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

Obstructive sleep apnea (OSA), daytime hypoxemia, and hypercapnia complicate obesity and are alleviated by weight loss. The flow-volume curve is a sensitive screening tool for most patients; the curve can monitor therapeutic efficacy of weight reduction.
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PMID:Weight loss and OSA and pulmonary function in obesity. 841 57

We report 16 adult men (age, 41 to 75 yr) with neuralgic amyotrophy (NA) who presented with dyspnea due to involvement of the diaphragm. All patients developed breathlessness after a prodrome of acute severe neck and shoulder pain. Bilateral diaphragm paralysis (BDP) was confirmed in 12 patients and unilateral diaphragm paralysis (UDP) in four by the absence of electrical and mechanical responses to percutaneous phrenic nerve stimulation. Global expiratory muscle strength was well preserved in all patients, but inspiratory muscle strength was reduced in proportion to the extent of diaphragmatic involvement. Lung function showed low lung volumes with preservation of carbon monoxide transfer coefficient in all patients. Two BDP patients were hypoxic (PaO2 = 67 and 54 mm Hg, respectively) on daytime arterial blood gas analysis; the latter patient with pre-existing chronic obstructive pulmonary disease and marked obesity also had borderline hypercapnia (PaO2 = 49 mm Hg). Overnight sleep studies in three BDP and two UDP patients showed frequent intermittent arterial oxygen desaturations apparently caused by obstructive sleep apneas, but there was no evidence of alveolar hypoventilation. Follow-up muscle studies in five BDP and four UDP patients between 2 and 4 yr after initial referral showed complete recovery of diaphragmatic function in only two UDP patients, one of whom relapsed a year later. We postulate that NA may be an important but underrecognized cause of diaphragmatic paralysis in otherwise normal patients. Diaphragmatic strength returns very slowly, if at all.
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PMID:Diaphragmatic dysfunction in neuralgic amyotrophy: an electrophysiologic evaluation of 16 patients presenting with dyspnea. 842 Apr 34

To determine whether moderately obese, normocapnic, sleep apnea patients are distinguished from normal obese individuals by differences in waking pulmonary function and respiratory chemosensitivity, we compared the waking pulmonary function, hypercapnic, and hypoxic ventilatory responses of 35 nonhypercapnic sleep apnea patients (32 men and 3 women) with those of 17 age-, sex-, weight-, and obesity-matched nonapneic control subjects (16 men and 1 woman). The waking ventilatory response to hypercapnia was lower among sleep apnea patients (mean +/- SD, 2.05 +/- 1.29 L/min/mm Hg) than control subjects (3.02 +/- 2.05 L/min/mm Hg, p < 0.05). Patients with sleep apnea demonstrated a higher waking PaCO2 (40.4 +/- 2.9 vs 37.0 +/- 2.7 mm Hg, p < 0.001), and a lower waking PaO2 (81.4 +/- 11.7 vs 89.7 +/- 10.4 mm Hg, p < 0.03). The waking hypoxic ventilatory response, however, was not significantly different between the groups. Moreover, control subjects had a higher total lung capacity than sleep apnea patients (6.99 +/- 1.12 L and 6.27 +/- 1.09 L, respectively, p < 0.05). The lower hypercapnic ventilatory response, higher waking PaCO2, and lower total lung capacity in the sleep apnea patients resemble the pattern observed in patients with pickwickian syndrome. This suggests that disturbances in pulmonary function and ventilatory control in moderately obese sleep apnea patients are intermediate along a continuum from normal obesity to the pickwickian syndrome.
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PMID:Pulmonary function and respiratory chemosensitivity in moderately obese patients with sleep apnea. 803 13

Patients with obstructive sleep apnea syndrome (OSAS) may have daytime pulmonary hypertension (PH). Transient and sometimes severe elevations of pulmonary arterial pressure during sleep as a result of intermittent upper airway obstruction may lead to daytime PH. We sought to study the factors involved in the development of daytime PH. Right-heart catheterization, pulmonary function tests, and arterial blood gas measurements were done in 25 patients in whom OSAS was diagnosed by whole-night polysomnography. Eight of the patients (32%) had PH, defined by a mean pulmonary arterial (PA) pressure > or = 20 mmHg. For the group as a whole, mean PA pressure was positively and significantly correlated with daytime PaCO2 (r = 0.79), percent of ideal body weight (r = 0.45), and Hb (r = 0.40). Mean PA pressure was negatively and significantly correlated with PaO2 (r = -0.54), FEV 1% (r = -0.52), and %FVC (r = -0.68). In contrast, mean PA pressure was not significantly correlated with apnea index or with sleep desaturation. These data indicate that daytime PH was not directly related to sleep-disordered breathing, but was related to daytime hypoxemia, daytime hypercapnia, obesity, obstructive and restrictive respiratory impairments, and secondary polycythemia.
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PMID:[Daytime pulmonary hypertension in the obstructive sleep apnea syndrome]. 854 78

