UOTW #54 Answer

Answer: acute pulmonary embolism (PE) with severe pulmonary hypertension, and an atrial septal defect (ASD) causing right to left shunting

This bedside echocardiogram demonstrates a severely dilated RV with a McConnell’s sign (akenetic RV free wall with spared function at the apical septum). During the apical view, the patient’s peripheral IV was being flushed with normal saline, resulting in a serendipitous bubble study. It is apparent that there is a significant right to left shunt.

The patient’s presentation and echocardiogram prompted an emergent CTA of the chest that demonstrated several segmental pulmonary emboli. The degree of severe hypoxia would typically not be explained by this finding in isolation. It can also be stated that a PE resulting in such severe hypoxia would typically not result in this patient’s relatively normal hemodynamics.

Subsequent history was obtained on this patient: he had had multiple previous pulmonary emboli. This patient’s right to left shunt was the result of an unfortunate combination of acute on chronic pulmonary hypertension and an ASD. The acute PE pushed the patient’s pulmonary artery pressures (and subsequent RV&RA pressures) above those being generated on the left heart, so the shunt suddenly become worse.

There are several important points in the management of this patient:

  • In patients who are having a right to left shunt, positive pressure ventilation will worsen the shunt.1,2 Once intubated, decreasing the inter-thoracic pressure associated with PPV can improve oxygenation.  This patient’s O2 sat increased to 90% (paradoxically) when the TV was decreased to 6 ml/kg and PEEP was decreased to 2.
  • Although this patient’s presentation did not meet all the criteria for acute submassive pulmonary embolism, he is someone who would benefit from thrombolysis given his severe PH and shunt.  He was subsequently administered thromblytics and over the next 24 hours was able to be weaned off the high oxygen requirements.
  • Patients who have an ASD, PFO in this case, are relatively protected from the expected hemodynamic compromise of massive pulmonary embolism because the right to left shunt allows for some LV filling and maintenance of systolic perfusion.3,4
  1. Védrinne JM, Duperret S, Gratadour P, Barthélémy C, Motin J. [Effects of mechanical ventilation with PEEP on right to left intra-cardiac shunt caused by patent foramen ovale]. Ann Fr Anesth Reanim. 1995;14:(5)387-92. [pubmed]
  2. Cujec B, Polasek P, Mayers I, Johnson D. Positive end-expiratory pressure increases the right-to-left shunt in mechanically ventilated patients with patent foramen ovale. Ann Intern Med. 1993;119:(9)887-94. [pubmed]
  3. Moua T, Wood KE, Atwater BD, Runo JR. Major pulmonary embolism and hemodynamic stability from shunting through a patent foramen ovale. South Med J. 2008;101:(9)955-8. [pubmed]
  4. Brydon C, Fawcett WJ, Treasure T, Clarke JT. Pulmonary embolus and patent foramen ovale: a rare cause of refractory hypoxaemia. Br J Anaesth. 1993;71:(2)298-300. [pubmed]

7 thoughts on “UOTW #54 Answer

  1. great case, I just had a patient who’s sat was registering below 50’s the other day and was wondering how this could be. Great explanation of shunt physiology

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