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At least 631 records · Page 35Linked to original sources
PubMed1979

Determination of liver intracellular pH in vivo and its homeostasis in acute acidosis and alkalosis.

An in vivo method is presented for the determination of liver intracellular pH (pHi) using [14C]dimethadione (DMO) in dogs. This method differs from those previously published in that hepatic venous and portal venous blood pH were selected as the extracellular reference pH, and liver blood space corrections are applied to whole liver tissue [14C]DMO activity. Using these corrections, a normal liver pHi of 6.99 +/- 0.03 (SE) was obtained. During acute metabolic acidosis and alkalosis, as well as during acute respiratory acidosis and alkalosis, the liver pHi remained normal; metabolic acidosis was 7.04 +/- 0.04; metabolic alkalosis was 6.92 +/- 0.08; respiratory acidosis was 6.98 +/- 0.04; and respiratory alkalosis was 7.00 +/- 0.10. None of these values was significantly different from normal (P greater than 0.05). Changes in intracellular bicarbonate and lactate appeared to account in part for the observed stability of the liver pHi despite acute manipulations resulting in a range of pH values between 7.09 and 7.63 in arterial blood.

Acid-Base Imbalance↗
PubMed1993

[Effect of intravenous lidocaine infusion on arterial baroreflex].

The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.

Acidosis, Respiratory↗
PubMed1987

The use of ketamine for the emergency intubation of patients with status asthmaticus.

We describe five patients with status asthmaticus whose respiratory acidosis persisted despite conventional treatment. Four were intubated with ketamine and succinylcholine and mechanically ventilated with immediate improvement of respiratory acidosis. One patient had been intubated previously with diazepam and succinylocholine and had a rise in pCO2 to 97. Ketamine was given IV with a rapid fall in pCO2. This improvement immediately after intubation is in contrast to previous reports of asthmatics whose respiratory acidosis and bronchospasm worsened immediately after intubation.

Asthma↗
PubMed1975

Central nervous system effects of local anaesthetic agents.

A review is given of an experimental study on cats where the influence of acid-base changes on central nervous system toxicity of local anaesthetic agents was studied. The conclusion of this study was that a respiratory acidosis increased the central nervous system toxicity of local anaesthetics and that the underlying metabolic conditions modified this increase. Thus a respiratory acidosis increased this toxicity more if it was based on a metabolic acidosis than on a metabolic alkalosis (Englesson, 1974; Englesson and Grevsten, 1974). An extended analysis is presented where automatic frequency analysis was performed on the e.e.g. recordings performed during the i.v. infusion of lignocaine, bupivacaine, L 134, HS 37 and its optical isomers. The preliminary results show that the electrical changes appearing in the e.e.g. from the start of the i.v. infusion until seizure activity were the same if this time interval was as short as 1 min or as long as 8 min. It also revealed remarkable individual differences between agents, for instance lignocaine displaying marked electrical changes already in the first third of this time period where bupivacaine showed no changes until shortly before seizures.

Acid-Base Equilibrium↗
PubMed1981

Respiratory acidemia and theophylline pharmacokinetics in the awake dog.

Recently, respiratory acidemia has been shown to be associated with an altered volume of distribution (Vd) of theophylline in patients during an acute exacerbation of chronic obstructive pulmonary disease. However, many factors other than acidemia could have altered the pharmacokinetics. Our purpose was to study the effects of respiratory acidemia alone. Six awake dogs had normocapnia and hypercapnia induced in a conditioned chamber. After intravenous injection (8 mg/kg), plasma theophylline concentrations were measured for 8 hours by means of quantitative enzyme immunoassay technique. There were no statistically significant effects of respiratory acidosis on Vd and total theophylline clearance. There was no significant correlation between these variables and pH, PCO2, PO2. We conclude that respiratory acidosis, per se, does not effect theophylline pharmacokinetics in dogs.

Acidosis, Respiratory↗
PubMed2001

Ventilator-induced lung injury and the evolution of lung-protective strategies in acute respiratory distress syndrome.

