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

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH less than 7-10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH less than 7-10 were judged to have "appropriate hypocapnia", and fifteen had "submaximal hypocapnia". Thirteen of the latter fifteen had circulatory failture and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate greater than 9 mmol/1. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.
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PMID:The ventilatory response in severe metabolic acidosis. 0 84

Chronic hypertrophied tonsils and adenoids causing partial airway obstruction produced serious illness and a confusing clinical picture in a 51/2-year-old boy. Cardinal signs were cor pulmonale, pulmonary oedema and marked cardio-respiratory changes due to hypoxaemia and hypercapnia, in addition to hypersomnia. Marked improvement of the clinical picture and the abnormal signs followed directly upon tonsillectomy and adenoidectomy. Chronic alveolar hypoventilation is presumably the main cause of the described condition and of others of extracardiac origin with similar signs and symptoms.
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PMID:[Chronic tonsillar hypertrophy as a cause of cor pulmonale, pulmonary oedema, and hypersomnia in children (author's transl)]. 89 99

After successful rescue from drowning there may develop a situation which is called secondary drowning, resulting in acute respiratory distress characterized by interstitial pulmonary oedema, hypoxaemia, hypercapnia and acidosis during drowning, direct alteration of the alveolar membrane by aspirated water and particulate matters and a volume overloading by adsorption and--not seldom--inept therapy. This situation requires mechanical ventilation and forced diuresis, combined with high doses of steroids, antibiotics and digitalis. We present the case of an eleven year old patient whose clinical course demonstrate the necessity of exact clinical observation after rescue from drowning. After development of acute respiratory distress only the immediate utilization of the therapeutic modalities of an intensive care may result in a satisfactory outcome. Four months later our patient had normal pulmonary function except for a moderate reduction of compliance.
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PMID:[Acute respiratory distress syndrome after near-drowning (author's transl)]. 90 76

Oxygen and carbon dioxide tensions of arterial blood and subcutaneous tissue were studied in rats during 84 h of continuous exposure to oxygen. O2 and CO2 tensions in the subcutaneous tissue were measured by means of an implanted Silastic tonometer. As pulmonary edema developed after 48 h of exposure to oxygen, Pao2 started to decline and PaCO2 rose. Tissue Po2 decreased below the normal level already after 24 h of exposure, probably due to O2-induced vasoconstriction. After 84 h of oxygen exposure, the mean tissue Po2 was 29 mm Hg. In general, a distinctly hypoxic tissue microclimate was not observed. After 48 h of exposure to oxygen, the tissue PCO2 exceeded the control level. An 84-h exposure resulted in a profound retention of CO2, both in peripheral tissues and arterial blood. It is concluded that, in contrast to earlier suggestions, hypercapnia rather than hypoxia is the final factor leading to death in oxygen toxicity.
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PMID:Arterial and tissue gas tensions in rats during development of pulmonary oxygen poisoning. 115 98

This paper reviews the principal aspects of the immediate management of patients suffering from spinal injury. An understanding of the pathophysiology of primary and secondary spinal cord injury enables appropriate initial care to be provided, thereby avoiding exacerbation and/or progressive deterioration of the lesion. It includes protective measures, restoration of vital functions to maintain adequate tissue perfusion and oxygenation, as well as pharmacological prevention of secondary injury. Protective measures include proper immobilisation of the spine with a semi-rigid collar and tape on a long backboard, or on vacuum mattress, taking great care to avoid deleterious in-line compression forces on the spinal column. The combination of cervical spine instability, a full stomach, unopposed vagal reflexes, hypoxia and hypercarbia makes airway management of these patients difficult. Tracheal intubation under fibroscopic control, with insertion of the tube only after topical anaesthesia of the airways under titrated intravenous sedation, offers safety and comfort to the patient. However, in cases of severe deterioration of vital functions, intubation must be performed without any delay at the site of the accident or in the emergency room. Three options are available: blind naso-tracheal intubation with spontaneous breathing, modified rapid sequence induction with orotracheal intubation under double protection, and immediate surgical airway if these techniques fail. Patients with cervical spine injury may demonstrate severe hypotension requiring sympathomimetic agents and careful fluid loading to avoid pulmonary oedema. To prevent aggravation of the spinal cord injury by systemic factors, the goal of initial resuscitation is to restore an adequate perfusion pressure of at least 60 mmHg, a PaO2 > 100 mmHg, and to keep PaCO2 below 45 mmHg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia of patients with injury to the cervical spine]. 130 64

Pulmonary edema is known to induce a rapid and shallow breathing pattern. However, its effects on the level and pattern of distribution of motor activity to the respiratory muscles is unclear. In the present study we evaluated the effect of oleic acid induced pulmonary edema on the electrical activity of the inspiratory muscles (costal and crural diaphragm and parasternal and external intercostal muscles) in the dog, and related it to the transdiaphragmatic pressure and ventilatory parameters over the course of CO2 rebreathing. Pulmonary edema, reflected by a 7.1 +/- 0.6 wet to dry ratio, decreased lung compliance by 57%, increased pulmonary shunt to 35%, and was associated with a rapid and shallow breathing pattern. When compared at equal levels of PCO2 during CO2 rebreathing before and during edema, ventilation and mean inspiratory flow were increased only at lower levels of hypercapnia and their responses to increasing levels of PCO2 were significantly diminished during edema. Transdiaphragmatic pressures were elevated during edema as compared to control values. The rate of rise of the electrical activity of all inspiratory muscles increased significantly during edema at all levels of PCO2. Peak activity, however, remained unchanged, due to shortening of the inspiratory duration. The EMG responses to progressive hypercapnia were not affected by edema. Pulmonary edema did not change the pattern of breathing and neural output to the inspiratory muscles in vagotomized dogs. We conclude that stimulation of pulmonary proprioreceptors during edema increases neural output to all inspiratory muscles. The neural response to hypercapnia is not altered by edema, and is additive to the vagal input. The ventilatory response to CO2 is blunted during severe edema, due to alterations in lung mechanics.
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PMID:Inspiratory muscle activity during pulmonary edema in anesthetized dogs. 141 Aug 42

