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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several well controlled epidemiologic and hemodynamic studies suggest that about 20% of sleep apnea syndrome (SAS) patients will have chronic obstructive pulmonary disease (COPD), and the majority of these patients (with combined diseases) will have pulmonary hypertension. Indeed it has been suggested that only patients with underlying hypoxemia, such as that from COPD, will develop right heart failure in the OSA setting. Experience shows that apnea/COPD patients will have severe hypersomnolence associated with the OSA, cough and dyspnea with the airways disease, and edema and plethora related to chronic hypoxemia. Many patients present with respiratory failure and are diagnosed at the time of initial intubation and mechanical ventilation. Episodic nocturnal hypoxemia may be worsened by a steeper rate of desaturation due to lower alveolar and blood oxygen stores, and longer apneas perhaps contributed to by depressed chemosensitivity. Daytime hypoxemia may also add to the severe hemodynamic disturbances. Since COPD cannot be cured, aggressive treatment of SAS is critical. Past studies have shown that tracheostomy or nasal CPAP in this setting not only leads to resolution of episodic nocturnal desaturation but may lead to rapid improvement in daytime oxygenation in many patients. Pulmonary hypertension and other measures of cardiopulmonary function improve when apnea is cured. Elimination of the SAS may disclose nonapneic REM related desaturation that could require supplemental oxygen therapy in addition to tracheostomy or nasal CPAP. Pulmonary function testing in SAS patients with smoking histories, followed by aggressive treatment of SAS, is recommended.
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PMID:Chronic lung disease in the sleep apnea syndrome. 211 88

The upper airway is not a simple solid conduit for respiratory airflow. It is also concerned with digestive and defense functions and vocalization. Therefore, it can be recognized as a complex organ to regulate these complex functions. There are three valve-like structures in the upper airway, i.e., the nasal cavity, pharynx and vocal cord. Therefore, airflow is controlled and sometimes obstructed in these particular regions, a phenomenon called airway collapse. In order to maintain the patency of the upper airway during inspiration, it is mandatory to elicit simultaneous activation of both respiratory and upper airway muscles. Even in normal healthy subjects, strong contraction of the respiratory muscles without accompanying activation of the upper airway muscles, such as in hiccups, results in airway collapse. In recent years, a number of physiological and pathophysiological studies have been accomplished to elucidate the mechanisms of the upper airway collapsibility. Particularly, the passive mechanism concept to explain obstructive sleep apnea during REM sleep advocated by Remmers and Guilleminault has substantially contributed to the recent development of research activities in this field. Important new findings related with this topic were presented by Drs. Fukuda, Kitagawa, Hida, Ohi and Kawakami in this symposium. In relation to the swallowing reflex and cough mechanism, interesting discoveries were also reported by Drs. Nishino and Sekizawa.
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PMID:[Respiratory functions of the upper airway with special reference to physiological implications of respiratory disease]. 235 83

Nineteen hydrocephalic patients were studied to determine factors affecting cerebrospinal fluid (CSF) flow through shunts. This study was based on our previously reported method by which fluctuations in CSF flow through a shunt of from 0.01 ml min-1 to 1.93 ml min-1 were identified, each having its own rhythmic pattern. While CSF flow in a supine position was less than 0.01 ml min-1, head elevation to 60 degrees led to increases in CSF flow from 0.12 ml min-1 to 0.17 ml min-1. Sudden respiratory changes such as coughing also affected CSF flow. CSF flows were higher than average between 10 pm and 7 am, and changes in CSF flow were related to slight increases in ICP during REM sleep. There is no relationship between CSF flow in a shunt and daily fluid intake which varied from 27 ml kg-1 to 103 ml kg-1, and no significant changes in CSF flow resulting from rapid intravenous injection of Glycerol and Ringer's solution.
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PMID:Factors affecting cerebrospinal fluid flow in a shunt. 326 43

In chronically implanted rats, we examined the respiratory EMG activity of the two parts of the diaphragm, costal and crural, during sleep and wakefulness. Their activity was compared and contrasted with that of the EMG activity of the cricothyroid muscle. Whether in wakefulness, while grooming and drinking, or in nonrapid eye movement (non-REM) sleep, and independent of the gas mixture breathed (4 to 5% CO2 or 10% O2 in nitrogen), the two parts of the diaphragm paused during REM apnea episodes whereas the cricothyroid muscle ceased its activity or exhibited sustained activity. We conclude that the diaphragm, mainly an inspiratory muscle, acts as a single functional unit when under the respiratory control system. The cricothyroid muscle functions as an inspiratory and/or expiratory muscle, also under the respiratory control systems. Both muscles in the rat come under other neural control mechanisms governing nonrespiratory functions, e.g., swallowing, defecation, and coughing, but not vomiting.
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PMID:Unity of costal and crural diaphragmatic activity in respiration. 393 Feb 80

A 9-year-old boy with respiratory disturbance associated with medullary lesions after pneumococcal meningitis is reported. Although he lives a normal daily life, he cannot cough or sneeze. A polysomnographic study revealed a low respiration rate and an irregular respiratory rhythm not only during REM sleep but also during slow wave sleep, and marked desaturation during sleep. Respiratory function tests including CO2 response revealed normal values. Magnetic resonance imaging demonstrated bilateral small lesions in the medulla. This patient is unusual because respiratory rhythm is impaired, without decreased ventilatory capacity or CO2 response, supporting the possibility that rhythmogenetic respiratory neurons are located in a limited area of the human medulla.
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PMID:Impairment of respiratory rhythmogenesis and sequelae of bacterial meningitis. 754 11

