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)

A 64-year-old man with multiple system atrophy complained of daytime sleepiness, fatigue, and snoring. Neurological examination revealed severe autonomic failure, mild cerebellar ataxia and akinesia. Daytime blood gas analysis showed respiratory acidosis with hypoxia and hypercapnia. MR imaging of the brain showed atrophy of the pons, cerebellum and bilateral frontal lobes. Although paralysis of the vocal cord abduction was not found by laryngoscopy during daytime examination, polysomnography (PSG) showed heavy snoring with paradoxical respiration associated with severe desaturation during sleep as well as reduced slow wave sleep and REM sleep. He was diagnosed as having sleep-related upper airway obstructive breathing disorder probably due to Gerhardt syndrome. Tracheostomy was considered, but we performed nasal CPAP therapy during sleep because this therapy is non-invasive and would not impair his daily life. After nasal CPAP therapy, daytime sleepiness, fatigue, and snoring with desaturation improved, and PSG showed increased slow wave sleep. These results demonstrate that nasal CPAP therapy improves the quality of sleep and should be considered in patients with early stages of multiple system atrophy who exhibit sleep-related breathing disorders.
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PMID:[Effective nasal CPAP therapy for heavy snoring and paradoxical respiration during sleep in a case of multiple system atrophy]. 1034 49

Morbidity and mortality derived from asthma continue to be a main public health problem in many countries, in spite of the advances in the knowledge on the disease and its treatment. There are several risk factors for asthma attack which have to be considered in the management of patients in order to prevent exacerbations and mortality. Smooth bronchial muscle constriction and inflammation with oedema of the bronchial wall are the facts that cause airway flow and resistance disturbances, with hyperinflation, leading to a bigger respiratory work. On the other hand, the bronchial obstruction leads to a ventilation-perfusion disequilibrium and hypoxia. At the beginning of the process there is hypocarbia, but when the attack progresses muscle fatigue happens, and retention of CO2, being a sing of alarm (predictive of respiratory failure) a normal and rising PaCO2. The evaluation of an acute asthmatic patient should accomplish a clinical and objective assessment (peak flow rate and saturation of O2), in order to classify the crisis in: mild, moderate or severe. Managing acute asthmatic patient includes: oxygen, bronchodilator ss2 agonists at high and even continuous doses and systemic corticosteroids to prevent the progression and to control inflammation. These procedures should be promptly instituted. Although there is less evidence on their beneficial effects other measures as intravenous aminophylline, nebulized anticholynergics, magnesium sulphate and intravenous ss2 agonists may be used when the conventional therapy is not quickly successful and the patient is in a critical situation, at a real risk of respiratory failure, and in order to avoid mechanical ventilation. If this is finally instituted, controlled hypoventilation with permissive hypercarbia is now recommended, to avoid barotrauma, which used to be a frequent complication when more aggressive attitude was the rule. Interaction between paralytic agents and corticosteroids may produce a miopathy, so the recommendation now is to try not to use paralytic agents, even with profound sedation of needed. Sixty four patients were treated on 77 occasions in the Pediatric Intensive Care Unit of our hospital. They were 0,5 to 13,9 years old, being 50% less than 5 years old. It was the first attack in 9 (14%) patients. The standard management consisted of oxygen, frequently or continuously nebulized salbutamol and intravenous methylprednisolone (1 to 6 mg/kg/day). Furthermore nebulized ipratropium bromide was administered 58 times (75%), as well as intravenous aminophylline 69 (89%), intravenous salbutamol 23 (30%), magnesium sulphate 16 (21%) and ketamine 10 (13%). Antibiotics were given 22 times (29%). Two 15 month old infants received mechanical ventilation in three occasions, and relevant complications happened (pneumothorax and myopathy, and pneumomediastinum and bronchiolitis obliterans respectively). Fifty six patients have been followed for a period of 3 to 110 months (median 48 months), and 16 (29%) have needed high doses (equal to or move than 800 mcg of budesonide or equivalent). There are data on lung function in 36 of them, FEV1 is normal (> 85% of predicted, between 86 and 127) in 26 (78%) and < 85% (65 to 84%) of predicted in 8 (22%) FEV1 rises more than 15% (16 to 23%) in four patients after the inhalation of a ss2 agonist. Inhaled anesthetic agents and heliox have been used in some pediatric cases. After a severe asthma attack the strategy of management should be reviewed, as well as the possible risk factors.
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PMID:[Round Table: Severe asthma in pediatrics: treatment of acute crises]. 1035 7

