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

Patients with morbid obesity present a series of functional and morphologic alterations and require a careful planning for anesthetic management. We report a case of a woman weighing 260 kg who was operated on twice for the treatment of her base condition. In the first operation, general anesthesia was carried out and in the second one, epidural anesthesia was conducted. Main complications included hypoxemia and hypercapnia which persisted during the first week after operation carried out under general anesthesia.
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PMID:[Anesthesia of a woman with extreme morbid obesity (260 kg)]. 209 82

1. To examine the relationship between eucapnic morbid obesity and ventilatory responsiveness to chemical stimuli, we measured hypercapnic and hypoxic ventilatory responses in 29 patients (26 women, three men) before and 3-6 months after gastroplasty. No subject demonstrated resting awake hypercapnia and non suffered from sleep-disordered breathing. 2. Mean weight fell significantly (122.8 +/- 21.4 vs 102.2 +/- 22.8 kg, P less than 0.0001) and functional residual capacity rose slightly but significantly (1.94 +/- 0.58 vs 2.18 +/- 0.64 litres; P less than 0.05) after weight loss. 3. The hypercapnic ventilatory response slope fell significantly after weight loss (2.88 +/- 2.27 vs 2.24 +/- 1.06 litres min-1 mmHg-1, P less than 0.05) with a significant shift of the ventilatory response curve to the right. There were no statistically significant changes in the patterns of ventilatory response. 4. In addition, isocapnic hypoxic ventilatory response slopes, measured at two levels of carbon dioxide partial pressure, fell significantly after weight loss. These changes were accompanied by significant shifts of the ventilatory response curves to the left, such that, for a given oxygen saturation, mean ventilation was significantly lower in the less obese state. Similarly to hypercapnic responses, there were no statistically significant changes in ventilatory pattern despite the changes in overall ventilatory response. 5. We conclude that ventilatory responsiveness to chemical stimuli is increased in obese subjects who maintain adequate alveolar ventilation while awake.
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PMID:Ventilatory responses to hypercapnia and hypoxia in patients with eucapnic morbid obesity before and after weight loss. 216 85

In December 1986 a 30-month-old female child with morbid obesity and respiratory failure was admitted to the Izaak Walton Killam Hospital for Children in Halifax. The etiology of the obesity was found to be dietary in origin after ruling out genetic, neurological and metabolic causes. This patient exhibited somnolence and cyanosis in association with hypercapnia and right ventricular overload. Her respiratory failure in the presence of a normal upper airway required ventilatory support, first with nasal endotracheal intubation, and then, tracheotomy. Weight reduction normalized her capillary blood gases and her somnolence disappeared. Subglottic stenosis hampered removal of the tracheotomy tube until 9 months after admission. The pathogenesis and management of obese hypoventilation syndrome are reviewed by the authors.
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PMID:Obese hypoventilation syndrome of early childhood requiring ventilatory support. 306 Apr 36

In morbid obesity, there is an increased hindrance to breathing caused by the effects of the increased mass on the chest wall and abdomen; subjects with morbid obesity can maintain eucapnia by increasing inspiratory neuromuscular drive and/or by altering central breath timing. We studied 23 eucapnic, obese subjects (greater than 190% predicted ideal weight), 7 males and 16 females with a mean age of 36.6 +/- 9.2 yr and 18 healthy, normal male subjects. Total lung capacity, functional residual capacity, and total thoracic compliance were significantly (p less than 0.05) reduced in the obese subjects. At rest, minute ventilation was significantly increased because of an increase in respiratory frequency, which in turn was due to a significant decrease in the expiratory time (TE) per breath; the ratio of inspiratory to expiratory time (TI/TE) was thus significantly altered, indicating an alteration in central breath timing. Resting inspiratory neuromuscular drive (as represented by mouth occlusion pressure) was significantly increased in the obese subjects, but tidal volume was not significantly altered. There was an increased ventilatory responsiveness to hypoxia and relatively decreased ventilatory responsiveness to hypercapnia in the obese subjects. These results indicate that morbidly obese subjects maintain eucapnia primarily by an alteration in central breath timing. Although these subjects have decreased responsiveness to CO2, putting them at some risk of developing respiratory failure under conditions of hypercapnic/hypoxic stress, it is possible that this is counteracted by the increased responsiveness to hypoxia.
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PMID:Ventilatory regulation in eucapnic morbid obesity. 642 20