Traditional ventilator management of acute respiratory distress syndrome (ARDS), emphasizing normalization of blood gases, promoted high rates of conventional barotrauma. Research revealed a broader range of ventilator-induced lung injury, physiologically and histopathologically indistinguishable from ARDS itself. It is now known that overdistention and cyclic inflation of injured lung can exacerbate lung injury and probably promote systemic inflammation, effects minimized by low tidal volumes/plateau pressures and by application of positive end-expiratory pressure. No compelling data suggest a safe interval for nonprotective ventilation in humans; historically defined "low" tidal volumes may remain excessive for certain patients. Protective ventilation, however, entails carbon dioxide accumulation ("permissive hypercapnia"). Despite extensive study, debate remains, even over whether consequent respiratory acidosis is harmful, tolerable with physiologic adaptation, or intrinsically adaptive. Its gross systemic effects seem generally tolerated by critically ill patients; however, subsets, including those with ischemic heart disease, left or right heart failure, pulmonary hypertension, or cranial injury, may be at higher risk. In controlled trials demonstrating mortality benefit from lung-protective ventilation, acidosis was more tightly controlled than in negative studies. Decreased acidosis-associated dyspnea probably explains reduced use of sedatives and paralytics noted in those trials. There may thus be disparate goals in ARDS management: rapid institution of a restrictive ventilatory strategy, and avoidance of significant acidosis. We review data pertaining to ARDS physiology, ventilator-induced lung injury, lung-protective ventilatory strategies, and the physiology of respiratory acidosis. Tracheal gas insufflation is considered as a means to reconcile the clinical goals of ventilatory reduction and control of acidosis.

Acidosis, Respiratory↗
PubMed1975

Continuous percutaneous monitoring of muscle pH and oxygen pressure. A new technique for in vivo use.

Newly developed all solid state catheter oxygen pressure (PO2) and pH electrodes were evaluated in dogs in respiratory acidosis and hemorrhagic shock. The electrodes were inserted into the blood vessels and thigh muscle by a percutaneous puncture technique. In animals with respiratory acidosis, arterial, venous, and intramuscular pH decreased in parallel as arterial carbon dioxide pressure (PCO2) increased. During severe acidosis, arterial and venous PO2 did not change appreciably, but intramuscular PO2 decreased moderately, indicating decreased tissue perfusion. In animals with hemorrhagic shock, intramuscular PO2 decreased in proportion to the blood loss, whereas the reduction in intramuscular pH and blood pressure lagged behind blood loss. A similar finding was observed during reinfusion of shed blood in surviving animals. In the animals that died, intramuscular PO2 AND PH remained low after the reinfusion of all shed blood, although arterial blood pressure did return to base line levels.

Acidosis, Respiratory↗
PubMed1995

Effects of carbonic anhydrase inhibition on the acid base status in lamprey and trout.

Inhibition of red cell carbonic anhydrase (CA) activity resulted in the rapid development of a respiratory acidosis (0.25 pH depression within 15 min post-injection) in the blood of trout. In the lamprey, however, the onset of the respiratory acidosis was delayed and its magnitude was less (0.18 pH depression at 6 h post-injection). Erythrocyte pH of both species decreased by about 0.12 units by 1 h after CA inhibition. These data, combined with the lack of rapid anion (Cl-/HCO3-) exchange in the red cells of agnathans but not in other lower vertebrates, support the hypotheses that (1) the majority of total CO2 in lamprey is transported within the erythrocyte, and (2) the limiting step in the evolution of a functioning Jacobs-Stewart cycle, and thus the evolution of the common mechanism of systemic CO2 transport in vertebrate blood, was the incorporation of the band-3 anion exchange protein into the membrane of the red cell.

Acetazolamide↗
PubMed1987

Successful direct extubation of very low birth weight infants from low intermittent mandatory ventilation rate.