Relatively little is known about the combined effects of hypercapnia and fatigue on the human diaphragm. We examined the effects of acute hypercapnia and fatigue in seven subjects by measuring changes in transdiaphragmatic pressure (Pdi) elicited by cervical magnetic stimulation after 2 min maximal voluntary ventilation (MVV) while breathing air and also with the inspired PCO(2) increased to 8% for 12 min before and during the MVV. Diaphragm strength was assessed before and at 0, 20, 40, 60, and 90 min after the MVV in both studies with the subjects breathing air. There was no difference in the level of ventilation for each run. Mean (+/- SD) twitch Pdi (TwPdi) fell significantly (p < 0.01) at 20 min after the control and hypercapnic MVV; (30.4 [7.8] to 27.0 [8.1] cm H(2)O control and 30.3 [4.1] to 27.3 [5.0] cm H(2)O CO(2)) and remained significantly (p < 0.01) below baseline. The changes in TwPdi at 20 to 90 min were not significantly different between the control and CO(2) runs. The decrease in TwPdi at 0 min after MVV, however, was greater (15%) in the hypercapnic run than in the control run (8.1%) (p < 0.05) when compared with baseline valves. Hypercapnia does not intensify long lasting fatigue but may reduce diaphragm contractility immediately after MVV.
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PMID:Effect of hypercapnia on maximal voluntary ventilation and diaphragm fatigue in normal humans. 1055 22

Alveolar hypoventilation associated with neuromuscular disease can occur in acute and chronic forms. In the acute form, progressive weakness of respiratory muscles leads to rapid reduction in vital capacity followed by respiratory failure with hypoxemia and hypercarbia. Symptoms are those of acute respiratory failure, including dyspnea, tachypnea, and tachycardia. In the chronic form, impairment of the respiratory muscles affects mechanical properties of the lungs and chest wall, decreases the ability to clear secretions, and eventually may alter the function of the central respiratory centers. Symptoms include orthopnea, fatigue, disturbed sleep, and hypersomnolence. Treatment and outcome of the disease's chronic form are dependent on the underlying clinical cause of the alveolar hypoventilation. For chronic but stable diseases such as old polio, quadriplegia, or kyposcoliosis, mechanical support of minute ventilation can reverse symptoms. For chronic and progressive disease such as muscular dystrophy and amyotrophic lateral sclerosis, mechanical support of minute ventilation provides only symptomatic relief and is usually associated with deterioration to the point of complete ventilator dependency for survival. For the chronic progressive forms of alveolar hypoventilation, there is currently a need for quality randomized controlled clinical trials to define physiologic indicators and appropriate timing for mechanical support of minute ventilation.
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PMID:Neuromuscular disease and hypoventilation. 1057 Jul 36

The effect of a COPD crisis on arterial blood gases, heart rate, lactate and indices of oxidative stress were investigated before, during and 1 h after a 'run up to fatigue' in 6 COPD horses. They were investigated twice, randomly: once in acute crisis (C) and once in clinical remission (R). Arterial and mixed venous blood samples were collected and analysed for partial pressures in O2 and CO2. The mixed venous blood was also analysed for plasma lactate (LA) and packed cell volume (PCV), as well as for indices of oxidative stress, i.e. reduced glutathione, glutathione disulphide, glutathione redox ratio (GRR) and lipid hydroperoxides (LPH). The exercise test was an effort of increasing intensity on a treadmill at 0% slope, which was stopped when the horses showed signs of exhaustion. Their performance was evaluated by the number of steps and the running time in the last step. Heart rate was monitored continuously during the test. Blood sampling was performed before, just after and 1 h after the end of the test. The COPD crisis significantly reduced the time to fatigue. However, despite the fact that the exercise intensity and length were lower, peak HR and peak LA were similar in C and R, while arterial hypoxaemia and hypercapnia, and PCV were significantly higher in C, indicating a higher physiological stress in this condition. By contrast, the oxidative stress seemed to be higher in R than in C as suggested by the fact that, 1 h after exercise, GRR and LPH were significantly increased with regards to their pre-exercise values in R and not in C. The fact that exercise did not induce an oxidative stress in C could be partly related to (1) the lower exercise intensity reached by the horses, and (2) to the more severe hypoxaemia experienced in this condition. In conclusion, COPD horses in acute crisis show a significant decrease in performance. The reasons for this exercise intolerance remain unclear, but do not appear to be related to any increase of the oxidative stress in C.
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PMID:Cardiorespiratory measurements and indices of oxidative stress in exercising COPD horses. 1065 28

