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

Acute respiratory distress syndrome is a common cause of morbidity and mortality in intensive care units. For the most part, the mortality of this syndrome has arguably not decreased since the syndrome was originally described. One of the major reasons for this lack of reduction in mortality may be related to adherence to more traditional ventilatory strategies that have the potential to cause ventilator-induced lung injury. Ventilator strategies that attempt to limit ventilator-induced lung injury and accept permissive hypercapnia have successfully demonstrated a marked reduction in mortality in uncontrolled settings. So encouraging are these reductions that there has been a subtle shift in philosophy of mechanical ventilation toward using lung-protective ventilatory strategies at all times. With broad acceptance of this shift in philosophy, and the use of recently standardized clinical definitions for controlled studies, we optimistically anticipate improved mortality rates for acute respiratory distress syndrome.
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PMID:Strategies of invasive ventilatory support in ARDS. 882 93

We have recently reported that in an anesthetized rat model, generation of oxygen free radicals (OFR) via i.v. administration of Xanthine plus Xanthine Oxidase [X + XO] resulted in death of about 90% of the animals within a 120-min observation period. Pretreatment of the rats with endogenous scavengers Superoxide Dismutase and Catalase, or with felodipine, a dihydropyridine calcium channel blocker, and/or with dopexamine, an agonist of beta 2 adrenoceptors as well as dopamine (DA-1) receptors significantly enhanced the survival rate to over 70%. The present study was designed to investigate whether lipid peroxidation and ensuing respiratory depression contributed to the lethal toxicity of the free radicals. In the control group, the death of the rats administered [X + XO] was proceeded by significant increases in the plasma lipid peroxides (PLP) and by a severe hypertensive response characteristic of an intense ischemic state, which was confirmed by the presence of hypercapnia, hypoxemia, and acidosis. Placement of the animals on the positive pressure ventilation prior to the administration of [X + XO] did not prevent increases in PLP but, prevented any adverse alterations in the respiratory markers and significantly enhanced survival rate up to 70%. In contrast, both felodipine as well as dopexamine prevented any increases in PLP, normalized blood gas profile, and significantly increased survival rate to 80 to 90%. These observations suggest that the lethal toxicity produced by oxygen free radical was due to respiratory distress. The relationship between increases in the PLP and respiratory depression and the mechanisms via which two pharmacologically distinct agents, felodipine and dopexamine, facilitated the salutary effects cannot be conclusively stated at this time. It is further suggested that although the doses of these two drugs employed in the present studies are not adequate to function as antioxidants, such a possibility cannot be entirely ruled out.
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PMID:Effect of pharmacological interventions in the prevention of lipid peroxidation and respiratory depression induced by oxygen free radicals in anesthetized rats. 890 25

Low volume ventilation with permissive hypercapnia is becoming widely used in the treatment of acute respiratory distress syndrome. A mathematical model was developed to examine the effects of hypoventilation on pulmonary gas exchange in lungs with a range of shunt fractions. Hypoventilation did not worsen gas exchange, provided the inspired oxygen concentration was high enough to maintain PAO2 at an adequate level. In lungs with a high shunt fraction, some improvement in gas exchange may result, but these effects are small. A rightwards shift of the oxygen-haemoglobin dissociation curve induced by hypercapnia, is likely to be beneficial rather than detrimental in patients with acute respiratory distress syndrome. This analysis was limited to the direct effects of hypoventilation in lungs with constant shunt fractions, and did not encompass a number of possible secondary effects such as changes in cardiac output with PaCO2, changes in shunt fraction associated with a reduction in mean airway pressure and possible direct effects of hypercapnia on the pulmonary vasculature or airways.
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PMID:Permissive hypercapnia and gas exchange in lungs with high Qs/Qt: a mathematical model. 895 93

