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At least 1,009 records · Page 56Linked to original sources
PubMed1998

Copper exposure impairs intra- and extracellular acid-base regulation during hypercapnia in the fresh water rainbow trout (Oncorhynchus mykiss).

In order to evaluate the impact of water-borne copper on acid-base regulation in fresh water rainbow trout, chronically cannulated fish were exposed to copper (0.6 mg 1(-1)), hypercapnia (water PCO2 of 6 mmHg) or a combination of copper and hypercapnia, while a fourth untreated group served as the control. Blood samples obtained at 0 h, 4 h and 24 h were analysed for acid-base status, ion concentrations and respiratory parameters. Tissue samples from caudal skeletal muscle, liver and gill filaments were examined for intracellular acid-base status, ion- and water contents, and copper concentration. Exposure to copper alone elicited a small extracellular metabolic alkalosis, no changes in arterial PO2, and a minor decrease in plasma ion concentrations. Hypercapnia alone increased arterial PCO2 from approximately 2 mmHg to 7.2 mmHg, but the extracellular respiratory acidosis present at 4 h was almost completely compensated at 24 h due to an increase in plasma bicarbonate concentration [HCO3-] from 8.1 mM to 24.4 mM. Combined exposure to hypercapnia and copper resulted in a slightly larger acidosis at 4 h, and the fish failed to restore extracellular pH at 24 h, because plasma [HCO3-] only increased to 16.3 mM. Fish exposed to hypercapnia and copper also showed a delayed recovery of intracellular pH in skeletal muscle, compared to fish exposure to hypercapnia only. Thus, copper exposure impaired both extracellular and intracellular acid-base regulation during hypercapnia. When seen in connection with only minor effects of copper on osmoregulatory and respiratory parameters, the reduced ability to regulate acid-base suggests that acid-base regulation may be one of the most copper-sensitive branchial functions.

Acid-Base Equilibrium↗
PubMed2006

The effects of apparatus dead space on P(aCO2) in patients receiving lung-protective ventilation.

BACKGROUND: Lung-protective ventilation using tidal volume (V(T)) of 4-6 mL/kg (predicted body weight) reduces mortality (compared with traditional V(T)) in patients with acute respiratory distress syndrome and acute lung injury. Standardized use of lower V(T) can result in respiratory acidosis and has raised new concerns about the appropriate configuration of the ventilator circuit, especially in regard to the dead space (V(D)) of the apparatus. We hypothesized that, with a patient receiving lung-protective ventilation, the removal of all apparatus dead space from the circuit would reduce P(aCO2) and allow a reduction in minute ventilation. METHODS: All the studied patients met the American-European consensus-conference criteria for acute respiratory distress syndrome/acute lung injury, were receiving a lung-protective ventilation strategy, were > 18 years of age, and were hemodynamically stable. We prospectively tested 3 different ventilator-circuit configurations, in random sequence, for 15 min each: (1) standard hygroscopic heat-and-moisture exchanger (HME) with 15-cm flexible tubing, (2) 15-cm flexible tubing only, (3) no HME or flexible tubing. V(T), respiratory rate, positive end-expiratory pressure, and fraction of inspired oxygen were maintained constant throughout the study, and exhaled CO2 was measured continuously. Physiologic dead space (V(D)/V(T)) was calculated using the Enghoff modification of the Bohr equation. RESULTS: Seven patients were studied. Removal of the HME from the circuit significantly decreased V(D)/V(T) (by approximately 6%) and P(aCO2) (by approximately 5 mm Hg). Removal of both the HME and flexible tubing from the circuit reduced V(D)/V(T) by an additional 5%, and P(aCO2) by an additional 6 mm Hg. With both circuit-configuration changes, minute ventilation fell from a mean of 11.51 L/min to 10.35 L/min, and pH increased from 7.30 to 7.38. Carbon-dioxide production did not change significantly. CONCLUSION: In patients receiving lower-V(T) ventilation, removing all the apparatus V(D) from the ventilator circuit reduces P(aCO2) and increases pH, at a lower minute ventilation. This information will help guide ventilator-circuit configuration for patients receiving lung-protective ventilation.

