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Acute haemodynamic effects of sodium bicarbonate administration in respiratory and metabolic acidosis in anaesthetized dogs.

Twenty-seven halothane-anaesthetized, mechanically ventilated adult mongrel dogs were randomly assigned to either respiratory acidosis group [pHa 7.22 (0.03, SD), PaCO2 9.6 (1.1) kPa, base excess -0.5 (1.4) mmol.l-1, n = 9], metabolic acidosis group [pHa 7.20 (0.05), PaCO2 5.5 (0.4) kPa, base excess -11.1 (2.1) mmol.l-1, n = 9], or nonacidosis group [pHa 7.37 (0.07), PaCO2 5.2 (0.4) kPa, base excess -1.1 (1.5) mmol.l-1, n = 9]. Respiratory acidosis and metabolic acidosis were induced by decreasing respiratory rate and continuous infusion of 2 mmol.l-1 hydrochloric acid, respectively. Sodium bicarbonate solution 1 mmol.kg-1 was injected into the right atrium over five seconds when haemodynamic stability was obtained. In all three groups, acute administration of sodium bicarbonate produced transient decreases in mean arterial pressure and RV dP/dtmax, and transient increase in right atrial pressure 30 seconds after injections, but these variables returned to the pre-injection values by the end of the three minutes observation period. Although no significant differences were seen in haemodynamic variables among the three groups at 30 seconds, one and three minutes, maximum reductions in both RV dP/dtmax and PBF in the metabolic acidosis group (260 (143) mmHg.s-1 and 0.38 (0.26) l.min-1) were significantly greater than those in the non-acidosis group (127 (34) mmHg.s-1 and 0.08 (0.09) l.min-1; P < 0.05).

Acidosis↗

Role of acidosis in early contractile dysfunction during ischemia: evidence from pHo measurements.

To investigate the contribution of acidosis to contractile dysfunction during early myocardial ischemia, miniature intramyocardial pH electrodes (0.2 mm tip diam) were used to correlate changes in extracellular pH (pHo) with tension in the isolated arterially perfused rabbit interventricular septum. A number of findings argue against acidosis as the major cause of contractile failure during early ischemia. During hypoxia without glucose present, the rate and pattern of tension decline was very similar to total ischemia, suggesting that a common mechanism is involved. Throughout the initial period in which tension declined by 50%, however, pHo increased in the six of eight preparations during hypoxia without glucose. During hypoxia with glucose present, tension fell less rapidly than during hypoxia without glucose despite a significantly greater fall in pHo in the former case. The maximal rate of relaxation (-dT/dt) was markedly more sensitive to ischemia, hypoxia, or exposure to inhibitors of aerobic metabolism (2,4-dinitrophenol and Na azide) than the maximal rate of force development (+dT/dt). In contrast, +dT/dt and -dT/dt decreased almost symmetrically during exposure to respiratory acidosis. During ischemia, the change in pHo associated with 50% reduction in tension was 0.11 +/- 0.04 units. During respiratory acidosis, this value was 0.45 +/- 0.02 units. From these observations we concluded that acidosis is unlikely to be a major factor in the early decline of tension during ischemia.

Acidosis↗

Assessing redox status in human plasma: experience in critically ill patients.

Clinical evaluation of metabolic acidosis has involved measurement of lactate (L), pyruvate (P), beta-hydroxybutyrate (BOHB), and acetoacetate (AcAc). We previously demonstrated that these metabolites are not at equilibrium in plasma. Their degree of disequilibrium is reflected in the ratio of apparent equilibrium constants (KLP/KBA) for the two redox couplets, L-P and BOHB-AcAc. The purpose of the study was to examine how well this ratio reflects disequilibrium in patients with metabolic acidosis. Measurements of the four metabolites were obtained in 23 critically ill patients. Disequilibrium was again observed, as manifested in an inconstant ratio (p less than .01). The ratio increased with clinical improvement. Patients were more likely to die during their ICU stay if the estimated ratio was low, particularly if metabolic acidosis was present. Patients with respiratory acidosis had both intermediate probabilities of death and intermediate ratios when compared to inpatient controls (ICU patients without acidosis). Our data indicate that changes in the L-P-BOHB-AcAc cycle reflect the degree of metabolic derangement in critically ill patients.