Profound periodic sleep hypoxemia (as low as 9-10% saturation) was observed in 41 morbidly obese patients with obstructive sleep apnea (OSA). Group 1 consisted of 14 patients with awake hypercapnia (mean PaCO2 54 +/- 8 torr, s.d.) and group 2 were 27 with eucapnia (PaCO2 38.6 +/- 2.9). Group 1 OSA patients were more obese (BMI 48.7 +/- 8.5 vs 38.3 +/- 6.8 kg/m2, had lower FEV1 (61 +/- 17% vs 86 +/- 15% pred.) and lower FVC (62 +/- 16% vs 77 +/- 13% pred.), all the differences insufficient per se to account for hypercapnia. Group I remained apneic longer in REM (100 +/- 50 s vs 65 +/- 32 s), and tolerated lower mean SpO2 (pulse oximeter SaO2) in NREM (71 +/- 16% vs 81 +/- 7%) and lower minimum SpO2 values in NREM (54 +/- 12% vs 69 +/- 11%) (all the differences were significant, p < 0.05). We conclude that daytime hypercapnia predicts more severe sleep desaturation in NREM in obese patients with OSA. The combination of morbid obesity and hypercapnia with OSA is associated with the most profound and repeated hypoxemia ever reported as occurring without evident brain damage or death.
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PMID:Profound sleep hypoxia in morbidly obese hypercapnic patients with obstructive sleep apnea. 807 11

To investigate the hypothesis that the impaired respiratory drive noted in morbid obesity was attributable to altered dopaminergic mechanisms acting on peripheral and/or central chemoreflex sensitivity, seven obese and seven lean Zucker rats were studied at 11 wk of age. Ventilation (VE) was measured by the barometric technique during hyperoxic (100% O(2)), normoxic (21% O(2)), hypoxic (10% O(2)), and hypercapnic (7% CO(2)) exposures after the administration of vehicle (control), haloperidol [Hal, 1 mg/kg, a central and peripheral dopamine (Da) receptor antagonist], or domperidone (Dom, 0.5 mg/kg, a peripheral Da receptor antagonist). In both lean and obese rats, Hal increased tidal volume and decreased respiratory frequency during hyperoxia or normoxia, resulting in an unchanged VE. In contrast, Dom did not affect tidal volume, frequency, or VE during hyperoxia or normoxia. During hypoxia, however, VE significantly increased from 1,132 +/- 136 to 1,348 +/- 98 ml. kg(-1). min(-1) (P < 0.01) after the administration of Dom in obese rats, whereas no change was observed in lean rats. Hal significantly decreased VE during hypoxia compared with control in lean but not obese rats. In both lean and obese rats, Hal decreased VE in response to hypercapnia, whereas Dom had no effect. Our major findings suggest that peripheral chemosensitivity to hypoxia in obese Zucker rats is reduced as a result of an increased dopaminergic receptor modulation in the carotid body.
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PMID:Dopaminergic modulation of ventilation in obese Zucker rats. 1174 39

