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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with chronic respiratory insufficiency the treatment of the underlying pulmonary disease is of primary importance. However, many patients often also need symptomatic management to recompensate or stabilize impaired pulmonary gas exchange. The most suitable measures for this purpose are (1) ventilatory support by periodic intermittent positive pressure breathing (IPPB), (2) long-term oxygen administration and (3) respiratory stimulant drugs. IPPB provides good results if restricted to well defined indications (paO2 below 60 mm Hg, paCO2 above 45 mm Hg, forced expiratory volume [FEV1] below 40% of vital capacity or below 1000 ml). Long-term domiciliary oxygen therapy for at least 15 h daily prevents the early decompensation of cor pulmonale and improves physical performance. With the introduction of industrial O2-concentrators this form of therapy becomes more practicable and less expensive compared with the conventional method delivering compressed oxygen. However, the indication should be confined to patients with chronic and severe hypoxemia (paO2 below 50 mm Hg), pulmonary hypertension and secondary polycythemia. Respiratory stimulant drugs are useful in protecting patients from central respiratory depression during oxygen breathing. Aminophylline seems to be the most suitable drug simultaneously acting as a bronchodilator and vasodilator in the pulmonary circulation. To achieve a potent stimulant effect, serum theophylline levels above 10 microgram/ml through repeated intravenous administrations of aminophylline are required. Individual differences in the pharmacokinetic action of theophylline may sometimes need drug monitoring to prevent toxic side effects.
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PMID:[Therapy of chronic respiratory insufficiency]. 701 May 78

During the period from 1961 to 1981, 40 pulmonary embolectomies were performed in 39 patients who were in extremis at the time of initiation of cardiopulmonary bypass. In a 460-bed hospital with more than 17,000 acute admissions and 4,000 operations per year, this small number represents the few patients who are potentially salvageable by urgent embolectomy. Preoperative angiography was performed in 57% of the cases, and in another ten patients suspected of having pulmonary emboli, angiography prevented unnecessary thoracotomy. Despite their moribund condition, 43% of the embolectomy patients lived. Excluding two patients with tumor occlusion of the pulmonary arteries and three patients with chronic cor pulmonale from old pulmonary emboli, the survival rate was 50%. Ten patients died because of hypoxemia and hypotension prior to initiation of cardiopulmonary bypass, and seven died of myocardial depression of multiple etiologies. Portable cardiopulmonary bypass affords the possibility of survival in moribund patients with acute massive pulmonary embolism. Preoperative angiography is recommended to guide appropriate surgical management.
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PMID:Pulmonary embolectomy for acute massive pulmonary embolism. 708 65

The presenting symptom complex, diagnostic features, and therapeutic alternatives for obstructive and central sleep apnea are discussed in relation to two illustrative patients. Heavy snoring and restlessness during sleep in an obese individual, usually a male, may indicate obstructive apnea. Daytime hypersomnolence, intellectual deterioration, mental depression, impotence, cardiac arrhythmias, cor pulmonale, systemic hypertension, and erythrocytosis are the most common complications. Tracheostomy, the classic form of therapy, can be replaced by pharmacologic intervention in most patients. The clinical presentation of central apnea is less dramatic, but neurological and cardiac complications can occur. Therapy is less well established for this entity. Knowledge of the increased incidence of these disorders and awareness of more subtle complications indicate that sleep apnea should be placed in the differential diagnosis of pulmonary and systemic hypertension, hypersomnolence states, mental deterioration, psychiatric illness, and even insomnia.
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PMID:Diagnosis and therapy of sleep apnea. 722 83

The high prevalence of obstructive sleep apnea (OSA) has only recently been appreciated, in part because the symptoms and signs of chronic sleep disruption are often overlooked in spite of their debilitating consequences. They typically develop insidiously during a period of years. We now know that the lives of millions of people each year are significantly impaired by the sequelae of OSA. Many of these patients go unrecognized, with tremendous medical and economic consequences for individual patients and for society. Evidence indicates that chronic, heavy snoring may be associated with increased long-term cardiovascular and neurophysiologic morbidity. Therefore considerable interest lies in the study of the epidemiology and the natural history of these related disorders. The fundamental problem in OSA is the periodic collapse of the pharyngeal airway during sleep. The pathophysiology of this phenomenon is reviewed in some detail. During apneas caused by obstruction, airflow is impeded by the collapsed pharynx in spite of continued effort to breathe. This causes progressive asphyxia, which increasingly stimulates breathing efforts against the collapsed airway, typically until the person is awakened. Hypopneas predominate in some patients and are caused by partial pharyngeal collapse. The clinical sequelae of OSA relate to the cumulative effects of exposure to periodic asphyxia and to sleep fragmentation caused by apneas and hypopneas. Some patients with frequent, brief apneas and hypopneas and normal underlying cardiopulmonary function may have considerable sleep disruption without much exposure to nocturnal hypoxia. Patients with sleep apnea often have excessive daytime sleepiness. As the disorder progresses, sleepiness becomes increasingly irresistible and dangerous, and patients develop cognitive dysfunction, inability to concentrate, memory and judgment impairment, irritability, and depression. These problems may lead to family and social problems and job loss. Cardiac and vascular morbidity in OSA may include systemic hypertension, cardiac arrhythmias, pulmonary hypertension, cor pulmonale, left ventricular dysfunction, stroke, and sudden death. The challenge for the clinician is to routinely consider the diagnosis and to incorporate several basic questions in the historical review of systems regarding daytime or inappropriate sleepiness. The diagnosis of OSA is made with polysomnography, and the decision to treat is based on an overall assessment of the severity of sleep-disordered breathing, sleep fragmentation, and associated clinical sequelae. The therapeutic options for the management of OSA are reviewed. Recognition and appropriate treatment of OSA and related disorders will often significantly enhance the patient's quality of life, overall health, productivity, and safety on the highways.
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PMID:Obstructive sleep apnea. 814 53