3-Hydroxybutyric Acid↗

Respiratory and acid-base physiology of the purple sea urchin, Strongylocentrotus purpuratus, during air exposure: presence and function of a facultative lung.

Upon exposure to air (emersion), the purple sea urchin Strongylocentrotus purpuratus releases an "emersion fluid" from its esophagus. Release of this fluid causes air to appear within the test (or calcareous theca), most likely inside the intestine. The air space is large, occupying 33.5% of the volume of the intrathecal space. The intestine containing air forms a facultative lung and contributes to the oxygenation of the perivisceral coelomic fluid (PCF) during emersion. During emersion, the mean partial pressure of oxygen (PO(2)) of the PCF declined from 56 to 24 torr (1 torr = 0.1333 kPa) after 2 h, remained relatively unchanged after 4 h, and rose to 39 torr after 8 h. The partial pressure of carbon dioxide (PCO(2)) rose from 2.6 to 3.8 torr after 2 h, remained unchanged after 4 h, and declined to 2.7 after 8 h. Due to the elevation of PCO(2) PCF pH declined from 7.41 to 7.17. PCF osmotic concentration, calcium ion concentration, chloride ion concentration, ammonium ion concentration, and protein concentration were unchanged by air exposure. Lactate levels in the PCF were undetectable. S. purpuratus was an osmoconformer and a chloride ion conformer at salinities down to 20.9 ppt. Below this salinity, the sea urchins died. The respiratory acidosis resulting from air exposure was uncompensated, supporting the hypothesis that compensation for a respiratory acidosis induced by air exposure does not occur in organisms that are unable to regulate ions in a dilute environment. We suggest that the facultative lung ensures a minimal PO(2) in the PCF, which may be especially important when the intrathecal space is full of ripe gonads, allowing the gonads to be more reliant on aerobic metabolism.

Acid-Base Equilibrium↗

Temporary acidosis during reperfusion limits myocardial infarct size in dogs.

We tested the hypothesis that myocardial extracellular acidosis during early reperfusion limits infarct size. The left anterior descending coronary artery was perfused with blood through a bypass tube in dogs. We occluded the bypass tube for 40 (protocol I; n = 24 hearts) and 90 min (protocol II; n = 36 hearts). In protocols I and II, we infused one group of hearts with HCl (60 micrograms.kg-1.min-1) for 60 min after the onset of reperfusion (the metabolic acidosis group), and another group of hearts were ventilated with 3 liters of 70% O2-30% CO2 mixed with room air 10 min before the onset of reperfusion for 70 min (the respiratory acidosis group). pH in the coronary venous blood and myocardial pH during reperfusion in the metabolic and respiratory acidosis groups were lower than those in the control groups. Infarct sizes in the metabolic (16.4 +/- 2.5 and 22.3 +/- 2.5%) and respiratory (16.7 +/- 2.6 and 22.3 +/- 2.5%) acidosis groups in protocols I and II, respectively, were smaller than those in the control groups (33.1 +/- 3.0 and 40.6 +/- 4.1%, respectively). Thus we conclude that temporary acidosis during reperfusion limits infarct size.

Acidosis↗

Carbon dioxide pneumoperitoneum induces fetal acidosis in a pregnant ewe model.

