Arterial base deficit in pulmonary embolism is an index of severity and diagnostic delay.

In acute pulmonary embolism, patients free from circulatory failure usually present a blood gas pattern consistent with respiratory alkalosis. We investigated whether the appearance of arterial base deficit in these patients indicates disease severity and diagnostic delay. Twenty-four consecutive patients with pulmonary embolism were retrospectively evaluated. Twelve patients had arterial base excess > or =0 mmol/L (Group 1), and 12 patients arterial base deficit <0 mmol/L (Group 2). No patient showed signs of circulatory failure. Group 1 was characterized by a mean base excess of 2.2 +/- 1.7 mmol/L, while in Group 2, the mean base deficit was -1.9 +/- 0.7 mmol/L (p < 0.0001). At 1 week since the embolism, 11 patients of Group 1 and 6 of Group 2 received a PE diagnosis (p < 0.05). The vascular obstruction index was more severe in Group 2 than in Group 1 (48 +/- 12 vs. 36 +/- 17%, respectively, p < 0.05). In Group 2, the PaCO(2) was lower (33 +/- 3 vs. 36 +/- 5 mmHg, respectively, p < 0.05), the arterial pH was decreased (7.442 +/- 0.035 vs. 7.472 +/- 0.050, respectively, p = 0.097), the Pv(50) was lower (28.3 +/- 1.7 vs. 29.8 +/- 1.6 mmHg, respectively, p < 0.05), the aHCO(3) (-) was lower (22.5 +/- 0.7 vs. 26.1 +/- 1.6 mmol/L, respectively; p < 0.0001), while between the Groups, O(2) delivery, O(2) mixed venous saturation, and O(2) extraction ratio were equivalent. Despite no signs of circulatory failure, an arterial Base deficit develops in patients with respiratory alkalosis subsequent to more severe pulmonary vascular obstruction. Diagnostic delay favors a base deficit. Depending on the degree of hypocapnia, there may be limitation of peripheral O(2) uptake despite adequate O(2) availability. Progressive bicarbonate deficit suggests an increased risk for underlying conditions such as cardio-respiratory disorders or cancer, and requires close control and treatment.