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At least 703 records · Page 39Linked to original sources
PubMed1981

Intraocular and intracranial pressure during respiratory alkalosis and acidosis.

Intraocular and intracranial pressures (IOP and ICP) were measured at four different arterial carbon dioxide tensions by direct continuous techniques in Rhesus monkeys during anaesthesia with halothane and nitrous oxide. Increases in IOP correlated significantly with PaCO2 ranging from 2.66 to 10.24kPa (P less than 0.001). Increases in ICP correlated significantly (P less than 0.001) with PaCO2 between 2.66 and 7.71 kPa, but plateaued thereafter. When PaCO2 was decreased rapidly, PaCO2, IOP and ICP decreased exponentially with similar half-times. The fast changes in IOP and ICP can probably be explained by an alteration of intraocular and intracranial blood volumes. IOP usually remained within the normal range, even at maximum PaCO2.

Acidosis, Respiratory↗
PubMed1986

Assisted ventilation in severe acute asthma.

During the period 1973-85 assisted ventilation was used for the treatment of severe asthma on 48 occasions in 18 patients (one patient was ventilated 29 times). On each occasion arterial blood gas abnormalities were restored to normal as quickly as possible irrespective of peak inflation pressures. One patient was thought to be brain dead on transfer from another hospital but was ventilated for 48 hours while this diagnosis was confirmed. There was one episode of mediastinal emphysema. There were no other complications apart from transient hypotension (blood pressure less than 100/60 mm Hg), which occurred on 17 occasions but did not have any sequelae. There was no relationship between hypotension and inflation pressure but there was an association between hypotension and rate of fall of arterial carbon dioxide tension. It is concluded that the risks of barotrauma during the ventilation of patients with severe asthma are theoretical or extremely small. Rapid correction of respiratory acidosis abolishes hypercapnic respiratory drive, allowing ventilation without use of muscle relaxants. It may also enable a shorter duration of ventilation, thus decreasing the likelihood of complications.

Acute Disease↗
PubMed1992

A combination of methotrimeprazine, midazolam and guaiphenesin, with and without ketamine, in an anaesthetic procedure for horses.

A combination of 0.5 mg/kg of methotrimeprazine, 0.1 mg/kg of midazolam and 100 mg/kg of a 10 per cent guaiphenesin solution was investigated for the induction of recumbency in 15 horses; the addition of 1.6 mg/kg of ketamine was also evaluated in 15 horses and anaesthesia was maintained with halothane in oxygen. The horses became recumbent quickly and smoothly and they recovered quietly, with little ataxia. Tachycardia occurred after induction, but no other changes from pre-operative values were observed until halothane in oxygen had been given, when hypothermia, hypotension, bradypnoea, hyperoxaemia, respiratory acidosis and decreased respiratory minute volume developed. Horses given ketamine in addition to methotrimeprazine, midazolam and guaiphenesin were easier to intubate and recovered more quickly than horses receiving only methotrimeprazine, midazolam and guaiphenesin.

Anesthesia↗
PubMed1996

Response of LLC-PK1-F+ cells to metabolic acidosis.

The role of extracellular glutamate formation as opposed to cellular glutamate removal in regulating monolayer glutamate content in response to metabolic acidosis was studied in LLC-PK1-F+ cells. Exposure to metabolic acidosis (14 mM bicarbonate; pH 7.1) for 18 h resulted in 24% fall in monolayer glutamate content. Of this, approximately one-half could be attributed to enhanced glutamate removal via glutamate dehydrogenase, consistent with a rise in ammonium production. The remainder appears due to reduced extracellular glutamate formation as a consequence of diminished gamma-glutamyltranspeptidase (gamma-Gt) activity. Metabolic acidosis, but not respiratory acidosis, resulted in a 33% fall in gamma-Gt activity and a proportional fall in extracellular glutamate formation; glutamate transport into these cells was not rate limiting in acidosis. Overall glutamine utilization decreased 36%, reflecting the fall in gamma-Gt activity as well as a decrease in a pH-sensitive glutamine uptake, whereas glutamine transport coupled to the phosphate-dependent glutaminase flux increased. It is noteworthy that the increased ammonium produced in metabolic acidosis was preferentially secreted into the apical compartment; acid secretion, but not production, was similarly increased. Thus reduced cellular glutamate appears to coordinate activation of intracellular glutaminase to the apical membrane exchanger, consistent with the functioning kidney response to metabolic acidosis.

