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Fig. 1 | Annals of Intensive Care

Fig. 1

From: The autonomic nervous system in septic shock and its role as a future therapeutic target: a narrative review

Fig. 1

Illustration of the short-term ANS regulatory mechanisms of the cardiovascular system. The arterial baroreceptors, usually known as high-pressure baroreceptors, are mainly located in the aortic arch and carotid sinuses. Cardiopulmonary baroreceptors—also known as volume-receptors or low-pressure baroreceptors—are located in the atria, ventricles, vena cava, and pulmonary vessels. The chemoreceptors are located both peripherally (carotid bodies and aortic arch) and centrally. The vasomotor center hosts the circulatory regulation and is part of the medulla oblongata located in the brainstem, next to the nucleus of the solitary tract that receives sensory nerves signals through the glossopharyngeal and the vagus nerves (green lines). The SNS fibers (blue lines) originate from the medulla oblongata and emerge from the spinal cord's upper thoracic segments as pre-ganglionic neurons, ending inside the sympathetic chain ganglia located next to the vertebral column. SNS post-ganglionic neurons leave the sympathetic chain ganglia towards their target organs, namely the heart, the vessels, and the adrenal glands. Note that adrenal medulla sympathetic activation also induces epinephrine and norepinephrine release (dashed light blue lines) into the bloodstream. The PNS fibers (red lines) also originate from the brain stem and are incorporated as pre-ganglionic neurons in the vagal nerve, ending on the parasympathetic cardiac ganglia lying in the heart fat pad. Very short post-ganglionic neurons arise from these parasympathetic cardiac ganglia towards the right and left atrium, the atrioventricular node, the interatrial septum, the ascending aorta, and the pulmonary trunk. During septic shock, hypotension and the inflammatory reaction inhibit the vagal centers—inducing vagal outflow reduction—whereas the sympathetic pathway is stimulated. Sepsis, therefore, provokes a striking imbalance in ANS activity with a shift towards the SNS

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