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)

Many animal studies have shown that high peak inspiratory pressures (PIP) during mechanical ventilation can induce acute lung injury with hyaline membranes. Since 1984 we have limited PIP in patients with ARDS by reducing tidal volume, allowing spontaneous breathing with SIMV and disregarding hypercapnia. Since 1987 50 patients with severe ARDS with a "lung injury score" greater than or equal to 2.5 and a mean PaO2/FiO2 ratio of 94 were managed in this manner. The mean maximum PaCO2 was 62 mmHg, the highest being 129 mmHg. The hospital mortality was significantly lower than that predicted by Apache II (16% vs. 39.6%, chi 2 = 11.64, p less than 0.001). Only one death was due to respiratory failure, caused by pneumocystis pneumonia. 10 patients had a "ventilator score" greater than 80, which has previously predicted 100% mortality from respiratory failure. Only 2 died, neither from respiratory failure. There was no significant difference in lung injury score, ventilator score, PaO2/FiO2 or maximum PaCO2 between survivors and non-survivors. We suggest that this ventilatory management may substantially reduce mortality in ARDS, particularly from respiratory failure.
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PMID:Low mortality associated with low volume pressure limited ventilation with permissive hypercapnia in severe adult respiratory distress syndrome. 224 18

Cardiorespiratory effects of tetrodotoxin (TTX) (15 micrograms/kg, i.p.) were investigated in urethane-anesthetized guinea pigs acutely instrumented for the recording of medullary respiratory-related units (RRUs), diaphragm electromyogram (DEMG), electrocorticogram (ECoG), electrocardiogram (ECG), blood pressure (BP), endtidal CO2, and arterial O2 and CO2. Respiratory system responses showed a hyperventilatory profile during the initial stage of intoxication. This was followed by an abrupt onset of a progressive decrease in the respiratory frequency, and a respiratory rate depression-related respiratory failure. The average time to TTX-induced respiratory arrest and death was 10.3 +/- 4.2 min. Concurrently recorded inspiratory and expiratory RRU activities indicated that respiration invariably failed in an end-expiratory position as manifested by a sustained period of expiratory RRU discharge. The progressive rate depression prior to respiratory arrest was temporally correlated only to a concomitantly augmenting expiratory RRU discharge duration. Inspiratory RRU discharge duration, on the other hand, did not display any significant change throughout the course of intoxication. The asymmetry in RRU response patterns indicates either an expiratory network component's particular sensitivity to perturbation by TTX or a dissociative trend in some bulbar respiratory rhythmogenic mechanisms. Peripheral cardiorespiratory changes were also quite profound. These included a gradual and steadfast decline in BP, a steadily decreasing amplitude in DEMG oscillations, and a state of progressive hypercapnia and hypoxemia. Changes in heart rate and ECG waveform attributes prior to respiratory arrest were not appreciable. In conclusion, in addition to a variety of TTX-induced peripheral cardiorespiratory effects, findings from this study have revealed a central respiratory system component that appears to show an unusual sensitivity to perturbation by TTX. The significance of this unique phenomenon as it relates to the nature and extent of TTX-induced central respiratory depression is discussed.
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PMID:Respiratory and cardiovascular effects of tetrodotoxin in urethane-anesthetized guinea pigs. 227 27

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

Respiratory disorders induce several pathophysiological changes involving gas exchange and acid-base balance, regional haemodynamics, and alterations of the alveolocapillary membrane. The consequences for the absorption, distribution and elimination of drugs are evaluated. Drug absorption after inhalation is not significantly impaired in patients. With drugs administered by this route, an average of 10% of the dose reaches the lungs. It is not completely clear whether changes in pulmonary endothelium in respiratory failure enhance lung absorption. The effects of changes in blood pH on plasma protein binding and volume of distribution are discussed, but relevant data are not available to explain the distribution changes observed in acutely ill patients. Lung diffusion of some antimicrobial agents is enhanced in patients with pulmonary infections. Decreased cardiac output and hepatic blood flow in patients under mechanical ventilation cause an increase in the plasma concentration of drugs with a high hepatic extraction ratio, such as lidocaine (lignocaine). On a theoretical basis, hypoxia should lead to decreased biotransformation of drugs with a low hepatic extraction ratio, but in vivo data with phenazone (antipyrine) or theophylline are conflicting. The effects of disease on the lung clearance of drugs are discussed but clinically relevant data are lacking. The pharmacokinetics of drugs in patients with asthma or chronic obstructive pulmonary disease are reviewed. Stable asthma and chronic obstructive pulmonary disease do not appear to affect the disposition of theophylline or beta 2-agonists such as salbutamol (albuterol) or terbutaline. Important variations in theophylline pharmacokinetics have been reported in critically ill patients, the causes of which are more likely to be linked to the poor condition of the patients than to a direct effect of hypoxia or hypercapnia. Little is known regarding the pharmacokinetics of cromoglycate, ipratropium, corticoids or antimicrobial agents in pulmonary disease. In patients under mechanical ventilation, the half-life of midazolam, a new benzodiazepine used as a sedative, has been found to be lengthened but the underlying mechanism is not well understood. Pulmonary absorption of pentamidine was found to be increased in patients under mechanical ventilation. Pharmacokinetic impairment does occur in patients with severe pulmonary disease but more work is needed to understand the exact mechanisms and to propose proper dosage regimens.
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PMID:The effect of respiratory disorders on clinical pharmacokinetic variables. 229 69

