Compare the compensatory mechanism employed in respiratory acidosis and alkalosi

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Compare the compensatory mechanism employed in respiratory acidosis and alkalosis

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Explanation / Answer

Respiratory acidosis is a clinical disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial arterial pressure of carbon dioxide (PaCO2).[1] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3-) / PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the lungs is less than the production of carbon dioxide in the tissues. Acute and chronic respiratory acidosis Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, > 45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate value (ie, > 30 meq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by: (1) cerebral disease or drugs, (2) an inability to ventilate adequately owing to a neuromuscular disease (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or (3) airway obstruction usually related to asthma or chronic obstructive pulmonary disease (COPD). Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including: (1) decreased responsiveness to hypoxia and hypercapnia, (2) increased ventilation-perfusion mismatch leading to increased dead space ventilation, and (3) decreased diaphragmatic function due to fatigue and hyperinflation. Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (ie, pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis (ALS), and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic skeletal deformities. Lung diseases that primarily cause abnormalities in alveolar gas exchange usually do not cause hypoventilation; however, they tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia typically occurs with severe pulmonary disease or when respiratory muscle fatigue is present. See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.

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