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

For over 15 years, upper respiratory tract obstruction due to adenotonsillar hypertrophy has been known to cause hypoxia, hypercapnia, increased pulmonary vascular resistance and thereby cor pulmonale and congestive heart failure. This is now an uncommon but not rare entity and three recent cases prompted this report. The typical patient is dyspneic with retractions, cyanosis, occasional periods of apnea and somnolence. Edema and hepatomegaly and at times splenomegaly are common. X-rays show cardiomegaly, which on electrocardiogram is found to involved mainly the right ventricle. The strict definition of cor pulmonale is right ventricular hypertrophy secondary to lung disease or abnormal pulmonary function, a definition that may logically be stretched to include abnormal respiratory function secondary to upper airway pathology. The mechanisms by which this occurs are generally agreed upon. Hypoxia has been demonstrated to cause pulmonary vasoconstriction. Acidosis and hypercapnia are thought by some to have the same effect. Pressure across the pulmonary vascular bed is also increased, as predicted by Poiseuille's law, by the high rate of blood flow required to maintain tissue oxygenation with poorly oxygenated blood. Conditions producing hypoxia of hypercapnia or both lead to hypertrophy and eventually to dilatation of the right ventricle. Three cases of children who underwent cardiac catheterization while suffering from cor pulmonale due to adenotonsillar hypertrophy are reported. Right ventricular pressure averaged 44/5, PAO2 72, pH 7.32, and PACO2 52. All were clinically improved following adenotonsillectomy. Cardiac catheterization was repeated in one case, with right ventricular pressure dropping from 44/5 to 21/2, pulmonary vascular resistance from eight units to three, and PACO2 from 62 to 44.
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PMID:Cardiac and pulmonary failure secondary to adenotonsillar hypertrophy. 95 48

A case of brain abscess in the right parietal lobe secondary to pulmonary arteriovenous malformation of the right lung is presented. A 27-year-old man was admitted for headache and left homonymous hemianopsia. CAG, VAG and brain scan detected brain abscess of the right parietal lobe which was successfully removed surgically. He had been noted to have generalized cyanosis and club finger which corresponded to polycytemia and hypercapnia on examination. Subsequently pulmonary arteriovenous malformation was found in the right lower lobe of the lung which was also successfully excised by thoracic surgeons. Brain abscess was caused by peptostreptococcus anaerobius.
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PMID:[Brain abscess secondary to pulmonary arteriovenous malformation, case report (author's transl)]. 98 96

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

The often perplexing clinical findings in acute epiglottitis are produced by the relative absence of cyanosis and hypercapnia in the face of severe hypoxemia, since expiration and CO2 elimination are not impaired. A serious situation arises when intubation is unseccessful. Six hundred otolaryngologists were polled to determine whether life-saving tracheotomy in such a situation could be performed within the time limits.
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PMID:Special considerations in epiglottitis in children. 123 71

Between October 6, 1986 and September 17, 1987, 11 patients underwent insertion of mandibular dental prostheses by the same oral surgeon. Three patients suffered cardiac arrest during surgery and subsequently died. Two of the patients who died had received general anaesthetics and the other had intravenous sedation given by three different anaesthetists. All three patients arrested suddenly, developing profound cyanosis and electrical mechanical dissociation, underwent prolonged resuscitative efforts, and had marked hypoxaemia and hypercapnia, despite cardiopulmonary resuscitation. Two other patients had signs of injection of air but survived, one suffering cardiac collapse and the other sustaining massive subcutaneous emphysema. Air embolism was produced by inadvertent injection of a mixture of air and water, passing through the hollow dental drill, directly into the mandible to the facial and pterygoid plexus veins and thence to the superior vena cava and right atrium.
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PMID:Fatal air embolism during dental implant surgery: a report of three cases. 227 34

A 2,980-gram female infant was born to a 25-year-old mother at the gestational age of 34 weeks with the chief problems of asphyxia and respiratory distress. Prenatal sonogram at 34th week of gestation showed significant pleural effusion, mediastinal shift, polyhydramnios and large for date. Soon after birth, she was put on intubation and ventilator therapy. Physical examination revealed poor chest wall excursion. Breathing sound was markedly decreased over the right lung field. Abdomen was soft and slightly distended with the liver palpable 0.5 cm below the right costal margin and 2 cm below the xyphoid process. Arterial blood gas with patient breathing 100% oxygen revealed severe acidosis and carbon dioxide retention. The first chest film showed right pleural effusion. Chest tap was performed, and 90 cc serosanguineous fluid was aspirated. The white cells of the effusion were 1,971 with lymphocyte predominant. No microorganism or malignant cell was found. Severe respiratory distress and cyanosis persisted inspite of these managements. Follow up chest film at the age of 11 hours revealed the right chest was occupied by intestinal loops. A thoracotomy was performed with the impression of right diaphragmatic hernia. The operation findings included a very redundant membranous portion of diaphragm formed a large sac containing the liver and some bowel loops, the lower lobe of the right lung collapsed and was located high in the posterior chest cavity. Diaphragmatic plication and excision were done with transient improvement of the skin color. The baby's condition deteriorated and expired at the age of 25 hours despite of postoperative vasodilator and ventilator therapies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congenital right diaphragmatic eventration manifested with pleural effusion. Report of one case]. 263 24

