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)

1-(2-Methoxy-2-phenyl)-ethyl-4-(2-hydroxy-3-methoxy-3-phenyl)-propyl-iperazine-dihydrochloride (zipeprol, Respilene) is a substance of non-phenanthrenic chemical structure. In the cat, it antagonised cough induced by stimulation of the superior laryngeal nerve or by direct mechanical excitation of the sensitive tracheo-bronchial receptors. The efficacy of zipeprol after enteral administration made it possible both to establish good intestinal absorption and to rank it favourably in relation to several major antitussive reference products; codeine, codethyline, dextromethorphan, diphenhydramine and pentoxyverine. The activity of zipeprol was superior or equal to that of all these substances, excdept codeine. The antitussive properties appeared to be due to a central action. Other properties have been demonstrated which suggest at least a supplementary mechanism in the inhibition of cough, in addition to the central action. These consisted of slight antihistamine and anticholinergic properties, marked local-anesthetic potency and bronchospasmolytic activity. This latter property was demonstrated by the inhibition of histamine and serotonin induced bronchospasm in the guinea-pig. In vitro, using human sputum, zipeprol had a mucolytic action, shown by a decrease in sputum vis viscosity and lysis of DNA and AMPS fibrils. In the dog, at high doses, zipeprol unlike codeine, did not inhibit central stimulation of respiration by hypercapnia, in addition no modification of ventilatory dynamics or blood gases was seen. On the basis of these results, zipeprol can be considered as possessing no respiratory depressant effect even in the upper ranges of its antitussive doses.
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PMID:General pharmacological properties of a new non-opiate antitussive: zipeprol (3024 CERM). I. Action on respiratory function and acute toxicity. 0 57

Because of the close anatomic and physiologic relationship between the heart and lungs, patients with chronic obstructive lung disease are at special risk of arrhythmias. Effective therapy hinges on identifying the mechanisms of the arrhythmias--hemodynamic, metabolic, or drug-induced. Impulsive use of antiarrhythmic agents may result only in a more complex and dangerous rhythm disorder. Extremes of pH are a major cause of arrhythmias in these patients. Respiratory alkalemia usually originates with inappropriate ventilation, often during mechanical respiration, while metabolic alkalemia generally can be traced to diuretic or bicarbonate therapy. Lidocaine or diphenylhydantoin are of little use, since the alkaline pH inside and outside heart muscle cells hampers drug distribution and activity. At the other extreme, the arrhythmias of acidemia strike patients who have severe respiratory failure with carbon dioxide retention or severe cardiac failure with shock and lactic acidemia. Arrhythmias may develop if vagal restraint is lost, which is especially likely in patients with potassium depletion. Irritant receptors along the bronchopulmonary tree can trigger arrhythmias if stimulated by cough, microembolism, or mechanical irritation, which is a hazard with endotracheal or tracheostomy tubes.
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PMID:Mechanisms of arrhythmias in chronic obstructive lung disease. 1 Feb 30

1. Patients should be divided preoperatively into low- or high-risk categories, depending on their probability of developing postoperative pulmonary complications. The evaluation should include spirometry as well as an assessment of the previously defined risk factors. 2. Patients in a low-risk category need only instruction in deep breathing pre- and postoperatively. Routine use of supplemented oxygen postoperatively is reasonable until it can be demonstrated whether such is necessary. 3. High-risk patients should be as free as possible of respiratory secretions at the time of surgery. A regimen for this purpose includes cessation of smoking, and administration of inhaled bronchodilators followed by chest percussion and postural drainage. 4. High-risk patients should be carefully instructed in deep breathing and coughing preoperatively. A mechanical device such as an incentive spirometer may be beneficial in this regard. If it is not possible to achieve spontaneous deep breathing, an attempt to accomplish this by IPPB may be undertaken. The tidal volume desired should be ordered. If IPPB does not result in large tidal volumes, it should be discontinued. 5. The deep breathing procedure found to be most successful preoperativelly should be continued postoperatively. 6. The patient should be as mobile as possible while in bed and ambulated as soon as is feasible. 7. Patients with preoperative expiratory flows of less than 20% of predicted values or with chronic hypercapnia should be carefully observed for postoperative ventilatory failure.
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PMID:Pulmonary complications of general surgery. 32 60

