PURPOSE: D-lactate, optical isomer of L-lactate is not a human metabolite. Once the D-lactate enters the human body, it is mainly metabolized in liver. The metabolism of D-lactate can be changed in patients with decompensated liver cirrhosis with the exposure of antibiotics and the frequent trial of lactulose, if neccessory. The aim of this study is to analyze blood D-lactate level in cirrhotic patients and it's relationship with the degree of hepatic insufficiency and acid-base imbalance. METHODS: Plasma L-lactate and D-lactate levels were measured in 40 cirrhotic patients classified by Child-Pugh system with L-LDH and D-LDH with comparison of their changes before and after the use of antibiotics and lactulose(n=14). Also, acid-base disorders were analyzed in 35 cirrhotic patients, and plasma L, D-lactate levels were determined in each acid-base disorder. RESULTS: Plasma D-lactate level was not significantly elevated in cirrhotic patients compared to the control group(2.34+/-.48 mmol/L vs. 1.63+/-.26 mmol/ L, p=NS), but some patients(n=4, 10%) revealed abnormally elevated D-lactate level. The plasma L, D- lactate levels were not different in subgroups classified by Child-Pugh system as well as by underlying causes of liver cirrhosis, and plasma D-lactate level was not sugnificnatly different before and after the exposure of antibiotics and lactulose. Plasma D-lactate level was significantly increased in 3 patients with respiratory alkalosis and metabolic acidosis(12+/-.98 mmol/L) compared to others(p<0.05). CONCLUSION: These results suggest that, regardless of its decompensated degree and exposure to drugs, a subset of patients with liver cirrhosis can develop elevation of D-lactate in blood, particularly when metabolic acidosis is accompanied.
Acid-Base Imbalance* ; Acidosis ; Alkalosis, Respiratory ; Anti-Bacterial Agents ; Hepatic Insufficiency ; Human Body ; Humans ; Lactic Acid ; Lactulose ; Liver ; Liver Cirrhosis ; Metabolism ; Plasma*

Action of neuromuscular blocking agents are known to be largely affected by acid-base imbalance. In general, acidosis potentiates and alkalosis antagonizes the action of the neuromuscular blockers. To evaJuate the effects of acid-base imbalance on the neuromuscular actions of atracurium or vecuronium in 24 cats, we induced respiratory and metabolic acid-base imbalance and performed cumulative dose response studies. The results are as follows; 1) ED(50) and ED(95) of the atracurium was smaller in metabolic acidosis than those of respiratory and metabolic alkalosis. 2) ED(50) of vecuronium was not affected by acid-base imbalance in either agent. 3) Duration and recovery index were not affected by acid-base imbalance in either agent. 4) In atracurium group, serum potassium and calcium values during respiratory or metabolic alkalosis were smaller than those of control, but did not influence the neuromuscular action of atracurium. 5) Dose-response curve of the atracurium shifted to the right with metabolic acidosis, respiratory acidosis, metabolic alkalosis and respiratory alkalosis in order, but acid-base imbalance did not influence the dose-response curve of the vecuronium. In conclusion, the potency might be increased in respiratory and metabolic acidosis with atracurium, but not with vecuronium. However, action and recovery were not influenced by a experimental imbalance in either agent.
Acid-Base Imbalance ; Acidosis ; Acidosis, Respiratory ; Alkalosis ; Alkalosis, Respiratory ; Animals ; Atracurium* ; Calcium ; Cats ; Neuromuscular Blockade* ; Neuromuscular Blocking Agents ; Potassium ; Vecuronium Bromide*

