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PubMed1996

[Evaluation of fetal condition in pregnancy complicated by hypertension--biochemical assessment of amniotic fluid. III. Acid-base balance].

Sixty two samples of amniotic fluid, collected by ultrasound guided amniocentesis, were submitted to biochemical investigation including 31 samples from women with pregnancy complicated by hypertension (studied group) and 31 samples deriving from healthy pregnant women (control group with). The following parameters of acid-base balance were measured in amniotic fluids of both groups: pH, pCO2, base deficiency, standard HCO3 and total CO2. Corning device type 168 was used. Distinct metabolic-respiratory acidosis was present in amniotic fluids of studied group showing the decrease of a pH, pO2, standard HCO3 values and an increase of CO2 values and base deficiency. Authors believe in pregnancy complicated by hypertension biochemical environment of intrauterine fetal development with regard to acid-base balance is highly unfavourable.

Acid-Base Equilibrium↗
PubMed1997

[Intraoperative malignant hyperthermia: apropos of a case].

Malignant hyperthermia (MHS) is a rare potentially fatal complication of general anesthesia. Anesthetic agents most frequently incriminated are succinylcholine and halogenated agents. Respiratory acidosis is the most specific and sensitive sign. Hyperthermia per se may occur secondarily or may stay totally absent. Tachycardia and/or arrhythmias often develop due to hyperkalemia and metabolic acidosis. Muscle rigidity whenever present is pathognomonic The "gold standard" test for the diagnosis of MHS is the halothane-caffeine contracture test. Dantrolene is the treatment of choice and prognosis depends on the early administration of this agent.

Dantrolene↗
PubMed1998

Joint NASA-ESA-DARA Study. Part three: cardiorespiratory response to elevated CO2 levels during sleep.

Long-term exposure to elevated ambient CO2-levels is a common condition for living in a closed environment such as a spacecraft. In this study, the cardio-respiratory system response to CO2-levels of 0.7% and 1.2% was assessed. The response was investigated during non-REM sleep when the sensitivity of the respiratory system to ambient CO2 is low and only subject to the metabolic respiratory drive. Four subjects were exposed to 0.7% and 1.2% CO2 for 23 d each. Respiration rate and heart rate were determined for the first two phases of slow wave sleep. In addition, the occurrence of central apneas was assessed. Data were analyzed by a repeated measure ANOVA. As a response to CO2 exposure two dynamic effects were observed. Heart rate increased initially with a peak between the second and the sixth night. Over the period of the exposure, respiration rate and heart rate decreased steadily. At least two mechanisms with different time constants must be considered for this dynamic behavior: an uncompensated respiratory acidosis, followed by a phase of relative compensation. At the end of the 23-d exposure, equilibrium in the physiological state had not been reached. Though the experiment did not show severe effects from CO2, it is too early to state that a long-term exposure does not have any consequences for health and well-being.

Adult↗
PubMed1998

[Evaluation of malignant hyperthermia episodes with the Clinical Grading Scale].

PURPOSE: The Clinical Grading Scale (CGS) was introduced to predict malignant hyperthermia (MH) susceptibility in adverse anaesthetic events. Because many of the clinical symptoms that occur during MH episodes are nonspecific, the CGS was designed as a tool to estimate the qualitative likelihood of MH. The purpose of this study was to compare the results of the CGS with the established in vitro contracture test (IVCT). METHODS: 92 patients with a personal history for MH were tested for MH susceptibility with the IVCT according to the protocol of the European MH Group. All patients were also evaluated with the CGS. Clinical indicators for the CGS are rigidity, muscle breakdown, respiratory acidosis, temperature increase and cardiac involvement. There are additional indicators in case of a family history for MH. For each indicator 3-15 points are added to build a raw score; this raw score corresponds to a MH rank in the CGS that describes the likelihood of MH in the suspected event. The higher the raw score rank, the higher the likelihood of MH and vice versa. RESULTS: From 92 patients, 32 (35%) were diagnosed as MH-susceptible (MHS) with the IVCT, 47 (51%) were MH-normal (MHN), and 13 (14%) were MH-equivocal (MHE). One patient with MH-rank 1 (MH almost never) in the CGS was diagnosed as MHS; on the other hand no patient with MH-rank 6 (MH almost certain) in the CGS was diagnosed as MHN. However, the majority of patients (72%) were assigned to ranks 3 and 4 (MH somewhat less than likely/MH somewhat greater than likely). The qualitative likelihood of MH could therefore not be clearly estimated. CONCLUSION: Our study shows that the MH-rank of the CGS corresponds poorly with the results of the IVCT. In any case the evaluation of an MH suspicious event depends on the availability of data of that event. It is often difficult to obtain sufficient data, especially if the event occurred a long while ago. In these cases the MH rank may underestimate the likelihood of MH susceptibility. On the other hand, overestimation is also possible because some of the scoring indicators depend on the anaesthesiologist's judgement only. At present, the use of the CGS is neither validated nor clinically feasible. The CGS cannot replace IVCT.

