Compare and contrast the pharmacology of carbicarb, Sodium bicarbonate and THAM.
Carbicarb is an equimolar combination of sodium carbonate and sodium bicarbonate, generates a smaller rise in CO2 than sodabicarb. More consistently increases intracellular pH, inconsistent effects on hemodynamics, not commonly used clinically.
Sodabicarb: 8.4% or 4.2% solution. Hyperosmolar, generates high CO2, can cause paradoxical acidosis in the presence of a low output, cause hypokalemia, alkalosis and left shift of the curve. Phlebitis when given peripherally. On the other hand, frequently used to treat a metabolic acidosis if pH < 7.1, improves vasopressor responsiveness, may have a role in decreasing contrast nephropathy.
THAM: commercially available weak alkali. Buffers H+ ions. Buffering not associated with a CO2 rise. Side effects include hyperkalemia, hypoglycemia, extravasation related necrosis, and hepatic dysfunction.
Sodium bicarbonate pharmacology is discussed at length elsewhere. It is a dear and familiar product to most ICU trainees. The other two products are somewhat more exotic, and deserve a brief digression. For instance, carbicarb does not seem to be available in Australia.
As a table, the answer would look like this:
Sodium bicarbonate | Carbicarb | THAM | |
Properties |
An 8.4% (1mol/L) solution of NaHCO3 which offers 1000mmol/L of HCO3- and Na+ions. |
An equimolar (300mmol/L) solution of Na2CO3 and NaHCO3which offers 666mmol/L of HCO3- ions, and 1000mmol/L of Na+ ions |
An organic amine buffer, otherwise known as tris-hydroxymethyl-aminomethane, or tromethamine. The 3mol/L solution offers |
Administration |
Ideally IV, but can be given orally |
IV only |
IV only |
Pharmacokinetics |
Eliminated renally, as well as being converted to CO2 and exhaled (in process of buffering reactions). These two substances differ mainly in the amount of bicarbonate anion they add. |
Rapidly eliminated by the kidney; 75% is excreted in the urine after 8 hours. |
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Adverse effects |
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Rationale for use |
Sodium bicarbonate contributes HCO3- which is a natural buffer, thus replenishing the buffer systems of the body in a state of acidosis. |
The sodium carbonate component is supposed to act as a bicarbonae precursor, regenerating HCO3- buffers without increasing the PaCO2. |
THAM is a "third buffer" to complement the buffering capacity of endogenous HCO3- and body protein. At pH of 7.40, 30% of THAM is not ionized and therefore may penetrate cells and act as an intracellular buffer. |
Indications |
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Contraindications (or, situations in which it is known to be useless) |
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In neonates it is |
Rhee, K. H., et al. "Carbicarb, sodium bicarbonate, and sodium chloride in hypoxic lactic acidosis. Effect on arterial blood gases, lactate concentrations, hemodynamic variables, and myocardial intracellular pH." CHEST Journal 104.3 (1993): 913-918.
Schmidt, G. A. "Treatment of Acidosis: Sodium Bicarbonate and Other Drugs."Anaesthesia, Pain, Intensive Care and Emergency Medicine—APICE. Springer Milan, 2002. 681-693.
Filley, G. F., and N. B. Kindig. "Carbicarb, an alkalinizing ion-generating agent of possible clinical usefulness." Transactions of the American Clinical and Climatological Association 96 (1985): 141.