Arterial Blood Lactate Levels Research Articles

The P50 is reduced in critically ill patients

A prospective study was designed to measure the P50 in 20 critically ill patients, and compare it with the P50 measured in 20 normal individuals. Arterial blood gases, lactate, haemoglobin (Hb) and phosphate (PO4) levels were also measured and compared with the P50 in the critically ill patients. The mean P50 of the critically ill patients was 24.5 mmHg (SD +/- 2.9) and was significantly lower than the mean P50 of 26.2 (SD +/- 2.2) in the normal individuals (p less than 0.05). In the critically ill patients, strong correlations were observed between the P50 and the arterial pH and base excess (BE) levels, with coefficients of 0.79 and 0.69 respectively whereas correlations between the P50 and arterial oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, Hb and PO4 levels were poor, with correlations of 0.001, 0.008, 0.07, 0.13 respectively. It is concluded that the P50 is commonly reduced in critically ill patients, and has a strong correlation with arterial pH and BE.

Continuous Monitoring of Mixed Venous Oxygen Saturation in Patients with Acute Myocardial Infarction

Continuous measurement of mixed venous oxygen saturation (SvO2) has been suggested as an adjunct in monitoring critically ill patients. We evaluated SvO2 monitoring in 24 patients suffering from complicated myocardial infarctions. Cardiac output and arterial lactate levels were measured when there were persistent 5 percent changes in SvO2, and otherwise, every 12 hours or as indicated clinically. Increases in SvO2 by 5 and 10 percent corresponded with an increase in cardiac index in 78.5 percent and 75 percent of measurements, respectively. Decreases in SvO2 by 5 and 10 percent corresponded with decreases in cardiac index in 45.5 percent and 61 percent of measurements. Twenty percent changes in cardiac index showed dissimilar directional changes with SvO2 in 62 percent of cases. Arterial blood lactate levels correlated poorly with SvO2. Survivors had significantly higher mean SvO2 and cardiac indices than nonsurvivors (p less than 0.01). The clinical management of patients with myocardial infarction may not be altered in view of the limitations of SvO2 in reflecting tissue hypoxia. We conclude that continuous monitoring of SvO2 may not be a sensitive measure of cardiac output after acute myocardial infarction.

Relation of arterial blood lactate to oxygen delivery and hemodynamic variables in human shock states

A retrospective study of 50 patients with circulatory shock and serial hemodynamic and metabolic measurements was undertaken. From the patient records, values for first measured cardiac index (CI) (t = 1) and highest CI (t = 2) with concomitantly obtained hemodynamic and metabolic variables and with arterial blood lactate levels (ABL), measured within 1.5 hours of t = 1 and t = 2 were taken. Nineteen patients had nonseptic shock (NSS), and 31 had septic shock (SS). Mortality rates were equivalent. At both t = 1 and t = 2, CI and O2 delivery (DO2) were higher and systemic vascular resistance index (SVRI) was lower in SS than in NSS. Although increases in DO2 were significant and not different between the groups and initial ABL values were similar, ABL had declined 50% in NSS but had not changed in SS (p less than 0.0001). From the hemodynamic and metabolic variables investigated in NSS, changes in ABL only correlated with changes in arterial oxygen content (CaO2; r = -0.65; p less than 0.01). Changes in ABL did not correlate with changes in DO2 in both groups. In SS, changes in ABL best correlated with changes in SVRI (r = -0.54; p less than 0.01). Our data suggest that anaerobic metabolism, reflected by ABL, decreases in response to an increase in CaO2, CI, and thus DO2 in NSS but not in hyperdynamic SS. Anaerobic metabolism in the latter may relate to peripheral vasodilation, associated with peripheral "functional" shunting of blood transported oxygen, rather than to insufficient DO2.

Effects of dichloroacetate following canine asphyxial arrest.

