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Alkalinization of the blood by administration of sodium bicarbonate or hyperventilation is widely recommended for treatment of cardiac toxicity due to tricyclic antidepressant overdose, yet its efficacy and mechanism of action are poorly defined. We studied the effects and possible mechanism of action of 1 M NaHCO3 on desipramine (DMI) toxicity in anesthetized, paralyzed rats. Administration of DMI (45 mg/kg i.p.) produced a mean increase in QRS duration of 142% and a mean decrease in mean arterial pressure of 46%. Treatments were administered i.v. 35 min after DMI and their effects were assessed 10 min later. NaHCO3 (1 M) at doses of 3 and 6 mEq/kg decreased mean QRS duration 15 +/- 5 and 24 +/- 6%, respectively (mean +/- S.D.) and was superior to no treatment (P less than .01). NaCl (1 M) was as effective as NaHCO3 in decreasing QRS duration, as was 1 M NaHCO3 supplemented with 48 mM KCl. Respiratory alkalosis and 10% mannitol did not decrease QRS duration. NaHCO3, NaCl and NaHCO3/KCl all produced comparable increases in mean arterial blood pressure. Respiratory alkalosis and mannitol did not increase mean arterial pressure, but did prevent the decline seen in control animals. Acidosis produced by ventilation with 10% CO2 exacerbated QRS prolongation due to DMI. In acidotic animals, NaHCO3 and NaCl were equally effective in reversing QRS prolongation and hypotension. Correction of respiratory acidosis by discontinuation of inhaled CO2 did not improve QRS duration or mean arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

A simple modification to the standard 'in-out' exchange transfusion technique is described which requires cannulation of the umbilical vein only, yet provides many of the theoretical and practical advantages of a 2-catheter arteriovenous technique. The advantages include a reduction of cardiovascular disturbance; a reduction of the inevitable pressure changes in the portal venous system (probably important in the pathogenesis of complicating necrotizing enterocolitis); administration of alkali or drugs diluted in donor blood; accurate assessment of balance; a more efficient exchange; and general ease of management allowing better clinical observation of the infant.

The effect of different drugs on the acid-base condition and gases of arterial blood was studied by Astrup's micromethod in 124 tests in patients with circulatory insufficiency. Cardiac glycosides correct the moderate decrease in blood oxygen tension and respiratory alkalosis in patients with left-ventricular failure. Morphine has a good arresting effect in attacks of cardiac asthma and corrects or reduces the respiratory alkalosis typical of the disease but at the same time reduces the saturation of blood with oxygen. The use of oxygen together with morphine removes this unfavourable effect of the drugs. Euphylline often intensifies respiratory alkalosis, while its effect on oxygen tension in the blood and its saturation with oxygen is poorly pronounced and diversely directed. Lasics causes a favourable correcting effect on the acid-base condition and oxygenation of blood in pulmonary edema marked by metabolic acidosis.

Two newborn infants with congenital diaphragmatic hernia, one of whom died, had significant improvement in arterial oxygen tension (Pao2) after intravenous administration of tolazoline (Priscoline) (1 to 2 mg. per kilogram). In both infants, systemic hypotension developed within minutes of administration of the drug and required pharmacologic and hemodynamic intervention. The response to tolazoline was more dramatic in the infant who survived, and his oxygen requirements were significantly reduced after the use of this drug. The infant who died also had a significant response to tolazoline. Tolazoline appears to be an important pharmacologic agent for use in the postoperative care of infants with diaphragmatic hernia and associated hypoxemia and acidosis.

Serial serum Ca values in 47 infants with intrauterine growth retardation were analyzed in relation to clinical and biochemical factors. Serum Ca concentrations in IUGR infants fell within the 95 percent confidence limits for serum Ca in infants whose birth weights were appropriate for gestational age. Serum Ca concentrations in IUGR infants were significantly correlated with birth asphyxia and bicarbonate therapy for acidosis. Serum Ca concentration at 24 hours of age was inversely correlated with serum P values. Thus the incidence of neonatal hyocalcemia in IUGR infants is not increased above the incidence expected from their respective gestational ages. Infants with IUGR who are well at birth do not appear to develop neonatal hypocalcemia, but IUGR infants who are asphyxiated at birth develop significant hypocalcemia.

The treatment of neonatal respiratory distress associates the improvement of lung ventilation with the correction of acid-base equilibrium (metabolic acidosis). In such a context we have considered 10 newborns with respiratory distress and we monitored pH, PCO2, B.E. and standard bicarbonate in capillary blood at 1, 5, 10, 25 hours after birth. The sodium bicarbonate doses given as a result of the emogasanalisis are above those usually recommended. We then give suggestions on how to use the sodium bicarbonate required to correct the acidosis without the aid of an emogasanaliser in order to avoid the iatrogenic alcalosis danger.

Cardiac arrhythmias have frequently been reported in association with respiratory failure. The possible additive role of pharmacologic agents in precipitating cardiac disturbances in patients with respiratory failure has only recently been emphasized. The effects of aminophylline on the ventricular fibrillation threshold during normal acid-base conditions and during respiratory failure were studied in anesthetized open chest dogs. The ventricular fibrillation threshold was measured by passing a gated train of 12 constant current pulses through the ventricular myocardium during the vulnerable period of the cardiac cycle. During the infusion of aminophylline, the ventricular fibrillation threshold was reduced by 30 to 40 percent of the control when pH and partial pressures of oxygen (PO2) and carbon dioxide (CO2) were kept within normal limits. When respiratory failure was produced by hypoventilation (pH 7.05 to 7.25; PC02 70 to 100 mm Hg: P02 20 to 40 mm Hg), infusion of aminophylline resulted in an even greater decrease in ventricular fibrillation threshold to 60 percent of the control level. These experiments suggest that although many factors may contribute to the increased incidence of ventricular arrhythmias in respiratory failure, pharmacologic agents, particularly aminophylline, may play a significant role.