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PubMed1981

Influence on cerebral blood flow of infusion of sodium bicarbonate during respiratory acidosis and alkalosis in the dog.

In anaesthetized dogs, a mixed acid-base disturbance was induced by adding a pronounced metabolic alkaline to an established respiratory acidosis or alkalosis. Cerebral blood flow (CBF) was measured by the radioisotope washout method. In the hypocapnic dogs, the addition of metabolic alkalosis did not significantly change cerebral blood flow. In the hypercapnic dogs, the intravenous infusion of alkali led to a substantial reduction of cerebral blood flow, parallelled by a reduction of cerebrovenous oxygen tension. Acid-base analysis of cerebrospinal fluid (CSF) indicated an increased bicarbonate concentration. Hypercapnia is suggested to facilitate the passage of bicarbonate over the blood-brain barrier, leading to cerebral vasoconstriction by means of increased extravascular pH.

Acidosis, Respiratory↗

PubMed2003

Integrated responses of Na+/HCO3- cotransporters and V-type H+-ATPases in the fish gill and kidney during respiratory acidosis.

Using degenerate primers, followed by 3' and 5' RACE and "long" PCR, a continuous 4050-bp cDNA was obtained and sequenced from rainbow trout (Oncorhynchus mykiss) gill. The cDNA included an open reading frame encoding a deduced protein of 1088 amino acids. A BLAST search of the GenBank protein database demonstrated that the trout gene shared high sequence similarity with several vertebrate Na(+)/HCO(3)(-) cotransporters (NBCs) and in particular, NBC1. Protein alignment revealed that the trout NBC is >80% identical to vertebrate NBC1s and phylogenetic analysis provided additional evidence that the trout NBC is indeed a homolog of NBC1. Using the same degenerate primers, a partial cDNA (404 bp) for NBC was obtained from eel (Anguilla rostrata) kidney. Analysis of the tissue distribution of trout NBC, as determined by Northern blot analysis and real-time PCR, indicated high transcript levels in several absorptive/secretory epithelia including gill, kidney and intestine and significant levels in liver. NBC mRNA was undetectable in eel gill by real-time PCR. In trout, the levels of gill NBC1 mRNA were increased markedly during respiratory acidosis induced by exposure to hypercarbia; this response was accompanied by a transient increase in branchial V-type H(+)-ATPase mRNA levels. Assuming that the branchial NBC1 is localised to basolateral membranes of gill cells and operates in the influx mode (HCO(3)(-) and Na(+) entry into the cell), it would appear that in trout, the expression of branchial NBC1 is transcriptionally regulated to match the requirements of gill pHi regulation rather than to match trans-epithelial HCO(3)(-) efflux requirements for systemic acid-base balance. By analogy with mammalian systems, NBC1 in the kidney probably plays a role in the tubular reabsorption of both Na(+) and HCO(3)(-). During periods of respiratory acidosis, levels of renal NBC1 mRNA increased (after a transient reduction) in both trout and eel, presumably to increase HCO(3)(-) reabsorption. This strategy, when coupled with increased urinary acidification associated with increased vacuolar H(+)-ATPase activity, ensures that HCO(3)(-) levels accumulate in the body fluids to restore pH.

Acidosis, Respiratory↗

PubMed1996

Iatrogenic "respiratory acidosis" during laparoscopic preperitoneal hernia repair.

This is the first report, to our knowledge, of a case of massive subcutaneous emphysema during totally preperitoneal laparoscopic hernia repair causing a "respiratory acidosis" with a systemic pH 7.20 and a pCO2 of 64 and PO2 of 84. The acidosis was corrected by increased mechanical ventilation. It appears that because of its lack of defined borders, the preperitoneal space is particularly vulnerable to the formation of massive subcutaneous emphysema. Thus, there is a large potential surface area for CO2 absorption. The complication may be prevented by increased attention to the length of fascial incisions, inflation of balloon expanding devices, and securing gripping devices in the port sites.

