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

Hypercapnic respiratory failure due to chronic obstructive pulmonary disease (COPD) is an indicator of poor prognosis compared to that for normocapnic patients. On the other hand, there exist particular patients who are hypercapnic during an acute exacerbation of COPD but revert to normocapnia after adequate therapy. The aims of this study were: 1) to document the admission characteristics of such patients in terms of clinical and laboratory findings; and 2) to analyse the long-term course and survival of chronic and reversible hypercapnic and normocapnic patients. Fifty-six consecutive patients, admitted with an acute exacerbation of COPD, were enrolled and divided into three groups according to arterial carbon dioxide tension (Pa,CO2) at first admission: 22 chronic hypercapnic (group 1), 15 reversible hypercapnic (group 2) and 19 normocapnic (group 3) patients. Age, sex, smoking history, white blood cell count, serum sodium, potassium, urea and albumin levels and pulmonary function tests at first admission were similar in the three groups. The haematocrit level was significantly higher in group 1 compared with the other groups. Groups 1 and 2 had lower pH, arterial oxygen tension (Pa,O2) and arterial oxygen saturation (Sa,O2) and a higher Pa,CO2 than group 3. The Pa,CO2 was also higher in group 1 than in group 2. The presence of cor pulmonale was significantly higher in group 1 compared with groups 2 and 3 (81.8 versus 60 and 10.5%, respectively). During the follow-up period, a significant increase was observed in airway obstruction associated with progressive hypercapnia and hypoxaemia in chronic hypercapnic patients, and 12 of 15 (80%) reversible hypercapnic patients progressed to a chronic hypercapnic status. The survival analyses after 10 yrs of follow-up revealed comparable survival durations in chronic and reversible hypercapnic patients (median of 8.86 versus 9.52 yrs, p > 0.05). In conclusion, despite careful monitoring of particular characteristics in chronic and reversible hypercapnic patients at the time of admission, no long-term predictivity of these features for either the course of the disease or survival could be found.
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PMID:Distinctive features and long-term survival of reversible and chronic hypercapnic patients with COPD. 1044 72

Idiopathic congenital central alveolar hypoventilation syndrome, otherwise known as Ondine's curse, is a rare neuropathologic syndrome characterized by an inadequate respiratory drive with hypoventilation and periods of prolonged apnea resulting in hypercarbia and hypoxemia. Although no definite pathologic abnormality has been identified to account for the disorder, it is thought to represent a primary defect related to altered function of central chemoreceptors resulting in defective control of minute ventilation. Associated problems related to neural crest cell migration, including neuroblastoma formation and Hirschsprung's disease, suggest that the primary defect is defective neural crest cell migration and function. Problems that may impact on perioperative care include the defective central control of ventilation and defective control of upper respiratory musculature, which may lead to upper airway obstruction. Although many patients will have previously undergone tracheostomy and chronic mechanical ventilation, problems in other organ systems can impact on perioperative care. Cardiovascular issues include the possible presence of cor pulmonale and autonomic nervous system dysfunction. Central nervous system issues include the frequent occurrence of seizures and mental retardation. The preoperative work-up, premedication, and the intraoperative/postoperative care and monitoring of these patients is reviewed.
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PMID:Anesthetic care for the child with congenital central alveolar hypoventilation syndrome (Ondine's curse). 1052 17

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake PaO(2) level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.
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PMID:Impact of sleep in COPD. 1067 75

Obesity is a well-known cause of upper airway narrowing, respiratory failure and resulting hypoxemia and hypercapnia, and cardiac arrhythmias during sleep. Obese patients are prone to snore loudly and to develop obstructive sleep apnea syndrome and also obesity-hypoventilation syndrome. Repeated nocturnal upper airway obstruction may cause respiratory failure and cor pulmonale and frequent awakenings, and result in nocturnal choking, with daytime drowsiness, somnolence and irritability. The purpose of this article is to review the evidence for these accepted facts and to consider a variety of new information that relates to the pathogenesis, symptomatology and treatment of sleep disorders caused by obesity.
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PMID:Sleep-related Disorders in the Obese. 1076 3

