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Query: UMLS:C0001127 (respiratory acidosis)
 1,501 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of pancuronium bromide (Pavulon) on maternal circulation and metabolism as well as on fetal metabolism and postnatal conditions were studied in 13 women in late pregnancy (between gestational weeks 33 and 40) requiring Caesarean section in general anaesthesia. A comparison with results of 50 spontaneous deliveries without analgetics was performed. The average dosage of 4 mg did not effect the maternal blood pressure, fetal muscle tonus and cardiorespiratory adaption of the newborn. According to general anaesthesia we found in acid-base status a pH decrease with respiratory acidosis in comparison with spontaneous deliveries without anaesthetics, but pH and pCO2 were normalized 30 min after delivery. On the contrary, the oxygen tension were higher as at delivery as 30 min after delivery by Caesarean section. Although 1 minute Apgar score was lower than after spontaneous delivery the heart rate and frequency of ventilation were normal in every time and in the following minutes Apgar score was 7 to 10, too. An effect of pancuronium bromide to maternal or fetal carbohydrate metabolism could not be found. The less side effects on maternal cardiovascular system and the missing influence in postnatal condition recommand pancuronium bromide as a suitable relaxant in obstetrical anaesthesia, too.
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PMID:[The effects of Pavulon (pancuronium bromide) on maternal circulation and metabolism as well as on fetal metabolism and postnatal condition at Caesarean section (author's transl)]. 4 Mar 68

Plasma renin activity in acute respiratory acidosis and the effect of hexamethonium bromide was studied. Fourteen mongrel dogs were anesthetized with sodium pentobarbiturate and given 5% and 15% carbon dioxide in room air, successively. Hexamethonium bromide was given to 8 dogs prior to carbon dioxide inhalation. Arterial carbon dioxide partial pressure, oxygen partial pressure and pH were measured in addition to the determination of plasma renin activity. Plasma renin activity was elevated in moderate respiratory acidosis induced by 5% carbon dioxide inhalation from 37.5 +/- 8.8 ng/ml to 52.8 +/- 7.0 ng/ml. In severe respiratory acidosis produced by 15% carbon dioxide inhalation, plasma renin activity elevated further to 85.8 +/- 8.6 ng/ml. Plasma renin activity of the hexamethonium bromide treated dogs was 19.0 +/- 3.5 ng/ml during room air breathing. The activity was elevated to 26.0 +/- 6.4 ng/ml by 5% carbon dioxide inhalation and further to 57.3 +/- 5.9 ng/ml by 15% carbon dioxide inhalation. These findings may suggest that the elevation of plasma renin activity in acute respiratory acidosis induced by carbon dioxide inhalation is independent from sympathetic stimulation.
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PMID:Plasma renin activity in acute respiratory acidosis. 125 23

The effects of spinal cord transection and acidosis on succinylcholine (SCC)-induced hyperkalemia were studied in Sprague-Dawley rats. The effectiveness of pretreatment with subparalyzing doses ("self-taming") of SCC or with the cholinesterase inhibitor hexafluorenium bromide in preventing hyperkalemia was also studied. The increase in plasma potassium after administration of SCC (1 mg/kg) was found to be significantly increased 10 days after spinal cord transection. This potassium increase could not be prevented by pretreatment with either hexafluorenium (0.3 mg/kg) or subparalyzing doses (0.15 mg/kg) of SCC. Respiratory acidosis caused an increase in plasma K+ in both normal and in spinal cord transected rats. Acidosis had a synergistic effect on succinylcholine-induced hyperkalemia. These findings support the clinical practice of not using succinylcholine in patients at risk of having a pathological sensitivity to SCC. Furthermore, SCC may be especially dangerous when administered to patients who are acidotic.
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PMID:Synergistic effect of acidosis and succinylcholine-induced hyperkalemia in spinal cord transected rats. 671 Dec 67

Pancuronium bromide, a neuromuscular blocking agent, was evaluated in canine cataract surgical patients under general anesthesia to determine its effects on respiratory function and globe position. Two paralytic, anesthetic regimes were studied: one using a standard dosage of 0.066 mg kg-1 pancuronium bromide, given intravenously while providing the patient with ventilatory support, and one using a dosage of 0.022 mg kg-1 in which no ventilatory support was provided. Eye position and anterior vitreal position/displacement were recorded by a surgeon who was blinded as to treatment group. Physiological parameters indicative of respiratory function were monitored. Both dosages of pancuronium produced comparable, neutral globe position within 30 s following administration which lasted for 20-30 min. All patients in the standard dose group experienced uneventful anesthetic episodes with physiological parameters well within the normal ranges. Within 5 min after administration, all patients in the low-dose group developed a pronounced respiratory acidosis (mean arterial pH = 7.07 +/- 0.08; mean PaCO2 = 79.8 +/- 10.7 mmHg), which exceeded a set of predetermined safety limits, and subsequently these dogs received ventilatory support. We conclude that 0.022 mg kg-1 pancuronium rapidly produces an unacceptable level of respiratory acidosis and, as a result, patients receiving neuromuscular blocking agents should routinely receive ventilatory support.
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PMID:Respiratory function and extraocular muscle paralysis following administration of pancuronium bromide in dogs. 1139 21

