A 28-year-old G1, PO 26-wk pregnant woman is seen in the OB clinic. She has a past history of bronchial asthma that has been well controlled for the last year by inhaled steroids. She states that she has noted increasing shoness of breath for the last 3 days. On examination, she appears tachypneic and moderately uncomfoable. On physical examination, she has a pulse of 110 bpm; normal temperature; respirations 32/min; blood pressure 160/90 mm Hg. Hea exam: NSR without any gallop. A grade 2/6 systolic murmur in the pulmonic area is heard. Lung exam is clear to auscultation; abdomen exam confirms a 26-wk gravid uterus. Laboratory data: Hb 12 g/dL; Hct 36%; WBCs 7.0/uL with normal differential; BUN 23 mg/dL; creatinine 0.9 mg/dL; sodium 136 mEq/L; potassium 4.2 mEq/l. ABGs on room air: pH 7.34; PCO2 34 mm Hg; PO2 68 mm Hg. PEFR 450 L/min. Chest x-rays are shown.The most likely diagnosis is
The PA show normal lung parenchyma. There are no mediastinal nodes or masses. The cardiophrenic and costophrenic angles are clear. Also, on the lateral view there is an enlarged left main pulmonary aery pressing over the LUL bronchus. Calcified hilar nodes are noted. This is a classic example of a clinical scenario with a high likelihood of pulmonary embolism in a high-risk patient. The chest radiograph is often unimpressive or normal, as in this case. However, congestive atelectasis, as mentioned in the previous question, moderate bloody pleural effusion, and nodular or patchy infiltrates can be seen. In some cases unilateral oligemia (Westermark sign) is recognized. Hampton's hump is a term used to define pulmonary lobules filled with blood. These are triangular pleural-based infiltrates with their apex toward the hilum. The increased alveolar aerial gradient seen on the aerial blood gas study suggests a ventilation-perfusion (V/Q) mismatch and rules out an acute anxiety state as the cause of the symptoms. Although the patient has a history of bronchial asthma, the lung exam reveals no wheezing or expiratory prolongation and symptoms have been well controlled. Peak flows are satisfactory and hence an acute asthmatic attack is unlikely. With a hemoglobin level of 12 g/dL and no clinical evidence of hea failure, a diagnosis of high-output hea failure is incorrect. The clinical diagnosis of pulmonary embolism warrants fuher diagnostic steps. A V/Q scan would be most helpful in reaching a diagnosis, especially in this case with a normal CXR. Other tests to assess respiratory function or exerciseinduced hypoxemia would be inappropriate in this clinical setting.
Acute anxiety
Pulmonary embolism
Acute exacerbation of bronchial asthma
High-output hea failure
Respiratory system