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

A brief review about the effects of hypothermia is presented, with regards to the difference between accidental hypothermia and controlled mild hypothermia (Core temperature = 33-35 degrees C). Mild hypothermia does not seem to affect the cardiac performance, while recent experimental reports show potential protective effects on the cardiac muscle during acute infarction. Mild hypothermia improve the outcome of brain function after cardiac arrest and head injury, while experimental reports show a potential protective effect of local spinal cord cooling during ischemic injury. Induced hypothermia of single organ is widely applied in liver resection and in other surgical procedures, further the cardiac ones. In the acute respiratory failure, mild hypothermia may induce a decrease in PaCO2, in sedated and muscle relaxed patients, due to the decrease of metabolic demand. In this setting a mild induced hypothermia potentially may decrease the side effects of therapeutic hypoventilation (permissive hypercapnia) both on haemodynamics and brain circulation. Preliminary data are presented about five ALI/ARDS patients, enclosed in a randomized trial, who were mechanically ventilated and cooled with an air-sheet: three patients died because of underlying disease and two patients survived with complete recovery. Mild controlled hypothermia seems to provide new interesting clinic uses.
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PMID:[Therapeutic applications of hypothermia in intensive care]. 1039 3

We report about a child with severe ARDS after burning trauma who did not respond to conventional treatment with controlled pressure ventilation under conditions of permissive hypercapnia and changing of the infants's body position. A combined treatment with high frequency oscillatory ventilation, inhalation of nitric oxide and surfactant replacement improved the pulmonary status. Twelve days after the accident the boy could be extubated and 5 weeks later he could be discharged without any pulmonary and neurologic handicap. The use of these therapeutic tools may help to avoid the necessity of the invasive extracorporeal life support.
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PMID:[Combination therapy of high frequency oscillatory ventilation, NO inhalation and surfactant replacement in a child with acute respiratory distress syndrome]. 1040 17

The underlying principle of the surgical treatment of non-small-cell lung cancer (NSCLC) is complete removal of the local/regional disease within the thorax. Pulmonary resection should be as conservative as possible without compromising the adequacy of tumor removal. A multitude of factors influence the incidence and severity of complications following pulmonary resection including the pre-operative physical and psychological status of the patient, the pathologic process requiring resection, the physiologic impact of the procedure, and the addition of pre-operative or postoperative adjuvant therapy. The insidious onset of interstitial changes on chest X-ray (CXR) 1 to 2 days after pulmonary resection forewarns of respiratory distress; however, the pathophysiology of adult respiratory distress syndrome (ARDS) with progression to respiratory failure requiring mechanical ventilation and advanced critical care often unfolds. Management of patients with severe respiratory failure remains primarily supportive. "Good critical care" is the mainstay of therapy: this includes gentle mechanical ventilation to avoid ventilator-induced barotrauma and over-extension of remaining functional alveoli, diuresis, infection identification and management, and nutritional support. New therapeutic strategies that may impact on outcomes in the adult population include pressure-limited ventilation (permissive hypercapnia), inverse ratio ventilation, high-frequency jet ventilation, high-frequency oscillatory ventilation, intratracheal pulmonary ventilation, and prone position ventilation. In addition, alternative therapies such as partial liquid ventilation, inhaled nitric oxide, and extracorporeal techniques including extracorporeal membrane oxygenation (ECMO), extracorporeal carbon dioxide removal (ECCO(2)R), intravascular oxygenation (IVOX), and arteriovenous carbon dioxide removal (AVCO(2)R), provide additional modalities. A component of some or all of these strategies is finding a role in clinical practice.
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PMID:Pathogenesis and management of respiratory insufficiency following pulmonary resection. 1065 20

