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Syncope: Physiology, Pathophysiology and Aeromedical Implications
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
David A. Low, Christopher J. Mathias
Reflex compensatory changes occur within the autonomic nervous system in response to alterations in blood pressure as part of the cardiopulmonary and arterial baroreflexes that participate continuously in the regulation of cardiovascular function to produce alterations in efferent sympathetic adrenergic and parasympathetic neural activity and subsequent haemodynamic adjustments (Figure 13.1). Arterial and cardiopulmonary baroreceptors respond to mechanical deformation via local changes in blood pressure and volume to correct alterations in blood pressure via changes in cardiac output and/or total peripheral resistance. There are two types of arterial baroreceptors: carotid baroreceptors, located in the internal carotid artery, and aortic baroreceptors, located in the aorta arch. Cardiopulmonary baroreceptors are mechanically sensitive receptors located in the four chambers of the heart that respond to changes in cardiac and pulmonary filling volumes (Ray and Saito, 2000). Afferent information from these baroreceptors is relayed to the cardiovascular centre in the brainstem. Efferent information via the parasympathetic and sympathetic neural pathways is then provided to effector organs, for example the heart and regional vascular beds, to correct the change in blood pressure and complete the baroreflex. The heart is under the dual control of the parasympathetic and sympathetic neural pathways, an increase in parasympathetic neural activity causing a reduction in heart rate. In contrast, increases in sympathetic nerve activity result in elevations in heart rate and vascular resistance of various regional vascular beds. In addition, increased sympathetic nerve activity is also directed to the adrenal gland, which stimulates the release of noradrenaline.
BP and HR Interactions: Assessment of Spontaneous Baroreceptor Reflex Sensitivity
Published in Herbert F. Jelinek, David J. Cornforth, Ahsan H. Khandoker, ECG Time Series Variability Analysis, 2017
Tatjana Lončar-Turukalo, Nina Japundžić-Žigon, Olivera Šarenac, Dragana Bajić
BP and HR interact on a beat-to-beat basis to maintain adequate circulation to all organs, especially the brain. The BP and HR fast interactions have been shown to be mediated via the ANS, that is, the BRR. Receptors that sense changes in BP, the baroreceptors, are located in large arteries of the thorax and the neck, most densely in the aortic arch and the carotid sinuses. The information about the change of BP is transmitted via the vagus nerve (X) and the glossopharyngeal nerve (IX) to the nucleus of the solitary tract (NTS) in the medulla oblongata and further to the hypothalamus. The main integration of the autonomic response directed to peripheral blood vessels and the heart occurs in the rostral ventrolateral medulla (RVLM) for the sympathetic outflow and in the vagal nuclear complex (nucleus ambiguus, dorsal vagal nucleus) for the parasympathetic outflow. There are two possible scenarios for BP changes (Figure 9.1). Scenario 1 assumes that BP increases. In this case, the BRR shifts the autonomic cardiovascular control to the vagus and withdraws sympathetic influence to the cardiovascular system. The vagal activation will slow down the heart and withdrawal of sympathetic influence will lead to arterial vasodilation and reduction of the peripheral resistance. Altogether, this will produce a decrease of BP and restoration of basal values. Scenario 2 supposes that BP decreases. In this case, the BRR shifts the autonomic balance to the sympathetic control of the cardiovascular system, which will increase HR and peripheral resistance, and restore the basal level of BP. As a consequence of the BRR, functioning BP and HR will oscillate around the set point. The period of BP and HR oscillations induced by the BRR ranges from seconds to hours, and contributes to both short-term and long-term BP and HR variability (HRV).
Baroreflex control model for cardiovascular system subjected to postural changes under normal and orthostatic conditions
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
V. L. Resmi, R. G. Sriya, N. Selvaganesan
On changing the position from supine to standing, blood pools towards the lower body due to gravity, which changes the distribution of the blood volume in the body, leading to change in venous pressure. The rapid blood pressure change is sensed by detecting the level of tension on vascular walls with the help of baroreceptors located in the carotid sinus and arch of the aorta. The Baroreceptors fire action potentials according to the blood pressure sensed through mechano-electrical transduction to the central nervous system. This information is processed in the medulla oblongata and its cardioinhibitory and vasomotor centers then create sympathetic and parasympathetic nerve activities, respectively (Solaro et al. 2019). The efferent pathways transmit these activities in the form of impulses to the various parts of the cardiovascular system which affects the blood pressure by changing the peripheral resistance, compliance, stroke volume and contractility.
