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

Patients with bronchial tree lesions feature, in particular, a high risk for developing bronchial fistulae after surgical repair when the clinical situation is complicated by acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and mechanical ventilation is needed. The current authors hypothesised that extracorporeal carbon dioxide removal would significantly decrease inspiratory airway pressures, thus promoting the protection of surgical bronchial reconstruction. Four patients were studied after surgical reconstruction of bronchial fistulae in whom ALI/ARDS developed and mechanical ventilation with positive end-expiratory pressure was required. Gas exchange, tidal volumes, airway pressures, respiratory frequency, vasopressor and sedation requirements were analysed before and after initiation of a pumpless extracorporeal lung assist device (pECLA; NovaLung, Talheim, Germany). Initiation of pECLA treatment enabled a reduction of inspiratory plateau airway pressures from 32.4 to 28.6 cmH(2)O (3.2 to 2.8 kPa), effectively treated hypercapnia (from 73.6 to 53.4 mmHg (9.8 to 7.1 kPa)) and abolished respiratory acidosis (from pH 7.24 to 7.41). All patients survived and were discharged to rehabilitation clinics. In patients after surgical bronchial reconstruction that was complicated by acute lung injury/acute respiratory distress syndrome, use of pumpless extracorporeal carbon dioxide removal was safe and efficient. Initiation of a pumpless extracorporeal lung assist device enabled a less invasive ventilator management, which may have contributed to healing of surgical bronchial repair.
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PMID:Bronchial fistulae in ARDS patients: management with an extracorporeal lung assist device. 1904 7

Dyspnea, or the uncomfortable awareness of respiratory distress, is a common symptom experienced by most people at some point during their lifetime. It is commonly encountered in individuals with pulmonary disease, such as chronic obstructive pulmonary disease (COPD), but can also be seen in healthy individuals after strenuous exercise, at altitude or in response to psychological stress. Dyspnea is a multifactorial sensation involving the brainstem, cortex, and limbic system, as well as mechanoreceptors, irritant receptors and chemoreceptors. Chemoreceptors appear to contribute to the sensation of dyspnea in two ways. They stimulate the respiratory control system in response to hypoxia and/or hypercapnia, and the resultant increase respiratory motor output can be consciously perceived as unpleasant. They also can induce the sensation of dyspnea through an as yet undetermined mechanism-potentially via direct ascending connections to the limbic system and cortex. The goal of this article is to briefly review how changes in blood gases reach conscious awareness and how chemoreceptors are involved in dyspnea.
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PMID:Role of chemoreceptors in mediating dyspnea. 1911 47

The effects of the combination of a 'lowest' lung ventilation with extracorporeal elimination of carbon dioxide by interventional lung assist are described in a patient presenting with severe acute respiratory distress syndrome due to fulminant pneumonia. Reducing tidal volume to 3 ml.kg(-1) together with interventional lung assist resulted in a decrease in severe hypercapnia without alveolar collapse or hypoxaemia but with a decrease in serum levels of interleukin-6. This approach was applied for 12 days with recovery of the patient, without complications. Extracorporeal removal of carbon dioxide by interventional lung assist may be a useful tool to enable 'ultraprotective' ventilation in severe acute respiratory distress syndrome.
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PMID:Pumpless extracorporeal removal of carbon dioxide combined with ventilation using low tidal volume and high positive end-expiratory pressure in a patient with severe acute respiratory distress syndrome. 1914 99

A 3-month-old boy was admitted to the intensive care unit because of septic shock; he required immediate intubation and placement of a nasogastric tube. A confirmatory chest radiograph showed that the nasogastric tube was looping in the hypopharynx and needed to be repositioned. During removal of the nasogastric tube, the infant experienced hypercapnia and respiratory distress. These complications were due to looping and knotting of the nasogastric tube around the nasotracheal tube.
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PMID:Knotting of nasogastric tube around a nasotracheal tube: An unusual cause of hypercapnia in a 3-month-old infant. 1938 61

Retinopathy of prematurity (ROP) is a complex disease of the developing retinal vasculature in premature infants. Clinical manifestations range from mild, usually transient changes of the peripheral retina to severe progressive vasoproliferation, and potentally blinding retinal detachment. With better standards in premature units and with increased survival rate of low gestational age and low birth weight infants the incidence of ROP also increased. The incidence of ROP has been decreasing in developed countries over the past decade, and ROP has become potentially confined to immature neonates with birth weights less than 1000 grams in these countries. Prematurity and retinal immaturity are the major risk factors. Oxygenation, respiratory distress, apnea, bradycardia, hearth disease, infection, hypercarbia, acidosis, anemia, and the need for transfusion are thought by some to be contributory factors. All of the preterm babies with a birth weight under 1500 grams and a gestational age under 32 weeks should be followed for ROP.
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PMID:[Retinopathy of prematurity]. 1940 50