BACKGROUND: Patients with cardiac diseases who have structural defects in their heart bring about metabolic insult such as preoperative acid-base imbalance. Cardiac operation requires many nonphysiologic procedures such as extracorporeal circulation, hypothermia, and hemodilution. We studied the acid-base status of surgical heart diseases pre-operatively, during extracorporeal circulation, and post-operatively and researched the treatment indications of acid-base disturbances. MATERIAL AND METHOD: From January 1997 to May 1999, fifty two cases of open heart surgery were carried out under extracorporeal circulation, which divided into a set of pediatric and adult groups, congenital and acquired groups, non-cyanotic and cyanotic groups, The alpha-stat arterial blood gas analysis was done in each group during the preoperative period, during the operation with extracorporeal circulation, and during the postoperative period. RESULT: Before surgery, all patients present metabolic acidosis, PaO2 was low in adult group and acquired group and compensatory respiratory alkalosis was noted in cyanotic group. During extracorporeal circulation, adult group revealed alkalosis and normal in acquired group. Pediatric group presents low PaCO2, metabolic acidosis and respiratory alkalosis. Congenital group and non-cyanotic group showed non-compensatory alkalosis trend and non-compensatory respiratory acidosis were observed in cyanotic group during extracorporeal circulation. Postoperative acid-base status of adult group was recovered to normal and the standard bicarbonate was increased in the acquired group. All of the pediatric, congenital non-cyanotic, and cyanotic groups revealed the lack of buffer base. CONCLUSION: In Preoperative period, correction of metabolic acidosis was required in pediatric, congenital and non-cyanotic groups, while treatment of metabolic acidosis and low PaCO2 were required in adult and acquired groups. In the cyanotic group, metabolic acidosis and respiratory alkalosis needed to be corrected preoperatively. Using the extracorporeal circulation, minimal correction was required except acquired group which showed normal acid-base balance. In postoperative period, restriction of bicarbonate was required for acquired group while increase of buffer base was required for pediatric, congenital, non-cyanotic, and cyanotic groups.
Acid-Base Equilibrium ; Acid-Base Imbalance ; Acidosis ; Acidosis, Respiratory ; Adult ; Alkalosis ; Alkalosis, Respiratory ; Blood Gas Analysis ; Extracorporeal Circulation* ; Gases* ; Heart Diseases* ; Heart* ; Hemodilution ; Humans ; Hypothermia ; Postoperative Period* ; Preoperative Period* ; Thoracic Surgery

No abstract available.
Acidosis, Respiratory* ; Alkalosis, Respiratory*

Intercalated cells play a major role in proton and bicarbonate secretion in the collecting duct of kidney. A third type of intercalated cell (non A-non B cell), besides type A and B intercalated cells, and a bipolar cell are known to exist in the kidneys of the rat or the mouse. The third type cell has H(+)-ATPase in the apical membrane like the type A intercalated cell, but has no Cl(-)-HCO(3)- exchanger (AE1) on the basolateral membrane. The bipolar cell was shown to express H(+)-ATPase on both the apical and basolateral membranes. The functions of these cells, however, are not determined yet. This study was intended to know the immunohistochemical changes of the intercalated cell subtypes in the acute respiratory acidosis and alkalosis. After midline tracheostomy, respiratory acidosis and alkalosis were induced and maintained for 4 hours in the Sprague-Dawley rats (450~500 g) using a Rodent Ventilator. The kidneys were preserved for immunohistochemical studies by in vivo perfusion fixation with periodate-lysine-paraformaldehyde solution through the abdominal aorta. To identify the subtypes of intercalated cells and the tubule segments in which they are located, a triple immunolabeling procedure was used. Distal convoluted tubule cells and principal cells in the collecting duct were identified using antibody to thiazide sensitive Na(+)Cl(-) cotransporter and antibody to aquaporin-2, respectively. Antibodies to H(+)-ATPase and AE1 were used to identify subpopulation of intercalated cells. Type A cells were activated in respiratory acidosis with enhanced AE1 activity on the basolateral membrane and H(+)-ATPase reactivity moved to the apical membrane, whereas inactivated in respiratory alkalosis with decreased AE1 reactivity and H(+)-ATPase reactivity moved to the supranuclear cytoplasm. The change in reactivity of type A cells in respiratory acidosis or alkalosis was shown to differ depending on the tubular segments: most of the intercalated cells were activated in the outer medullary collecting duct while only a portion of the type A cells activated in the distal convoluted tubule, connecting tubule and cortical collecting duct. No changes were observed in type B cells in respiratory acidosis and alkalosis. In non A-non B cell which was increased in size in respiratory acidosis, H(+)-ATPase reactivity was seen on the apical membrane in respiratory acidosis, while seen in the supranuclear cytoplasm in respiratory alkalosis. These findings indicated that the renal compensation for respiratory acid-base imbalance was mediated mainly by type A cells rather than by type B or non A-non B cells. Among type A cells, more of those of outer medullary collec-ting duct were thought to be recruited compared with those of the cortical collecting duct and connecting tubule.
Acid-Base Imbalance ; Acidosis, Respiratory* ; Alkalosis* ; Alkalosis, Respiratory ; Animals ; Antibodies ; Aorta, Abdominal ; Aquaporin 2 ; B-Lymphocytes ; Compensation and Redress ; Cytoplasm ; Immunohistochemistry ; Kidney* ; Membranes ; Mice ; Perfusion ; Proton-Translocating ATPases ; Protons ; Rats* ; Rats, Sprague-Dawley ; Rodentia ; Tracheostomy ; Ventilators, Mechanical

