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PubMed1981

[Home-respirator treatment in idiopathic hypoventilation (author's transl)].

A report is given on a 66 years old patient with severe idiopathic hypoventilation. Two years ago the disease had developed rather suddenly with severe hypoventilation during sleep, accompanied by marked hypoxemia and hypercapnia with pCO2-values above 100mm Hg and respiratory acidosis. No pulmonary, cardiac or neurological disease was found. After failure of two attempts of stimulation of the phrenic nerve the patient was admitted to a respiratory intensive care unit and ventilated by a respirator during sleep. After improvement of this general condition he was discharged at first only in the daytime, later he could be discharged fully from the unit, after a respirator had been installed in his home. Now the patient is connecting himself to the respirator during sleep and since 20 months is so in a tolerable condition. The indications for home-respirator treatment are discussed.

Aged↗
PubMed1991

Compensatory mechanisms induced by high oropharyngeal airway resistance in rats.

Acid base balance changes were observed during 72 h following bilateral nasal obstruction in rats. Mouth breathing caused acute respiratory acidosis and marked aerophagia, leading to spontaneous death of the experimental animal 80 to 90 h postoperatively. Stenotic oropharyngeal airway, due to palatal-epiglottic approximation, is supposed to be responsible for respiratory insufficiency in the nose obstructed rats. The compensatory changes in respiratory mechanics caused by high oropharyngeal airway resistance, together with some possible reflex changes, may have caused either air swallowing or aspiration. As changes in acid base balance parameters did not show breakdown of the compensatory mechanisms during the first 72 h postoperatively, it is supposed that the increased air volume in stomach and guts, causing elevation of the diaphragm and paralytic ileus, contributed to the experimental animals' death.

Acidosis↗
PubMed1985

Pathogenetic factors in erosive gastritis.

Under physiologic conditions, luminal acid and pepsin are absolute requirements in the development of erosive gastritis and ulceration. Even the injurious effects of most drugs are potentiated by acid and pepsin. Although the importance of luminal acid has long been recognized, only in the last 10 years has evidence accrued showing the detrimental effects of tissue acidosis in producing injury to the gastric mucosa. It now seems clear that by whatever means it is produced, e.g., through reduced mucosal blood flow, metabolic or respiratory acidosis, or inhibition of acid secretion with subsequent decreased "alkaline tide," tissue acidosis plays a profound role in the pathogenesis of erosive gastritis and ulceration. The gastric mucosal barrier is now recognized as the anatomic integrity of the surface epithelium, rather than as an ethereal physiologic barrier. This barrier is maintained as an intact layer under physiologic conditions by a newly described rapid repair process called restitution.

Acid-Base Imbalance↗
PubMedDate not supplied

Respiratory and behavioural compensation during chronic severe loading in a hypoxic rat model.

1. Respiratory load compensation plays an important role in the maintenance of an appropriate level of ventilation. We investigated the ventilatory and behavioural responses to a severe load causing both hypercapnia and hypoxaemia in a rat model. 2. A thin silicone tube (15 mm in length, 1 mm ID) was implanted surgically in the trachea. Arterial blood gases and ventilatory and motor activities were assessed serially and non-invasively over a period of 8 weeks. 3. Ventilatory loading produced severe respiratory acidosis with concomitant hypoxaemia immediately after imposition of the load, but there was a considerable improvement of arterial blood gases at 1 day after the start of respiratory loading. Ventilatory loading also caused a gradual increase in ventilatory activity, requiring 7 days to reach the maximum level. There was a reduction in daily motor activity immediately after the ventilatory loading, but this reduction recovered gradually, together with recovery of reduced food and water intake. Administration of a hyperoxic gas mixture during the ventilatory loading decreased ventilatory activity while improving reduced motor activity. 4. These observations suggest that severe chronic ventilatory loading may induce adaptive responses that compensate rapidly for the disturbed acid-base balance with slow and gradual increases in ventilatory activity while matching the increase in motor activity/metabolic rate.

Animals↗
PubMed1988

Delayed muscular rigidity and respiratory depression following fentanyl anesthesia.

