Kussmaul respiration

Intoxication may present as inebriation and drowsiness similar to ethanol use. Other symptoms are vomiting, diarrhea, delirium and agitation, back and abdominal pain, and clammy skin. Toxic effects usually follow a latent period of several hours. Formate inhibits mitochondrial cytochromes resulting in neurotoxicity. Ocular signs include blurred vision, dilated pupils, and direct retinal toxicity with optic disc hyperemia and ultimately permanent blindness [91]. Cerebral hemorrhagic necrosis has been reported [92]. Severe poisoning may result in Kussmaul respiration, inspiratory apnea, coma, and death. Urine samples may have the characteristic smell of formaldehyde. An elevated serum osmolal gap from methanol will be evident early in presentation but may disappear after approximately 12 hours. At this time, an elevated anion gap metabolic acidosis from retained formate may be evident. 

Comatose patients in diabetic ketoacidosis have the smell of acetone (a derivative of the ketone body acetoacetate) on their breath. In addition, DKA patients have deep, relatively rapid respirations typical of acidotic patients (Kussmaul respirations). These respirations result from an acidosis-induced stimulation of the respiratory center in the brain. More CO2 is exhaled in an attempt to reduce the amount of acid in the body H -1- HCO3 — H2CO3 H2O + CO2 (exhaled). 

Compensation the low pH stimulates the respiratory centre In the brain causing hyperventilation, This expires CO2 in an attempt to lower the pC02. This dram tii hyperventilation has been described as air hunger or Kussmaul respiration ... 

Pulmonary edema Kussmaul respirations (to decrease COj to balance metabolic acidosis)... 

Deep, rapid breathing (Kussmaul respirations to blow off CO )... 

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). 

---