Kussmaul’s respirations

The manifestations of acute severe metabolic acidemia (pH less than 7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. Respiratory compensation may occur as Kussmaul s respirations (i.e., deep, rapid respirations characteristic of diabetic ketoacidosis). 

A further consequence of thiamine depletion during parenteral nutrition can be severe lactic acidosis (44). Six cases have been described from Japan with associated hypotension, Kussmaul s respiration, and clouding of consciousness, as well as abdominal pain not directly related to the underlying disease. During parenteral nutrition administration there was blockade of oxidative decarboxylation of alpha-keto acids such as pyruvate and alpha-ketoglutarate, resulting in pjruvate accumulation and massive lactate production. None of the patients responded to sodium bicarbonate or other conventional emergency treatments for shock and lactic acidosis. Thiamine replenishment with intravenous doses of 100 mg every 12 hours resolved the lactic acidosis and improved the clinical condition of three patients. 

After administration Monitor for acidosis (headache, lethargy progressing to drowsiness, CNS depression, Kussmaul s respiration). 

Severe metabolic acidosis is usually associated with acute processes. The manifestations of severe acidemia (pH <7.15 to 7.20) involve the cardiovascular, respiratory, and central nervous systems. Hyperventilation is often the first sign of metabolic acidosis. At a pH of 7.2, pulmonary ventilation increases about fourfold and an eightfold increase has been noted at a pH of 7. Respiratory compensation may occur as Kussmaul s respirations—the deep, rapid respirations seen commonly in patients with diabetic ketoacidosis. In extremely severe acidosis (pH <6.8), central nervous system (CNS) function is disrupted to such a degree that the respiratory center is depressed. 

The level of total ketone bodies in Lofata Burne s blood greatly exceeds normal fasting levels and the mild ketosis produced during exercise. In a person on a normal mealtime schedule, total blood ketone bodies rarely exceed 0.2 mM. During prolonged fasting, they may rise to 4 to 5 mM. Levels above 7 mM are considered evidence of ketoacidosis, because the acid produced must reach this level to exceed the bicarbonate buffer system in the blood and compensatory respiration (Kussmaul s respiration) (see Chapter 4). 

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