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

Noninvasive long-term ventilation is consensually advocated when daytime hypercapnia > 6 kPa at steady state in chronic restrictive pulmonary syndromes. Several mechanisms can cause the occurrence of hypercapnia in these diseases. They may involve impairment of lung mechanics or airway function and cough, ventilation-perfusion mismatching, blunted central ventilatory drive or respiratory muscle fatigue. These abnormalities may occur while awake or during sleep. From a practical point of view, imperative ventilation, a palliative technique that aims to supply respiratory muscle weakness, and preventive ventilation, aimed at delaying respiratory handicap, should be distinguished between. The latter is offered to patients who do not fulfil any criteria for mechanical ventilation. Otherwise, the underlying disease markedly influences both pathophysiology and outcome. This implies that the available modes of ventilatory support should be assessed in each disease. Several findings have been published about Duchenne's muscular dystrophy. Mechanical ventilation, usually using noninvasive methods, is offered to patients with either hypercapnia or a forced vital capacity < 20% of the predicted value. Nevertheless, based on our experience, deterioration of the restrictive syndrome should be followed by a tracheostomy. By contrast, early ventilation, offered to patients free of symptoms and whose forced vital capacity are within 20-50% pred and with normal arterial blood gas levels, achieves no benefit.
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PMID:Is early noninvasive mechanical ventilation of first choice in stable restrictive patients with chronic respiratory failure? 1021 81

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

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

Chronic expiratory flow limitation and hyperinflation are the mechanical hallmarks of chronic obstructive pulmonary disease (COPD). Although carbon dioxide retention is dependent on the severity of airflow limitation, there is considerable variability in the relationships between arterial carbon dioxide tension (Pa,CO2) and forced expiratory volume in one second (FEV1) or total lung resistance (RL). In stable COPD patients with severe airflow obstruction, shallow breathing and inspiratory muscle weakness are the main factors associated with CO2 retention. In stable COPD patients, the diaphragm is less effective than in normal subjects and, with increasing airflow obstruction and hyperinflation, the contribution to the generation of ventilatory pressure of the ribcage inspiratory muscles increased. Abdominal muscles are recruited during expiration in severe COPD patients and the expiratory rise in gastric pressure is directly related to intrinsic positive end-expiratory (alveolar) pressure (PEEPi). During acute bronchoconstriction, COPD patients with severe airflow obstruction recruited the rib cage inspiratory muscles proportionally more than the diaphragm. The associated recruitment of abdominal muscles results in a reduction in abdominal volume at end-expiration and contributes to a significant extent to PEEPi. Dynamic hyperinflation can be overestimated during chronic and acute airway obstruction if abdominal muscle function is not evaluated.
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PMID:Physiological changes during severe airflow obstruction in chronic obstructive pulmonary disease. 1074 Nov 1

To evaluate ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia with paralysis of abdominal muscles, we studied seven patients with complete transection of the midthoracic cord (Th6-Th7) and six normal subjects. Minute ventilation (V E) and mean inspiratory flow responses to hypercapnia were similar in normal subjects and patients with paraplegia, but in the latter, at any given level of end-tidal CO(2) partial pressure (PET(CO(2))), tidal volume (VT) was reduced and frequency was increased. In normal subjects during hypercapnia, end-expiratory transpulmonary pressure (PL) and abdominal volume at end expiration decreased markedly, whereas end-expiratory volume of the rib cage (Vrc,E) remained constant, suggesting progressive recruitment of abdominal muscles. In patients with paraplegia compared to normal subjects the decrease in end-expiratory PL was reduced, and it was associated with a decrease in Vrc,E, suggesting recruitment of rib cage expiratory muscles. For a PET(CO(2)) of 70 mm Hg the estimated expiratory muscle contribution to VT was 10.3 and 28.4% (p < 0.02) in patients with paraplegia and normal subjects, respectively. We conclude that the V E-CO(2) relationship is preserved in patients with paraplegia with the development of a rapid and shallow pattern of breathing. This suggests that expiratory muscle paralysis elicits adaptation of the ventilatory control system similar to that observed in patients with generalized respiratory muscle weakness.
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PMID:Ventilatory and respiratory muscle responses to hypercapnia in patients with paraplegia. 1090 42

