Abstract Hypoxia secondary to pulmonary embolisms (PE) is primarily due to the ventilation to perfusion (V/Q) mismatch. As blood cannot flow past the point of obstruction, there is a low V/Q ratio in areas of no obstruction and high V/Q ratio in areas past the obstruction. This V/Q mismatch is partly caused by an increase in physiologic dead space. In the following case, we will present an example in which a concurrent ventilatory impairment led to the improvement of the patient’s V/Q mismatch in the setting of a massive PE. The patient is a 68-year-old male with past medical history significant for tobacco use disorder, cerebrovascular accident, and necrotizing pneumonia. He presented with shortness of breath and left lower extremity swelling. Patient was alert and oriented to person and place and denied shortness of breath, chest pain, and lower extremity pain. Vitals were significant for tachycardia, hypertension, and hypoxia, which improved with 2 liters nasal cannula. Labs were remarkable for negative troponins, elevated brain natriuretic peptide at 8677 picograms per milliliter, and lactic acid at 2.6 millimoles per liter. Left lower extremity venous duplex showed acute deep venous thrombosis. Computed tomography scan for PE showed acute saddle PE with large clot burden extending bilaterally and right heart strain. It also showed interval total collapse of the left lung with superimposed aspiration or opacification with worsening leftward shift of mediastinal structures due to lung volume loss and right sided pulmonary edema versus aspiration pneumonia. The PE response team was consulted, and the patient was determined not to be a candidate for thrombectomy as the clot was felt to be subacute given the negative troponins and lack of right ventricular dysfunction on echocardiogram despite the large clot burden. The patient was subsequently started on therapeutic anticoagulation. Despite an extensive saddle PE, the patient remained hemodynamically stable, and oxygen requirements were minimal. Of note, this patient had a recent case of necrotizing pneumonia and aspiration resulting in bronchial occlusion that led to complete collapse of the left lung. This phenomenon would cause V/Q mismatch through a physiologic shunt. Theoretically, the collapsed lung would have minimal ventilation, reducing the amount of physiologic dead space due to PE, and conversely, with a PE, there would be redirection of blood flow, minimizing the physiologic shunt from the collapsed lung. The presence of both pathologies occurring simultaneously likely actually resulted in the improvement of the patient’s V/Q mismatching. This abstract is funded by: None
Panicker et al. (Fri,) studied this question.