Experimental and clinical evidence has led to a revision of conventional techniques used for mechanical ventilation in the treatment of respiratory failure due to severe asthma and acute respiratory distress syndrome. A common feature in these two clinical situations is the heterogeneous nature of the lesions, causing mechanical alterations which vary from one region to another. Thus the tidal volume is not equally distributed throughout the lungs and can lead to overdistension in some regions or functional exclusion in others. Hyperinflation then exposes the patient to barotrauma, cardiocirculatory and/or alveolocapillary complications. Controlled hypoventilation-or permissive hypercapnia-is a new approach aimed at preventing complications by supplying adequate oxygen while accepting or provoking a certain degree of hypercapnia by alveolar hypoventilation. The technique is based on restricting tidal volume and respiratory rate as long as is necessary to recover more favorable mechanical conditions. Results obtained with this method have been convincing for the treatment of decompensated asthma but preliminary data obtained in acute respiratory distress syndrome remain to be validated.
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PMID:[Permissive hypercapnia. From choice to unavoidable decision]. 895 67

Artificial ventilation plays a key role in the treatment of acute respiratory distress syndrome (ARDS). Initially, the goal is to normalize gas exchange compromised by the lung disease. Positive pressure ventilation can however aggravate prior lesions of the pulmonary parenchyma, at least in areas of the lung accessible to ventilation. Computed tomography of the lung has given us a better understanding of the pathogenesis of these ventilation-induced lesions, leading to new ventilatory strategies aimed at assuring adequate oxygenation without damaging the parenchyma. These ventilatory modes may tolerate a certain degree of hypercapnia to avoid lung injury. Improved oxygenation relies on optimizing the ventilation/perfusion ratio, either with inhaled nitric oxide or a supine position to improve alveolar recruitment. In the most severe cases, extra-corporal gas exchange systems have shown their efficacy for patients whose lungs cannot be ventilated. Thus ventilation should be carefully adapted to each patient based on the severity of the ARDS and its clinical course. We present a practical protocol based on a hierarchy rationale for each ventilation mode and indicate the explorations required to adapt each mode to a specific patient.
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PMID:[Artificial ventilation in acute respiratory distress syndrome in adults. Towards an individual optimization]. 895 78

Complications may occur when nutritional support is administered either parenterally or enterally. Inappropriate nutritional formulas with high carbohydrate loads can precipitate respiratory failure in patients with compromised lung function, induce respiratory distress which manifests as dyspnea and tachypnea in an originally normal lung condition, produce hypercapnic acidosis in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD) as well as patients recovering from acute respiratory distress syndrome (ARDS) without chronic lung disease, or result in difficult weaning. Hypercaloric mixed substrates administered either parenterally or enterally can also have profound impacts on gas exchange and energy expenditure. This report describes a patient who experienced exacerbation of respiratory distress and hypercapnic acidosis during recovery from septic ARDS as the result of a nutritionally-related increase in CO2 production. As carbohydrate calories were decreased, CO2 production diminished and the hypercapnia was resolved. The importance of indirect calorimetry cannot be overemphasized during tailoring of nutritional support for the critically ill patients.
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PMID:Hypercapnic respiratory acidosis precipitated by hypercaloric carbohydrate infusion in resolving septic acute respiratory distress syndrome: a case report. 903 53

Pulmonary contusion is a common lesion occurring in patients sustaining severe blunt chest trauma. Alveolar hemorrhage and parenchymal destruction are maximal during the first 24 hours after injury and then usually resolve within 7 days. The diagnosis of traumatic lung injury is usually made clinically with confirmation by chest x-ray films. The chest computed tomography scan is highly sensitive in identifying pulmonary contusion and may help predict the need for mechanical ventilation. Respiratory distress is common after lung trauma, with hypoxemia and hypercarbia greatest at about 72 hours. Although management of patients with pulmonary contusion is supportive, pneumonia and adult respiratory distress syndrome with long-term disability occur frequently.
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PMID:Pulmonary contusion: review of the clinical entity. 919 84

