress, it’s just an ECG…

EKG Characteristics

• Rate

  66

• Rhythm

  Normal Sinus Rhythm

• Intervals

  Normal PR, QRS, QT Intervals

• Axis

  Normal

• ST Segments

  ST segment elevations in I, aVL, V1, V2 and reciprocal ST depressions in II, III and aVF

Diagnosis

Diagnosis:

Takotsubo’s Cardiomyopathy (also known as stress-cardiomyopathy, stress-induced cardiomyopathy, broken heart syndrome, and apical ballooning syndrome)

Questions

1. What is your differential diagnosis for this patient?

   Acute coronary syndrome (ACS), cardiomyopathy, cardiogenic shock, aortic dissection, pulmonary embolism, myocarditis/pericarditis, cardiac tamponade, coronary artery dissection, coronary vasospasm, ventricular aneurysm

2. What are your next steps in management for this patient?

   EKG is concerning for acute STEMI with STE in lead I and aVL with reciprocal changes. The patient is also hypotensive and hypoxic, concerning for cardiogenic shock. Initial management steps include dual antiplatelet therapy, heparin, and STEMI activation for emergent catheterization. Consider serial EKGs, which may demonstrate evolution of disease. If the patient remains hypotensive, consider starting vasopressors. Use caution with inotropes, such as dobutamine, as they have mild vasodilatory effects and can worsen hypotension if given prior to vasopressors.

Discussion

Case Discussion:

This patient’s initial EKG was concerning for a STEMI, given the anterolateral ST-elevations with reciprocal ST-depressions in the inferior leads. 

EKG two months prior to presentation is grossly normal:  

Additionally, she presented with signs of cardiogenic shock, given her hypotension and syncope.  Point of care ultrasound (POCUS) revealed global decreased contractility with an enlarged LV and scattered B-lines on lung exam. The ED team emergently notified cardiology and loaded her with aspirin, ticagrelor, and heparin. She was given a small amount of IV fluids; however given the concern for cardiogenic shock and persistent hypotension, she was started on a norepinephrine drip with good response. She was taken urgently to cardiac catheterization, which revealed mild diffuse coronary artery disease without occlusion and an estimated Ejection Fraction (EF) of 45%. High-sensitivity troponin peaked at 61 and BNP was normal.

 

Upon transfer to the MICU, she remained hypotensive and CXR revealed multifocal pneumonia. She was presumed to be in septic shock and was started on broad spectrum antibiotics and continued on norepinephrine drip. Upon further workup, TTE showed abnormal LV relaxation, mid and apical segments of LV akinesis, and an EF of 34% — a pattern consistent with Takotsubo’s Cardiomyopathy. The patient was ultimately diagnosed with Takotsubo’s cardiomyopathy and multifocal pneumonia, leading to mixed cardiogenic and septic shock. She was weaned off of pressors and discharged four days after presentation to the ED with close cardiology follow up.

 

Epidemiology:

• First described in Japan in 1990
• Present in 1-2% of patients with troponin-positive suspected ACS
• Incidence of stress cardiomyopathy among patients undergoing physical or emotional stress is not known
• More common in women than men, predominantly in older population
  • 90% of cases occur in postmenopausal women

Pathophysiology:

 

The pathophysiology of Takotsubo’s cardiomyopathy is not completely understood.  Currently it is hypothesized to be a combination of sympathetic nervous system activation and microvascular spasm. When a patient undergoes a significant stressor, the sympathetic nervous system sends  a catecholamine surge, which leads to coronary microvascular spasms. The cardiac apex has the highest number of sympathetic fibers – therefore, the apex is primarily affected in this syndrome.

 

Typical EKG Findings:

ST elevation mimicking STEMI/OMI:

The acute phase of Takotsubo’s cardiomyopathy shows ST-elevations +/- Q-waves due to ischemia secondary to microvascular spasms. Given the concern for ischemia and STEMI, there are no emergent tests in the ED that can exclude coronary occlusion, apart from taking the patient to emergent angiography. Because Takotsubo’s usually affects the apex, isolated ST-elevations in leads V2-5 and II, without inferior ST-depressions, are typical. Variability in this pattern is present, as this case demonstrates.  Some patients may also present with a new left bundle branch block.

 

T-wave inversion with long QT intervals: 

After the acute phase, T-wave inversions and Q-waves develop, reflecting myocardial reperfusion. The T-wave inversions are typically diffuse and deep, with a prolonged QT interval. In this particular case, repeat EKG seven days later showed diffuse T-wave inversions in inferior and anterolateral leads with a mildly prolonged QTc interval of 464ms. 

 

This patient’s EKG seven days after initial ED presentation: 

Diagnosis:

 

Takotsubo’s cardiomyopathy is a retrospective diagnosis of exclusion contingent on the following findings:  

-Angiogram without coronary artery occlusion

-TTE with apical ballooning

-Follow-up TTE with Left Ventricle recovery 

 

Modified Mayo Clinic criteria:

• Absence of coronary artery disease >50% on angiography
• Transient dyskinesis, hypokinesis, or akinesis of the left ventricle midsegments with or without apical involvement
• Regional wall motion abnormalities beyond a single epicardial vascular distribution
• New ECG changes (ST elevation or T wave inversion) or moderate troponin rise
• Absence of myocarditis or pheochromocytoma

Management:

• Supportive care and resolution of the stressor usually results in full resolution of symptoms
• Heart failure management:
  • Beta-blocker
  • Ace-inhibitor / ARNI
  • Diuretic
• In patients with hypotension and signs of cardiogenic shock:
  • Perform TTE. It’s important to determine if patient has left ventricular outflow tract (LVOT) obstruction, as giving inotropes to a patient with underlying LVOT obstruction may induce worsening LVOT obstruction and exacerbate cardiogenic shock
  • Without LVOT obstruction
    • Mild fluid resuscitation
    • Inotropes (ie. Dobutamine, Milrinone, Dopamine)
    • Vasopressors (ie. Norepinephrine)
  • With LVOT obstruction
    • Do not use inotropes
    • Beta-blockers may help with resolution of the obstruction
    • Increase preload with mild fluid resuscitation and leg raise
    • Consider alpha agonists (ie. Phenylephrine) to increase afterload, therefore improving hemodynamics
      • Use caution as this can lead to worsening coronary vasospasm

Pearls

• EKG findings are typically consistent with anterolateral ST elevations in leads II, V2-V5 without reciprocal depressions, however each patient presentation differs - as you can see in this case!
• You can’t definitively make a diagnosis of Takotsubo’s cardiomyopathy in the ED, therefore, it’s important to have a high clinical suspicion for ACS and to activate your hospital’s STEMI protocol as indicated
• Management is typically supportive and tailored to the patient’s presentation

Sources

• Buttner, R., Burns, E., & Burns, R. B. and E. (2021, April 29). Takotsubo cardiomyopathy. Life in the Fast Lane • LITFL. https://litfl.com/takotsubo-cardiomyopathy-ecg-library/ 
• Khalid, N. (2023, March 6). Pathophysiology of takotsubo syndrome. StatPearls [Internet]. https://www.ncbi.nlm.nih.gov/books/NBK538160/ 
• McLaren, J. (2022, September 13). ECG approach to takotsubo syndrome: ECG cases: EM cases. Emergency Medicine Cases. https://emergencymedicinecases.com/ecg-cases-takotsubo-syndrome/ 
• Reeder GS, Prasad A. Management and prognosis of stress (takotsubo) cardiomyopathy. In: UpToDate, Connor RF (Ed),