There is intriguing evidence suggesting pathophysiologic relationships among dyspnea, hyperventilation, and panic anxiety. The symptoms of panic attacks and pulmonary disease overlap, so that panic anxiety can reflect underlying cardiopulmonary disease and dyspnea can reflect an underlying anxiety disorder. The pathogenesis of panic may be related to respiratory physiology by several mechanisms: the anxiogenic effects of hyperventilation, the catastrophic misinterpretation of respiratory symptoms, and/or a neurobiologic sensitivity to CO2, lactate, or other signals of suffocation. In a subset of patients with PD, incipient pulmonary dysfunction may also contribute to their anxiety symptoms. Patients with pulmonary disease, particularly those with obstructive lung disease, have a high rate of panic symptoms and PD. There is reason to believe that pulmonary disease constitutes a risk factor for the development of panic related to repeated experiences with dyspnea and life-threatening exacerbations of pulmonary dysfunction, repeated episodes of hypercapnia or hyperventilation, the use of anxiogenic medications, and the stress of coping with chronic disease. Panic in pulmonary patients may carry significant morbidity, including phobic avoidance of activity, overly aggressive treatment with anxiogenic medications, and more prolonged and frequent hospitalization. Successful treatment of panic in these patients can improve functional status and quality of life by relieving anxiety and dyspnea. Nonpharmacologic treatment of panic, including cognitive-behavioral approaches, can be useful in patients with concomitant respiratory disease. Sedating medications such as benzodiazepines should be used with caution in patients with pulmonary disease to avoid respiratory depression. Serotonergic antidepressants (SSRIs) and anxiolytics (buspirone) may be effective treatments for panic or generalized anxiety in pulmonary patients and have relatively little potential for significant adverse effects.
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PMID:Panic anxiety, dyspnea, and respiratory disease. Theoretical and clinical considerations. 868 Jul

Based on a case report, we offer brief guidelines on the perioperative management of patients with Sleep-Apnea-Syndrome (SAS) who present with a high incidence of a difficult airway and a high risk of respiratory depression during the perioperative period. A 39 year old male patient with a body mass index of 34.22 kg/m2 and receiving continuous-positive-airway-pressure-(CPAP) therapy for known SAS was scheduled for elective plastic surgery. After induction of anaesthesia and direct laryngoscopy no adequate airway could be established and the patient became hypoxic, hypercapnic and developed hypotension and bradycardia. With the use of a laryngeal mask airway the patient was stabilized and did not show neurologic sequale after immediate awakening. The following fiberoptic intubation of the awake patient, still showing tendency of upper airway obstruction, confirmed the difficult anatomical structures. The subsequent general anesthesia was uneventful. The patient received CPAP therapy and was monitored during the first postoperative night in the Intensive Care Unit. He made an uneventful recovery. He was advised to have regional anaesthesia or planned fiberoptic intubation, where possible, in the case of further anesthetic intervention. SAS has major implications for the anaesthesiologist and whenever patients exhibiting the high risk factors (obesity, male sex, history of intense snoring, impaired daytime performance, nonrefreshing daytime naps) are presented for surgery this condition should be considered. Elective surgery should be postponed until after adequate examination and treatment when necessary. Patients with SAS should always be suspected of having cardiopulmonary dysfunctions such as hypertension, cardiac dysrhythmia or cor pulmonale. It is most important to avoid sedative premedication, to initiate CPAP therapy preoperatively, to encourage regional anaesthesia if possible and to ensure close monitoring over the complete perioperative period. Planned fiberoptic intubation, preferably with surgical personnel available for an emergency airway, is a safe method for the induction of anaesthesia. Postoperatively, patients are at high risk from respiratory depression, even in the awake state. Postoperative opioid analgesia, no matter what route, should only be given under close monitoring. Independently of regional or general anaesthesia there is an increased risk of respiratory depression in the middle of the first postoperative week, suspected to be caused by the catching up on lost REM-sleep, due to shifts in the normal sleep pattern during the first postoperative days.
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PMID:[Induction of anesthesia for a patient with sleep apnea syndrome]. 1084 May 41