Acidosis, Respiratory↗

PubMed1989

Furosemide and cerebrospinal fluid ions during acute respiratory acidosis.

The purpose of this study was to investigate the effects of furosemide, an inhibitor of NaCl cotransport, on cisternal cerebrospinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (n = 7 in each) of anesthetized, paralyzed, and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After base-line samples were obtained (-1 h), furosemide (50 mg/kg) was administered intravenously within 15 min (group II); group I received an equal volume of half-normal saline. ARA was induced 1 h later (0 h) and arterial CO2 tension was maintained between 55 and 60 Torr for 5 h. Mean cisternal CSF PCO2 was 42.8 +/- 2.6 and 39.5 +/- 1.7 Torr, respectively in groups I and II and rose approximately 20 Torr during ARA. In group I, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 meq/l, respectively at 0, 2.5, and 5 h. Respective values for group II were 22.2 +/- 1.3, 24.3 +/- 1.8, and 24.6 +/- 1.0 meq/l. These values were not significantly different from each other. In each group, CSF [Na+-Cl-] increased significantly during ARA, but the changes were not significantly different when the two groups were compared. We conclude that furosemide at the dose used in the present study does not change ionic composition and acid-base balance of cisternal CSF compared with control. Because changes in CSF [Na+-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by furosemide should have been proportional to that of Na+.

Acid-Base Equilibrium↗

PubMed1982

Effect of respiratory acidosis on metabolism in exercise.

Five healthy males took part in two separate studies. In one study subjects breathed air (control, C) and in the other 5% CO2 in 21% O2 (respiratory acidosis, RA). Measurements were made at rest, during exercise at 30 and 60% maximal O2 uptake (VO2 max), (20 min each) and in recovery. RA was associated with higher arterial CO2 partial pressure (PCO2) and bicarbonate and lower pH than C. The increase with exercise in plasma lactate (mmol . l-1) was less in RA than C from 1.0 +/- 0.15 (SE) (C = 1.1 +/- 0.17) at rest to 5.3 +/- 1.25 (C = 6.8 +/- 0.98) at 60% VO2 max (P less than 0.10). Plasma pyruvate, alanine, and glycerol concentrations increased with exercise; free fatty acids did not change. There were no significant differences between RA and C in any of these metabolites. Norepinephrine concentrations were similar at rest but increased to a greater extent during exercise in RA than C (P less than 0.02). Epinephrine levels were also higher in RA than C at 60% VO2 max (NS); the two subjects in whom lactate was not lower with RA showed the greatest increase in epinephrine. Exercise in RA was associated with higher heart rates (P less than 0.05), blood pressures (NS), and ventilation (P less than 0.01). In hypercapnia the metabolic effects of acidosis are modified by increased levels of circulating catecholamines.

Acidosis, Respiratory↗

PubMed2002

Clinical predictors of acute respiratory acidosis during exacerbation of asthma and chronic obstructive pulmonary disease.

Mechanical ventilation (MV) during exacerbation of asthma or chronic obstructive pulmonary disease (COPD) is unequivocally needed when apnoea, cardiorespiratory arrest, coma, hypoxia or treatment failure is present. The need is less clear when the patient can respond, has intact airway reflexes and spontaneous respiration. In this situation, acidosis is an important factor in the decision to institute MV. This study aimed to provide a clinical means of identifying patients with acute respiratory acidosis (ARA) in a setting where blood gas analysis is unavailable. We undertook a prospective, observational study of consecutive patients who presented to two emergency departments with severe and life-threatening exacerbation of asthma or COPD. Each underwent clinical assessment, treatment and blood gas analysis. The outcome measure was ARA or mixed ARA and metabolic acidosis. A total of 127 episodes in patients aged 15-90 years (65.3% males and 34.7% females) were included in the study. Of these, 62.2% had asthma and 37.8% had COPD; 71.7% had life-threatening and 28.3% had severe attacks. Overall, the adjusted odds ratio (and 95% confidence intervals) for predictors of ARA were 7.09 (1.79-28.06) for drowsiness, 4.11 (1.31-12.88) for flushing, 3.34 (1.01-11.02) for having COPD and 2.86 (1.01-8.07) for intercostal retractions. In conclusion, with drowsiness, the likelihood of ARA is about seven times higher. The presence of flushing, COPD and intercostal retractions also increase the risk of ARA.

