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

To study pulmonary transvascular filtration of fluid and the normal adaptive response of newborn animals to excessive water in the lungs, we measured lung lymph flow, pulmonary vascular pressures, and the concentration of protein in lymph and plasma of nine unanesthetized 1- to 3-wk-old lambs, before, during, and after a rapid iv infusion of isotonic saline, 130-250 ml/kg.hr for 3-4 hr. During infusions, lung vascular pressures increased, the transvascular gradient of protein osmotic pressure decreased, and there was a 2- to 5-fold increase of lung lymph flow. When infusions stopped, lymph flow decreased, as the concentration of protein in plasma increased and pulmonary vascular pressures decreased to new steady-state levels. The concentration of protein in lymph did not change for several hours after the infusions. Body weight increased by 28% and extravascular lung water content was 19% above normal after saline; these changes were associated with mild tachypnea, hypercarbia, and hypoxemia. Sections of lung from these lambs had prominent cuffs of fluid surrounding large blood vessels.
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PMID:Lung fluid balance in awake newborn lambs with pulmonary edema from rapid intravenous infusion of isotonic saline. 50 55

During sleep some patients with airways obstruction and hypoxaemia developed tachypnoea. This could not be explained by the severity of their abnormality of lung function, their CO2 responsiveness, the nature of their lung disease or their personality. This nocturnal tachypnoea correlated best with a raised resting arterial blood PCO2, and was not seen hypoxaemic patients with a normal PCO2 who showed the usual fall in respiratory rate when asleep. We suggest that in patients with both hypoxaemia and hypercapnia sleep removes a cortical inhibitory mechanism which slows breathing durigng waking hours, and is linked to the arterial blood PCO2.
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PMID:Sleeping ventilatory patterns in patients with severe chronic airflow obstruction causing respiratory failure. 95 25

The first case of "idiopathic" persistence of the fetal cardiopulmonary circulatory pathway with survival after a prolonged course is documented by serial cardiac catheterizations. All previously reported infants have either markedly improved within the first week of life or subsequently died. This entity has been described in term infants with prenatal or perinatal distress who present with tachypnea and cyanosis from birth. The chest radiograph is remarkable for the absence of pulmonary parenchymal pathology and the hemoglobin and hematocrit are normal. Blood gas determinations indicate hypoxia and acidosis with or without hypercarbia. Cardiac catheterization and angiography reveal an anatomically normal heart with severe pulmonary hypertension, left ventricular pressure lower than right ventricular pressure, and right-to-left venoarterial shunting through the fetal channels (atrial and or ductal levels). It is postulated that this entity may result from antenatal factors that affect the pulmonary vasculature and its subsequent adjustment to extrauterine life. These factors may include abnormal intrauterine stress resulting in excessive hypertrophy of the pulmonary arteriolar smooth muscle, or abnormal pulmonary vascular responsiveness to the usual vasoactive stimuli before or after birth, or an immature or dysfunctioning enzyme system necessary for the normal decrease in pulmonary artery pressure.
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PMID:Persistence of the fetal cardiopulmonary circulatory pathway: survival of an infant after a prolonged course;. 116 63

To clarify the mechanisms involved in the ventilatory response to the inhalation of low concentrations of CO (0.18-0.22% in air), the roles of the arterial chemoreceptors and the forebrain structures have been investigated in unanesthetized adult cats. The ventilatory response was observed in conscious animals intact, after carotid denervation (CD), and after midcollicular decerebration. The results show that the initial small ventilatory depression was unaffected by CD but that the subsequent characteristic tachypnea was blunted after CD even after more prolonged exposure to CO. The CO tachypnea was not observed after decerebration, but a residual hyperventilation was noted with the higher concentration used. It may be concluded that carotid chemoreceptors do not mediate the CO tachypnea, which may then originate in suprapontine structures as shown by comparison of intact and decerebrate animals. The blunting of the tachypnea after CD may be caused by the relative hypercapnia observed in CD animals. The residual hyperventilation observed in decerebrate animals may be caused by central acidosis and/or some peripheral potentiation of chemoreceptor activity resulting from the decrease in arterial blood pressure that accompanied CO inhalation in decerebrate animals.
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PMID:Effects of carotid denervation and decerebration on ventilatory response to CO. 226 65

During the 1987 through 1988 seasonal peak of respiratory syncytial virus (RSV), 177 courses of ribavirin were administered at St Christopher's Hospital for Children, a tertiary care medical center in Philadelphia, Pa. Charts were reviewed on 100 treated patients with proved or suspected RSV disease to determine adherence to American Academy of Pediatrics treatment guidelines. Ninety-four percent fulfilled criteria for the risk of significant morbidity: cardiac, pulmonary, or immunodeficiency conditions (38%); an age of 6 weeks or younger (35%); or severe illness (21%). Severe illness was defined as hypoxemia, hypercapnia, or marked tachypnea. Of those treated because of underlying conditions, 71% had RSV documented, as did 71% of patients aged 6 weeks or younger and 81% of patients with severe disease. A study of 80 consecutive patients who were hospitalized with illness compatible with RSV infection revealed that 56% of patients were treated with ribavirin. Adherence to guidelines led to ribavirin use in half of the hospitalized patients with suspected RSV infection. The majority of these patients received therapy because of underlying conditions or very young age.
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PMID:Impact of treatment guidelines on use of ribavirin. 239 11