Cough responses evoked by mechanical stimulation of the tracheobronchial mucosa in anesthetized and tracheostomized dogs were studied. The most common response was a group of coughs. Phase relationships between coughing and spontaneous respiration during the cough initiation and resolution periods were categorized as either synchronized or unsynchronized. We defined the synchronization as the coincidence of an expiratory thrust and the early-expiratory phase of respiration. During the cough initiation period, the incidence of synchronization increased as central respiratory activity was enhanced by hypercapnia or as the cough center's activity was suppressed by deep anesthesia. Synchronization decreased as central expiratory activity was enhanced by expiratory threshold loading. During the cough resolution period, synchronization occurred in conjunction with a gradual decrease in the cough center's activity. Coughing could be evoked when the dog was made apneic either by hyperventilation or by the Hering-Breuer reflex. In either case, apnea persisted after coughing subsided. These findings suggest that mechanical stimulation directly activates the cough center rather than the respiratory center; and that synchronization is determined by the relative strengths of the respiratory and cough center's activities.
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PMID:Influence of central respiratory activity on the cough response in anesthetized dogs. 180 71

In experiments on 10 adult anaesthetized cats (pentobarbital 30 mg.kg-1 i.p.) the effect of stimultaneous hypoxia and hypercapnia was studied on the defence respiratory reflexes of the airways. Expiratory reflex and cough were elicited by mechanical stimulation of the airways mucosa, and the obtained values were evaluated on basis of the intrapleural pressure. Inhalation of the hypoxic-hypercapnic gas mixture (11% + 7% CO2 in N2) for 15 minutes led to a significant decrease of respiratory frequency, tidal volume and PaCO2, while pHa and PaCO2 also decreased significantly together with the intensity of the expiratory reflex and that of cough. Recent studies, showed that in the course of the effect of hypoxia (11% O2) and of hypercapnia (5% CO2), cough intensity decreased, but the change was not significant. The decrease of the intensity of respiratory defence reflexes under hypoxic-hypercapnic conditions might have been due to the changes of centrally controlling structures, or to the effector part of the reflex arc, resulting from fatigue of the respiratory muscles. The possible effect of anaesthesia exerting a significant influence on the intensity and character of airways defence reflexes could not be excluded.
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PMID:Effect of hypoxia and hypercapina on the airways defence reflexes. 312

The impulse activity of bulbar respiratory neurons and the electrical activity of main respiratory muscles were studied stereotaxically and electromyographically on 21 male and female cats anesthetized with pentobarbital (40 mg/kg, i.p.) during defensive respiratory (expiratory and coughing) reflexes. During stimulation of laryngopharyngeal and tracheobronchial receptors, a pronounced focus of excitation appears in the bulbar respiratory centre, its peripheral manifestation being powerful electrical activity of expiratory muscles (expiratory reflex) or of both expiratory and inspiratory muscles (coughing). Respiratory defensive reflexes are very powerful and stable and are retained in hypercapnia and hypoxia.
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PMID:[Electrophysiological evaluation of the intensity of protective respiratory reflexes]. 362 Jun 50

To evaluate the contribution of vagal airway receptors to ventilatory control during hypercapnia, we studied 11 normal humans. Airway receptor block was induced by inhaling an aerosol of lidocaine; a preferential upper oropharyngeal block was also induced in a subgroup by gargling a solution of the anesthetic. Inhalation of lidocaine aerosol adequate to increase cough threshold, as measured by citric acid, did not change the ventilatory response to CO2, ratio of the change in minute ventilation to change in alveolar PCO2 (delta VI/delta PACO2), compared with saline control. Breathing pattern at mean CO2-stimulated ventilation of 25 l/min showed significantly decreased respiratory frequency, increased tidal volume, and prolonged inspiratory time compared with saline. Resting breathing pattern also showed significantly increased tidal volume and inspiratory time. In nine of the same subjects gargling a lidocaine solution adequate to extinguish gag response without altering cough threshold did not change delta VI/delta PACO2 or ventilatory pattern during CO2-stimulated or resting ventilation compared with saline. These results suggest that lower but not upper oropharyngeal vagal airway receptors modulate breathing pattern during hypercapnic as well as resting ventilation but do not affect delta VI/delta PACO2.
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PMID:Effects of upper or lower airway anesthesia on hypercapnic ventilation in humans. 405 88

