Am. J. Respir. Crit. Care Med., Vol 155, No. 3, 03 1997, 957-963.
Tris-hydroxymethyl aminomethane and sodium bicarbonate to buffer metabolic acidosis in an isolated heart model
D Sirieix, S Delayance, M Paris, S Massonnet-Castel, A Carpentier and JF Baron
Department of Anesthesiology and Intensive Care, Broussais Hospital, Paris, France.
Metabolic acidosis induces a decrease in the developed force of cardiac
muscle by affecting every step of the excitation--contraction coupling
pathway. Due to transient worsening in intracellular acidosis, the value of
administering sodium bicarbonate therapeutically during acute acidosis has
been questioned. An alternative therapeutic drug, Tris- hydroxymethyl
aminomethane (THAM) has the advantage of diffusing into the intracellular
space. This study was designed to evaluate the effects of metabolic
acidosis on myocardial performance and to determine the effects of
alkalinization with sodium bicarbonate, THAM, and their combination. Using
a blood-perfused isolated heart preparation, left ventricular contractility
and relaxation were measured at normal pH and during metabolic acidosis (pH
= 7.0). Acidosis dramatically impaired myocardial contractility and
relaxation. After buffering with sodium bicarbonate, although plasma
bicarbonate concentration was normalized, pH remained below normal owing to
an increased PaCO2. Contractility and relation were initially worsened,
then slightly improved to return to control values. THAM uncompletely
buffered acidosis but significantly improved contractility and relaxation.
The combination of THAM with sodium bicarbonate perfectly buffered acidosis
without modifying PaCO2 and significantly improved contractility. The
combination of THAM with sodium bicarbonate is based on the ability of THAM
to capture the CO2 produced by the sodium bicarbonate buffer. This
combination achieves a perfect correction of metabolic acidosis and
improves myocardial performance.
