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

Eleven cases of cor pulmonale secondary to tonsil and adenoid hypertrophy and upper airway obstruction were reviewed. These patients presented with a spectrum disease ranging from mild, with only abnormal ECG or chest X-ray findings, to severe with hypercarbia, hypoxia, and right heart failure. One patient with severe disease suffered a postoperative respiratory arrest. We have successfully managed 4 patients with severe cor pulmonale with postoperative intubation and assisted ventilation. Hypoxia is the driving stimulus for respiration in patients with upper airway obstruction and hypercarbia. Relief of respiratory obstruction by tonsillectomy and adenoidectomy with postoperative oxygen administration may remove the hypoxic drive, resulting in respiratory arrest. Patients undergoing tonsillectomy and adenoidectomy for upper airway obstruction disease should be screened for cor pulmonale. Affected patients should be managed after surgery in an intensive care unit (ICU) environment with careful monitoring of the respiratory status. Patients with severe cor pulmonale can be successfully managed with planned postoperative intubation and mechanical ventilation to prevent respiratory arrest.
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PMID:Cor pulmonale secondary to tonsillar and adenoidal hypertrophy: management considerations. 306 49

Studies are reported of four patients (all lifetime non-smokers) who presented with right heart failure as a consequence of unrelieved asthmatic airways obstruction. These patients demonstrated severe airways obstruction with crackles on auscultation and hypercapnia. As shown here, such a presentation, without the usual pattern of dyspnoea and wheeze, tends to obscure the diagnosis and delays effective treatment. In three of the patients, treatment to relieve airways obstruction improved gas exchange, and the heart failure resolved. In the remaining patient, improvement was limited, and death ensued from respiratory failure. In patients who present with right heart failure, a relationship with airways obstruction and respiratory failure should be considered and assessed by objective tests. Delays in the effective treatment of these patients may result in the progression of their disease to a stage at which airways obstruction no longer responds to medical therapy.
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PMID:Malignant asthma presenting as right heart failure. 360 Apr 57

Acute respiratory acidosis results in increases in cardiac output and in systemic and pulmonary arterial blood pressures. The aim of this investigation was to determine if isoflurane modifies these effects. Nine patients (ASA II or III) scheduled for major surgery took part in the investigation. After the induction of general anesthesia, CO2 was added to the inspiratory gas mixture. After 15 min, ventilation with addition of CO2 (PaCO2 8-9 kPa) isoflurane (3%) was added. Hemodynamic measurements were made to study the effects of acute hypercapnia and the effects of isoflurane during hypercapnia. The addition of carbon dioxide resulted in increases in cardiac output, systemic and pulmonary arterial blood pressures, and right and left ventricular stroke work. The addition of isoflurane during hypercapnia decreased systemic arterial blood pressure, but pulmonary arterial blood pressure was unaffected, cardiac output and stroke volume did not change, and left but not right ventricular stroke work decreased. In conclusion, acute pulmonary hypertension induced by hypercapnia was not affected by isoflurane but, despite increased right ventricular stroke work, there were no signs of right ventricular failure.
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PMID:Circulatory effects of isoflurane during acute hypercapnia. 368 95

This paper analyzes the craniofacial morphology in a patient with typical Hallermann-Streiff syndrome (HSS) who developed symptomatic cardiorespiratory deficiency at the age of 48 years. The patient had obstructive sleep apnea (OSA), hypoxia, hypercarbia, pulmonary hypertension, tricuspid insufficiency, and right ventricular failure. Analysis of cephalometric roentgenograms, done 15 years earlier, revealed severe mandibular hypoplasia with marked underdevelopment of the ramus and body. The gonial angle was abnormally obtuse. The condylar and coronoid processes were reduced in size. The anteroposterior dimension of the upper airway was markedly narrowed. Cephalometric roentgenograms of six other HSS patients from our clinic were compared to those of the reference patient. Considerable variation in the features of the syndrome were noted. None of the other patients showed definitive airway obstruction. Comparison was also made with cephalometric roentgenograms of a patient with Treacher Collins syndrome and of a patient with progeria. The former showed airway obstruction associated with a deformed hypoplastic mandible; the latter had an unobstructed airway despite a small mandible because of associated hypoplasia of the maxilla and tongue. The HSS reference patient improved after oxygen therapy, diuretics, antibiotics, and relief of OSA. Patients with HSS, as well as those with Treacher Collins syndrome, appear to be at risk for the development of cardiopulmonary disease if they have obstructed airways. OSA has been shown to have developed in two patients with HSS. The resultant cardiopulmonary insufficiency of such patients may be preventable if airway obstruction can be relieved relatively early in life.
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PMID:Cardiorespiratory disease associated with Hallermann-Streiff syndrome: analysis of craniofacial morphology by cephalometric roentgenograms. 387 95

