Respiratory Alkalosis

Usually you caused it - Iatrogenic hyperventilation in the intubated patient is a leading cause. An ABG showing alkalemia with a low PaCO2 in a patient you are ventilating means the fix is the ventilator, not a drug: acute respiratory alkalosis under anesthesia is corrected by decreasing minute ventilation. Direct pH reduction with acidic agents is described but is not routinely done and carries no mortality benefit.

Cerebral vasoconstriction is the main lever - Lowering PaCO2 constricts cerebral arterioles and drops cerebral blood flow and volume. That is the mechanism behind hyperventilation for acute intracranial hypertension, but below a PaCO2 of about 25 mmHg the vasoconstriction is already maximal and further hypocapnia buys nothing. In anyone at risk for cerebral ischemia, that same vasoconstriction steals flow from the parenchyma that can least afford it.

The ICP benefit expires - The brain readjusts to the reduced CO2 within 6 to 18 hours, so sustained hyperventilation stops helping. Treat it as a bridge to a definitive intervention, not a plan.

Potassium and phosphate shift intracellularly - Acute hypocapnia drives both into cells. The serum potassium will read lower than total body stores actually are, so a hypokalemia you find while actively hyperventilating a patient is partly an artifact of your ventilator settings. Fix the ventilation before chasing it with replacement.

Ionized calcium falls - Alkalemia increases calcium binding to albumin, dropping ionized calcium even when total calcium is normal. That is what produces the perioral tingling, paresthesias, and carpopedal spasm, and it is why a Trousseau or Chvostek sign can appear on exam. Send an ionized calcium rather than a total.

Left shift of the oxyhemoglobin curve - Alkalemia raises hemoglobin's oxygen affinity and decreases oxygen release to tissue. The pulse oximeter can look reassuring while delivery at the cell is worse.

Acute or chronic, off the bicarbonate - Use the compensation rules to date the process. A near-normal HCO3 with a low PaCO2 is acute. A low HCO3 with a low PaCO2 is either chronic respiratory alkalosis or a metabolic acidosis hiding underneath, and those two need very different responses.

The number is not the problem, the cause is - Respiratory alkalosis by itself is not life-threatening; the etiology can be. Get an ABG to confirm the disturbance, then work the differential with directed tests: a wide A-a gradient points at pulmonary embolism, chest x-ray sorts anatomic and infectious causes and rules pulmonary edema in or out, and CT or MRI of the head with lumbar puncture goes with a suspected neurologic insult.

Check the electrolytes, all of them - Sodium, potassium, and calcium are the ones that cause trouble here, and magnesium and phosphate are worth drawing at the same time given the transcellular shifts.

In the spontaneously ventilating patient, think light - Pain, fear, and anxiety are central drivers of hyperventilation. A patient who starts blowing off CO2 under a spontaneous technique is more often underdosed on analgesia than exotic. Rule out hypoxia at the same time, since hypoxic stimulation drives ventilation at the cost of CO2 and the alkalosis is a symptom of it.

Respiratory alkalosis is an arterial pH above 7.45 driven by a fall in PaCO2. Since CO2 production essentially never drops on its own, in practice this is always hyperventilation blowing the CO2 off. Causes group into central (pain, fear, anxiety, head injury, stroke, hyperthyroidism, salicylates), hypoxemic (hypoxia driving ventilation at the expense of CO2), pulmonary (pulmonary embolism, pneumothorax, pneumonia, asthma or COPD exacerbation), and iatrogenic — overventilating a patient on the ventilator.

Renal compensation drops bicarbonate but takes days, which is what separates acute from chronic: HCO3 falls 1 to 2 mEq/L per 10 mmHg drop in PaCO2 acutely, 4 to 5 mEq/L per 10 mmHg once chronic. Acute hypocapnia drives potassium and phosphate into cells and increases calcium binding to albumin, so ionized calcium falls. Alkalemia also shifts the oxyhemoglobin dissociation curve left, raising hemoglobin's affinity for oxygen and cutting what it releases to tissue.