Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Methotrexate, an antifolate cytotoxic drug, is used in anticancer chemotherapy as well as an immuno suppressive in rheumatoid arthritis. It is responsible for numerous secondary effects, amongst which is a characteristic acute pneumonia known since 1969. This pneumonitis has been described in detail, up to the present time in 78 cases gathered in this review. The prevalence of this complication is estimated at around 7%. This pneumonia may occur whatever the age, indication for which methotrexate is prescribed, the route of administration of the product (including the intra-thecal route) and the dose. It includes dyspnoea, fever, (sometimes quite marked) and frequently an acute reversible respiratory failure. Radiologically the opacities are usually diffuse interstitial and symmetrical with a basal predominance with sometimes some confluence and occasionally a pleural reaction. In a small number of cases a transient mediastinal adenopathy has been described. Respiratory function tests show a rapidly developing restrictive syndrome accompanied by hypoxia and hypocapnia. Broncho-alveolar lavage is characterised by hypercellularity with a frank and apparently transitory lymphocytosis. Histologically the most frequent lesion sighted is an extensive acute granulomatous reaction with or without oedema. Most often the outcome is favourable (75% of cases). However 6 deaths due to respiratory failure have been reported. Even though there has not been any formal test, steroid therapy in high dosage seems to accelerate recovery. Progress to an irreversible pulmonary fibrosis is possible but rare. The mechanism of this drug related acute pneumonia is not known but would seem to resemble that of other granulomatosis. Besides this rapidly progressive pneumonitis, methotrexate is responsible for a very small number of cases of severe pulmonary oedema and of acute painful pleurisies.
Rev Mal Respir 1990
PMID:[Pneumopathy caused by methotrexate]. 225 35

The respiratory function of pregnant women is changed for more than one reason. There is a mechanical effect due to the increase in the uterine volume and the elevation of the diaphragm. However, there are only modest functional consequences, because the pulmonary volumes are only little changed, with the exception of a reduction in the functional residual capacity. Bronchial permeability is unaltered due to the balancing of constrictors (mechanical, hypocapnia) and dilators (hormonal influences). As regards pulmonary haemodynamics, the hypovolaemia of the pregnant woman has no repercussions on pulmonary vascular pressure. Gas exchange and alveolar-capillary diffusion are normal or even improved as a consequence of chronic hyperventilation. The latter is the most important functional change, sometimes expressed as a sensation of dyspnoea. The origin of this hyperventilation relates to the diminution of the threshold of sensibility in the respiratory centres to CO2 due to the effect of raised progesterone levels.
Rev Mal Respir 1988
PMID:[Pregnancy and the respiratory function]. 304 98

Arterial blood gases (pH, pO2, p CO2) were studied in 100 patients with documented pulmonary embolism (Group A), confirmed by pulmonary angiography (n = 51) or scintigraphy ( n = 49). The pO2 ranged from 32 to 97 mm Hg (average 60,5 +/- 13 mm Hg). Hypoxaemia was found in 97 cases and would therefore seem to be a reliable sign of pulmonary embolism. In the three cases in which it was absent, the embolism was small. Hypoxaemia was associated with hypocapnia and alkalosis in 91 cases. However, hypoxaemia was not a specific finding; it was also present in 49 patients with suspected pulmonary embolism (Group B) in whom the diagnosis was excluded by pulmonary angiography or scintigraphy. A previous history of cardiovascular disease was found in 37 patients (76%) in this group: of the 12 remaining patients, 6 were heavy smokers and 4 were significantly obese. No correlation was found between the degree of hypoxaemia and the extent of amputation of the vascular bed on pulmonary angiography or scintigraphy. Nevertheless, a pO2 of under 50 mm Hg was always associated with a severe embolism with amputation of over 40% of the pulmonary vascular bed. A significant correlation was found between the severity of hypoxaemia and the degree of cyanosis (p less than 0,05) and ECG changes (p less than 0,01). The average pO2 was 59 +/- 12 mm Hg in patients with cardiovascular disease ( n = 21) and 55 +/- 11 mm Hg with known pulmonary disease ( n = 6). A higher average pO2 was found when these conditions were absent (61,5 +/- 13 mmHg). The difference was not statistically significant unless previous cardiac and pulmonary disease were associated (pO2 = 51 +/- 14 mm Hg, p less than 0,05).
Arch Mal Coeur Vaiss 1981 Feb
PMID:[Arterial blood gas analysis in acute pulmonary embolism]. 678 77

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
Rev Mal Respir 1999 Apr
PMID:[Sleep-related cardiac insufficiency and respiratory disorders. Prevalence, physiopathology, and treatment]. 1033 59

Pulmonary embolism alters the distribution of ventilation/perfusion relationships, and increases pulmonary vascular resistance. These changes lead to hypoxemia and hypocapnia, and eventually, to right heart failure. The thin-walled and compliant right ventricle adapts to any increase in afterload by dilatation and decreased stroke volume, but this is largely prevented or delayed by the pulmonary circulation being a low resistance, recruitable and distensible circuit. Pulmonary embolism cannot be associated with a mean pulmonary artery pressure higher than 40 mmHg. More severe pulmonary hypertension indicates the presence of a hypertrophied right ventricle in the context of preexistent cardiac or pulmonary disease. Gas exchange is initially affected because of increased ventilation/perfusion ratios in embolized lung areas, and decreased ventilation/perfusion ratios in remaining non embolized lung areas. Both physiologic shunt and physiologic dead space increase accordingly, resulting in hypoxemia and hypocapnia. However, these changes are rapidly affected by an increase in ventilation, and by a "pneumoconstriction" which decreases physiologic dead space in embolized areas. In addition, a series of secondary alterations contribute to increase perfusion to lung units with low ventilation/perfusion ratios, thereby aggravating hypoxemia, while hypocapnia persists.
Rev Mal Respir 1999 Nov
PMID:[Physiopathology of pulmonary arterial hypertension and gas exchange in acute pulmonary embolism]. 1090 37

Cheyne-Stokes respiration occurs during sleep in 40-45% of patients with NYHA class III and IV heart failure. Such patients experience repeated episodes of progressively diminishing ventilation associated with desaturation followed by periods of increasing-amplitude ventilation. The mechanism appears to be related to hyperventilation leading to hypocapnia which occurs near a critical threshold of apnea during sleep stages I and stage II and interrupts central ventilatory control. The total duration of the periodic respiration cycle would depend on the increased circulation time subsequent to lowered cardiac output. Brief periods of waking provoked by Cheyne-Stokes respiration, accentuating sympathetic nervous system activity, are an unfavorable prognostic factor in heart failure. Activation of the sympathetic system may be corrected by CPAP although the long-term effect on heart failure remains controversial. Other treatments, such as oxygen therapy or theophylline, combined with optimized treatment of heart failure, have been proposed.
Rev Mal Respir 2000 Jun
PMID:[Heart failure and sleep respiratory disorders. Prevalence, physiopathology and treatment]. 1093 1