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).

Doxapram is a central and peripheral respiratory stimulant that has been primarily used to counteract postanesthetic respiratory depression.

Administration of opioid in doses sufficient to produce anesthesia is invariably associated with respiratory depression.

While opioid-induced depression can be reversed by appropriate specific opioid antagonists, it has not been possible to ify the respiratory depressant effects of a opioid without simultaneously ifying the analgesic effects.

The purpose in the present study was to determined whether doxapram is able to reverse the respiratory depressant effects of balanced anesthesia with pethidine-diazepam-nitrous oxide.

Of a total of 30 patients. the control group of 15 patients was given saline lml, and the other 15 patients(doxapram group) were given doxapram hydrochloride 20mg intravenously, and observed blood pressure, heart rate, tidal volume, respiratory rate and arterial blood gas analysis.

In doxapram group(group II). systolic arterial pressure was significantly increased 1minute after administration and heart rate increased 3minute after administration.

Tidal volume significantly increased from 4.8±1.0 to 6.0±l.0ml/kg, but little change in respiratory rate in doxapram group.

PaO₂ significantly decreased in control group(group I) compared to doxapram group 30minute after administration, but not difference in pH, PaCO₂, base excess and oxygen saturation between control and doxapram group.

Postoperative hypoxemia in elderly patients caused to suffer tissue hypoxia and injury to vital organs.

Thirty-two elderly patients over 65 years age with normal or abnormal findings in pulmonary function test were at random either epidural analgesia with 2% lidocaine and 0.5% bupivacaine or general anesthesia with diazepam, pethidine, pancuronium or vecuronium. N₂0 / 0₂ for lower abdominal or lower extremity surgery. The arterial blood gas analysis was performed at preanesthetic, 30min after extubation(or 30min after the end of surgery in epidural analgesia groups) and postoperative lday.

The results were as follows:

1) In general anesthesia group with normal findings in pulmonary function test(PET). the PH decreased, and PaCO₂ increased on 30min after extubation compared to preanesthetic values, but the PH increased, and base excess decreased significantly on the postoperative lday.

2) In epidural analgesia group with normal findings in PFT, the values of arterial blood gas analysis were no changed on 30min after the end of surgery and postoperative lday compared to preanesthetic values.

3) In general anesthesia group with abnormal findings in PFT, the PaCO₂ increased, and Pa0₂ and oxygen saturation decreased significantly on 30min after extubation, but the PH increased, Pa0₂ remained reduced on the postoperative lday compared to preanesthetic values.

4) In epidural analgesia group with abnormal findings in PFT, the values of arterial blood gas analysis were no changed on 30min after the end of surgery, but the PH increased, PaCO₂ decreased significantly on the postoperative lday compared to preanesthetic values.

It appears from these findings that epidural analgesia is preferable to general anesthesia in lower abdominal or low extremity surgery for elderly patients with abnormal findings in PFT.