Permissive hypercapnia, achieved using low tidal volume ventilation, has been an effective protective strategy in patients with acute respiratory distress syndrome. To date, no such protective effect has been demonstrated for the chronic neonatal lung injury, bronchopulmonary dysplasia. The objective of our study was to determine whether evolving chronic neonatal lung injury, using a rat model, is resistant to the beneficial effects of hypercapnia or simply requires a less conservative approach to hypercapnia than that applied clinically to date. Neonatal rats inhaled air or 60% O2 for 14 days with or without 5.5% CO2. Lung parenchymal neutrophil and macrophage numbers were significantly increased by hyperoxia alone, which was associated with interstitial thickening and reduced secondary crest formation. The phagocyte influx, interstitial thickening, and impaired alveolar formation were significantly attenuated by concurrent hypercapnia. Hyperoxic pups that received 5.5% CO2 had a significant increase in alveolar number relative to air-exposed pups. Increased tyrosine nitration, a footprint for peroxynitrite-mediated reactions, arteriolar medial wall thickening, and both reduced small peripheral pulmonary vessel number and VEGF and angiopoietin-1 (Ang-1) expression, which were observed with hyperoxia, was attenuated by concurrent hypercapnia. We conclude that evolving chronic neonatal lung injury in a rat model is responsive to the beneficial effects of hypercapnia. Inhaled 5.5% CO2 provided a significant degree of protection against parenchymal and vascular injury in an animal model of chronic neonatal lung injury likely due, at least in part, to its inhibition of a phagocyte influx.
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PMID:Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats. 1974

The objective of this case-based review is to identify and summarize the relevant evidence for the clinical utility of peripheral venous blood gas (pVBG) analyses in patients with acute exacerbations of chronic obstructive pulmonary disease (COPD) treated in the emergency department. Relevant studies were identified using the Cochrane Library, Medline, Embase, and CINAHL databases and by hand searching of references of published articles. Included studies were prospective trials comparing arterial and pVBG results in patients with COPD or respiratory distress that reported at least average differences and/or limits of agreement between the two results in English. Outcomes of interest were agreement between arterial and pVBG values for pH, pCO2, pO2, and HCO3. Eighty-nine studies were identified of which six were relevant. The weighted average difference for pCO2 was 5.92 mmHg, whereas those for pH, pO2, and HCO3 were 0.028, 18.65 mmHg, and 1.34 mEq/l, respectively. Using Bland-Altman analysis, the 95% limits of agreement were in the range of -0.10 to 0.08, -17 to 26 mmHg and, -3.5 to 3.5 mEq/l for pH, pCO2, and HCO3, respectively. Reported cutoff pVBG pCO2 values for screening of arterial hypercarbia ranged from 30 to 46 mmHg. No studies investigated the role of pVBG analysis in treatment alteration or clinical outcomes. Available evidence suggests that there is good agreement for pH and HCO3 values between arterial and pVBG results in patients with COPD, but not for pO2 or pCO2. Widespread clinical use is limited because of the lack of validation studies on clinical outcomes.
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PMID:A meta-analysis on the utility of peripheral venous blood gas analyses in exacerbations of chronic obstructive pulmonary disease in the emergency department. 1999 74

There have been contradictory reports suggesting that CO(2) may constrict, dilate, or have no effect on pulmonary vessels. Permissive hypercapnia has become a widely adopted ventilatory technique used to avoid ventilator-induced lung injury, particularly in patients with acute respiratory distress syndrome (ARDS). On the other hand, respiratory alkalosis produced by mechanically induced hyperventilation is the mainstay of treatment for newborn infants with persistent pulmonary hypertension. It is important to clarify the vasomotor effect of CO(2) on pulmonary circulation in order to better evaluate the strategies of mechanical ventilation in intensive care. In the present study, pulmonary vascular responses to CO(2) were observed in isolated rat lungs (n = 32) under different levels of pulmonary arterial pressure (PAP) induced by various doses of endothelin-1 (ET-1). The purposes of this study were to investigate (1) the vasodilatory effect of 5% CO(2) in either N(2) (hypoxic-hypercapnia) or air (normoxic-hypercapnia) at different PAP levels induced by various doses of endothelin-1, and (2) the role of nitric oxide (NO) in mediating the pulmonary vascular response to hypercapnia, hypoxia, and ET-1. The results indicated that (1) CO(2) produces pulmonary vasodilatation at high PAP under ET-1 and hypoxic vasoconstriction; (2) the vasodilatory effect of CO(2) at different pressure levels varies in accordance with the levels of PAP, the dilatory effect tends to be more evident at higher PAP; and (3) endogenous NO attenuates ET-1 and hypoxic pulmonary vasoconstriction but does not augment the CO(2)-induced vasodilatation.
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PMID:Effect of carbon dioxide on pulmonary vascular tone at various pulmonary arterial pressure levels induced by endothelin-1. 2021 11

Pulmonary contusion is a common finding after blunt chest trauma. The physiologic consequences of alveolar hemorrhage and pulmonary parenchymal destruction typically manifest themselves within hours of injury and usually resolve within approximately 7 days. Clinical symptoms, including respiratory distress with hypoxemia and hypercarbia, peak at about 72 h after injury. The timely diagnosis of pulmonary contusion requires a high degree of clinical suspicion when a patient presents with trauma caused by an appropriate mechanism of injury. The clinical diagnosis of acute parenchymal lung injury is usually confirmed by thoracic computed tomography, which is both highly sensitive in identifying pulmonary contusion and highly predictive of the need for subsequent mechanical ventilation. Management of pulmonary contusion is primarily supportive. Associated complications such as pneumonia, acute respiratory distress syndrome, and long-term pulmonary disability, however, are frequent sequelae of these injuries.
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PMID:Pulmonary contusion: an update on recent advances in clinical management. 2040 67

The authors present their experience in treating 142 patients with severe viral respiratory infection caused by influenza A (H1N1), describe its clinical picture, and identify major syndromes observed in the treatment of these patients at an intensive care unit. A rapid development of acute respiratory distress syndrome, significant hypoxemia and hypercapnia with the low efficiency of various therapeutic measures and hence progressive organ dysfunction determine the essence of the severe course of the disease. Uniform guidelines for intensive care in this patient population are presented.
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PMID:[Experience in treating severe viral respiratory infection caused by influenza A (H1N1)]. 2073 42


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