Adult↗
PubMed2000

Acid-base balance following Tityus serrulatus scorpion envenoming in anaesthetized rats.

In the present work the pH and arterial blood gases were measured in fasted and fed male albino rats, weighing 297 +/- 13 g, anaesthetized with urethane (1.4 g/kg, i.p.) before and after injection of T1 fraction from Titys serrulatus scorpion venom, during 60 min. Arterial blood samples were collected at 0, 5, 15, 30 and 60 min for pH, pCO2, pO2, bicarbonate and base-excess analysis. The data showed that the scorpion toxin induced a continuous drop in the blood pH along the time. Hypercapnia and hypoxemia peaking at 30 min and followed by a recovery towards normal values at 60 min were also observed. A pronounced decrease in the blood bicarbonate levels at 60 min and negative base-excess values along with time were evident at 60 min. The comparisons between fasted and fed animals have shown that in the last group the effects of scorpion toxin on the arterial blood gases were less pronounced. We conclude that T1 fraction of Tityus serrulatus scorpion venom induces in anaesthetized rats an acute respiratory acidosis followed by metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1996

Predictors of extubation success and failure in mechanically ventilated infants and children.

OBJECTIVE: To predict extubation success and failure in mechanically ventilated infants and children using bedside measures of respiratory function. DESIGN: Prospective collection of data. SETTING: A university-affiliated children's hospital with a 51-bed critical care unit. PATIENTS: All infants and children who were mechanically ventilated for at least 24 hrs, except neonates < or = 37 wks gestation and patients with neuromuscular disease. INTERVENTIONS: Bedside measurements of cardiorespiratory function were obtained immediately before extubation. MEASUREMENTS AND MAIN RESULTS: Extubation failure was defined as reintubation within 48 hrs of extubation in the absence of upper airway obstruction. Failure rates were calculated for different ranges (selected a priori) of preextubation measures of breathing effort, ventilatory support, respiratory mechanics, central inspiratory drive, and integrated indices useful in adults. Effort of spontaneous breathing was assessed by the respiratory rate standardized to age, the presence of retractions and paradoxical breathing, inspiratory pressure, maximal negative inspiratory pressure (maximal negative inspiratory pressure), inspiratory pressure/maximal negative inspiratory pressure ratio, and tidal volume indexed to body weight of a spontaneous breath. Ventilatory support was measured by the fraction of inspired oxygen (F10(2)), mean airway pressure, oxygenation index, and the fraction of total minute ventilation provided by the ventilator. Respiratory mechanics were assessed by determination of peak ventilatory inspiratory pressure and dynamic compliance. Central inspiratory drive was assessed by mean inspiratory flow. Frequency to tidal volume ratio and the compliance, rate, oxygenation, and pressure indexed to body weight, the integrated indices useful in predicting extubation failure in adults, were also calculated. Thirty-four of the 208 patients who were studied were reintubated for an overall failure rate of 16.3% (95% confidence interval 11.3% to 21.4%). The reasons for reintubation were poor effort (n = 8), excessive effort (n = 14), altered mental status or absent airway reflexes (n = 2), cardiovascular instability (n = 3), inadequate oxygenation (n = 3), respiratory acidosis (n = 3), and undocumented (n = 1). Extubation failure increased significantly with decreasing tidal volume indexed to body weight of a spontaneous breath, increasing F10(2), increasing mean airway pressure, increasing oxygenation index, increasing fraction of total minute ventilation provided by the ventilator, increasing peak ventilatory inspiratory pressure, or decreasing mean inspiratory flow (p < .05). Dynamic compliance showed a trend of increasing failure rate with decreasing dynamic compliance but did not reach statistical significance (p = .116). Respiratory rate standardized to age, inspiratory pressure, maximal negative inspiratory pressure, inspiratory pressure/maximal negative inspiratory pressure ratio, frequency to tidal volume ratio, and compliance, rate, oxygenation, and pressure did not show any trend in failure rate with increasing or decreasing values. Threshold values that defined a low risk (< or = 10%) and a high risk (> or = 25%) of extubation failure could be determined for tidal volume indexed to body weight of a spontaneous breath, F10(2), mean airway pressure, oxygenation index, fraction of total minute ventilation provided by the ventilator, peak ventilatory inspiratory pressure, dynamic compliance, and mean inspiratory flow. Neither a low nor a high risk of failure could be defined for frequency to tidal volume ratio or the compliance, rate, oxygenation, and pressure (CROP) index. CONCLUSIONS: Bedside measurements of respiratory function can predict extubation success and failure in infants and children. Both a low risk and a high risk of failure can be determined using these measures. Integrated indices useful in adults do not reliably predict extubation success or failure in

