Hypocapnia is common in ventilated preterm infants. This can be seen as a result of improved lung compliance and/or function, or aggressive ventilatory support (accidental or intentional). Several studies have reported associations between hypocapnia and PVL, neurodevelopmental disorders, and CP. In one study, time-averaged PaCO₂ on day 3 of life was lower in preterm infants who developed PVL than in preterm infants who did not develop PVL. And those longer and more frequent episodes of hypocapnia are associated with more severe brain injury. In a retrospective study of nearly 250 neonates, hypocapnia is associated with adverse outcomes after perinatal hypoxia-ischemia in term infants. This was also found in a National Institute of Child Health and Human Development Neonatal Research Network study on systemic hypothermia. Early blood gas assessment (hypothermia 12 hours after birth) revealed that dead or disabled infants had significantly lower trough Pco₂ concentrations (median 22 vs. 26 mmHg, p=0.15), which was a predictor of outcome. This relationship also held true for infants with longer cumulative durations of hypocapnia, which also had poorer outcomes. Despite these correlations, it remains unclear whether hypocapnia leads to brain damage or is merely an early marker of increased risk. Hypocapnia is when Paco₂ levels fall below the normal range of 35-45 mmHg. Seen in hyperventilation syndrome. Such situations occur with spontaneous or iatrogenic hyperventilation or are caused by systemic or central nervous system disorders. Patients present with a variety of neurological symptoms, including lightheadedness, tinnitus, lip paralysis, blurred vision, tetany, and seizures. These symptoms are mediated by several mechanisms. Hyperventilation-induced respiratory alkalosis induces calcium shifts and hypocalcemia that cause peripheral paresthesia and tetany. Hypocapnia shifts the hemoglobin-oxygen dissociation curve to the left, reducing oxygen supply to tissues and causing tissue hypoxia. Hypocapnia also induces cerebral vasoconstriction and reduces cerebral blood flow. This phenomenon is used therapeutically to reduce the increase in intracranial pressure during hyperventilation. 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. Hypocapnia also called hypocapnia, sometimes mistakenly called acania, is a condition of reduced carbon dioxide in the blood. Hypercapnia and hypocapnia often complicate the condition seen in critically ill patients. Both conditions have important physiological implications that may influence the clinical management of these patients. For example, hypercapnia results in increased bronchodilation and hypoxic vasoconstriction, leading to improved ventilation/perfusion adaptations. These effects have also been exploited for therapeutic purposes. Hypocapnia is commonly used to control intracranial pressure in patients with traumatic brain injury (TBI). 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.