Acidosis↗
PubMed1990

Triggering of erythropoietin production by hypoxia is inhibited by respiratory and metabolic acidosis.

Erythropoietin (EPO) production in response to hypoxic hypoxia is known to be attenuated by simultaneous hypercapnia. This study aimed to investigate whether this inhibitory effect of hypercapnia is 1) a direct effect of carbon dioxide or mediated by changes in pH or bicarbonate, 2) affects also carbon monoxide hypoxia, and 3) influences either the synthesis and release of EPO or the mechanisms by which hypoxia triggers an increase in EPO production rate. We found that EPO formation in mice exposed to normobaric hypoxia (8% O2) or to carbon monoxide (0.1%) was reduced by 30 and 42% when animals were simultaneously exposed to hypercapnia (7% CO2), by 35 and 38% when subjected to metabolic acidosis (NH4Cl), and unchanged when subjected to metabolic alkalosis (NaHCO3). In animals exposed to brief hypoxia (15 min) and subsequent normoxia (2 h), metabolic acidosis did not affect EPO levels when initiated after the hypoxic period. The results indicate that acidosis inhibits hypoxia-induced triggering of EPO formation independently of PCO2 and HCO3 levels. Because this inhibitory effect is also present during carbon monoxide hypoxia, it appears not solely due to potentiated hyperpnea. Alternatively, it may result from a facilitated intrarenal oxygen release or a direct effect at the EPO production sites.

Acid-Base Equilibrium↗
PubMed1999

Pulmonary vascular responses during acute and sustained respiratory alkalosis or acidosis in intact newborn piglets.

Acute alkalosis-induced pulmonary vasodilation and acidosis-induced pulmonary vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro studies have found that relatively brief periods of sustained alkalosis can enhance, and sustained acidosis can decrease, vascular reactivity. In this study of intact newborn piglets, effects of acute (20 min) and sustained (60-80 min) alkalosis or acidosis on baseline (35% O2) and hypoxic (12% O2) pulmonary vascular resistance (PVR) were compared with control piglets exposed only to eucapnia. Acute alkalosis decreased hypoxic PVR, but sustained alkalosis failed to attenuate either baseline PVR or the subsequent hypoxic response. Acute acidosis did not significantly increase hypoxic PVR, but sustained acidosis markedly increased both baseline PVR and the subsequent hypoxic response. Baseline PVR was similar in all piglets after resumption of eucapnic ventilation, but the final hypoxic response was greater in piglets previously exposed to alkalosis than in controls. Thus, hypoxic pulmonary vasoconstriction was not attenuated during sustained alkalosis, but was accentuated during sustained acidosis and after the resumption of eucapnia in alkalosis-treated piglets. Although extrapolation of data from normal piglets to infants and children with pulmonary hypertension must be done with caution, this study suggests that sustained alkalosis may be of limited efficacy in treating acute hypoxia-induced pulmonary hypertension and the risks of pulmonary hypertension must be considered when using ventilator strategies resulting in permissive hypercapnic acidosis.

Acidosis, Respiratory↗
PubMed2006

[Non-invasive ventilation support in patients with acute exacerbation of chronic obstructive pulmonary disease (COPD)].

AIM: To verify that the use of noninvasive ventilatory support in acute exacerbation of chronic obstructive pulmonary disease leads to decreasing the number of deaths, shortening in-hospital stay and decreasing number of endotracheal intubations (ETI). SETTING: The study was conducted at a respiratory department's ICU in 2002-2004. METHODS: Patients hospitalized on ICU with acute exacerbation of COPD, respiratory acidosis and global respiratory failure were randomised into two groups. Patients in group A were treated by conservative medical therapy (oxygen, bronchodilator, corticosteroid), patients in group B received noninvasive ventilation with face mask. The parameters followed were: decrease in the number of deaths, shortening of ICU stay, reduction of ETI, faster improvement of breathing frequency, heart rate, pH, PaO2, PaCO2, lactate, dyspnoea symptom score and lung functions. RESULTS: Each group consisted of 30 randomised patients. There were 10 intubated patients in group A, as opposed to 3 in group B (N = 60; P = 0.034). Average length of ICU stay was 9.8 days in group A and 7.1 days in group B (N = 60; P = 0.756). Mortality rate was identical in both groups: 3 patients survived, 7 patients died. We found faster decrease of breathing frequency after one hour of noninvasive ventilation in group B (28.3 +/- 7.1 vs. 24.6 +/- 6.3, N = 59, p = 0.03). CONCLUSION: No difference was found in mortality rate. We observed decreasing of ETI rate with NIV. We found a tendency to shortening of ICU stay. There was faster improvement of breathing frequency after one hour of NIV.

