Direct Vasodilator Effect of Hyperventilation-Induced Hypocarbia in Autonomic Failure Patients

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Hypocapnia is a drop in the level of carbon dioxide (CO2) in the alveoli and blood below the normal reference range of 35 mmHg. CO2 is a metabolite of many cellular processes in the body involved in the processing of lipids, carbohydrates and proteins. The major organ systems involved in regulating CO2 homeostasis are the pulmonary and renal systems. Additionally, CO2 is regulated by a CO2/HCO3 pH buffer system. Abnormalities that lead to hypocapnia usually also lead to respiratory alkalosis. This activity reviews the assessment and management of hypocapnia and highlights the role of professional teams in educating patients with this condition about follow-up care. Hypocapnia, also known as hypocapnia, is a drop in the level of carbon dioxide (CO2) in the alveoli and blood below the normal reference range of 35 mmHg. CO2 is a metabolite of many cellular processes in the body involved in the processing of lipids, carbohydrates and proteins. The major organ systems involved in regulating CO2 homeostasis are the pulmonary and renal systems. Additionally, CO2 is regulated by a CO2/HCO3 pH buffer system. Abnormalities that lead to hypocapnia usually also lead to respiratory alkalosis. Fundamentally, hypocapnia is caused by either decreased CO2 production or increased CO2 loss. The main event is loss of CO2 through changes in the pH buffering system or the pulmonary system, as metabolic demand usually does not decrease sufficiently to adjust CO2 levels to meaningful hypocapnic levels. The pulmonary system is very efficient at removing CO2 from the body by gas diffusion. This requires a diffusion gradient from the high concentration of arteriolar blood to the relatively low concentration of ambient air. This gradient is maintained by continuously flushing CO2 from the alveolar space regardless of absolute PaCO2 concentration. Thus, a CO2 gradient is generated and maintained. In this case, arterial PaCO2 is directly proportional to the rate of metabolic CO2 production and inversely proportional to the rate of CO2 excretion by the lungs due to increased alveolar ventilation. Alveolar ventilation is the distance from the alveolar air to the environment defined as the exhaled minute ventilation reaching the alveoli, determined by the ratio of dead space to minute ventilation and tidal volume. From these relationships, it can be concluded that respiratory rate and tidal volume are two components of ventilation that are physiologically or artificially controlled to mitigate CO2 excretion. Hypocapnia-inducing etiology is therefore any disease that increases the ventilation rate or tidal volume. Increased breathing rate is often the cause. Various diseases can provoke this. In almost all scenarios, hypocapnia is synonymous with respiratory alkalosis. Both are induced by processes that involve hyperventilation. Hypocapnia is the result of hyperventilation. Increased ventilation of the alveolar spaces removes gaseous CO2 rapidly. This increases the diffusion gradient of CO2 from the blood to the alveoli. CO2 is then more easily removed from the body. Other than reduced respiratory rate, there is virtually no mechanism to regulate this loss. The partial pressure of carbon dioxide (PaCO2) is maintained between 35 and 45 mmHg using a feedback controller. Central chemoreceptors (in the brain) and peripheral chemoreceptors (in the carotid artery) sense hydrogen concentration and influence ventilation to regulate pH and PaCO2. For example, when these receptors sense an increased concentration of hydrogen ions, ventilation increases to flush CO2. Continued hyperventilation eventually leads to hypocapnia as alveolar ventilation exceeds the amount of CO2 generated.