An uncommon cause of acute severe respiratory failure: a case report

Abstract

Hypoxemia is an abnormally low arterial oxygen tension [1].Hypoxemia can result from any combination of the following causes:• hypoventilation • ventilation-perfusion mismatch • diffusion impairment • right to left shunt • low inspired air oxygen content.In the literature there are some case reports of hypoxemia due to right to left blood shunting [2][3][4]. Most causes of right to left shunting through a patent foramen ovale are attributed to right atrial pressure exceeding that of the left, forcing open a potentially patent foramen ovale. A patent foramen ovale is present in 25-30% of healthy subjects [5], and is responsible for a right to left shunt when pulmonary hypertension is present. In the absence of pulmonary hypertension there are three main pathophysiologic mechanisms [6]: extrinsic compression of the right atrium (right hydrothorax or a localized pericardial effusion) causing an increase in the right heart pressure; a decrease in the compliance of the right ventricle (due to right ventricle ischemia or after pneumonectomy); and an abnormal anatomic relationship between the vena cava and the atrial septum or an anatomic distortion of the heart with downward displacement of the right atrium due to the enlargement of the thoracic aorta with distortion of the position of the atrial septum relative to caval inflow and favouring interatrial flow. Case reportAcute respiratory failure with hypoxemia is commonly seen in the emergency department (ED). While there are many causes of hypoxemia, in patients with refractory hypoxemia, we must remember right to left shunt.We describe the case of a 86-year-old man, who presented to our ED with progressive dyspnea. He had been recently discharged from another hospital with a diagnosis of pneumonia. He had a history of previous myocardial infarction, chronic atrial fibrillation, mechanical aortic prosthetic valve replacement, an ascending aortic aneurysm, as well as chronic obstructive pulmonary disease with cor pulmonale. He was on the following therapy: picotamide, warfarin, digoxin, methylprednisolone, furosemide, nitrates, proton pump inhibitors, and an inhaled bronchodilatator.The patient was admitted to the hospital for progressive dyspnea, without fever, cough or thoracic pain. On physical examination the vital signs were: blood pressure 120/ 80 mmHg, heart rate 80 beats/min, respirations 18 breaths/ min, and arterial oxygen saturation 65% in room air. The heart sounds were of normal intensity without audible murmurs. The breath sounds were diminished bilaterally. There was no pedal edema, no hepatomegaly, and no jugular vein distension.The ECG showed a sinus rhythm, a right bundle branch block, and left anterior hemi-block. The arterial blood gas analysis on room air showed: pH 7.50, PaO 2 33 mmHg, PaCO 2 31 mmHg, HCO 3 22.6 mmol/L, sat. 71%. Increasing the inhaled FiO 2 did not correct hypoxemia: with a