Permissive hypercapnia, involving tolerance to elevated Pa(CO(2)), is associated with reduced acute lung injury (ALI), thought to result from reduced mechanical stretch, and improved outcome in ARDS. However, deliberately elevating inspired CO(2) concentration alone (therapeutic hypercapnia, TH) protects against ALI in ex vivo models. We investigated whether TH would protect against ALI in an in vivo model of lung ischemia-reperfusion (IR). Anesthetized open chest rabbits were ventilated (standard eucapnic settings), and were randomized to TH (FI(CO(2)) 0.12) versus control (FI(CO(2)) 0.00). Pa(CO(2)) and arterial pH values achieved in the TH versus CON groups were 101 +/- 3 versus 44.4 +/- 4 mm Hg and 7.10 +/- 0.03 versus 7.37 +/- 0.03, respectively. Following left lung ischemia and reperfusion, TH versus control was associated with preservation of lung mechanics, attenuation of protein leakage, reduction in pulmonary edema, and improved oxygenation. Indices of systemic protection included improved acid-base and lactate profile, in the absence of systemic hypoxemia. In the TH group, mean BALF TNF-alpha levels were 3.5% of CON levels (p < 0.01), and mean 8-isoprostane levels were 30% of CON levels (p = 0.02). Western blot analysis demonstrated reduced lung tissue nitrotyrosine in TH, indicating attenuation of tissue nitration. Finally, preliminary data suggest that TH may attenuate apoptosis following lung IR. We conclude that in the current model TH is protective versus IR lung injury and mechanisms of protection include preservation of lung mechanics, attenuation of pulmonary inflammation, and reduction of free radical mediated injury. If these findings are confirmed in additional models, TH may become a candidate for clinical testing in critical care.
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PMID:Therapeutic hypercapnia reduces pulmonary and systemic injury following in vivo lung reperfusion. 1111 2

Acute respiratory distress syndrome (ARDS) is an acute form of severe alveolar-capillary injury that evolves after a direct or indirect lung insult. It begins as noncardiogenic pulmonary edema and develops into a neutrophilic alveolitis, and, later, pulmonary fibrosis. Mortality remains high among children with ARDS, particularly when serious underlying conditions co-exist, sepsis occurs, and when there is multi-organ failure. Lung function improves with time among survivors, but pulmonary fibrosis may persist. Advances in the care of children with ARDS include the use of lung-protective ventilator strategies, permissive hypercapnia, inhaled nitric oxide, high-frequency ventilation, and extra-corporeal life support. These approaches reduce ventilator-associated lung injury and may improve survival when used in combination with one another. Interventions that reduce alveolar inflammation, enhance alveolar fluid removal, and reduce pulmonary fibrosis will further improve survival and recovery from ARDS in the future.
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PMID:Current concepts in adult respiratory distress syndrome in children. 1138 62

The ARDS (acute respiratory distress syndrome) Network study found 22% lower mortality in acute lung injury and ARDS patients ventilated with low tidal volumes (V(T)) than in those ventilated with traditional V(T) ventilation. Several points should be considered when using the low V(T) protocol for clinical practice. Prior to implementation, hemodynamic and acid-base status, minute ventilation, and adequacy of sedation should be assessed to minimize the potential for intolerance. The volume-preset, assist-control mode is recommended for better control of V(T), and the respiratory rate should be increased as V(T) is reduced, so as to maintain minute ventilation and prevent acute hypercapnia. When unavoidable, hypercapnia should be induced slowly. Ventilator inspiratory flow (V(I)) and trigger sensitivity settings should be optimized to limit the increase in work of breathing and dyspnea. When dyspnea results in double-triggered breaths, V(T) can be titrated to 7-8 mL/kg, provided end-inspiratory plateau pressure is < or = 30 cm H(2)O. In severe acidosis (pH < 7.15) V(T) also can be increased. However, every effort should be made to maintain plateau pressure and V(T) goals by buffering severe acidosis and treating patient-ventilator asynchrony with sedation. Evaluation for weaning should occur when adequate oxygenation can be maintained on 40% oxygen and a positive end-expiratory pressure of 8 cm H(2)O. Pressure support levels between 5 and 20 cm H(2)O (above 5 cm H(2)O positive end-expiratory pressure) are used for weaning and titrated to keep the respiratory rate < 35 breaths/min. Pressure support levels should be weaned aggressively, as long as the protocol's weaning tolerance criteria can be maintained.
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PMID:Implementation of a low tidal volume ventilation protocol for patients with acute lung injury or acute respiratory distress syndrome. 1157 55

Initial Implementation of Mechanical Ventilation was focused on providing adequate oxygenation and relief of work of breathing. Over the last few decades it has become apparent that stretch-induced lung injury, associated with normocapnia or hypocapnia, is a real phenomenon. Attempts to reduce stretch-induced injury led to development of permissive hypercapnia in the neonatal population, and later to its acceptance as a standard of care in adult patients with ARDS. Here, the elevated CO2 was a result of reduced minute ventilation, and was considered to be a by-product of the technique that could be tolerated in most instances. It is now apparent that hypercapnia by itself can be protective. In addition, hypocapnia can be harmful. These observations led to the hypothesis of therapeutic hypercapnia, i.e., deliberate production of high CO2 as a goal in the care of critically ill patients.
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PMID:Normocapnia vs hypercapnia. 1202 43

