Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Persons residing at high altitude who develop excessive polycythemia are more hypoxemic than normal high-altitude residents. We investigated the causes of hypoxemia in 20 patients with excessive polycythemia residing at an altitude of 3,100 m. Lung disease evidenced by abnormal spirometric features and results of a respiratory questionnaire was present in 10 of 20 patients and resulted in increased alveolar-arterial difference for PO2 [(A-a)PO2]. The excessive hypoxemia in the patients with normal lungs was not due to increased (A-a)PO2. We measured ventilatory responses to hypoxia and to hypercapnia to determine whether blunting of these responses was a cause of this excessive hypoxemia. We found, however, that chemical drives to breathe, although blunted, were the same in patients with polycythemia as in high-altitude control subjects. However, an abnormal breathing pattern was observed; the polycythemic patients had a smaller tidal volume and a greater ratio of dead space to tidal volume than did the normal subjects. In addition, the polycythemic patients had increased minute ventilation on breathing 100 percent O2, whereas the normal subjects did not. Thus, hypoxic depression of ventilation may have been present. Our findings suggested that blunted chemical drives are not causative in this disease, and that some other cause of hypoxemia must be present.
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PMID:Excessive polycythemia of high altitude: role of ventilatory drive and lung disease. 70 89

The percentage of the patients with PaCO2 more than 60 Torr and PaO2 more than 50 Torr were 13% in the patients with tuberculosis sequela (N = 502) and 4% in the patients with chronic obstructive lung disease (COLD, N = 727), who were treated with home oxygen therapy in the western region of Japan. Patients with chronic respiratory failure caused by tuberculosis sequela have higher PaCO2 than patients with COLD. Although the prognosis of patients with hypercapnia and moderate hypoxemia is not necessarily poor, some patients may need treatment for severe hypoventilation to prevent respiratory muscle fatigue and abnormal breathing during sleep. In this study, nine patients with hypercapnic chronic respiratory failure caused by tuberculosis sequela were ventilated by Chest Negative Pressure Ventilation (CNPV). The patients were monitored as in polysomnography by transcutaneous PCO2 (PtcCO2) electrode and Respiratory Inductance Plethysmography (RIP). Tidal volume induced by CNPV was larger during mouth breathing (504 +/- 128 ml, mean +/- s.d.) than during nose breathing (438 +/- 109 ml) calculated from RIP in awake state (N = 7). Oxygen saturation measured by ear oximeter and PtcCO2 were 94.4 +/- 2.9% and 57.8 +/- 12.2 Torr in awake state. Following CNPV SaO2 and PtcCO2 were 95.7 +/- 3.0%, 42.7 +/- 12.1 Torr in awake state (N = 9) and 93.0 +/- 4.4%, 57.0 +/- 15.7 Torr in Non-REM sleep (N = 5), respectively. CNPV is effective in these patients in awake state. During Non-REM sleep, CNPV maintains the PtcCO2 level only in awake state.
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PMID:[Tuberculosis sequelae: pathophysiological aspect (ventilation)]. 207 61

We studied hypoxic and hypercapnic ventilatory drives in 22 eucapnic obese subjects (14 female and eight male subjects) referred for weight reduction therapy and 23 normal subjects (eight female and 15 male subjects). In the female subjects, both occlusion pressure, currently used as an indicator of ventilatory drive, and ventilatory responses to hypoxia, as well as occlusion pressure response to hypercapnia, were significantly greater in the obese than in the normal subjects; however, no significant differences in these responses between male obese and male normal subjects were observed, except for the hypoxic occlusion pressure response. We also studied disordered breathing during sleep in the obese subjects, and male predominance in abnormal breathing and oxygen desaturation was noted. These results showed that obese female subjects increased their hypoxic and hypercapnic chemosensitivities against their body mass loading, which was not evident in obese male subjects. The relatively depressed chemosensitivities of the latter may be related to disordered breathing and oxygen desaturation during sleep.
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PMID:Sex differences in awake ventilatory drive and abnormal breathing during sleep in eucapnic obesity. 335 50

