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 62 year-old woman with a bilateral carotid body paraganglioma presented, 2 years after the removal of the right one, with signs of right-heart failure. Hypoxemia, hypercapnia, polycythemia and pulmonary hypertension with normal ventilatory capacity were found. Central alveolar hypoventilation was diagnosed on the basis of absence of ventilatory response and sensation of provoked hypercapnia, prolonged breath-holding time and correction of hypercapnia by voluntary ventilation. Progesterone (200 mg/d during 3 weeks) or naloxone did not improve either arterial blood gases (ABG) or the P 0.1/PCO2 curve. Hypoxemia and hypercapnia were not corrected during metabolic acidosis provoked by acetazolamide (250 mg/d). Nasal CPAP did not control hypoventilation periods. Mechanical ventilation was initiated with negative pressure (NPV) through a poncho. The patient presented severe discomfort with NPV and obstructive apneas were verified during it. She refused to continue NPV. Mechanical ventilation was initiated with positive intermittent pressure (IPPV) through a nasal mask. The patient had excellent tolerance to the procedure. SpO2 during IPPV was always higher than 95%. During sleep induction (under IPPV), respiration in phase with the ventilator 1: 1 was observed; instead, during consolidated sleep there was a complete dependence of the ventilator with apnea for over 2 min when IPPV was interrupted (Fig. 1). After 2 months of treatment, a relief of right ventricular failure occurred and hematocrit fell to 39%. There was an improvement of day-time ABG (Table I). The P. 0.1/PaCO2 curve 3 months after IPPV was the same as the previous one (Fig. 2). The patient has been for 18 months on home ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Central alveolar hypoventilation with cor pulmonale: successful treatment by non-invasive intermittent positive pressure ventilation]. 771 33

Patients in hypercapnic respiratory failure have got a poor prognosis. The recognition of pathophysiological mechanisms is required in order to choose adequate therapy. During the past years it has been shown that pathological respiratory events during sleep occur early in the disease process and that blood gas changes are usually most pronounced during sleep. Minute ventilation and functional residual capacity (FRC) decrease during sleep even in normal subjects and upper airway resistance increases markedly. PO2 slightly decreases and paCO2 increases. In most patients with hypercapnic respiratory failure episodes of marked hypoxemia and hypercapnia occur, mainly during REM sleep. Suggested pathomechanisms are worsening ventilation-/perfusion mismatching, impaired respiratory muscle function and a reduction in ventilatory drive, the latter two being of major importance. The relation between load and capacity is shifted towards an increased load and ventilatory drive is decreased at the same time. Therapeutic strategies that reduce the load of the respiratory pump, increase minute ventilation and prevent sleep related hypoventilation, thus noninvasive ventilation should be used. Symptoms of hypercapnic respiratory failure are often unspecific. Dyspnea, headache and awakening from sleep with dyspnea are often reported. Signs of right heart failure will be present in advanced disease stages. Early diagnosis and treatment provided, noninvasive ventilation achieves excellent improvement of both quality of life and life expectancy, especially if the primary disease progress is not rapidly progressive.
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PMID:[Pathophysiology and clinical aspects of global respiratory insufficiency]. 923 56

Chronic lung disease (CLD) of prematurity is a common disorder in preterm infants who were ventilated for respiratory distress syndrome (RDS) at birth. Premature birth, mechanical ventilation and supplemental oxygen are the major risk factors for the development of CLD. Although the exact pathophysiology is unclear, recent evidence suggests that pulmonary inflammation may play a pivotal role in the development of CLD. Histologically, the evolution of CLD can be divided into an early inflammatory phase followed by a subacute and chronic fibroproliferative phase. The early, inflammatory phase of CLD is clinically indistinguishable from RDS. In bronchoalveolar lavage fluid an influx of inflammatory cells and increased levels of cytokines can be found. Pathological examination of the lungs reveals persisting hyaline membranes, necrosis of airway and alveolar epithelium and an influx of inflammatory cells in the lung. In the subacute fibroproliferative or reparative phase of CLD, persistent respiratory distress and hypercapnia are seen and patients require oxygen with or without ventilatory support. Histologically, this phase is characterized by hyperplasia of type II pneumocytes, hypertrophy of bronchial and bronchiolar smooth muscle and interstitial and perialveolar fibrosis. In the chronic fibroproliferative phase (up to 1 yr), airway remodelling occurs. Respiratory distress continues and many patients remain oxygen dependent. Cyanotic spells are frequently seen and chronic hypoxia may lead to pulmonary hypertension and right heart failure. Many patients have severe feeding problems and somatic growth is poor. In surviving patients, persisting lung function abnormalities are found. Airway resistance and airway responsiveness are increased and residual volume (RV) and RV/total lung capacity ratios remain elevated, indicating air trapping. Although lung function improves during childhood, residual abnormalities are still found in young adults, raising concerns about the evolution of pulmonary function in old age.
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PMID:Evolution and natural history of chronic lung disease of prematurity. 927 Feb 56

