There was no evidence of new infiltrates, pneumothorax, or pulmonary edema, the likely alternative explanations for this sudden onset of respiratory distress hypoxemia had resolved with supplemental oxygen, and Pa CO 2 was not measured. We posit this was the principal cause of this patient’s worsening respiratory distress other possible contributing factors are discussed here.

On the basis of the patient’s acute respiratory decompensation, audible wheezing, and hyperinflation on chest imaging, we inferred that bronchospasm with airflow limitation led to acute dynamic hyperinflation. A respiratory code was called for urgent endotracheal intubation. An electrocardiogram demonstrated sinus tachycardia. Imaging showed no evidence of pneumothorax, pulmonary edema, or new infiltrates. Auscultation of the chest revealed diffuse bilateral inspiratory and expiratory wheezes.Īn urgent chest radiograph was obtained and demonstrated enlarged lung volumes and a flattened diaphragm these findings were new compared with prior exam. She was extremely anxious and was using accessory muscles of ventilation. With increase in the F i o 2, oxygen saturation improved to 92%, but respiratory distress persisted. Her oxygen saturation was measured at 82% with 2 L/min supplemental oxygen by nasal cannula. Her vital signs were notable for tachycardia, with a heart rate of 125 beats/min, blood pressure of 150/90 mm Hg, and tachypnea with a respiratory rate of 28 breaths/min.

However, within minutes after the procedure, the patient developed acute respiratory distress and fever to 103☏. A diagnostic ultrasound-guided liver biopsy was performed for further evaluation of the hepatic mass. Treatment with empiric antibiotics was initiated all culture data were negative. A 70-year-old woman nonsmoker, with a history of asthma (no prior pulmonary function tests, not treated with chronic bronchodilators) and gastroesophageal reflux disease presented with abdominal pain, anorexia, and fever.

Antidote for morphine sulfate