Recently, several investigators have begun to question the routine use of sodium bicsrbonate in metabolic acidosis, based on a failure to clearly demonstrate the efficacy of alkali therapy, which includes the production of carbon dioxide and variability of the effect on hemodynamic state. We studied the use of sodium bicarbonate in a canine model of hemorrhagic shock to determine its effect on arterial, mixed venous blood gases and hemodynamic states. Nine adult mongrel dogs were anesthetized with pentothal sodium and mechanical ventilation was adjusted to maintained the PaCO2 at 30 to 35mmHg. Ar Swan-Ganz catheter was inserted via a right femoral vein and the right femoral artery was cannulated for continuous pressure monitoring and intermittent blood sampling. 30 minutes after hemorrhagic shock, sodium bicarbonate (1mEq/kg) was administered and 1, 5, 15, 30 and 60 minutes after administration of sodium biearbonate we analyzed the arterial, mixed venous blood gases and measured hemodynamic states. The results were as follows, 1) The arterial carbon dioxide tensions(PaCO2) of 1,5,15,30 and 60 minutes after administration of sodium bicarbonate were 44,42,41,42 and 46mmHg which increased significantly compared to control value, 33mmHg. 2) The mixed venous carbon dioxide tensions(PvCO2) ofr 1, 5, 15, 30 and 60 minutes after administration of sodium bicarbonste were 57, 55, 56, 55 and 55mmHg which also increased significantly compared to control value, 46mmHg. 3) The mean arterial pressures of 1, 5, 15, 30 and 60 minutes after administration of sodium bicarbonate were 61, 60, 64, 68 and 70mmHg which increased significantly compared to control value, 50mmHg, but there were no increasements of cardiac output. It is undesirable to use sodium bicarbonate routinely during hemorrhagic shock because the use of sodium bicarbonate in metabolic acidosis increased arterial and mixed venous carbon dioxide tension and did not show the improvement of hemodynsmic derangement.
Acidosis ; Adult ; Alkalies ; Animals ; Arterial Pressure ; Carbon Dioxide* ; Carbon* ; Cardiac Output ; Catheters ; Dogs ; Femoral Artery ; Femoral Vein ; Gases ; Hemodynamics* ; Humans ; Research Personnel ; Respiration, Artificial ; Shock, Hemorrhagic* ; Sodium Bicarbonate* ; Sodium* ; Thiopental

The change of venous capacitance has an influence on venous return to the heart and cardiac output, and causes the alteration of preload, cardiac filling pressure and myocardial wall tension. Venous capacitance is assesed by measuring the mean circulatory filling pressure (MCFP), and MCFP is measured during brief periods of circulatory arrest produced by inflating an indwelling balloon in the right atrium It is important to know the effects of vasodilator and anesthetic drugs on venous capacitance. Therefore, this study was performed to know the effects of nitroglycerin and diltiazem on venous capacitance in rats. Rats were anesthetized with ketamine 125 mg/kg given intraperitoneally and added 10 mg/kg every 30 minutes. Their mean arterial pressure (MAP) was lowered to 60 mmHg by intravenous injection of 0.82+/-0.36 mg/kg nitroglycerin and/or 6.7+/-1.5 mg/kg diltiazem. Hemodynamic parameters such as MAP, heart rate, central venous pressure and MCFP were measured before and after drug-injection. Hemodynamic values measured before drug-injection in two groups were little differences statistically. However, the MCFP of nitroglycerin was significantly decreased (p<0.01) from 7.3+/-0.61 mmHg to 5.4+/-0.58 mmHg after drug-injection, and that of diltiazem was not significantly changed from 7.1+/-0.54 mmHg to 6.9+/-0.63 mmHg. The results suggested that nitroglycerin was predominantly a venous dilator in terms of MCFP but diltiazem had little effect of venodilation.
Anesthetics ; Animals ; Arterial Pressure ; Cardiac Output ; Central Venous Pressure ; Diltiazem* ; Equidae ; Heart ; Heart Atria ; Heart Rate ; Hemodynamics ; Injections, Intravenous ; Ketamine ; Nitroglycerin* ; Rats*

OBJECTIVE: To analyze the clinical characteristics of intrauterine fetal death. METHODS: A retrospective cross sectional analysis was done on 269 cases of intrauterine fetal death, among 44,453 deliveries over 20 weeks of gestation or weighs more than 500gm, at Ghil Hospital, Gacheon Medical School from April 1994 to December 2001. RESULTS: The incidence of intrauterine fetal death was 0.06$. The average maternal age was 28 +/- 4.6 years old. There were 52 cases(19.3%) with previous history of spontaneous abortion and 3 cases(1.1%) with previous history of intrauterine fetal death. There were 28 cases(10.4%) of fetal anomaly, and of which central nervous system defect, hydrops fetalis, abdominal anomaly were common. The maternal disease was accompanied by 69 cases(25.7%) and most common maternal disease was preeclampsia. In 74 cases(27.5%), we could not find the suspected cause of intrauterine fetal death. The suspected causes of intrauterine fetal death were intrauterine growth retardation(13.8%), cord complication(12.6%), preeclampsia(11.5%), fetal anomaly(10.4%), and placental abruption(8.2%). There were 12 cases(4.5%) of peripartum maternal complications. CONCLUSION: Intrauterine growth retardation and cord complications were the most common suspected causes, we could not find the cause of intrauterine fetal death in 74 cases(27.5%) out of 269 cases.
Abortion, Spontaneous ; Central Nervous System ; Cross-Sectional Studies ; Female ; Fetal Death* ; Fetal Growth Retardation ; Humans ; Hydrops Fetalis ; Incidence ; Maternal Age ; Peripartum Period ; Pre-Eclampsia ; Pregnancy ; Retrospective Studies ; Schools, Medical

