Correct Answer: B. Respiratory alkalosis
Hyperventilation in hysteria (now termed conversion disorder in ICD-11) causes excessive CO₂ elimination, leading to respiratory alkalosis. The pathophysiology is straightforward: increased minute ventilation → ↓ PaCO₂ → ↑ pH. Alkalosis shifts the ionized calcium equilibrium; increased protein binding of calcium reduces free (ionized) Ca²⁺ in blood, causing hypocalcemia. This triggers neuromuscular hyperexcitability, manifesting as carpo-pedal spasm (Trousseau's sign). The spasm is a classic clinical sign of hypocalcemia-induced tetany. In Indian clinical practice, hysteria-induced hyperventilation tetany is a well-recognized presentation in emergency departments, particularly in young women. The diagnosis is confirmed by arterial blood gas showing pH >7.45 with PaCO₂ <35 mmHg, and serum ionized calcium is low despite normal total calcium. Management involves reassurance, rebreathing into a paper bag to restore CO₂, and addressing the underlying psychological stressor. This is a high-yield concept because it links a psychiatric presentation to a specific acid-base disorder and its electrolyte consequence.
Why the other options are wrong
A. Metabolic acidosis — Metabolic acidosis would cause hyperkalemia and hypercalcemia (increased ionized Ca²⁺), not hypocalcemia. Carpo-pedal spasm is a sign of hypocalcemia, not hyperkalemia. Hyperventilation in hysteria causes CO₂ loss, not metabolic acid accumulation. This is a trap for students who confuse the acid-base disorder with the electrolyte consequence. C. Metabolic alkalosis — Metabolic alkalosis does cause hypocalcemia and can trigger tetany, but it arises from loss of H⁺ (vomiting, diuretics) or HCO₃⁻ retention, not from hyperventilation. Hyperventilation is a respiratory process (CO₂ loss), not a metabolic one. The primary disorder here is respiratory, not metabolic. NBE may lure students who know alkalosis causes tetany but miss the respiratory mechanism. D. Respiratory acidosis — Respiratory acidosis occurs with hypoventilation (CO₂ retention), not hyperventilation. Hyperventilation causes CO₂ loss and alkalosis, not acidosis. Respiratory acidosis would cause hypercalcemia (increased ionized Ca²⁺), not the hypocalcemia needed for tetany. This is a direct contradiction to the clinical scenario.
High-Yield Facts
- Hyperventilation → ↓ PaCO₂ → respiratory alkalosis with pH >7.45 and PaCO₂ <35 mmHg
- Alkalosis increases protein binding of Ca²⁺ → ↓ ionized calcium → neuromuscular hyperexcitability and tetany
- Carpo-pedal spasm (Trousseau's sign) is the classic clinical sign of hypocalcemia-induced tetany in hyperventilation
- Hysteria-induced hyperventilation tetany is a common emergency presentation in India, especially in young women with conversion disorder
- Paper bag rebreathing restores CO₂ and corrects respiratory alkalosis; reassurance addresses the psychological trigger
- Ionized calcium is low despite normal total calcium in respiratory alkalosis; total calcium may appear normal on routine labs
Mnemonics
HALT for Hyperventilation Tetany Hyperventilation → Alkalosis → Low ionized Ca²⁺ → Tetany (carpo-pedal spasm). Use this when you see hyperventilation + spasm in an anxious patient. Alkalosis = Hypocalcemia Tetany Both metabolic and respiratory alkalosis cause hypocalcemia tetany (increased protein binding of Ca²⁺). But hyperventilation is respiratory, not metabolic. Remember: hyperventilation = respiratory alkalosis, not metabolic.
NBE Trap
NBE pairs "hysteria + hyperventilation" with tetany to test whether students know the acid-base consequence (respiratory alkalosis) versus confusing it with metabolic alkalosis or acidosis. The trap is that students may correctly identify alkalosis but pick metabolic instead of respiratory, missing the mechanism of CO₂ loss.
Clinical Pearl
In Indian emergency departments, a young woman presenting with anxiety, hyperventilation, and sudden carpo-pedal spasm is a classic hysteria-induced tetany case. Quick bedside confirmation: ask her to rebreathe into a paper bag for 2–3 minutes; spasm resolves as CO₂ rises and pH normalizes. This simple maneuver is both diagnostic and therapeutic, avoiding unnecessary calcium infusions.
_Reference: Harrison Ch. 48 (Acid-Base Disorders); Guyton & Hall Ch. 30 (Acid-Base Balance); KD Tripathi Ch. 8 (Respiratory Physiology)_