Orthostatic hypotension due to arterial baroreflex failure

The acute form of baroreflex failure is encountered following loss of glossopharyngeal or carotid sinus nerve function due to surgical intervention or accidental injury [1][3][4]. It is characterized by severe, unremitting hypertension, tachycardia, and headache. The systolic blood pressure can exceed 250 mmHg, which may lead to hypertensive encephalopathy and (fatal) cerebral haemorrhage [5]. Hypertensive crisis may evolve over days and weeks into the more chronic volatile hypertensive phase [1][6]. In addition, volatile hypertension may result from a gradual decline in baroreflex function due to neck irradiation [7]. Volatile hypertension due to baroreflex failure is characterized by paroxysms of abrupt sympathetic activation, including excessive increments in plasma catecholamine levels. Surges of blood pressure and tachycardia may occur spontaneously or are elicited by mental stress or physical stimuli like exercise, cold and sexual arousal. These bouts of sympathetic activation may be accompanied by severe headaches, palpitations, diaphoresis, lightheadedness and anxiety. In addition, emotional instability appears to be a prominent feature in this phase of baroreflex failure.

Apart from hypertensive surges, hypotensive episodes may occur during sleep. In rare cases, inadequate baroreflex buffering of cardiovagal efference is the most prominent feature, resulting in malignant vagotonia with hypotension, bradycardia, and asystole [8]. Accompanying symptoms of this so-called “selective baroreflex failure” include fatigue and dizziness, with possible progression to frank syncope. In the patient presented here, orthostatic lightheadedness due to initial orthostatic dizziness and orthostatic hypotension was a prominent feature of baroreflex failure. Orthostatic hypotension was originally claimed not to be part of the baroreflex failure syndrome [1]. However, compensatory mechanisms were later shown to fail after squatting [7]. In other cases, orthostatic hypotension may not become apparent until years after baroreceptor denervation [9]. In addition, persistent orthostatic hypotension was found in patients after bilateral carotid body tumor surgery [10]. Afferent baroreceptor denervation in these patients was shown to result in abnormal control of cardiovagal efference and as well as of efferent muscle sympathetic nerve activity [11]. Abnormal orthostatic control of blood pressure and heart rate following lesion of afferent baroreceptors may occur through abnormal baroreflex-mediated adjustments of both efferent pathways during active standing. In the patient presented here, orthostatic hypotension resolved within 1 year after the onset of baroreflex failure, whereas initial orthostatic dizziness and hypotension persisted. Remaining aortic baroreceptors, as well as cardiopulmonary baroreceptors may in time (partially) compensate for the loss of carotid sinus baroreceptors.