Effect of Sodium Bicarbononate on Acid-Base Status in Apneic Rabbit

Sodium bicarbonate (NaHCO₃) has been used in the treatment of metabolic acidosis for more than 50 years until about 1980. and has almost become a matter or routine. But in most patients with cardiac arrest, shock or sepsis, impaired tissue oxygen delivery is the primary cause of lactic acid accumulation and the administration of sodium bicarbonate dose not appear to affect the underlying tissue hypoxia and is generally not successful in improving either acidotic state or clinical status.

The purpose in the present study was to examine the effect of sodium bicarbonate on acid base start in case of resuscitation of cardiopulmonary arrest state due to apnea combined with respiratory and metabolic acidosis.

Of a total of 12 rabbits, the control group(n=6) was given normal saline 3ml. and the experimental group(n=6) was given 5% sodium bicarbonate 3ml immediately after the induction of apnea intravenously.

Arterial and venous blood gas analysis was done. and arterial hemoglobin. K⁺. uric acid. lactic acid and glucose levels were measured immediately before the induction of apnea. immediately after the induction of apnea. 10 min and 30 min after the cardiopulmonary resuscitation (CPR).

The data were statistically compared & analysed with following results

1) In the control group arterial and venous blood gas analysis showed decreased values of pH. P0₂, oxygen saturation and base excess and increased value of PCO₂ immediately after the induction of apena(p<0.001) compared to contol values(preapnea values), and all measures except bicarbonate concentration and base excess returned to normal ranges after CPR. Arterial K⁺ levels increased, glucose levels decreased compared to contol values immediatelv after the induction of apnea(p<0.05).

2) In the experimental group, arterial and venous blood gas analysis showed similar changes in all parameters immediately after the induction of apnea. and at 10 mm after CPR, pH, PO₂, oxygen saturation arid base excess decreased compared to control value, But PCO₂ increased(p<0.001). At 30 min after CPR. pH remained decreased but PCO₂ remained increased compared to the control values(p<0.001). Arterial K⁺ level increased immediately after the induction of apena and lactic acid level increased immediately after the induction of apnea. 10 and 30 min after CPR compared to control values(p<0.05).

3) In the experimental group. arterial and venous blood pH. P0₂ oxygen saturation were lower. but PCO₂ was higher at 10 min after CPR compared to control group(p<0.05). At 30 min after CPR. venous blood pH was lower. and arterial and venous PCO₂ were higher compared to control group(p<0.05). Arterial K⁺ level at 10 min after CPR and lactic acid level at 10 and 30 min after CPR were higher compared to control group(p<0.05).