Acute Disease↗
PubMed1991

Arterial and mixed venous blood acid-base balance during hypoperfusion with incremental positive end-expiratory pressure in the pig.

The authors sought to determine how hypoperfusion influences acid-base balance in arterial and mixed venous blood. In anesthetized, ventilated pigs (n = 12), we determined hemodynamics, O2 uptake, CO2 output, dead-space ventilation, arterial and mixed venous blood acid-base balances, and lactate concentrations during graded reductions in cardiac output by incremental positive end-expiratory pressure (PEEP, 0-20 cm H2O). Cardiac output decreased from 3.2 +/- 0.2 (mean +/- SEM) to 1.2 +/- 0.1 L/min at 20 cm H2O PEEP. Oxygen delivery declined more than O2 uptake did by 60% +/- 2% and 27% +/- 2%, respectively. The decrease in CO2 output (by 21% +/- 2%) was less than that in O2 uptake. Fractional dead-space ventilation increased. At a slight increase in carbon dioxide tension (PCO2) of 4 +/- 1 mm Hg, pH decreased in arterial blood from 7.54 +/- 0.01 to 7.47 +/- 0.02 mmol/L, and standard bicarbonate decreased from 30.3 +/- 0.5 to 27.5 +/- 0.6 mmol/L. The decrease in standard bicarbonate exceeded the increase in blood lactate concentrations. At a similar decrease in standard bicarbonate, the decrease in pH was larger (P less than 0.005) in mixed venous blood than in arterial blood owing to a larger increase in PCO2 (from 40 +/- 2 to 50 +/- 2 mm Hg, P less than 0.005). The changes were reversed after discontinuing PEEP. The authors conclude that ischemia after incremental PEEP results in tissue metabolic acidosis with superimposed respiratory acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMedDate not supplied

Ledacrine effect on free fatty acids and glycerol mobilization from rat adipose tissue in vivo.

In rats receiving intraperitoneally Ledacrine in toxic doses the free fatty acids (FFA) and glycerol serum levels and the amount of fatty acids and glycerol released from the epididymal tissue of the rats were determined during one-hour incubation in vitro. It was found that Ledacrine in toxic doses stimulated the process of lipolysis as evidenced by raised serum FFA and glycerol levels and increased amount of FFA and glycerol released from the epididymal adipose tissue in vitro in relation to the values in control rats. The results of investigations of acid-base equilibrium parameters indicated that Ledacrine in toxic doses caused in rats metabolic acidosis associated with respiratory acidosis.

Acid-Base Equilibrium↗
PubMed1997

[Evaluation of hyperkinetic cardiac arrhythmia in chronic obstructive bronchopneumopathy].

Patients with chronic obstructive pulmonary disease (COPD), especially during acute exacerbations of their disease, show a greater incidence of cardiac arrhythmias than healthy subjects of the same age. The type of arrhythmias found may be supraventricular (premature atrial beats, paroxysmal supraventricular tachycardia, multifocal atrial tachycardia, atrial flutter, atrial fibrillation) or ventricular (premature ventricular beats, sustained ventricular tachycardia, torsades de pointes, ventricular fibrillation) that may lead to sudden cardiac death. The pathogenesis of arrhythmias is complex and many factors may be involved such as hypoxemia, hypercapnia, respiratory acidosis, metabolic and respiratory alchalosis, hypokalemia, concomitant ischemic heart disease, chronic cor pulmonale, left ventricular diastolic dysfunction. Remarkable attention has been drawn to the possible arrhythmogenic effect of drugs such as theophylline, beta-adrenergic stimulants and digitalis which are commonly used in the therapy of COPD. Both of the main classes of bronchodilators (methylxanthynes and beta-adrenergic agonists), even when used together, apparently do not increase the incidence of dangerous cardiac arrhythmias. However, these drugs should be used with caution in the elderly, in patients with preexisting cardiac arrhythmias, with heart disease or with reduced hepatic function. In these cases Holter monitoring, repeated measurements of plasma drugs concentration and prompt hospitalization of high risk patients in Intensive Care Unit may be needed.

Adrenergic beta-Agonists↗