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

For over 15 years, upper respiratory tract obstruction due to adenotonsillar hypertrophy has been known to cause hypoxia, hypercapnia, increased pulmonary vascular resistance and thereby cor pulmonale and congestive heart failure. This is now an uncommon but not rare entity and three recent cases prompted this report. The typical patient is dyspneic with retractions, cyanosis, occasional periods of apnea and somnolence. Edema and hepatomegaly and at times splenomegaly are common. X-rays show cardiomegaly, which on electrocardiogram is found to involved mainly the right ventricle. The strict definition of cor pulmonale is right ventricular hypertrophy secondary to lung disease or abnormal pulmonary function, a definition that may logically be stretched to include abnormal respiratory function secondary to upper airway pathology. The mechanisms by which this occurs are generally agreed upon. Hypoxia has been demonstrated to cause pulmonary vasoconstriction. Acidosis and hypercapnia are thought by some to have the same effect. Pressure across the pulmonary vascular bed is also increased, as predicted by Poiseuille's law, by the high rate of blood flow required to maintain tissue oxygenation with poorly oxygenated blood. Conditions producing hypoxia of hypercapnia or both lead to hypertrophy and eventually to dilatation of the right ventricle. Three cases of children who underwent cardiac catheterization while suffering from cor pulmonale due to adenotonsillar hypertrophy are reported. Right ventricular pressure averaged 44/5, PAO2 72, pH 7.32, and PACO2 52. All were clinically improved following adenotonsillectomy. Cardiac catheterization was repeated in one case, with right ventricular pressure dropping from 44/5 to 21/2, pulmonary vascular resistance from eight units to three, and PACO2 from 62 to 44.
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PMID:Cardiac and pulmonary failure secondary to adenotonsillar hypertrophy. 95 48

Since February 1990, five children, aged 10 days to 6.5 years, were treated with extracorporeal lung support at our hospital for acute, unrelenting pulmonary failure. Two had viral pneumonia: one with respiratory syncytial virus (RSV) bronchiolitis, and one with herpes simplex virus pneumonia, encephalitis, and disseminated intravascular coagulation. One presented with a febrile illness followed by a pulmonary hemorrhage. Two patients had adult respiratory distress syndrome (ARDS) complicating severe systemic illnesses, toxic epidermal necrolysis in one and cat scratch disease with encephalitis in the other. All children had diffuse parenchymal lung disease by chest x-ray. On maximum medical management all patients were developing carbon dioxide retention and progressive hypoxemia, exceeding previously established NIH study criteria for extracorporeal treatment. Three children (10 days, 2 months, 13 months) were placed on venoarterial support and two children (20 months and 6.5 years) were placed on venovenous extracorporeal support (ECCO2R). Three of the five had open lung biopsies performed, which showed findings consistent with a moderate to severe cellular phase of ARDS. No viral inclusions were found in the patient with RSV infection. One hundred percent immediate survival was achieved in this patient population. Average duration of support was 330 hours (range, 89 to 840). Following completion of extracorporeal support, all children were successfully weaned from the ventilator with an average time to extubation of 23.2 days (range, 2 to 58 days). One child died of congestive heart failure following palliative surgery for a complex noncyanotic congenital cardiac lesion 35 days after successfully weaning from extracorporeal support for an acute febrile illness and pulmonary hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of acute pulmonary failure with extracorporeal support: 100% survival in a pediatric population. 132 87

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

Cardiopulmonary complications such as sudden death, congestive heart failure and hypercapnia are now recognized to punctuate the refeeding course of malnourished hospitalized patients; these effects in particular occur early in the recovery period. Data that indicate a time-dependent dose and composition effect of continuously infused formula on gas exchange, metabolic rate, ventilation and cardiac-related indexes are discussed. Unlike the interrupted feeding of regular meal ingestion, continuous feeding produces a sustained physiologic response. Delineation of continuous feeding effects on host metabolism provides a rational basis for managing the untoward cardiac and pulmonary complications of nutrition support.
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PMID:Physiologic response and clinical implications of nutrition support. 311 92

Blood gas and haemodynamic changes caused by chronic respiratory insufficiency affect the right ventricle and produce chronic cor pulmonale. Equally important but less well known modifications affect the left ventricle and the general circulation and are the subject of the present report. Hypoxemia, hypercapnia and acidosis caused by severe hypoxia create functional disturbances in both ventricles that are manifested in a volume overload that added to other major malfunctions provoke congestive heart failure. The coronary circulation is affected by metabolic factors, perfusion alterations, right ventricular hypertrophy and concomitant coronary lesions. Advanced respiratory insufficiency caused by poorly compensated respiratory acidosis and metabolic acidosis reduces cardiac output and frequency so that tissue perfusion is compromised. Furthermore alterations in transmembrane electrolytic concentrations produce repeated multifocal ventricular arrhythmias that expose the patient to the risk of sudden death. Cardiac failure is reflected in other organs like the kidney and the central nervous system and also contributes to tissue and cerebral hypoxia. The later depresses the respiratory centres and develops into often irreversible coma. A better knowledge of these elements may contribute to the development of appropriate treatment.
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PMID:[General cardiocirculatory effects in chronic respiratory insufficiency]. 354 42