Child↗
PubMed1984

Influence of lidocaine and bupivacaine on isolated guinea pig atria in the presence of acidosis and hypoxia.

In an isolated guinea pig atrial preparation, the bathing solution pH, PO2, and PCO2 were manipulated to mimic normal, acidotic, and hypoxic conditions. The effect of lidocaine and bupivacaine on spontaneous heart rate (HR) and contractile force (CF) was determined for 60 min under conditions of normal pH, PO2, and PCO2. Lidocaine (50 micrograms/ml) reduced HR by a maximum of 34.2 +/- 1.5% and CF by 38.9 +/- 8.1% (mean +/- SEM). Bupivacaine (5 micrograms/ml) reduced HR by a maximum of 30.1 +/- 1.9% and CF by 48.0 +/- 6.5%. Bupivacaine (10 micrograms/ml) caused a maximum HR reduction of 61.7 +/- 9.5% and CF reduction of 66.0 +/- 8.6%. Hypoxia or metabolic or respiratory acidosis did not further enhance the local anesthetic induced atrial depression. However, conditions of combined acidosis/hypoxia, while not significantly altering the HR and CF depression caused by lidocaine, did enhance bupivacaine-induced depression of HR and CF (93.6 +/- 6.3% and 95.2 +/- 4.8%, respectively). The effect of a protein-free bathing solution on the relative toxicities of lidocaine and bupivacaine is discussed.

Acidosis↗
PubMed1993

Death from a morphine infusion during a sickle cell crisis.

A 15-year-old boy died during a vaso-occlusive sickle cell crisis after having received a prolonged infusion of morphine. Even in therapeutic doses, narcotics may cause significant respiratory acidosis and hypoxemia, enhancing polymerization of hemoglobin SS and thereby promoting sickling and vaso-occlusion. When narcotics are used during a sickle cell crisis, the best method is pharmacokinetically based patient-controlled analgesia.

Adolescent↗
PubMed1990

Respiratory syncytial viral infection in infants: nursing implications.

Respiratory syncytial viral infection is the leading cause of acute lower respiratory tract disease in infants and young children. Presenting symptoms include rhinorrhea, nasal congestion, a low grade fever, and a cough. Hypoxemia and respiratory acidosis are the most common presentation for infants requiring intensive care. Critical care nurses must skillfully assess the infant's clinical status and response to medical treatment, implement and enforce isolation procedures, and remain sensitive to the emotional and psychologic needs of RSV-infected infants and their families. They must be knowledgeable regarding the latest research and recommendations concerning isolation policies and safe administration of ribavirin therapy in order to maximize the care for infants experiencing acute respiratory distress caused by RSV infection.

Child, Preschool↗
PubMed2003

Ventilator-induced lung injury.

Ventilator-induced lung injury has been established as a significant risk to patients receiving PPV. Animal studies have provided definitive experimental data that support the existence of VILI. Clinical studies have implied the role of VILI in ARDS and ALI patients. In patients who have ARDS or ALI, however, VILI cannot be distinguished from exacerbation of the primary condition. Animal and clinical studies that clearly show elevated levels of cytokines when PPV is applied beyond certain limits support the concept that an inflammatory process is activated by PPV. Whether the induction of inflammatory mediators contributes to the mortality or morbidity of the ventilated patient has not been established. A potential role for anti-inflammatory therapeutic agents is promising. Therefore, the following considerations can guide the clinical care of ventilator patients: Alveolar pressure exposure (plateau pressure) should be limited to less than 32 cm H2O. Positive end-expiratory pressure should be applied to avoid end-expiratory collapse and reopening. Tidal volume should be set at approximately 6 mL/kg or further guided by plateau pressure limitation. Although studies suggest that reducing Ti, flow, and f may be important in avoiding VILI, there are no current guidelines. The results of preliminary studies investigating the preventative potential of respiratory acidosis, prone positioning, or careful vascular pressure management seem promising. Inflammatory response in VILI has been established, but a role for intervention, such as general or specific suppression of the response, has not been established.

