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)

Since hypoxemia is not known to be a sensitive indicator of acute pulmonary embolism, we performed a retrospective study to determine whether an increased P(A-a)O2 gradient or hypocapnia improved the sensitivity of blood gas analysis in acute embolism. The study group consisted of 78 patients with angiographically documented emboli who had blood gas samples obtained while breathing room air. None had a prior history of cardiopulmonary disease. Hypoxemia was present in 59 patients (76 percent), hypoxemia or hypocapnia in 73 patients (93 percent), an increased P(A-a)O2 gradient in 74 patients (95 percent), and an increased P(A-a)O2 gradient or hypocapnia in 77 patients (98 percent). Only one patient with acute embolism showed a normal P(A-a)O2 gradient and normal PaCO2 breathing room air. These results suggest that a normal P(A-a)O2 gradient and a normal PaCO2 obtained in a patient during room air breathing can be used as evidence against the presence of pulmonary emboli.
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PMID:Improved use of arterial blood gas analysis in suspected pulmonary embolism. 279 99

We have emphasized the mechanisms and consequences of sleep state effects on the manifestation of a sensitive apneic threshold. In the absence of the stabilizing influences of wakefulness, even the healthy person is vulnerable to instabilities and ventilatory control as maintenance of a rhythmic breathing pattern becomes overwhelmingly dependent on CO2. This sleep-induced unmasking of the depressant effects of hypocapnia contrasts with the relatively minor effects of sleep on the ventilatory response to a wide variety of other acute or chronic ventilatory stimuli or inhibitors. This combination of an apneic threshold with a maintained hypoxic (and asphyxic) responsiveness during non-REM sleep probably explains much of the periodic breathing in hypoxic sleep in adults and in newborns. Furthermore, applying acute hypoxia to persons with upper airways that are susceptible to collapse, i.e., snorers, showed that fluctuating chemical stimuli and the accompanying instability in ventilatory control during sleep can cause obstructive apnea, at least under conditions where chemoreceptor stimuli are sufficient to initiate some inspiratory effort but insufficient to insure a completely patent upper airway. We emphasize that chemoreceptor-induced instability and/or apnea probably plays little or no role in the induction of many other varieties of sleep apnea including most obstructive sleep apneas and perhaps even in some types of nonobstructive apnea. The consequences of these chemoreceptor-induced instabilities are, of course, substantial in terms of impairment of pulmonary gas exchange and the precipitation of events that contribute significantly to the development of chronic cor pulmonale.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A sleep-induced apneic threshold and its consequences. 371 65

In kyphoscoliosis restrictive ventilatory defect occurs. In idiopathic scoliosis vital capacity failure is significantly correlated with Cobb angle, vertebral rotation, and thoracic lordosis. Maximum voluntary ventilation is the most affected measurement. Forced expiratory volume in 1 second is reduced. Residual volume remains longtime normal. Hypoxemia due to decrease of diffusing capacity occurs, with initially reflex hyperventilation hypocapnia, and secondary hypercapnia. Pulmonary hypertension and cor pulmonale is related to hypoventilation and hypoxia. The lung situated on the concave side of the scoliosis curve shows a more functional derangement. Ventilatory pattern consists of low tidal volume and high respiratory rate with increase of ventilatory work. Scoliosis that appears in the earlier stage of the life has the worst respiratory prognosis (before 5 years of age) with impairement of lung and thoracic growth. To stimulate pulmonary and thoracic growth, intermittent ventilatory assistance by pressure preset ventilator should be performed as soon as possible and pursued up to 8 years of age, at least, more if necessity. In over 60 degrees angle idiopathic scoliosis, respiratory failure appears after 40 to 50 years of age. Non invasive ventilatory assistance with preset pressure ventilator by oral way in moderate cases and nocturnal nasal ventilation by volume ventilator or inspiratory assistance ventilator, in the most severe cases are efficient. In very severe and acute respiratory insufficiency (scoliosis over 90 degrees) ventilation by intubation then tractheostomy may be required. Earlier orthopedic management and surgical procedure to correct and stabilize spinal deformities is the best to prevent respiratory insufficiency. For scoliosis below 60 degrees, post operative pulmonary complications are very low, with no requirement of post operative ventilatory support. In very severe respiratory insufficiency treatment of respiratory failure precedes, and follows, orthotic treatment and surgical procedures; it shouldle pursued afterwards.
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PMID:[Respiratory problems in severe scoliosis]. 1043 94

Examining the parameters of the blood oxygen-transport system and oxygen tissue balance in 71 patients with bronchial asthma (BA) and in 60 patients with BA concurrent with varying carbohydrate metabolic disturbances (CMDs) revealed differences in oxygen transport. In asthmatic patients without CMDs, the pattern of changes in oxygen balance permitted identification of arteriohypoxemic hypoxia. The high frequency of factors (alkalosis, hypocapnia) that enhance hemoglobin affinity for oxygen, which are compensated for by the increase in 2,3-DPH, as well as hypoxia of peripheral shunting are the specific features of impaired oxygen balance in asthmatic patients with concomitant CMDs that predispose to the development and progression of pulmonary hypertension and cor pulmonale which cause early disability. The determination of the leading link in impaired oxygen transport individualizes treatment approaches and provides evidence for a need for earlier use of metabolic and antihypoxic agents in asthmatic patients with CMDs.
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PMID:[The blood oxygen-transport system and oxygen tissue balance in patients with bronchial asthma (BA) concurrent with carbohydrate metabolic disturbances]. 1588 65

Pulmonary hypertension (PH), i. e. an increase of mean pulmonary artery pressure above 20 mm Hg under resting conditions, can be observed in different forms of sleep-disordered breathing (SDB). In obstructive sleep apnea (OSA) the apnea-associated triggers of hypoxia and intrathoracic pressure swings lead to repetitive rises of pulmonary artery pressure during sleep. In 20 - 30 % of these patients daytime PH occurs. PH in the setting of OSA is usually mild and rarely causes clinically evident cor pulmonale. Effective CPAP therapy has a beneficial influence on pulmonary hemodynamics in OSA. Severe congestive heart failure (i. e. with a LVEF < 40 %) might provoke pulmonary venous hypertension and thereby stimulation of pulmonary stretch and irritant receptors. The ensuing hyperventilation leads to a decrease of pCO (2) levels below the apneic threshold and thus contributes to the emergence of Cheyne Stokes respiration (CSR) in up to one half of the affected patients. Patients suffering from advanced idiopathic pulmonary arterial hypertension (IPAH) might show a similar breathing pattern while asleep. Possible pathogenetic factors of the nocturnal periodic breathing occurring in end-stage IPAH are prolonged circulation times and hypocapnia. In conclusion, SDB might cause PH (OSA-associated PH). On the other hand, PH might lead to the development of SDB (CSR in congestive heart failure, periodic breathing in IPAH).
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PMID:[Pulmonary hypertension and sleep-related breathing disorders]. 1594 1