Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Respiratory muscle failure. 634 27

From 1967 to 1972 12 patients were operated on for emphysematous bullae in the Liverpool regional cardiothoracic centre. The patient with the poorest lung function died in the immediate postoperative period but the remainder survived for more than five years. All but one of the survivors showed evidence of benefit three to six months after surgery and all those not retired returned to full-time employment for at least five years. Nine patients were reviewed 5-10 years after surgery. These all reported a gradual return of dyspnoea, which was matched by a falling one-second forced expiratory volume (FEV1) (mean fall 82 ml a year); but five were still maintaining some of their postoperative improvement. When mean preoperative lung function values were compared with the values obtained 5-10 years later there was still a significant improvement in forced vital capacity; but FEV1, residual volume, transfer coefficient, and arterial oxygen and carbon dioxide tensions were unchanged. Chest radiographs showed no new bullae or (except in one case) any increase in size of pre-existing bullae. We conclude that the removal of large emphysematous bullae did not hasten the progress of the underlying emphysema and that in most patients some benefit lasted for more than five years after the operation. Patients treated by lobectomy fared at least as well as those treated by bullectomy alone. It may be relevant to the relatively good progress of patients in this series that only three had suffered from chronic bronchitis before operation or smoked after operation, all but two had bullae occupying half or more of one hemithorax, and none had hypercapnia.
 ...
PMID:Surgical treatment of emphysematous bullae: late outcome. 640 36

Five male volunteers served as subjects for exercise studies during three dives to pressures of 47 and 66 ATA while breathing gases containing 0.5 ATA PO2 and varying amounts of N2 and He. The inspired gas density ranged from 1.1 g/l (BTPS) at the surface to 17.1 g/l at the highest pressure. Dyspnea at rest and during exercise was evident in all divers and was predominantly inspiratory in nature. Despite the dyspnea, divers were able to perform work requiring an O2 consumption larger than 2 l/min STPD at each depth. Compared with surface measurements, moderate work at depth was associated with alveolar hypoventilation, arterial hypercapnia, very large physiological dead space, and higher levels of arterial lactate and signs of simultaneous respiratory and metabolic acidosis. The increase of ventilation that accompanies the onset of acidemia at the surface was not present at depth. Acidemia at depth was more severe, and its onset occurred at lesser work rates than at 1 ATA. No large differences could be ascertained when a variety of responses obtained with inspired gas having a density of 7.9 g/l at 47 ATA were compared with those obtained with an inspired gas density of 17.1 g/l at 66 ATA. It appears that the major impact of the environment on the physiological responses to work was almost fully manifested at a pressure of 47 ATA with a He-O2 gas mixture. It is cautioned that maximum work tolerance may be an insufficient assessment of the physiological condition of a diver exposed to these high pressures.
 ...
PMID:Physiological responses to exercise at 47 and 66 ATA. 643 26

Seven patients are described who had a distinctive syndrome of chest wall restriction caused by asbestos-induced pleural fibrosis. All had severe dyspnea and predominant pleural disease on radiographic examination, with pulmonary function findings of reduced vital capacity, total lung capacity (measured in five patients), and maximal voluntary ventilation. Five patients had ventilatory failure with carbon dioxide retention; four of these have died and one is close to death. Examination of the thoracic organs in five patients showed minimal or no parenchymal fibrosis in three and less severe involvement of the parenchyma than of the pleura in the remaining two. Neoplasms were suspected in three patients because of extension of the pleural fibrosis into the lung. Two of these patients had pleural uptake of 67-gallium citrate attributable to the inflammatory reaction. With the increasing duration since onset of exposure in the nine million workers who have been exposed to asbestos, as well as in other exposed persons, it is expected that additional cases of ventilatory failure caused by asbestos-induced pleural fibrosis will be encountered.
 ...
PMID:Ventilatory failure due to asbestos pleurisy. 665 May 44

Fifteen out of 18 "pink and puffing" patients completed a double-blind, placebo-controlled cross-over trial of diazepam and promethazine for breathlessness and reduced exercise tolerance. Dosages were 25 mg and 125 mg daily, respectively, and each course lasted two weeks. Patients with psychiatric or other major medical histories were excluded. Of the three patients who did not complete the trial, one died during an exacerbation of breathlessness while taking diazepam, one was withdrawn because of mild hypercapnia while taking placebo, and one suffered intolerable drowsiness while taking diazepam. Of the remaining 15 patients, six needed a reduction in dosage because of drowsiness: one of these was taking promethazine and five diazepam. Diazepam had no effect on breathlessness and noticeably reduced exercise tolerance. Promethazine reduced breathlessness and improved exercise tolerance without altering lung function. From these results diazepam is contraindicated for breathlessness and reduced exercise tolerance in fixed airways obstruction, but promethazine may be beneficial.
 ...
PMID:Drug treatment of breathlessness: contrasting effects of diazepam and promethazine in pink puffers. 678 19