The ventilatory response to CO hypoxia (FICO = 0.0025), hypercapnia, and hypoxia was studied in a group of intact, conscious cats before and during chronic administration of phenobarbital (60 mg/day). It was found that the ventilatory response to hypercapnia or hypoxia was not significantly modified during phenobarbital administration. However, the ventilatory response to CO hypoxia was markedly blunted with phenobarbital: the initial ventilatory inhibition was still observed but the subsequent hyperventilation was delayed. Furthermore, the tachypnea was less intense and the decrease in tidal volume was smaller during CO hypoxia. In addition, the behavioral reactions which usually accompanied the tachypnea were attenuated and unconsciousness was often noted. These results indicate that the modifications caused by phenobarbital do not result from a general inhibition of the respiratory control network but rather from a selective inhibition of the structures rostral to the brain stem. As a consequence, the behavioral reactions and resulting respiratory activation were attenuated. Since the hypoxic tachypnea and behavioral reactions are observed only during central hypoxemia, it is concluded that arterial chemoreceptor afferents normally inhibit the supra-pontine structures which are otherwise stimulated by central hypoxemia.
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PMID:Effects of chronic administration of phenobarbital in low doses on control of breathing in the cat. 309 Jun 65

This study tests three hypotheses regarding mechanisms that produce rapid shallow breathing during a severe inspiratory resistive load (IRL): 1) an intact vagal afferent pathway is necessary; 2) diaphragm fatigue contributes to tachypnea; and 3) hypoxia may alter the pattern of respiration. We imposed a severe IRL on pentobarbital sodium-anesthetized dogs, followed by bilateral vagotomy, then by supplemental O2. IRL alone produced rapid shallow breathing associated with hypercapnia and hypoxia. After the vagotomy, the breathing pattern became slow and deep, restoring arterial PCO2 but not arterial PO2 toward the control values. Relief of hypoxia had no effect, and at no time was there any evidence of fatigue of the diaphragm as measured by the response to phrenic nerve stimulation. We conclude that an intact afferent vagal pathway is necessary for the tachypnea resulting from a severe IRL, neither hypoxia nor diaphragm fatigue played a role, and, although we cannot rule out stimulation of vagal afferents, the simplest explanation for the increased frequency in our experiments is increased respiratory drive due to hypercapnia.
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PMID:Vagal afferents, diaphragm fatigue, and inspiratory resistance in anesthetized dogs. 313 22

The measurement of pulmonary mechanics has been developed extensively for adults, and these techniques have been applied directly to neonates and infants. However, the compliant chest wall of the infant frequently predisposes to chest wall distortion, especially when there is a low dynamic lung compliance (CL,dyn). We describe a technique of directly measuring the static chest wall compliance (Cw,st), developed initially in the newborn lamb and subsequently applied to the premature neonate with chest wall distortion. The mean CL,dyn in seven intubated newborn lambs in normoxia was 2.45 +/- 0.41 ml.cmH2O-1.kg-1, whereas Cw,st was 11.81 +/- 0.25 ml.cmH2O-1.kg-1. These values did not change significantly in seven animals breathing through a tight-fitting face mask or with hypercapnia-induced tachypnea. For the eight premature infants the mean CL,dyn was 1.35 +/- 0.36 ml.cmH2O-1.kg-1, whereas the mean Cw,st was 3.16 +/- 1.01 ml.cmH2O-1.kg-1. This study shows that, under relaxed conditions when measurements of static compliance are performed, the chest wall is more compliant than the lung. The measurement of Cw,st may thus be used to determine the contribution of the respiratory musculature in stabilizing the chest wall.
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PMID:Direct measurement of static chest wall compliance in animal and human neonates. 318 79

We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.
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PMID:Effect of ozone on breathing in dogs: vagal and nonvagal mechanisms. 355 75

The effects of halothane anesthesia have been investigated in intact and in decerebrated cats. Pulmonary ventilation and breathing pattern were studied during room-air breathing, hypercapnia, and O2 inhalation. The following results have been demonstrated. First, halothane anesthesia does not modify pulmonary ventilation, but a tachypnea much more intense in intact than in decerebrated cats is observed. This indicates that halothane-induced tachypnea originates mainly in structures rostral to the brain stem. Second, decerebrated animals exhibit a breathing pattern and a ventilatory response to CO2 similar to those of intact conscious cats, suggesting that forebrain facilitatory and inhibitory influences on brain stem are cancelled out by decerebration. However, the tidal volume vs. inspiratory duration relationship observed in decerebrated cats differs from that in conscious cats. Finally, during halothane anesthesia, ventilatory response to CO2 is markedly depressed. Third, during O2 inhalation, except in decerebrated, anesthetized animals, ventilation is only slightly depressed. This suggests that central stimulatory effect of O2 is enhanced and/or that peripheral chemoreceptor drive is reduced.
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PMID:Influence of halothane on control of breathing in intact and decerebrated cats. 365 12


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