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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 respiratory acidosis on the pancreas were studied in 25 Wistar rats. Ligation of the duct combined wiht respiratory acidosis resulted in the development of acute pancreatitis. In explantation of the results it is suggested that exhaustion of the buffering capacity causes a dramatic fall in pH of the pancreatic juice. The clinical relevance of findings is discussed.
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PMID:[The role respiratory acidosis in the development of acute pancreatitis (author's transl)]. 3 13

The present work was undertaken to elucidate the underlying causative factors limiting survival in hypothermic rats (non-hibernator) and hamsters (hibernator). A variety of physiological and biochemical parameters were measured for 28 male Wistar rats (205-286 g) and 26 male golden hamsters (85-118 g) before and during induction of hypothermia to colonic temperature (Tco) of 18 degrees C. With progressive decreases in Tco, parallel falls in VO2, VCO2, and heart rate were observed. In rats, plasma pH (pHp) in arterial blood was significantly lowered from 7.453 at Tco of 38 degrees C to 7.327 at Tco of 18 degrees C (p less than 0.001). From the observations of increased arterial PCO2 and bound CO2 (bicarbonate ion) concentration, together with the unchanged blood lactate, respiratory acidosis caused by hypoventilation was suggested to be responsible for the decrease in pHp. In contrast to rats, in hamsters pHp was almost unchanged during the induction of hypothermia, while nearly complete depletion of blood glucose (-84.6%) and liver glycogen (-99.5%) were observed when Tco of 38 degrees C was lowered to 18 degrees C. It is concluded that the decrease in pHp is a limiting factor for rats to survive the deep hypothermia at Tco of 18 degrees C and the exhaustion of carbohydrates as an energy supply for hamsters.
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PMID:Difference in the mode of acute cold-induced hypothermia between rat and hamster. 311 20

Non-invasive continuous positive airway pressure (CPAP) seems to decrease the need for intubation in patients with severe cardiogenic pulmonary oedema (CPO) in the intensive care unit. The goals of our study were to delineate indications for CPAP in the emergency department, and to confirm its usefulness in such a setting. We retrospectively assess the evolution of all patients ventilated under CPAP for an acute hypoxaemic respiratory failure over a 1-year period (n = 64 patients). Hypercarbia and respiratory acidosis were present in most patients with CPO (PaCO2 = 54.4+/-22.3 mmHg; pH = 7.27+/-0.13), according to respiratory exhaustion, although initial PaCO2 was low in the pneumonia group. There was a significant improvement of arterial blood gases after 1 hour of ventilation in the CPO group (PaO2 = 254.1+/-121.0 mmHg; PaCO2 = 44.0+/-12.6 mmHg; pH = 7.34+/-0.08; p < 0.0001 for both parameters). In the pneumonia group, oxygenation was also improved but with the persistence of a significant shunt (PaO2 = 157.6+/-84.4 mmHg). Fifty-four patients (84%) were considered as successfully ventilated under CPAP, with no need for intubation and a favourable evolution, mainly in the CPO group. No side effects were reported. In conclusion, CPAP is a useful and easy-to-use ventilatory device in the emergency department. It is now one of our first line treatments during prehospital and emergency care of patients with CPO.
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PMID:Non-invasive continuous positive airway pressure in acute hypoxaemic respiratory failure--experience of an emergency department. 982 33

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

Chronic heart failure (CHF) is a common condition and is associated with excess morbidity and mortality, in spite of the many advances in its treatment. Chronic stable heart failure is also associated with an increased incidence of sleep-related breathing disorders, such as central sleep apnoea (CSA) and Cheyne Stokes respiration (CSR). Continuous positive airways pressure (CPAP) has been shown to alleviate the symptoms of CHF, improve left ventricular function and oxygenation. To a certain extent, CPAP also abolishes sleep-related breathing disorders in patients with chronic heart failure. In patients with acute pulmonary oedema, the use of positive pressure ventilation improves cardiac haemodynamic indices, as well as symptoms and oxygenation, and is associated with a lower need for intubation. However, some studies have cast doubts about its safety and suggest a higher rate of myocardial infarction associated with its use. In our opinion, non-invasive positive pressure ventilation and CPAP offers an adjunctive mode of therapy in patients with acute pulmonary oedema and chronic heart failure, who may not be suitable for intubation and in those not responsive to conventional therapies. Non-invasive ventilation also helps to improve oxygenation in those patients with exhaustion and respiratory acidosis. Many trials are still ongoing and the results of these studies would throw more light on the present role of non-invasive ventilation in the management of CHF.
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PMID:Positive pressure ventilation in the management of acute and chronic cardiac failure: a systematic review and meta-analysis. 1638 32

The present study examined the effects of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exhaustive exercise. Six male subjects underwent exercise of increasing intensity until exhaustion: (1) breathing air = MAX (maximal exercise), or (2) under hypercapnia (HC: 21% O(2), 6% CO(2)) that had been maintained from 60 min before to 30 min after exercise = HC; and (3) exercise of the same intensity as HC in air = SUB (submaximal exercise). Arterialized blood was drawn from a superficial vein. Blood pH in HC was significantly lower than in MAX or SUB at rest, at the end of exercise and throughout recovery (P<0.05). Plasma lactate and ammonia concentration in HC was significantly lower than in MAX (P<0.05), and similar to that in SUB at the end of exercise and throughout recovery. Respiratory acidosis resulting from hypercapnia shifted the linear lactate to blood pH relationship during exhaustive exercise below that at normocapnia (P<0.001). The reduced slope of linear blood pH to ammonia relationship under hypercapnia (P<0.001) is attributed to lactic acidosis that is less, due to the lesser work intensity at the end of exhaustion, than that of normocapnia. From these results we conclude that (1) hypercapnia-induced respiratory acidosis promoted the decrease in blood pH due to lactate production throughout recovery; (2) plasma lactate concentration at maximal exercise was lowered under hypercapnia; (3) plasma ammonia concentration at maximal exercise was reduced, probably due to a less intense lactic acidosis.
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PMID:Effect of hypercapnia on changes in blood pH, plasma lactate and ammonia due to exercise. 1619 39