UMLS:C0011570 - FACTA Search

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

The feasibility of employing a recently developed pulmonary assist membrane oxygenator for partial respiratory support in arteriovenous perfusion was studied using small mongrel dogs rendered hypoxic by oxygen depression. The unit is employed along with the conventional ventilation techniques (such as CPAP and PEEP) when the latter alone cannot maintain adequate gas exchange in the lung. The results indicate that poorly oxygenated arterial blood can be upgraded to life-sustaining levels when the bypass flow rate through the oxygenator is in the range of 18-33% of the total cardiac output. No cardiovascular derangements were noted at these arteriovenous flow rates for perfusion periods of four to six hours. The present results demonstrate the feasibility of providing partial support to pulmonary function using the pulmonary assist membrane oxygenator.
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PMID:Arteriovenous perfusion with the pulmonary assist membrane oxygenator. 27 77

Intermittent Mandatory Pressure Release Ventilation (IMPRV) is a positive pressure spontaneous breathing ventilatory mode in which airway pressure is released intermittently and synchronously with patient's spontaneous expiration in order to provide ventilatory assistance. Eight critically ill patients free of any factor known to alter chest wall mechanics (group 1) and 8 critically ill patients whose spontaneous respiratory activity was markedly altered by a flail chest, or by a C5 quadraplegia and/or by the administration of opioids (group 2) were studied prospectively. CPAP and IMPRV were administered to each patient in a random order during a 1 h period using a CESAR ventilator. Gas flow, tidal volume, tracheal pressure, esophageal pressure, end-expiratory lung volume and hemodynamic parameters were measured. In group 1 patients, the ventilatory assistance provided by IMPRV was associated with a significant decrease in spontaneous tidal volume whereas all other respiratory parameters remained unchanged. In group 2 patients, IMPRV increased minute ventilation from 8.0 +/- 2.61/min to 12.2 +/- 1.81/min (p less than 0.05), decreased PaCO2 from 46 +/- 7.3 mmHg to 38 +/- 6.8 mmHg (p less than 0.05) and reduced respiratory frequency from 21 +/- 10 bpm to 14 +/- 5.7 bpm (p less than 0.07). These results show that IMPRV provides significant ventilatory assistance to patients with mild acute respiratory failure either by decreasing patient's contribution to minute ventilation or by increasing alveolar ventilation in presence of respiratory depression of central or peripheral origin.
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PMID:Continuous positive airway pressure (CPAP) vs. intermittent mandatory pressure release ventilation (IMPRV) in patients with acute respiratory failure. 161 99

Single pass extraction of a new iodinated inhibitor of angiotensin-converting enzyme (ACE) was measured by means of indicator-dilution techniques applied to rabbit lungs, perfused in situ at 20 ml/min with Krebs bicarbonate solution containing 3% bovine serum albumin. A bolus containing the inhibitor, N-[1(S)-carboxy-(4-OH-3-125I-phenyl)ethyl]-L-Ala-L-Pro (CPAP), and an intravascular marker, [14C]dextran, was injected and extraction calculated at the peak of the resulting venous outflow-time curve. In 13 of 21 lungs used, a synthetic substrate for ACE, [3H]benzoyl-phenylalanyl-alanyl-proline (BPAP), was added to the bolus and appearance of its hydrolysis product, [3H]benzoyl-Phe, measured in effluent samples. When low amounts (0.15 nmol) of [125I]CPAP were injected, pulmonary extraction (E) of CPAP was 67 +/- 14% (X +/- S.D; n = 21) and metabolism (M) of BPAP was 56 +/- 9% (n = 13). Addition of unlabeled CPAP (3, 34 or 340 nmol) to the Addition of unlabeled CPAP (3, 34 or 340 nmol) to the injected bolus caused dose-dependent reduction of E(CPAP) and M(BPAP) that was no longer evident 10 min after the largest dose of CPAP. Coadministration of the ACE inhibitor, captopril (3, 6, 8 and 28 nmol), also caused dose-dependent, reversible depression of both E(CPAP) and M(BPAP). Accordingly, extraction of CPAP by perfused rabbit lung is saturable. Inasmuch as CPAP inhibits ACE activity (as reflected by BPAP metabolism) and CPAP uptake is inhibited by captopril (which also inhibits BPAP hydrolysis), it appears that a large portion of this saturable process probably reflects binding to vascular ACE.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uptake of N-[1 (S)-carboxy-(4-OH-3-125I-phenyl)ethyl]-L-Ala-L-Pro, an inhibitor of angiotensin-converting enzyme by rabbit lungs in situ. 301 13

Of 22 patients investigated for sleep disorders, habitual snoring and/or daytime hypersomnolence, 12(10 men) had obstructive sleep apnea syndrome (OSAS). 3 OSAS were mild, 5 moderate and 4 severe. The leading symptoms were daytime hypersomnolence and habitual snoring. As risk factors we found retro-micrognathia in 2 patients, macroglossia secondary to acromegaly in 1, alcohol abuse in 7 and obesity in 6. Conservative measures improved the disorder subjectively in 6 patients. One patient had a relapse 6 months after uvulopalatopharyngoplasty. 4 patients were successfully treated by nasal CPAP. Other diagnoses were idiopathic alveolar hypoventilation (2), Cheyne-Stokes breathing secondary to low cardiac output (1), monosymptomatic narcolepsy (2), sleep disturbances secondary to depression (2), chronic benzodiazepine abuse (1) and chronic bronchitis without nocturnal hypoxemia (1). History, clinical observation and oxymetry make diagnosis possible in most cases of OSAS severe enough to require treatment. Polysomnography is time-consuming and should be reserved for selected cases.
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PMID:[Sleep-apnea syndrome. Elucidation, therapy and course]. 305 35