The objective of this study was to evaluate the physiologic consequences of a pneumoperitoneum (pneumo) to the midterm fetus in a pregnant sheep model. The performance of laparoscopic cholecystectomy (LC) during pregnancy is controversial. The primary concern regarding the safety of LC during pregnancy is the physiologic consequences of the CO2 pneumo to the fetus. Eight ewes with singlet pregnancies between 100 and 120 days of gestation were anesthetized and intubated. Carotid artery and internal jugular catheters were placed in the ewe and in the fetus. Two trocars were placed through the abdominal wall of the ewe and the abdomen was inflated with CO2 or N2O at 15 mmHg pressure for 90-120 min. Hemodynamic and blood gas data were obtained every 15 min before, during, and after the pneumo. In two ewes attempts were made to keep maternal Pco2 constant with hyperventilation. In two other animals the pneumo was increased stepwise in five mmHg increments to 25 mmHg. One fetus succumbed during the CO2 pneumo, but this animal appeared to be ill during the establishment of invasive monitoring. Fetal respiratory acidosis occurred, reproducibly, after establishment of CO2 pneumo but did not occur before insufflation or under N2O pneumo (P < 0.0001). Hemodynamic changes were minimal with all agents but it appeared that there a was greater prevalence of fetal tachycardia and hypertension during CO2 pneumo than during N2O pneumo. Alterations in ventilator settings based on maternal capnography resulted in late and incomplete correction of respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗

Effect of acidosis on intracellular pH and calcium concentration in the newborn and adult rabbit myocardium.

This study investigated developmental changes in the effect of acidosis on intracellular pH (pHi) and [Ca]i in the isolated heart and isolated myocyte preparations. The whole heart or myocytes of newborn (5-7 days old) and adult rabbits were loaded with the fluorescent pH indicator 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein (BCECF) or calcium indicator fura-2. Left ventricular pressure in the isolated heart preparation and the magnitude of cell contraction in the single-cell preparation were monitored. The heart and single cell were illuminated with excitation lights (340 and 380 nm, respectively, for fura-2 and 438 and 490 nm for BCECF). The intensity of fluorescence from the ventricular surface or from the cell was detected. [Ca]i was estimated from the following ratio: fluorescence at 505 nm during excitation at 340 nm/fluorescence at 505 nm during excitation at 380 nm. pHi was estimated from the following ratio: fluorescence at 530 nm during excitation at 490 nm/fluorescence at 530 nm during excitation at 438 nm. In the newborn, depression of contractile function during respiratory acidosis or metabolic acidosis was less than in the adult. Diastolic and systolic [Ca]i increased during respiratory acidosis in both the newborn and adult, and the net changes in [Ca]i were similar in the two age groups. During respiratory or metabolic acidosis, pHi decreased, but the decrease in the newborn was significantly less than in the adult. These data suggest that the greater resistance of the newborn myocardium to acidosis is due to the smaller change of pHi in this age group and not due to the difference in [Ca]i alteration.

Acidosis↗

The effect of respiratory and lactic acidosis on diaphragm function.

The relative effects of respiratory and metabolic acidosis on diaphragm function are not known. To determine these effects, we compared the effects of respiratory and lactic acidosis on the contractile properties of the diaphragm. We estimated diaphragmatic performance from the change in transdiaphragmatic pressure after supramaximal stimulation of the phrenic nerves in an open-chested, casted-abdomen dog. Similarly, we stimulated the gastrocnemius motor nerve and examined force production and relaxation rate to determine if there was a difference in the response of this skeletal muscle. There was a fall in diaphragm performance with respiratory acidosis (77.1 +/- 16.9 cm H2O versus 93.8 +/- 15.0 cm H2O baseline), but not with lactic acidosis (96.7 +/- 15.7 cm H2O versus 93.8 +/- 15.0 cm H2O baseline); and the gastrocnemius was unaffected by either acidosis. The changes with respiratory acidosis were similar to those seen with diaphragmatic fatigue and had similar relaxation rate changes, suggesting that intracellular pH may play a mechanistic role in respiratory muscle fatigue. In addition, the absence of a respiratory acidosis effect on a non-diaphragmatic skeletal muscle's function represents another physiologic difference between the diaphragm and other skeletal muscles.

Acidosis, Lactic↗

Pulmonary function in dogs after intercostal thoracotomy: comparison of morphine, oxymorphone, and selective intercostal nerve block.