A delayed effect of fentanyl used for anesthesia may be respiratory distress several hours after surgery. The findings are muscular rigidity, fall in chest wall compliance, hypoventilation, respiratory acidosis, and hypotension. In the past, to our knowledge, this complication was exclusively reported in patients undergoing cardiac surgery, when large fentanyl dosages are employed. This article describes three general surgical patients in whom respiratory distress developed three to five hours following colon surgery when a moderate dose of fentanyl citrate, 55 to 75 micrograms/kg, was used. Initially, all patients had a normal recovery from anesthesia. Later, respiratory distress was successfully treated with a fentanyl antagonist and ventilatory assistance. This delayed toxic phenomenon is thought to be due to the reentry of fentanyl into plasma from deposits in adipose tissue, muscle, and the gastrointestinal tract, leading to a secondary rise in the plasma concentration. It is more likely to be encountered when hypothermia, rewarming, and acidosis are present in the postoperative period. This life-threatening complication is treacherous, since it may occur when the patient has been transferred to the surgical ward and is less closely monitored.

Aged↗
PubMed2000

Effect on lung function of continuous positive airway pressure administered either by infant flow driver or a single nasal prong.

UNLABELLED: The aim of this study was to assess if continuous positive airways pressure (CPAP) delivered by an infant flow driver (IFD) was a more effective method of improving lung function than delivering CPAP by a single nasal prong. A total of 36 infants (median gestational age 29 weeks, range 25-35 weeks) were studied, 12 who received CPAP via an IFD, 12 who received CPAP via a single nasal prong and 12 without CPAP. CPAP was administered post extubation if apnoeas and bradycardias or a respiratory acidosis developed or electively if the infant was of birth weight <1.0 kg. Lung function was assessed by the supplementary oxygen requirement and measurement of compliance of the respiratory system using an occlusion technique. Assessments were made immediately prior to and after 24 h of CPAP administration and at similar postnatal ages in the non-CPAP group. The infants who did not require CPAP had better lung function (non significant) than the other two groups before they received CPAP. After 24 h, lung function had improved in both CPAP groups to the level of the non CPAP infants. The supplementary oxygen requirements of all three groups decreased over the 24 h period, but this only reached significance in the single nasal prong group (P<0.05). Four infants supported by the IFD, but none with a single nasal prong, became hyperoxic. CONCLUSION: Continuous positive airways pressure administration via the infant flow driver appears to offer no short-term advantage over a single nasal prong system when used after extubation in preterm infants.

Humans↗
PubMed2005

Respiratory pathogenesis of amoebic gill disease (AGD) in experimentally infected Atlantic salmon Salmo salar.

The aim of this study was to investigate the respiratory responses of Atlantic salmon, Salmo salar, experimentally affected with amoebic gill disease (AGD). In Series I, arterial blood samples were taken over a 96 h period following amoebae addition to examine potential respiratory effects associated with initial exposure. No major significant treatment effects were found between fish exposed to amoebae and control (non-exposed) fish. Arterial pH (pHa) was seen to be significantly elevated at 48 h in AGD fish relative to the 0 h time point. To investigate the long-term respiratory effects associated with infection, fish were similarly exposed to amoebae and sampled over a 16 d period. As for Series I, caudal blood pH was significantly elevated by Day 2 (48 h) compared to the pre (Day 0)-time point, suggesting that initial exposure to amoebae and/or amoebae attachment may have induced an initial respiratory alkalosis via increased ventilation frequency and/or amplitude. From Day 7 onwards, and coinciding with a significant increase in the percentage of affected gill filaments, blood pH decreased significantly, possibly indicating the onset of the characteristic respiratory acidosis that has previously been described for experimentally AGD-affected Atlantic salmon. Although fish in this study showed up to 90% AGD-affected filaments, the corresponding respiratory results do not reflect a major acid-base disturbance. Therefore, the findings from the present study support the contention that, although AGD only affects the gill, AGD-associated mortality in Atlantic salmon may not be primarily associated with respiratory failure.

Acid-Base Equilibrium↗
PubMed1993

[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment].

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)

Arrhythmias, Cardiac↗
PubMed1993

Characterization of serum lysosomal enzymatic activities. III. Effect of infectious influenza in Egyptian equines.