Non-invasive positive pressure ventilation (NIPPV) has been discussed comprehensively in the last years, but usage of non-invasive ventilation in Intensive Care Units is rare. The reasons may be uncertainty in indications and difficulties in handling the masks and ventilators. In the last years the introduction of full face masks and respiratory helmets has made it possible to ventilate patients with unusual facial forms and to avoid problems of pressure necrosis. Software components designed for NIPPV are available for standard respirators. Indications for NIPPV (neuromuscular diseases, spinal abnormalities, chest wall malformations, COPD, cardiogenic pulmonary edema) have been ensured in clinical trials. No sufficient data are available for the application of NIPPV in weaning and respiratory failure following extubation. Indication for NIPPV becomes apparent when therapy starts in early stage with sufficient ventilation pressure. Compared to standard therapy, no reliable advantage has been seen for NIPPV in hypoxic hypercapnia respiratory failure except for malignant diseases. However, prophylactic use in patients with high risk might be conceivable. For these patients strict criteria of termination are required to avoid missing the time point for intubation. Gas exchange disturbances in advanced lung fibrosis, pneumonia and ARDS are not amenable to NIPPV. Contraindications for NIPPV are non-compliant patients, absence of cough- and pharyngeal reflexes as well as retention of secretions and malignant ventricular arrhythmia. Relative contraindications are catecholamine-dependent circulatory collapse and acute myocardial infarction, since sufficient data for NIPPV are missing.
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PMID:[Noninvasive ventilation in the intensive care unit -- is it still negligible?]. 1267 84

"Permissive hypercapnia" is an inherent element of accepted protective lung ventilation. However, there are no clinical data evaluating the efficacy of hypercapnia per se, independent of ventilator strategy. In the absence of such data, it is necessary to determine whether the potential exists for an active role for hypercapnia, distinct from the demonstrated benefits of reduced lung stretch. In this review, we consider four key issues. First, we consider the evidence that protective lung ventilatory strategies improve survival and we explore current paradigms regarding the mechanisms underlying these effects. Second, we examine whether hypercapnic acidosis may have effects that are additive to the effects of protective ventilation. Third, we consider whether direct elevation of CO(2), in the absence of protective ventilation, is beneficial or deleterious. Fourth, we address the current evidence regarding the buffering of hypercapnic acidosis in ARDS. These perspectives reveal that the potential exists for hypercapnia to exert beneficial effects in the clinical context. Direct administration of CO(2) is protective in multiple models of acute lung and systemic injury. Nevertheless, several specific concerns remain regarding the safety of hypercapnia. At present, protective ventilatory strategies that involve hypercapnia are clinically acceptable, provided the clinician is primarily targeting reduced tidal stretch. There are insufficient clinical data to suggest that hypercapnia per se should be independently induced, nor do outcome data exist to support the practice of buffering hypercapnic acidosis. Rapidly advancing basic scientific investigations should better delineate the advantages, disadvantages, and optimal use of hypercapnia in ARDS.
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PMID:Permissive hypercapnia--role in protective lung ventilatory strategies. 1472 44

Acute respiratory distress syndrome (ARDS) is a clinically defined entity describing the severity of diffuse alveolar injury caused by direct or indirect injury to the lung. Pathophysiology, clinical course and outcome of ARDS depend on the underlying cause, the severity of the disease and co-morbidities. Pulmonary function tests show restrictive lung disease, which is characterised by a reduction in lung compliance and functional residual capacity, resulting in marked ventilation-perfusion inequality. Current ventilator strategies aim to minimise ventilator-induced lung injury by targeting mechanical ventilation between the lower and upper inflection point of the pressure volume curve. This includes recruitment manoeuvres and the use of high PEEP to open the atelectatic lung and the use of permissive hypercapnia and the limitation of peak inspiratory pressure below 35 cm H2O to avoid overinflation. The clinical benefit of newer modes of ventilatory support such as inverse ratio ventilation, high frequency oscillatory ventilation, surfactant replacement, prone positioning and inhaled nitric oxide has yet to be determined in children.
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PMID:Acute lung injury: pathophysiology, assessment and current therapy. 1626 76


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