Acid-Base Balance and Respiratory Disorders: An Updated Review

Background: Acid–base homeostasis is vital for maintaining physiological stability, enzymatic activity, and cellular metabolism. The respiratory system is central to this regulation through control of arterial carbon dioxide tension (PaCO₂), a major determinant of blood pH.Aim: This review summarizes updated knowledge on the mechanisms, control, and clinical disorders of respiratory acid–base balance, emphasizing ventilatory responses to hypercapnia and hypocapnia, physiological adaptations, and implications for clinical management.Methods: A comprehensive synthesis of recent physiological, experimental, and clinical literature was undertaken, integrating data on chemoreceptor function, ventilatory control, cellular mechanisms of CO₂ regulation, and the pathophysiology of respiratory alkalosis and acidosis.Results: The review highlights the dynamic coordination between central and peripheral chemoreceptors that sustain pH homeostasis. The ventilatory response to hypercapnia exhibits linear proportionality to PaCO₂ over most physiological ranges but is influenced by factors such as circadian rhythm, obesity, pharmacological agents, and anesthesia. Acute and chronic alterations in PaCO₂ trigger adaptive renal and central nervous mechanisms, shifting bicarbonate buffering and ventilatory set points. Disorders such as respiratory alkalosis arise from excessive ventilation, while respiratory acidosis results from hypoventilation, increased dead space, or elevated CO₂ production. The review also elucidates the dual-edged cellular and systemic effects of hypercapnia—anti-inflammatory yet potentially injurious—particularly under lung-protective ventilation strategies.Conclusion: Acid–base balance represents a multi-system equilibrium involving chemical, neural, and renal pathways. Understanding these interactions enhances clinical management of respiratory failure, anesthesia, and critical care ventilation