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

Congenital central alveolar hypoventilation syndrome (CCAHS) is a disorder of ventilatory control that occurs without neuromuscular blockade or pulmonary disease. It is characterized by a lack of response to habitual respiratory stimulants, especially hypercapnia. In this article, the management of this syndrome by diaphragmatic pacing is discussed. Paralysis of the phrenic nerve in small children usually results from injury during birth or during a cardiothoracic operation and results in eventration of the hemidiaphragm. Alternatively, eventration of the diaphragm may be a congenital condition. In both cases it may lead to respiratory distress in the newborn. In this article, we review the diagnosis of these conditions and their management, focusing on the surgical indications. We also discuss outcome.
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PMID:Central hypoventilation and diaphragmatic eventration: diagnosis and management. 1252 Apr 71

Although permissive hypercapnia improves the prognosis of patients with acute respiratory distress syndrome, it has not been conclusively determined whether hypercapnic acidosis (HA) is harmful or beneficial to sustained inflammation of the lung. The present study was designed to explore the molecular mechanism of HA in modifying lipopolysaccharide (LPS)-associated signals in pulmonary endothelial cells. LPS elicited degradation of inhibitory protein kappaB (IkappaB)-alpha, but not IkappaB-beta, resulting in activation of nuclear factor (NF)-kappaB in human pulmonary artery endothelial cells. Exposure to HA significantly attenuated LPS-induced NF-kappaB activation through suppressing IkappaB-alpha degradation. Isocapnic acidosis and buffered hypercapnia showed qualitatively similar but quantitatively smaller effects. HA did not attenuate the LPS-enhanced activation of activator protein-1. Following the reduced NF-kappaB activation, HA suppressed the mRNA and protein levels of intercellular adhesion molecule-1 and interleukin-8, resulting in a decrease in both lactate dehydrogenase release into the medium and neutrophil adherence to LPS-activated human pulmonary artery endothelial cells. In contrast, HA did not inhibit LPS-enhanced neutrophil expression of integrin, Mac-1. Based on these findings, we concluded that hypercapnic acidosis would have anti-inflammatory effects essentially through a mechanism inhibiting NF-kappaB activation, leading to downregulation of intercellular adhesion molecule-1 and interleukin-8, which in turn inhibits neutrophil adherence to pulmonary endothelial cells.
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PMID:Hypercapnic acidosis attenuates endotoxin-induced nuclear factor-[kappa]B activation. 1260 Aug 32

Congenital lobar emphysema (CLE) is characterized by overdistension and air-trapping in the affected lobe, and is one of the causes of infantile respiratory distress. In this report, we review our 27 years of experience with 30 CLE patients. Patients' medical records were evaluated with regard to age, clinical presentation, diagnostic methods, associated diseases, treatment, histopathologic findings, and final clinical and laboratory findings at the end of a long-term period. The mean age of 30 patients (18 male) at diagnosis was 4.9 +/- 6.7 months (range, 2 days-2.5 years). Tachypnea, dyspnea, cough, cyanosis, wheezing, hoarseness, and decreased breath sounds on the affected side were the main symptoms and clinical findings. On chest X-rays, emphysema was seen in all patients; shift/herniation to the opposite lung, atelectasis, and pneumothorax were observed in 16, 5, and 2 cases, respectively. Computerized tomography of the thorax was performed in 16 cases and revealed emphysema at affected lobe/lobes in all, a shift/herniation to the opposite side in 12 cases, and atelectasis of neighbor lobe/lobes in 7 cases. All 8 patients who had perfusion scintigraphy showed reduced perfusion in the affected lobe. Narrowed and flaccid bronchi were detected in one patient by using flexible bronchoscopy. Blood gas analysis was performed in 11 patients, and hypoxia and hypercarbia were revealed in 9 and 7 of these patients, respectively. The most common affected lobe was the left upper lobe (57%), followed by the right upper lobe (30%) and right middle lobe (27%). Two lobes were involved in 4 patients. Associated abnormalities were observed in 5 patients. Twenty-one patients underwent lobectomy; 9 were followed conservatively. Ages at diagnosis were significantly younger in surgically treated patients. Emphysema was detected in all pathological specimens, with an additional bronchial cartilage deficiency in 2 patients. In the surgically treated group, 2 patients died and 2 patients were lost to follow-up. In the conservatively treated group, one patient was lost to follow-up. Mean follow-up duration of all patients was 63.2 +/- 56.2 months (range, 1-209 months). At follow-up visits, all patients were doing well. In surgically treated patients, chest X-rays were normal (9 cases), or showed hyperlucency on the operated side (6 cases) or chronic changes in the operation area (2 cases). Hyperexpansion in the affected lobe was found to be reduced in all cases in the conservatively treated group.
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PMID:Congenital lobar emphysema: evaluation and long-term follow-up of thirty cases at a single center. 1268 96

The application of high thoracic epidural anesthesia (TEA) as an adjunct to general anesthesia is increasingly being used for coronary artery bypass grafting (CABG) with extracorporeal circulation. Recent developments in beating heart techniques rendered the sole use of TEA in conscious patients possible, and have been reported for single-vessel beating heart CABG via lateral thoracotomy. For multi-vessel revascularization, the heart is usually approached via sternotomy; therefore, the sole use of TEA was applied in awake patients who underwent CABG via sternotomy. A total of 7 patients scheduled for awake coronary artery bypass grafting (ACAB) received TEA via an epidural catheter placed at the levels of T1-2 or T2-3, respectively. Total arterial myocardial revascularization was performed after partial lower sternotomy. Besides standard monitoring, anesthetic levels were determined using an epidural scoring scale for arm movements (ESSAM). While 6 patients were awake and spontaneously breathing during the entire procedure, one patient had to be intubated intraoperatively because of respiratory distress caused by phrenic nerve palsy. Hemodynamics were stable throughout the operation. No significant arterial hypercarbia occurred. All patients rated TEA as "good" or "excellent." We could demonstrate that the single use of TEA for CABG via sternotomy was feasible and that the patients felt well, were painfree, and remained hemodynamically stable. High patient satisfaction in our small and highly selected cohort can be reported. Because beating heart surgery in a conscious patient still carries a significant risk, further randomized controlled trials are mandatory to definitively evaluate the role of sole TEA in cardiac surgery.
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PMID:Coronary artery bypass grafting via sternotomy in conscious patients. 1271 18