The findings of this clinical study suggest that the ETTS/MH procedure could be safely performed upon patients with severe closed head injuries whose baseline measurements of MICP were within the range of 0 to 20 mm Hg, provided the CPP was maintained at 50 mm Hg or greater. The advantages of performing the ETTS/MH procedure upon intubated patients far outweigh the possible disadvantages. The removal of pulmonary mucus plugs and secretions, which subsequently prevents hypercarbia and hypoxemia, is very important to the patient's recovery. In most situations, stimulation of the cough reflex through ETTS or even MH can help prevent atelectasis, a frequent pulmonary complication of neurologically depressed patients. Atelectasis can result in hypoxia that may adversely affect the cerebrovascular status. In addition, the results of this study suggest that multiple MHs after the third and subsequent ETTSs should be extended to a longer time interval, perhaps 60 seconds, in order that the physiologic measurements of MABP, MICP, CPP, and HR more closely approach the baseline levels. Also it is suggested that nurses performing the ETTS/MH procedure delay initiation of levels of physiologic function used to assess cerebrovascular status are reached.
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PMID:The effects of the endotracheal tube suctioning/manual hyperventilation procedure on patients with severe closed head injuries. 656 6

In early phases of neuromuscular disease, patients are either free of respiratory symptoms or have exertional dyspnea not explained by obvious obstructive or restrictive lung disease. Physical examination may be negative because generalized muscle weakness does not correlate with the degree of respiratory muscle involvement. When the diaphragm is involved, one may detect the absence of outward excursion during inspiration or even paradoxic inward inspiratory movement of the abdomen on one side. A substantial loss of respiratory muscle strength is typically accompanied by little or no change in spirometry or arterial blood gas composition. Other characteristics are moderate loss of maximal voluntary ventilation and an increase in residual volume, yet PImax and PEmax may be as low as 50% of the predicted value. In more advanced neuromuscular disease, patients may have severe symptoms if the onset is acute or subacute; however, patients with chronic advanced generalized muscle weakness do not exercise and, therefore, may not be breathless. Many patients with advanced neuromuscular disease present with daytime somnolence as a manifestation of a sleep-related breathing disorder. Physical examination may reveal generalized muscle weakness and difficulty with speech or swallowing. Signs specific to respiratory involvement include tachypnea, use of neck inspiratory muscles and abdominal expiratory muscles, and loss of chest-abdomen synchrony. Sometimes paradoxic bilateral inward movement of the abdomen with inspiration is overt. Patients may be unable to cough effectively, have scoliosis, and lack a gag reflex. At this advanced stage, PImax and PEmax are lower than 50% of the predicted value, and the vital capacity is reduced. Maximal voluntary ventilation increases, and residual volume increases further. Patients may not yet exhibit CO2 retention during the day and may even have a low PaCO3. A sleep study may reveal significant hypopneas with severe desaturation and hypercapnia, especially during REM sleep. It is important to be aware that overt ventilatory failure can occur abruptly and that measurement of arterial blood gas composition is not a reliable indicator of this danger. Therefore, it is critically important to heed clinical phenomena, such as increasing dyspnea and tachypnea, and symptoms of sleep disturbance, such as morning headache and daytime somnolence. Physicians should make serial measurements of VC and respiratory muscle strength in patients considered to be at risk for further deterioration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Assessment of ventilatory function in patients with neuromuscular disease. 786 89

The upper airway performs three distinct functions that must be coordinated to allow maximal operation of each individual system. We tested the ventilatory response to progressive hypercapnia in seven normal adults during continuous swallowing. Swallowing was induced by oral infusion of water while the subject breathed through the nose. Infusion of 40 ml/min resulted in repetitive swallows (rate: 8.1 +/- 4.1 swallows/min, mean +/- SD), but this did not cause a single incidence of coughing or aspiration. Swallows interrupted inspiration and expiration and resulted in compensatory changes in tidal volume and breathing frequency. Continuous drinking did not significantly change the slope of the ventilatory response to hypercapnia. The test was repeated in three subjects swallowing water infused at 60, 80, and 100 ml/min. The slope of the response was also not significantly different from control in these tests. We conclude that continuous swallowing does not override ventilatory control mechanisms in human adults.
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PMID:Control of ventilation during continuous swallowing. 795 52


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