Well put Sebastian! If you are thinking massive PE then you are correct!

(Follow this LINK to the initial post, with ECGs and question.)

 

Definition of massive pulmonary embolism (PE) is a PE with cardiac arrest, systemic hypotension (SBP < 90mmHg or drop in SBP of at least 40mmHg from baseline for at least 15 minutes), or shock (evidence of tissue hypoperfusion).

There are many ECG findings in PE, including but not limited to:

  • Normal sinus rhythm
  • Sinus tachycardia
  • Low voltage in limb leads
  • New or incomplete right bundle branch block, including tall terminal R’ in V1
  • Right axis deviation
  • S1Q3T3 (S-wave in lead I, Q-wave in lead III, and inverted T-wave in lead III)
  • Peaked P-waves in II, III, aVF (P pulmonale)
  • Deep inverted T-waves with or without ST-depressions in V1-V3, may also include leads II, III, aVF

You can see three of these findings on the above ECG. There is an incomplete RBBB, S1Q3T3, and deep T-wave inversions in V1-V4 & II,III, aVF. In addition, there are also ST-depressions in V1-V4. The ST-segment and T-wave changes in the anterior and inferior leads are consistent with right ventricular strain. A brief bedside echo may further increase your suspicion for PE if you see an enlarged RV, bowing of the interventricular septum towards the LV (‘D-sign’), or akinesis of mid-RV free wall with normal motion at apex (McConnell’s sign).

The patient became hypotensive shortly after the ECG was taken, which by definition, means we are dealing with a massive PE. Patients such as this are too unstable to go for a CTA of their pulmonary arteries to confirm the diagnosis. In a patient with risk factors, physical findings, characteristic ECG & bedside echo findings consistent with PE, the appropriate thing to do is manage the patient for presumptive PE.

The key to management is recognizing the signs of PE early on and thrombolysis for hemodynamic instability. If there are no absolute contraindications present, tPA is the mainstay of treatment for massive PE. In most cases systemic thrombolytics are given, however we may see more of a trend toward catheter-directed thrombolysis in the future.

If there are absolute contraindications for thrombolytics or if a patient remains hemodynamically unstable after thrombolysis, consider getting your interventional radiologists and/or surgeons involved for possible percutaneous catheter thrombectomy or surgical thrombectomy, depending on your institution and available resources. Percutaneous catheter interventions include thrombolysis, aspiration thrombectomy, and/or thrombus fragmentation, which converts a massive PE into many smaller PEs.

See EM-CCM Pulmonology: Managing Massive PE critical care blog post for more information regarding massive PE management.

 

References:

Ferrari E, Imbert A, et al. The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads—80 case reports. Chest. 1997. March;111(3):537-543.

Kucher N, Goldhaber S. Management of massive pulmonary embolism. Circulation. 2005;112:e28-e32.

Jaff M, McMurtry M, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension. A scientific statement from the American Heart Association. Circulation. 2011;123:1788-1830.

Martindale, Jennifer and Brown, David. “Chapter 9: Voltage Abnormalities”. Rapid Interpretation of ECGs in Emergency Medicine. Philadelphia, PA: Lippincott Williams & Williams, 2012.

 

 

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