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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An anaesthetic circle system without a carbon dioxide absorber is described. The efficiency of the circle, i.e., the fraction of alveolar gas in the outflow from the circle, was measured in 15 patients during halothane anaesthesia or neurolept analgesia. The fraction ranged from 0.88 to 0.95 (mean 0.91), while the ratio between the alveolar ventilation and the fresh gas inflow ranged from 0.97 to 1.71. The efficiency was not correlated to this ratio. There was no need for hyperventilation if the fresh gas inflow was 10% higher than the alveolar ventilation required to maintain normal PaCO2. The circle was used in 50 patients manually ventilated by nurse anaesthetists. Mean fresh gas inflow was 60 ml/kg. Mean PaCO2 was 5.47 kPa (41 mmHg). In a similar group of 50 other patients, in which the standard circle used in the department was employed, the mean PaCO2 was 4.80 kPa (36 mmHg). The frequency of hypercapnia was equal in the two groups, but hypocapnia was not seen when the circle without absorber was used.
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PMID:A circle system without carbon dioxide absorption. 67 46

A retrospective clinico-pathological analysis of 78 cases of fatal subarachnoid hemorrhage (SAH) was carried out: 71% had a pathological diagnosis of pulmonary edema (PE), and of these 31% had a clinical diagnosis of PE. Patients with pathological PE were younger and died sooner after their SAH than those without. The incidence of PE fell with the passage of time following SAH, while the occurrence of pneumonia and embolism increased. There were hypoxemia and hypocapnia in both groups, more severe in the group that had pathological PE. The pathophysiology of neurogenic PE is discussed and possible therapeutic approaches indicated.
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PMID:Pulmonary edema following fatal aneurysm rupture. 69 Jun 77

1. Electromyography was used to measure the response of the diaphragm and intercostal muscles to CO2 in artificially ventilated decerebrate cats. 2. Hypocapnia produced tonic activity in either inspiratory or expiratory muscles or both, according to the preparation. 3. A graded effect of CO2 on both rhythmic and tonic activity was observed and for the latter this could be seen at as low as 10 torr PA,CO2. 4. In one human subject tonic firing of expiratory motoneurones was also induced by hypocapnia and this activity showed a graded increase with increasing (CO2. 5. A saggital incision of the medulla aimed at interrupting inspiratory bulbospinal axons abolished activity in inspiratory muscles and at eupnoeic levels of CO2 converted the activity of expiratory muscles from a periodic to a topic firing pattern. 6. Following such lesions the threshold for rhythmic excitation of expiratory muscles was elevated and this revealed that the graded effect of CO2 on tonic expiratory activity extends to as high as 60 torr. 7. The tonic activation of respiratory muscles in response to CO2 ceased after cervical cord transection or when the saggital incision in the medulla was extended caudally to the first cervical segment. 8. It is concluded that the CO2 dependent activation of spinal respiratory motoneurones is conveyed by bulbospinal axons which decussate in the vicinity of the obex and that this activation can be rhythmic or tonic. 9. It is suggested that the rhythmic excitation of expiratory muscles derives from a periodic inhibition of expiratory bulbospinal neurones which are subjected to a tonic CO2 dependent excitation which is continuously variable over the physiological range.
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PMID:On the transmission of the stimulating effects of carbon dioxide to the muscles of respiration. 69 Aug 72

The alveolar-capillary gas metabolism was studied in 60 patients with acute myocardial infarction. Arterial hypoxemia and hypocapnia were observed in the majority of the patients. Those disturbances are more pronounced in the presence of cardiac insufficiency. The combination of shunt effect with the diminution of cardiac volume is admitted to be the possible pathogenetic mechanism for arterial hypoxemia. The first mechanism is associated with the disturbances of the systemic hemodynamics. Both types of hemodynamic disturbances are conditioned by the weakness of the left ventricle.
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PMID:[Disordered alveolar-capillary gas metabolism in the acute stage of myocardial infarct]. 69 28

Previous studies have demonstrated a significant pressure gradient from carotid artery to pial or middle cerebral arteries. This pressure gradient suggests that large cerebral arteries contribute to cerebral resistance. We have tested the hypothesis that large cerebral arteries contribute to regulation of cerebral blood flow during changes in blood gases and arterial pressure. Microspheres were used to measure brain blood flow in anesthetized dogs. Resistance of large cerebral arteries was estimated by determining the pressure gradient between common carotid and wedged vertebral artery catheters. Systemic hypercapnia and hypoxia dilated large cerebral arteries, and hypocapnia constricted large cerebral arteries. Resistance of large arteries was 0.6+/-0.1 (mean +/- SE) mm Hg per ml/min per 100 g during normocapnia. During hypercapnia and hypoxia, large artery resistance decreased significantly to 0.2 +/- 0.03 and 0.3 +/- 0.05, respectively. During hypocapnia large artery resistance increased significantly to 1.0 +/- 0.1. In other experiments, we found that large cerebral arteries participate in auto-regulatory responses to hemorrhagic hypotension. When arterial pressure was reduced from 110 to 58 mm Hg, autoregulation maintained cerebral blood flow constant, and resistance of large cerebral arteries decreased significantly from 1.0 +/- 0.2 to 0.6 +/- 0.1 mm Hg per ml/min per 100 g. In absolute terms, we calculated that 20-45% of the change in total cerebral resistance during these interventions was accounted for by changes in large artery resistance. These studies indicate that large cerebral arteries, as well as arterioles, participate actively in regulation of cerebral blood flow during changes in arterial blood gases and during autoregulatory responses to hemorrhagic hypotension.
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PMID:Role of large arteries in regulation of cerebral blood flow in dogs. 70 75