An outbreak of infectious influenza was recognized in Menofeia governorate in October 1989. Eight naturally influenza infected as well as 8 healthy control horses, mules and donkeys were selected for collection of blood and sera separation to estimate four lysosomal enzymatic activities and to describe the clinical findings, which were fever, congested nasal, conjunctival membranes and cough. Bronchopneumonia followed later with bilateral purulent nasal discharge as a complication in 2 donkeys. Thereafter laboured breathing occurred. Therefore a therapeutic penicillin-streptomycin dose was injected to safeguard against the secondary bacterial invasion. All lysosomal enzyme levels in serum of diseased equines were subjected to consistent regression except N-acetyl-beta-glucosaminidase -beta-NAG) that behaved very highly significant activity, probably due to the acid pH resulting from bronchopneumonia and respiratory acidosis which override the inhibitory action of the antibiotics. Influenza virus may inhibit the synthesis of the pulmonary surfactant in alveolar and bronchial epithelium, thereafter, the animals suffered from respiratory distress and bronchospasm with resultant decreased acid phosphatase (ACP) value which was histochemically located in both sites. The disappearance of alpha- and beta-galactosidases (alpha-GAL & beta-GAL) from the serum of diseased animals can be attributed to the antibiotic dose.

Animals↗
PubMed1975

Influence of the neuroleptanalgesic combination of etorphine and acepromazine on the horse: blood gases and acid-base balance.

Respiratory function and acid-base variables were studied in Welsh Mountain ponies before and at predetermined times after the intravenous injection of Immobilon and Revivon.A marked depression of respiratory rate was accompanied by large reductions in arterial blood oxygen tension and saturation and the development of a mild respiratory acidosis following the injection of Immobilon. It was concluded that at least three factors contributed to the hypoxic hypoxia produced by Immobilon; the posture of lateral recumbency, the decrease in respiratory rate and the laboured character of the respiration. Arterial oxygen and carbon dioxide tensions returned towards control levels soon after administering Revivon. Mixed venous oxygen tensions were little affected by either Immobilon or Revivon, and mixed venous carbon dioxide tensions were increased to smaller degrees that those of arterial blood. Haemoglobin was increased initially by Immobilon, had returned to the control level by 30 min and fell below the control following the administration of Revivon.

Acepromazine↗
PubMed1986

The promotion of catecholamine release in rainbow trout, Salmo gairdneri, by acute acidosis: interactions between red cell pH and haemoglobin oxygen-carrying capacity.

A fall in blood pH was generated either by infusion of HCl or by reducing gill ventilation and raising blood PCO2 in rainbow trout, Salmo gairdneri Richardson. The acute acidosis resulting from HCl infusion caused an increase in plasma adrenaline and noradrenaline concentrations, the adrenaline increase being proportional to the decrease in blood pH. Fish subjected to a prolonged respiratory acidosis, caused by a reduction in gill ventilation, showed no increase in catecholamines 24 h after the change in gill ventilation. We suggest that catecholamine levels increase in response to a pH decrease, but if acidotic conditions are maintained, circulating catecholamines return to low levels. There was a much smaller decrease in erythrocytic pH with a fall in plasma pH when catecholamine levels were high. This ameliorating effect of catecholamines on erythrocytic pH during a plasma acidosis maintains the oxygen-carrying capacity of the haemoglobin. If erythrocytic pH was decreased by increasing blood PCO2 in vitro, then there was a fall in haemoglobin oxygen-carrying capacity which was proportional to the reduction in pH. We conclude that catecholamines are released into the blood in proportion to the fall in blood pH but if the pH is maintained the circulating catecholamines return to their initial low levels. The elevated catecholamine concentrations in blood safeguard against any impairment of haemoglobin oxygen-carrying capacity by maintaining erythrocytic pH in the face of a plasma acidosis.

Acidosis↗
PubMed1994

[A case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with bilateral recurrent nerve palsy and primary alveolar hypoventilation--comparative studies of the histological findings of the two sural nerve biopsies with 9 years interval].

