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

Decreased ventilatory responses to carbon dioxide (CO2) correlate with elevated scores on tests for depression in normal subjects and with episodes of endogenous depression in psychiatric patients. Patients with severe chronic obstructive pulmonary disease (COPD) frequently develop resting hypercapnia due to impaired ventilatory mechanics or drive, and may also have elevated scores on tests for depression. Tricyclic antidepressant drugs can improve ventilatory mechanics and possibly drive. We hypothesized that antidepressant drugs might enhance ventilatory drive and improve arterial blood gases in patients with severe COPD and that these improvements might correlate with improvement in depression scores. Therefore, we studied the effects of desipramine versus placebo on spirometry, resting arterial blood gases, hypercapnic ventilatory and mouth occlusion pressure responses, and scores on the Beck and Zung self-rated depression scales. In our patients the resting arterial CO2 (PaCO2) was found to depend almost equally on ventilatory mechanics and drive. In addition, patients with higher depression scores tended to have a lower PaCO2 when the severity of airways obstruction was taken into consideration. In a 16-week, double-blind, crossover comparison of desipramine with placebo, both treatments led to significant improvement in depression scores. Desipramine had no effects on resting PaCO2, spirometry, or ventilatory control.
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PMID:Effect of desipramine on control of ventilation and depression scores in patients with severe chronic obstructive pulmonary disease. 392 77

The objective of this study was twofold: (1) to document the prevalence of depression and anxiety in patients with moderate or severe chronic obstructive pulmonary disease; and (2) to determine whether the presence of depression or anxiety adversely affected the functional capabilities of the patient as reflected by the distance he could walk in 12 minutes. Forty-five patients with an FEV1 less than 1,250 ml underwent pulmonary function testing including spirometry, single breath diffusing capacity, and arterial blood gas determinations. The degree of depression was assessed by the Beck depression inventory, while the degree of anxiety was assessed by the State-Trait anxiety inventory. Forty-two percent of the patients had significant depression, while only 2 percent of the patients had significant anxiety. There was a highly significant correlation between the depression scores and the anxiety scores (r = 0.81, p less than 0.001). There was no significant correlation between the level of depression or anxiety and the distance that the patient could walk in 12 minutes. From this study, we conclude that the prevalence of depression in patients with moderate or severe COPD approaches 50 percent while the incidence of anxiety is much lower (2 percent).
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PMID:Prevalence of depression and anxiety in patients with COPD. Relationship to functional capacity. 396 63

The effects on the respiratory function of two tranquillising drugs, lorazepam and diazepam, have been compared in 20 patients with chronic obstructive lung disease. Both drugs induce a respiratory depression (decrease in tidal volume and minute ventilation with acceleration of the respiratory frequency) with slight respiratory acidosis, but lorazepam causes no significant hypoxemia and has a shorter duration of action than diazepam. Nevertheless, if tranquillisers are indicated in such patients, they have to be used with care.
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PMID:Double-blind comparison of the respiratory effects of parenteral lorazepam and diazepam in patients with chronic obstructive lung disease. 415 89

The physical and pharmacological properties of the structural isomers isoflurane and enflurane differ from each other and from those of other potent inhaled anaesthetics. The minimum alveolar concentration (MAC) for isoflurane (1.15%) is one-and-one-half times that for halothane (0.75%) and two-thirds that for enflurane (1.7%). The blood/gas partition coefficient (1.4) for isoflurane is lower than the coefficients for all other potent inhaled agents. Despite this lower blood solubility, induction of anaesthesia is slightly faster with halothane because of isoflurane's mild pungency. Enflurane depresses ventilation more than isoflurane, which in turn is slightly more depressant than halothane. All these agents dilate constricted bronchi, and thus are useful in the anaesthetic management of patients who have asthma or chronic obstructive pulmonary disease. Isoflurane has the largest circulatory margin of safety of all potent halogenated agents; it produces the least myocardial depression at a given multiple of MAC. Isoflurane may increase heart rate, particularly in younger patients, and occasionally is associated with tachycardia. It decreases total peripheral resistance, thereby decreasing systemic arterial pressure. Although results from one study suggest that isoflurane may produce a "steal" or coronary blood flow in patients with coronary artery disease, results from other studies suggest that, even in the presence of coronary artery disease, coronary blood flow to all parts of the heart remains as adequate with isoflurane as with other anaesthetics. Greater concentrations of isoflurane (1.6 MAC) increase cerebral blood flow less than does halothane. Isoflurane does not produce convulsive activity, but can produce profound muscle relaxation. It enhances the action of tubocurarine or pancuronium, and (to a lesser extent) vecuronium or atracurium. The enhancement is comparable to that produced by enflurane. Less enhancement is produced by halothane or nitrous oxide-narcotic. Only 0.17% of isoflurane taken up in man appears as urinary metabolites. This resistance to biodegradation may explain the minimal or absent hepatotoxicity and nephrotoxicity of isoflurane.
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PMID:The pharmacology of isoflurane. 639 30

