Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve rhesus monkeys were delivered prematurely at 129, 130, or 131 days. The first breath was inhibited while tracheotomy was performed and a catheter introduced into the umbilical artery. Into the tracheal tubes of six of the newborn monkeys was instilled 0.20 to 0.27 ml. of a natural surfactant (SA) suspension, obtained from lung wash of adult rabbits. Nothing was given to six control monkeys. Breathing was then supported with a ventilator. Although its settings were adjusted in attempts to maintain normal blood gases, the control monkeys developed severe hypercapnia and acidosis, and two died after 4 1/2 and 5 1/2 hours. The remaining four control monkeys and the six treated monkeys were killed after six hours. Pulmonary pressure-volume characteristics were conspicuously better following SA treatment. It was concluded that instillation of SA in the upper airways of premature primates prior to their first breath holds promise as an effective way of preventing respiratory distress.
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PMID:Improved ventilation of prematurely delivered primates following tracheal deposition of surfactant. 3 Oct 91

Some renal parameters have been studied in newborns with respiratory distress syndrome (RDS). During the first 24 h, the serum creatinine level of the severe cases of RDS are significantly increased, decreasing gradually with improvement of the RDS and reaching normal values within 10 days. Blood urea nitrogen remained unchanged. In the milder cases of RDS, the serum creatinine also showed a slighter increase, which became normal within 4 days after birth. During the acute phase of RDS, there is a reversible impairment in the renal function, which correlates with the degree of hypoxia, hypercapnia and acidosis determined by the primary disease.
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PMID:Alterations in creatinine clearance during respiratory distress syndrome. 3 62

This report describes a syndrome of delayed respiratory distress occurring in premature infants usually under 1,250 gm at birth. Unlike hyaline membrane disease, this syndrome occurs after four to seven days in a previously healthy infant; also unlike hyaline membrane disease, it persists for two to four weeks. Chronic pulmonary insufficiency of prematurity (CPIP) carries a 10% to 20% mortality rate. The infants are frequently apneic, require supplemental oxygen, but lack the radiologic findings of hyaline membrane disease or bronchopulmonary dysplasia. When compared with nondistressed infants of similar birthweight, infants with CPIP demonstrate slowly progressive atelectasis, hypoxemia, and hypercapnia. Recovery is usually complete by 60 days of age. The importance of CPIP is that an awareness of its existence can eliminate a false sense of security, often communicated to anxious parents, during the four-to-seven-day grace period before its appearance is clinically obvious. The physiologic similarities between CPIP and hyaline membrane disease suggest that lack of surfactant may play a role in the pathogenesis of CPIP.
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PMID:Chronic pulmonary insufficiency of prematurity (CPIP). 23 87

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

In a series of 102 patients with multiple injury including a blunt lesion of the chest treated in 1970 through 1973 the mortality rate could be reduced to 17 per cent. This compares favourably with a mortality of about 34 per cent in a similar group of patients treated in the same hospital during 1965 through 1969. The improvement is partly due to increasing experience of the surgical and anaesthesiological teams and especially to a better appreciation of the importance of ventilatory pulmonary insufficiency and acute respiratory distress syndrome which are frequent in these patients. Early respiratory assistance is indicated in all cases with an instability of the chest wall. The imminence of a respiratory distress syndrome may announce itself by the classical symptoms of an increased breathing rate with hypocarbia before hypoxia becomes manifest. In the majority of patients with a thoracic lesion however the syndrome starts with a combination of increasing dyspnoea and normo- or even hypercarbia. This should be recognized and promptly treated by artificial respiration before acidosis and hypoxia with cardiac arrest can occur.
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PMID:Blunt thoracic trauma in multiple injury. 124 43

In order to establish more objective criteria for surgical intervention, the literature and our clinical experience with operative closure of patent ductus arteriosus in 11 premature infants was reviewed. A wide range of age at the time of operation underscored the spectrum of clinical presentation and the difficulty of interpreting the course of therapy. The presence of a typical continuous murmur established the diagnosis of patent ductus arteriosus in patients with respiratory distress syndrome. Cardiac catheterization confirmed the diagnosis and provided quantitation of the left-to-right shunt flow through the ductus arteriosus in 6 patients but did not influence the decision to operate. Progress of the clinical course as determined by the heart size on chest roentgenogram and the presence of hypercarbia (Paco2greater than60 mm. Hg) after respiratory assistance and medical decongestive measures were the two most helpful signs indicating the need for surgical intervention.
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PMID:Patent ductus arteriosus in premature infants. Indications for surgery. 124 43

