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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Animal studies have demonstrated that mechanical ventilation with high peak inspiratory pressure (PIP) results in acute lung injury characterised by hyaline membranes, granulocyte infiltration and increased pulmonary and systemic vascular permeability. This can result in progressive respiratory failure and death. In surfactant deficient lungs this occurs with tidal volumes (Vt) as low as 12 ml/kg, and PIP as low as 25 cm H2O, values which are frequently used clinically. The mechanisms resulting in this form of ventilator induced lung injury are not clear, but it appears to result from global or regional overdistension of the lung or terminal airways. It can be prevented or reduced in severity in some animal models by the use of PEEP. It is suggested that the use of high PIP in some patients may result in progressive deterioration of their ARDS, possibly contributing to mortality both from respiratory failure and other causes. It may be very important to limit PIP by reducing Vt even if this results in hypercapnia and a deterioration of oxygenation in the short term.
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PMID:Ventilatory management of ARDS: can it affect the outcome? 219 41

Three children developed severe respiratory distress at days +12, +11, and +11 following allogeneic bone marrow transplantation from donors. The first child was a 13-year-old Hispanic boy transplanted in relapse of Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL). At day -14, a bronchial washing done for a streaky pulmonary infiltrate was negative for acid-fast bacilli. Miliary tuberculosis was discovered at postmortem examination. A second child, transplanted in remission of null-cell ALL, developed severe hypoxia and hypercarbia on day +11 but recovered fully following prolonged mechanical ventilation. An open-lung biopsy showed a pattern of nonspecific, diffuse alveolar damage compatible with respiratory distress syndrome. The third child was transplanted in remission of B-cell ALL and developed fatal fungal and cytomegalovirus pneumonia on day +12. In these latter two cases, it is likely that open-lung biopsy would have missed the diagnosis because of the uneven pulmonary involvement and multiple etiologies observed. All three children received cyclosporine, granulocyte transfusions, and multiple antimicrobials, including amphotericin B. Hyperfractioned total-body irradiation with lung shielding was used in the latter two patients.
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PMID:Difficulty in establishing diagnosis from lung biopsies and bronchial washing analysis in children with leukemia following bone marrow transplantation. 331 45

To clarify the evolution of acute lung injury induced by endotoxin, the progression of lung damage in 26 rats submitted to intratracheal instillation of 5 mg/kg body weight endotoxin was examined by blood gas analysis, computerized tomography, light and electron microscopy. Hypoxaemia, hypercapnia, acidosis and inhomogeneous bilateral infiltrates developed gradually within 48 hours. Monocytes appeared within blood capillaries and the instertitium by 12 hours after treatment, then migrated into alveoli and underwent progressive differentiation into macrophages by 24 hours after treatment. Granulocytes were found within blood capillaries at an early stage, but outside capillaries only at 48 hours. Hyperplasia of type II pneumocytes and hypertrophy of interstitial fibroblasts also occurred at 48 hours. These data suggest that the pathogenesis of endotoxin induced pulmonary injury proceeds through an early phase of granulocyte migration inside capillaries and monocyte extravasation, an intermediate phase of monocyte differentiation into macrophages inside alveoli and a late phase of diffuse infiltration of alveoli by newly differentiated macrophages and late-extravasated neutrophils.
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PMID:Evolution of endotoxin induced acute lung injury in the rat. 748 52

Many animal studies have demonstrated that mechanical ventilation with high peak inspiratory pressures (PIP) can result in a form of acute lung injury closely resembling ARDS, ie characterised by hyaline membranes, granulocyte infiltration, increased pulmonary and systemic vascular permeability, and eventually proliferation of fibroblasts and type II pneumocytes. These studies have led to a concern that, in some patients, orthodox ventilatory management in severe ARDS may result in additional lung injury and, possibly, remote organ dysfunction. Mortality may be increased as a consequence. In an attempt to avoid such ventilator-induced lung injury in severe ARDS, several modifications of ventilatory management have been evaluated. We have previously reported the technique of low volume pressure limited ventilation with permissive hypercapnia, using tidal volumes of 5-7 ml/kg and allowing the PaCO 2 to rise substantially (maximum PaCO 2 17.2 kPa [129 mmHg]), mean maximum 8.3 kPa [62 mmHg]). In an uncontrolled study the mortality was significantly lower than that predicted by Apache II (16% vs 39.6%, p less than 0.01). Acute hypercapnia can cause many physiological disturbances but most of these appear to be due to the resulting intracellular acidosis and should not occur in hypercapnia of gradual onset, allowing the intracellular pH to be normalised. The time scales for compensation of intracellular and extracellular acidosis are markedly different. However, even severe acute hypercapnia appears to be remarkably well tolerated. Several clinical studies suggest that the avoidance of high PIP may reduce mortality in ARDS, but a randomised trial will be required to establish whether pressure limitation and permissive hypercapnia do improve outcome.
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PMID:Low volume ventilation with permissive hypercapnia in the Adult Respiratory Distress Syndrome. 1014 4