A thoracotomy was performed at the left 5th intercostal space in 24 dogs. Dogs were assigned to 4 groups of 6 dogs each. Postoperative analgesia was administered as follows: group 1--control, no analgesia; group II--morphine (0.5 mg/kg of body weight); group III--oxymorphone (0.1 mg/kg); group IV--selective intercostal nerve block with bupivacaine HC1. Respiratory rate, minute volume (VE), and arterial blood gases were measured during the recovery period. Ventilation-perfusion mismatch was estimated by calculation of the alveolar-arterial oxygen tension difference. Arterial carbon dioxide tension (Paco2) in the control and selective intercostal nerve block groups remained within the normal range and did not differ significantly (P less than 0.05) between groups. During the first 60 to 90 minutes after surgery, Paco2 tension was increased significantly (P less than 0.05) in the groups given morphine and oxymorphone. Hypoventilation in the groups given narcotics resulted from significant reductions (P less than 0.05) in the respiratory rate and VE and produced significant (P less than 0.05) respiratory acidosis and hypoxemia. Three dogs in the groups given narcotics had a panting response that resulted in increased respiratory rates and VE. This response did not improve alveolar ventilation in these dogs, which was evidenced by increased Paco2 values. Hypoventilation, respiratory acidosis, and hypoxemia in the groups given narcotics improved significantly with time, presumably because of drug clearance. Values for alveolar-arterial oxygen tension difference indicated moderate ventilation-perfusion mismatch secondary to anesthesia in all groups; however, significant differences (P less than 0.05) between the groups were not observed.

Animals↗

Breathing pattern and arterial blood gases during Nd-YAG laser photoresection of endobronchial lesions under general anesthesia: use of negative pressure ventilation: a preliminary study.

STUDY OBJECTIVE: To evaluate the efficacy of negative pressure ventilation (NPV) in avoiding or reducing apneas and related hypoxemia and respiratory acidosis during laser therapy (LT) of endobronchial lesions. DESIGN: A prospective, controlled, randomized study. SETTING: An operating theater of a respiratory endoscopy and laser therapy unit. POPULATION AND INTERVENTION: Twenty-seven consecutive patients referred to LT were entered into the study. Fourteen patients were randomly assigned to LT under general anesthesia and spontaneous assisted ventilation (control group) whereas in 13 cases, NPV by a poncho-wrap ventilator (NPV group) was added to the procedure. MEASUREMENTS AND RESULTS: The prevalence and the duration of apnea/hypopnea periods assessed by respiratory inductive plethysmography during LT were significantly reduced under NPV, compared to the control group. As compared to baseline, during LT, all control patients developed mild to severe hypercapnia (PaCO2 ranging from 55 to 76 mm Hg) and respiratory acidosis (pH from 7.33 to 7.19), whereas only three patients undergoing NPV (23%) developed hypercapnia (PaCO2 from 52 to 68 mm Hg) and related acidosis (pH from 7.29 to 7.21). Optimal oxygenation was achieved in all of the patients; nevertheless, patients under NPV needed a lower mean oxygen supply; five of them (38%) could be treated at a fraction of inspired oxygen of 0.21 for the whole procedure. CONCLUSION: NPV may be useful in reducing apneas during laser therapy under general anesthesia, thus reducing hypercapnia, related acidosis, and need of oxygen supplementation.

Adult↗

Postasphyxial lung disease in newborn infants with severe perinatal acidosis.

The pulmonary course and respiratory management of 65 asphyxiated infants with at least one arterial pH less than or equal to 7.00 within the first 2 hours of life was determined. Asphyxia in the preterm and term infants in the absence of respiratory distress syndrome or meconium aspiration syndrome was associated with a transient respiratory insufficiency requiring assisted ventilation which markedly improved in the first 24 hours of life. In contrast, infants with asphyxia complicated by respiratory distress syndrome or meconium aspiration syndrome developed profound lung disease including pulmonary hemorrhage and persistence of the fetal circulation. The course of their illness was significantly worse than control infants without asphyxia. Ineffective neonatal resuscitation allowing for the development of meconium aspiration syndrome and persistent respiratory acidosis contributed to the severity of illness in more than 50% of the infants. Central nervous system pathologic conditions were present in asphyxiated infants with and without severe pulmonary disease. We conclude that severe asphyxia in the absence of underlying lung disease results in a predictable postasphyxial transient respiratory insufficiency, with marked improvement in the first 24 hours of life.