To ascertain whether any routine practices or clinical manipulations in a neonatal intensive care unit could induce intraventricular hemorrhage (IVH) in preterm infants, we performed ultrasonic monitoring of the germinal layer continuously for 48 hours in 33 extremely premature infants with respiratory distress. Intraventricular hemorrhage developed in 16 of these infants. In four infants the timing of the germinal layer hemorrhage was confirmed with ultrasonic monitoring. Three of the four cases were apparently associated with clinical events occurring at the moment of IVH: manual ventilation for improvement of hypercapnia associated with primary pulmonary hypertension of the newborn; correction of hyperkalemia, which was causing an arrhythmia, with administration of calcium gluconate and sodium bicarbonate; and administration of surfactant-TA to improve respiratory failure caused by pulmonary hemorrhage. In these three infants it appeared that one of the basic factors inducing IVH might be an increase in blood pressure with or without hypercapnia, causing cerebral reperfusion after ischemic damage of the germinal layer.
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PMID:Clinical events in association with timing of intraventricular hemorrhage in preterm infants. 140

Neonates with congenital diaphragmatic hernia (CDH) are known to be susceptible to stress-induced persistent pulmonary hypertension (PPHN). Congenital cystic adenomatoid malformations (CCAMs) may also present as respiratory distress in the newborn. Intubation and mechanical ventilation cause clinical deterioration because of air trapping within cystic spaces; these patients require prompt lobectomy. PPHN has not been commonly associated with CCAM. Three patients with CCAM were encountered who developed PPHN postlobectomy. Three newborns, 36 to 38 weeks' gestation, presented with respiratory distress. Two had diagnosis of thoracic tumors on fetal ultrasound (22 and 33 weeks). Chest x-ray at birth confirmed cystic intrathoracic tumors in all and they underwent immediate thoracotomy and lobectomy (1 right upper, 1 left lower, 1 left upper). The patients were stable for 4 hours to 5 days postoperatively and then developed findings consistent with PPHN by cardiac echocardiography and required extracorporeal membrane oxygen (ECMO) support. ECMO was required for 66.5 to 120 hours. Each patient was successfully weaned to conventional ventilatory support. The clinical course of these patients was similar to those with CDH who undergo immediate surgery. The stress of surgical intervention combined with hypoxia and hypercarbia stimulates a hyperactive pulmonary vasculature and the development of PPHN. ECMO provides an effective adjunct to support patients with PPHN on the basis of congenital cystic adenomatoid malformations.
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PMID:Persistent pulmonary hypertension complicating cystic adenomatoid malformation in neonates. 155 45

In vivo anaphylaxis is associated with respiratory distress and cardiovascular failure. The present investigation was designed to further characterize respiratory and cardiac anaphylactic events. In guinea pigs, sensitization was produced by subcutaneous application of ovalbumin together with Freund's adjuvant. Fourteen days after sensitization, the effects of an intravenous infusion of ovalbumin were tested in the anesthetized artificially ventilated guinea pigs. The renewed application of the antigen induced an initial increase of left ventricular pressure which was followed by a rapid decrease 5 min after antigenic challenge. Enddiastolic left ventricular pressure increased within 3 min, thus indicating left ventricular pump failure. In the same time range, ECG recordings uniformly showed signs of acute myocardial ischemia. In addition, heart rate steadily decreased. All animals died within 15 min. Simultaneously with cardiac anaphylactic malfunction, severe arterial hypoxia and carbon dioxide retention occurred, revealing respiratory distress. Histamine is known as a potent bronchoconstrictor via histamine H1-receptor stimulation. Administration of H1-receptor antagonists to improve respiration may therefore provide further information on the contribution of pulmonary malfunction to anaphylactic cardiovascular shock. Therefore, additional experiments were performed with sensitized guinea pigs pretreated with the histamine H1-receptor blocker mepyramine. In these experiments the antigenic challenge induced a dissociation of cardiac and respiratory manifestation of anaphylaxis. Despite inhibition of hypoxia and carbon dioxide retention, left ventricular pump failure and occurrence of myocardial ischemia were delayed but not suppressed. It is concluded that histamine is an important mediator of anaphylactic respiratory distress. However, vasoactive anaphylactic mediators other than histamine are primarily involved in anaphylactic cardiac malfunction occurring during the later phase of systemic anaphylaxis.
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PMID:Effects of histamine H1-receptor blockade on respiratory and cardiac manifestation of systemic anaphylaxis. 168 6

Infants with esophageal atresia and a distal tracheoesophageal fistula are predisposed to respiratory failure on the basis of prematurity, respiratory distress syndrome, aspiration of saliva, and reflux of gastric contents into the tracheobronchial tree. Thoracotomy and primary repair may be delayed to allow time for complete evaluation of the infant and respiratory stabilization. Poorly compliant lungs and a large distal fistula can result in selective passage of ventilatory gases into the gastrointestinal tract with resultant hypercarbia. Fogarty balloon occlusion of the distal esophageal segment halts this air shunt and facilitates effective mechanical ventilation.
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PMID:Esophageal atresia, distal tracheoesophageal fistula, and an air shunt that compromised mechanical ventilation. 194 74


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