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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radiographic pattern associated with respiratory distress, distinct from hyaline membrane disease and transient tachypnea of the newborn, is described in eight infants of diabetic mothers. The radiographic findings demonstrate a regional distribution of reticulogranular densities accompanied by increased lung volumes. Clinical features were gestationally mature infants in moderate respiratory distress with tachypnea, hypercapnia, and hypoxemia requiring supplemental oxygen, with steady improvement and uneventful recovery within 2 weeks. There was no bacteriologic evidence of infection or radiographic evidence of delayed lung fluid absorption. The mothers had mild diabetes. These features characterize a newly recognized entity in diabetes-related idiopathic lung disease of the newborn. Possible causative factors are discussed.
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PMID:A newly recognized profile in neonatal lung disease with maternal diabetes. 387 61

Respiratory muscle weakness is considered to be a factor in the inability to wean from mechanical ventilation. To assess this possibility, the present study examined the mechanical behavior of the diaphragm by measuring the change in transdiaphragmatic pressure (delta Pdi) during weaning. Nine "T-piece" weanings were carried out in seven patients with prior weaning failure and were terminated with the development of hypercapnia, hypoxemia, or severe tachypnea. Serial measurements of delta Pdi during these weans revealed that (1) in no case was there a decrease in delta Pdi at termination of weaning, and (2) in the subgroup of patients whose weaning failed because of hypercapnia, the increase in arterial carbon dioxide tension (mean increase of 12 mm Hg) was associated with a significant increase in delta Pdi, from the beginning (21.1 +/- 12.1 cm H2O) to the end (24.8 +/- 13.4 cm H2O) of the trial (p less than 0.05). We conclude that failure to wean in these patients, in particular the development of carbon dioxide retention, was not due to failure of the diaphragm as a pressure generator.
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PMID:Diaphragmatic strength during weaning from mechanical ventilation. 393 89

We determined the effects of denervating the hilar branches (HND) of the vagus nerves on breathing and arterial PCO2 (PaCO2) in awake ponies during eupnea and when inspired PCO2 (PICO2) was increased to 14, 28, and 42 Torr. In five carotid chemoreceptor-intact ponies, breathing frequency (f) was less, whereas tidal volume (VT), inspiratory time (TI), and ratio of TI to total cycle time (TT) were greater 2-4 wk after HND than before HND. HND per se did not significantly affect PaCO2 at any level of PICO2, and the minute ventilation (VE)-PaCO2 response curve was not significantly altered by HND. Finally, the attenuation of a thermal tachypnea by elevated PICO2 was not altered by HND. Accordingly, in carotid chemoreceptor-intact ponies, the only HND effect on breathing was the change in pattern classically observed with attenuated lung volume feedback. There was no evidence suggestive of a PCO2-H+ sensory mechanism influencing VE, f, VT, or PaCO2. In ponies that had the carotid chemoreceptors denervated (CBD) 3 yr earlier, HND also decreased f, increased VT, TI, and TT, but did not alter the slope of the VE-PaCO2 response curve. However, at all levels of elevated PICO2, the arterial hypercapnia that had persistently been attenuated, since CBD was restored to normal by HND. The data suggest that during CO2 inhalation in CBD ponies a hilar-innervated mechanism influences PaCO2 by reducing physiological dead space to increase alveolar ventilation.
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PMID:Effect of hilar nerve denervation on breathing and arterial PCO2 during CO2 inhalation. 393 17

1. The effects of asphyxia, hypoxia, hypercapnia, stimulation of peripheral chemoreceptors, pneumothorax and breathing through resistances have been investigated on laryngeal resistance to airflow in anaesthetized cats, with and without bilateral vagotomy below the origin of the recurrent laryngeal nerves.2. Resistance to airflow of the innervated larynx was usually measured with the larynx isolated in situ with constant flow from the trachea to a pharyngeal opening, and expressed by the relationship between translaryngeal pressure and airflow.3. Asphyxia, hypoxia and hypercapnia each stimulated breathing and decreased laryngeal resistance to airflow, in both the inspiratory and expiratory phases. After vagotomy the effect was reduced, abolished or (usually) reversed to a laryngeal constriction, especially in expiration.4. Intra-arterial injections of potassium cyanide (to stimulate carotid body chemoreceptors) caused a short apnoea or an augmented breath followed by hyperpnoea, concurrently with expiratory constrictions of the larynx. The responses were usually stronger after bilateral vagotomy.5. Pneumothorax caused tachypnoea, inspiratory dilatations and expiratory constrictions of the larynx. The responses were abolished by vagotomy.6. Imposition of respiratory resistances dilated the larynx, in inspiration and expiration, while complete closure of trachea caused expiratory constrictions of the larynx. These changes did not depend on intact vagal pathways.7. The results are discussed in terms of nervous control of the larynx in the different conditions.
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PMID:Studies on laryngeal calibre during stimulation of peripheral and central chemoreceptors, pneumothorax and increased respiratory loads. 441 40