Some patients with obesity show chronic hypercapnia while awake. Such patients are referred to as obesity hypoventilation syndrome(OHS). Particularly, patients with profound obesity who have clinical features of sleep disordered breathing, hypersomnolence, cor pulmonale and so on represent the Pickwickian syndrome. The mechanisms of hypoventilation in OHS are multifactorial. The level of the blunted chemosensitivity, mechanical impairments of the respiratory system, the severity of the sleep-disordered breathing, and chronic hypoxemia may be important determinants of chronic hypoventilation. In this paper, the characteristics of pulmonary functions in obesity and the possible mechanisms of hypoventilation in patients with OHS were reviewed. Furthermore, the definition of OHS and descriptions of thr severity of OHS as recommended by Respiratory Failure Research Committee of Japanese Ministry of Health and Welfare are introduced.
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PMID:[Obesity and obesity hypoventilation syndrome]. 1094 42

Cor pulmonale is defined as "hypertophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, as congenital heart disease". Pulmonary hypertension is a frequent hemodynamic complication associated with a wide variety of respiratory systems disorders whose only common physiologic abnormalities are alveolar hypoxia and consequent arterial hypoxemia of longterm duration. The sustained elevation in pulmonary arterial hypertension is thought to be mediated through two pathophysiologic vascular mechanism: 1) persistent vasoconstriction and 2) vascular structural remodeling. The combination of these processes causes vascular luminal narrowing and vessel obliteration that reduce pulmonary vascular surface area to the critical degree necessary for the development of the pulmonary hypertension. Cor pulmonale may be difficult to diagnose, particularly early in its course, when they symptoms manifested may be interpreted as representing progression of an underlying pathophysiological state, such as chronic obstructive airways disease. The treatment of cor pulmonale is directed toward reversing the pathogenetic process that can be directly treated, while at the same time relieving the hypoxemia, hypercapnia or acidosis. At present long-term oxygen therapy is the best treatment for pulmonary hypertension. Heart failure in cor pulmonale is usually transient once the initiating mechanism is controlled. The usual therapeutic measures for heart failure apply: a low-salt regimen, and diuretics.
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PMID:[Chronic cor pulmonale]. 1114 67

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.
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PMID:[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. 1156 26

Chronic obstructive pulmonary disease (COPD) often leads to massive oedema and the development of what is usually called cor pulmonale. The mechanisms by which patients with COPD retain salt and water are not completely understood. Several abnormalities have been found including reduced renal blood flow with relatively preserved glomerular filtration rate and elevated levels of renin, aldosterone, arginine vasopressin and atrial natriuretic peptide. Generally, these abnormalities worsen with the severity of COPD and are most marked during the oedematous phases. Cardiac output is remarkably normal, suggesting that "cor pulmonale" is not primarily a cardiac disorder but rather a condition of volume overload due to activation of sodium-retaining mechanisms. The stimulus for this activation could be underfilling of the arterial system (reduced effective circulating volume) secondary to a fall in total peripheral vascular resistance. The latter is caused by hypercapnia-induced dilation of the precapillary sphincters. Apparently, the massive sodium retention by the kidney is not able to restore the circulating volume and a vicious cycle ensues ultimately leading to a clinical picture which resembles right-sided heart failure. Predictably, only blockade of the effects of carbon dioxide at the level of the precapillary sphincters would be able to halt this process.
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PMID:Fluid homeostasis in chronic obstructive lung disease. 1462 Nov 5

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

The authors report the results of a study on patients with chronic cor pulmonale hospitalized in the Departement of Cardiology (Dakar), from 1990 to 1998. The hospital prevalence is 0.9% with a male predominance (73.5%). The clinical signs were dominated by dyspnea and cough. The right heart failure is noted in 85.29% of cases. As far as the biological factor is concerned, it exists an polycythemia about 75% of cases, hypoxia (88.8%), hypercapnia (55.5%) and a respiratory acidoses (55.5%). The spirometry showed in 66% of cases, a mixed syndrom with obstructive predominance. The echocardiography showed in all cases right heart dilatation with pulmonary hypertension. The etiological factors are dominated by tobacco (21 cases). The hospital evolution has been favorable in 19 cases underoxygentherapy, lowdosediuretic, expectorant, bronchodilatators and salt restriction. However, 14 patients have died.
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PMID:[Chronic cor pulmonale: a study of 34 cases in the Dakar University Hospital Center Cardiology Department]. 1577 62


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