Animals↗
PubMed1989

Ketoacid production in acute respiratory and metabolic acidosis and alkalosis in rats.

Metabolic acidosis inhibits and alkalosis enhances ketoacid production in ketotic humans and animals. To compare these effects with those of superimposed respiratory acid-base disturbances, ketone output was evaluated in awake ketotic rats during metabolic (intravenous infusions of HCl or NaHCO3) or respiratory (hyper or hypocapnia) disorders. With decreases in blood pH of 0.1-0.2 units over 3 h, blood ketone concentrations significantly decreased an average of 1.9 mM (metabolic) and 1.1 mM (respiratory) and urinary ketone excretion rates significantly decreased by 1.3 mumol/min (metabolic). With increases in systemic pH, blood ketone concentrations and urinary ketone excretion rates were significantly increased. Changes in blood pH correlated with changes in urinary ketone excretion rates in both metabolic (r = 0.87) and respiratory (r = 0.67) acid-base disturbances. The alterations occurred promptly and were rapidly reversible. These findings indicate that modest changes in systemic pH from metabolic or respiratory acid-base disturbances modify net ketoacid production in ketotic rats, confirm pH control of endogenous acid output as an acid-base regulator, and show that systemic pH, not bicarbonate concentration, mediates the process.

Acetoacetates↗
PubMed1993

Acute ventilatory failure from massive subcutaneous emphysema.

A 66-year-old woman developed massive subcutaneous emphysema following intubation. Acute thoracic restriction developed resulting in life-threatening respiratory acidosis. The patient could not be ventilated with conventional means. A tracheostomy was performed to decompress the chest and mediastinum with rapid resolution following. Although ventilatory failure from subcutaneous emphysema is very unusual, decompression with tracheostomy can be life saving.

Acute Disease↗
PubMed1994

Continuous monitoring of blood gases during hypercapnia in a patient with severe acute lung failure.

We report about our first experiences with a new device for continuous intra-arterial monitoring of blood gases in a patient with severe acute respiratory failure. This device facilitated continuous monitoring of PaO2, PaCO2 and pH while weaning the patient from extracorporeal membrane oxygenation (ECMO). Although sufficient oxygenation at FIO2 0.45 could be achieved after disconnection from ECMO, carbon dioxide elimination remained inadequate and resulted in severe respiratory acidosis. Within six hours, PaCO2 increased to 95 mmHg. Continuous monitoring of pH and PaCO2 helped to monitor CO2 retention and assisted the decision making process for reinstitution of ECMO.

Acute Disease↗
PubMed1995

Pathophysiological response of bovine pulmonary function to gastric distension.

The purpose was to determine whether gastric overdistension leads to life-threatening perturbations of pulmonary gas exchange in healthy calves. Six animals were studied with normal (0 kPa) and increased (1, 2, 3, 4 and 5 kPa) intragastric pressure (IGP). Changes in pleural pressures and peak expiratory flow paralleled those of IGP. Inspiratory pressure-time index remained stable throughout the insufflation process. Pulmonary function values were characterized by abrupt changes with increasing IGP. Tidal volume declined as IGP increased and, along with inspiratory flow, decreased abruptly with the highest pressure (5 kPa). Respiratory rate progressively increased up to an IGP of 4 kPa, then decreased by 30%, due to breath-holding at the end of inspiration. Minute volume increased with IGP up to 4 kPa, but dramatically declined at 5 kPa. Total pulmonary resistance remained stable throughout the insufflation process, whereas lung dynamic compliance fell abruptly to one-half of its baseline value at IGPs of 1 kPa and above. Arterial oxygen tension was maintained at an IGP of 1 kPa, slightly diminished at 2-3 kPa, and markedly decreased at 4-5 kPa. Hypercapnia and respiratory acidosis developed progressively with increasing IGP. Changes in arterial gases were probably due to a combination of (1) alveolar hypoventilation, caused by altered tidal to dead space volume ratio, inadequate central nervous system "drive", altered effectiveness of inspiratory muscle action, or end-inspiratory breath-holding, and (2) ventilation to perfusion mismatch, caused by perfusion of collapsed lung units. In the range of IGPs used, standardized arterial pH did not decline below the control value, which suggests that perfusion of peripheral tissues remained sufficient, and that respiratory failure rather than cardiovascular failure may be the principal physiopathological effect of increased gastric pressure.