When the ventilatory muscles are unable to develop the required force as it occurs during fatigue, hypercapnic respiratory failure ensues. We present evidence that when the respiratory muscles work in a fatiguing load domain the central controllers respond at an early stage with tachypnea, while when the muscles fail bradypnea ensues which is followed by apnea. Although bradypnea and apnea in addition to muscle inability to develop force may reduce alveolar ventilation by virtue of reducing the total minute ventilation, tachypnea may also be followed by hypercapnia at constant total minute ventilation by virtue of a reduction in tidal volume (VT). Such a strategy will increase the ratio of dead space (VD) to tidal volume (VD/VT) and PCO2 will rise. It is argued that this mechanism could satisfactorily explain the high levels of CO2 in patients with chronic obstructive lung disease, as well as the CO2 retention at an early stage in acute cases of fatigue during, for example, the weaning period of a patient from the respirator. Bradypnea and apnea contribute to CO2 retention at a later stage, when the muscles are exhausted and total ventilation decreases. This sequence in frequency of breathing is explained as an advantageous strategy adopted for the respiratory muscles, because it allows the muscles to operate at an optimal length. It is also hypothesized that muscle afferents, probably via the small fibers III and IV and/or Golgi and tendon organs, are responsible for this interaction of CNS and respiratory muscles.
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PMID:Ventilatory muscle fatigue governs breathing frequency. 650 21

In carotid body-denervated cats, moderate hypoxia, or even normoxia when compared to hyperoxia, provokes a significant depression of the respiratory output. This is observed in conscious or anesthetized or decerebrated animals. On the other hand, more severe hypoxia induces tachypnea (hypoxic tachypnea of Miller and Tenney, Respir. Physiol. 23: 31-39, 1975) in conscious cats, whereas the same hypoxia is followed by marked respiratory depression or apnea in the anesthetized or decerebrated animals. Hypoxic tachypnea can be partly or completely reversed by injection of dopa or xanthines such as caffeine or aminophylline. This suggests that alterations in brain monoamine metabolism by hypoxia may be responsible for the alterations in suprapontine respiratory control systems, resulting the tachypnea. Mild hypercapnia can also reverse hypoxic tachypnea. It is concluded that the ventilatory response to hypoxia of conscious animals results from stimulation of peripheral chemoreceptors, inhibition of brain stem neurons, and finally involvement of suprapontine structures that seems to be mediated by depletion of monoamines.
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PMID:Possible alterations in brain monoamine metabolism during hypoxia-induced tachypnea in cats. 677 76

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.
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PMID:Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors. 680 50

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.
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PMID:Clinical manifestations of inspiratory muscle fatigue. 681 17

In 10 dogs the authors studied the effect of increasing doses of alfathesin on ventilation (VE, frequency, VT, blood gases), on the ventilatory pattern (TI, TE, TI/Ttot), on the neurological initiation of ventilation (VT/TI, occlusion pressure at 0.5 seconds), and on the Hering-Beurer reflex (duration of apnoea after occlusion of the airway at the end of inspiration). The results were compared with normal values taken from the literature. The correlation between the dose of alfathesin and the measured or calculated parameters was examined. Ventilation was stimulated by low doses of alfathesin, a stimulation, characterized by tachypnoea without change in tidal volume. Deepening of anaesthesia was accompanied by progressively increasing depression of respiration (diminution of VE, of frequency, of VT/TI and increase of PaCO2 and of the duration of apnoea). The mechanisms of the initial stimulation of ventilation and of respiratory depression are discussed. The authors conclude that the action of alfathesin on the central nervous system is biphasic, with stimulation during light anaesthesia followed by depression with associated depression of ventilation, despite increasing hypoxia and hypercapnia.
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PMID:[Respiratory effects of increasing doses of alfathesin in the dog]. 681 35

To study the effect of hypercapnia on net transvascular filtration of fluid in newborn lungs, we measured pulmonary arterial and left pressures and collected lung lymph from 11 awake 2-wk-old lambs as they spontaneously breathed a gas mixture rich in carbon dioxide. After a 2-h control period in air, the lambs breathed 8-11% carbon dioxide mixed with air and nitrogen for 2-6 h. Average pulmonary arterial pressure and blood flow to the lungs increased during hypercapnia, but pulmonary vascular resistance did not change. In all cases, hypercapnia led to an acute transient increase in lymph flow. During sustained hypercapnia, however, flow of lymph was not significantly different from flow measured during the control period. The concentration of protein in lymph decreased at the onset of hypercapnia and remained low during sustained hypercapnia. These results suggest that acute hypercapnia increases net filtration by increasing the transvascular gradient of hydraulic pressure, whereas, in a "steady-state," neither hypercapnia nor the tachypnea that accompanies it alters net transvascular filtration of fluid in the lungs of unanesthetized newborn animals.
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PMID:Effect of hypercapnia on net filtration of fluid in the lungs of awake newborn lambs. 726 49


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