Human lung transplantation was successfully performed in the early eighties and is now an option for patients with endstage lung disease, which is associated with poor survival. Most frequent indications for lung transplantation are emphysema, cystic fibrosis, fibrosing alveolitis, primary pulmonary hypertension and Eisenmenger's syndrome. Single lung transplantation (SLT) is most often performed in emphysema, fibrosing alveolitis and other diseases which are not associated with chronic infection of the lung. Double lung transplantation was recently replaced by the technique of sequential single lung or bilateral lung transplantation (BLT). Cardiopulmonary bypass can often be avoided and problems of the airway anastomosis are less frequent using BLT. Main indications for this procedure are cystic fibrosis, bronchiectasis and primary pulmonary hypertension (PPH). In PPH often only SLT is performed. Cor pulmonale is reversible following SLT or BLT even if the heart is not replaced. Combined heart-lung transplantation (HLT) is reserved for some cases of Eisenmenger's syndrome and few centers still prefer HLT in patients with cystic fibrosis. Patients are usually accepted for transplantation when they are considered to have life expectancy of 12 to 24 months. Quality of life and physical working capacity are severely decreased and patients suffer dyspnea NYHA grade III or IV. Most of the patients are hypoxic and need continuous oxygen therapy. Hypercapnia is also a negative predictive factor for survival without transplantation. In PPH cardiac index of less than 2 litres/m2 is associated with poor outcome. Not only absolute values for FEV1 and pO2 have to be considered in finding the best moment for assessment for transplantation but the clinical course of the disease during previous months and years also has to be taken into account. Contraindications to transplantation include acute infection, concomitant diseases of other organs, bronchial carcinoma and psychiatric disorders if noncompliance is likely. To achieve good results after lung transplantation, proper donor and recipient selection, experienced surgery and careful postoperative management are essential. Complications must be diagnosed early to provide effective treatment. Most complications occur within the first months after surgery. Early complications include primary organ failure, pleural bleeding, problems at the site of the airway anastomosis, infection and acute rejection. Acute rejection is common but can be treated successfully if diagnosed early.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:[Lung transplantation]. 778 72

Vocal cord paralysis can produce extrathoracic airway obstruction with severe respiratory failure, post-surgical traumatism being the most frequent. Definitive treatment can require aritenoidectomy. For emergency treatment tracheal intubation of tracheotomy are frequently needed. We report a patient with acute post-surgical upper airway obstruction successfully treated with CPAP application through nasal mask. A 29 year-old female showed stridor and retraction of the supraclavicular, intercostal and epigastric region following an uncomplicated tracheal extubation immediately after surgery (radical thyroidectomy with nodal dissection). Pulsosaturometry showed O2 desaturation despite high flow O2 administration. She received intravenous steroids and O2 through intermittent positive pressure by nasal mask (manual resuscitator) increasing SpO2 to 90%. Laringoscopy showed both vocal cords fixed at medium line. CPAP through a nasal mask was initiated with a 5 cm H2O pressure and high FIO2. Immediately afterwards, dyspnea, stridor, supraclavicular retraction and respiratory accessory muscles use disappeared. Heart rate decreased (120 to 92 x min.) and SpO2 increased to 99%. Arterial blood gases did not show hypercapnia. Dyspnea and physical signs of upper airway obstruction appeared immediately after interrupting CPAP application, with a marked decrease in SpO2. So the mask was reinstalled keeping the same pressure level during 18 hs. The procedure was well tolerated. There were no local or hemodynamic complications. CPAP was progressively discontinued.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Treatment of respiratory insufficiency secondary to vocal cord bilateral paralysis with continuous positive pressure]. 785 91

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

Arterial blood gas data were correlated with clinical variables including patients' perception of dyspnea and spirometry in 79 episodes of acute asthma attacks. Among several variables that showed univariate significance with severity, only subjective degree of dyspnea rated on a modified Borg scale (MBS) remained predictive to discriminate the presence or absence of hypoxia/hypercapnia in multivariate analyses. MBS alone could predict the arterial blood gas status with accuracy of approximately 75%. Therefore, patients' sensation of dyspnea seemed to be an important factor in the evaluation of acute asthma in an emergency room.
 ...
PMID:Clinical features to predict hypoxia and/or hypercapnia in acute asthma attacks. 792 36

Weaning patients from mechanical ventilation constitutes a major portion of the workload in an intensive care unit, as over 40% of total ventilator time is consumed by the weaning process. Several pathophysiological mechanisms may be responsible for weaning failure, but the precise role of each is incompletely understood. Patients who fail a weaning trial commonly develop hypercapnia, which appears to be due to decreased tidal volume rather than a primary decrease in respiratory drive. Respiratory muscle performance is impaired as a result of dynamic hyperinflation and paradoxic motion of the rib cage and abdomen. Worsening of pulmonary mechanics will cause further embarrassment of the respiratory muscles. However, the clinical importance of respiratory muscle fatigue remains unclear. Afferent stimuli arising in the lung parenchyma, respiratory muscles, or as a consequence of impaired gas exchange will be transmitted to the respiratory control centers and result in severe dyspnea in patients who fail a weaning trial.
 ...
PMID:Pathophysiology of failure to wean from mechanical ventilation. 799 29


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>