Sodium dichloroacetate (DCA) has been shown to lower elevated serum lactate levels produced by hypoxia, exercise, and phenformin. We conducted a study to investigate the effect of DCA treatment on lactic acidosis following resuscitation from asphyxial cardiac arrest. Conditioned dogs were anesthetized with pentobarbital (30 mg/kg), endotracheally intubated, and mechanically ventilated to maintain an arterial pCO2 of 30 to 40 mm Hg. Asphyxial cardiac arrest was produced by endotracheal tube occlusion for six to eight minutes. After five minutes of cardiac arrest, the endotracheal tube was unclamped and closed-chest CPR was begun. Six animals received DCA 100 mg/kg IV push after one minute of CPR. Control animals (n = 6) received an equal volume of saline. CPR was continued until the return of a spontaneous pulse, when mechanical ventilation was resumed. Arterial and venous blood gases, glucose, and lactate levels were obtained at baseline and 15, 30, 45, 60, 90, and 120 minutes after resuscitation. Mean arterial blood pressure, pulse, and glucose, and venous and arterial blood gases were similar in both groups throughout the study. By 45 minutes after resuscitation, the DCA-treated group showed a significantly faster rate of decline in lactate levels that continued to the final sampling period. By 90 minutes, arterial lactate in DCA animals was not significantly different from baseline (pre-arrest) values. DCA given during cardiac arrest will cause a more rapid normalization of arterial lactate after successful resuscitation. Further studies are needed to evaluate the effects of lowered lactic acid on survival and neurological outcome following cardiac arrest.

Peripheral vascular resistance in septic shock: its relation to outcome.

To support the concept that patients who die of septic shock have a persistent defect in peripheral vascular tone irrespective of cardiac index (CI), a retrospective study was undertaken of 42 patients with documented septic shock. From the patient records, the single lowest CI (t = 2) measured after initial values (t = 1) with concomitantly obtained haemodynamic and metabolic variables was taken. Group 1 consisted of 21 survivors and group 2 of 21 patients, who had died in shock. Initial haemodynamic and metabolic variables were comparable between the groups, reflecting shock with a hyperdynamic circulation and lactic acidemia. At t = 2, median CI measured 3.21.min-1.m-2 in both groups, but mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) were higher in group 1 than 2 (p less than 0.0005). Changes in arterial blood lactate levels also differed significantly. The rankcorrelation between CI and SVRI at t = 2 was significant in group 1 (rs = -0.69, p less than 0.005) but not in group 2 (rs = -0.34). Our data suggest that when CI decreases in septic shock, patients with a fatal outcome have less capability to augment vascular resistance than survivors. Hence, peripheral vascular failure, even if complicated by inability to maintain an elevated CI, may be a major haemodynamic determinant of mortality in septic shock.

Net hepatic lactate balance following mixed meal feeding in the four-day fasted conscious dog

The present experiments were undertaken to determine whether four days of fasting and marked hepatic glycogen depletion would alter the effect of mixed meal feeding on net hepatic lactate balance in the conscious dog. Dogs were fasted for four days and were then fed a mixed meal over a ten-minute period. Net hepatic glucose and lactate balance were monitored for the next eight hours using the A-V difference technique. The arterial plasma glucose level rose to a maximum of 121 ± 3 mg/dL three hours after feeding and then decreased. Net hepatic glucose output declined to 0.44 ± 0.44 mg/kg/min but the liver never became a net consumer of glucose. The arterial blood lactate level rose from 678 ± 71 to 1000 ± 158 μmol/L as the liver switched from net lactate uptake (12.2 ± 2.0 μmol/kg/min) to net lactate production (4.3 ± 1.7 μmol/kg/min). Over the course of the eight-hour postprandial period 25 g of glycogen were deposited in the liver. The net hepatic uptake of the gluconeogenic amino acids rose from 6.1 ± 1.2 μmol/kg/min to a peak of 15.4 ± 4.3 μmol/kg/min one hour after feeding. Net hepatic uptake of glycerol fell from 3.0 ± 0.3 μmol/kg/min to an average of 1.5 ± 0.4 μmol/kg/min. The plasma insulin level increased from 13 ± 2 μU/mL to a peak of 50 ± 4 μU/mL at 3.5 hours and fell to 32 ± 7 μU/mL by 8 hours. The plasma glucagon level rose from 22 ± 3 pg/mL to 93 ± 12 pg/mL 1.5 hours after feeding and fell to 68 ± 6 pg/mL 8 hours after feeding. It is concluded that in the long-fasted dog fed a mixed meal, (1) the liver switches from net lactate uptake to net lactate output, (2) net hepatic glucose production decreases, but net hepatic glucose uptake does not occur, and (3) hepatic glycogen synthesis occurs despite the absence of net glucose and lactate uptake by the liver.

Prognostic significance of ventricular CSF lactic acidosis in severe head injury.

