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

Respiratory acidosis of severe acute asthma is a severity factor. In this paper the treatment of associated metabolic acidosis is discussed. Among 34 consecutive episodes of severe acute asthma with acidosis (pH < 7.35) treated with continuous adrenaline perfusion, theophylline and hydrocortisone hemisuccinate, respiratory acidosis was observed in 12, metabolic acidosis in 2 and mixed respiratory and metabolic acidosis in 20. The association of hypercapnic acidosis with hypochloraemic acidosis reflected a time of installation longer than when respiratory acidosis only was present (p < 0.05). Among the 22 patients who had metabolic acidosis on admission, 14 were treated with 168 +/- 82 mmol of sodium bicarbonate, the remaining 8 patients being untreated and acting as controls. The rapidity with which pH was corrected was the same in the treated and untreated groups (9.1 +/- 5.5 hours vs 6.7 +/- 3.7 hours), whereas dyspnoea (respiratory rate < 18/min) was more rapidly corrected in the treated group that in controls (11.6 +/- 5.7 hours vs 5.9 +/- 5.9 hours; p < 0.05). It is concluded that in more than 50% of the cases respiratory acidosis of severe acute asthma is associated with a metabolic acidosis. Correcting this metabolic acidosis with sodium bicarbonate results in improvement of respiration, perhaps by facilitating the action of bronchodilator catecholamines.
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PMID:[Metabolic acidosis in severe acute asthma. Effect of alkaline therapy]. 133 76

Problems facing a patient with severe dyspnea secondary to diaphragmatic herniation are hypoxia, hypercarbia and respiratory acidosis, and cardiovascular instability. It is easy to precipitate a crisis in these patients during anesthetic induction as a result of stress, bad positioning, induction of pneumothorax, or inappropriate anesthetic technique. These patients require a smooth, stress-free perianesthetic period with preoxygenation, positioning with the affected side down, rapid intravenous induction, endotracheal intubation, and mechanical ventilation. Maintenance with isoflurane is preferred, and nitrous oxide should be avoided. Close monitoring of the cardiovascular and pulmonary systems is essential. Recovery from anesthesia should include oxygen supplementation, pleural drainage, and local analgesia if required.
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PMID:Anesthesia for patients with diaphragmatic hernia and severe dyspnea. 158 3

The report describes seven SMA-cases in descendents of crossbreeds of American Brown Swiss x Deutsches Braunvieh. Symptoms and course: After initially normal development of the calves for one to six weeks the disease set in suddenly followed by a rapid lethal course of one to one and a half weeks duration due to asphyxia and/or secondary diseases. Only one case was reported having been sick since birth (?). Characteristic signs were rapidly progressing muscular atrophy, paresis and paralysis of the limbs, the trunk and the diaphragm, usually accompanied by progressive dyspnoea. Signs of congenital neuromyodysplasia (arthrogryposis) of different degree were present in four of the seven calves. Six calves had contracted a secondary pneumonia. Blood gas analysis (6/7) revealed a compensated (1x) or decompensated (4x) respiratory acidosis. Neurohistological findings: Degeneration and loss of motor neurons in the ventral horns of the spinal cord and neurogenic muscular atrophy. Immunohistochemistry revealed a pronounced accumulation of type 200 kD-neurofilaments in perikarya and dendrites of ventral horn motoneurons indicating disturbed mechanisms of the axonal transport. The disease seems to be inherited as a recessive trait.
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PMID:[Spinal muscle atrophy in Brown Swiss x Braunvieh cross calves]. 163 59

Three patients presented respiratory abnormalities following Crotalus durissus snakebite. These abnormalities appeared in the first 48 h after the snake bite and consisted of dyspnea, tachypnea, use of accessory muscles of respiration (cases 1 and 2) and flaring of the nostrils (case 2). Cases 1 and 2 developed acute respiratory failure. Case 2, 24 h after the snakebite presented difficult breathing and periods of apnea. He was intubated in the emergency room and transferred to the intensive case unit where he arrive with spontaneous breathing. His respiratory pattern worsened and measurement of arterial pH and blood gases showed metabolic and respiratory acidosis with partial carbon dioxide pressure increasing from 40 to 50.3 mmHg compatible with acute ventilatory failure. Both patients needed mechanical ventilation. Weaning from the ventilator was accomplished after 33 days in case 1 and after 15 days in case 2. Both patients also presented acute renal failure treated with peritoneal dialysis with full recovery of the renal function. Measurements of forced vital capacity (FVC) and forced expiratory volume in the first second (FEV 1.0) was carried out 58 hours after the snakebite in case 3. Both FVC and FEV 1.0 were reduced in relation to the predicted values (60 and 67% respectively) but the ratio FEV 1.0/FVC was in the normal range. These findings were compatible with a restrictive pattern of ventilatory failure. Serial measurements showed progressive increase of both FVC and FEV 1.0 reaching 72 and 79% of the predicted values, respectively, in the 10th day after the snakebite.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Respiratory involvement secondary to crotalid ophidian bite (Crotalus durissus)]. 184 45

A 15-months-old boy underwent the intra-cardiac repair with a glutaraldehyde-preserved equine pericardium for total anomalous pulmonary venous connection (Darling's type IIb). Because of rapidly progressive dyspnea, tachycardia and respiratory acidosis, he required emergent reoperation at 234 postoperative days. The pseudointima was thickened heavily and detached from glutaraldehyde-preserved equine pericardium. New channel was created with a piece of EPTFE sheet to prevent obstruction of pulmonary venous flow. However, about four months after second surgery, cough and tachycardia progressed again remarkably. Intra-atrial channel was obstructed between EPTFE sheet and the partition from pulmonary venous orifice to the atrial septal defect in the third operation. The intra-atrial channel was enlarged by cut-back method using EPTFE sheet again. His postoperative hemodynamics were satisfactory
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PMID:[Recurrent surgery for pulmonary venous obstruction after total correction of TAPVC (IIb)]. 189 90