Metabolic acid-base disorders are comnom clinical problems in ICU patients. Arterial blood gas analysis and anion gap (AG) are important laboratory data in approaching acid-base interpretation. When measuring the AG, several factors such as albumin have influence on unmeasured anions and unmeasured cations. If a patient has hypoalbuminemia, the AG should be adjusted according to the albumin level. High AG metabolic acidoses including lactic acidosis, ketoacidosis, and ingestion of toxic alcohols are common in ICU patients. The treatment target of lactic acidosis and ketoacidosis is not the acidosis, but the underlying condition causing acidosis. Gastric acid loss, diuretics, volume depletion, renal compensation for respiratory acidosis, hypokalemia, and mineralocorticoid excess are common causes of metaboic alkalosis. In chloride responsive metaboic alkalosis, volume and potassium repletion are mandatory.
Acid-Base Equilibrium ; Acidosis ; Acidosis, Lactic ; Acidosis, Respiratory ; Alcohols ; Alkalosis ; Anions ; Blood Gas Analysis ; Cations ; Compensation and Redress ; Diuretics ; Eating ; Gastric Acid ; Humans ; Hypoalbuminemia ; Hypokalemia ; Ketosis ; Potassium

BACKGROUND: Intraoperative acid-base imbalance frequently occurs during liver transplantation (LT). The purpose of this study was to compare the acid-base changes between cadaveric whole LT and a LT from a living relative using a strong ion approach. METHODS: Twenty-four patients undergoing LT were allocated to a group receiving a LT from a brain dead donor (BD group, n = 12) or a LT from a living, related donor (LD group, n = 12) according to the surgical technique required. Acid-base parameters such as PaCO2, pH, base excess, and serum concentrations of bicarbonate, albumin, lactate, phosphate, and other electrolytes were measured at 30 min after skin incision (T1), 30 min after reperfusion (T2), and 1 h after the arrival at the intensive care unit (T3). The apparent strong ion difference (SIDa), the effective strong ion difference (SIDe), and the strong ion gap (SIG) were calculated using the Stewart equation. RESULTS: There were no significant differences in pH, PaCO2, base excess, SIDa, and SIG between the two groups throughout the entire period of investigation. pH was decreased from T1 to T2, and increased significantly from T2 to T3 in both groups. The serum concentration of lactate was significantly increased from T1 to T2 and T3 in both groups without any intergroup differences. The strong ion gap was significantly increased from T1 to T2 only in the BD group. CONCLUSIONS: During LT from both cadaveric and living related donors, there is a biphasic acid-base change that is characterized by an initial metabolic acidosis and then a metabolic alkalosis, with no significant intergroup differences in acid-base variables.
Acid-Base Equilibrium ; Acid-Base Imbalance ; Acidosis ; Alkalosis ; Brain Death ; Cadaver ; Electrolytes ; Humans ; Hydrogen-Ion Concentration ; Intensive Care Units ; Lactic Acid ; Liver ; Liver Transplantation ; Reperfusion ; Skin ; Tissue Donors

Capnometer has been used in anesthesia for the evaluation of pulmonary ventilation because of its nonivasive and continuous monitoring advantges. We studied pulmonary ventilation effects with arterial blood gas parameter between normoventilation and hyperventilation with capnometric control during 1 hr duration. We devided two group. Control group was maintained PetCO2 38 mmHg and experimental group PetCO2 28 mmHg and four times arterial blood gas sample were done. The results were as follows. 1) Serum K+ concentration was decreased siginifcantly in hyperventilation group. 2) Arterial pH changes were observed respiratory alkalosis in experimental group and respiratory acidosis in control group. 3) (a-t)PCO2 differnce were increased in both group and especially control group with correlation of time duration. 4) No arrhythmia were detected in both group. We conclude that only capnometric control of pulmonary ventilation is not suffieient and it has to be combined periodic ABGS and resetting of ventilation mode.
Acidosis, Respiratory ; Alkalosis, Respiratory ; Anesthesia ; Arrhythmias, Cardiac ; Hydrogen-Ion Concentration* ; Hyperventilation* ; Pulmonary Ventilation ; Ventilation