Brain-tissue acidosis inferred by cerebrospinal fluid (CSF) lactic acidosis is considered to play an important role in the clinical course of severe head injury. Ventricular CSF lactate concentration was studied in 19 patients during the first 5 days after severe head injury. All patients were intubated, paralyzed, and artificially ventilated so that PaCO2 was kept at 33.2 +/- 5.0 mm Hg and PaO2 at 122 +/- 18 mm Hg (mean +/- standard deviation). The mean Glasgow Coma Scale score on admission was 5.73 +/- 2.42. The first CSF sample was drawn within 18 hours after head injury. Over the first 4 days postinjury, patients with a poor outcome had significantly higher ventricular CSF lactate levels than did those with moderate disabilities or a good outcome. Patients showing favorable outcome had a significant decrease in ventricular CSF lactate levels 48 hours after injury. This decrease was not observed in patients with a poor outcome. Increased ventricular CSF lactate concentration was also reliably associated with increased intracranial pressure (ICP). Ventricular CSF lactate levels did not correlate with the magnitude of intraventricular bleeding. Arterial and jugular venous blood lactate levels, although high after head injury, were usually lower than the levels in the ventricular CSF and reached a normal range by the 3rd day following head trauma. At that time, the ventricular CSF lactate concentration was still above normal in patients with a poor outcome but had decreased to normal in patients with moderate disabilities or a good outcome. Ventricular CSF pH did not generally correlate with the ventricular CSF lactate concentration in patients under controlled ventilation; however, in a few patients close to death or with ventricular infection, a correlation was noted. Ventricular CSF lactate levels were not related to cerebral blood flow. In this study, profiles of ventricular CSF lactate concentration are defined in relation to the patients' clinical course and outcome. High ventricular CSF lactate concentration is present within 18 hours after severe head injury. Its decrease to normal in the following 48 hours is a reliable sign of clinical improvement; however, ventricular CSF lactate levels that are persistently high or that increase over time indicate the patient's deterioration. Serial assessment of ventricular CSF for acid-base status and metabolites in head-injured patients with a ventricular catheter already placed for ICP monitoring is useful in the evaluation of prognosis and clinical course.

Intracellular and extracellular acid-base status and H+ exchange with the environment after exhaustive exercise in the rainbow trout.

Exhaustive exercise induced a severe short-lived (0-1 h) respiratory, and longer-lived (0-4 h) metabolic, acidosis in the extracellular fluid of the rainbow trout. Blood 'lactate' load exceeded blood 'metabolic acid' load from 1-12 h after exercise. Over-compensation occurred, so that by 8-12 h, metabolic alkalosis prevailed, but by 24 h, resting acid-base status had been restored. Acid-base changes were similar, and lactate levels identical, in arterial and venous blood. However, at rest venous RBC pHi was significantly higher than arterial (7.42 versus 7.31). After exercise, arterial RBC pHi remained constant, whereas venous RBC pHi fell significantly (to 7.18) but was fully restored by 1 h. Resting mean whole-body pHi, measured by DMO distribution, averaged approx. 7.25 at a pHe of approx. 7.82 and fell after exercise to a low of 6.78 at a pHe of approx. 7.30. Whole-body pHi was slower to recover than pHe, requiring up to 12 h, with no subsequent alkalosis. Whole-body ECFV decreased by about 70 ml kg-1 due to a fluid shift into the ICF. Net H+ excretion to the water increased 1 h after exercise accompanied by an elevation in ammonia efflux. At 8-12 h, H+ excretion was reduced to resting levels and at 12-24 h, a net H+ uptake occurred. Lactate excretion amounted to approx. 1% of the net H+ excretion and only approx. 2% of the whole blood load. Only a small amount of the anaerobically produced H+ in the ICF appeared in the ECF and subsequently in the water. By 24 h, all the H+ excreted had been taken back up, thus correcting the extracellular alkalosis. The bulk of the H+ load remained intracellular, to be cleared by aerobic metabolism.