Six horses were randomly assigned to receive either frusemide (F) (0.5 mg/kg i.v.) or an equivalent volume of saline (S) i.v., 4 h prior to treadmill exercise. Horses were instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) carotid arterial pressures, pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), blood gases, and cardiac output (CO). Plasma (PV) and blood volumes (BV) were measured using 2 injections of Evan's Blue dye. Baseline parameters were recorded while the horse stood quietly. Horses were then administered F or S. Four hours later, they were warmed up for 3 min at 4 m/s and then exercised to the point of fatigue at 115% VO2max. Horses were anaesthetised immediately following exercise by administration of detomidine (0.04 mg/kg bwt i.v.) followed 5 min later by tiletamine-zolazepam (1.25 mg/kg bwt i.v.). After transporting the horse to a recovery stall, anaesthesia was maintained with isoflurane in 100% O2. Data were analysed using a 2-way ANOVA with repeated measures with post hoc differences identified using the Student-Newman-Keul's procedure. Exercise was associated with increases in HR, SAP, MAP, DAP, PAP, CVP, TEMP, PCV, and BV, and decreases in PV, pH, arterial bicarbonate and base excess. Anaesthesia was associated with marked hypercapnia, a decrease in HR following detomidine administration, and persistent pulmonary hypertension despite carotid arterial pressure which returned to baseline. No effects attributable to F were identified at any time during the study.
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PMID:Effects of pre-exercise frusemide administration and post exercise anaesthesia on cardiopulmonary and acid-base parameters and blood and plasma volumes in horses exercised supramaximally to fatigue. 1065 46

Diaphragm fatigue may contribute to respiratory failure. (31)P-nuclear magnetic resonance spectroscopy is a useful tool to assess energetic changes within the diaphragm during fatigue, as indicated by P(i) accumulation and phosphocreatine (PCr) depletion. We hypothesized that loaded breathing during hypoxia would lead to diaphragm fatigue and inadequate aerobic metabolism. Seven piglets were anesthetized by using halothane inhalation. Diaphragmatic contractility was assessed by transdiaphragmatic pressure (Pdi) at end expiration with the airway occluded. A nuclear magnetic resonance surface coil placed under the right hemidiaphragm measured P(i) and PCr during four conditions: control, inspiratory resistive breathing (IRB), IRB with hypoxia, and recovery (IRB without hypoxia). IRB alone resulted in hypercarbia (32 +/- 7 to 61 +/- 21 Torr) and respiratory acidosis but no change in diaphragm force output or aerobic metabolism. Combined IRB and hypoxia resulted in decreased force output (Pdi decreased by 40%; from 30 +/- 17 to 19 +/- 11 mmHg) and evidence of metabolic stress (ratio of P(i) to PCr increased by 290%; from 0.19 +/- 0.09 to 0.74 +/- 0.27). We conclude that diaphragm fatigue associated with inadequate aerobic oxidative metabolism occurs in the setting of loaded breathing and hypoxia. Conversely, aerobic metabolism and force output of the diaphragm remain unchanged from control during loaded normoxic or hyperoxic breathing despite the onset of respiratory failure.
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PMID:Effects of loaded breathing and hypoxia on diaphragm metabolism as measured by (31)P-NMR spectroscopy. 1071 Mar 88