A 27-year-old man noticed a tingling sensation in his fingers and toes in early 1982, at the age of 18 years, and his symptom gradually progressed in the following several months. In December 1982, based on neurological and laboratory examinations including the first sural nerve biopsy on the right side, a diagnosis of axonal sensory neuropathy of unknown etiology was made. During the following years, muscle weakness in the distal limbs and hoarseness developed and progressed, and the sensory impairments became gradually evident. On the second neurological examination in July 1991, he showed soft palate palsy and bilateral recurrent nerve palsy. The intrinsic muscles of hands and feet were atrophic, and pes cavus was noted bilaterally. There was mild to moderate weakness in the distal muscles of both limbs. Ankle jerk was absent and other tendon reflexes were decreased in both limbs. A mild to moderate decrease of both superficial and deep sensations with mild paresthesia was noted in both hands and feet. Routine laboratory findings were unremarkable. In blood gas analysis, hypercapnea and respiratory acidosis were found. Spirometry showed an increase of residual volume, and alveolar CO2-pulmonary ventilation response test suggested the presence of primary alveolar hypoventilation caused by hypofunction of the medullary respiratory center. In nerve conduction studies, motor nerve conduction velocities were moderately reduced in bilateral median and ulnar nerves. Distal latencies of M-waves were prolonged in bilateral median nerves. Temporal dispersion of M-wave was found in the left tibial nerve. The amplitudes of sensory action potentials were moderately reduced in bilateral median and sural nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2005

Cerebral and plasma kinetics of a high dose of midazolam and correlations with its respiratory effects in rats.

Benzodiazepine poisoning causes coma and respiratory depression. Our objective was to determine whether, and to what extent, arterial blood gas disturbances correlated with blood or cerebral kinetics of midazolam. A 160 mgkg(-1) single dose of midazolam was infused intravenously over 20 min in catheterized male Sprague-Dawley rats. Midazolam kinetics was simultaneously determined in plasma and brain using striatal microdialysis. Midazolam concentrations were measured using a high-performance liquid chromatographic assay with ultraviolet detection. Midazolam (160 mgkg(-1)) reproducibly induced deep coma with respiratory acidosis. Plasma midazolam kinetics was well described by a bi-exponential model, with an elimination half-life of 6.4+/-1.8 h. The striatal dialysate concentration peaked at 50.0+/-8.9 min after the end of infusion, with a significant delay to peak concentration compared to plasma. Respiratory depression, assessed by the elevation in PaCO2, was more closely correlated with midazolam striatal dialysate rather than plasma kinetics. These results suggest a central mechanism for midazolam respiratory effects at toxic doses in rats. In conclusion, our study showed a delayed onset in peak PaCO2 and pH effects after the slow infusion of a toxic dose of midazolam in rats. The effects on arterial blood gases were better correlated with midazolam striatal concentrations than with plasma concentrations. This study may contribute to better understanding of benzodiazepine-induced respiratory depression in poisonings.

Acidosis↗
PubMed1988

Delayed respiratory depression following fentanyl anesthesia for cardiac surgery.

High-dose fentanyl anesthesia is widely used in cardiac surgery. Its immediate side-effects are well known. However, its late adverse effect manifested by extreme truncal rigidity, decreased chest wall compliance, hypoventilation, respiratory acidosis and hemodynamic instability is not sufficiently appreciated. Of 380 patients who underwent aortocoronary artery bypass under high-dose (100 micrograms/kg) fentanyl anesthesia, 29 (7.6%) developed the sudden onset of extreme thoracic and abdominal rigidity, leading to respiratory depression 2 to 6 h postoperative, after an apparently normal recovery from the anesthesia. In 15 patients, a high plasma level of fentanyl (5.2 to 7.8 ng/ml) correlated with the clinical events. Administration of naloxone or a muscle relaxant rapidly reversed this late complication of fentanyl, thought to be due to re-entry of fentanyl into plasma from deposits in adipose tissue, muscle and the GI tract, leading to a secondary peak in plasma fentanyl. It is more likely to be encountered when hypothermia, rewarming, and acidosis occur in the postoperative period. Awareness of this life-threatening complication is critical in patients undergoing surgery with fentanyl anesthesia.

Aged↗
PubMed2000

Elective use of nasal continuous positive airways pressure following extubation of preterm infants.