It is common practice to use endotracheal continuous positive airway pressure for various time periods up to 24 hours before attempting extubation in infants who are mechanically ventilated. A few studies in newborns have indicated that airway resistance is increased through small endotracheal tubes. This increases the work of breathing and the likelihood of subsequent ventilatory failure. In this study, 27 very low birth weight infants who were 1/2 to 28 days old at the time of extubation were randomly divided into two groups. One group of 13 study infants were extubated directly from intermittent mandatory ventilation rates of six to ten per minute, and the other 14 control infants were placed on continuous positive airway pressure through endotracheal tubes for six hours prior to an attempt to extubate. There was no difference between the two groups in gestational age, postnatal age, weight, or severity of lung disease at the time of extubation. All 13 study infants were successfully extubated without significant apnea or respiratory acidosis. Of the 14 control infants, only seven were successfully extubated; six infants had significant apnea and in one infant respiratory acidosis with pH 7.13 and PCO2 65 developed while receiving continuous positive airway pressure (13/13 v 7/14, P less than .005). The seven infants who failed the preextubation trial of continuous positive airway pressure were later extubated from low intermittent mandatory ventilation rates without significant apnea or respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1994

Acidosis and bone.

Acidosis has important effects on the bone mineral which can be investigated utilizing neonatal mouse calvariae in organ culture. When calvariae are cultured for 3 h in physiologically acidic medium produced by a reduction of the bicarbonate concentration, a model of acute metabolic acidosis, there is net calcium efflux from bone in addition to net proton influx into bone which lessens the severity of the acidosis. Utilizing a high resolution scanning ion microprobe to study the bone during acidosis we have found that the protons exchange for sodium and potassium on the bone surface. In acute experiments the calcium efflux is the result of mobilization of carbonated apatite through an alteration in the physicochemical driving forces for bone mineral accretion and dissolution. In the more chronic cultures (greater than 48 h) metabolic acidosis induces calcium efflux by stimulating osteoclastic bone resorption and inhibiting osteoblastic bone formation. When calvariae are cultured for 3 h in acidic medium produced by an increase in the partial pressure of carbon dioxide, a model of respiratory acidosis, there is also calcium efflux; however, at the same decrement in pH the net flux is far less than that observed during metabolic acidosis. During acute respiratory acidosis there is no measurable influx of protons into bone and during chronic studies there is no measurable calcium efflux.

Acidosis↗
PubMed1991

Intracellular acid-base responses to environmental hyperoxia and normoxic recovery in rainbow trout.

Exposure of rainbow trout to environmental hyperoxia (PIO2 approximately 530 Torr) resulted in an extracellular respiratory acidosis which was fully compensated by 72 h; return to normoxia (PIO2 approximately 145 Torr) at this time induced a metabolic alkalosis which was corrected by 24 h. Intracellular pHi ([14C]DMO method), fluid volumes [3H]PEG-4000 method), and electrolytes were monitored. Environmental hypercapnia (PICO2 approximately 6.5 Torr) was employed to confirm that intracellular responses were specific to respiratory acidosis. Gill pHi did not change during respiratory acidosis despite a very low non-HCO3- buffer capacity, but gill ICFV decreased markedly. A large loss of gill intracellular [Cl-]i in excess of [Na+]i, combined with a substantial gain in [K+]i, contributed to gill pHi regulation by raising branchial [SID]i. In weakly buffered brain tissue, active adjustment of pHi started within 3 h, but two well buffered tissues, RBC and white muscle, exhibited compounding metabolic acidoses during the first 12-24 h. The muscle response was associated with small increases in ICFV and [Cl-]i, and a large decrease in [K+]i which reduced muscle [SID]i. We hypothesize that this initial export of K+ and basic equivalents served to regulate pH in more critical compartments (e.g. gills, brain) at the expense of muscle acidosis. By 48 h, pHi restoration in all tissues was complete, in advance of pHe regulation (72 h). Return to normoxia at 72 h elevated muscle, brain, and gill pHi, but there was no evidence of a comparable 'altruistic' role of muscle during this metabolic alkalosis. Regulation of pHi was complete by 24 h recovery, accompanied by partial or complete restoration of intracellular ions and fluid volumes.

Acid-Base Equilibrium↗
PubMed1997

[Efficacy of acetazolamide treatment of patients with hypercapnia and superimposed metabolic alkalosis].

