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

To go back to a period more than five decades ago to talk about the health left is to enter not just another time, but another world. Between the Great Depression and the postwar period, challenging and contradictory social, political, and professional developments were brought to the surface in U.S. life. The health left shared in the opportunities and confusion, enriching the American spirit and participating in both the pleasures and the pain. The 1930s saw economic depression, wars, the birth of fascism, and fears of social collapse. In medicine, despite sporadic scientific advances, the social response was remote and narrow. But social activism motivated medical students and medical practitioners. The 1940s marked a change in both attitudes and values. The left was divided, and bitter factionalism stymied cooperative action. Participation in the war against fascism promoted solidarity, despite the sadness of the evidence of brutality and lack of humanity. The 1950s are sometimes considered regressive, but seeds germinated as the complexity of medical life engendered new approaches to meeting sociomedical needs. As we entered the 1960s a different and more hopeful story unfolded as the rebellions of the poor, blacks, and women brought about a new era of social action.
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PMID:The health left in the 1930s, 1940s, and 1950s. 772 65

Dextropropoxyphene overdose may be complicated by serious cardiovascular manifestations, including conduction abnormalities and collapse. We report two patients in whom cardiac toxicity developed. Cardiovascular depression seemed to be improved after naloxone infusion in these two cases. Possible mechanisms are briefly discussed.
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PMID:Adverse cardiac manifestations following dextropropoxyphene overdose: can naloxone be helpful? 783 61

In an investigation of 2 closely related Miniature Horses with a history of excessive sleepiness, depression and episodes of collapse, a diagnosis of narcolepsy was made on the basis of neurological examination and pharmacological testing. Further investigations included electroencephalographic examination (EEG), and analysis of protein content, cell count and monoamine metabolite concentrations of lumbosacral cerebrospinal fluid (CSF). There were no abnormalities noted in the EEGs, and no consistent changes in CSF neurotransmitter metabolites in the narcoleptic horses when compared with 3 normal, unrelated Miniature Horses and 2 related, clinically unaffected animals. The breeding background of the 2 affected horses was investigated and a limited survey of Miniature Horse breeders in North America was conducted. These investigations have shown that narcolepsy is a rare but distinct syndrome in the Miniature Horse, and that the cases described here appear to represent a familial occurrence of the disease.
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PMID:Familial occurrence of narcolepsy in miniature horses. 827 92

Acute myocarditis is usually a self-limiting viral illness. Rarely, however, myocardial depression can be profound leading to circulatory collapse. Mechanical cardiac support in the form of intraaortic balloon pumps or ventricular assist devices have been used in these unusual cases to maintain systemic perfusion until transplantation or left ventricular recovery occurs. We report a young patient with acute myocarditis who required left heart mechanical support and who, however, was successfully weaned despite only minimal myocardial recovery.
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PMID:Temporary left-sided mechanical cardiac support during acute myocarditis. 803 10

Common tiger snake (Notechis scutatus) venom was injected into mice and dogs at various dose rates calculated on the known lethal dose (LD) for each species. The larger the dose of venom, the earlier was the onset of clinical signs and the more rapid and severe the course of the disease in both species. In dogs injected with 32 LD of venom, there was sudden collapse and death in about one hour from the time of injection without recovery from premonitory depression and before mydriasis occurred. Dogs given 5 to 16 LD of venom developed preparalytic signs (vomition, salivation or defaecation) in 5 to 30 min, mydriasis in 2 to 4 h, became paralysed and died in about 2.5 to 5 h. When doses of venom of about 1 LD were injected, vomition and salivation occurred within 2 h and mydriasis in about 4 h. The dogs were unable to close the mouth completely despite retention of jaw muscle tone. Sublethally envenomed dogs did not show preparalytic signs nor did they have general skeletal muscle paralysis. Even at the lowest dose tested (0.25 LD), however, they developed mydriasis and photophobia, which persisted for several days. At the site of injection of venom there was occasional but slight erythema and oedema.
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PMID:Common tiger snake envenomation in dogs and mice--relationship between the amount of venom injected and the onset of clinical signs. 806 44

