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

Severe head trauma patients frequently develop pulmonary failure. The aetiology of this respiratory distress may be central (neurogenic pulmonary oedema, delayed neurogenic pulmonary dysfunction, abnormal respiratory patterns) or peripheral, due to chest trauma, multiple trauma or lung infection. Hypoxia and hypercarbia alter cerebral haemodynamics, increase intracranial pressure and cause secondary deterioration of neurological function. Ventilatory support is of utmost importance in supportive care of head trauma patients. Continuous mechanical ventilation and intermittent mandatory ventilation are most frequently employed. Hyperventilation is used to lower intracranial pressure and positive end-expiratory pressure (PEEP) is applied in lung disorders characterized by interstitial oedema and alveolar collapse. The effects of PEEP on cerebral perfusion pressure and on intracranial pressure depend on the interaction of pulmonary compliance, cerebral pressure/volume relationship and cerebral vascular autoregulation. High levels of PEEP may be deleterious in patients with altered cerebral autoregulation. High frequency ventilation theoretically has less influence on intrathoracic pressures and on cerebral haemodynamics but has not been shown superior in the respiratory support of severe head trauma patients.
 ...
PMID:Ventilatory support for pulmonary failure of the head trauma patient. 389 Sep 90

The aim of the present study was to determine whether the diversion of blood flow away from a collapsed pulmonary lobe is due to hypoxic pulmonary vasoconstriction alone, or whether hypercapnia and mechanical factors also contribute. Hypoxic pulmonary vasoconstriction was tested in a canine pulmonary left lower lobe. Alveolar hypoxia was produced by absorption collapse or by ventilation with 7% oxygen, which has previously been shown to produce an end-pulmonary capillary pO2 similar to mixed venous pO2. The proportion of the cardiac output flowing to the lobe was reduced in both hypoxic states but was significantly lower during collapse than during ventilation hypoxia. The beta 1-adrenergic agonist dobutamine hydrochloride (30 micrograms X kg-1 X min-1 iv) produced a significant increase in the proportion of the cardiac output flowing to the lobe during collapse but no significant change during ventilation hypoxia. It is concluded that changes in local pCO2 during collapse may account for the greater diversion of blood flow from the lobe when compared with ventilation hypoxia.
 ...
PMID:Pulmonary lobe blood flow during ventilation hypoxia and lobar collapse in the dog. 399 22

1. Exposure to glass of whole blood from anaesthetized foetal lambs (at 0.6-0.95 of term) causes the rapid development of a potent pulmonary vasodilator agent.2. The formation of the vasodilator agent on exposure to glass, its disappearance with time, and the inhibition of its production by soya bean trypsin inhibitor, suggest that it is bradykinin.3. Small doses of bradykinin ( approximately 1 ng/kg) cause pulmonary vasodilatation on close arterial injection. Neither this, nor the vasodilatation caused by glass-exposed whole blood, are affected by agents which block the vasodilator actions of acetylcholine, isoprenaline or histamine.4. Exposure of foetal plasma and/or red cells to glass rarely caused the development of a pulmonary vasodilator agent. Maternal plasma was always active. Injection of the buffy coat from foetal blood caused pulmonary vasodilatation.5. The capacity of plasma from sheep at different ages to produce kinin(s) was examined by assay on the isolated rat's uterus. In the foetus activity was very low; it increased with age.6. In adolescent lambs 5-14 weeks after birth injection of approximately 10 ng/kg bradykinin into the pulmonary artery caused only a trifling vasodilatation; this was greater when pulmonary vasoconstriction was induced by lung collapse, hypoxaemia and hypercapnia.7. The possible physiological consequences of these findings are discussed.
 ...
PMID:The release of a bradykinin-like pulmonary vasodilator substance in foetal and new-born lambs. 563 4

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.
 ...
PMID:[Tracheal dyskinesia (tracheomalacia) in infants and children. Study of 127 cases diagnosed through endoscopic examination (author's transl)]. 626 18