Conventional pharmacotherapy of severe asthma and status asthmaticus includes beta2-sympathomimetics, theophylline, corticosteroids and occasionally topical anticholinergics (ipratropium bromide). Since hypoxemia is the most severe phenomenon in status asthmaticus the administration of oxygen is mandatory. However, if the bronchodilating therapy fails and hypoxemia continues, usually respiratory failure develops due to progressive respiratory muscle failure. An increasing PaCO(2) and respiratory acidosis are indications for mechanical ventilatory support to unload the failing respiratory pump. Nowadays, there is increasing consensus that ventilatory support should be administered primarily as non-invasive ventilation (NIV) via a face mask1. However, in a significant number of patients with severe asthma NIV is either contraindicated or insufficient. In this case usually the patient must be endotracheally intubated and mechanically ventilated "invasively". Intubation and ventilation of patients with severe asthma or status asthmaticus is associated with a high incidence of complications compared to patients ventilated for other causes of respiratory failure2,3. Therefore the risks of invasive mechanical ventilation have to be weighted carefully to ongoing conservative therapy and NIV. Cardiopulmonary arrest and severe hypoxemia in spite of O2 supplement and NIV are absolute criteria for intubation and ventilation. Mostly deterioration in mental status and exhaustion are the clinical findings leading to mechanical ventilation. Decision is guided rather by the course of the deterioration (how fast the patient's condition is worsening) than by pathological values alone. An increased PaCO(2) with moderate respiratory acidosis alone is not per se an indication for mechanical ventilation. However, a continuously rising PaCO(2) or the development of a severe metabolic acidosis after 1 hour of NIV is a strong argument for invasive mechanical ventilation. Other criteria are evidence of cardiac failure with fall in pulse volume and dysrhythmias, pneumomediastinum or pneumothorax (which has to be drained before mechanical ventilation!).
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PMID:Ventilating the patient with severe asthma: nonconventional therapy. 1276 62

A 39-year-old man presented to the emergency department (ED) in severe respiratory distress. He had a prior diagnosis of brittle asthma and had been admitted on several occasions but never previously ventilated. Therapy given in the first 3 hours of arrival included nebulized salbutamol (5 mg, x5), ipratropium bromide (0.5 mg), intravenous hydrocortisone (200 mg), and magnesium sulfate (2 g). His arterial blood gases continued to deteriorate. He was then given an intravenous bolus of salbutamol (250 microg) and heliox via facemask. His worsening status necessitated invasive ventilation. His hypercapnia and resultant respiratory acidosis improved rapidly, but there was a concurrent accumulation of lactic acid resulting in acidemia. This patient had lactic acidosis as a direct effect of administration of salbutamol. The development of hazardous salbutamol-induced toxicity in acute severe asthma is discussed.
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PMID:An under-recognized complication of treatment of acute severe asthma. 1841 Aug 27

Bromine (Br2 ) gas inhalation poses an environmental and occupational hazard resulting in high morbidity and mortality. In this review, we underline the acute lung pathology (within 24 h of exposure) and potential therapeutic interventions that may be utilized to mitigate Br2 -induced human toxicity. We discuss our latest published data, which suggest that an increase in heme-dependent tissue injury underlies the pathogenesis of Br2 toxicity. Our study was based on previous findings that demonstrated that Br2 upregulates the heme-degrading enzyme heme oxygenase-1 (HO-1), which converts toxic heme into bilverdin. Interestingly, following Br2 inhalation, heme levels were indeed elevated in bronchoalveolar lavage fluid, plasma, and whole lung tissue in C57BL/6 mice. High heme levels correlated with increased lung oxidative stress, lung inflammation, respiratory acidosis, lung edema, higher airway resistance, and mortality. However, therapeutic reduction of heme levels, by either scavenging with hemopexin or degradation by HO-1, improved lung function and survival. Therefore, heme attenuation may prove a useful adjuvant therapy to treat patients after Br2 exposure.
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PMID:Role of heme in bromine-induced lung injury. 2724 63