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

Because of the neonate's susceptibility to pulmonary hypertension (PHN) and his inefficiency in invoking the compensatory mechanisms often used by adults to maintain stable levels of O2 consumption (VO2) in the face of changes in O2 delivery (DO2) and metabolic demand, we have attempted to define the O2 handling capabilities of the newborn piglet affected with various types of pulmonary vasoconstriction. Hemodynamically similar levels of PHN were generated in 18 newborn piglets (six through group B beta-hemolytic Streptococci infusion; six through hypoxia; six through hypercarbia) and O2 transport was studied. At 60 min VO2 was similar in all groups, although DO2 was different (10.7 +/- 6.7, 7.2 +/- 1.6, and 21.7 +/- 8.9 ml/kg.min, in the septic, hypoxic, and hypercarbic groups, respectively). Extraction efficiency varied in an inverse fashion (43 +/- 12%, 72 +/- 12%, and 27 +/- 16%, in the septic, hypoxic, and hypercarbic groups, respectively). Supply dependency and a critical DO2 were observed in the septic and hypoxic PHN groups (18.4 and 12.2 ml/kg.min, respectively). Both of these were elevated as compared to healthy adult levels. Hypercarbic pulmonary hypertension was supply independent at the levels studied; however, DO2 remained elevated in these animals and may never have reached the critical DO2 level.
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PMID:Oxygen transport in newborn piglets with pulmonary hypertension. 313 50

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.
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PMID:Effects of He-O2 breathing during experimental decompression sickness following air dives. 357 43

There is a wide clinical spectrum in chronic obstructive pulmonary disease (COPD). The extremes of this spectrum, the "pink puffer" (PP) and "blue bloater" (BB) stereotypes differ in their degree of sleep hypoxemia and pulmonary hypertension. Most patients cannot be characterized as either PP or BB. The data amassed in the recent nocturnal oxygen therapy trial provide an opportunity to see to what extent differences in sleep oxygenation and hemodynamics in a large hypoxemic COPD population are related to awake hypoxemia and hypercapnia. From a large hypoxemic COPD population sleep SaO2 was examined in those with (PaCO2 greater than 44 mm Hg) and without (PaCO2 less than or equal to 44 mm Hg) hypercapnia. Hypercapnic patients (mean PaCO2 49.8 mm Hg) had the same PaO2 and degree of airflow obstruction as normocapnic patients (PaCO2 37.4 mm Hg) but had far greater sleep hypoxemia (measured by mean sleep SaO2, low sleep SaO2, and awake-low sleep SaO2, p less than 0.05). In addition, arterial blood gases of the large sleep O2 desaturaters were compared with those of the small desaturaters; PaO2 was similar in both groups, whereas PaCO2 was different (p less than 0.01). Two common subsets of hypoxemic patients were also compared; one was hypercapnic and overweight, the other normocapnic and hyperinflated. We found that patients in the hypercapnic group had far worse sleep hypoxemia, although they had better lung function. We conclude that hypercapnia is a marker for sleep O2 desaturation in hypoxemic COPD.
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PMID:Hypercapnia and sleep O2 desaturation in chronic obstructive pulmonary disease. 362 83

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

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

This study describes the case of a 58 year old man who presented with an episode of acute respiratory failure and right heart decompensation. After recovery from the acute illness, hypoxaemia, hypercapnia and pulmonary arterial hypertension remained, the causes of which were not known. There was no airway obstruction, only a moderate restrictive ventilatory defect, a little weight increase and a unilateral diaphragmatic paralysis. Obstructive sleep apnoea was finally suspected and confirmed by sleep recording. The obstructive sleep apnoea probably explained the respiratory insufficiency and the pulmonary hypertension. Loss of weight was associated with the disappearance of hypercapnia and pulmonary hypertension. As a result of this study, the value of sleep recording is emphasized. When respiratory failure or pulmonary hypertension seem unexplained, think of obstructive sleep apnoea.
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PMID:[Value of sleep polygraph examination in the etiological diagnosis of apparently inexplicable respiratory insufficiency]. 404 63

1. Almitrine, an agonist of peripheral chemoreceptors, has been shown to be effective in lowering PaCO2 in patients with chronic obstructive lung disease. The aim of this investigation was to evaluate the pulmonary haemodynamic response to almitrine in clinically stable patients with chronic airflow obstruction and chronic hypercapnia (PaCO2 7.1 +/- 0.5 kPa, mean +/- SD). 2. Seven men, aged from 55 to 64 years, had the following values for pulmonary function (means +/- SD): FEV1.0 0.67 +/- 0.16 litre; VC 2.12 +/- 0.52 litres; FEV1.0/VC 33 +/- 8%. They had haemodynamic monitoring during 1 h of almitrine (1 mg/kg intravenously) and solvent (placebo) in a random fashion while receiving 28% oxygen. Before infusion, six patients had evidence of pulmonary hypertension and the mean pulmonary artery pressure (PAP) for all seven patients was 4.3 +/- 1.6 kPa (mean +/- SD); the pulmonary vascular resistance (PVR) was 0.61 +/- 0.22 kPa 1(-1)s (mean +/- SD). 3. There were no significant changes from baseline values during placebo. During almitrine, however, the PAP and right ventricular stroke work (mean +/- SD) increased significantly at 30 min (6.0 +/- 2.1 kPa, P less than 0.001, 0.38 +/- 0.12 J, P less than 0.05, respectively) with maximum increase of PVR at 45 min (1.01 +/- 0.34 kPa 1(-1)s, P less than 0.001, mean +/- SD). The lowest PaCO2 (mean +/- SD) was observed at the end of the infusion (5.7 +/- 0.5 kPa, P less than 0.001). 4. These results confirm the benefit of almitrine in lowering PaCO2 in patients with chronic airflow obstruction who have chronic hypercapnia but also demonstrate significant pulmonary vasoconstriction.
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PMID:The pulmonary haemodynamic effects of almitrine infusion in men with chronic hypercapnia. 612 33

The status of long-term, outpatient oxygen therapy is reviewed, particularly as it is applied to patients with chronic obstructive pulmonary disease. Recent clinical trials have shown that in stable hypoxemic patients (arterial O2 tension less than 60 torr) with obstructive disease, survival is prolonged by chronic O2 therapy, and that the more continuous the therapy is, the better the survival rate. The mechanism of the improved survival rate is not clear, although O2 therapy decreases the hematocrit and pulmonary vascular resistance and may improve neuropsychological function. In such patients, nocturnal decreases in arterial O2 saturation are associated with carbon dioxide retention and may contribute to pulmonary hypertension. Nocturnal hypoxemia is eliminated by the usual continuous O2 therapy. The incidence of nocturnal hypoxemia without upper airway obstruction or daytime hypoxemia is not known but may be small. Nocturnal O2 treatment for such patients may be indicated, but further studies are needed. Oxygen therapy during exercise in patients who are not hypoxemic at rest should be done only when benefits cannot be attributed to a placebo effect of O2 therapy.
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PMID:Long-term oxygen therapy. 635 31

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


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