Cerebrospinal fluid (CSF) in a shunt does not have a constant flow rate. The flow fluctuates from 0.01 ml/min to 1.93 ml/min according to each patient's own daily supine rhythmic pattern. We determined and evaluated the factors influencing CSF flow in a shunt in 19 cases of hydrocephalus. Postural changes, such as head elevation, led to increases by over 0.04 ml/min in inshunt CSF flow, while inshunt CSF flow in the supine position was less than 0.04 ml/min. Respiratory changes, such as coughing and apnea-hyperventilation, also influenced inshunt CSF flow. Changes in intracranial pressure (ICP) corresponded to changes in inshunt CSF flow. Inshunt CSF flows were higher than average during the night, the flows being stimulated by increases in ICP especially during REM sleep.
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PMID:CSF shunt physics: factors influencing inshunt CSF flow. 762 80

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

Charcot-Marie-Tooth disease (CMT) is a slowly progressive hereditary neuropathy characterised by degeneration of motor and sensory peripheral nerves resulting in distal muscle weakness with atrophy and sensory impairment. We report a 35-year-old woman with CMT presenting with respiratory failure due to a pneumonia, sputum impaction and insufficient cough reflex. After recovery, we diagnosed a very severe restrictive lung function disturbance caused by muscle weakness and a possible coexistent unilateral diaphragm paralysis. A very severe REM (Rapid Eye Movement Sleep) related sleep hypopnea syndrome was successfully treated with Nasal Intermittent Positive Pressure Ventilation (NIPPV).
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PMID:Intermittent positive airway pressure by nasal mask as a treatment for respiratory insufficiency in a patient with Charcot-Marie-Tooth disease. 1709 14

Hypercapnic respiratory failure is usually caused by an overload of the respiratory muscles (respiratory pump). After treatment of the underlying disease, mechanical ventilation will achieve optimal treatment success and higher degrees of respiratory muscle unloading will improve the outcome in terms of lower PaCO (2) levels and improved exercise performance. Routinely assisted modes are being used for ventilation, where the patient has to trigger the ventilator with his effort. Controlled ventilation is usually applied in sedated patients lacking spontaneous breathing efforts that are necessary to trigger the ventilator. Controlled ventilation, however, is feasible in awake patients but requires operator expertise. In this process, the respiratory pattern of the ventilator has to be adapted to the patient's own respiratory pattern. Changing conditions require a re-adaptation of parameters. In order to automatise this complex and time-consuming operation, a time-adaptive mode (TA-mode) has been developed. This programmed mode incorporates a self-learning algorithm, primarily detecting the patient's respiratory pattern. The software then calculates a matching flow profile using a motion equation that gives consideration to resistance and compliance. The operator has to pre-select allowed ranges of parameters (especially in- and expiratory pressures, IPAP and EPAP). After detection of a stable respiratory pattern (usually after 10 - 20 breaths), the ventilator will slowly increase the calculated flow profile and achieve controlled ventilation without irritating respiratory centres of the brain. Respiratory drive will cease usually within three to five minutes. Restart of the respiratory drive, for example, after coughing or during REM sleep with an altered respiratory pattern will be detected as ventilator fighting and the programme will return to the analysis algorithm again. After the respiratory pattern has become stable, the ventilator will take over ventilation again. The new mode has been validated in an accreditation study. For this purpose we selected 21 patients with stable hypercapnic respiratory failure, most of whom (20) had previously been ventilated with a controlled T-mode and only one patient had previously been ventilated with an assisted mode and adapted them to the new ventilator under polygraphic surveillance. Each time seven patients were adapted to a T-, ST- and TA-mode, respectively. Two patients, however, could not be adapted to ST-mode ventilation and were switched to TA-mode. PCO (2) values before and after ventilation were not significantly different between modes. Patient satisfaction was rated very good in 34 %, good in 45 % and non-gratifying in 21 % of cases ventilated with TA-mode. Consideration has to be given to the fact that patients previously had been receiving optimal ventilator treatment. The TA-mode is a self-learning system, capable of copying the patients own breathing pattern while awake, in order to achieve complete unloading of the respiratory muscles through controlled ventilation during a circumscribed period.
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PMID:[Time-adaptive mode, a new ventilation form for the treatment of respiratory insufficiency--a self-learning system]. 1843 1

Cough and sleep are vital functions. The effects of cough on sleep and vice versa are important for a number of reasons. Sleep disruption is common in patients with cough and is often the reason why they seek medical attention. Sleep suppresses cough and the biological mechanisms for this action are poorly understood. Cough has recently been reported as a presenting symptom of obstructive sleep apnea. It is uncommon for healthy people to cough at night; however, approximately 50% of patients with chronic cough report sleep disruption due to cough. Cough frequency is much lower at night than during the day. There is reduced exposure to tussive stimuli at night and decreased cough reflex sensitivity. Cough is more difficult to induce in REM sleep compared to slow-wave sleep. Studies of anesthetized humans have shown that the cough reflex is suppressed; however, the expiratory reflex is less affected. The sleep-cough interaction has implications for the physician. The measurement of cough frequency with 24-h ambulatory cough monitors in patients with chronic cough suggests that the presence or absence of nocturnal cough is not helpful in establishing the etiology. Nocturnal cough may be a useful outcome parameter for clinical trials of antitussive drugs since it is under less voluntary control than daytime cough. Most antitussive drugs are sedatives. This suggests that part or all of their action may be through an effect on cortical neural pathways. Unexplained chronic cough has recently been reported as a presenting feature of obstructive sleep apnea. Patients are likely to be female and report gastroesophageal reflux and rhinitis. Continuous positive airway pressure therapy is effective in alleviating cough. Greater awareness of this condition is needed.
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PMID:Cough and sleep. 1982 13


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