Three patients with mitochondrial myopathies and progressive external ophthalmoplegia had repeated episodes of respiratory failure requiring assisted ventilation. Studies in these patients and asymptomatic family members, as well as a sporadic case of Kearns-Sayre syndrome, demonstrated markedly depressed ventilatory drive responses to hypoxia. In 2 patients, there was also decreased drive to hypercapnia. The reduced ventilatory drive appears to be due to an altered neural control system that may cause episodic life-threatening hypoventilation occurring especially in relation to surgery, sedation, or intercurrent infection.
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PMID:Recurrent respiratory insufficiency and depressed ventilatory drive complicating mitochondrial myopathies. 229 55

Respiratory arrests occur in the clinical setting of respiratory failure, but the mechanism is unclear. We used a dog model with increased inspiratory resistance and hypoxemia to explore the cause. We hypothesized that respiratory muscle fatigue (RMF) played a role in these respiratory arrests, and that the combination of hypoxia and resistive loading would produce respiratory arrest by the mechanism of RMF. Our preparation had transdiaphragmatic pressures that were 40% of maximum (Pdimax = 46.3 +/- 10.0 cm H2O) and progressive hypoxia resulting in a final arterial PO2 of 38 +/- 9 mm Hg and a phrenic vein O2 content of 1.8 +/- 1.1 mg/dl. Instead of failure associated with carbon dioxide retention and RMF, we saw a rapid decrease in tidal volume and respiratory rate, leading to apnea over 30 to 60 s while the diaphragm still responded with significant pressure generation when externally stimulated. These results suggest that respiratory muscle fatigue may not be a major factor in respiratory arrests associated with inspiratory loading and hypoxia, but that suppression of central drive, induced by the combination of inspiratory loading and hypoxemia, may be important.
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PMID:The mechanism of respiratory arrest in inspiratory loading and hypoxemia. 232 56

Previous reports have disclosed a high morbidity and mortality in hospitalized asthmatics, especially those treated in the intensive care unit. Recently, it has been questioned whether the benefits of treating asthmatics in the intensive care unit outweigh the potential hazards. To address this issue, we examined the outcome of status asthmaticus in our medical intensive care unit between January 1, 1978, and December 31, 1987. Eighty episodes of status asthmaticus occurred in 64 patients. In 50 episodes, respiratory failure (PaCO2 greater than 50 mm Hg) was present. In half of these episodes, mechanical ventilation was avoided despite severe acidosis and hypercapnia; in the remainder mechanical ventilation was required as a lifesaving measure. Most patients improved rapidly and required only a short stay in the intensive care unit. There were no deaths and few complications. This was accomplished by close monitoring and repetitive blood gas analysis. We believe that the previous high complication rates and mortality associated with the hospital care of status asthmaticus can be avoided.
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PMID:Intensive care of status asthmaticus. A 10-year experience. 236 33

This study analyzed the history, clinical characteristics, and acid-base data in relation to the speed of decompensation in 34 patients intubated and mechanically ventilated for severe asthma. Three patterns of decompensation were established according to the delay between the onset of symptoms and endotracheal intubation: Group I, rapid decompensation (less than 3 hours); Group II, gradual development of respiratory failure (9.2 +/- 7.7 days); Group III, acute exacerbation after unstable asthma (4.2 +/- 3.6 days). Patients who developed sudden asphyxia (Group I) showed features distinct from those with a gradual worsening. Sudden asphyxic asthma is more frequent in young men and is characterized by a severe mixed acidosis with extreme hypercapnia (mean PaCO2 = 112.8 +/- 43.9 mm Hg), a higher incidence of respiratory arrest, and silent chest upon admission. Recovery is more rapid, with a shorter duration of mechanical ventilation (33.7 +/- 25.3 h versus 91.4 +/- 64.1 h in Group II). Several arguments suggest that bronchospasm plays the primary role in the pathogenesis of sudden asphyxic asthma.
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PMID:Sudden asphyxic asthma: a distinct entity? 236 57

On the basis of literature analysis and clinical experience, a classification of external respiratory failure (ERF) is suggested. The types of ERF can be as follows: 1) pulmonary ventilation failure; 2) gas diffusion failure; 3) pulmonary blood flow failure; 4) respiration control failure; and 5) ambient air gas composition change. The forms of ERI can be classified as acute, subacute and chronic. The stages of ERF include the following: I (compensatory) with pulmonary ventilation function drop of degree I-III (of an obstructive, restrictive and mixed type) and without hypoxemia, normo- or hypocapnia; II (subcompensatory) with the same pulmonary ventilation failures, moderate or serious hypoxemia, normo- or hypocapnia; III (decompensatory) with hypoxemia and hypercapnia or extremely severe hypoxemia in combination with normo- or hypocapnia.
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PMID:[Pathophysiological classification of external respiratory failure]. 239 45

The ability to manage acute airway obstruction can be life-saving. Airway relief should be expeditious and immediate, with low morbidity and mortality. It should not interfere with future definitive therapy. In patients with terminal malignancy, it should be economical in cost and should minimize hospitalization. We used biopsy forceps and the rigid bronchoscope to "core out" 56 patients with obstructing airway neoplasms. The location of the obstruction was trachea in 16 patients, carina in 24, main bronchi in 8, and distal airway in 8. Improvement in the airway was accomplished in 90% of patients. A single bronchoscopy was sufficient in 96%. Nineteen complications occurred in 11 patients: pneumonia in 5, bleeding in 3, pneumothorax in 2, hypoxia/hypercarbia in 2, arrhythmias in 6, and laryngeal edema in 1. There were four deaths within 2 weeks of core-out related to respiratory failure. Further therapy consisted of resection in 28.6% (tracheal in 9, carinal in 3, pulmonary in 4), irradiation alone or in combination with chemotherapy in 60.7%, and no therapy in 10.7%. Palliation of symptoms and establishment of an airway in acute obstruction is the goal. Survival depends on the effectiveness of the proposed treatment. We find this time-honored method superior to use of the laser.
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PMID:Endoscopic relief of malignant airway obstruction. 247 87


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