BACKGROUND: Metabolic alkalosis usually complicates the evolution of patients with hypercapnia under diuretic or steroid therapy. The objective of this study was to analyze the efficiency of therapy with acetazolamide, a reversible carbonic anhydrase inhibitor, in this condition. PATIENTS AND METHODS: Prospective study conducted at our hospital from June 1994 to March 1996, with 45 patients who had chronic respiratory acidosis and metabolic alkalosis. After a previous stabilization of the patient and eventually the discontinuation of diuretic or corticosteroid drugs fro 24-48 hours, 500 or 750 mg of acetazolamide were administered daily for 48 hours. Later, variations both in arterial gasometry and venous electrolytes were analyzed by comparing two means of paired data. RESULTS: After therapy with acetazolamide a clinical improvement was observed in patients, a decrease in PaCO2, pH and CO3H (p < 0.001) and an increase in PaO2 (p < 0.001). Hypochloremia (82.2%) and hypopotassemia (33.3%) were the most common electrolytic abnormalities before therapy. Both abnormalities improved significantly after the administration of acetazolamide. In five patients (11.1%) acetazolamide was discontinued when metabolic acidosis appeared, which only in three cases was associated with acidemia. No secondary effects were observed. CONCLUSIONS: Acetazolamide is an efficient alternative for treatment of patients with respiratory acidosis and metabolic alkalosis, particularly when other more common measures in this condition (discontinuation of diuretics and/or volemic replacement) have failed or are contraindicated. On the other hand, the emergence of relevant secondary effects is unlikely.

Acetazolamide↗
PubMed1986

Persistent bronchopleural air leak during mechanical ventilation. A review of 39 cases.

Bronchopleural fistula (BPF), or bronchopleural air leak, is regarded as an ominous complication of ventilator management in acute respiratory failure, but data on its natural course and prognosis are lacking. We reviewed all instances of mechanical ventilation at a major trauma center during a four-year period, and found that 39 of the 1,700 mechanically-ventilated patients developed BPF lasting at least 24 hrs. Overall mortality in these 39 patients was 67 percent, and this was higher when BPF developed late in the illness (16 of 17, or 94 percent, when mean onset was hospital day 13), than when it occurred within 24 hours of admission (ten of 22, or 45 percent, p = 0.002). Survival in patients with chest trauma (12 of 27, 44 percent), most of whom had air leaks on or just after admission, was better than in those with other primary diagnoses (one of 12, 8 percent, p less than 0.005). All eight patients whose maximum air leak exceeded 500 ml per breath died, whereas 13 of 30 with smaller maximum leaks survived (p less than 0.05). Despite leaks as large as 900 ml per breath, however, conventional ventilator adjustments permitted avoidance of severe respiratory acidosis (pH less than 7.30) in all but two patients. We conclude that the occurrence of BPF during mechanical ventilation identifies patients with high mortality, but that unmanageable respiratory acidosis from this complication is rare.

Acidosis, Respiratory↗
PubMedDate not supplied

Nasal continuous positive airway pressure: an alternative method for respiratory assistance.

STUDY OBJECTIVE: To examine the efficacy of a nasal continuous positive airway pressure (CPAP) system for respiratory support in patients who have respiratory insufficiency but are able to maintain spontaneous breathing without hypercapnia, respiratory acidosis, or deteriorated mental status. DESIGN: Prospective study. SETTING: Medical and surgical patients admitted to the intensive care unit (ICU) at the Hillel Yaffe Medical Center. PATIENTS: Nineteen patients with acute respiratory insufficiency and intact mental status who were able to maintain spontaneous breathing without hypercapnia or respiratory acidosis. Additional entry criteria were as follows: arterial oxygen tension (PaO2) less than 65 mmHg on inspired oxygen tension (FIO2) greater than or equal to 0.45, PaO2/FIO2 less than 150, respiratory rate greater than 35 breaths/minute, and inability to tolerate mask CPAP. INTERVENTIONS: Nasal CPAP (10 cmH2O) was applied to patients through two nasopharyngeal airways with an internal diameter (ID) of 8 mm each, inserted in both nostrils. During CPAP application, the patients were requested to breathe through their nose with their mouth closed. Even if they breathed through their open mouth, however, CPAP was maintained despite an observed pressure decrease of 4 cmH2O. MEASUREMENTS AND MAIN RESULTS: All patients showed a constant improvement in arterial blood gases, PaO2/FIO2, and respiratory signs during nasal CPAP of 10 cmH2O. PaO2 increased from 52 +/- 5.3 mmHg to 131 +/- 20 mmHg with CPAP administration (p less than 0.05), while arterial carbon dioxide tension (PaCO2) increased from 32 +/- 2 mmHg to 36 +/- 2 mmHg (p less than 0.05) and respiratory rate decreased from 39 +/- 2.3 breaths/minute to 31 +/- 1.6 breaths/minute (p less than 0.05). CONCLUSIONS: Nasal CPAP (10 cmH2O) is a reliable alternative to support arterial oxygenation in patients with respiratory failure who are alert and vigorous enough to avoid hypercapnia and respiratory acidosis while breathing spontaneously. In addition, since the patients are able to speak and thus are capable of expressing their feelings, the anxiety observed during respiratory support can be reduced.

