Profound Metabolic Acidosis Research Articles

Functional and Metabolic Effects of Anoxic Cardiac Arrest

Myocardial changes were studied in 12 dogs and 5 patients to determine whether anoxic, normothermic cardiac arrest, a simple, effective adjunct in open-heart surgery, is detrimental to cardiac function. After 30 minutes of aortic occlusion the dogs showed uniform depression of left ventricular function with profound metabolic acidosis and elevation of lactate of the coronary sinus blood. Five patients who had 21 to 45 minutes of anoxic cardioplegia also showed marked respiratory acidosis, elevation of the lactate/pyruvate ratio, and a progressive rise in lactate of the coronary sinus blood. The effects of anoxia on the human heart are comparable to those observed in the dog. We believe that anoxic cardioplegia of 45 minutes is tolerated by patients but that coronary perfusion should be employed after that length of time.

Poisoning with ethylene glycol monomethyl ether. Report of two cases.

Abstract. The clinical and laboratory features of two patients with ethylene glycol monomethyl ether poisoning are presented. By accident, both patients concomitantly had ingested about 100 ml of the toxic agent. After a symptom‐free interval of 8–18 hours, they became mentally confused and complained of general weakness and nausea. In addition, a deep and frequent respiration together with a profound metabolic acidosis was found. One of the patients, in whom a marked oxaluria was demonstrated, initially had a transitory rise in the serum creatinine level. Both cases made an uneventful recovery. The similarities between the clinical picture described and that of poisoning with pure ethylene glycol and also methanol are emphasised and might support the assumption that ethylene glycol monomethyl ether is hydrolysed in man with formation of the two former compounds.

Platelet counts in healthy premature infants

Summary Fatal myocardial infarction occurring in the first day of life is reported. Coronary artery occlusion resulted from a paradoxical embolus, the thrombus having arisen in the ductus venosus. Severe circulatory failure resulted in profound metabolic acidosis, and death occurred at the age of 23 hours.

Methylmalonic aciduria. An inborn error leading to metabolic acidosis, long-chain ketonuria and intermittent hyperglycinemia.

An eight-month-old boy was seen with profound metabolic acidosis, developmental retardation and a very unusual biochemical triad: methylmalonic aciduria; long chain ketonuria; and intermittent hyperglycinemia. Ingestion of a diet high in protein or one with a moderate amount of protein supplemented with valine or isoleucine accentuated the methylmalonic aciduria and precipitated ketoacidosis and long-chain ketonuria. There was no temporal association between these clinical and biochemical abnormalities and the elevated plasma glycine concentrations. The findings suggest that the methylmalonic aciduria, acidosis and ketonuria are the result of an inborn enzymatic defect in the conversion of methylmalonyl coenzyme A to succinyl coenzyme A. These studies also demonstrate that methylmalonic aciduria and idiopathic hyperglycinemia are two distinct but very closely related disorders.

Extracorporeal Dialysis for Methanol Intoxication

THE TOXIC effects of methanol in man are well recognized. The most severe consequences are blindness and a profound metabolic acidosis, which occur characteristically after a latent period of several hours or days after ingestion. Success in treatment depends on the correction of the acidosis and the prevention of the metabolism of methanol. The following report describes the combined use of early extracorporeal dialysis with alkalization and anhydrous alcohol (ethanol) therapy in a case of methanol poisoning, with an uneventful recovery. Report of a Case A 59-year-old white man was referred to the Charleston Memorial Hospital six hours after drinking about 16 oz of a commercial paint thinner containing methanol. The patient had a 40-year history of heavy alcohol intake, and he admitted having consumed 2 pt of whiskey daily during the week prior to admission. Results from physical examination revealed that

A Method for the Control of Severe Alterations in Acid-Base Equilibrium

Tris buffer was utilized in the prevention or treatment of profound metabolic acidosis which developed during, and immediately after, extended periods of extracorporeal circulation. In 16 patients (group I), buffer was added to the 24-hour-old heparinized priming blood prior to initiation of bypass, to counteract a low pH and high lactic acid concentration. The success of this therapy was manifested by the stability of all acid-base parameters during and following operation. In the second group of 11 patients (group II), severe metabolic acidosis developed despite preliminary buffering of the priming blood. Here, the administration of additional buffer successfully restored acid-base equilibrium prior to the termination of perfusion. The buffer also proved effective in the treatment of two patients who developed severe respiratory acidosis in the immediate postperfusion period, and was instrumental in the resuscitation of a final patient following a prolonged period of cardiac arrest. It is suggested that tris buffer is a safe, potent agent for use in the prevention and treatment of acidosis from whatever cause.

Acute Intestinal Iron Intoxication: II. Metabolic, Respiratory and Circulatory Effects of Absorbed Iron Salts

Abstract Following oral or rectal administration of toxic doses of dissociable iron salts in dogs and rabbits, the rapidly and excessively absorbed iron produced a profound metabolic acidosis with blood pH values as low as 6.7. The acidosis was mainly due to the hydrolysing effect of ferric ions and partly due to an increase in lactic and citric acid. The latter findings suggest a possible interference of the absorbed iron with enzymes in the Krebs cycle. The respiratory changes were those seen in metabolic acidosis: greatly increased respiratory rate and minute volume, lowering of the blood CO2, excessive CO2 output. The cardiac output decreased progressively due to diminished venous return, but a normal blood pressure was maintained by arteriolar constriction until the final collapse occurred, which was preceded by respiratory failure. A marked capillary congestion and increased capillary permeability were noted, the latter possibly being the result of a direct action of the high non-protein bound serum iron upon the capillary wall. The increased capillary permeability caused a reduction in plasma volume and hemoconcentration. No abnormal hemoglobin derivatives were found.