A Model of Blood Pressure, Heart Rate, and Vaso-Vagal Responses Produced by Vestibulo-Sympathetic Activation

Abstract

Blood Pressure (BP), comprised of recurrent systoles and diastoles, is controlled by central mechanisms to maintain blood flow. Periodic behavior of BP was modeled to study how peak amplitudes and frequencies of the systoles are modulated by vestibular activation. The model was implemented as a relaxation oscillator, driven by a central signal related to Desired BP. Relaxation oscillations were maintained by a second order system comprising two integrators and a threshold element in the feedback loop. The output signal related to BP was generated as a nonlinear function of the derivative of the first state variable, which is a summation of an input related to Desired BP, feedback from the states, and an input from the vestibular system into one of the feedback loops. This nonlinear function was structured to best simulate the shapes of systoles and diastoles, the relationship between BP and Heart Rate (HR) as well as the amplitude modulations of BP and Pulse Pressure. Increases in threshold in one of the feedback loops produced lower frequencies of HR, but generated large pulse pressures to maintain orthostasis, without generating a VasoVagal Response (VVR). Pulse pressures were considerably smaller in the anesthetized rats than during the simulations, but simulated pulse pressures were lowered by including saturation in the feedback loop. Stochastic changes in threshold maintained the compensatory Baroreflex Sensitivity. Sudden decreases in Desired BP elicited non-compensatory VVRs with smaller pulse pressures, consistent with experimental data. The model suggests that the Vestibular Sympathetic Reflex (VSR) modulates BP and HR of an oscillating system by manipulating parameters of the baroreflex feedback and the signals that maintain the oscillations. It also shows that a VVR is generated when the vestibular input triggers a marked reduction in Desired BP.

Do patients with Ménière’s disease have attacks of syncope?

“…We hypothesize that a sudden change in environmental pressure would lead to pressure changes in the endolymph/ perilymph system and distort the otolith membrane, provoking a Tumarkin attack and eventually leading to syncope. We also found that syncope was negatively correlated with rotatory vertigo attacks, indicating that the role of semicircular canals may not be important, confirming the findings in animals [27,30]. Our findings indicate that the main reason for syncope in patients with MD is the malfunctioning otolith organ, which disturbs the vestibular sympathetic reflex originating from the otoliths, thus provoking the paradoxical vasovagal attack leading to syncope.…”

“…The syncope attacks in experimental animals were very much the same as the neurogenically mediated vasovagal syncope [26] occurring in association with Tumarkin attacks. We hypothesize in line with Raphan et al that the vestibular sympathetic reflex interferes with the medullary rostral and caudal lateral medullary nucleus and interferes with the function of the vasoregulatory center and causes syncope [27]. The output would cause vasovagal attack with reduced muscle sympathetic vessel tonus with simultaneous paradoxical bradycardia, leading to falls and also syncope for a variable time [28].…”

“…The patient had higher anxiety scores and experienced more fatigue. Loss of vitality has also been reported as a consequence in patients with orthostatic disorder [8]. The therapeutic possibilities seem to be limited.…”

“…Recent experiments on space flights confirm that the inner ear otolithic input is an important regulator of blood pressure and heart rate in humans [7] and leads to orthostatic dizziness and also syncope due to a sudden drop in blood pressure. The otoliths detect a position change with respect to gravity within milliseconds, and play a key role in the activation of the vascular tone through the vestibular sympathetic reflex [8]. In an experimental animal model, researchers demonstrated that the otolith input influenced mechanisms regulating blood pressure and heart rate, and seemed to be one of the key operators in regulating the homeostatic control of blood pressure during stance [9].…”

Electrical Vestibular Nerve Stimulation for the Management of Tension Headache

“…This may be due to different effects of vestibular stimulation on auditory and visual reaction time, which has to be further studied. Stimulating the vestibular system was reported to influence the blood pressure and heart rate by modulating the baroreceptor reflex [14]. Further, dysregulation of blood pressure was reported followed by damage of vestibular system [15].…”