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

Patients with end-stage lung disease are at significant risk of hypoxia and dynamic hyperinflation during mechanical ventilation, particularly during one-lung ventilation. This article describes aspects of care such as patients, including acceptance of permissive hypercapnia, adjustment of ventilator settings, and methods to optimize recovery from anesthesia.
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PMID:Lessons from lung transplantation for everyday thoracic anesthesia. 1157 7

Advances in neonatology have resulted in an increase in the absolute number of survivors with chronic lung disease (CLD), though its overall incidence has not changed. Though the single most important high-risk factor for CLD is prematurity, the focus of attention has recently changed over to minimizing the impact of other two risk factors: baro/volutrauma related to mechanical ventilation, and oxygen toxicity. Permissive hypercapnia (PHC) or controlled ventilation is a strategy that minimizes baro/volutrauma by allowing relatively high levels of arterial CO(2), provided the arterial pH does not fall below a preset minimal value. The benefits of PHC are primarily mediated by the reduction of lung stretch that occurs when tidal volumes are minimized. PHC can be a deliberate choice to restrict ventilation in order to avoid overdistention, while application of high airway pressures and large tidal volumes would permit normocapnia, or relative hypocapnia (PaCO(2), < or = 25-30 mmHg), but may result in CLD and be harmful to the developing lung. The current concept that PaCO(2) levels of 45-55 mmHg in high-risk neonates are "safe" and "well tolerated" is based on limited data. Further prospective trials are needed to study the definition, safety and efficacy of PHC in ventilated preterm and term neonates. However, designing disease/gestational-postnatal age-specific clinical trials of PHC will be difficult in neonates, given the diverse pathophysiology of their diseases and the various ventilatory modes/variables currently available. The potential benefits and adverse effects of PHC are reviewed, and its relationship to current ventilatory strategies like synchronized mechanical ventilation and high-frequency ventilation in high-risk neonates is briefly discussed.
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PMID:Permissive hypercapnia in neonates: the case of the good, the bad, and the ugly. 1174 61

The experience of using noninvasive ventilation (NIV) in 113 adult cystic fibrosis (CF) patients with chronic respiratory failure, during episodes of acute deterioration in respiratory function is reported. The patients aged 15-44 yrs were divided into three groups. Group A consisted of 65 patients (median forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) 0.7/1.4 L) who were on a lung transplant waiting list. Group B consisted of 25 patients (median FEV1/FVC 0.7/1.4 L) who were being evaluated for lung transplantation. Group C consisted of 23 patients (median FEV1/FVC 0.6/1.2 L) who were not being considered for lung transplantation. The mean duration of NIV support for groups A, B and C was 61 (range: 1-600) days, 53 (1-279) days and 45 (0.5-379) days respectively. Twenty-three patients in group A subsequently received lung transplantation and 12 of these patients had a median survival of 39 months postsurgery. Thirty-nine patients died and three awaited transplantation. Five patients in group B received a transplant four of whom survived; thirteen patients died and seven awaited transplantation. Twenty patients in group C died. Noninvasive ventilation improved hypoxia but failed to correct hypercapnia in these cystic fibrosis patients. Noninvasive ventilation is useful in the treatment of acute episodes of respiratory failure in cystic fibrosis patients with end-stage lung disease who have been accepted, or are being evaluated, for lung transplantation. For these patients, there is a possibility of prolonging life if they are successfully treated for their acute episode of respiratory failure until transplantation. In this group, treatment is not merely prolonging the process of dying.
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PMID:Noninvasive ventilation in cystic fibrosis patients with acute or chronic respiratory failure. 1186 11

Pressure-limited (controlled) ventilation is commonly employed to provide mechanical ventilation in the intensive care unit when lung compliance is poor or when airway resistance is irreversibly high. Modification of the inspiratory-expiratory ratio to include inspiratory-expiratory ratio reversal and permissive hypercapnia can also be used when lung disease or injury is severe. Because other donor organs often can be saved for transplantation even when the lungs have been badly damaged, the organ procurement coordinator should adopt pressure-limited ventilation as well as inspiratory-expiratory ratio reversal and permissive hypercapnia as potentially helpful methods while providing mechanical ventilation to selected donors.
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PMID:Using pressure-limited mechanical ventilation in caring for organ donors. 1194 59

