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

Studies of the arterial blood gas tensions and pH in 21 children during 24 acute attacks of asthma showed that all were hypoxic on admission to hospital, and in 10 there was evidence of carbon dioxide retention. Cyanosis, invariably present when the So(2) was below 85%, and restlessness in patients breathing air were the most reliable indices of the severity of hypoxia. There were no reliable clinical guides to the Pco(2) level. Conventional oxygen therapy in tents (25-40%) did not always relieve hypoxia, and in three cases the administration of oxygen at a concentration of 40% or over failed to produce a normal arterial oxygen tension. Uncontrolled oxygen therapy may aggravate respiratory acidosis, and three of our patients developed carbon dioxide narcosis while breathing oxygen. The necessity for blood gas measurements in the management of severe acute asthma in childhood is emphasized.
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PMID:Arterial blood gas tensions and pH in acute asthma in childhood. 566 2

127 cases of tracheal dyskinesia were seen in infants and children out of which 87 were 1 to 12 months of age. The diagnosis was based on the existence of a collapse reducing the tracheal diameter of more than 50% on endoscopy. Endoscopic examination was performed without general anesthesia. This material represents 5,8% of the patients submitted to this procedure. 85 patients had "primitive" dyskinesia and 42 had major associated abnormalities. Uni or bilateral bronchial dyskinesia was associated in 43% of the cases. The four commonest presenting symptoms were a stridulous or wheezing respiration, recurrent bronchitis, chronic cough, cyanosis. The frequency of associated digestive troubles: gastroesophageal reflux aspiration was noteworthy. Several functional consequences were encountered: hypoxemia, hypercapnia, abnormalities of FRC, increased RL, lowering of dynamic compliance, alterations of perfusion and ventilation on scintiscans. The prognosis was good in primitive cases. Two deaths occurred, in the group with associated abnormalities. The pattern of the patient with primitive dyskinesia and that of the patient with dyskinesia and associated abnormalities are outlined. Some features remarkable in this series of patients are pointed out in a discussion of the pathophysiology of the syndrome. Increased transmural pressure is not a common cause of tracheal dyskinesia and infection as well. The possibility of a temporary intrinsic anomaly of the tracheal wall is suggested. Even if its exact mechanism remains unknown, tracheal dyskinesia is a distinct entity observed in infants and children. It appears as a common cause of recurrent bronchopulmonary disease in the young.
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PMID:[Tracheal dyskinesia (tracheomalacia) in infants and children. Study of 127 cases diagnosed through endoscopic examination (author's transl)]. 626 18

We studied diaphragmatic muscle function during inspiratory flow resistive (IFR) loaded breathing in unanesthetized sheep. We measured the change in transdiaphragmatic pressure (dPdi) and arterial blood gas tensions and recorded diaphragmatic electromyogram (EMG) from electrodes implanted on the muscle. We found that, with IFR loads less than 150 cmH2O X l-1 X s, dPdi and the integrated EMG increased, reached a plateau, and were maintained at high levels. The centroid frequency (fc) of the EMG power spectrum did not consistently change. With IFR loads greater than 150 cmH2O X l-1 X s, O2 was administered to prevent hypoxia, cyanosis, and agitation. With these loads, dPdi increased severalfold above base line, reached a plateau, and then started to decrease. Arterial PCO2 increased sharply at the time when dPdi decreased. The integrated EMG (iEMG) and fc started to decrease gradually 10-20 min before dPdi started to decrease. We conclude that 1) the diaphragm is capable of generating large pressures for prolonged periods with no evidence of fatigue; 2) with very high IFR loads, mechanical failure of the diaphragm can occur in the unanesthetized awake sheep; 3) diaphragmatic fatigue is associated with acute hypercapnia and therefore failure of the entire respiratory pump; and 4) a decrease in iEMG and a concommitant shift in the power spectrum density towards lower frequencies precede the mechanical failure of the diaphragm.
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PMID:Diaphragmatic fatigue in unanesthetized adult sheep. 646 79

We postulated that parents of infants who sustain near-death episodes associated with defective chemical regulation of breathing might share a similar defect. We, therefore, measured the ventilatory responses to progressive hypoxia and hypercapnia individually in eight sets of parents of infants who had sustained at least one near-death episode (apnea, cyanosis, pallor, limpness, and responsive only to mouth-to-mouth resuscitation); each infant had a ventilatory response to CO2 which was more than 2 S.D. below the mean normal. Ventilatory function measured by vital capacity forced expiratory volume 1.0 and flow curves was normal in each group. Responses to hypercapnia and hypoxemia in both fathers and mothers were similar to 11 pairs of controls. Ventilation during CO2 rebreathing normalized for surface area increased 0.87 liter/min/mm Hg in fathers, 0.94 in controls, 0.87 in mothers, and 0.75 in controls. Ventilation during progressive hypoxemia increased 88 liter/min/1 divided by mm Hg in fathers, 92 in controls, 86 in mothers, and 101 in controls. None of these differences was significant.
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PMID:Ventilatory chemoreceptor response in parents of children at risk for sudden infant death syndrome. 679 81

