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KMID : 0374019920150040405
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Ewha Medical Journal
1992 Volume.15 No. 4 p.405 ~ p.412
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Effects of Sodium Bicarbonate on Acid-Base Status in Apneic Rabbit
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Abstract
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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 of 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 of clinical status.
The purpose in the present study was to examine the effect of sodium bicarbonate on acid-base status in cases 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. PO2. Oxygen saturation and base excess and increased value of PCO2 immediately after the induction of apena(p<0.001) compared to control
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 control values immediately 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 min after CPR. pH. PO2. Oxygen saturation and 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 apnea 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. PO2 and oxygen saturation were lower. But PCO2 was higher at 10 min after CPR compared to control group(p<0.05). At 30min 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).
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