CLINICAL SIGNIFICANCE OF DEEP BODY TEMPERATURE DIFFERENCE DURING OPEN HEART SURGERY

The correlation between the deep body temperature difference (DBT•Diff) immediately after the end of cardiopulmonary bypass (CPB) and the carbohydrate and tissue metabolism early after open heart surgery was studied in 22 cases consisted of 10 cases operated upon under nonpulsatile CPB cases consisted of 10 cases operated upon under nonpulsatile CPB and 12 cases under pulsatile CPB. In the cases that DBT•Diff immediately after the end of CPB represented more than 4°C, arterial blood lactate level was higher, insulin-glucagon ratio and c-peptide were significantly lower than the cases with DBT•Diff less than 4°C. These facts strongly suggested that the cases with DBT•Diff more than 4°C might possibly fall into the deterioration of tissue metabolism, the suppression of insulin secretion and then catabolic response early after surgery. Therefore, these cases were thought to be require the proper correction of tissue underperfusion as soon as possible. Continuous infusion of hydralazine at a rate of 1.0-1.5γ/kg/min effectively resulted in the reduction of DBT•Diff, lactate level and the increase in cardiac index. It is concluded that the monitoring of DBT•Diff was very helpful for the early detection of metabolic disorder after open heart surgery.

Dichloroacetate--its in vivo effects on carbohydrate metabolism in the conscious dog.

The effects of sodium dichloroacetate (DCA) on carbohydrate metabolism in conscious, 48-h-fasted dogs were examined using the hepatic A-V difference technique and a double isotope infusion technique (3H-glucose to measure glucose production and 14C-alanine to assess gluconeogenesis). DCA infusion (0.4 mg/kg-min) resulted in an 82 +/- 1% fall in the arterial plasma alanine level and a 53 +/- 8% fall in the arterial whole blood lactate level. Hepatic uptake of alanine and lactate fell 67 +/- 5% and 59 +/- 15%, respectively, although the fractional extraction of these intermediates was not altered. DCA decreased the conversion of circulating alanine and lactate to glucose but by only 41 +/- 7%, suggesting that a slight increase in the efficiency of the intrahepatic gluconeogenic process took place. This may be explained by the decrease in the plasma insulin level (39 +/- 9%) that occurred in the presence of an unchanged plasma glucagon concentration. Despite the substantial fall in the levels of gluconeogenic precursors in blood and the considerable decrease in their rate of conversion to glucose, the overall rates of glucose production and the blood glucose concentration were not altered by DCA. These data indicate that the alanine and lactate supplied by the periphery after a 48 h fast in the dog are not essential for the acute maintenance of glucose production or euglycemia. They suggest, further, that a compensatory increase in glucose production can occur by drawing on an alternate intrahepatic carbon source, the nature of which and signal for which remain unclear.

Arterial blood levels of energy substrates and evidence for renal glucose production in the baboon infant.

The age-related changes in fasting arterial levels of energy substrates and insulin were studied at birth and/or 6 wk in eleven baboon infants. In addition, the renal contribution to glucose release in the primate infant was estimated. Arterial blood glucose levels were similar in six fasted newborns and in nine fasted 6-wk-old infants. Arterial blood lactate, alanine, pyruvate, glutamate, and glutamine levels were significantly higher (P < 0.01) in the new born animals, and beta-hydroxybutyrate was significantly higher in the older animals (P < 0.001). Arterial plasma insulin levels were low in both groups. Levels of blood glucose in the inferior vena cava below the renal vein were significantly lower than levels in the aorta (P < 0.01). In contrast, levels of blood glucose in the inferior vena cava above the renal vein were significantly higher than in the aorta (P < 0.05). Computed renal vein glucose levels were higher than those in the aorta (P < 0.01). In the newborn infants, there was significant renal uptake of lactate, pyruvate, glycerol, and glutamine (P < 0.01), and release of beta-hydroxybutyrate (P < 0.05). In the older animals, there was renal uptake of alanine, lactate, pyruvate, and glycerol (P 0.01). Mean cardiac output per kg body weight did not differ significantly in the newborn and 6-wk-old infants. Lactate uptake was potentially responsible for 59% of mean renal glucose output in the newborn and 76% of mean renal glucose output in the older infant. Net renal glucose release in eight 6-wk-old infants was estimated to be 3.5 +/- 1.1 microM/min . kg (95% confidence limits, 0.7 < 3.5 < 6.2). Net renal glucose release in three newborn infants was 4.7, 5.4, and 19.8 microM/min . kg. There was a significant linear relationship between arterial lactate levels and renal glucose production in the older infants (P < 0.05). Extremely low arterial pH was associated with increased renal glucose release in the newborn, and high arterial pH with decreased or absent glucose release in the 6-wk-old animals.