A progressive pulmonary disease resulting in severe respiratory failure and death in an average of 3 weeks was diagnosed in 11 young Dalmatian dogs. The dogs were from 4 litters, all genetically related by a common ancestor. The initial clinical signs were tachypnea and noisy respiration. Respiratory distress developed shortly before death and was characterized by strenuous and rapid respirations, along with cyanosis and vomiting. On blood gas analysis, there were severe arterial hypoxemia, hypercapnia, and marked alveolar-arterial oxygen difference. Radiographically, a diffuse pattern of alveolar, interstitial, and peribronchial densities was observed in the lungs. Most dogs developed pneumomediastinum and gastroesophageal intussusception in the terminal phase of the disease. There was no response to treatment with antibiotics, corticosteroids, diuretics, or oxygen. At necropsy, the lungs were wet, heavy, and relatively airless. Absence of 1 kidney in 2 dogs and severe internal hydrocephalus in 2 dogs were additional necropsy findings. Pulmonary histopathology included metaplasia and atypia of the alveolar and bronchiolar epithelium, a nonpurulent inflammatory reaction characterized mainly by mononuclear cells and macrophages, eosinophilic hyaline membrane formation, and focal pulmonary fibrosis. The histological manifestations were typical of acute lung injury. Clinically, the findings were consistent with adult respiratory distress syndrome (ARDS), except for the relatively long course. No known risk factors for ARDS, such as trauma, toxin exposure, infection, or endotoxemia could be identified. The relationship of the other abnormalities (ie, renal aplasia, hydrocephalus) to the pulmonary disease also remains obscure. An inherited defect is suspected, because segregation analysis of the 4 litters suggests autosomal recessive inheritance.
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PMID:Lung injury leading to respiratory distress syndrome in young Dalmatian dogs. 767 17

A 3700-g male infant born at 37 weeks' gestation presented with cyanosis at birth. He was diagnosed as having persistent pulmonary hypertension of the newborn (PPHN) on the basis of persistent hypoxemia, despite continuous mechanical ventilatory support with 100% O2, and right-to-left shunting through the foramen ovale shown by Doppler echocardiography. Treatment with hyperventilation, and administration of tolazoline, prostaglandin E1 and MgSO4 failed to reverse his hypoxemia. High ventilator settings were required, and pneumothoraces ensued. Airway resistance increased gradually with development of hypercapnia and deterioration of hypoxemia. Bradycardia unresponsive to resuscitation occurred, and he died at eight days of age. Postmortem examination of the lungs revealed increased peripheral connective tissue and diffuse extension of medial smooth muscle to the precapillary pulmonary arteries. Excessive antenatal muscularization of the peripheral pulmonary arteries and resultant increased vasoconstriction capacity may have played an important role in the pathogenesis of PPHN in this case.
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PMID:Persistent pulmonary hypertension of the newborn associated with excessive pulmonary arterial muscularization: report of an autopsy case. 790 70

Heroin lung is the most frequent complication of heroin intoxication. In September 1991 and January 1993, two young men aged 19 and 22 years presented with a sudden loss of consciousness and cyanosis after injecting heroin. They were both brought to our emergency department in the night and were immediately intubated and given 100% oxygen. Following intravenous naloxone, they both regained consciousness. The first patient's chest X ray revealed increased bilateral perihilar lung markings and mild patchy alveolar edema while the second patient showed a bat's wing shaped confluent alveolar edema. The blood gases in both cases revealed hypoxemia and hypercapnia. Follow-up chest roentgenograms on the second hospital day in case 1 and the third hospital day in case 2 revealed partial clearing of the lung fields. Fever developed on the second hospital day and they both received two weeks of antibiotics prior to discharge. Case 1 had normal pulmonary function testing, but case 2 developed mild restrictive lung changes. Review of the literature shows that heroin can cause a fulminant but rapidly reversible form of pulmonary edema. The treatment for this noncardiogenic pulmonary edema is adequate ventilation, good pulmonary toilet, and naloxone to reverse the respiratory and central nervous system depression. Diuretics, digitalis and morphine are not recommended in the treatment of heroin lung.
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PMID:Heroin lung: report of two cases. 791 90

