Kussmaul's Breath

Specialty: Endocrine and metabolic.

• acidotic breathing
• hyperventilatory metabolic hyperpnea
• breathing of air hunger

Why it occurs

• Diabetic ketoacidosis (DKA, excess circulating keto acids activate central and peripheral chemoreceptors that stimulate the respiratory center to scavenge carbon dioxide and compensate for acidosis)
• Severe lactic acidosis (secondary to septic, cardiogenic shock or metformin accumulation in the context of acute renal failure)
• Terminal uremia due to renal failure (accumulation of fixed non-volatile organic acids)
• Intoxication by salicylates or methanol (severe metabolic acidosis with elevated anion gap due to toxic metabolites)
• Decompensated type 1 renal tubular acidosis (inability of the distal tubules to secrete protons)

Initial workup

Immediate arterial blood gases to assess pH, pCO2, real bicarbonate and base excess; plasma electrolytes (sodium, potassium, chlorine) to accurately calculate the anion gap; blood lactate levels; plasma glycemia and determination of beta-hydroxybutyrate; urea nitrogen (BUN) and serum creatinine; and complete urinalysis with toxic screening if alcohol intake is suspected.

Standard management

• 8.4% baking soda — administered by slow intravenous route only if arterial pH is strictly less than 6.9, due to the risk of paradoxical intracellular acidosis, hypokalemia, and delayed recovery from ketoacidosis
• Regular insulin — continuous intravenous infusion of 0.1 IU/kg/hour to stop ketogenesis and correct the underlying metabolic acidosis in diabetic ketoacidosis
• 0.9% saline solution — intravenous infusion to restore peripheral cellular and tissue perfusion, helping to reverse lactic acidosis due to poor perfusion
• Potassium chloride — supplementation if the potassium level is less than 5.2 mEq/L, since the correction of acidosis decreases extracellular plasma potassium