Nasal obstruction is associated with abnormal breathing during sleep. To investigate this we measured ventilation and isocapnic hypoxic and rebreathing hypercapnic ventilatory responses in 9 awake normal men, with and without artificial nasal occlusion. Resting breathing frequency was lower (P less than 0.05) with mouth (12.5 +/- 1.0 [SEM]) than with nose (15.1 +/- 1.3 b/min) breathing, due to prolongation (P less than 0.05) of expiratory time with mouth breathing (mouth 3.25 +/- 0.35, nasal breathing 2.41 +/- 0.37 sec). Resting tidal volume was similar for both routes, thus minute ventilation was lower (P less than 0.01) mouth breathing (8.43 +/- 0.44) compared with nose breathing (9.37 +/- 0.47 L/min). Ventilatory responses were greater with mouth than nose breathing both for hypercapnia (mouth 2.29 +/- 0.21, nose 1.58 +/- 0.18 L/min/mm Hg CO2; P less than 0.01) and for hypoxia (mouth 1.08 +/-0.16, nose 0.91 +/- 0.21 L/min/% SaO2; P = 0.10). In 6 subjects measurements were repeated before and after upper airway lignocaine anaesthesia, which abolished the differences in respiratory timing and drive between the breathing routes. It is suggested that there may be upper airway flow receptors which influence respiratory timing.
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PMID:Effect of breathing route on ventilation and ventilatory drive. 684 56

Four morbidly obese men who had been found to have significant sleep-disordered breathing and oxygen desaturation were restudied after an average weight loss of 108 kg (range 53-155 kg). In all subjects, weight loss was accompanied by a significant reduction in the number of episodes per hour of sleep-disordered breathing events. In three of the four subjects, there was improvment in the severity of desaturation accompanying abnormal breathing. The two subjects with daytime somnolence and hypercapnia prior to weight loss showed the most dramatic improvement in desaturation. This suggests that obesity is a cause, rather than an effect, of the sleep apnea syndrome.
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PMID:The effect of weight loss on sleep-disordered breathing and oxygen desaturation in morbidly obese men. 710 55

The objective was to examine whether abnormal breathing during sleep may affect regulation of ventilation after awakening in patients with obstructive sleep apnoea (OSAS). In 19 patients with OSA and 12 normal subjects we examined ventilatory responses to hypoxia (HVR) and to hypercapnia (HCVR) before and after sleep (BS and AS), and compared the changes in ventilatory responses with respiratory events during sleep. In the OSA group, the values of resting ventilation were significantly smaller in AS than those in BS and end-tidal partial pressure of CO2 in arterial blood (Pco2) (PETCO2) rose significantly from BS to AS. The slopes of the HVR or HCVR did not differ between BS and AS. However, both the response lines shifted downward and minute ventilation (VE)80 (VE at arterial oxygen saturation (Sao2) of 80%) in HVR and VE60 (VE at PETCO2 of 60 mmHg) in HCVR decreased significantly from BS to AS. The percentage changes of VE80 and VE60 were significantly correlated with mean Sao2, total sleep time below Sao2 of 90% and lowest Sao2 during sleep. However, in normal subjects we observed no circadian variation in their ventilatory responses. These data support the hypothesis that repeated episodes of nocturnal hypoxia and hypercapnia may modify the regulation of ventilation after awakening in patients with OSA.
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PMID:Regulation of ventilation before and after sleep in patients with obstructive sleep apnoea. 1038 30

The causes of obstruction to airflow in the pediatric upper airway include craniofacial disorders, subglottic stenosis, choanal atresia, syndromes associated with neuromuscular weakness, and the most common, hypertrophy of the tonsils and adenoids. Abnormal breathing can adversely affect craniofacial growth, and abnormal craniofacial development can promote upper airway obstruction. Chronic upper airway obstruction often presents with evidence of obstructive sleep apnea syndrome; in severe cases these children also present with pulmonary hypertension and cor pulmonale. The development of pulmonary hypertension and right heart dysfunction from chronic upper airway obstruction is complex. Hypoxemia and hypercarbia-induced respiratory acidosis are potent mediators of pulmonary vasoconstriction that can lead to reversible and irreversible chronic changes in the pulmonary vasculature. It is likely that production of various neurohumoral factors in response to hypoxemia and respiratory distress may further promote pulmonary hypertension, right ventricular dysfunction, and consequent impairment of systemic cardiac output. The anesthetic considerations for children undergoing adenotonsillectomy for chronic airway obstruction are significant. These children are at high risk for complications such as laryngospasm, desaturation, stimulation of pulmonary hypertension and cardiac dysfunction, pulmonary edema, postoperative upper airway obstruction, and respiratory arrest. Because of underlying condition(s) (facial abnormalities, neuromuscular disease, etc.), successful adenotonsillar surgery may not improve upper airway obstruction significantly, especially in the immediate postoperative period when edema, bleeding and the effects of anesthetics and analgesics are present.
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PMID:Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthetic implications. 1471 77