Adolescent↗
PubMed1998

[Emergency room visits by patients with exacerbations of asthma].

We retrospectively analyzed patterns of emergency room visits by patients with exacerbations of asthma from December 1995 through November 1996. A total of 591 episodes in 198 patients were reviewed. The average age was 35.8 years, ranging from 15 to 71. The largest number of visits occurred in September. The number of visits per year ranged from 1 to 22; the mean was 2.9 per year. In patients who were followed on a regular basis at our institution, serve attacks accounted for 7.1% of the total, compared with 21.6 percent at other hospitals or outpatient clinics. We suspect that this difference was related to differences in the use of inhaled steroids. At our institution, 89% of patients were taking inhaled steroids; at other hospitals or clinics, only 21% were taking inhaled steroids. Of the 198 patients, 33 fulfilled one of the following criteria: (1) endotracheal intubation for respiratory failure or respiratory arrest, (2) respiratory acidosis (pH < 7.35) without endotracheal intubation; 27% of those patients had been given a diagnosis of mild asthma before the acute exacerbation. We conclude that patient education and standard guidelines for treatment of asthma, are very important for appropriate management of asthma, to prevent exacerbations and asthma-related deaths.

Administration, Inhalation↗
PubMed1998

Suspected malignant hyperthermia during isoflurane anesthesia--a case report.

We present a patient with thyroid cancer, who developed respiratory acidosis, tachycardia and hyperthermia during isoflurane anesthesia. Malignant hyperthermia was suspected on the basis of clinical manifestation and laboratory finding. With early diagnosis and treatment the patient survived the episode.

Adult↗
PubMed1973

Evolution of the acid-base status in cardiac arrest.

In a study of the evolution of acid-base status in 26 patients who had cardiopulmonary arrest in the operating room, it appeared that:The determination of acid-base status within the first hour post-cardiac arrest is useful in differentiating final survivors from non-survivors. Respiratory or combined acidosis carries a poor prognosis not evidenced for metabolic acidosis. Late respiratory complications are more frequent in patients with initial combined acidosis. Treatment should be instituted on the basis of frequent determinations of acidbase status, since accurate diagnosis of degree and type of acidosis cannot be done on clinical grounds only. Recovery of consciousness is influenced by the type and severity of acidosis, less so by duration of arrest; and that high pCO(2) is associated frequently with unconsciousness after recovery of circulatory function.

Acidosis, Respiratory↗
PubMed1999

Role of nitric oxide in rat coronary flow regulation during respiratory and metabolic acidosis.

A rat Langendorff heart preparation, perfused at constant pressure, was used to evaluate the role of nitric oxide in the increases in coronary vessel flow during hypercapnic and metabolic acidosis. Prior administration of the nitric oxide synthase (NOS) inhibitor N6-nitro-L-arginine methyl ester (100 microM) significantly reduced the basal, resting, rate of coronary flow but did not attenuate the increases in flow during brief (2-min) periods of perfusion with acidotic solutions. These results suggest that nitric oxide is not a significant contributor to rat heart coronary flow regulation during respiratory or metabolic acidosis.

Acidosis↗
PubMed1985

Effect of acidosis on contractile function in the newborn rabbit heart.

