Improved hemodynamic function during hypoxia with Carbicarb, a new agent for the management of acidosis.

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Abstract
Carbicarb is a mixture of Na2CO3/NaHCO3 that buffers similarily to NaHCO3, but without net generation of CO2. We studied the effects of carbicarb in an animal preparation of hypoxic lactic acidosis (HLA). HLA was induced by ventilating dogs with an hypoxic gas mixture (8% O2/92% N2). Dogs with HLA (n = 28) were then treated with 2.5 meq/kg of either NaHCO3 or carbicarb over 1 hr. Measurements were made, after 1 hr of hypoxia and 1 hr of therapy, of: cardiac hemodynamics, blood gases, liver intracellular pH (pHi), oxygen consumption, and regional lactate production. After therapy, the arterial pH rose with carbicarb (7.22 to 7.27, p < .01), and fell with NaHCO3 (7.18 to 7.13, p < .01). Mixed venous PCO2 did not change with carbicarb but increased with NaHCO3 (p < .05). Artreial lactates stabilized with carbicarb but rose with Na HCO3 (by 3.1 mmol/liter, p < .005). Lactate use by muscle, gut, and liver all improved with carbicarb and decreased with NaHCO3. The liver pHi (normal = 6.99, hypoxia = 6.80) improved the carbicarb (to 6.92), but decreased further with NaHCO3 (to 6.40). Muscle O2 consumption rose with carbicar, whereas it decreased with NaHCO3. Arterial pressure fell less with carbicarb (-12 vs -46 mm Hg, p < .006) and the cardiac output was stable with carbicarb but decreased with NaHCO3 (from 143 to 98 ml/kg/min, p < .004). Stroke volume also improved with carbicarb but there was no change in pulmonary capillary wedge pressure, suggesting that carbicarb had a beneficial effect on myocardial contractility. These data demonstrate that admininistration of carbicarb to dogs with HLA results in improvements in the arterial blood gases, tissue pHi, lactate production, and cardiac hemodynamics. These findings are in contrast to the effects of NaHCO3 and may be related to less systemic CO2 generation by carbicarb. Carbicarb thus appears to be superior to NaHCO3 for the treatment of hypoxic states in the presence of lactic acidosis.