Corticosteroids may produce mood changes. This could account for improvement in patients with chronic airflow limitation following trials of oral corticosteroid treatment as mood elevation might improve performance in objective measurements. This proposition was tested in 21 patients with chronic airflow limitation, who underwent detailed psychological assessment during a randomised controlled double blind crossover trial of the effect of prednisolone 40 mg daily compared with that of a placebo. Self rating visual analogue scales for various qualities of mood were completed before the study and after each phase in addition to depression and psychological symptom questionnaires. After treatment with the placebo, patients showed increases in cheerfulness (p less than 0.01) and sociability (p less than 0.01) and a decrease in depression (p less than 0.01). After treatment with prednisolone there were increases in cheerfulness (p less than 0.01), optimism (p less than 0.01), activity (p less than 0.05), and sociability (p less than 0.02) and there was a decrease in depression (p less than 0.01). When placebo and prednisolone values were compared, however, there were no significant differences. Some patients showed improvements (greater than 20%) in peak expiratory flow, FEV1 or forced vital capacity (FVC) after prednisolone, but nearly all had improvements in at least one psychological test. There were no detectable associations between changes in objective measurements and changes in psychological test ratings. This study suggests that in patients with chronic obstructive lung disease significant psychological changes are no more likely to follow treatment with a corticosteroid than treatment with a placebo and that physiological improvement after corticosteroid treatment is not tied to psychological changes.
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PMID:Psychological changes and improvement in chronic airflow limitation after corticosteroid treatment. 639 17

Using a dual isohypercapnic technique, the authors compared the effect on ventilatory control of midazolam (0.2 mg/kg) and thiopental (3.5 mg/kg) in normal volunteers and in subjects with chronic obstructive pulmonary disease (COPD). In normal volunteers the slope of the CO2 response curve decreased from 1.77 +/- 0.16 l . min-1 . mmHg-1 (mean +/- SEM) to a minimum of 1.14 +/- 0.17 l . min-1 . mmHg-1 3.5 min after midazolam, returning to 1.32 +/- 0.21 l . min-1 . mmHg-1 15 min after injection. In the same subjects, the slope of the CO2 response curve fell from 1.89 +/- 0.18 l . min-1 . mmHg-1 to a minimum of 1.37 +/- 0.29 l . min-1 . mmHg-1 one minute after injection of thiopental, returning to 1.69 +/- 0.22 l . min-1 . mmHg-1 15 min after injection. These changes were not statistically significant. In subjects with clinical COPD, the slope of the CO2 response curve decreased from 1.89 +/- 0.63 l . min-1 . mmHg-1 to a minimum of 0.39 +/- 0.19 l . min-1 . mmHg-1 two minutes after injection of midazolam (P less than 0.05 compared with control), while 15 min after injection, the slope recovered to only 0.62 +/- 0.40 l . min-1 . mmHg-1 (P less than 0.05 compared with control). In the same subjects, the slope of the CO2 response curve decreased from 1.53 +/- 0.17 to a minimum of 0.69 +/- 0.25 l . min-1 . mmHg-1 0.5 min after injection of thiopental, recovering to 1.47 +/- 0.28 l . min-1 . mmHg-1 15 min after injection. This was significantly greater than the corresponding slope after midazolam (P less than 0.05). The authors conclude that while the time course of ventilatory depression after thiopental is similar in normal volunteers and in patients with COPD, the ventilatory depression 15 minutes after midazolam is more profound in patients with COPD than in normal subjects.
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PMID:Time course of ventilatory depression after thiopental and midazolam in normal subjects and in patients with chronic obstructive pulmonary disease. 640 63

Impaired pulmonary mechanics or depression of the respiratory centers can limit the ventilatory response to inhaled carbon dioxide in patients with chronic obstructive pulmonary disease (COPD). We devised a method able to detect depressed neurogenic and chemical ventilatory drive during expiratory airflow obstruction. In 14 normal subjects, we impeded expiratory airflow while measuring the resultant decline in maximum voluntary ventilation (MVV) and the ventilatory response to rebreathing 7 percent CO2 (delta V/delta PCO2). The MVV and delta V/delta PCO2 fell proportionately and were closely correlated (r = 0.88). The lower limit for delta V/delta PCO2 during airway obstruction equalled 1.2 L/min/mm Hg X (observed MVV divided by predicted MVV). Nine patients with COPD and normal arterial carbon dioxide tension (PaCO2) all had normal values for delta V/delta PCO2 corrected for MVV; however, nine of 12 patients with COPD and elevated PaCO2 and bicarbonate levels had depressed values for delta V/delta PCO2. These data indicate that neurogenic and chemical depression to ventilation can be detected in patients with mechanical obstruction to expiratory airflow if delta V/delta PCO2 is corrected for changes in MVV.
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PMID:"Won't breathe" vs "can't breathe". Detection of depressed ventilatory drive in patients with obstructive pulmonary disease. 640 8