The adult (acute) respiratory distress syndrome is a significant cause of morbidity in children. The mortality rates remain elevated, greater than 50%, and even greater than 80% in patients with underlying malignancies. The therapeutic interventions remain mainly supportive. Strategies of conventional mechanical ventilation are directed toward the use of high positive end-expiratory pressures, low positive inspiratory pressure, and permissive hypercapnia. High-frequency oscillatory ventilation and tracheal insufflation are not yet used extensively, although they should contribute to less aggressive ventilation. Surfactant replacement, nitric oxide inhalation, and partial liquid ventilation seem to be promising technologies, but controlled clinical studies are necessary before their wide-spread use. Extracorporeal membrane oxygenation remains the alternative technology in case of failure of conventional support.
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PMID:Acute respiratory distress syndrome in children. 922 57

Congenital diaphragmatic hernia (CDH) is associated with pulmonary hypoplasia. The pulmonary vascular bed may be extremely reactive to various stimuli, and in the treatment it is important to avoid pulmonary vasospasm. The strategy in our institution since 1990 has involved a prolonged preoperative stabilization with gentle mechanical ventilation. Pressures have been kept as low as possible, and slight hypercarbia has been accepted. Peak inspiratory pressures exceeding 35 cm H2O have been avoided. Extracorporeal membrane oxygenation (ECMO) has been used according to standard inclusion criteria. Nitric oxide and high-frequency oscillation have been added to the therapeutic modalities during the study period. When the patient was considered stabilized, surgical repair was undertaken after a delay of 24 to 96 hours. In patients on ECMO who could not be decannulated, surgical repair was undertaken while on ECMO. From 1990 through 1995, 52 patients were admitted with a diagnosis of CDH. Forty-three of these were risk group patients presenting with respiratory distress within 6 hours after birth. A total of 48 patients survived (survival rate 92%), and 39 of the risk group patients (survival rate 91%). There were only four hospital deaths, all with contraindications to ECMO. It is suggested that the adopted protocol is beneficial in the treatment of CDH and that the fraction of patients who have pulmonary hypoplasia incompatible with life is smaller than previously believed.
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PMID:Improved results in patients who have congenital diaphragmatic hernia using preoperative stabilization, extracorporeal membrane oxygenation, and delayed surgery. 926 67

Chronic lung disease (CLD) of prematurity is a common disorder in preterm infants who were ventilated for respiratory distress syndrome (RDS) at birth. Premature birth, mechanical ventilation and supplemental oxygen are the major risk factors for the development of CLD. Although the exact pathophysiology is unclear, recent evidence suggests that pulmonary inflammation may play a pivotal role in the development of CLD. Histologically, the evolution of CLD can be divided into an early inflammatory phase followed by a subacute and chronic fibroproliferative phase. The early, inflammatory phase of CLD is clinically indistinguishable from RDS. In bronchoalveolar lavage fluid an influx of inflammatory cells and increased levels of cytokines can be found. Pathological examination of the lungs reveals persisting hyaline membranes, necrosis of airway and alveolar epithelium and an influx of inflammatory cells in the lung. In the subacute fibroproliferative or reparative phase of CLD, persistent respiratory distress and hypercapnia are seen and patients require oxygen with or without ventilatory support. Histologically, this phase is characterized by hyperplasia of type II pneumocytes, hypertrophy of bronchial and bronchiolar smooth muscle and interstitial and perialveolar fibrosis. In the chronic fibroproliferative phase (up to 1 yr), airway remodelling occurs. Respiratory distress continues and many patients remain oxygen dependent. Cyanotic spells are frequently seen and chronic hypoxia may lead to pulmonary hypertension and right heart failure. Many patients have severe feeding problems and somatic growth is poor. In surviving patients, persisting lung function abnormalities are found. Airway resistance and airway responsiveness are increased and residual volume (RV) and RV/total lung capacity ratios remain elevated, indicating air trapping. Although lung function improves during childhood, residual abnormalities are still found in young adults, raising concerns about the evolution of pulmonary function in old age.
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PMID:Evolution and natural history of chronic lung disease of prematurity. 927 Feb 56


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