Acute Disease↗
PubMed1981

CSF acid-base regulation and ventilation during acute hypercapnia in the newborn dog.

We studied the response of blood, cerebrospinal fluid (CSF), and brain ionic composition and acid-base status as well as ventilation to acute respiratory acidosis (FICO2 0.08) in lightly anesthetized newborn puppies. Control puppy plasma ions and CSF-plasma ionic distribution ratios were essentially adultlike while in blood a mild, compensated respiratory acidosis was present, and in CSF, PCO2 and [HCO3-] were slightly higher than in adults. Brain tissue water content was higher in puppy vs. adult; the Cl- space was greater; the content of [Na+], [Cl-], and [HCO3-] were higher and [K+] lower. During respiratory acidosis, CSF [HCO3-] increased 2.0 mmol/l by 15 min and 6.2 mmol/l by 3 h, a response quantitatively like that observed in the adult. The quantity, CSF [Na+] -- [Cl-], increased stoichiometrically with CSF [HCO3-], indicating the mechanistic involvement of these ions in the CSF [HCO3-] response. In brain tissue, water content, [Cl-], and the [Cl-] space were unchanged, but by 3 h [Na+] and [HCO3-] were increased. Ventilation was stimulated but the response expressed as ml.min-1.Torr-1.body wt-1 was less in puppy than in adult.

Acid-Base Equilibrium↗
PubMed1977

Effect of metabolic alkalosis on respiratory function in patients with chronic obstructive lung disease.

Eleven instances of a mixed acid-base disorder consisting of chronic respiratory acidosis and metabolic alkalosis were recognized in eight patients with chronic obstructive lung disease and carbon dioxide retention. Correction of the metabolic alkalosis led to substantial improvement in blood gas values and clinical symptoms. Patients with mixed chronic respiratory acidosis and metabolic alkalosis constitute a common subgroup of patients with chronic obstructive lung disease and carbon dioxide retention; these patients benefit from correction of the metabolic alkalosis.

Acetazolamide↗
PubMed1998

Permeability of the developing and mature blood-brain barriers to theophylline in rats.

1. In the present study, the uptake of theophylline and L-glucose into the adult and neonatal rat brain has been investigated. Steady state cerebrospinal fluid (CSF) and brain concentrations of theophylline were reached within 1 h following a single intraperitoneal (i.p.) injection, whereas steady state CSF and brain concentrations of L-glucose were not approached until after 5 h. 2. Steady state brain:plasma and CSF:plasma concentration ratios for theophylline and L-glucose in neonatal rats were significantly higher than ratios in adult rats. Erythrocyte:plasma ratios for theophylline in neonatal rats were also significantly higher than ratios in adult rats. Steady state ratios for theophylline were significantly higher than those for L-glucose in both neonatal and adult rats. 3. Respiratory acidosis (pH 6.9-7.0) did not affect steady state CSF:plasma or brain:plasma ratios for theophylline in neonatal or adult rats. In contrast, steady state CSF:plasma and brain:plasma ratios for L-glucose were increased by respiratory acidosis. 4. The lower steady state CSF:plasma, brain:plasma and erythrocyte:plasma ratios for theophylline in adult rats are likely to be due to a higher concentration of plasma proteins in adult blood compared with neonates, with a greater retention of protein-bound (non-exchangeable) theophylline in adult blood, and are unlikely to be due to p-glycoprotein-mediated efflux of theophylline at the adult blood-brain barrier.

Acidosis, Respiratory↗