Disturbance in acid-base balance is commonly observed in patients with heart failure. The most common disturbance is metabolic alkalosis combined with hypokalemia, as a result of the excessive use of loop diuretics. Occasionary, hypoxia due to pulmonary edema stimulates ventilation, resulting in respiratory alkalosis. When pulmonary edema develops, carbon dioxide retention occurs, resulting in respiratory acidosis. Decreased tissue oxygen delivery may also produce lethal lactic acidosis. Compensatory mechanisms, coexistence of independent acid-base disorders and changes in electrolytes complicate acid-base balance in the individual patients. As acid-base disturbances have harmful effects on the cardiovascular system, precise diagnosis and proper treatment are highly important.
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PMID:[Acid-base disturbances in heart failure]. 143 8

Extracorporeal Membrane Oxygenation (ECMO) has been adopted as a means of strong respiratory support. In lung transplantation, reimplantation response is still a serious problem. It causes severe respiratory failure which is refractory to mechanical ventilation in some cases. The purpose of this study was to evaluate the effects of veno-venous ECMO after lung transplantation using a canine autotransplantation model. The autotransplantation model was created by keeping the left lung in a warm ischemic state for 2 h. After reperfusion, the right pulmonary artery was ligated. The following two groups were studied: Group 1, Control group, (no ECMO group) (n = 6). After reperfusion, both lungs were ventilated without ECMO. Group 2, ECMO group (n = 7). After reperfusion, veno-venous ECMO support was introduced with reduction of mechanical ventilation. In the no ECMO group, four of the animals died within 210 min after reperfusion. In the ECMO group, two of the animals died of severe pulmonary edema. Data of blood gas analyses (PaO2, PaCO2, and SvO2) after reperfusion were significantly better in the ECMO group, whereas there were no significant differences in both shunt fraction and pulmonary vascular resistance index. In this model with severe pulmonary edema induced by warm ischemia, veno-venous ECMO contributed to the improvement of hypoxemia and hypercapnia, but did not improve pulmonary hemodynamics.
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PMID:Experimental study on veno-venous extracorporeal membrane oxygenation for respiratory failure after lung transplantation. 150 26

Rats injected intravenously with oleic acid developed pulmonary edema leading to hypoxia and hypercarbia. These changes were accompanied by an increase in immunoreactive endothelin (ir-ET) in plasma as early as 15 min after injection. At 45 min after injection plasma levels peaked at 114 +/- 19 pg/ml plasma (n = 8) and reached basal levels again after 240 min. In contrast, much larger amounts of ir-ET were found in the bronchoalveolar lavage fluid, with a peak at 120 min (2878 +/- 258 pg/lung, n = 7) preceding the maximum hypoxia observed at 180 min. In both plasma and bronchoalveolar lavage fluid samples ir-ET was characterized by reverse-phase HPLC as a mixture consisting mainly of ET-1 and smaller amounts of big ET-1, ET-2 and ET-3. In light of the biological effects of ET, the data suggest that these peptides might be of pathophysiological significance in this model of adult respiratory distress syndrome.
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PMID:Release of endothelin in the oleic acid-induced respiratory distress syndrome in rats. 161 74

The effects of acidosis and alkalosis on pulmonary gas exchange were studied in 32 pentobarbital sodium-anesthetized intact dogs after induction of oleic acid (0.06 ml/kg) pulmonary edema. Gas exchange was assessed at constant ventilation and constant cardiac output, by venous admixture calculations and by intrapulmonary shunt measurements using the sulfur hexafluoride (SF6) method. Metabolic acidosis (pH 7.20) and alkalosis (pH 7.60) were induced with HCl and Carbicarb (isosmolar Na2CO3 and NaHCO3), respectively. Hypercapnia was induced by adding inspiratory CO2, whereas pH was allowed to change (respiratory acidosis, pH 7.20) or maintained constant (isolated hypercapnia). Mean intrapulmonary shunt and pulmonary arterial minus wedge pressure difference, respectively, changed from 44 to 33% (P less than 0.05) and from 9 to 10 mmHg (P greater than 0.05) in metabolic acidosis, from 44 to 62% (P less than 0.001) and from 12 to 8 mmHg (P less than 0.01) in metabolic alkalosis, from 40 to 42% (P greater than 0.05) and from 13 to 16 mmHg (P less than 0.05) in respiratory acidosis, from 42 to 52% (P less than 0.05) and from 8 to 12 mmHg (P less than 0.01) in isolated hypercapnia. These results indicate that acidosis, alkalosis, and hypercapnia markedly influence pulmonary gas exchange and/or pulmonary hemodynamics in dogs with oleic acid pulmonary edema.
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PMID:Acid-base status affects gas exchange in canine oleic acid pulmonary edema. 201 14


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