The second group is anything that increases physiologic dead space (part of the lung that does not participate in gas exchange) this is ventilation without perfusion. Deformity of the thoracic cage can impact tidal volumes, therefore decreasing minute ventilation. Notable etiologies include Guillain-Barre, myasthenia gravis, amyotrophic lateral sclerosis, myositis, multiple sclerosis, phrenic nerve injury, tetanus, botulism, organophosphates, and ciguatera. Decreased respiratory neuromuscular function can decrease minute ventilation. Although the medulla functions to control the respiratory drive, many peripheral nerves and respiratory muscles are needed to perform respirations. Notable etiologies include overdose of sedative medications (narcotics, benzodiazepines, tricyclic antidepressants, etc.), stroke, and hypothermia. Anything that affects the central respiratory center can affect the minute ventilation. The central respiratory center in the medulla takes feedback from multiple inputs and integrates them into a respiratory drive, which functions to control our minute ventilation. The first group is anything that causes decreased minute ventilation (respiratory rate x tidal volume). The etiology can be extensive, but it can be helpful to divide the potential causes into three groups: decreased minute ventilation, increased physiologic dead space, increased carbon dioxide production. Overall, the driving mechanism of CO2 narcosis is acute hypercapnia.
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