After a brief historical recall, this review states the needs for an accurate diagnosis of the neonatal respiratory distress syndrome (RDS). The clinical features consist of disturbances of respiratory rate, grunting, intercostal retractions, and cyanosis, but early mechanical ventilation tends to suppress most of them. Laboratory findings include hypoxemia, hypercapnia, and mixed acidosis. Positive radiological diagnosis remains an important criterion but early ventilation with positive end-expiratory pressure has made grading obsolete. The biochemical diagnosis addresses the basic lung surfactant deficiency, by determination of the lecithin/sphingomyelin ratio and phosphatidylglycerol ("modified lung profile") in lung effluents at birth. If clinical and radiological diagnosis remains adequate for daily practice and epidemiological studies, biochemical diagnosis should be mandatory for therapeutic trials. However, the problem of atypical RDS in very low birth weight infants has not been totally solved. RDS has now been known for more than 80 years; yet its diagnosis is still a matter of controversy.
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PMID:Neonatal diagnosis of respiratory distress syndrome. 266 94

In December 1986 a 30-month-old female child with morbid obesity and respiratory failure was admitted to the Izaak Walton Killam Hospital for Children in Halifax. The etiology of the obesity was found to be dietary in origin after ruling out genetic, neurological and metabolic causes. This patient exhibited somnolence and cyanosis in association with hypercapnia and right ventricular overload. Her respiratory failure in the presence of a normal upper airway required ventilatory support, first with nasal endotracheal intubation, and then, tracheotomy. Weight reduction normalized her capillary blood gases and her somnolence disappeared. Subglottic stenosis hampered removal of the tracheotomy tube until 9 months after admission. The pathogenesis and management of obese hypoventilation syndrome are reviewed by the authors.
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PMID:Obese hypoventilation syndrome of early childhood requiring ventilatory support. 306 Apr 36

To determine the clinical features and outcome of patients with hypercapnia from acute asthma, we examined 229 (62 men, 167 women) consecutive episodes of acute asthma over a 6-yr period. Sixty-one episodes were associated with hypercapnia at presentation (PaCO2 greater than 38 mm Hg). Men more commonly presented with hypercapnia: 31 of 62 (50%) men with acute asthma had hypercapnia compared with only 30 of 167 (18%) women (p less than 0.001). Patients with hypercapnia had a longer duration of chronic asthma and were more likely to be steroid-dependent. Hypercapnic patients had greater airway obstruction, respiratory rate, and pulsus paradoxus than did nonhypercapnic patients. Findings of a quiet chest on auscultation, inability to talk, and cyanosis also suggested the presence of hypercapnia. Five hypercapnic patients required mechanical ventilation, but hypercapnia did not prolong hospitalization. In nonventilated patients, hypercapnia resolved in a mean time of 5.9 h; 50% of hypercapnic episodes resolved by 4 h, and all resolved by 16 h. No patient presenting with normocapnia progressed to hypercapnia with therapy, and there were no deaths in either the hypercapnic group or the nonhypercapnic group. In patients with more than one admission, the PaCO2 of one episode correlated with the PaCO2 on a subsequent admission, suggesting a role for individual variation in ventilatory control. With appropriate medical therapy, most patients with hypercapnia from acute asthma have rapid reversibility, and mechanical ventilation usually can be avoided. However, these patients require close inhospital observation until it is certain that the acute asthmatic episode has resolved.
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PMID:Clinical features and outcome in patients with acute asthma presenting with hypercapnia. 320 9

The clinical and physiologic features of 28 infants with Pierre Robin syndrome and those of 20 infants with various types of nasal obstruction were reviewed to determine whether different causes of upper airway obstructure may lead to a common syndrome. The patients had no significant differences in distribution of main clinical manifestations. Their features included cyanosis with respiratory distress, apneic spells, oropharyngeal dysphagia, vomiting, failure to thrive, cor pulmonale, brain damage, and sudden death during sleep. The common physiologic manifestation appeared to be an oropharyngeal obstruction caused by glossoptosis, which occurred mainly during wakefulness. Upper airway obstruction led to hypoxemia, which, in many instances, was not associated with hypercapnia and was not relieved by oxygen administration. It is concluded that regardless of a specific cause, any airway obstruction that results in a decreased inspiratory pressure overcoming the airway maintaining genioglossus action causes a glossoptosis-apnea syndrome.
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PMID:Glossoptosis-apnea syndrome in infancy. 399 Dec 69


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