OBJECTIVE: The biochemical data of 10 patients admitted with diabetic ketoacidosis(DKA) during the last 2 years were analyzed for the disturbances of serum potassium(K) and acid-base balance with a special interest to look for the underlying causes of potassium(K) disorder, retrospectively. METHODS: Arterial blood gas analysis was done and electrolytes, serum glucose, serum osmolality, BUN, creatinine were checked on admission and recovery in 10 patients with diabetic ketoacidosis. RESULTS: The mean(+/-SE) serum K at diagnosis and on recovery was 4.9+/-0.9mEq/L(range, 3.2-6.5 mEq/L) and 3.8+/-0.2mEq/L(range, 3.0-4.3mEq/L), respectively. Hyperkalemia(>5.0mEq/L) in 30%(3/10) and hypokalemia(<3.5mEq/L) in 10%(1/10) was noted on admission, whereas, on recovery, hyperkalemia in none and hypokalemia in 40%(4/10). Initial K levels showed a negative correlation with pH(gamma= -0.62, P=0.05) but no significant correlation was found between the initial K levels with anion gap (AG), with serum glucose value and with blood osmolality. Only 40%(4/10) had a simple metabolic acidosis while 60%(6/10) had a mixed acid-base disorder DKA with respiratory alkalosis, mostly(5/6). The ratio of delta AG over delta HCO3 was not significantly different between patients with a simple metabolic acidosis(0.95) and with a mixed acid-base disorder(0.92). CONCLUSION: The degree of acidosis must be one of the predominant factors in the pathogenesis of the initial hyperkalemia rather than hyperglycemia resulting from insulinopenia itself. Also, we observed that patients with DKA commonly develop mixed acid- base disorders, and delta AG/delta HCO3 ratio would not be an useful tool to look for a mixed acid-base disorder.
Acid-Base Equilibrium* ; Acidosis ; Alkalosis, Respiratory ; Blood Gas Analysis ; Blood Glucose ; Creatinine ; Diabetic Ketoacidosis ; Diagnosis ; Electrolytes ; Humans ; Hyperglycemia ; Hyperkalemia ; Hypokalemia ; Osmolar Concentration ; Potassium* ; Retrospective Studies

The effects of acidosis and alkalosis on vascular smooth muscle contractions were studied. Ring segments(3-4 mm in length) of rabbit abdominal aorta and pulmonary artery were mounted in the tissue bath(for respiratory study) and superfusion device(for metabolic study) for isometric tension recording. Respiratory acidosis and alkalosis were obtained by increasing and lowering the PCO2(80 and 15 mmHg, respectively). Metabolic acidosis and alkalosis were obtained by lowering and increasing the HCO3 concentration(12 and 50 mEq/l, respectively). After precontraction with norepinephrine(10-7 M), Vessels were exposed to acidosis and alkalosis for 30 minutes. The study was done with and without endothelium. The mechanism of vasorelaxation and vasoconstriction were confirmed with Ca2+ activated K+ channel blocker and Ca2+ free Krebs solution. The results were as follows: 1) Respiratory and metabolic acidosis induced significant vasorelaxation in both group of abdominal aorta and pulmonary artery(p<0.05). In endothelium intact group, vasorelaxation was greater than endothelium removed group. especially in respiratory acidosis was statistically significant(p<0.05). 2) Respiratory and metabolic alkalosis induced significant vasoconstriction in both group of abdominal aorta and pulmonary artery(p<0.05). In endothelium intact group, vasoconstriction was lesser than endothelium removed group, but was not statistically significant. 3) Acidosis induced vasorelaxation was blocked by tetraethylammonium(TEA). 4) Alkalosis induced vasoconstriction was blocked by Ca2+ free Krebs solution. These results suggested that: 1) Acidosis induced vasorelaxation. 2) alkalosis induced vasoconstriction 3) Vasorelaxation during acidosis was induced by K+ efflux through the Ca2+ activated K' channel. 4) Vasoconstriction during alkalosis was induced by Ca2+ influx.
Acid-Base Equilibrium* ; Acidosis ; Acidosis, Respiratory ; Alkalosis ; Aorta, Abdominal ; Endothelium ; Muscle, Smooth, Vascular ; Pulmonary Artery ; Vasoconstriction ; Vasodilation