Search

Bicarbonate infusion is traditionally used to increase pH during metabolic acidosis, but it has been also suggested to increase the pH during permissive hypercapnia. In this paper we will discuss the physicochemical effect of adding (Na+ HCO3-), first in a closed system (venous blood) and then in an open system (the blood after the lung). According to Stewart model, in the closed system two independent variables are changed (CO2 and strong ion difference). As a first result changes in pH are negligible. If the CO2 is cleared by the lung and the PCO2 is maintained as before the infusion, the rise in pH is due to the SID increase caused by the (Na+) rise. The effect is independent on (HCO3-) infusion and equivalent to adding (Na+ OH-) instead of (Na+ HCO3-).

Sodium bicarbonate has been thought to be effective for hypoxic lactic acidosis, but recently its adverse reactions have been pointed out. Therefore, the effects of NaHCO3 therapy in hypoxic lactic acidosis were evaluated in the anesthetized dog. Studies were carried out in four groups of adult mongrel dogs. The first group received control ventilation with hypoxic gas (5%O2 + 95%N2) and NaHCO3 therapy to adjust blood base excess. The second group did not receive NaHCO3 therapy after control ventilation with hypoxic gas. The third group breathed hypoxic gas spontaneously and received NaHCO3 therapy. The fourth group did not receive NaHCO3 therapy during spontaneous breathing of hypoxic gas. The changes of acid-base balance, CO2 and lactate of arterial blood and cerebrospinal fluid (CSF) were analysed in each dog. The conclusions were as follows; 1. The NaHCO3 therapy is not necessary for hypoxic lactic acidosis under proper ventilation, if arterial blood pH does not fall extremely. 2. The CSF acid-base balance is kept within normal ranges, so that the NaHCO3 therapy is not necessary from this point of view.

Nineteen infants with acidosis associated with RDS were studied following the infusion of: (1) 0.58M (7%) THAM over 30 seconds; (2) molar bicarbonate over 30 seconds; (3) molar bicarbonate over 2 minutes; and (4) molar bicarbonate over 5 minutes. PaC02 fell after THAM; PaC02 rose sharply after bicarbonate and remained elevated 10 minutes after infusion. The pH rose abruptly in all infants and remained significantly elevated 10 minutes after infusion. Pa02 changes were variable; no infant had immediate improvement in Pa02. The changes in osmolality, hematocrit, and colloid osmotic pressure describe the immediate osmotic hemodilution following the infusion of hypertonic base.

The administration of sodium bicarbonate solution, which has been advocated for the treatment of metabolic acidosis, may have detrimental side effects. We evaluated oxyhemoglobin saturation and oxygen tensions in eight anesthetized swine before and after freshwater near-drowning and after a rapid intravenous infusion of 7.5% sodium bicarbonate solution (8 mEq/kg). After freshwater aspiration, arterial and venous oxygen tensions and oxyhemoglobin saturation decreased. Administration of sodium bicarbonate resulted in decreased venous and increased arterial, oxygen tensions. Arterial, but not venous, oxyhemoglobin saturation increased. These findings suggest that sodium bicarbonate caused a distinct leftward shift in the oxyhemoglobin dissociation curve, which could impair tissue oxygenation. Therefore, to avoid detrimental effects, sodium bicarbonate should be administered slowly and in a dose sufficient just to correct metabolic acidosis.

In summary, infusion of bicarbonate in the treatment of neonatal acidosis has limited value. Although it may be useful adjunct in the resuscitation of severely depressed and acidotic infants, its efficacy in the management of postasphyxia acidosis or RDS is not supported by any data. The clear risks and disadvantages of such infusions should warn against its current indiscriminate use.

Carbicarb (Na2CO3 0.33 molar NaHCO3 0.33 molar), a mixture formulated to avoid the objections to sodium bicarbonate therapy, has been compared with 1 mol/L NaHCO3 and 1 mol/L NaCl in the treatment of mixed respiratory and metabolic acidosis (pH 7.17) produced by asphyxia in rats. In clinically appropriate doses, intravenous NaHCO3 raised arterial pH only 0.03 unit, elevated arterial carbon dioxide pressure, and doubled lactate concentration. With Carbicarb, the pH rise was three times as great and the blood lactate level was unchanged. The new drug should be effective in treating the acidosis of cardiopulmonary failure without raising blood carbon dioxide pressure or lactate levels and at lower sodium doses than required for NaHCO3.

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)

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.