Lethal pulmonary embolism is associated with hypoxemia and hypocapnia in the vast majority of cases. The easily calculated ventilation corrected oxygen tension was a very sensitive test in patients breathing air. It yielded no normals, four percent mild hypoxemia, and 96 percent moderate to extreme hypoxemia. The alveolar-arterial oxygen tension difference and oxygen ratio were equally sensitive during air breathing. During oxygen inhalation, alveolar-arterial oxygen difference was most sensitive; oxygen ratio was second best; and oxygen saturation was the least sensitive test.
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PMID:Ventilation corrected oxygen tension in lethal pulmonary embolism. 70 44

Experiments on anesthetized chickens were conducted to study interactions between afferent activity from the intrapulmonary and systemic CO2-sensitive chemoreceptors in the generation of respiratory amplitude (RA) and respiratory frequency (f). The thoracoabdominal cavity was opened, air sacs ruptured and each lung independently and unidirectionally ventilated. Intrapulmonary chemoreceptor activity was altered by changing the PCO2 of the ventilatory gas (PICO2) to the vascularly isolated right lung (VIL); systemic chemoreceptor activity was altered by changing the PICO2 to the denervated left gas exchange lung (GEL). Respiratory amplitude and frequency responses to changes in intrapulmonary PCO2 were determined at four levels of systemic arterial PCO2 (PaCO2). The results indicate that elevating PaCO2 shifts the pulmonary CO2-response curves for both RA and f to the left and increases the sensitivity of the RA-CO2 response curve but decreases the sensitivity of the f-CO2 response curve. We conclude that (1) interaction occurs between intrapulmonary and systemic afferent activity in the generation of RA and f, (2) the nature of the interaction is synergism with respect to RA and interference with respect to f, and (3) the interaction is greater during hypocapnia than hypercapnia.
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PMID:Intrapulmonary and systemic CO2-chemoreceptor interaction in the control of avian respiration. 70 70

We have attempted to identify the afferent endings responsible for the pulmonary-CO2 ventilatory reflex. We recorded afferent vagal impulses arising from the left lung in anesthetized dogs with separately ventilated lungs. When the left pulmonary artery was occluded, left lung PCO2 fell to 3 mm Hg and slowly-adapting pulmonary stretch receptor activity increased 46%. Firing declined to its original intensity when left lung PCO2 was raised in steps by administration of CO2, firing decreasing most between 2 and 19 mm Hg, and least between 30 and 50 mm Hg. Irritant receptor activity also increased (from 2.8 to 7.4 impulses/sec) after pulmonary arterial occlusion, the effect being reversed by administration of CO2. These procedures caused trivial changes in pulmonary and bronchial C-fiber activity. Effects on both slowly-adapting stretch receptors and irritant receptors appeared to result from a direct action of CO2 on the endings themselves, rather than from mechanical changes in the lung. Changes in slowly-adapting stretch receptor activity provide an adequate explanation for the pulmonary-CO2 ventilatory reflex, the relationship between impulse frequency and lung PCO2 suggesting that these afferents may have a role in limiting CO2 loss under conditions causing hypocapnia, but be less effective in stimulating breathing during hypercapnia.
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PMID:II. Effect of CO2 on afferent vagal endings in the canine lung. 70 75

The joint response of the respiratory and panting centres of fully-conscious unidirectionally-ventilated chickens to simultaneous combinations of hyperthermia and hypo-/hypercapnia was examined. The response was monitored by changes in the rate and amplitude of movements of the body wall and gular apparatus respectively. The response to a combination of hyperthermia plus hypercapnia bore indications of a linear summation of the individual responses of the panting centre and respiratory centre to the respective thermal and chemical stimuli. A more complex response was elicited by a combination of hyperthermia plus hypocapnia. In this case the inhibition of respiratory movements induced by the hypocapnia (hypocapnic apnea) permitted a more forceful manifestation of the component of the thermoreflex which acts via the hyoid muscles and which is responsible for the synchronous 'gular flutterin'. The rate of gular fluttering increased by up to 150% as compared to normal panting. The experimental procedure therefore provided a technique for breaking the central linkage which normally constrains the rhythm of the hyoid muscles to the more dominant rhythm of the respiratory muscles.
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PMID:Experimentally induced antagonism of chemical and thermal reflexes in the respiratory system of fully conscious chickens. 70 90

Ventilation may bypass obstructed airways through collateral channels, including interalveolar pores of Kohn, bronchiole-alveolar communications of Lambert, and interbronchiolar pathways of Martin. Resistance through these channels, like resistance through small airways, increases with decreasing lung volume and with hypocapnia. But whereas the distention of collateral channels and small airways by a variety of factors is similar, the efficiency of ventilation through collateral channels is less than the efficiency through airways. Gas inspired through collateral channels is contaminated with alveolar gas from surrounding lung so that the dead space for collateral ventilation is increased. When one part of the lung ventilates out of phase with the surrounding lung, pulmonary interdependence promotes more homogeneous ventilation. In the presence of airways obstruction, interdependence may be a primary factor governing the rate of collateral ventilation. In man, collateral ventilation is unimportant in normal lungs. However, with disease, it may be critical in producing or compensating for abnormalities. For example, the long time constant for collateral ventilation in the middle lobe may be responsible for atelectasis, which results in the middle lobe syndrome. On the other hand, the short time constant for collateral ventilation in emphysema may be essential for the distribution of ventilation beyond obstructed airways.
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PMID:Collateral ventilation. 75 33


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