Five infants with Pierre Robin syndrome developed evidence of carbon dioxide retention and congestive cardiac failure despite measures to alleviate upper airway obstruction. Investigations included chest radiography, electrocardiography, echocardiography, and cardiac catheterization; pulmonary hypertension was diagnosed. In two cases raised main pulmonary artery pressures of 40 mm Hg and 120 mm Hg were recorded. Relief of upper airway obstruction was achieved by tracheostomy in three cases and nasopharyngeal intubation in two cases, with reversal of signs of cor pulmonale in each. Four patients progressed well with no recurrence of cardiac problems but one died suddenly one month after apparently successful management by tracheostomy.
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PMID:Pierre Robin syndrome and pulmonary hypertension. 388 27

A controlled trial of long term domiciliary oxygen therapy has been carried out in three centres in the U.K. The 87 patients, all under 70 years of age, who took part had chronic bronchitis or emphysema with irreversible airways obstruction, severe arterial hypoxaemia, carbon dioxide retention, and a history of congestive heart failure. The patients were randomised to oxygen therapy (treated) or no oxygen (controls). Oxygen was given by nasal prongs for at least 15 h daily, usually at 2 1/min. The two groups were well matched, both clinically and in terms of lung function and other laboratory findings. 19 of the 42 oxygen treated patients died in the five years of survival follow-up compared with 30 out of 45 controls: in the 66 men in this trial the survival advantage of oxygen did not emerge until 500 days had elapsed. Survival for the 12 female controls was surprisingly poor, 8 of them being dead at 3 years. Mortality was not easy to predict, though a summation of arterial carbon dioxide tension and red cell mass was helpful. Neither time spent in hospital because of exacerbations of respiratory failure nor work attendance were affected by oxygen therapy, but these patients were very ill at the start of the trial and many had already retired on grounds of age or ill-health. Physiological measurements suggested that oxygen did not slow the progress of respiratory failure in those who died early. However, in longer term survivors on oxygen, arterial oxygenation did seem to stop deterioration.
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PMID:Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party. 611 Sep 12

We describe continuous positive airway pressure (CPAP) by mask to reduce hypercarbia in two patients who had pulmonary edema due to congestive heart failure. In such patients, beside reducing venous return and filling pressures, CPAP improves compliance and decreases the work of breathing, thereby improving effective ventilation. Hence, CPAP may be useful to combat not only hypoxemia but also hypercarbia that is associated with pulmonary edema.
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PMID:Effectiveness of CPAP by mask for pulmonary edema associated with hypercarbia. 633 82

A review of the relevant literature was stimulated by recent publications urging extensive laboratory assessment of elderly patients presenting with intellectual impairment. Published data regarding reversible causes of impairment are limited and exist only for hospitalized patients, with rare exceptions. The frequencies of azotemia, hyponatremia, volume depletion, hypoglycemia, cardiac arrhythmia, cerebrovascular disease, sensory impairment, hypercarbia, congestive heart failure, infections, subdural hematoma, and chemical intoxications as causes of the intellectual impairment are entirely unknown. It is reported that 8 per cent of patients hospitalized for dementia are depressed; alcoholism is causative in 8 to 13 per cent of patients with mental impairment; normal pressure hydrocephalus is reported in 7 to 12 per cent. The frequency of the latter conditions in outpatients is not known. While estimates exist for the frequencies of hypothyroidism, hyperparathyroidism, neurosyphilis, and vitamin B12 and folate deficiencies among the elderly, no prevalence data exist for these disorders among the intellectually impaired.
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PMID:Reversible intellectual impairment: an internist's perspective. 711 32

With airway obstruction there is a decrease in inspiratory intrathoracic pressure. This could lead to increased venous return to the right ventricle (RV) and increased afterload imposed on the left ventricle (LV). Chronic upper airway obstruction, caused by either upper airway lesions or obstructive sleep apnea, is a cause of congestive heart failure because of a chronic resistive load imposed on the respiratory system. To determine the effects of chronic upper airway obstruction on RV and LV in adolescent rats, we chronically obstructed the trachea so as to considerably increased inspiratory esophageal pressure excursion (-3.7 +/- 2.2 to -29.4 +/- 10.1 cm H2O). Rats were studied at 7 wk (Group 1) and at 1 yr (Group 2) after tracheal banding. Sham-operated time-matched rats served as controls. In neither group was there evidence of arterial hypoxemia, but in both groups there was chronic hypercapnia (PCO2, approximately 51 mm Hg; bicarbonate, 27 to 28 mEq/ml). Hemoglobin was also normal in both groups, confirming the absence of chronic hypoxia. There were no significant differences between obstructed and control rats in lung, liver, and LV weight to body weight ratio. However, RV weight to body weight ratio was increased in obstructed rats compared with that in control rats in both groups by approximately 50% (p < 0.005). Thus, chronic normoxic airway obstruction leads to evidence of RV but not LV hypertrophy. We conclude that the mechanical effects of airway obstruction impose a chronically increased afterload on the RV, probably caused by venous return effects, but they have relatively little effect on the LV.
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PMID:Chronic upper airway obstruction produces right but not left ventricular hypertrophy in rats. 823 74


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