Idiopathic congenital central hypoventilation syndrome (CCHS) is a rare disorder in which affected children have a decreased sensitivity of their respiratory centers to hypercarbia and hypoxia, as well as evidence for generalized autonomic nervous system dysfunction. A genetic origin has long been hypothesized for CCHS. Previous reports of the syndrome among twins, siblings, and half siblings, as well as an established association with Hirschsprung disease and neural crest tumors support this genetic hypothesis. Here, we present the first reported offspring born to four women diagnosed with idiopathic CCHS. Their children display a spectrum of abnormalities with one child being diagnosed with CCHS, one child with recurrent apparent life threatening events, one infant born prematurely with severe chronic lung disease and diminished ventilatory responses to carbon dioxide, and one infant who is apparently healthy with no clinical manifestations suggestive of disordered respiratory control to date. Two and potentially three of these patients illustrate transmission of altered respiratory control by CCHS patients into the next generation, furthering the evidence that CCHS is part of a broadly based inherited syndrome of autonomic nervous system dysfunction.
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PMID:Idiopathic congenital central hypoventilation syndrome: the next generation. 1223 19

Prevention of acute hypercapnia during obstructive events in obstructive sleep apnea requires a balance between carbon dioxide (CO(2)) loading during the event and CO(2) unloading in the interevent period. Earlier studies have demonstrated that acute CO(2) retention may occur despite high interevent ventilation when the interevent duration is short relative to the duration of the preceding event. The present study examines the relationship between apnea and interapnea durations and relates this assessment of ventilatory periodicity to the degree of chronic hypercapnia in subjects with severe sleep apnea. A total of 18 subjects with sleep apnea (> 40 apnea/hour; chronic awake Pa(CO2) 36-62 mm Hg) and without underlying lung disease underwent polysomnography. For each event, apnea duration, interapnea duration, and apnea/interapnea duration ratio were determined. No relationship was observed between chronic Pa(CO2) and mean apnea or interapnea duration (p > 0.1). However, Pa(CO2) was directly related to apnea/interapnea duration ratio (r = 0.48; p < 0.05) such that with increasing chronic hypercapnia the interapnea duration shortens relative to the apnea duration. The present study suggests that control of the interapnea ventilatory duration relative to the duration of the preceding apnea, is an important component of the integrated ventilatory response to CO(2) loading during apnea and may contribute toward the development and/or maintenance of chronic hypercapnia in obstructive sleep apnea/hypopnea syndrome.
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PMID:Hypercapnia and ventilatory periodicity in obstructive sleep apnea syndrome. 1237 56

Long-term MV, delivered by way of a tracheostomy or noninvasive mask, often is indicated in patients with restrictive or neuromuscular pulmonary diseases and occasionally in patients with severe obstructive hypercapnic respiratory failure. Regardless of the mode of ventilation, respiratory physiology seems to be significantly impacted in these patients. Although the effects of ventilation can be unpredictable, they often seem to be favorable. Selected patients can develop increased sensitivity to hypercapnia, with subsequent improvements in blood gas tensions and decreased pulmonary artery pressures, which result in augmented cardiac function and greater tolerance to exercise. The patient-ventilator interaction, mode of ventilation, and degree of support should be considered when managing these patients. For some patients, particularly patients with fibrotic lung disease or COPD, chronic MV likely does not alter pathophysiology or improve prognosis.
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PMID:Physiologic responses to long-term ventilation. 1248 66

