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

Intravenous amiodarone (5 mg/kg) was administered to 10 patients with chronic obstructive airways disease, hypercapnia and hypoxia, and pulmonary hypertension. Respiratory function tests, arterial blood gases, ECG, blood pressure and subjective tolerance were monitored. Subjective tolerance was excellent. The parameters investigated showed no significant changes either biologically or statistically, excepting a slowing of the cardiac rhythm. The authors conclude that amiodarone has no undesirable cardiopulmonary side effects.
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PMID:[Use of injectable amiodarone in patients with chronic respiratory insufficiency]. 676 11

Hypoxemia, hypercarbia, and cor pulmonale ultimately occur in most patients with chronic lung disease. Although oxygen therapy may reduce or delay the development of pulmonary hypertension and myocardial failure in these patients, its use is thought to lead to CO2 narcosis and apnea. The effect of O2 administration during sleep has been examined in 12 patients (seven with cystic fibrosis, three with bronchopulmonary dysplasia, one with bronchiolitis obliterans, and one with severe hypersensitivity pneumonitis) using skin surface O2 (Roche) and CO2 (Radiometer) electrodes. Both electrodes were calibrated over wet gas and applied at 44 C. Ten patients had chronic hypercarbia (PaCO2 62 +/- 19 torr; range 46 to 103 torr) when awake. Humidified oxygen was administered by nasal cannula, Venturi mask, or head hood. Oxygen flow was increased every 20 minutes from 80 minutes or until the patient awoke. In eight of ten patients with hypercarbia and in the two normocarbic patients, skin surface carbon dioxide tension (PsCO2) increased by 10% or less as the skin surface oxygen tension (PsO2) was increased. In the remaining two patients with hypercarbia (both had cystic fibrosis) PsCO2 increased 18% and 24% as PsO2 was increased. These last two patients with depressed responsiveness to CO2 could not be separated from the other patients by clinical or laboratory criteria. It is concluded that the skin surface blood gas tensions are a simple and reproducible method for adjusting oxygen therapy in patients with chronic lung disease, and although the response to oxygen varies from patient to patient, most patients with chronic hypercarbia retain their central responsiveness to CO2 during sleep and for them O2 therapy is probably safe.
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PMID:Effect of oxygen administration during sleep on skin surface oxygen and carbon dioxide tensions in patients with chronic lung disease. 678 98

Baroreceptor sensitivity, reflected by the slope of the linear regression of the electrocardiographic R-R interval on the rise of systolic blood pressure after injection of phenylephrine, was significantly lower in 27 patients with chronic obstructive pulmonary disease (4.67 +/- 2.67) than in 10 normal subjects (12.07 +/- 3.3) of comparable age (p less than 0.001). In 20 patients in whom right heart catheterisation was performed, pulmonary artery pressure was inversely related to baroreflex sensitivity (r = - 0.603, p less than 0.01). Independent variables such as arterial Po2, Pco2, and mean pulmonary artery pressure were examined in order to assess their ability to predict baroreflex sensitivity. The independent variable that made the most significant contribution was mean pulmonary artery pressure. It seems that the attenuation of baroreflex response in patients with chronic obstructive pulmonary disease is caused mainly by pulmonary hypertension and partly by the central effects of hypoxia and hypercapnia.
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PMID:Reduced baroreceptor sensitivity in patients with chronic obstructive pulmonary disease. 711 59

The effect of repeated lung inflammation on the pulmonary vascular bed was studied in rats. Nonbacterial lung inflammation was induced by repeated carrageenan instillations into the lungs. Three days after the single carrageenan injection, the mean pulmonary arterial blood pressure was only slightly raised [16.3 +/- 0.6 (mean +/- SE) Torr in controls and 19.5 +/- 0.5 Torr in rats with lung inflammation, P less than 0.001]. A substantial pulmonary hypertension was found in rats 3 days after the sixth lung inflammation (24.6 +/- 1 Torr). In this group, arterial hypoxemia, hypercapnia, and right-heart hypertrophy were found. In the 14th day of recovery after the last injection of carrageenan, the mean pulmonary artery blood pressure decreased (18.5 +/- 0.9 Torr) but remained higher than in the control group. There was no difference in cardiac output measured by dye-dilution technique between the experimental and control groups. After repeated inflammation, the media of distal pulmonary vessels thickened and the number of pulmonary arterioles with distinct media increased.
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PMID:Pulmonary hypertension induced by repeated pulmonary inflammation in the rat. 732 77