Sixty outpatients with chronic obstructive pulmonary disease underwent nutritional, physiologic, and psychologic evaluation to determine the prevalence of nutritional depletion and the relationship to physiologic and psychologic factors. Weight loss was reported in 27 percent. Triceps skinfolds (TSF) were less than 60 percent of standard in 33 percent, none had mid-arm muscle circumference (MAMC) less than 60 percent of standard, and 5 percent had body weight (BW) less than 60 percent of ideal. Values for BW-percent of ideal, TSF-percent of standard, and MAMC-percent of standard were inversely correlated with the percent of estimated caloric expenditure ingested. Also, BW percent was correlated with FEV1 percent predicted, diffusion capacity percent predicted, and oxygen consumption/kg at rest (VO2 percent/kg). There were five variables that explained 62.6 percent of the variation in BW percent: VO2/kg at rest explained 22.2 percent; ventilatory equivalent 13.5 percent; PaCO2 9.8 percent; log vital capacity percent predicted 9.2 percent; and depression 7.8 percent. It is concluded that increased caloric utilization without adequate compensation in dietary intake is the reason for nutritional depletion.
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PMID:The prevalence and determinants of nutritional changes in chronic obstructive pulmonary disease. 647 94

We evaluated the accuracy of a new device for continuous noninvasive measurement of cutaneous PCO2. The Hewlett-Packard capnometer (model 47210/HA) works by means of an infrared transducer applied to the forearm over an area of skin that has been stripped of the stratum corneum. Capnometer transcutaneous carbon dioxide pressure (CPCO2) was compared with arterial carbon dioxide pressure (PaCO2) during 60 simultaneously obtained measurements in 13 hemodynamically stable patients. Each patient was studied for 1 1/2 to 5 hours, and a wide range of PaCO2 values (21 to 82 mm Hg) was represented. The data show a clinically significant relationship whereby PaCO2 = CPCO2 - 4.13, with a SE of +/- 2.19 mm Hg. Clinical usefulness of noninvasive cutaneous CO2 monitoring can be foreseen in patients whose ventilatory support is being tapered, in those with respiratory depression caused by various neuromuscular disorders, and in patients with chronic obstructive pulmonary disease and acute respiratory failure. Our results indicate that continuous transcutaneous CPCO2 measurements are safe and accurate and strongly suggest that they can be of clinical usefulness in a select group of hemodynamically stable patients.
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PMID:Transcutaneous noninvasive monitoring of carbon dioxide tension. 679 84

We studied 20 men (ages 46 to 69, mean 45 years) with chronic obstructive pulmonary disease (FEV1 of 0.55 to 2.1 L), to determine the relative importance of pulmonary impairment vs other occult physical or psychologic factors in the genesis of sexual dysfunction. Seven subjects had ceased sexual activity concomitant with worsening of their pulmonary symptoms; six because of erectile impotence and one due to dyspnea. Frequency of intercourse for the remaining 13 was 16 percent of prelung disease levels, and libido was decreased to 25 percent of premorbid levels. Nocturnal penile tumescence monitoring disclosed that six subjects had organogenic erectile impotence (OEI). None of the subjects showed signs of peripheral vascular disease as assessed by Doppler examination of peripheral pulses (including penile). The mean bulbocavernosus reflex latency (BCRL) for the OEI group (N = 5) was 40.2 msec, while that for the group with full nocturnal erections (N = 10) was 34.5 msec (P less than 0.005). Four subjects had occult diabetes mellitus evident on oral glucose tolerance tests, and one had evidence of an androgen deficit. The correlation coefficient for rank by sexual dysfunction vs pulmonary impairment and age was 0.66 (P less than 0.005) and 0.24 P greater than 0.05), respectively. Subjects with OEI tended to have the worst pulmonary function test results and the highest T-scores on the hypochondriasis, depression, and hysteria scales of the Minnesota Multiphasic Personality Inventory. Data suggest that sexual dysfunction worsens as lung disease worsens and that chronic obstructive pulmonary disease may be associated with male impotence in the absence of other commonly known causes.
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PMID:Sexual dysfunction and erectile impotence in chronic obstructive pulmonary disease. 680 73


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