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Shock Management
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
The sympathetically induced circula-tory responses to hypovolaemia are markedly affected by the degree of tissue damage. Minimal tissue damage, typically associated with a penetrating wound (for example, a stab wound) will result in tachycardia and vasoconstriction. Initially, this may be sufficient to maintain a relatively normal blood pressure. However, continued blood loss causes a reduction in venous return which leads to stimulation of the cardiac c-fibre reflex. This inhibits the vasomotor centre, resulting in a vagally mediated reduction in heart rate and loss of sympathetic tone (particularly in skeletal muscle and kidneys) and a profound fall in blood pressure.
The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The medulla oblongata contains the vasomotor centre, also called the cardiovascular centre. This regulates the heartbeat and controls the diameter of blood vessels, thereby controlling blood pressure. The medulla is also responsible for the rhythmical pattern of breathing. The medulla contains ascending sensory pathways and descending motor pathways connecting the spinal cord with other parts of the brain. The area where the medulla joins the spinal cord is where most of the ascending and descending pathways (tracts of axons within the CNS) cross over; as a result, each cerebral hemisphere is responsible for sensation and voluntary movement on the opposite side of the body.
Paroxysmal Autonomic Syncope
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Ronald G. Victor, C.M.T. Jost, R. L. Converse, Tage N. Jacobsen
In addition to emotional activation of hypothalamic vasodilator pathways, two other specific central mechanisms have been implicated in triggering sympathetic inhibition during hypovolaemic hypotension. The first is that reduction in sympathetic vasomotor outflow occurs only in the terminal stage of decompensated, irreversible hemorrhagic shock when the severity and duration of brainstem ischaemia are sufficient to directly depress the firing of the central sympathetic neurons (Rothe, Schwendenmann and Selkurt, 1963; Lundgren, Lundwall and Mellander, 1964). This concept is stated concisely in the latest edition of the Textbook of Medical Physiology: “... there comes a point at which diminished blood flow to the vasomotor center itself is so depressed that the center becomes less active and finally totally inactive.... Fortunately, though the vasomotor center does not usually fail in the early stage of shock — only in the late stages” (Guyton, 1991).
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.
Recent advances in the understanding of enterovirus A71 infection: a focus on neuropathogenesis
Published in Expert Review of Anti-infective Therapy, 2021
Han Kang Tee, Mohd Izwan Zainol, I-Ching Sam, Yoke Fun Chan
The main cause of death was attributed to neurogenic pulmonary edema (stage III in EV-A71 infection) [27,33]. The onset of neurogenic pulmonary edema was postulated to link to prominent damage of the vasomotor center of brainstem, leading to autonomic nervous system dysfunction [34]. Kao et al. reported that damage of medial, ventral and caudal medulla causes sympathetic overactivation, resulting in systemic vasoconstriction with resulting shift of blood to the lungs [35]. Several studies found that neurogenic pulmonary edema was associated with widespread inflammation observed in spinal cord and brain stem [24,33,36]. Consistently, no virus damage nor viral antigens can be detected in the lungs suggesting that pulmonary edema is more likely to be neurologically induced [28,29,36]. Increased pulmonary vascular permeability caused by brainstem lesions or/and systemic inflammatory responses could play an important role in pathogenesis of fatal pulmonary edema [37]. In rare cases, acute heart dysfunction due to left ventricular failure was also reported to be a cause of death in EV-A71-infected patients [38,39].
Responsiveness of α2-adrenoceptor/I1-imidazoline receptor in the rostral ventrolateral medulla to cardiovascular regulation is enhanced in conscious spontaneously hypertensive rat
Published in Clinical and Experimental Hypertension, 2019
Masanobu Yamazato, Minori Nakamoto, Atsushi Sakima, Yoriko Yamazato, Shuichi Takishita, Yusuke Ohya
Recent advances in therapeutic strategies that target the neural component of hypertension, such as renal denervation therapy for patients with treatment-resistant hypertension (1), have refocused attention on the altered tone of the sympathetic nervous system in these patients. Centrally acting antihypertensive agents elicit sympatholytic and sedative effects by acting on the α2-adrenoceptor/I1-imidazoline (α2-/I1-) receptors in the central nervous system (2,3). The sympathoinhibitory effect of α2-/I1-receptor agonists is believed to result from the actions on the cardiovascular nuclei of the medulla oblongata. The rostral ventrolateral medulla (RVLM) is a vasomotor center wherein cardiovascular sympathetic premotor neurons are located (4,5). The RVLM neurons directly innervate sympathetic preganglionic neurons in the intermediolateral cell column of the spinal cord and provide supraspinal excitatory input to these neurons (4). The RVLM neurons also participate in the reflex control of the cardiovascular system. Microinjection of clonidine into the RVLM was shown to induce long-lasting hypotensive and sympathoinhibitory effects (6–9). The RVLM is therefore regarded as an important target site that mediates the hypotensive effect of α2-/I1-receptor agonists (5).