BACKGROUND: During hemorrhagic shock, acidosis was frequently treated with sodium bicarbonate, but various adverse reactions were reported. Most adverse effects of sodium bicarbonate have been attributed to increased CO2 production and paradoxical intracellular acidosis. This study was designed to compare the effects of Carbicarb and sodium bicarbonate on hemodynamics and acid base states in canine hemorrhagic shock. METHODS: 12 mongrel dogs were randomly divided as sodium bicarbanate group (group 1, n=6) and Carbicarb group (group 2, n=6). The study was divided into three successive phases as prehemorrhagic phase (I), hemorrhagic shock phase (II), acid-base correctoin phase (III+1 min, III+5 min, III+15 min, III+30 min). At the beginning of phase III, group 1 received sodium bicarbonate 2.5 ml/kg and group 2 received Carbicarb 2.5 ml/kg. During each phase a complete set of hemodynamic parameters, arterial and mixed venous blood gas measurements were recorded. RESULTS: 1) Arterial and end-tidal CO2 of sodium bicarbonate treated group were increased significantly compared with that of Carbicarb treated group after treatment. 2) Acidosis was improved in both groups, but pH of Carbicarb treated group showed more increase compared with pH of sodium bicarbonate treated group (P <0.05). 3) There was significant hemodynamic improvement on both group after treatment, but there was no statistical significance between groups. CONCLUSION: The treatment of Carbicarb shows more increase in arterial pH and less increase in carbon dioxide compared with sodium bicarbonate to treat metabolic acidosis due to hemorrhagic shock in mongrel dogs. So we suggest that Carbicarb is useful in the treatment of metabolic acidosis during hemorrhagic shock.
Acidosis ; Animals ; Carbon Dioxide ; Dogs ; Hemodynamics* ; Hydrogen-Ion Concentration ; Shock, Hemorrhagic* ; Sodium Bicarbonate* ; Sodium*

BACKGROUND: Lidocaine is used for suppressing circulatory responses to endotracheal intubation. In this study the investigated changes of middle cerebral artery blood flow velocity (Vmca) before and after intravenous lidocaine injection by transcranial doppler. METHODS: Fifteen healthy volunteers received a bolus dose of intravenous lidocaine 1.5 mg/kg. Vmca's were measured on the temple using a bidirectional 2-MHz transcranial doppler probe before and after lidocaine injection. Vmca's were recorded continually every 10 sec for 10 minutes after lidocaine injection. RESULTS: Mean Vmca was 67.6 +/- 7.6 cm/sec before lidocaine injection. Maximal Vmca's (70.7 +/- 7.5 cm/sec, P<0.05) occurred 35 +/- 16 sec after lidocaine injection, and then the Vmca decreased gradually. Minimal Vmca's (56.6 +/- 7.4 cm/sec, P<0.05) were measured at 164 +/- 40 sec after lidocaine injection. CONCLUSIONS: We suggest that lidocaine generally causes the decreases in Vmca, excepting the temporarily increase in Vmca about 35 sec after a single bolus administration of intravenous lidocaine.
Blood Flow Velocity* ; Healthy Volunteers ; Injections, Intravenous* ; Intubation, Intratracheal ; Lidocaine* ; Middle Cerebral Artery*

BACKGROUND: Although modified Mapleson D systems connected to ventilators have been used for controlled ventilation of anesthetized infants and children, the complexity of factors affecting rebreathing within the Mapleson D circuit has resulted in a variety of recommendations for fresh gas flow and minute ventilation. We constructed a formula for ventilator settings which would provide normal tidal volume, respiratory rate, and minute ventilation without rebreathing during mechanical ventilation in pediatric anesthesia and would like to compare this method to commonly recommended Bain-Spoerel's method. METHODS: Seventy eight infants and small children who anesthetized with enflurane and nitrous oxide were studied. We performed controlled ventilation with each method and measured SpO2, PETCO2 at 10, 20, 30 min after anesthetic induction. At 20 min after anesthetic induction, we drew a arterial blood sample to evaluate PaCO2 and PaO2. RESULTS: In patients above 10 kg, mean PaCO2 was within normal range. But in patients below 10 kg, PaCO2 was significantly higher(p<0.01) with the Bain-Spoerel's method than with the Paik Hosp.'s method. CONCLUSIONS: We conclude that our method for ventilator settings can be safely and competently applied to mechanical ventilation with Modified Mapleson D circuit in pediatric anesthesia.
Anesthesia* ; Child ; Enflurane ; Humans ; Infant ; Nitrous Oxide ; Reference Values ; Respiration, Artificial* ; Respiratory Rate ; Tidal Volume ; Ventilation ; Ventilators, Mechanical