Effects of respiratory and metabolic acidosis (pH approximately 6.8) on myocardial function were studied in the newborn and adult rabbits. Mechanical function was studied in the isolated arterially perfused heart preparation. Acidosis was induced either by increase of the perfusate PCO2 or by decrease of the bicarbonate content. During respiratory acidosis, developed tension (DT) decreased to 43 +/- 3% of control (n = 18) in the adult and this depression was significantly greater than in the newborn (DT = 92 +/- 4%, n = 6). Depression of DT by respiratory acidosis was observed even at high extracellular Ca. During metabolic acidosis, mechanical function decreased gradually and DT at 30 min into acidosis in the adult was 78 +/- 3% of control (n = 6). This depression of DT in the adult was significantly greater than in the newborn (DT at 30 min = 96 +/- 1% of control, n = 6). Statistical analysis using paired t test showed that respiratory acidosis, but not metabolic acidosis, caused significant negative inotropism in the newborn. Myofibrils were isolated and the ATPase was measured at 10(-8) to 10(-4) M Ca and at pH of 7.1 (control), 6.5, and 6.0. Reducing pH depressed the ATPase activity similarly in the newborn and adult. Intracellular buffer capacity was determined by titrating muscle homogenate with HCI. Although the initial pH was not different, addition of HCl to the homogenate caused less decrease in pH in the newborn. These data indicate that contractile function in the newborn heart is more resistant to acidosis and this may be due partly to the greater intracellular buffer capacity.

Acidosis↗
PubMed1980

The metabolic and respiratory alterations of heat stroke.

The metabolic and respiratory changes of 21 patients with heat stroke were studied. Admission arterial blood gas levels were measured, and serum bicarbonate, lactate, calcium, phosphorus, and anion gap determinations were performed. Seven patients had a metabolic acidosis (pH 7.20 +/- 0.04, PCO2 32 +/- 2 mm Hg, and bicarbonate 12 +/- 1 mEq/L), seven a combined metabolic acidosis and respiratory alkalosis (pH 7.39 +/- 0.01, PCO2 25 +/- 1 mm Hg, and bicarbonate 15 +/- 1 mEq/L), four a respiratory alkalosis (pH 7.45 +/- 0.01, PCO2 30 +/- 1 mm Hg, and bicarbonate 20 +/- 1 mEq/L), one a metabolic and respiratory acidosis (pH 7.13, PCO2 52 mm Hg, and bicarbonate 17 mEq/L), and one a respiratory acidosis (pH 7.30, PCO2 56 MM Hg, and bicarbonate 27 mEq/L). The 15 patients with a metabolic acidosis had a pH of 7.28 +/- 0.03, PCO2 of 30 +/- 2 mm Hg, bicarbonate level of 14 +/- 1 mEq/L, lactate concentration of 6.5 +/- 1.0 mEq/L, and an anion gap of 26 +/- 4 mEq/L. Nine patients were hypocalcemic (7.8 +/- 0.3 mg/dL), and five patients were hypophosphatemic (2.0 +/- 0.2 mg/dL). The predominant metabolic change in heat stroke is a metabolic acidosis secondary to increased lactate content and/or a respiratory alkalosis. Hypocalcemia is common and hypophosphatemia is not infrequent.

Acidosis↗
PubMed1965

Respiratory failure.

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Acidosis, Respiratory↗
PubMed1986

Effect of acute acidemia on phosphate uptake by renal proximal tubular brush-border membranes.

Prolonged metabolic acidosis is associated with depressed phosphate (Pi) uptake by the brush-border membrane (BBM) of the proximal tubule. To examine if changes in systemic pH underlie this inhibition, we measured Pi transport by renal cortical BBM from thyroparathyroidectomized rats with respiratory or metabolic acidosis of 1 or 3 h, respectively, and in appropriate controls. Also, Pi transport was measured in BBM prepared using tissue slices from nonacidotic rats that were preincubated for 20 or 45 min at either pH 6.9 (HCO3 = 10 mM, CO2 = 10%) or 7.4 (HCO3 = 10 mM, CO2 = 2.5%). Despite comparable acidemia (pH 7.06 +/- 0.05 with respiratory acidosis and 7.10 +/- 0.03 with metabolic acidosis), Na-dependent Pi uptake at 5 s incubation was reduced by 15.2 +/- 3.5% with respiratory acidosis compared with paired controls. It was not altered with metabolic acidosis. Vmax in respiratory acidosis (1.2 nmol X mg protein-1 X 5 s-1) was less than in controls (1.6); Kt was similar in both groups. 22Na transport and Na-dependent glucose transport were unchanged. Plasma phosphorus (P) increased from 8.75 +/- 0.35 mg/dl to 12.42 +/- 1.9 with respiratory acidosis. Therefore BBM vesicles transport was measured in controls after plasma P was raised. Under these conditions, Pi transport was similar to that with respiratory acidosis. Also Pi transport by BBM was unchanged when tissue slices were preincubated in vitro at high CO2 concentrations for 20 or 45 min. Thus respiratory acidosis specifically inhibits Na-dependent Pi transport by decreasing the number or rate of the BBM Pi carrier.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1987

