Respiratory Alkalosis

The anxious post-op patient breathing 28 times per minute has a pH of 7.52 — but the real danger isn't the anxiety. It's what the alkalosis does to calcium and potassium.

Respiratory alkalosis occurs when the client hyperventilates, blowing off excess CO2 and driving the pH above 7.45 with a PaCO2 below 35 mmHg. The root problem is always alveolar hyperventilation — anxiety and pain are the most common triggers on the NCLEX, but fever, sepsis, hypoxemia, high altitudes, mechanical over-ventilation, and early salicylate toxicity also cause it. The critical downstream effect: alkalosis drops extracellular H+ concentration, so H+ shifts out of cells to buffer the blood; to maintain electrical neutrality, K+ shifts into cells, producing hypokalemia. Simultaneously, more calcium binds to albumin in alkalotic blood, dropping ionized (free) calcium levels and causing neuromuscular irritability — tingling, numbness, carpopedal spasms, and a positive Chvostek or Trousseau sign. Nursing priorities center on treating the underlying cause: coaching slow breathing, using a calm environment for anxiety-driven cases, adjusting ventilator rate/tidal volume for iatrogenic causes, and monitoring for cardiac dysrhythmias related to the electrolyte shifts. Rebreathing into a paper bag is outdated and no longer recommended because it can worsen hypoxia.

Key Distinctions

Don't confuse respiratory alkalosis (low CO2, high pH, patient is hyperventilating) with metabolic alkalosis (high HCO3, high pH, usually from vomiting or NG suction). Students often attribute numbness and tingling to the anxiety itself — it's actually the alkalosis-induced drop in ionized calcium. Iatrogenic respiratory alkalosis from mechanical ventilation is corrected by decreasing rate or tidal volume, not by adding sedation alone.

Clinical Pearl

Fast breathing blows off CO2, blows up the pH, and blows calcium and potassium into hiding — think 'blow off three things at once.'