Chronic respiratory failure (CRF) is a major cause of morbidity and mortality. It is estimated that in France at least 60,000 patients exhibit severe CRF and that about 15,000 patients die each year from CRF. Chronic obstructive pulmonary disease (COPD) (chronic obstructive bronchitis, emphysema and their association) is by far the first cause of CRF (90% of the cases). The clinical picture of CRF depends on the causal disease, but exertional dyspnea is observed in almost all patients. Pulmonary function testing allows to assess whether the ventilatory defect is obstructive (COPD), restrictive or mixed. Severe CRF is usually defined by a Pa02 < 55 mmHg, in a stable state of the disease, with or without hypercapnia (PaC02 > 45 mmHg). The two major complications of CRF are acute exacerbations of the disease, with clinical and gasometric worsening, and pulmonary hypertension which may lead with time to right heart failure. Prognosis is poor in CRF since the 5 year survival rate is of 50% in COPD patients. Under long-term oxygen therapy (LTOT) the survival rate has been somewhat improved, being of 60-65% at 5 years. The best prognostic indices in CRF complicating COPD are the level of FEV1, Pa02, PaC02, the level of pulmonary artery mean pressure (PAP) and age. In COPD patients under LTOT the best prognostic indices are PAP and age.
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PMID:[Chronic respiratory insufficiency: evaluation, evolution, prognosis]. 981 2

The prevalence of sleep apnea syndrome (SAS) is approximately 7.5% in Japanese adults aged 18-68 years old. SAS is characterized by repeated episodes of apnea, especially obstructive apnea, during sleep. Severe SAS has life-threatening complications such as pulmonary hypertension, arrhythmias, right heart failure or brain damage, which could be caused by hypoxemia and/or hypercapnia. Upper airway relaxation is responsible for the obstruction during apnea, and an increase in the activities of the upper airway muscles dilates and stiffens the upper airway wall. Maintaining the activities of the upper airway muscles may contribute to keeping the airway patent. Submental electrical stimulation of the upper airway muscles would be a novel treatment method for obstructive apnea.
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PMID:New strategies of screening and treatment for sleep apnea syndrome. 1032 56

Respiratory insufficiency appearing during chronic lung diseases leads to hypoxemia, hypercapnia, acidosis, right ventricular failure and secondary polyglobulia. These disturbances lead to respiratory encephalopathy which is characterized by the appearance of various types of neurological syndromes. We present here the case of a patient suffering from chronic spastic bronchitis accompanied by pulmonary emphysema, whose consciousness disturbances, a generalized epileptic seizure and hemiparesis were connected with his respiratory insufficiency intensifying during the basic disease. Removal of metabolic disturbances caused by respiratory insufficiency has a key role in preventing secondary neurological syndromes.
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PMID:[A case of hypoxic encephalopathy in the course of chronic spastic bronchitis and pulmonary emphysema]. 1110 77

Circulating and urinary levels of endothelin (ET), an endothelium-derived vasoconstrictive and mitogenic peptide have been reported to increase in patients with chronic obstructive pulmonary disease (COPD), but the mechanisms of these abnormalities are not fully understood. Our study objectives were to evaluate pulmonary and renal ET clearance in COPD patients during an acute exacerbation. Our participants included nine consecutive patients with moderate to severe COPD without signs of right heart failure admitted for acute exacerbation and ten healthy volunteers (HV) as controls. ET was detected by radioimmunoassay in venous and arterial blood as well as in a timed urine specimen. For each subject, arterial/venous immunoreactive ET ratio (ir-ETart/ir-ETven) was evaluated as an index of its pulmonary clearance. Creatinine clearance was employed in each case to obtain a corrected renal ir-ET clearance. Glomerular filtration rate (GFR) was also assessed by dynamic(99m)Tc-diethylenetriamine pentaacetic acid renal scintigraphy in six COPD patients during acute exacerbation and at recovery. The ratio ir-ETart/ir-ETven was comparable in COPD patients (0.75+/-0.12) and in HV (0.82+/-0.09). A significant difference was found with respect to 24 h ir-ET urinary excretion between COPD patients during exacerbation as well as at recovery (respectively 142.1+/-12.8 ng/24 h and 89.0+/-15.1 ng/24 h) and HV (65.1+/-10.1 ng/24 h). ET renal clearance was higher in COPD patients than in HV (29.2+/-5.2 ml min(-1)in COPD during exacerbation; 17.5+/-3.9 ml min(-1)at recovery and 13.6+/-2.4 ml min(-1)in HV, P<0.001). GFR was 69.4+/-10.0 ml min(-1)in COPD patients during exacerbation and it significantly increased at the recovery (95.5+/-20.9 ml min(-1)P<0.001). Corrected renal clearance of the peptide was significantly correlated to GFR values during the exacerbation (r=-0.81, P<0.05). Furthermore change in renal ET production resulted associated with changes in paCO(2)(r=0.83, P<0.001) and in paO(2)(r=-0.73, P<0.05). Acute exacerbation in COPD patients causes an increase in renal ET production which is partially reversible at the recovery, in the absence of significant changes in ET-1 circulating levels. ET might contribute to the renal response to hypoxaemia and hypercapnia in COPD.
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PMID:Abnormalities of renal endothelin during acute exacerbation in chronic obstructive pulmonary disease. 1144 May 61