Acidosis↗

Miconazole therapy for systemic candidiasis in a conjoined (Siamese) twin and a premature newborn.

A 2.5 kg thoracopagus (Siamese) twin and a 0.73 kg premature newborn developed systemic candidiasis and were treated with intravenous miconazole. The conjoined twin was in a state of severe metabolic acidosis, respiratory distress, jaundice, anuria, abdominal distension, and shock. The 0.73 kg premature infant was also in a state of severe metabolic acidosis, respiratory distress, and oliguria. Miconazole was used in this desperate situation for the treatment of life-threatening candidiasis. Both infants responded well to treatment and recovered. All parameters of their diseases improved during therapy despite pre-existing multiple organ dysfunction. Miconazole can be a safe alternative to amphotericin B for the treatment of systemic candidiasis in neonatal infants, including those with impaired renal function.

Candida albicans↗

A comparison of four different blood gas analysers.

Four automatic blood gas analysers from four different manufactures were evaluated and compared. The measurements were performed on blood representing respiratory acidosis and hypoxemia, normal conditions, and respiratory alkalosis and hyperoxemia. On each level nine complete runs were carried out, each run consisting of six replicates of each parameter (pH, Pco2 and Po2) on each instrument (six rounds). Only the directly measured parameters (pH, Pco2, Po2) were compared. The main conclusion is that the four instruments can be used alternatively, and that the differences between the values measured by the four instruments are of little clinical significance.

Acidosis, Respiratory↗

Effects of acidosis on rat muscle metabolism and performance during heavy exercise.

The metabolism and performance of a perfused rat hindquarter preparation was examined during heavy exercise in three conditions: control (C), metabolic acidosis (MA, decreased bicarbonate concentration), and respiratory acidosis (RA, increased CO2 tension). A one-pass system was used to perfuse the hindquarters for 30 min at rest and 20 min during tetanic stimulation via the sciatic nerve. The isometric tension generated by the gastrocnemius-plantaris-soleus muscle group was recorded, and biopsies were taken pre- and postperfusion. Initial isometric tensions were similar in all conditions, but the rate of tension decay was largest in acidosis; the 5-min tensions for C, MA, and RA were 1,835 +/- 63, 1,534 +/- 63, and 1,434 +/- 73 g, respectively. O2 uptake in C was greater than in MA and RA (23.4 +/- 1.3 vs. 17.0 +/- 1.4 and 16.5 +/- 2.3 mumol X min-1), paralleling the tension findings. Hindquarter lactate release was greatest in C, least in MA, and intermediate in RA. Acidosis resulted in less muscle glycogen utilization and lactate accumulation than during control. Muscle creatine phosphate utilization and ATP levels were unaffected by acidosis. Acidosis decreased the muscle's ability to generate isometric tension and depressed both aerobic and anaerobic metabolism. During stimulation in this model lactate left the muscle mainly as a function of the production rate, although a low plasma bicarbonate concentration at pH 7.15 depressed muscle lactate release.

Acidosis↗

Clinical, laboratory and X-ray findings of drowning and near-drowning in the Gulf of Aqaba.

Clinical, laboratory and X-ray findings in 34 victims of submersion are presented. Five people died and 29 survived (age range 12-60 years). Severe hypoxia was found in all patients (mean PO2 of 58 mmHg with some oxygen support). Arterial blood gas analysis showed significant metabolic acidosis in 19 patients and significant respiratory acidosis in 15 patients. Pulmonary oedema was the most common X-ray finding. Fourteen patients were put on mechanical ventilation on the basis of their clinical picture and blood gases analysis. Clinical and laboratory data are very similar to those reported in international studies.

Acidosis, Respiratory↗

Is ischemia-induced pH decrease of dog myocardium respiratory or metabolic acidosis?