A patient with Prader-Willi syndrome developed bronchospasm during anesthesia. The patient was a 9-year-old boy and was scheduled for orchiopexy. His psychomotor development was delayed, and at 12 months of age he was diagnosed as Prader-Willi syndrome by chromosomal examination. The patient weighed 17 kg, was 111 cm tall, and had no symptom of upper respiratory infection preoperatively. Preoperative examinations were normal except supraventricular extrasystole in electrocardiogram. Following administration of scopolamine 0.15 mg intramuscularly as preanesthetic medication, anesthesia was induced smoothly by slow induction using N2O-O2-sevoflurane. However, right after endotracheal intubation with vecuronium 2 mg, remarkable stridor was noticed. Despite hyperventilation, the patient exhibited hypercapnia, and the diagnosis of bronchospasm was made. Aminophylline and steroid were administered intravenously and halothane was inhaled instead of sevoflurane. The bronchospasm was improved gradually and surgery was finished. Prader-Willi syndrome is an uncommon disease first reported by Prader in 1956 and characterized by hypotonia, hypomentia, hypogonadism and obesity. In the perioperative management for a patient with Prader-Willi syndrome, special attention must be paid to the abnormalities in the upper and lower respiratory systems.
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PMID:[Bronchospasm during anesthesia in a patient with Prader-Willi syndrome]. 858 65

The clinical course and changes in hypercapnic ventilatory drive over time were serially assessed before and after tracheostomy placement in a 14 year old, morbidly obese female patient with Prader-Willi syndrome, severe obstructive sleep apnoea, and obesity-hypoventilation syndrome. A tracheostomy became necessary after supplemental oxygen and continuous positive airway pressure (CPAP) had failed to improve the severity of nocturnal hypoventilation. Continued improvement in the slope to rebreathing hyperoxic hypercapnia occurred from 2-10 weeks after tracheotomy in conjunction with night-time bilevel pressure ventilation, and remained unchanged thereafter. In contrast, increases in mean resting minute ventilation at an end-tidal carbon dioxide tension (PET,CO2) of 8 kPa (60 mmHg) were documented even after 30 weeks. This case study illustrates the time-frame of dynamic ventilatory changes occurring after removal of upper airway resistance and normalization of nocturnal alveolar ventilation.
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PMID:Longitudinal assessment of hypercapnic ventilatory drive after tracheotomy in a patient with the Prader-Willi syndrome. 883 75

5 cases with obesity-hypoventilaion syndrome were reported. The clinical manifestations were obesity, palpitation, dyspnea, lethargy, cyanosis, distention of cervical vein, edema, enlargement of liver and hypertension. All of them were initially diagnosed as chronic bronchitis or heart diseases. Pulmonary function test showed restrictive ventilative defect and hypercapnia with hypoxemia. Mouth oclusion pressure at 0.1 second was higher than the normal value. The response to CO2 was decreased. Hypertrophy of right heart was shown in ECG and X-ray film improvement in symptoms and blood gases analyses were found to be associated with body weight decrease in a follow up period of one year.
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PMID:[Obesity-hypoventilation syndrome]. 927 46

Sleep is characterized by many changes in the respiratory system, including a reduction in respiratory motor output associated with the loss of wakefulness, increased upper airway resistance, and blunted protective reflexes (such as load compensation), that result in reduced alveolar ventilation. The development of carbon dioxide retention appears to be linked to the exaggeration of sleep-related changes on ventilation by coexistent respiratory system disorders. Sleep-disordered breathing is becoming increasingly recognized in subjects with neuromuscular diseases, who may be prone to nocturnal respiratory events due to diaphragm and bulbar muscle weakness, abnormal central respiratory control, obesity, and sleep position restrictions. Nocturnal gas exchange deterioration may occur in patients with chronic obstructive pulmonary disease, particularly during rapid eye movement sleep when activity of the respiratory muscles other than the diaphragm is inhibited. Concurrent obstructive sleep apnea syndrome may further compromise nocturnal ventilation, thereby contributing to the development of acute or chronic respiratory failure. The use of noninvasive nocturnal ventilation at night has resulted in significant improvements in symptoms of hypoventilation and daytime carbon dioxide retention in various clinical settings, yet important questions remain about implementation of this modality.
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PMID:Sleep-wake cycles and the management of respiratory failure. 936 92

