Abstract

The carotid body (CB) is an interoceptive organ that transmits afferent information to the brain via the carotid sinus nerve (CSN) to maintain homeostasis, i.e., the regulation of internal equilibrium despite external changes. It functions as a complex polymodal receptor capable of sensing multiple stimuli, including blood flow, osmolarity, pO2, pH, pCO2, CO2/H+, and temperature. In addition, the CB responds to a wide range of circulating molecules such as angiotensin II, endothelin-1, aldosterone, insulin, histamine, and leptin, and expresses receptors for interleukins (ILs) and tumor necrosis factor-α (TNF-α) (1). CB dysfunction has been associated with conditions such as obstructive sleep apnea (OSA), in which intermittent hypoxemia induces an inflammatory response mediated, among other mechanisms, by reactive oxygen species (ROS). This process contributes to alterations in respiratory drive and enhanced sympathetic nervous system activity. Following streptococcal toxic shock syndrome due to Streptococcus Pyogenes, severe abdominal septic shock, and multiple infectious complications, our patient developed an altered respiratory pattern and a hypercatabolic state that precluded weaning from mechanical ventilation (MV) despite respiratory physiotherapy. Given treatment failure, we hypothesized underlying carotid body (CB) hyperexcitability, likely pre-existing due to obstructive sleep apnea (OSA) and exacerbated by cytokine storm and severe systemic inflammation related to Strept. Pyogenes toxins and subsequent abdominal sepsis from colonic perforation. This may have contributed to sustained sympathetic overactivation and immune dysregulation. Clinically, the patient exhibited increased respiratory drive (30–35 breaths/min), excessive inspiratory effort, and marked patient–ventilator asynchrony in the absence of hypoxemia. Non-targeted physiotherapy may have acted as a second inflammatory hit, perpetuating the inflammatory cycle.

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