OBJECTIVE: The authors report what they believe is the first reported use of etomidate to assist in the reduction of a major joint in an outpatient setting. METHODS: The authors review the case of an elderly woman with a total hip arthroplasty who experienced four spontaneous posterior hip dislocations in a 5-month period. Etomidate was successfully used in two dislocations where previous methods had failed. RESULTS: A 68-year-old woman, who 13 months earlier had an uncomplicated total left hip replacement, was transported to the same ED on four separate occasions for a spontaneous left hip dislocation. Radiographs in each instance were significant only for a posterior dislocation of the implant articulation. The first reduction in the ED was unsuccessful and required a closed reduction in the operating theater. Seventy-two hours later the second dislocation and subsequent reduction occurred in the ED using etomidate to facilitate muscle relaxation. The patient was subsequently discharged home. Similar scenarios were replayed in the next few months. CONCLUSIONS: Muscle relaxation is the key characteristic for the reduction of dislocated major joints. The risks of respiratory depression and hemodynamic alterations with sedation are not insignificant, especially at the extremes of age. In the present case, intravenous narcotics and sedative-amnestic agents did not result in sufficient muscle relaxation. Larger or repeated doses may have resulted in undesirable or dangerous side effects. Etomidate is a useful adjunct when cardiopulmonary disease is present. The rapid onset and recovery from etomidate make it an excellent choice for facilitating the reduction of hip dislocations in elderly patients with prior total hip replacements.
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PMID:Etomidate-facilitated hip reduction in the emergency department 1101 54

In the UK the prevalence of chronic obstructive pulmonary disease has been estimated at one per cent, rising to five per cent of men aged 65-74 years and 10 per cent of men aged over 75 years. It is thought that only a quarter of COPD cases are diagnosed (Calverley and Bellamy, 2000). The symptoms of breathlessness, chronic cough, and regular sputum production usually develop insidiously. However, COPD not only affects the lungs but has extra pulmonary effects such as muscle wasting and weight loss, pulmonary hypertension, cor pulmonale (enlargement of the right side of the heart), anxiety, and depression.
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PMID:NICE guidelines for chronic obstructive pulmonary disease--a review. 1522 93

Obstructive sleep apnea (OSA) occurs commonly in the U.S. population and is seen in both obese as well as non-obese individuals. OSA is a disease characterized by periodic upper airway collapse during sleep, which then results in either apnea, hypopnea, or both. The disorder leads to a variety of medical complications. Neuropsychiatric complications include daytime somnolence, cognitive dysfunction, and depression. Increased incidence of motor vehicle accidents has been documented in these patients and probably reflects disordered reflex mechanisms or excessive somnolence. More importantly, vascular disorders such as hypertension, stroke, congestive cardiac failure, arrhythmias, and atherosclerosis occur frequently in these patients. The lungs may be affected by pulmonary hypertension and worsening of asthma. Recent data from several laboratories demonstrate that obstructive sleep apnea is characterized by an inflammatory response. Cytokines are elaborated during the hypoxemic episodes leading to inflammatory responses as marked clinically by elevated C-reactive protein (CRP). As elevated CRP levels are considered markers of the acute phase response and characterize progression of vascular injury in coronary artery disease, it is likely that obstructive sleep apnea could lead to worsening of vasculopathy. Moreover, as inflammatory mechanisms regulate bronchial asthma, it is also likely that cytokines and superoxide radicals generated during hypoxemic episodes could exacerbate reactive airway disease. Patients with Cough, Obstructive sleep apnea, Rhinosinusitis, and Esophageal reflux clustered together can be categorized by the acronym, "CORE", syndrome. The purpose of this manuscript is to review the inflammatory responses that occur in patients with obstructive sleep apnea and relate them to the occurrence of cardiopulmonary disease.
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PMID:Obstructive sleep apnea, inflammation, and cardiopulmonary disease. 1535 23

A 53-year-old right-handed man was scheduled to receive 6 treatments of electroconvulsive therapy (ECT) for intractable depression. He was being treated for long-standing hypertension with nadolol and had no history of cardiopulmonary disease. Six months previously, he received 6 nondominant, unilateral ECT treatments. During each of these treatments, his blood pressure increased transiently to as high as 250/150, but he experienced no adverse consequence. He commenced the current course of ECT with well-controlled blood pressure (145/90). During his first bilateral treatment, his blood pressure rose to 280/160, and pulmonary edema ensued. Clinically evident pulmonary edema after ECT is an uncommon event that rarely has been described in the literature.
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PMID:Excessive hypertension and pulmonary edema after electroconvulsive therapy. 1612 8


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