Hypercapnic acidosis protects against direct lung injury in in vivo and ex vivo models, however, lung injury/acute respiratory distress syndrome commonly occurs after a nonpulmonary etiology. We investigated whether therapeutic hypercapnia (TH)-deliberate elevation of carbon dioxide (CO2) tension-would protect against lung injury after splanchnic ischemia-reperfusion injury in an in vivo model. TH was associated with preservation of lung mechanics, attenuation of protein leakage, and improved oxygenation compared with control conditions. Lung protection was therapeutic as well as prophylactic. Protection was dose-dependent, but inspired CO2 concentrations above 5.0% were associated with little additional lung protection. Before lung injury, increasing FICO2 resulted in a dose-dependent increase in PaO2. Lung protection with hypercapnia occurred despite pulmonary artery pressures that were greater than observed with normocapnia. Reperfusion increased lipid peroxidation (tissue 8-isoprostane concentration) in the bowel, liver, and lung, and caused histologically apparent bowel injury; however, none of these effects was altered by TH. Therefore, TH-induced by adding CO2 to inspired gas-provides consistent protection against lung injury in terms of lung permeability, oxygenation, and lung mechanics after mesenteric ischemia-reperfusion. These data further support the emerging evidence for ongoing physiologic study of TH at the bedside.
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PMID:Effects of therapeutic hypercapnia on mesenteric ischemia-reperfusion injury. 1464 26

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

The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.
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PMID:Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthetic implications. 1471 77

We experienced 2 patients with acute respiratory distress syndrome (ARDS) from pneumonia after intervention for subarachnoidal hemorrhage. We applied lung protective ventilation strategy (LPVS) on both cases: a tidal volume less than 6 ml x kg(-1) ideal body weight and PEEP at 10-15 cmH2O. Although etiology and degree of hypoxia were very similar in two patients when ARDS was diagnosed, clinical course was quite different. The patient in whom LPVS had been started on the 5th day of ARDS required mechanical ventilation of 23 days. In contrast, another patient in whom LPVS had been started on the 16th day of ARDS required mechanical ventilation of 219 days. PaCO2 during LPVS with permissive hypercapnia in the latter patient increased up to 161 mmHg but no adverse effect was observed. These cases suggest that early application of the LPVS may be important to improve respiratory outcomes of ARDS patients.
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PMID:[Early application of the lung protective ventilation strategy at different stages in two ARDS patients]. 1519 34

Mechanical ventilation is necessary for treating patients with severe brain injury because it guarantees the airway (through endotracheal intubation), permits sedation (and even curarization), and prevents hypoxemia and/or hypercapnia. Hyperventilation continues to be a focus of debate in the current literature. Nevertheless, the weight of scientific evidence to date suggests that it should not be applied prophylactically during the first 24 hours and that patients should not be hyperventilated for prolonged periods in the absence of intracranial hypertension. Acute lung injury and respiratory distress are among the most frequent and serious complications related to severe brain injury that benefit from the use of positive end-expiratory pressure (PEEP) and ventilation to protect the lung. Gas insufflation through the trachea is a promising therapeutic option for correcting hypercapnia secondary to ventilation for lung protection in such patients. Finally, multimodal monitoring (intracranial pressure, central venous pressure, oxygen saturation detected in the jugular bulb, cerebral oxygen pressure) is recommended for adjusting PEEP and controlling hyperventilation.
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PMID:[Ventilatory management of the severely brain-injured patient]. 1520 Jan 86

Congenital central hypoventilation syndrome (CCHS) is a rare syndrome, present from birth, and is defined as the failure of automatic control of breathing. Patients have absent or negligible ventilatory sensitivity to hypercapnia and hypoxaemia during sleep and wakefulness. Therefore, especially while asleep, children with CCHS experience progressive hypercapnia and hypoxaemia. They lack arousal responses and sensations of dyspnoea to the endogenous challenges of isolated hypercapnia and hypoxaemia and to the combined stimulus of hypercapnia and hypoxaemia. Patients with CCHS do not exhibit signs of respiratory distress when challenged with hypercarbia or hypoxia. The diagnosis is one of exclusion, ruling out any primary pulmonary, cardiac, metabolic or neurologic cause for central hypoventilation. CCHS is associated with other manifestations of autonomic nervous system dysfunction, including Hirschsprung's disease. All patients with CCHS require lifelong ventilatory support during sleep but some will be able to maintain adequate ventilation without assistance while awake once past infancy. However, some CCHS patients require ventilatory support for 24h/day. Modalities of home mechanical-assisted ventilation include positive pressure ventilation via tracheostomy, non-invasive positive pressure ventilation (bi-level ventilation), negative pressure ventilation and diaphragmatic pacers. Supplemental oxygen alone is inadequate treatment. With early diagnosis and adequate ventilatory support, these children can have good outcomes and lead productive lives.
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PMID:Congenital central hypoventilation syndrome: not just another rare disorder. 1527 29


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