Animals↗
PubMed1992

Failure of pulmonary acidosis to increase respiratory drive.

Experiments were performed to determine whether increases in acidity isolated to the pulmonary circulation would stimulate hypothesized pulmonary chemoreceptors and increase respiratory drive in the anesthetized paralyzed mechanically ventilated cat (n = 9). Respiratory drive was assessed by measuring the frequency and amplitude of the integrated phrenic neurogram. To create an isolated pulmonary acidosis, blood returning to the lung was acidified by infusion of 0.3 M lactic acid (1.91 ml/min) into the inferior vena cava, while systemic arterial pH was restored to near normal levels by simultaneous infusion of base (0.3 M NaOH) into the left atrium. Six minutes after the start of this dual infusion of acid and base, right ventricular (pulmonary) pH decreased from 7.286 to 7.179 and PCO2 increased 7 Torr. Systemic arterial pH and PCO2 were unchanged from measurements immediately before the infusion. This level of pulmonary acidosis failed to increase respiratory drive as assessed by phrenic activity. To test the sensitivity of the preparation to known systemic arterial chemical stimuli, a combined pulmonary and systemic acidosis was elicited by infusion of 0.3 M lactic acid into the inferior vena cava and 0.3 M NaCl into the left atrium. This infusion significantly lowered both systemic arterial and pulmonary arterial pH (7.343 to 7.155 for systemic arterial pH and 7.286 to 7.067 for pulmonary pH) and increased phrenic efferent activity 45%. We conclude that phrenic efferent activity is unaffected by moderate reductions in the pH of the pulmonary circulation in the absence of a significant systemic arterial acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed2004

Heliox administration during high-frequency jet ventilation augments carbon dioxide clearance.

We report the combined use of heliox and high-frequency jet ventilation to augment carbon dioxide clearance, with a focus on the important technical considerations. Our case is a 5-month old infant with acute respiratory failure associated with gas trapping, hypercarbia, respiratory acidosis, and air leak. Despite maximal conventional ventilation, bronchodilator therapy, corticosteroids, and sedation, the infant continued to demonstrate worsening gas exchange necessitating an escalation of support to high-frequency oscillatory ventilation. After the development of an air leak and continued difficulties with carbon dioxide clearance, the patient was transitioned to high-frequency jet ventilation. Persistent hypercarbia resulted in the addition of heliox to facilitate ventilation. Improvements in gas exchange occurred rapidly. The combination of heliox and high frequency jet ventilation resulted in improved carbon dioxide clearance, respiratory stabilization, and the ability to wean ventilator settings.

Acute Disease↗
PubMed1986

Oxyhemoglobin affinity in patients with chronic obstructive pulmonary disease and acute respiratory failure: role of mechanical ventilation.

Oxyhemoglobin affinity was assessed in 20 subjects with chronic obstructive pulmonary disease, all of whom experienced acute respiratory failure. PaCO2, pH, and 2,3-diphosphoglycerate (2,3-DPG) were measured 24 and 48 h after admission, and then during weaning (for the ten patients on mechanical ventilation) or on discharge (for the ten nonventilated patients). At 24 h, nonventilated patients had a lower pH (p less than .001) and 2,3-DPG concentration (p less than .05) and a higher PaCO2 (p less than .01) than ventilated patients; 48 h later only PaCO2 was higher (p less than .01) in the former, and there were no differences between the two groups in the final set of measurements. There was a persistent left shift in the oxyhemoglobin dissociation curve (P50 at pH 7.4) in both groups throughout the study period. In contrast, the in vivo P50 was significantly lower in ventilated patients only at 24 h (22.7 +/- 2.2 vs. 25.8 +/- 1.5 torr, respectively, p less than .005). Our results suggest that changes of in vivo P50 in ventilated patients are probably related to the Bohr effect induced by mechanical ventilation. The latter swiftly corrects severe respiratory acidosis, causing an intra-erythrocytic alkalotic pH and raising the levels of 2,3-DPG.