Acute cold exposure and the metabolism of blood glucose, lactate and pyruvate, and plasma amino acids in the hind leg of the fed and fasted young ox.

1. Young steers were fed either 3-4 or 20 h before exposure to a thermoneutral or a moderately cold environment. Measurements were made of total oxygen consumption (total V 0-2), respiratory quotient (rq), blood packed cell volume (PCV), and hind-leg blood flow (leg Q) and oxygen uptake (leg VO-2). The arteriovenous differences in whole blood glucose, lactate and pyruvate, and individual amino acid and urea concentrations across the leg were also measured. Net exchange and fractional uptake of these metabolites by the leg were calculated from these results. 2. Cold exposure doubled total VO-2, significantly decreased RQ and significantly increased PCV. Leg Q and leg VO-2 increased 3- to 5-fold and 4- to 13-fold respectively in both feeding groups. Arterial blood glucose increased slightly but significantly in both 20 h- and 3 h-fed steers. There was a substantial increase in mean net leg uptake of glucose in both feeding groups. This was much greater in the 20 h-fed group because of the significant increase in fractional uptake occurring only in this group. Cold did not significantly affect arterial blood lactate or pyruvate levels, but the net leg output of lactate found in both feeding groups in thermoneutrality was increased in the 20 h-fed steers, and reversed to a net uptake in the 3 h-fed animals. Cold caused a small but significant decrease in the total plasma amino acid level in the 20 h-fed but not in the 3 h-fed group; individual amino acid levels or leg uptakes were not affected. 3. Feeding before the experiment caused a significant increase in RQ. Leg Q, leg uptake of glucose and leg output of lactate increased after feeding in the thermoneutral environment only. Arterial pyruvate increased significantly, but net leg output was not significantly affected by feeding. Arterial plasma concentration of several individual, but not of total amino acids, increased significantly in both environments, and the net output of many individual amino acids in the 20 h-fed steers was decreased or reversed to a net uptake in the 3 h-fed group in thermoneutrality only. 4. The results suggest that blood glucose could be a significant fuel for oxidation in shivering skeletal muscle in young steers, and that output of amino acids from skeletal muscle could not contribute significantly to this increased glucose supply by hepatic gluconeogenesis.

Influence of phenformin on fat and lactate metabolism and insulin production in starved normal subjects

In starved but not in fed, normal subjects, phenformin increases the level of plasma FFA and β-hydroxybutyrate and augments the plasma triglyceride increase that occurs during starvation. These findings suggest that phenformin increases the release and degradation of fatty acids in starved subjects. Arterial blood lactate levels were increased by phenformin in fed subjects. In starved persons phenformin inhibited the fall in blood lactate values induced by i.v. glucose administration. Neither in fed nor in starved, normal subjects, did phenformin decrease the insulin response to i.v. glucose administration. A higher insulin response was found in the phenformintreated, starved subjects than in the controls.

Serum enzymes in combat casualties.

Lactic dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT), and glutamic pyruvic transaminase (GPT) are intracellular enzymes which do not normally appear in appreciable concentrations in the serum. Serum levels are elevated in a variety of conditions in which cellular necrosis or changes of cellular permeability have occurred. 1-4 The elevation of serum enzymes is proportional to the extent and duration of cellular damage. The present study was undertaken to evaluate serum enzyme levels in combat casualties: specifically, the effects of (1) wound type, (2) shock, and (3) transfusion therapy. Materials and Methods All patients were American or South Vietnamese soldiers wounded less than two hours prior to admission to a front line hospital. No therapy had been given before the first sampling of serum. At admission, blood was drawn for arterial blood lactate, arterial pH, pO 2 , pCO 2 , and serum enzyme levels. 5 Thereafter, blood was drawn at least once

Circulatory and metabolic effects of oxygen in myocardial infarction.

The circulatory and metabolic effects of inhalation of oxygen in high concentration were investigated in 50 patients with acute myocardial infarction. The heart rate, arterial blood pressure, cardiac out-put, blood gas tensions, pH, and lactate and pyruvate levels were measured. In general, oxygen inhalation produced a fall in cardiac output and stroke volume and a rise in blood pressure and systemic vascular resistance. In a small number of patients with very low cardiac out-puts there was a rise in output. A substantial rise in arterial oxygen tension was obtained even in patients with low initial values. The raised arterial blood lactate levels which were frequently present were reduced after oxygen. The therapeutic implications of these effects are discussed.