Respiratory compensation and acidosis in endotoxin shock: effects of naloxone in conscious rats.

Naloxone treatment of endotoxin shock has been shown to alter many cardiovascular parameters. However, since opioids can affect ventilatory function we thought it important to assess the effects of naloxone on some respiratory variables during endotoxin shock. Male Sprague-Dawley rats (300-400 g) were surgically prepared with carotid artery and jugular vein cannulas 24 hours before experiments were begun. Conscious, unrestrained rats were challenged with 10 mg/kg E. coli endotoxin or saline. Measurements of blood gases, pH, respiratory rate, serum lactate, and medullary/pontine blood flow (radio labelled microsphere method) were made 0, 10, 30, and 60 minutes postchallenge. Rats were treated with either 2 mg/kg naloxone or saline at 25 minutes postchallenge. Arterial PO2 rose and PCO2 fell in a stepwise fashion in saline-treated endotoxic rats. These changes were unrelated to medullary/pontine perfusion or to arterial pH (up to 30 minutes postchallenge). In naloxone-treated endotoxic rats the increased ventilatory drive at 60 minutes was attenuated, apparently as a result of prevention of acidosis at this time. These data further support uncoupling of ventilatory drive and arterial pH reported earlier and also indicate that naloxone's ability to prevent acidosis in these animals is not mediated through respiratory compensation.

Acid-Base Equilibrium↗
PubMed1988

Effects of respiratory and metabolic alkalosis and acidosis on pipecuronium neuromuscular block.

Acute respiratory and metabolic acidosis as well as metabolic alkalosis increased (by 11, 11, 21%) whereas respiratory alkalosis antagonized (by 10%) the partial steady state block produced by pipecuronium infusion on the anterior tibialis muscle of the cat. The duration of neuromuscular block following six successive doses of pipecuronium was prolonged 1.4-fold during long-lasting metabolic alkalosis while this parameter was shortened to half of that in control cats during acidosis. Pipecuronium block could be fully antagonized by neostigmine.

Acidosis↗
PubMed1983

Importance of medullary events in ammonium excretion: studies in acute respiratory and acute metabolic acidosis.

The renal medulla can play an important role in acid excretion by modulating both hydrogen ion secretion in the medullary collecting duct and the medullary PNH3. The purpose of these experiments was to characterize the intrarenal events associated with ammonium excretion in acute acidosis. Cortical events were monitored in two ways: first, the rates of glutamine extraction and ammoniagenesis were assessed by measuring arteriovenous differences and the rate of renal blood flow; second, the biochemical response of the ammoniagenesis pathway was examined by measuring glutamate and 2-oxoglutarate, key renal cortical metabolites in this pathway. There were no significant differences noted in any of these cortical parameters between acute respiratory and metabolic acidosis. Despite a comparable twofold rise in ammonium excretion in both cases, the urine pH, PNH3, and the urine minus blood PCO2 difference (U-B PCO2) were lower during acute hypercapnia. In these experiments, the urine PCO2 was 34 mmHg (1 mmHg = 133.322 Pa) lower than that of the blood during acute respiratory acidosis while the U-B PCO2 was 5 +/- 3 mmHg in acute metabolic acidosis. Thus there were significant differences in medullary events during these two conditions. Although the urine pH is critical in determining ammonium excretion in certain circumstances, these results suggest that regional variations in the medullary PNH3 can modify this relationship.

Acidosis↗