This report describes a young woman with unexplained chronic hypoventilation that was greatly exacerbated during sleep. Treatment with nocturnal O2 during a 2-yr period was associated with stable cardiovascular function but severe morning headaches and lethargy, presumably related to nightly bouts of hypercapnia and acidosis during sleep. A subsequent 2-yr period in which ventilation was assisted during sleep by means of a rocking bed, but supplementary O2 was not used, was associated with disappearance of the headaches and improved psychosocial function, but with the insidious development of signs of pulmonary hypertension and right ventricular hypertrophy. This patient's clinical course demonstrates the separate adverse effects of intermittent hypoxemia and hypercapnia and emphasizes the importance of preventing both hypoxemia and hypercapnia during sleep.
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PMID:Idiopathic hypoventilation syndrome: importance of preventing nocturnal hypoxemia and hypercapnia. 735 98

A 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation]. 771 33

Detection of nocturnal hypoxaemia, defined as a mean arterial oxygen saturation below 90%, in normoxic or mildly hypoxic chronic obstructive pulmonary disease (COPD) patients seems clinically relevant, since this feature may precede pulmonary hypertension. Nocturnal studies are expensive and time-consuming procedures. The current study investigates to what extent it is possible to predict nocturnal hypoxaemia from daytime parameters. Forty two COPD patients with a daytime arterial oxygen tension (PaO2) above 8 kPa participated. Nocturnal oxygenation, daytime blood gas values, and ventilatory responses to hypercapnia were measured. In 10 patients, enough desaturations occurred to qualify as nocturnal hypoxaemia. They had a significantly lower daytime PaO2 value, and a lower steady-state hypercapnic ventilatory response. They also smoked more often, and complained about daytime sleepiness. Multiple linear regression analysis demonstrated that daytime PaO2 (32%) was the best independent predictor. Sleepiness (12%), and number of cigarettes smoked (5%) also contributed independently, but in a minor way. Patients with a high daytime PaO2 (> 11 kPa) did not develop nocturnal hypoxaemia. The hypercapnic ventilatory response was used to distinguish nocturnal hypoxaemic from normoxaemic patients. Only patients with a low response (< 3.5 l.min-1.kPa-1) appeared to run a risk of developing nocturnal hypoxaemia. The sensitivity of this test was 80%, and the specificity 70%. It is concluded that daytime PaO2, hypercapnic ventilatory response and sleepiness are helpful in predicting nocturnal hypoxaemia.
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PMID:Predictors for nocturnal hypoxaemia (mean SaO2 < 90%) in normoxic and mildly hypoxic patients with COPD. 774 97

The mortality rate for infants severely affected with congenital diaphragmatic hernia (CDH) remains high despite significant advances in surgical and neonatal intensive care including delayed repair and extracorporeal membrane oxygenation (ECMO). Because of the increasingly successful experience with single-lung transplantation in adults; this approach has been suggested as a potential treatment for CDH infants with unsalvageable pulmonary hypoplasia. The authors report on a newborn female infant who was the product of a pregnancy complicated by polyhydramnios. At birth, she was found to have a right-sided CDH and initially was treated with preoperative ECMO, followed by delayed surgical repair. Despite the CDH repair and apparent resolution of pulmonary hypertension, the infant's condition deteriorated gradually after decannulation, and escalating ventilator settings were required as well as neuromuscular paralysis and pressor support because of progressive hypoxemia and hypercarbia. A lung transplant was performed 8 days after decannulation, using the right lung obtained from a 6-week-old donor. The right middle lobe was excised because of the size discrepancy between the donor and recipient. After transplantation, the patient was found to have duodenal stenosis and gastroesophageal reflux, which required duodenoduodenostomy and fundoplication. The patient was discharged from the hospital 90 days posttransplantation, at 3 1/2 months of age. Currently she is 24 months old and doing well except for poor growth. This case shows the feasibility of single-lung transplantation for infants with CDH, and the potential use of ECMO as a temporary bridge to transplantation. Lobar lung transplantation allowed for less stringent size constraints for the donor lung.
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PMID:Lobar lung transplantation as a treatment for congenital diaphragmatic hernia. 787 27