Acidosis, Respiratory↗

PubMed1982

Brain water and electrolytes in response to respiratory acidosis and brain edema in the mutant mouse, jimpy.

Compared to littermate controls, unstressed Jimpy mice have higher brain water, sodium, potassium and chloride contents and lower carbonic anhydrase activity. When stressed by CO2 to produce a respiratory acidosis or by injection of distilled water to produce brain edema, the Jimpy mouse brain has water and ionic responses essentially like those in controls.

Acidosis, Respiratory↗

PubMed1989

The use of helium-oxygen mixtures in the support of patients with status asthmaticus and respiratory acidosis.

Ten patients with status asthmaticus and respiratory or combined respiratory and metabolic acidosis were treated with a mixture of helium-oxygen (He-O2) in addition to the usual bronchodilator therapy and corticosteroids. A significant reversal of the acidosis was noted within the first 20 minutes, and no patient required subsequent intubation. The He-O2 mixture was started after the aerosolized and subcutaneous bronchodilators, but before intravenous corticosteroids and aminophylline had reached their peak effects. There were no untoward reactions and most of the patients sensed an immediate reduction in their dyspnea with the onset of He-O2 therapy. We conclude that He-O2 may be a useful adjunct to the usual medications employed in the treatment of status asthmaticus and may allow some patients to avoid intubation and mechanical ventilation.

Acidosis, Respiratory↗

PubMed1994

Respiratory acidosis and subcutaneous emphysema during laparoscopic cholecystectomy.

A case is presented of a healthy 69-year-old woman who underwent elective laparoscopic cholecystectomy under general anaesthesia. As surgery proceeded she developed hypercapnia (arterial blood PaCO2 = 100 mmHg) and a related respiratory acidosis (arterial blood pH 7.07). The cause was attributed to subcutaneous insufflation and absorption of CO2, directly related to the surgical pneumoperitoneum.

Acidosis, Respiratory↗

PubMed1987

Hypokalaemia and respiratory acidosis following partial obstruction of the airway.

An 87-year-old female, with a history of hypertension controlled with hydrochlorothiazide, was scheduled for excision of a cystic mass of the left lobe of the thyroid. In the course of the anaesthetic, she developed partial airway obstruction that resulted in respiratory acidosis (PaCO2 108 mmHg, pH 7.06), developed premature ventricular contractions and experienced a reduction in plasma potassium concentration from 3.9 to 2.9 mmole X L-1. We interpret this hypokalaemia as a consequence of the epinephrine discharge due to hypercapnia. The case is reported to emphasize the importance of minimizing the sympathetic response to induction of anaesthesia, intubation and surgery in patients with marginal potassium stores.

Acidosis, Respiratory↗

PubMed2001

Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain.

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.

Acidosis, Respiratory↗

PubMed1984

Effects of changes of blood pressure, respiratory acidosis and hypoxia on blood flow in the sciatic nerve of the rat.