Chronic obstructive pulmonary disease (COPD) is a leading cause of death, and constitutes a major medical and an increasing economic problem for acute and long term care. A low level of irreversible airway obstruction when in stable condition, hypercapnia, hypoxia, the presence of comorbid heart disease, right ventricular failure, and low serum albumin are the main factors related to risk of exacerbations. Bronchial infections, bronchospasm, left ventricular failure, pneumonia, pneumothorax and thromboembolism are described as the most frequent relapsing causes of COPD. During exacerbation, the inflammatory process, the ventilation/perfusion (V'A/Q') mismatching, an increased airflow resistance and dynamic hyperinflation (PEEPidyn) expose the respiratory muscles to the risk of fatigue, eventually leading to ventilatory pump failure and rising hypercapnia. Prevention of exacerbations and subsequent hospitalisations may be obtained with careful rehabilitation programs, a strict drug protocol, long term oxygen therapy and sometimes using home noninvasive mechanical ventilation (NMV). During exacerbation proper management of infection and lung mechanics derangement has to be adopted using an accurate assessment of severity and standardized treatment protocols. Patient history and examination and functional tests are beneficial to decide how and where to treat these patients. Mechanical ventilation (possibly noninvasive) may be required to reverse the acute episode. The aims of all these procedures remain: i) to prolong length and quality of life; ii) to save costs. Both hospital and post-discharge mortality of exacerbated COPD remain high while quality of life appears to be poor. Future studies will elucidate the relation between number and severity of exacerbations and prognosis.
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PMID:Exacerbations of COPD: predictive factors, treatment and outcome. 1149 3

The present review is focused on chronic RV pressure overload or Cor Pulmonale as it may occur in the setting of two distinct disorders: those associated with abnormal pulmonary gas exchange (hypoxemia and/or hypercapnia) where chronic obstructive pulmonary disease (COPD) is the leading cause, and those associated with pulmonary vascular obstruction where primary pulmonary hypertension (PDDH) is the representative example. The clinical curse, prognostic, implications, and therapeutic strategies differ considerably in these two clinical entities. Right ventricular failure (RVF) may adversely influence the natural history and prognosis of patients with diverse cardiopulmonary disorders. It has been long established that right ventricular (RV) ischemia, RV overload, and RV pressure overload, alone or in combination, are the main factors involved in the pathogenesis of RVF. From the pathophysiologic point of view, RVF of COPD is more a congestive type of failure, in which activation of renin-angiotensin system is involved. In PPH, a low cardiac output state is predominant and the precise mechanism of RVF remains unknown. Current evidence in favor of the pathogenetic role of ischemia, adrenergic overdrive, and genetic determination are all reviewed during the course.
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PMID:[Right ventricle insufficiency in pulmonary arterial hypertension. Physiopathologic considerations]. 1156 26

Chronic alveolar hypoventilation is a classic feature of the "pickwickian syndrome" (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients. Most recent studies having included large numbers of unselected, consecutive OSAS patients agree on a prevalence of 10-20% of alveolar hypoventilation. The mechanisms of hypercapnia in OSAS are not fully understood but the determining factors of daytime respiratory insufficiency are probably the presence of a marked obesity, leading to the obesity hypoventilation syndrome and, principally, the association of OSAS with chronic obstructive pulmonary disease. This association (the so-called "overlap syndrome") is observed in >10% of OSAS patients. Bronchial obstruction is generally mild to moderate and may be asymptomatic. The severity of the nocturnal events (apnoeas, hypopnoeas) and a (possible) diminished chemosensitivity to hypercapnic and hypoxic stimuli do not appear to be determining factors of hypercapnia. The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure. When nasal continuous positive airway pressure fails to correct sleep-related hypoxaemia, supplementary O, must be given or another way of assisted ventilation (BIPAP) must be considered. In the most severe patients (diurnal PaO(2) <55 mmHg) conventional O(2) therapy (>or=16h/24h) is required in addition to nocturnal ventilation.
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PMID:Daytime hypoventilation in obstructive sleep apnoea syndrome. 1531 Apr 91


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