The authors have studied chemical control of breathing in 37 normocapnic patients with OSA. These patients had increased apnea-hypopnea index (AHI = 51 +/- 22), obesity (BMI = 32.4 +/- 5.6 kg/m2) and normal lung function tests. Control group consisted of 20 healthy subjects with normal weight (BMI = 23.1 +/- 2.4 kg/m2). Respiratory responses (ventilatory and P0.1) to hypercapnic and hypoxic stimulation during rebreathing tests were measured with computerized methods. The obtained results in OSA patients were compared with the data of the control group. The results exceeding mean values of the control group above 1.64 SD were recognized as hyperreactive responses. The majority e.g. 26 patients (OSA-N) had normal respiratory responses during hypercapnic stimulation. delta V/delta PCO2 = 16.8 +/- 4.5 L/min/kPa, P0.1/delta PCO2 = 3.5 +/- 2.4 cm H2O/kPa/. In remaining 11 patients (OSA-H) respiratory responses were significantly increased delta V/delta PCO2 = 39.1 +/- 18.8 L/min/kPa, P0.1/delta PCO2 = 8.6 +/- 3.9 cm H20/kPa). During isocapnic hypoxic stimulation majority e.g. 25 patients (OSA-H) had significantly increased respiratory responses delta V/delta SaO2 = 3.28 +/- 1.63 L/min/%, delta P0.1/delta SaO2 = 0.54 +/- 0.43 cm H2O/%/. In remaining 12 patients (OSA-N) respiratory responses were within normal limits delta V/SaO2 = 1.2 +/- 0.28 L/min/%, delta P0.1/ delta SaO2 = 0.21 +/- 0.07 cm H2O/%/. The above results indicated, that majority OSA patients (67.5%) had increased ventilatory and P0.1 responses to hypoxic stimulation. Among them also 11 patients had increased respiratory responses to hypercapnia. It seems, that increased respiratory responses to hypoxic stimulus in OSA patients are symptoms of protective reaction to hypoxaemia occurring during repetitive sleep apnoea and reveals increased neuro-muscular output.
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PMID:[Chemical control of breathing in patients with obstructive sleep apnea]. 941 Feb 80

In contrast to the obstructive sleep apnoea syndrome (OSA) the obesity-hypoventilation syndrome (OHS) is characterized by persistent hypercapnia during the day. After positive pressure ventilation (PPV) patients with OHS the daytime blood gases normalize after a short time. The aim of this study was to investigate whether blood gases at the end of a standardized exercise test separate both OSA and OHS after 3 months of PPV. Fourteen patients with OHS (12 males, 53.2 +/- 9.5 years, BMI: 41.7 +/- 9.6 kg/m2, PCO2: 50.7 +/- 4.5 mmHg) and 28 patients with severe OSA (27 males, 54.5 +/- 8.3 years, BMI: 35.7 +/- 4.9 kg/m2, PCO2: 37.3 +/- 3.3 mmHg) were studied. Blood gases before and after 4 minutes constant load exercise test were measured. The exercise level for patients with OSA was 2/3 of the predicted maximal work load. Since in OHS the load tolerance was compromised, the exercise test was performed at 2/3 of the maximal exercise level which was investigated before. The identical exercise load was done before and 3 months after beginning the PPV. Compared to the OSA-group the load tolerance of the OHS-group was lower (112 +/- 20 Watt [2/3 of predicted maximal work load] versus 81 +/- 26 Watt [39.9 +/- 8.3% of predicted maximal work load], p < 0.0001). Both before and after 3 months of PPV all patients with OHS showed an exercise induced increase of PCO2 (Before PPV: from 50.7 +/- 4.5 to 56.6 +/- 5.8 mmHg; after PPV: from 39.1 +/- 2.7 to 45.6 +/- 2 mmHg, each p < 0.0001). Correspondingly the PCO2 decreased significantly. In OSA neither before nor after 3 months PPV the blood gases changed significantly during the exercise test. We conclude that the OHS associated hypercapnia during exercise is further on a reliable indicator for the diagnosis despite the daytime normocapnia during rest after PPV. However after PPV the PCO2-values of patients with OHS at rest are in the normal range.
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PMID:[Ergometry separates sleep apnea syndrome from obesity-hypoventilation after therapy positive pressure ventilation therapy]. 948 73


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