During an 18-month period, 11 preterm infants with birthweights between 700 and 1560 g (mean 1.2 kg) developed excessive tracheobronchial secretions during intensive care. No single obstetric factor was incriminated. Copious, viscous, tracheobronchial secretions were noted at about 5 days during mechanical ventilation via endotracheal tube causing recurrent segmental collapse, hypoxia, and hypercapnia (median peak PCO2 13.5 kPa). All infants were treated with frequent bronchial lavages and continued intermittent positive pressure ventilation, together with high concentrations of oxygen. No infant died, but morbidity was high. Tracheostomy was performed on 2 infants (one at age 3 months, because of severe croup) and 2 others had clinical or physiological evidence of upper airways narrowing. Follow-up studies showed that this group had more problems of airways obstruction throughout the first year of life as well as increased lung stiffness. The hypersecretion group showed a higher incidence of chronic lung disease. Likely aetiological factors were sought. Contamination of the mechanical ventilation equipment by detergent and activated glutaraldehyde was found; this could have been a contributory factor.
 ...
PMID:Bronchial hypersecretion in preterm neonates. 706 6

Recent insights into the pathophysiology of acute lung injury have led to changes in our routine approach to mechanical ventilation in this population of patients. Heterogeneous alterations in the anatomy and function of the lung are characteristic of acute lung injury. Experimental evidence strongly suggests that traditional approaches to mechanical ventilation with normal tidal volumes applied uniformly to the injured lungs will result in repetitive alveolar overdistention in regions with normal compliance. This process, termed volutrauma, impedes lung healing and may extend damage to previously unaffected areas. This realization has led to a strategy that is designed to avoid tidal alveolar collapse using physiologic transalveolar pressures while allowing alveolar hypoventilation and hypercapnia. Debate continues regarding the risks and benefits of pressure-limited versus volume-limited mechanical ventilation to achieve this goal. Research is ongoing regarding the role and techniques for nonconventional methods of cardiorespiratory support for this severely ill group of patients.
 ...
PMID:New approaches to ventilation in infants and children. 766 11

In acute respiratory failure interstitial oedema, alveolar collapse, and multiple atelectasis are the main mechanisms which lead to increased venous admixture and impaired oxygenation. Thus the lung volume available for pulmonary gas exchange is considerably reduced. Since there is strong evidence that alveolar overdistension causes lung damage ('barotrauma/volutrauma') large tidal volumes and high airway pressures in mechanical ventilation have to be strictly avoided, even allowing hypoventilation ('permissive hypercapnia'). Recruitment of the collapsed alveoli by external or intrinsic PEEP, or by changing body position, is often possible. However, alveolar recruitment takes much longer than previously assumed: instead of occurring within one respiratory cycle ('inflection point'), it seems to take hours. This slow recruitment process can be effectively supported by a deliberate use of intrinsic PEEP as with inverse ratio ventilation, either in volume or pressure controlled mode. Assisted spontaneous breathing makes ventilatory support less invasive and offers considerable advantages for many patients, but there are still some restrictions. Individual adaptation may be difficult in some patients. New principles of assistance control ('proportional assist ventilation') may improve individual adaptation. New concepts for weaning in COPD patients seem to offer better clinical strategies.
 ...
PMID:Artificial ventilation: some unresolved problems. 814 15

Many experimental studies have shown that mechanical ventilation with high tidal volumes (Vt) or with a low end-expiratory volume allowing repeated end-expiratory collapse, can result in acute parenchymal lung injury and probably an inflammatory response. Low volume ventilation with permissive hypercapnia has been used in an attempt to avoid such injury in ARDS. Such management can affect oxygenation in many complex ways. The right-shift of the haemoglobin-oxygen dissociation curve during acute respiratory acidosis may increase venous oxygen tension (PvO2) which could allow increased O2 uptake in ischaemic tissues. Acidosis may reduce intrapulmonary shunt (Qs/Qt) by potentiating hypoxic pulmonary vasoconstriction, and there may also be direct and autonomically mediated effects of hypercapnia both on the lung vasculature and on the airways. Cardiac output usually increases as a consequence of hypercapnia and perhaps as a result of reduced intrathoracic pressure, further increasing PvO2 and CvO2, but the increase in cardiac output (CO) may tend to increase Qs/Qt as flow increases preferentially in unventilated lung. The reduction of mean airway pressure may directly increase Qs/Qt. Hypercapnia may affect the distribution of systemic blood flow both within organs and between organs. Limited clinical studies suggest that tissue oxygenation is usually unchanged or improved during permissive hypercapnia with increased CO, reduced arterio-venous O2 content difference and reduced blood lactate concentration. However, acute hypercapnia per se can reduce lactate production. Further studies are required of this complex issue.
 ...
PMID:Permissive hypercapnia in ARDS and its effect on tissue oxygenation. 859 78