Although right heart failure is a recognized complication of obstructive sleep apnea, the incidence and pathogenesis of this complication have not been established. We therefore studied 50 consecutive patients with obstructive sleep apnea to determine the incidence of right heart failure and the factors involved in its development. Six patients (12%) were found to have right heart failure. There were no differences in the number of apneas between those with right heart failure (mean +/- SE, 30 +/- 10 per h sleep) and those without right heart failure (33 +/- 4 per h sleep). In contrast, mean nocturnal oxygen saturation was lower in patients with right heart failure (76 +/- 3%) than in those without right heart failure (90 +/- 1%; p less than 0.001). Furthermore, patients with right heart failure also had a substantially lower awake arterial PO2 (52 +/- 4 mmHg versus 75 +/- 2 mmHg; p less than 0.001) and a higher PCO2 (51 +/- 2 mmHg versus 36 +/- 1 mmHg; p less than 0.001) than those without right heart failure. Severe nocturnal hypoxemia in the absence of diurnal hypoxemia was not associated with right heart failure. Daytime hypoxemia in the patients with right heart failure was associated with a higher residual volume (p less than 0.001) and lower forced expiratory volume in one second (p less than 0.001) than in the patients without right heart failure. The findings suggest that sustained hypoxemia and/or hypercapnia over a 24-h period is a necessary prerequisite for the development of right heart failure in patients with obstructive sleep apnea, and that diffuse airway obstruction plays a major role in causing such hypoxemia.
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PMID:Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome. 400 33

The relation between daytime and nocturnal hypoxaemia on one hand and right ventricular failure (RVF) and hypertrophy (RVH) on the other was studied in 21 patients with severely reduced ventilatory capacity. RVH was assessed by myocardial scintigraphy, vector cardiography and echocardiography. Seven patients had suffered from acute RVF at least once. They had lower vital capacity and PaO2 and higher PaCO2 than patients without a history of RVF. They also had a more severe nocturnal hypoxaemia. They did not, however, have more severe RVH than patients without a history of RVF. Blood gases during daytime were not related to RVH. Oxygen saturation during sleep had a weak inverse relationship to RVH determined with scintigraphy, but not with the other methods. Nocturnal hypoxaemia was closely related to hypoxaemia and hypercapnia during daytime. A difference between daytime PaO2 and PaCO2 less than 2 kPa could with reasonable accuracy identify patients with nocturnal hypoxaemia.
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PMID:Nocturnal hypoxaemia and cor pulmonale in severe chronic lung disease. 407 59

Hypoxaemia secondary to chronic bronchopulmonary disease may lead to total invalidity and be complicated by right heart failure. Consistent and meticulous medical care may produce a notable improvement by not smoking, using bronchodilators, mucolytics and physiotherapy. If, despite these measures, frank hypoxaemia persists, then domiciliary oxygen should be considered. The need for prolonged oxygen therapy of more than 15 hours is often countered by the scepticism and lack of discipline of the patient and family. In cases of hypoxaemia which are partially refractory or are associated with hypercapnia prolonged mechanical ventilation with a tracheotomy will ensure considerable salvage in those with severe restrictive defects and right heart failure. The supervision of oxygen therapy requires not only adequate control of blood gases, but also collaboration between the family doctor, the respiratory physician and home visitors such as the nurse or technician.
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PMID:[General problems posed by the domiciliary treatment of chronic respiratory insufficiency]. 641 Apr 69

Left ventricular function was studied at rest and during post-extrasystolic potentiation (PESP) in 18 patients with chronic obstructive lung disease. The contractility indices were obtained from pressures recorded in the osovolumetric period and from volume variations during ejection. All patients were hypoxic; six of them had cor pulmonale (group B); the remaining 12 patients constituted group A. Left ventricular function was similar in both groups; it is concluded that right heart failure in cor pulmonale is not secondary to left ventricular failure. Left ventricle was hypertrophied and pump function altered, but left ventricular kinetics was normal or increased. Isovolumetric phase contractility indices were decreased; they may increase during PESP. Left ventricular compliance was altered due to left and right ventricular hypertrophy and to paradoxical movement of interventricular septum which impeded diastolic expansion of left ventricle. The impairment of left ventricular function seems to be related to both intrinsic (hypoxia, hypercapnia, hypertrophy) and extrinsic factors (right ventricular hypertrophy with deviation of interventricular septum, lowering of left ventricular preload).
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PMID:Left ventricular function in chronic obstructive pulmonary disease. 645 29

The development of right ventricular failure due to pulmonary hypertension is a common complication of severe chronic bronchitis and emphysema (Renzetti et al. 1976) but is rare in bronchial asthma (Clark 1977). We report a 20-year-old extrinsic asthmatic with persistent hypoxaemia and carbon dioxide retention, secondary polycythaemia and cor pulmonale and describe his further investigation.
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PMID:Cor pulmonale in asthma. 661 6

An unusual patient with hypoxemia, hypercapnia, and right ventricular failure is presented. Minimal skeletal muscle weakness, although present, cannot explain hypercapnia. Muscle biopsy revealed diabetic microangiopathy. Carbon dioxide stimulation demonstrated a diminished hypercapnic ventilatory response. The patient benefited from progesterone therapy. In this unusual patient, mild muscular weakness, caused by diabetes, and central alveolar hypoventilation have acted in synergism to cause abnormal ventilation and right ventricular failure.
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PMID:Right ventricular failure in a patient with diabetic neuropathy (myopathy) and central alveolar hypoventilation. 664 56


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