Patients with restrictive lung disease, owing to respiratory muscle dysfunction, have no parenchymal involvement. Their vital capacity (VC) and total lung capacity (TLC) are reduced to less than 50% and can lead to pneumonia and nocturnal hypercapnia and hypoxia. Their diffusion capacity is normal. With maximal static mouth pressure (Pimax) < 80 cm H2O and/or Pemax < 100 cm H2O, patients are referred to the national centres. Here, inspiratory muscular insufficiency is confirmed by sniff nasal inspiratory pressure and oesophageal pressure < 70 cm H2O. Expiratory muscular insufficiency is confirmed by a cough peak flow < 3-4 L/sec. and cough gastric pressure < 100 cm H2O. Sleep studies reveal nocturnal hypoventilation. Phrenic nerve stimulation is to be introduced in the diagnostic approach. Twitch mouth or oesophageal pressure < 10 cm H2O and twitch gastric pressure < 7 cm H2O are pathognomonic for neuromuscular respiratory insufficiency.
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PMID:[Hypodynamic respiratory insufficiency. Diagnostic investigation]. 1252 42

In the perinatal period, glucocorticoids are frequently administered to enhance pulmonary maturity or prevent chronic lung disease of prematurity. Recently, it has been suggested that the perinatal exposure to glucocorticoids can be associated with unfavorable neurologic development. We studied the hypothesis that 24-h pretreatment with glucocorticoid might modify cerebrovascular responses to high and low partial arterial CO(2) tension in newborn animals in vivo. A closed cranial window was implanted over the left parietal cortex of 20 anesthetized ventilated newborn (<3 d old) pigs. The actual experiments were carried out in 15 pigs: eight pretreated with a total dose of 6 mg/kg of dexamethasone and seven controls. Five pigs were used for preliminary experiments as described in the text. Pial arteriolar diameters were measured during 1) baseline conditions (normocapnia), 2) hypercapnia induced by ventilating the animals with a gas mixture containing 10% CO(2), or 3) hyperventilation with resultant hypocapnia. Under these conditions, the concentrations of 6-keto-PGF(1alpha) in the CSF were measured in five experimental animals and six controls. In summary, the dexamethasone pretreatment 1) attenuated the hypercapnia-induced dilator responses of pial arterioles and prevented the hypercapnia-associated fall in mean arterial blood pressure; 2) caused moderate, although not statistically significant, diminution in 6-keto-PGF(1alpha) levels in the CSF during baseline; 3) blocked hypercapnia-induced elevation of 6-keto-PGF(1alpha); and 4) enhanced vasoconstrictive arteriolar responses to hyperventilation. We speculate that in the clinical setting, the dexamethasone effects may compromise the adjustments of global or regional cerebral blood flow to changing physiologic states in neonates.
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PMID:Dexamethasone pretreatment attenuates cerebral vasodilative responses to hypercapnia and augments vasoconstrictive responses to hyperventilation in newborn pigs. 1253 84

Chronic lung disease of the neonate sometimes occurs as a residual condition following respiratory distress in preterm infants. Improvements in neonatal intensive care treatment will in future lead to a greater number of children surviving chronic lung disease and reaching adulthood. The symptoms of the disease are hypoxaemia, hypercapnia, tachypnoea, subcostal and intercostal retractions, fluid retention, a reduced exertion tolerance and hyperreactive airways. The treatment after the first weeks of life is symptomatic and consists of: providing supplemental oxygen via a nasal mask or cannula (0.1-1 l/min); rapid downward adjustment of oxygen therapy may lead to more complaints and poorer growth; a normal fluid therapy; if there is a tendency towards fluid retention, then diuretic therapy is indicated and in severe cases fluid restriction as well; in the case of bronchial hyperreactivity: inhaled corticosteroids (the lowest effective dose for a period of several months) and a trial treatment with beta-agonists; in the case of persistent complaints or functional limitations, lung function tests can distinguish obstructive and restrictive disorders; vaccinations according to the national programme; consider vaccinations against influenza (age: 6-12 months) and respiratory syncytial virus (age < 2 years).
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PMID:[Chronic lung disease of the neonate; pathophysiology and treatment after the first weeks of life]. 1469 49


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