Severe obesity is a chronic condition that is difficult to treat through diet and exercise alone. Gastrointestinal surgery for obesity (bariatric surgery) alters the digestive process by either restrictive surgical alterations or malabsorptive operations. Some 10-20% of patients who have weight-loss surgery require follow-up operations to correct complications. Hypoxemia after gastric bypass surgery for morbid obesity, a reported complication, can occur as early as 24 h post surgery. Two patients presented with severe hypoxia and were placed on veno-venous extracorporeal membrane oxygenation (ECMO). Patient No. 1 had an obstruction of the alimentary limb of the gastric bypass due to suture adhesions, and patient No. 2 had an incarcerated diaphragmatic hernia. While on ECMO, ventilation using a protective strategy (60% FiO2, pressure-controlled ventilation inspiratory pressure (PCV) IP 25-27, positive end-expiratory pressure (PEEP) 10-14, permissive hypercapnia) was employed. An inflow cannula to the level of the right atrium served as arterial outflow from the circuit to the patient, while the femoral vein served as venous inflow to the ECMO circuit. Although ECMO in adult respiratory failure is often used as the last resort due to serious associated adverse events, we report two patients with life-threatening complications from gastric bypass who were rescued, resuscitated to day 7, and uneventfully discharged from the hospital to home.
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PMID:Respiratory failure of two sp gastric bypass patients and subsequent rescue with extracorporeal membrane oxygenation. 1648 3

The prevalence of childhood obesity has more than tripled over the past five decades. Obesity results in low lung volumes, likely through increased loading of the chest wall and abdomen. The prevalence of asthma in children has paralleled the rise in obesity; obesity may increase the severity of asthma, but a direct link has been difficult to establish. Obesity is a risk factor for obstructive sleep apnea (OSA) in children as well as adults. Obese children may be at increased risk for persistent OSA following adenotonsillectomy treatment for OSA. Severe obesity and OSA may lead to the obesity-hypoventilation syndrome, with hypoxia, hypercapnia, and reduced ventilatory drive. Obesity can increase a child's risk for complications of anesthesia and recovery from surgery.
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PMID:Obesity and respiratory diseases in childhood. 1970 55

Obstructive sleep apnea (OSA) may occur in association with obesity-hypoventilation (Pickwickian) syndrome, a disorder of ventilatory control affecting individuals with morbid obesity. Through the pressor effects of chronic hypercapnia and hypoxemia, this syndrome may result in pulmonary hypertension, right heart failure, and massive peripheral edema. We present a case of severe scrotal edema in a 36-year-old male with OSA and obesity-hypoventilation syndrome. A tracheostomy was performed to relieve hypoxemia and led to dramatic improvement of scrotal edema. No scrotal surgery was necessary. Followup at two months showed complete resolution of scrotal edema, improvement in mental status, and normalization of arterial blood gas measurements. This case demonstrates that OSA and obesity-hypoventilation syndrome may present with massive scrotal edema. Furthermore, if OSA is recognized as the cause of right heart failure, and if the apnea is corrected, the resultant improvement in cardiac function may allow reversal of massive peripheral, including scrotal, edema.
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PMID:Massive scrotal edema: an unusual manifestation of obstructive sleep apnea and obesity-hypoventilation syndrome. 2353 35

Morbid obesity plays an increasingly important role in healthcare. Patients who are severely obese often suffer from a range of medical problems. One problem is obesity-related hypoventilation syndrome with its resulting hypercapnia. We report a case of a 33-year-old female patient who was in an extraordinarily bad medical state, with severe hypercapnia (pCO2 15.1 kPa), sepsis, acute anuric kidney failure and resulting acidosis (pH 6.96). Her body mass index was 84 kg/m2. Her chances of survival were considered very low after failed attempts at noninvasive ventilation. Based on prior research, we refrained from intubation and chose venovenous extracorporeal membrane oxygenation to treat the hypercapnia. In the entire medical literature, we are not aware of a similarly extraordinary case of obesity-related hypoventilation syndrome that could finally be treated successfully. The idea behind this case report is to consider venovenous extracorporeal membrane oxygenation as an alternative to intubation in this patient collective.
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PMID:Venovenous extracorporeal membrane oxygenation to treat hypercapnia in a morbidly obese patient. 3004 77


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