A case is reported of acute respiratory failure occurring during upper abdominal surgery in a patient not previously known to have chronic respiratory failure. Preoperatively, this 68 year old patient presented with mild obesity, slight effort dyspnoea and paralysis of the right hemidiaphragm, a sequela of polytrauma she suffered the year before. Respiratory tests were not considered useful with regard to the results of clinical examination. Moreover, she had already several previous general anaesthetics without any problems. A thoracic epidural anaesthesia was performed with a mixture of 150 mg lidocaine, 37.5 mg bupivacaine with adrenaline and 100 micrograms fentanyl, injected in the T8-T9 epidural space via a catheter. Ten minutes after the starting of surgery, the patient became agitated and complained of difficulty in breathing. Blood gas analysis showed hypercapnia, with respiratory acidosis (Pao2: 28.19 kPa; Paco2: 9.2 kPa; pH 7.273). Clinical examination revealed a bilateral Horner syndrome (T1-T4 sympathetic blockade). The patient was intubated and ventilated after adequate sedation. She was extubated 3 h 30 min after the initial epidural injection. Epidural analgesia was maintained during 72 h, with 0.1% bupivacaine, with no recurrence of respiratory failure.
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PMID:[Transient acute respiratory failure and thoracic epidural anesthesia]. 273 73

The clinical experience of 661 children with bronchiolitis is reported in four-years period to gain a better understanding of diagnosis and pathogenesis of bronchiolitis. Upper airways infections, expiratory dyspnea, clear sound by chest percussion, vesicular rales and whistling by chest auscultation, air trapping on the chest radiography were considered as essential data of diagnosis. It was found in 595 patients: expiratory dyspnea, air trapping, vesicular r. and whistling in 85% and whistling only in 15%; hypoxemia in 20% combined with hypercapnic acidosis in 10%; normoxemia in 80% combined with hypocapnia in 54%; hyperlactemia in 64% combined with an increment in the serum of CPK in 50% and of GPT in 30%; virus were cultured in 27%, adenovirus and RSV were identified in 90%. Instead it was found in 66 patients: air trapping but no difficult breath, with normal chest auscultation; crisis of cyanosis or paleness-cyanosis chilly sweat in 80% were motive of admission. The clinical and/or radiological features of "air trapping" were considered as essential symptoms and signs of bronchiolitis. The insufficient systemic perfusion was considered as a frequent occurrence and as cause for sudden respiratory and circulatory emergency.
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PMID:[Bronchiolitis. Our clinical experience in the 4 years from 1981 to 1984]. 383 40

The diseases which are commonly complicated by hypercapnic respiratory failure also compromise the respiratory muscles in several ways. Increased work of breathing, mechanical disadvantage, neuromuscular disease, impaired nutritional status, shock, hypoxemia, acidosis, and deficiency of potassium, magnesium, and inorganic phosphorus are the major non-neurologic factors which contribute to respiratory muscle fatigue and failure. Respiratory muscle fatigue has two components. High frequency fatigue occurs rapidly with intense contractile efforts but is usually not severe. It also recovers rapidly with rest. Low frequency fatigue develops more slowly but is severe and requires hours for recovery. Since the spontaneous rate of neural stimulation is predominantly in the low frequency range, this component of fatigue is of particular clinical importance. Fatigue of the inspiratory muscles leads to acute respiratory acidosis, but before carbon dioxide retention occurs, it can be recognized from characteristic symptoms and signs. These include dyspnea which responds to mechanical ventilation, rapid shallow breathing, and asynchronous movements of the chest and abdomen. Inspiratory muscle fatigue must be treated by putting these muscles to rest, by mechanically supporting ventilation. In addition, underlying metabolic nutritional and circulatory abnormalities must be corrected and infection treated. Aminophylline and isoproterenol can restore inspiratory muscle contractility, but controlled clinical trials remain to be done regarding their application in acute and chronic respiratory failure. Inspiratory muscle training improves strength and endurance in patients with obstructive lung disease, cystic fibrosis, and spinal cord injury, but does not always improve physical exercise performance. Again, more work is needed to develop the indications for inspiratory muscle training and to determine the optimum type and duration of the training regimen.
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PMID:Respiratory muscle failure. 634 27

Three elderly patients with established chronic obstructive airways disease were admitted with a short history of increasing dyspnoea and tiredness and (in two cases) a deterioration in mental state. Acute respiratory acidosis was diagnosed and mechanical ventilation instituted. Two hours after beginning mechanical ventilation the mean arterial pH had risen to 7.40, but all patients showed a dramatic fall in the serum phosphate concentration (lowest value 0.3 mmol/l (0.9 mg/100 ml] accompanied by a low urinary excretion of phosphate. No patient could tolerate withdrawal of mechanical ventilation until the serum and urinary concentrations of phosphate had returned to normal. Recovery from acute respiratory acidosis should be added to the list of conditions associated with severe hypophosphataemia.
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PMID:Severe hypophosphataemia during recovery from acute respiratory acidosis. 643 41

Serious acute complications can occur in relation to anastomotic insufficiency or re-opening of the fistula in patients with tracheo-oesophageal fistula and atresia, even if the repair has been carried out extra-pleurally. For this reason the patient should not be nursed flat and the important life-threatening signs to watch for are increasing tachypnoea and dyspnoea with respiratory acidosis and a central air shadow in the mediastinum.
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PMID:[Mediastinal complications following retropleural operation for oesophageal atresias (author's transl)]. 745 83


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