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 ≥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 PaCO₂ 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 Pv₅₀ was lower (28.3 ± 1.7 vs. 29.8 ± 1.6 mmHg, respectively, p < 0.05), the aHCO₃ ⁻ was lower (22.5 ± 0.7 vs. 26.1 ± 1.6 mmol/L, respectively; p < 0.0001), while between the Groups, O₂ delivery, O₂ mixed venous saturation, and O₂ 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 O₂ uptake despite adequate O₂ availability. Progressive bicarbonate deficit suggests an increased risk for underlying conditions such as cardio-respiratory disorders or cancer, and requires close control and treatment.