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

Conventional treatment of the adult respiratory distress syndrome (ARDS) includes pressure-limited ventilation, permissive hypercapnia, posture changes, aggressive dehydration, selective lung ventilation, and extracorporeal gas exchange. New strategies such as nitric oxide inhalation, the implantation of an intravenous membrane oxygenator (IVOX), and surfactant replacement are currently under evaluation. Nitric oxide (NO) is an important endothelium-derived relaxing factor that is rapidly inactivated by binding to haemoglobin. Inhaling this substance has been shown to induce selective vasodilatation of ventilated lung regions. Thus, inhaled NO reduces pulmonary hypertension, increases right heart ejection fraction, and improves arterial oxygenation by redistributing blood flow away from areas with intrapulmonary shunts to areas with a normal ventilation/perfusion ratio. Dose-response analysis has revealed that effective doses for improvement of oxygenation are lower than for reduction of mean pulmonary artery pressure. The use of a miniaturised membrane lung, IVOX, for intracaval oxygen and carbon dioxide exchange is a new approach to augment gas exchange. The IVOX is inserted via an introducer into the femoral vein and is designed for placement in the full length of the vena cava. Initial experiences with this device show that the currently used prototype provides a maximum of one-third of basal gas exchange. Therefore, a more efficient device will be needed to significantly reduce high inspired oxygen concentrations and airway pressures. Moreover, there exists evidence that IVOX causes caval obstruction. Lung surfactant recovered in BAL from patients with ARDS demonstrates that fractional contents of phosphatidylcholine and phosphatidylglycerol are reduced, and that the total concentration of apoproteins is decreased. Furthermore, the surfactant surface tension-lowering activity is abnormal. Thus, administration of exogenous surfactant may have therapeutic benefits. However, the optimal surfactant preparation, the optimal amount required to restore lung surfactant activity, and the optimal method to deliver it to patients with ARDS are unknown and currently under evaluation.
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PMID:[Therapy of ARDS. 2. New management methods--first clinical experiences]. 804 71

Pregnancy often poses a risk to patients with neuromuscular and skeletal disorders when these affect the respiratory muscles or the rib cage. The outlook is determined both by the severity of the underlying condition and the physiological changes during pregnancy. Patients with a vital capacity of less than 1 to 1.5 litres, hypercapnia, severe scoliosis, diaphragm weakness or pulmonary hypertension before pregnancy are particularly at risk. Pregnancy may adversely affect the conducting airways, respiratory pump and gas exchange in the lungs. Close monitoring of high risk patients during pregnancy is required and either a termination of pregnancy or mechanical respiratory support may be indicated if ventilatory or cardiac failure develops.
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PMID:Pregnancy in neuromuscular and skeletal disorders. 808 20

A 62-year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation to provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary hyperventilation.
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PMID:Bilateral carotid body paraganglioma and central alveolar hypoventilation. 826 82

The recent surge in enthusiasm for laparoscopic surgery has created concern that abdominal insufflation with carbon dioxide produces a respiratory acidosis. This may be because of both transperitoneal gas absorption and impaired ventilation with increased dead space from elevated intraabdominal pressure. To examine the relative contributions of these factors, we developed an animal model of surgical pneumoperitoneum that evaluated the cardiorespiratory effects of abdominal insufflation. Helium was chosen as an alternative to CO2 because it is both chemically and biologically inert. Carbon dioxide absorption during CO2 pneumoperitoneum caused arterial PCO2 to increase from 41.3 +/- 3.0 to a maximum of 58.3 +/- 4.0 mm Hg, with pH descending from 7.46 +/- 0.02 to a nadir of 7.31 +/- 0.02 (p < 0.05). Pulmonary artery pressure increased to twice baseline levels during CO2 insufflation (p < 0.05). Helium did not cause hypercarbia, acidemia, or pulmonary hypertension despite insufflation under identical conditions. These results indicate that transperitoneal absorption of CO2, not increased dead space, is responsible for the respiratory acidosis observed. Helium merits further study as an agent to induce pneumoperitoneum, especially when concerns of underlying acidosis or impaired gas exchange are present.
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PMID:Comparative cardiopulmonary effects of carbon dioxide versus helium pneumoperitoneum. 848 70

Patients with obstructive sleep apnea syndrome (OSAS) may have daytime pulmonary hypertension (PH). Transient and sometimes severe elevations of pulmonary arterial pressure during sleep as a result of intermittent upper airway obstruction may lead to daytime PH. We sought to study the factors involved in the development of daytime PH. Right-heart catheterization, pulmonary function tests, and arterial blood gas measurements were done in 25 patients in whom OSAS was diagnosed by whole-night polysomnography. Eight of the patients (32%) had PH, defined by a mean pulmonary arterial (PA) pressure > or = 20 mmHg. For the group as a whole, mean PA pressure was positively and significantly correlated with daytime PaCO2 (r = 0.79), percent of ideal body weight (r = 0.45), and Hb (r = 0.40). Mean PA pressure was negatively and significantly correlated with PaO2 (r = -0.54), FEV 1% (r = -0.52), and %FVC (r = -0.68). In contrast, mean PA pressure was not significantly correlated with apnea index or with sleep desaturation. These data indicate that daytime PH was not directly related to sleep-disordered breathing, but was related to daytime hypoxemia, daytime hypercapnia, obesity, obstructive and restrictive respiratory impairments, and secondary polycythemia.
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PMID:[Daytime pulmonary hypertension in the obstructive sleep apnea syndrome]. 854 78