Using the hydrogen clearance technique, we have measured blood flow in the sciatic nerves of healthy, anaesthetized rats at rest, at various arterial blood pressures, and during respiratory acidosis and hypoxia. The majority of hydrogen clearance curves were bi-exponential. The slower component appears to reflect nerve blood flow more accurately than either the fast component or the composite value obtained from both components. Mean nerve blood flow estimated from the slow component of the seventeen bi-exponential hydrogen clearance curves and from the seven mono-exponential curves was 15.8 +/- 1.1 ml min-1 100 g-1 (+/- S.E. of the mean). The mean value of the fast component of the bi-exponential curves was 118 +/- 6 ml min-1 100 g-1 and that obtained from both components was 25.9 +/- 2.6 ml min-1 100 g-1. Sciatic nerve blood flow was measured over a range of arterial blood pressures of 60-160 mmHG. There is a curvilinear relationship between pressure and flow suggesting that the nerve vascular bed responds passively to changes in perfusion pressure. Respiratory acidosis resulted in no significant change in nerve blood flow. The mean flow was 15.5 +/- 1.9 ml min-1 100 g-1. During hypoxia, nerve blood flow decreased to 7.5 +/- 1.4 ml min-1 100 g-1 as a result of a reduction in arterial blood pressure and an increase in vascular resistance. These findings suggest that normal nerve blood flow is high in relation to metabolic activity, especially when compared with the brain.

Animals↗

PubMed2004

Tracheal double-lumen ventilation attenuates hypercapnia and respiratory acidosis in lung injured pigs.

OBJECTIVE: Evaluation of ventilatory and circulatory effects with coaxial double-lumen tube ventilation for dead-space reduction as compared with standard endotracheal tube ventilation. DESIGN: Experimental study in a pig model of lung lavage induced acute lung injury. SETTING: University research laboratory. MEASUREMENTS AND RESULTS: Tidal volumes of 6, 8 and 10 ml/kg body weight with a set respiratory rate of 20 breaths per minute were used in a random order with both double-lumen ventilation and standard endotracheal tube ventilation. Measurements of ventilatory and circulatory parameters were obtained after steady state at each experimental stage. With a tidal volume of 6 ml/kg, PaCO(2) was reduced from 10.9 kPa (95% CI 9.0-12.9) with a standard endotracheal tube to 8.2 kPa (95% CI 7.0-9.4) with double-lumen ventilation. This corresponds to a reduction in carbon dioxide levels by 25%. At 6 ml/kg, pH increased from 7.17 (95% CI 7.09-7.24) with a standard endotracheal tube to 7.27 (95% CI 7.21-7.32) with double-lumen ventilation. Tracheal pressure was monitored continuously and no difference between single- or double-lumen ventilation was noted at corresponding levels of ventilation. There was no formation of auto-PEEP. Partial tube obstruction due to secretions was not observed during the experiments. CONCLUSIONS: Coaxial double-lumen tube ventilation is an effective adjunct to reduce technical dead space. It attenuates hypercapnia and respiratory acidosis in a lung injury pig model.

Acidosis, Respiratory↗

PubMed1979

Respiratory acidosis with the small Storz-Hopkins bronchoscopes: occurrence and management.

Carbon dioxide retention in the Storz rigid ventilating bronchoscope with the Hopkins lens system was investigated in the laboratory. The 3.5, 4.0, and 5.0 30-cm Storz bronchoscopes with a 3.95-mm (outside diameter) telescope lens were used in 10 mongrel dogs weighing between 8 and 15 kg. Significant (p less than 0.01) accumulation of arterial carbon dioxide tension (PaCO2) (respiratory acidosis) was observed after 5 and 10 minutes of ventilation through the 3.5 and 4.0 bronchoscopes, but no significant increase in PaCO2 was noted with the 5.0 bronchoscope. There was no significant change in arterial oxygen tension under the same conditions. Manual compression of the upper anterior abdominal wall during expiration was applied during bronchoscopy in 6 children. Arterial blood samples were taken before insertion of the bronchoscope and 5 minutes later with and without abdominal compression during expiration. A significant increase (p less than 0.05) in PaCO2 and a decrease in pH were observed after 5 minutes of the bronchoscopic procedure without manual compression of the abdominal wall, while no significant changes in PaCO2 were observed with abdominal compression.

Abdominal Muscles↗

PubMed1992

Greater unidirectional calcium efflux from bone during metabolic, compared with respiratory, acidosis.