A case of severe accidental hypercapnia during anesthesia is presented. A 44-year-old woman underwent laparotomy under general anesthesia. Forty minutes after the start of the operation, BP rose slightly and HR increased from 110 to 140 x min-1. Then ST segment depression was noted on ECG monitor. Therefore, nitrous oxide was discontinued for 20 minutes. Frequent oxygen supply with oxygen flush was needed to inflate the collapsed bag. The operation was concluded without additional clinical problems. The patient remained unconscious after the anesthetics were discontinued. Cyanosis was observed despite the delivery of 100% oxygen. Cardiac arrest occurred following abrupt bradycardia, but she responded immediately to resuscitation. She was in a deep comatose state and did not respond to painful stimuli. The pupils were fully dilated with absent light reflex. Arterial blood gas analysis revealed; pH 6.720, PaCO2 277 mmHg, PaO2 159 mmHg, and BE-16.2. Disconnection of anesthetic circuit was noted, thereafter, and hyperventilation was performed. Then, the pupils became promptly constricted and the response to painful stimuli appeared within 30 minutes. Her level of consciousness recovered completely after 4.5 hours of hyperventilation. She suffered from refractory hypotension (BP70-85 mmHg in systolic pressure) in spite of catecholamine administration, tachycardia (HR 140-160 x min-1) and ARDS in the ICU, but all the symptoms disappeared by the 16 hours after ICU admission.
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PMID:[A patient who manifested various symptoms following severe accidental hypercapnia]. 899 34

Noninvasive mechanical ventilation (NMV) now represents the first step in the management of acute on chronic respiratory failure (A/CRF). During the last 5 yrs, many studies have confirmed the feasibility of NMV in an acute setting, either by facial or nasal interface, used in addition to volumetric or barometric respirators, to manage A/CRF. The best indications for NMV are slowly progressive A/CRF, frequently represented by chronic obstructive pulmonary disease (COPD), or restrictive pulmonary disease. The criteria to initiate NMV in such patients are worsening of respiratory status and arterial blood gas (ABG) values, with increased hypoxia, hypercapnia and respiratory acidosis, despite optimal management with medication, physiotherapy and oxygen therapy. Respiratory encephalopathy is not an absolute contraindication; however, bronchial hypersecretion indicates that care is needed under NMV. Invasive mechanical ventilation with endotracheal (ET) intubation is discussed in the case of failure of NMV, when clinical status and ABG values worsen in spite of it. The signal for ET intubation is then obvious, represented by severe dyspnoea leading to respiratory pauses or arrest, severe cyanosis, and signs of haemodynamic instability. Despite immediate evidence of ominous cardiorespiratory inefficiency, ET intubation may be delayed and often avoided with the help of NMV. Criteria should be studied to identify guidelines for cessation of NMV, in order not to continue with the technique too long considering the safety of the patient. Indications for NMV in other kinds of ARF have received less study and are more controversial.
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PMID:Noninvasive mechanical ventilation and acute respiratory failure: indications and limitations. 915 23

A 4-month-old baby girl, after a period of apparent good health, began to have aphonia, dyspnea, difficulties with swallowing, cyanosis, apnea, and hypopnea during sleep that resulted in admission to an intensive care unit for intubation and mechanical ventilation. At the age of 9 months she was admitted to our hospital with a possible diagnosis of central hypoventilation syndrome. A polysomnographic study showed apnea and hypopnea (apnea + hypopnea index = 47.1), hypercapnia (mean end-tidal PCO2 89 +/- 15.0 mmHg), and arterial desaturation (mean SaO2 91 +/- 1.7%; lowest SaO2 < 50%; 68% of total sleep time at SaO2 below 93%); the study also showed an absent ventilatory response to CO2, absent cardiac responses to apnea during sleep, and right ventricular hypertrophy. Nocturnal nasal bi-level positive airway pressure (BIPAP), applied initially at 6 cmH2O and gradually increased to 16 cmH2O, caused the sleep-related abnormal respiratory events to disappear. End-tidal PCO2 decreased to 39 mmHg, and SaO2 increased to 94%. After 6 months of nocturnal BiPAP ventricular right hypertrophy reversed and arrested growth and hypotonia normalized. The child has tolerated and has remained on BiPAP support up to her current age of 3 years and continues to use this form of ventilatory assistance without difficulties.
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PMID:Bi-level positive airway pressure (BiPAP) ventilation in an infant with central hypoventilation syndrome. 926 57


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