The most frequent form of lung emphysema leading to respiratory failure is the tobacco bronchitis-induced type of emphysema the so called chronic obstructive pulmonary (lung) disease (COPD). Histologically the centrilobular or centriacinar emphysema is believed to develop due to elastase and oxidant overload with concomitant antiprotease deficiency. The alpha1-antitrypsin deficiency is a rare genetic defect leading also in non-smoking patients to early death due to panlobular or panacinar emphysema. The functional pattern of both emphysema types shows irreversible lung overinflation with severe mainly expiratory bronchial obstruction with various degrees of pulmonary hypertension alpha1-proteinaseNinhibitor deficiency emphysema is prophylactically treated with prolastine and if hypoxia (PaO2 > 55 mm/Hg) is present with long term oxygen therapy. If hypercapnia develops O2 Therapy is combined with non invasive pressure supported ventilation. Volume reducing surgery may precede. In nonsmoking emphysema patients long term oxygen therapy and later unilateral lung transplantation improves quality of life as well as life expectancy.
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PMID:[Pulmonary emphysema--lung transplantation]. 857 95

A 48-year-old man was referred to our hospital because of hypoxemia (PaO2 = 43 mmHg), hypercapnia (PaCO2 = 70 mmHg), complete atrio-ventricular block, and heart failure. He also had limitation of spine flexion, scoliosis, deformity of the rib cage, and constriction of the ankle joints, complicated by cor pulmonale. These findings were compatible with rigid spine syndrome. To avoid progressive pulmonary hypertension and hypoxemia, nasal BiPAP and home oxygen therapy (0.5 liters/minute) were begun. Rigid spine syndrome is clinically characterized by limitation of spine flexion, and the limitation of thoracic movement often causes severe constrictive respiratory dysfunction. This syndrome should be considered when evaluating patients who have both thoracic deformity, especially scoliosis, and respiratory failure.
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PMID:[Rigid spine syndrome associated with marked hypoxemia and hypercapnia]. 875 23

Acutely tightening a snare around one pulmonary artery previously was shown to trigger a reversible ventilation-perfusion (V/Q) mismatch in broilers, as reflected by decreases in the partial pressure of oxygen in arterial blood (hypoxemia), accompanied by increases in the hydrogen ion concentration (acidosis) and partial pressure of carbon dioxide (hypercapnia). In the present study, snares were loosely implanted around the right pulmonary artery and the right extrapulmonary primary bronchus in anesthetized male broilers. These snares were tightened and released independently and then simultaneously to evaluate the possibility that directing the entire respiratory minute volume toward the left lung might attenuate the V/Q mismatch caused by forcing the entire cardiac output (CO) through the left lung. Fully reversible arterial blood hypoxemia, acidosis, and hypercapnia occurred when either snare was tightened independently. Presumably, tightening the bronchial snare restricted ventilation but not blood flow to the right lung, thereby permitting blood to perfuse poorly ventilated gas exchange surfaces. Simultaneously tightening both snares triggered arterial blood hypoxemia, acidosis, and hypercapnia similar to or greater in magnitude than the responses obtained by tightening the pulmonary artery snare independently. Tightening either snare independently or both snares simultaneously caused pulmonary arterial pressure to increase (pulmonary hypertension), and permanent obstruction of one bronchus in a separate experiment caused an increase in the right:total ventricular weight ratio, which is indicative of chronic pulmonary hypertension. The mean systemic arterial pressure decreased when the pulmonary artery snare was tightened independently or in combination with the bronchial snare, but not when the bronchial snare was tightened independently. The respiratory rate increased and the heart rate decreased when the pulmonary artery snare was tightened independently, but not when the bronchial snare was tightened independently or in combination with the pulmonary artery snare. These results demonstrate that the V/Q mismatch caused by forcing all the CO to perfuse one lung cannot be attenuated by simultaneously directing the entire respiratory minute volume toward the same lung.
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PMID:Independent and simultaneous unilateral occlusion of the pulmonary artery and extra-pulmonary primary bronchus in broilers. 893 96

Even if different mechanisms of various interactions during sleep are known, it is still unsolved by which mechanisms physiological reactions during sleep may start a pathophysiological course. Hypoxia, Hypercapnia and repetitive sympathetic elevations are well known elements in the control of the arterial resistance. Furthermore investigations in patients with sleep apnea showed changes of the pulsatile secretion pattern within the renin-angiotensin-system and the antinatriuretic peptides. These changes were reversible under nasal CPAP-therapy, nycturia as a frequent symptom disappeared. Nevertheless neither hypoxia nor intrathoracic pressure changes nor the arousals can assert the longterm influence on the blood pressure alone, a multifactorial confluence must be assumed. Further it is unclear how a tonic increase of the arterial blood pressure may occur in dependence of the REM- and NREM-sleep cycle changes as well as during daytime. First investigations in sleeping man seem to indicate, that a disturbance of the physiological coupling of breathing and circulation may present a pathogenetic element. Finally it remains open, whether the changes of the cardiorespiratory coupling during sleep of control persons and of patients with OSA are comparable, and whether they may be procured for an explanation of the pathogenesis of arterial and pulmonary hypertension. Further investigations in the control mechanisms of breathing and circulation related to the circuits of chemo- and baroreception, thresholds during wakefulness and sleep may be of decisive help to process the question, to what extent clinical states find a correlate in a disturbed cardiorespiratory coupling and, much more significantly, whether a disturbance in the physiological cardiorespiratory coupling appears already in early states of a disease. Sleep with ist complex physiology as well as with its characteristic pathophysiological phenomenon of sleep related breathing disorders has opened a new interdisciplinary field where tools like the polysomnography and electronic data analysis are used by physiologists, pathophysiologists as well as by physicians.
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PMID:[Cardiorespiratory coupling in obstructive sleep apnea (OSA)]. 924 90

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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