Seizures followed by cardiac arrest after obstetrical epidural anaesthesia are induced by either low cerebral perfusion due to cardiovascular collapse after too excessive sympathetic blockade or after accidental total spinal anaesthesia, or by toxic accident due to accidental intravascular administration of local anaesthetic drugs. In case of toxic accident, convulsions usually occur before haemodynamic changes. Whatever the mechanism of the accident, excessive sympathetic blockade or toxic accident, when epidural anaesthesia is performed with lidocaine, bradycardia with normal QRS complexes occurs. Respiratory depression has to be treated and ephedrine has to be administered. In contrast, when bupivacaine is used, in case of toxic accident, there are dysrhythmias or bradycardia but QRS complexes are widened. The treatment is firstly to oxygenate, to stop convulsions and then to intubate the trachea and to ventilate the lungs.
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PMID:[Convulsions and cardiac arrest after epidural anesthesia. Prevention and treatment]. 808 41

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

The objective of this study was to test our hypothesis that pregnancy modifies the central nervous and cardiovascular toxicity of cocaine. Ten chronically catheterized term pregnant rats and 13 chronically catheterized nonpregnant female rats were infused with cocaine (2 mg/kg/min) intravenously to observe the sequential toxic manifestation of cocaine from mild central nervous stimulation (hyper-locomotor activities) to fatal cardiovascular collapse. Arterial blood samples were withdrawn at the onset of major toxic signs or symptoms--namely convulsion, hypotension, and circulatory collapse--for determination of cocaine concentrations and plasma cholinesterase activity. The dosage and plasma concentrations of cocaine associated with the onset of convulsions and cardiovascular depression were significantly lower in pregnant rats when compared with the nonpregnant animals. The mean time required to develop convulsions in the pregnant rat was significantly shorter (21 minutes) than that in the nonpregnant animal (33 minutes). However, once convulsive activity had developed, the time interval to achieve circulatory collapse was similar in both groups. Although the baseline plasma cholinesterase activity was higher in the pregnant rats than in the nonpregnant ones, the values in the samples obtained from the pregnant group at the onset of circulatory collapse were similar to the baseline values for the nonpregnant group. These findings suggest that a higher enzyme activity does not protect the development of toxic manifestations in the pregnant rat as compared to the nonpregnant animal when cocaine was administered at the same infusion rate.
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PMID:Pregnancy decreases the threshold for cocaine-induced convulsions in the rat. 824 93

Two-dimensional Doppler echocardiography was used as an intraoperative cardiac function monitor in anesthetic management of a 79-year-old male with hypertrophic obstructive cardiomyopathy (HOCM) who underwent pulmonary lobectomy for lung cancer. Circulatory collapse occurred after thoracic epidural anesthesia (TEA), and was aggravated with following induction of general anesthesia. The collapse did not improve with phenylephrine nor atropine and necessitated ethylephrine and dopamine. During the above course, left ventricular outflow tract pressure gradient measured with continuous wave Doppler method was almost in proportion to cardiac output measured with thermo-dilution method. This means that TEA and the administration of inotropics did not worsen the left ventricular outflow tract obstruction. Left ventricular filling property estimated by trans-mitral flow velocity spectra improved when hemodynamics was stabilized with continuous infusion of dopamine, while it had been impaired during preoperative period and at the beginning of anesthesia. Our observation suggests that TEA for HOCM patient is a relative indication because it may exert negative inotropic effect, and that careful titration with inotropics is not contraindicated when undesired cardiac depression is proved by echocardiography.
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PMID:[Echocardiographic observation of intraoperative circulatory collapse in a patient with hypertrophic obstructive cardiomyopathy]. 830 35

The medical records of five dogs diagnosed with infectious pericardial effusion were reviewed. Clinical signs included anorexia, depression, respiratory distress, abdominal distension, collapse, coughing, and vomiting. Anemia and leukocytosis were present in three dogs. Grass awn migration was confirmed as the cause of the pericardial effusion in two dogs and suspected in the other three. Surgery, followed by continuous chest drainage, and appropriate antibiotic therapy was the treatment in four dogs. Chest drains were removed within 4 days of surgery. One dog did not have chest drainage after surgery. Antibiotic treatment was continued for up to 6 months. The dogs were monitored postsurgically for a period ranging from 3 to 24 months. All dogs recovered well without apparent complications.
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PMID:Infectious pericardial effusion in five dogs. 858 48


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