If chronic hypercapnia in patients with severe COPD occurs as a consequence of respiratory muscle (RM) weakness or fatigue, we would expect that ventilatory muscle recruitment (VMR) and exercise performance in stable hypercapnic patients would differ from those in eucapnic patients. We evaluated exercise performance and RM function at rest and during exercise in 19 eucapnic (PCO(2) 40 +/- 3 mm Hg), and 13 hypercapnic (PCO(2) 52 +/- 10 mm Hg) patients with severe COPD. A metabolic cart was used to determine V E, V O(2), V CO(2), and HR. Gastric (Pg) and esophageal (Ppl) balloons were used to measure Pg, Ppl, and Pdi. Ventilatory muscle recruitment pattern (VMR) was partitioned using end-inspiratory and end-expiratory Pg and Ppl. Hypercapnic patients had lower FEV(1) (0.60 +/- 0.24 versus 0.95 +/- 0.31 L, p < 0.001), MVV (28 +/- 11 versus 41 +/- 13 L, p < 0.001), resting PO(2) (61 +/- 11 versus 70 +/- 11 mm Hg, p < 0.001), peak PO(2) (60 +/- 20 versus 75 +/- 22 mm Hg, p < 0.005), and V E(max) (24 +/- 10 versus 32 +/- 12 L/min, p < 0.001). Patients in both groups had similar FRC (5.7 +/- 1.6 versus 5.0 +/- 1.5 L), V O(2)max (0.58 +/- 0.30 versus 0.76 +/- 0.32 L/min), Watts (45 +/- 48 versus 71 +/- 59), V E/MVV (88 +/- 33 versus 79 +/- 14), and HRmax (117 +/- 17 versus 128 +/- 18 beats/min). PI(max) (67 +/- 28 versus 65 +/- 32 cm H(2)O) and PE(max) (98 +/- 34 versus 96 +/- 40 cm H(2)O) were also similar in both groups. VMR (DeltaPg/DeltaPpl) at rest (-0.28 +/- 0.51 versus 0 +/- 0.35) and during exercise (0.4 +/- 0.2 versus 0.39 +/- 0.15) was equally affected in both groups. We conclude that exercise capacity and ventilatory muscle recruitment are similarly impaired in eucapnic and hypercapnic patients with severe COPD. These findings make inability of the lung to increase ventilation and not respiratory muscle dysfunction a more attractive explanation for CO(2) retention in stable hypercapnic patients.
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PMID:Respiratory muscle recruitment and exercise performance in eucapnic and hypercapnic severe chronic obstructive pulmonary disease. 1071 37

Complaints of poor sleep are very common in people with chronic respiratory disorders. In patients with chronic obstructive pulmonary disease (COPD), poor sleep may be due to many causes, including cough, excess mucous production, and frequent arousals from sleep caused by hypercapnia, as well as secondary to medications used to manage the lung disease. Patients with obstructive sleep apnea (OSA) also complain of excessive daytime sleepiness and fatigue due to poor-quality sleep, although the mechanism of sleep disruption is somewhat different from that in patients with COPD. Although benzodiazepines are often the drugs of choice for the management of insomnia, caution is suggested with the use of these agents in patients with chronic obstructive respiratory disease due to the reduction in upper airway muscle tone and blunting of the arousal response to hypercapnia. However, controlled trials with short-acting benzodiazepine receptor antagonists, including triazolam, zolpidem, and zaleplon, suggest that these agents may be safely used in selected patients who have mild to moderate COPD without daytime hypercapnia. Less data are available on the use of these agents for patients with OSA, but a preliminary trial using zaleplon suggests that respiratory function is not adversely affected in patients with mild to moderate OSA. Studies are needed to further define the benefit-risk ratio of the use of benzodiazepine receptor agonists for the management of insomnia in patients with chronic obstructive lung disease.
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PMID:Perspectives on the management of insomnia in patients with chronic respiratory disorders. 1075 6

Sleep-related breathing disorders, ranging from habitual snoring to the increased upper airway resistance syndrome to sleep apnea, are now recognized as major health problems. The majority of patients have excessive daytime sleepiness and tiredness. Neuropsychological dysfunction results in poor work performance, memory impairment, and even depression. Until recently, the coexistence of cardiovascular and cerebrovascular diseases with sleep-related breathing disorders was thought to be the result of shared risk factors, such as age, sex, and obesity. However, in the past 5 years several epidemiologic studies have demonstrated that sleep-related breathing disorders are an independent risk factor for hypertension, probably resulting from a combination of intermittent hypoxia and hypercapnia, arousals, increased sympathetic tone, and altered baroreflex control during sleep. Sleep apnea may lead to the development of cardiomyopathy and pulmonary hypertension. Early recognition and treatment of sleep-related breathing disorders may improve cardiovascular function.
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PMID:Sleep-related breathing disorders and cardiovascular disease. 1075 96


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