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)

Administration of sodium bicarbonate during cardiopulmonary resuscitation (CPR) is controversial, and our aim was to elucidate whether or not its administration is beneficial by analyzing the acid-base status and the level of carbon dioxide in central venous blood during CPR, and their changes following administration of sodium bicarbonate. Six patients were studied. They had all been admitted to the intensive care unit (ICU), had already had pulmonary arterial or central venous catheters inserted, and had acute episodes of circulatory collapse during their stay in the ICU. The following phenomena were observed: 1) hypercapnia and acidosis of central venous blood were prominent during both cardiogenic shock and CPR, although arterial hypocapnia was maintained by hyperventilation; 2) administration of sodium bicarbonate during cardiogenic shock and CPR induced exacerbation of hypercapnia and acidosis of central venous blood; 3) when arterial hypercapnia was present due to disturbed ventilation, administration of sodium bicarbonate exacerbated hypercapnia and acidosis of both arterial and central venous blood; 4) administration of sodium bicarbonate did not induce hypercapnia of central venous blood in a septic shock patient in whom the septic hyperdynamic state was prevalent in spite of low systemic perfusion pressure. It was concluded that hypercapnia and acidosis of the central venous blood and tissues were exacerbated by administration of sodium bicarbonate during CPR, and that such an effect might be dependent on the severity of the decrease in tissue perfusion.
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PMID:Exacerbation of hypercapnia and acidosis of central venous blood and tissue following administration of sodium bicarbonate during cardiopulmonary resuscitation. 254 21

In pentobarbitalized rats, hypoxia induced by inhalation of O2 8%-N2 92%, produces a transient hyperventilation which is followed by a respiratory depression and an apnea. A cardiovascular collapse is then observed. Correction of the hypocapnia depending on the initial hyperventilation, by inhalation of a gas mixture containing 4% CO2 maintains the hyperventilation and suppresses the cardiovascular collapse. Carbon dioxide activity is both a direct one by stimulation of respiratory centers and an indirect one by increasing the sensitivity of the peripheral arterial chemoreceptors to hypoxia. Four percent carbon dioxide just compensating hypocapnia are sufficient to prevent apnea and vascular collapse. The increase of this concentration up to hypercapnia complicates the interpretation of the results by addition of hypoxic and hypercapnic effects.
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PMID:[Effects of the addition of carbon dioxide on manifestations of acute hypoxia in rats]. 297 Feb 83

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

We report on an 83 yr old man with hypersomnia and central sleep apnoea (CSA). He had several possible causes for CSA, including a central nervous system lesion, hypocapnia and anatomical narrowing of the airway at the hypopharyngeal level. We postulate that reduced central respiratory drive occurring in conjunction with upper airway narrowing may have led to central apnoeas. These in turn could have facilitated a complete passive hypopharyngeal collapse at the end of each apnoea, as visualized by somnofluoroscopy. The CSA could also have been favoured by respiratory instability due to chronic hypocapnia.
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PMID:Central sleep apnoea syndrome with upper airway collapse. 849 10

We wished to determine the effect of reduced ventilatory drive (hypopnea) on upper airway patency in humans during non-rapid-eye-movement (NREM) sleep. We studied nine subjects (58 trials) spanning the spectrum of susceptibility to upper airway collapse including normals, snorers and patients with mild sleep apnea. Hypocapnic hypopnea was induced by abrupt cessation of brief (1 min) nasal mechanical hyperventilation. Surface inspiratory EMG (EMGinsp) was used as an index of drive. Upper airway resistance and supraglottic pressure-flow plots were used as indexes of upper airway patency. Termination of nasal mechanical ventilation resulted in reduced VE to 4904 of pre-mechanical ventilation eupneic control. Upper airway resistance at a fixed flow did not change significantly in inspiration or expiration. Likewise, pressure-flow plots showed no increase in upper airway resistance except in one subject. However, maximum flow (Vmax) decreased during hypopnea in four subjects who demonstrated inspiratory flow-limitation (IFL) during eupneic control. In contrast, no IFL was noted in subjects who showed no evidence of IFL during eupnea. We concluded: (1) Reduced ventilatory drive does not compromise upper airway patency in normal subjects during NREM sleep; (2) the reduction in Vmax during hypopnea in subjects with IFL during eupneic control, suggests that reduced drive is associated with increased upper airway compliance in these subjects; and (3) upper airway susceptibility to narrowing/closure is an important determinant of the response to induced hypopnea during NREM sleep.
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PMID:Effect of induced hypocapnic hypopnea on upper airway patency in humans during NREM sleep. 936 Nov 50

Lung injury in ventilated premature infants occurs primarily through the mechanism of volutrauma, often due to the combination of high tidal volumes in association with a high end-inspiratory volume and occasionally end-expiratory alveolar collapse. Tolerating a higher level of arterial partial pressure of carbon dioxide (PaCO2) is considered as 'permissive hypercapnia' and when combined with the use of low tidal volumes may reduce volutrauma and lead to improved pulmonary outcomes. Permissive hypercapnia may also protect against hypocapnia-induced brain hypoperfusion and subsequent periventricular leukomalacia. However, extreme hypercapnia may be associated with an increased risk of intracranial hemorrhage. It may therefore be important to avoid large fluctuations in PaCO2 values. Recent randomized clinical trials in preterm infants have demonstrated that mild permissive hypercapnia is safe, but clinical benefits are modest. The optimal PaCO2 goal in clinical practice has not been determined, and the available evidence does not currently support a general recommendation for permissive hypercapnia in preterm infants.
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PMID:Permissive hypercapnia to decrease lung injury in ventilated preterm neonates. 1897 27

Objectives: The critical closing pressure (CrCP) defines arterial blood pressure below which cerebral arteries collapse. It represents a clinically relevant parameter for the estimation of cerebrovascular tone. Although there are few methods to assess CrCP, there is no consensus which of them estimates this parameter most accurately. The aim of present retrospective, experimental study was to compare three methods of CrCP estimation: conventional Aaslid's formula and methods based on the cerebrovascular impedance: the established continuous flow forward (CFF) and a new pulsatile flow forward (PFF) model.Methods: The effects of the following physiological manoeuvres on the CrCP were studied in New Zealand white rabbits: lumbar infusion of Hartmann's solution to induce mild intracranial hypertension, sympathetic blockade to induce arterial hypotension, and modulation of respiratory tidal volume to induce hypocapnia or hypercapnia.Results: During intracranial hypertension, all CrCP estimates were significantly higher than at baseline, decreased with decreasing ABP and increased with gradual hypocapnia. During hypercapnia, all CrCP estimates were significantly decreased but only in the case of CrCPA the negative, non-physiological values were observed (16% of the cases). The Bland-Altman analysis revealed that a good agreement between each impedance method and Aaslid's method deteriorated significantly in the low range of the average numerical value of the estimates.Discussion: Our results confirm the limited usage of Aaslid's formula for the calculation of CrCP. Although both impedance methods seem to be equivalent, the fact that PFF model better describes cerebrovascular hemodynamic allows the recommendation of this model for the calculation of CrCP.
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PMID:Critical closing pressure during experimental intracranial hypertension: comparison of three calculation methods. 3216 31