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Platypnea-orthodeoxia.
Platypnea-orthodeoxia (PO) is a syndrome where upright brachial blood pressure is high in supine position and low in upright position. Its cardinal features are lack of a compensatory increase in heart rate (HR), usually an increase in arterial partial pressure of oxygen (pO2), and orthostatic hypotension. PO is often associated with Parkinson’s disease and orthostatic dysautonomia and leads to significant disability. A low sitting and supine pO2 may explain the high prevalence of PO in patients with Parkinson’s disease. PO is commonly misdiagnosed as obstructive sleep apnea with compensatory hypoventilation, since low sitting and supine pO2 is often seen in patients with obstructive sleep apnea. The “normal response” to hypoxia seen in some patients with PO could be explained by a sleep-related respiratory disturbance, or by non-respiratory factors such as orthostatic dysautonomia. In patients with obstructive sleep apnea, the “normal” response to increasing oxygen could be explained by ventilatory inefficiency, reduced somatic afferent drive, and increased sympathetic outflow with activation of arterial chemoreceptors. The combination of orthostatic and hypoxemia in patients with PO is likely to decrease their ability to “reset” chemoreceptor sensitivity and increase their sympathetic activity. Some patients with PO have a normal compensatory rise in HR but increased pO2, which has been attributed to an autonomic cholinergic hyperresponsiveness. Alternatively, there could be an increased sensitivity to hypoxia in the brainstem hypoxia sensing neurons. Other possible explanations include reduced arterial chemoreceptor sensitivity, altered chemoreceptor sensitivity, increased post-hypoxic vasodilation, and disturbed respiratory drive. We need to understand the mechanism of the “normal response” to hypoxia in PO in order to develop novel therapies for the management of this condition.Q:
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