2,3-Diphosphoglycerate↗
PubMed1998

Prognostic indicators of survival in ALS. ALS CNTF Treatment Study Group.

We analyzed data from the 245-patient placebo group of the ALS CNTF Treatment Study Group study, a large, prospective, multicenter study of recombinant human ciliary neurotrophic factor to determine prognostic factors for length of survival in ALS. Variables examined included baseline demographic characteristics, indices of disease severity, pulmonary function, and clinical laboratory tests. Shorter survival was associated with greater age, lower percent-predicted forced vital capacity (FVC%), and lower serum chloride at study entry. A shorter interval from symptom onset to diagnosis of ALS and greater weight loss in the 2 months before study entry also predicted shortened survival times. The rate of muscle strength loss before study entry did not predict risk of mortality. Serum chloride, reflecting the degree of respiratory acidosis, was identified for the first time as being correlated with prognosis in ALS. The relationship between a patient's FVC% and the probability of survival is described.

Acid-Base Equilibrium↗
PubMed1995

Clinical characteristics of adult asthmatics requiring intubation.

Fifty eight admissions for 52 adult asthmatics who required intubation were reviewed for the years of 1988-1995 to examine factors related to specific clinical patterns and profile the course of these patients. Of the 56 admissions where patients were intubated for respiratory failure and/or cyanosis, 5 were associated with significant complications of mechanical ventilation/intubation (pneumothorax, subcutaneous emphysema, aspiration pneumonia, and laryngeal edema) and there were no fatalities. Patients > or = 35 years of age had significantly more profound respiratory acidosis in initial arterial blood gases (pH = 7.14 versus 7.23, p = 0.03). In contrast, patients with a history of drug abuse or psychiatric disorders had lower mean pCO2 (p < = 0.01). The overall mean length of intubation was 17.6 hours, while the overall mean hospital stay was 6.6 days. Longer intubation times were associated with the occurrence of major complications, female gender, and hospital administration of ipratropium. Hospital stay was correlated with length of intubation, later month of admission, and earlier year of admission. Common precipitating factors noted for first admissions were upper respiratory infections (61%), followed by allergy or smoke exposure (13%), compliance related problems (12%), and drug abuse/inhalation (6%). Inhaled anti-inflammatory drugs, oral steroids or either were taken at the time of admission by 35%, 35% and 65% of the patients, respectively. There was an even distribution of patients with respect to medical insurance coverage type, admissions per season or year, ethnicity, marital status, and gender. We conclude that severe asthma resulting in respiratory failure is common despite the frequent use of anti-inflammatory asthma medications. Mechanical ventilatory support can be administered safely in the majority of these patients and should be considered early in acute asthma.

Adult↗
PubMed1990

Measurement of tidal volume using a pneumotachometer during high-frequency oscillation.

To assess the accuracy of a pneumotachometer (PN) for tidal volume (VT) measurements during high-frequency oscillation (HFO), we determined simultaneously VT using a PN and a full body plethysmograph (PL) in 12 rabbits. HFO was delivered with an oscillator at a frequency of 10 Hz, mean airway pressure of 8 cm H2O, and inspiratory time of 50%. Pressure amplitude (delta P) was varied as follows: 40, 60, 80, 20, 100, 40 cm H2O. Finally, in ten rabbits a spacer equal in deadspace (VD) to that of the PN (15 ml) was left in-line for 5 min. Blood gases were obtained before and after the spacer was added. We found that VT-PN correlates well with VT-PL (r = .92), although the difference between VT-PN and VT-PL is greater at large VT. Significant respiratory acidosis developed with the spacer in-line. PN may be used to trend VT during HFO but PN must not be left in-line, as increased VD seriously affects ventilation.

Animals↗