Hypercarbia during the postoperative period following repair of congenital heart defects in children has been associated with acute pulmonary hypertension. Because decreases in respiratory rate (RR) and digital pulse oximetry (SpO2) have been observed after preanesthetic medication of similar children, it is possible that hypercarbia and pulmonary hypertension may be unappreciated risks in premedicated children during the preoperative period. As the first step in addressing this question, changes in transcutaneous and end-tidal PCO2 (PtcCO2 and PetCO2) were examined after preanesthetic medication of children prior to cardiac surgery. Forty-four children were randomly assigned to receive either intramuscular morphine, 0.2 mg/kg, and scopolamine, 0.01 mg/kg, or oral midazolam, 0.75 mg/kg, 1 hour before anesthetic induction. PtcCO2, PetCO2, SpO2, RR, and sedation score were monitored. Significant sedation occurred after both premedication regimens. Following morphine/scopolamine, PtcCO2 increased from 36 +/- 4 (mean +/- SD) to 43 +/- 6 mmHg (P < 0.01), PetCO2 increased from 35 +/- 3 to 40 +/- 5 mmHg (P < 0.01), SpO2 decreased from 93 +/- 2 to 91 +/- 4% (P < 0.01), and RR decreased from 30 +/- 10 to 24 +/- 7 breaths/minute (P < 0.01). After midazolam, PtcCO2 increased from 35 +/- 4 to 40 +/- 6 mmHg (P < 0.01), PetCO2 increased from 34 +/- 5 to 39 +/- 3 mmHg (P < 0.01), SpO2 decreased from 93 +/- 6 to 90 +/- 7% (P < 0.01), and RR decreased from 33 +/- 13 to 30 +/- 13 breaths/minute (P < 0.01). Clinically significant increases in PtcCO2 (> 45 mmHg) occurred in nine patients, including five with pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of preanesthetic medication on carbon dioxide tension in children with congenital heart disease. 794 97

Obstructive sleep apnoeas (OSA) exert immediate marked cardiovascular effects, and may favour the development of systemic and pulmonary hypertension in the long-term. As for the pathogenesis of the acute cardiovascular changes, the first studies high-lighted the role of OSA-induced hypoxia and mechanical changes. However, more recent work pointed to the role played by the arousal reaction terminating OSA, and to the activity of the autonomic nervous system during apnoea and inter-apnoeic phase. As for the pathogenesis of chronic cardiovascular changes, recent findings suggest that the link between OSA and systemic hypertension may be through an abnormal function of the carotid body and underline the importance of chronic intermittent hypoxia versus continuous hypoxia in the development of stable systemic hypertension. On the other hand, OSA do not appear to enhance strongly the development of stable pulmonary hypertension. In this review, we analyze OSA-induced cardiovascular changes with particular emphasis on to the interplay of the possible pathogenic mechanisms involved. Acute OSA-induced cardiovascular alterations during the apnoeic phase appear to result mainly from the mechanical effects of OSA, while during the interapnoeic phase they seem mostly determined by chemical factors (hypoxia, hypercapnia) and by the arousal reaction. In addition, the role of reflex changes elicited by resumption of ventilation should be reconsidered, since lung inflation seems to exert a positive effect on the cardiovascular changes occurring at the end of OSA. This would be in contrast with the inhibitory effects described as "lung inflation reflex", and deserves further study.
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PMID:The cardiovascular effects of obstructive sleep apnoeas: analysis of pathogenic mechanisms. 800 63


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