Также фрагмент кейса, где говорится о вероятных механизмах SIADH при неопухолевой легочной недостаточности:
Several investigators have shown that hypoxaemia or hypercapnic acidosis results in an elevation of plasma ADH levels in man,6 sheep,10 and dog.11 Rosenow et al.6 reported that inadequate filling of the left atrium due to decreased blood flow through the pulmonary vascular bed could be the cause of the elevated blood ADH levels in the patients who have pneumonia and SIADH. There have also been several reports that the plasma ADH level was significantly higher in mechanically ventilated patients of diverse causes with hypoxaemic and/or hypercapnic respiratory failure. It has been assumed this was secondary to intermittent positive pressure ventilation, causing an increase in intrathoracic pressure, impeding the filling of the left atrium, and thus stimulating ADH release.12,13 In our case, the diagnosis of SIADH was made before mechanical ventilation was started, and the hyponatraemia and high level of plasma ADH returned to normal ranges when PaO2 and PaCO2 were normalized by mechanical ventilation, so that such therapy was not causative. Thus, it seems quite reasonable to speculate that hypoxaemia and hypercapnaemia due to respiratory muscle weakness may be responsible for the occurrence of SIADH in this patient. The precise mechanism for the association of SIADH and respiratory failure is still unclear, but clinicians should be aware that acute respiratory failure should be included in the differential diagnosis of SIADH.
Respirology. 1999 Jun;4(2):185-7.
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