There is a smaller net calcium efflux from bone in vitro during respiratory (increased PCO2) than metabolic (decreased [HCO3-] acidosis. This could be due to the elevated PCO2, which would lessen the driving force for mineral dissolution and increase the driving force for mineralization with respect to carbonated apatite in the bone mineral. To test this hypothesis, we injected neonatal mice with 45Ca and dissected the radiolabeled calvariae 24 h later. The live calvariae were then cultured for 24 h under conditions simulating respiratory acidosis (Resp, pH = 7.225 +/- 0.003, PCO2 = 87.5 +/- 0.1 mmHg), severe respiratory acidosis (SResp, pH = 7.072 +/- 0.004, PCO2 = 103.0 +/- 0.5 mmHg), metabolic acidosis (Met, pH = 7.212 +/- 0.003, HCO3- = 15.5 +/- 0.1 meq/l), or normal acid-base status (Ctl, pH = 7.452 +/- 0.003, PCO2 = 40.0 +/- 0.2 mmHg, HCO3- = 27.8 +/- 0.2 meq/l) and bidirectional net calcium flux (JCa) and unidirectional 45Ca release were determined. There was greater JCa from bone during Met than Resp, and JCa was not different from Met during SResp despite the latter having a significantly lower pH. There was greater unidirectional 45Ca release from bone during Met than Resp, SResp, or Ctl. There was a similar direct correlation between JCa and 45Ca efflux in the respiratory and metabolic groups. However, when calvarial osteoclast activity was inhibited with calcitonin,although there was again greater JCa and 45Ca release with a metabolic compared with respiratory acidosis, there was a greater proportion of 45Ca release than JCa from bone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1975

[Study of P50 in patients under continuous O2 inhalation and during chronic respiratory acidosis].

In vitro, the affinity of Hb for O2 depends on pH and capnia by the intermediate of the 2-3 DPG level, the concentration of which lowers in the case of acidosis and hypercapnia. Thus, an increase in the affinity results, but while Bohr's effect is immediate, on the contrary the 2-3 DPG effect is slow. Authors have verified the importance of this modification by studying the affinity of Hb for O2 thanks to the P50 technique in 15 normal non-smokers subjects and in 10 subjects with compensated or not respiratory acidosis but normally saturated thanks to continuous O2 administration.

Acidosis, Respiratory↗

PubMed2002

[Partial occlusion of the Bain circuit causes respiratory acidosis under general anesthesia].

The Bain circuit is a modification of the Mapleson D ventilation system used in general anaesthesia in children and adults. It has several advantages over other systems as it is light in weight, convenient, and has no valves. But it contains the risk of undetected leak or occlusion, because of its construction with a small inner tube, which provides the patient with fresh gas, inside a larger corrugated tube. We report a partial occlusion in the T-piece of the Bain circuit, leading to high peak pressure and respiratory acidosis under controlled ventilation in a 15-year-old boy.

Acidosis, Respiratory↗

PubMedDate not supplied

[Kinetics of the compensation of respiratory acidosis induced by experimental chronic hypercapnia in man (author's transl)].

Four groups of male volunteers have been exposed in a tight climatical chamber to PICO2 of 14, 21, 28 and 32 torr; exposure periods varied from two to 30 days, between two reference periods in normal air. The results deal with the evolution of arterial blood acid-base equilibrium and that of renal response in relation to PICO2. In all exposures, the carbon dioxide alveolar overload increases by several torr during the first 24 hours on account of attenuation of the initial hyperventilation. Kinetics of the respiratory acidosis compensation differs according to hypercapnia which is moderate (PICO2 of 14 and 21 torr) or relatively severe (PICO2 of 28 and 32 torr). The decrease in arterial pH lessens as early as the 24th hour at PICO2 28 and 32 torr, and only after two days at PICO2 14 and 21 torr. The renal response is characterized by a significant increase in aciduria during the first 24 hours at PICO2 28 and 32 torr; the changes are smaller and start latter at PICO2 14 torr.

Acidosis, Respiratory↗