Although ventilatory failure is the most common cause of death in amyotrophic lateral sclerosis (ALS) and measurement of respiratory muscle strength (RMS) has been shown to have prognostic value, no single test of strength can predict the presence of hypercapnia reliably. RMS was measured in 81 ALS patients to evaluate the relationship between tests of RMS and the presence of ventilatory failure, defined as a carbon dioxide tension > or = 6 kPa. We studied the predictive value of vital capacity (VC), static inspiratory and expiratory mouth pressures (MIP, MEP), maximal sniff oesophageal (sniff P(oes)), transdiaphragmatic (sniff P(di)) and nasal (SNP) pressure, cough gastric (cough P(gas)) pressure and transdiaphragmatic pressure after bilateral cervical magnetic phrenic nerve stimulation (CMS P(di)) to identify the risk of ventilatory failure in the whole group and in subgroups of patients with and without significant bulbar involvement. For patients without significant bulbar involvement, sniff P(di) had greatest predictive power [odds ratio (OR) 57] with specificity, sensitivity and positive and negative predictive values (PPV, NPV) of 87, 90, 74 and 95%, respectively Of the less invasive tests, per cent predicted SNP had greater overall predictive power (OR 25, specificity 85%, sensitivity 81%) than per cent predicted VC (9, 89%, 53%) and per cent predicted MIP (6, 83%, 55%). No test had significant predictive power for the presence of hypercapnia when used to measure RMS in a subgroup of patients with significant bulbar weakness. Thirty-five patients underwent polysomnography. CMS P(di), sniff P(di) and per cent predicted SNP were significantly correlated with the apnoea/hypopnoea index (AHI) (P = 0.035, 0.042 and 0.026, respectively). The correlations between AHI and per cent predicted MIP and VC were less strong (both non-significant). In ALS patients without significant bulbar involvement, novel tests of RMS have greater predictive power than conventional tests to predict hypercapnia. In particular, the non-invasive SNP is more sensitive than VC and MIP, suggesting that it could usefully be included in tests of respiratory muscle strength in ALS and will be helpful in assessing the risk of ventilatory failure. In patients with significant bulbar involvement, tests of respiratory muscle strength do not predict hypercapnia. Sleep-disordered breathing is correlated with RMS and the novel tests of RMS having the strongest relationship with the degree of sleep disturbance.
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PMID:Respiratory muscle strength and ventilatory failure in amyotrophic lateral sclerosis. 1157 Dec 18

We report a 55-year-old woman with typical clinical, biochemical and radiological features of Cushing's disease, who developed a severe respiratory insufficiency as the main symptom. She also complained of proximal muscle weakness over the last year and progressive dyspnea over the last four months. Bronchospasm, respiratory infection or cardiologic dysfunction were excluded. Arterial blood gas analysis showed severe respiratory insufficiency with hypoxemia and hypercapnia, respiratory acidosis and a normal alveolar-arterial oxygen gradient. Spirometry and plethysmography showed a restrictive ventilatory failure and maximum inspiratory and expiratory pressures were reduced. These findings were strongly suggestive of neuromuscular disease. Serum creatine kinase, aldolase, sodium, potassium and thyroid function tests were normal. An electromyogram and a muscle biopsy confirmed myopathic disease. Ketoconazole therapy improved her symptoms and respiratory function tests. In conclusion although proximal myopathy is a frequent presenting symptom of Cushing's syndrome, involvement of respiratory muscles with severe restrictive ventilatory dysfunction has not been previously reported as the main initial feature of Cushing's disease. Medical treatment of hypercortisolism improves muscle strength and resolves the respiratory insufficiency.
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PMID:Severe respiratory failure secondary to Cushing's myopathy. 1168 45