Baroreflex activation therapy systems: current status and future prospects
Published in Expert Review of Medical Devices, 2019
Gino Seravalle, Raffaella Dell’Oro, Guido Grassi
It has been clearly shown that carotid baroreceptors represent an intriguing target to treat not only hypertension but also several pathophysiological conditions characterized by a hyperadrenergic tone and an impairment in baroreflex sensitivity. Clinical studies and trials have underlined the potential of the carotid baroreceptor devices to improve blood pressure control. These results have been obtained both with ‘old’ and new devices. It is necessary to underline that the efficacy was accompanied by an improvement in the safety. In particular a reduction in procedure time for implantation and procedure related events were observed through the progresses in minimally invasive devices technology. This allows reducing the discomfort at the level of chest, throat, teeth, ears, and the number of perioperative infections at the insertion site [73]. These aspects were less evident with EBA which is a more simple and efficient interventional strategy although it showed, in the preliminary study [64], a 13% of serious adverse effects and in particular transient ischemic attack. Of course the risk-to-benefit balance of passive reshaping of the carotid remains unclear because the dynamic physiology of the baroreceptor reflex and the resetting phenomenon and also the possible late local atherosclerosis. The answers on these topics are attended from the ongoing trials and trials starting in these years.
Peat smoke inhalation alters blood pressure, baroreflex sensitivity, and cardiac arrhythmia risk in rats
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Brandi L. Martin, Leslie C. Thompson, Yong Ho Kim, Charly King, Samantha Snow, Mette Schladweiler, Najwa Haykal-Coates, Ingrid George, M. Ian Gilmour, Urmila P Kodavanti, Mehdi S. Hazari, Aimen K. Farraj
Exposure to low peat increased BRS gain during exposure, indicating dysregulation of the baroreflex. When functioning normally, the baroreceptor reflex maintains homeostatic control of BP by producing reflex decreases in HR when BP rises and elevation in HR when BP falls, changes that are mediated by the autonomic nervous system (Hazari et al. 2014). Exposure to a variety of air pollutants was largely linked with a reduction in BRS including exposure to sulfur dioxide in humans (Routledge et al. 2006), and acrolein (Hazari et al. 2014), cigarette smoke (Valenti et al. 2010) and carbon nanotubes in rodents (Legramante et al. 2009). In contrast, exposure to ambient PM in dogs elevated both arterial BP and BRS (Bartoli et al. 2009). One potential explanation for the BRS effects with low peat relates to altered autonomic tone as increased BRS was previously linked with thoracic sympathectomy (Bygstad et al. 2013)) and drug-induced decreases in sympathetic nervous system activity (Lewandowski et al. 2010). Although heart rate variability was not measured in the current study, the immediate decrease in HR at the beginning of the exposure period with low peat suggests increased parasympathetic tone consistent with early exposure effects reported in previous studies (Farraj et al. 2012). Further, Lamb et al. (2012) previously demonstrated that exposure to low, but not high concentrations of particle-free DE increased markers of heart variability that reflect enhanced parasympathetic tone. Thus, low, but not high peat may have elevated parasympathetic tone, which in turn increased BRS. These findings contrast with findings that point to sympathetic mediation of responses to low PM concentrations and mediation by pulmonary neural reflex-triggered elevated parasympathetic tone with repeated exposure or exposure to higher PM concentrations (Carll et al. 2017). The precise reasons for this divergence are unclear but may relate to the greater complexity of responses to whole combustion emissions containing multiple pollutants relative to responses to single pollutants. This is illustrated in findings from previous investigations that noted that whole and particle-free DE produced divergent cardiovascular responses (Carll et al. 2012; Hazari et al. 2011; Lamb et al. 2012). The uncertainty resulting from the potential elicitation of unique mechanisms by particulate and gaseous constituents of combustion emissions is enhanced when factoring in that when compared to higher exposure levels, lower exposure levels at least in the present experimental findings contained smaller particle size and higher particle number, both linked to worse cardiovascular responses than their counterparts (Brook et al. 2010).