UNLABELLED: The aim of this study was to determine whether elective use of nasal continuous positive airways pressure (CPAP) following extubation of preterm infants was well tolerated and improved short- and long-term outcomes. A randomized comparison of nasal CPAP to headbox oxygen was undertaken and a meta-analysis performed including similar randomized trials involving premature infants less than 28 days of age. A total of 150 infants (median gestational age 30 weeks, range 24-34 weeks) were randomized in two centres. Fifteen nasal CPAP infants and 25 headbox infants required increased respiratory support post-extubation and 15 nasal CPAP infants and nine headbox infants required reintubation (non significant). Eight infants became intolerant of CPAP and were changed to headbox oxygen within 48 h of extubation; 19 headbox infants developed apnoeas and respiratory acidosis requiring rescue nasal CPAP, 3 ultimately were re-intubated. Seven other trials were identified, giving a total number of 569 infants. Overall, nasal CPAP significantly reduced the need for increased respiratory support (relative risk, 0.57, 95% CI 0.43-0.73), but not for re-intubation (relative risk 0.89, 95% CI 0.68-1.17). Nasal CPAP neither influenced significantly the intraventricular haemorrhage rate reported in four studies (relative risk 1.0, 95% CI 0.55, 1.82) nor that of oxygen dependency at 28 days reported in six studies (relative risk 1.0, 95% CI 0.8, 1.25). In two studies nasal CPAP had to be discontinued in 10% of infants either because of intolerance or hyperoxia. CONCLUSION: Elective use of nasal continuous positive airways pressure post-extubation is not universally tolerated, but does reduce the need for additional support.

Female↗
PubMed1980

Maternal halothane anesthesis reduces cerebral blood flow in the acidotic sheep fetus.

Cerebrovascular autoregulation is lost during fetal asphyxia as cerebral vessels undergo compensatory vasodilation. In such a situation, maternal anesthetics, which decrease fetal arterial blood pressure and cardiac output, may further aggravate cerebral hypoxia. To examine this possibility, we prepared six pregnant ewes in such a manner as to be able to measure fetal regional cerebral blood flow in utero during acidosis produced by partial umbilical cord compression both before and after 15 minutes of halothane anesthesia given to the mother. Umbilical cord compression in the absence of anesthesia caused fetal metabolic and respiratory acidosis as evidenced by a decrease in arterial pH from 7.34 to 7.05; fetal arterial oxygen saturation simultaneously decreased from 29 to 17%. Halothane anesthesia administered to the mother of the acidotic fetus caused further aggravation of fetal acidosis (arterial pH 6.85) and oxygen desaturation (10%) and the fetus became markedly hypotensive. Blood flow to four cerebral areas increased 27 to 69% above control levels in the fetus during acidosis in the absence of maternal anesthesia but decreased to levels 30 to 42% below acidosis values when maternal anesthesia was combined with fetal acidosis. These data suggest that potent cardiovascular depressant anesthetics administered to the mother in the presence of fetal acidosis could decrease fetal cerebral oxygen delivery by interfering with fetal cardiovascular compensation during acidosis and reducing fetal cerebral blood flow.

Acid-Base Equilibrium↗
PubMed1986

Myocardial intracellular pH in a perfused rainbow trout heart during extracellular acidosis in the presence and absence of adrenaline.

Myocardial intracellular pH was measured in a perfused rainbow trout, Salmo gairdneri, with DMO (5,5-dimethyl-2,4-oxazlidinedione), to test the hypothesis that catecholamines promote active regulation of myocardial pH in order to protect contractility during a respiratory acidosis comparable to that observed after exercise. Under control conditions (extracellular pH = 8.0; PCO2 = 2 Torr), myocardial pH was 7.53 +/- 0.01 (N = 5). Acidosis (extracellular pH = 7.45; PCO2 = 8.6 Torr) reduced contractility, mechanical efficiency and intracellular pH (7.25 +/- 0.04), but did not affect myocardial O2 consumption. The addition of 0.5 mumol l-1 adrenaline during extracellular acidosis prevented the loss of contractility, restored mechanical efficiency, but did not change intracellular pH significantly. Thus, adrenaline enabled cardiac contractility to recover, without intracellular pH regulation, possibly by modulation of sarcolemmal calcium changes. The absence of a myocardial acidosis after exercise in vivo is discussed with respect to possible intracellular pH regulation via lactate uptake and metabolism.

Acidosis↗
PubMed2004

Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthetic implications.

The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.

Airway Obstruction↗