Deviation of end-expiratory lung volume from the elastic equilibrium volume of the respiratory system is recognized as a cardinal feature in mechanically-ventilated patients with severe chronic obstructive pulmonary disease (COPD) and acute ventilatory failure (AVF). The presence of dynamic hyperinflation implies that alveolar pressure remains positive throughout expiration. At the end of the expiration, this positive pressure is named intrinsic positive end-expiratory pressure (PEEPi). Recent studies have suggested that, in COPD patients with expiratory flow limitation, the application of external PEEP during assisted mechanical ventilation, or the use of continuous positive airway pressure (CPAP) in spontaneously breathing patients, can counterbalance and reduce the inspiratory threshold load imposed by PEEPi, without causing further increase in lung volume and alveolar and intrathoracic pressures until a critical value of PEEP (Pcrit) is reached. Above this critical limit further hyperinflation is observed. A specific and characteristic role of PEEPi in compromising the heart function in COPD patients during AVF may be identified based on: 1) an increase in right ventricular impedance due to lung hyperinflation; 2) an increase in the venous return to the right ventricle and, consequently, a leftward shift of the septum caused by the large negative deflections in intrathoracic pressure due to the inspiratory threshold load; 3) a further increase in venous return to the right ventricle, with the eventual collapse of the vena cava caused by the expiratory recruitment of abdominal muscles; and 4) hypoxia and hypercapnia consequent to acute ventilatory failure, which may further increase right ventricular impedance and venous return to the right ventricle. All these phenomenon are directly correlated to the large negative intrathoracic pressure developed by the respiratory muscles to overcome the inspiratory threshold caused by intrinsic positive end-expiratory pressure (preload effect), and to the increase in lung volume (afterload effect). Application of positive end-expiratory pressure/continuous positive airway pressure in chronic obstructive pulmonary disease patients during acute ventilatory failure may, hence, unload the respiratory muscles as well as the heart.
 ...
PMID:Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. 880 50

Suffocation by bedclothes became a popular diagnosis in the 1940s but gradually became replaced with the diagnostic label of Sudden Infant Death Syndrome (SIDS). In 1991 a paper purported that, instead of SIDS, pillows filled with polystyrene beads had caused death by rebreathing suffocation; this conclusion was reached on the basis of experiments with anesthetized rabbits breathing through a doll's head that was placed face down on the pillow. Because of the anesthesia, rabbits could not change their face down position. The doll's nares could not collapse, which would have resulted in rapid death due to conventional suffocation. The rabbits required up to 3 hours or more to die of hypercarbia and hypoxia. Studies in normal infants revealed that they turned from the face-down position after only 2 minutes. (The only infant who retained CO2 soon died of a fatal neurologic disorder, with central hypoventilation). Using the rabbit/doll's head and mechanical models, a wide range of bedding was indicted, including cushions, sheepskins, pillows, comforters, foam mattresses, and even simple blankets and sheets as potentially causing fatal rebreathing. Except for the use of pillows in general, as well as mattresses filled with kapok and bark, there has been no epidemiologic support for these indictments. Although normal infants are unlikely to succumb to rebreathing suffocation, infants with blunted ventilatory responsiveness and delayed arousal due to prior hypoxia were hypothesized to be at increased risk. Support for this concept was found in the pathology of the brain stem in victims of SIDS that was attributed to prior hypoxic injury. In infants who survived prolonged apnea, less than 20% have demonstrated a diminished ventilatory responsiveness to hypercarbia, but, more significantly, none had an absent response. Arousal to hypercarbia, an abnormality which is crucial to the hypothesis of rebreathing suffocation, is regularly present in normal subjects, but the threshold is higher in near-SIDS infants; however, no instances of failure to arouse have been reported in near-SIDS. If the infant is placed on his or her back or side, the issue of bedding could become moot; unfortunately, a sizable percentage of infants are still being placed prone for sleep. Instead of confusing parents with an ever-expanding list of "dangerous bedding," the message "Back to Sleep" should be emphasized.
 ...
PMID:Are bedding and rebreathing suffocation a cause of SIDS? 901 66


<< Previous 1 2 3 4 5 6 7 8 Next >>