Ischemia causes myocardial acidosis and elevation of myocardial CO2 tension (PCO2). We performed the present study to examine whether accumulation of hydrogen ion is a cause or result of accumulation of CO2. The myocardial pH and PCO2 were measured simultaneously in the dog heart, and the concentration of HCO-3 [( HCO-3]) was calculated according to the Henderson-Hasselbalch equation. Ischemia was induced by either partial or complete occlusion of the left anterior descending coronary artery (LAD). After LAD occlusion, the myocardial pH decreased with a marked decrease in [HCO-3], indicating that metabolic acidosis occurred. We ascertained in experiments with blood sample in vitro that an addition of lactic acid into blood decreased both [HCO-3] and pH (metabolic acidosis), whereas an addition of CO2 gas into blood increased [HCO-3] and decreased pH (respiratory acidosis). These findings suggest that ischemic acidosis is not respiratory in nature, but metabolic. The myocardial pH decrease due to ischemia, however, cannot be explained by the tissue lactate accumulation alone, because the decrease of [HCO-3] is far greater than the increase of lactic acid during ischemia.

Acidosis↗

Intracellular potential and K+ activity in rat kidney proximal tubular cells in acidosis and K+ depletion.

Techniques were developed for the measurement of intracellular potentials and potassium activities in rat proximal tubule cells using double barreled K+ liquid-ion-exchanger microelectrodes. After obtaining measurements of stable and reliable control values, the effects of K+ depletion and metabolic and respiratory acidosis on the intracellular potential and K+ activity in rat kidney proximal tubular cells were determined. At a peritubular membrane potential of -66.3 +/- 1.3 mV (mean +/- SE), intracellular K+ activity was 65.9 +/- 2.0 mEq/liter in the control rats. In metabolic acidosis [70 mg NH4Cl/100 g body wt) the peritubular membrane potential was significantly reduced to -47.5 +/- 1.9 mV, and cellular K+ activity to 53.5 +/- 2.0 mEq/liter. In contrast, in respiratory acidosis (15% CO2) the peritubular membrane potential was significantly lowered to -46.1 +/- 1.39 mV, but the cellular K+ activity was maintained at an almost unchanged level of 63.7 +/- 1.9 mEq/liter. In K+ depleted animals (6 weeks on low K+ diet), the peritubular membrane potential was significantly higher than in control animals, -74.8 +/- 2.1 mV, and cellular K+ activity was moderately but significantly reduced to 58.1 +/- 2.7 mEq/liter, Under all conditions studied, cellular K+ was above electrochemical equilibrium. Consequently, an active mechanism for cellular K+ accumulation must exist at one or both cell membranes. Furthermore, peritubular HCO3- appears to be an important factor in maintaining normal K+ distribution across the basolateral cell membrane.

Acidosis↗

Monitoring of acid-base status of workers at a methyl methacrylate and polymethyl methacrylate production plant in Bulgaria.

This study was carried out on 104 workers at three work operations and a control (nonproduction) area, within a methyl methacrylate (MMA)/polymethyl methacrylate (PMMA) production facility in Bulgaria. Airborne monitoring was conducted over a 10-year period for MMA and the reactant chemicals methanol and acetone cyanhydrine at the MMA operation, and MMA was monitored at the PMMA operation. Acid-base status of the workers was evaluated using traditional criteria (pH, pCO(2), pO(2), and HCO(3) in plasma). Data from retrospective monitoring of air levels of the chemicals were compared with the acid-base status of workers at the plant. In some cases air concentrations exceeded the threshold limit value, with the highest percentage of overexposure occurring with airborne MMA in the PMMA production operation. Acid-base disruption indicated by reductions in plasma pH and HCO(3) was found for all groups except the control population. The highest percentage reduction was associated with PMMA production workers. Additionally, respiratory acidosis, indicated by increased pCO(2), was noted in the MMA production and maintenance groups, implying that the response to MMA exposure may involve both the metabolic and respiratory acidosis component. This study was unique in that the combined exposure to MMA and the precursor chemical (methanol) were shown to produce the same effects in workers. It is suggested that when combined exposure occurs, disruption of acid-base status may occur. Enforcement of PPM requirements for coveralls and gloves should prevent skin contamination. Additionally, improvement of equipment in MMA and PMMA production areas is recommended: (1) automation of some manual operations; (2) use of respiratory protection during equipment cleaning; and (3) installation of local ventilation when applicable.

Acid-Base Imbalance↗