Tetrodotoxin (TTX) poisoning, although uncommon, is frequently seen in Taiwan, Japan, and Southeast Asia. It is rare but significant in the United States as well. Only three cases have been reported in the EM literature. We report an outbreak of six cases of TTX poisoning from eating puffer fish. On April 17, 2001, an outbreak of TTX poisoning occurred among Mainland Chinese fishermen who shared puffer fish on their boat in the Taiwan Strait. All six cases were middle-aged men (aged 32-49 yr). Onset of symptoms began approximately 2 to 3 hours after ingestion; symptoms included orolingual numbness, acroparesthesia, and breathlessness. As a result of delayed transportation and initial resuscitation, one patient presented in full cardiac arrest, with recovery of spontaneous circulation after successful cardiopulmonary resuscitation. With the exception of this patient, the initial acid-base abnormalities were inconsistent with severity of illness and mild hypercapnia was common (4 out of 5). The patient who presented in full arrest died 1 day after admission as a result of intractable bradycardia (complete atrioventricular block), a finding rarely mentioned in the literature, despite intravenous atropine and dopamine infusion. The remaining patients survived without significant sequelae and were discharged after short-term observation and supportive care, although some had neurologic and cardiopulmonary manifestations (muscle weakness, hypotension, hypoxemia, and hypercapnia). Some mildly hypoventilated patients recovered well without endotracheal intubation and ventilatory support. Favorable outcomes in most patients can be obtained if aggressive supportive treatment is provided in time. Thus, appropriate prehospital and ED ventilatory support (the implementation of a bag-valve mask or endotracheal intubation with good ventilatory support) is mandatory for those patients with respiratory failure. Most patients experience onset of symptoms within 6 hours of ingestion, but a few have a delayed onset up to 20 hours. Therefore, for those TTX-intoxicated patients without immediate prominent respiratory insufficiency, at least 24 hours of intensive monitoring of their respiratory state is necessary because of the different susceptibility and unpredictability of an individual course.
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PMID:Tetrodotoxin poisoning. 1256 82

A 62-year-old man with well-controlled diabetes mellitus developed numbness of the bilateral feet and hands, followed by subacutely progressive weakness and amyotrophy of extremities. He became bed-ridden state, and dyspnea also appeared, so he was referred to our hospital. Physical examination revealed a lean man, with dark-reddish skin pigmentation, crabbed fingers, bilateral pretibial pitting edema, and bristles in extremities. Thoracoabdominal paradoxical respiration was observed and pulmonary vesicular sounds was decreased markedly in the both lungs. Laboratory data revealed hypoproteinemia, abnormalities of endocrine system, but M-protein was not detected. Serum vascular endothelial growth factor level was quite high. Chest radiography revealed elevation of the bilateral diaphragm, the % vital capacity (%VC) was 24%, and arterial blood gas analysis showed marked hypoxia with hypercapnia. These findings suggested that his respiratory failure was induced by bilateral diaphragmatic paralysis caused by bilateral phrenic nerve palsy due to Crow-Fukase syndrome. He became somnolent because of hypercapnic narcosis, so non-invasive positive pressure ventilation (NIPPV) was started. We treated him with intravenous immunoglobulin and oral corticosteroids therapies, and after these therapies, his symptoms were remarkably recovered and NIPPV became unnecessary soon. The most frequent causes of respiratory failure in Crow-Fukase syndrome are pleural effusion and pulmonary hypertension, and only two cases of this syndrome with respiratory failure caused by bilateral diaphragmatic paralysis were reported until now. When the patients with Crow-Fukase syndrome complain of dyspnea, we should take the diaphragmatic paralysis into consideration, which may be improved by appropriate therapies.
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PMID:[A case of Crow-Fukase syndrome with respiratory failure due to bilateral diaphragmatic paralysis]. 1266 Nov 11

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


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