In a 27-year-old patient with a severe obstructive sleep apnea syndrome documented by a polysomnographic study, an oral dose of 15 mg midazolam caused life-threatening obstructive apnea and excessive sedation. Therapy with nasal CPAP eliminated the pharyngeal obstruction, but marked central hypoventilation persisted. Benzodiazepines are known to aggravate the obstructive sleep apnea syndrome. Dangerous central hypoventilation occurring after this medication during treatment with nasal CPAP has not yet been reported. Excessive susceptibility to depression of chemoresponsiveness to pCO2 is suspected. The potentially dangerous and life-threatening side effects of sedatives in patients with obstructive sleep apnea syndrome are discussed.
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PMID:[Life-threatening apnea after midazolam administration in a patient with obstructive sleep apnea syndrome]. 329 65

The aim of the research was to discover the level of change observed in cognitive functions and personality variables in patients ill with obstructive sleep apnea prior to and after CPAP treatment. Data was collected from 20 male patients ill with a severe form of obstructive sleep apnea whose physiological symptoms were correlated with the results of cognitive functions and personality variables. It was concluded that obstructive sleep apnea patients have lowered; attention, concentration, speed of learning verbal and visual stimuli and speed of learning visual-motor tasks. An increased level of depression was noted together with increased anxiety and psychological tension. In half of the group irregular EEG recordings and a pathological result on the Benton Test suggests organic damage to the CNS. These changes were negatively correlated with amounts of REM and 3 + 4 NREM sleep, but were positively correlated with the level of sleep hypoxemia. The results suggest that after 3 months of CPAP treatment affect improved significantly. The observed tendency for cognitive functions to improved was not statistically significant.
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PMID:[Psychopathological characteristics of the consequences of obstructive sleep apnea prior to and 3 months after therapy]. 848 1

Stress and shortage of sleep may cause daytime somnolence and impaired vigilance at the wheel, especially among those suffering from sleep disturbances. According to the international consensus meeting in Stockholm in May of 2000 on "The sleepy driver and pilot--causes, risks and countermeasures", drowsy driving is an underestimated risk factor in official statistics, and as many as 15-30 percent of today's traffic accidents are related to drowsiness; thus it is an even greater risk factor than alcohol. Drowsy drivers suffer from inattention, impaired concentration and may even fall asleep at the wheel. Accidents during dozing result in three times as many fatalities as other accidents. There are a number of reasons for habitual drowsiness at the wheel aside from sleep deprivation, including rhonchopathy, shift work and jet lag, mental depression, insomnia, narcolepsy, endocrinological diseases, periodic limb movement disorder, medication, pain-disordered sleep, and heart disease. Among the most active drivers, i.e. middle aged men, obstructive sleep apnea syndrome (OSAS) has been found to be the most common reason for habitually drowsy driving. OSAS causes a 2-3 fold increased risk of traffic accidents, and it impairs simulated driving. Palatoplasty as well as nasal CPAP have been shown to improve vigilance and driving performance to an extent that the increase in risk is eliminated. Drivers suffering from habitual drowsiness and micro-sleep attacks forcing them to take repeated rests are at special risk. Even if they are as dangerous as drivers with unlawful blood alcohol levels they cannot be caught in a police checkpoint. However they often seek medial advice, and properly treated they may often return safely to traffic. If not, there could be a need to report them to the authorities so as to limit or prohibit their driving.
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PMID:[Drowsiness--greater traffic hazard than alcohol. Causes, risks and treatment]. 1146 75

A patient in stage 3-4 of the Unified Parkinson's Disease Rating Scale (UPDRS), or in stage 4-5 of Hoehn and Yahr staging scale, or a patient with 0-50% activities of daily living scale of Schwab and England is considered a Late Parkinson's Disease (LPD) patient. The prevalence of disturbed sleep in Parkinson's Disease (PD) was found to vary according to an objective rating, from 60 to 98%. The factors predicting the quality of life in PD patients are: depression, sleep disturbances and dependence. The present article proposes the insertion of the following items as a chapter in a revised UPDRS based on updated knowledge in sleep arousal disturbances in PD. V. SLEEP-AROUSAL DISTURBANCES: Sleep disturbances 43. Light fragment sleep (LFS) 44. Sleep-related breathing disorders (SRBD) 45. Restless legs-periodic leg movements during sleep (RLS-PLM) 46. REM behavioral disorders (RBD) 47. Sleep-related hallucinations (SRH) 48. Sleep-related psychotic behavior (SRPB) Arousal disturbances 49. Sleep attacks (SA) 50. Excessive daytime sleepiness (EDS). Approaching the treatment of disturbed sleep in LPD means postponement of the institutionalization of the LPD patient, allowing the spouse or the caregiver a quiet nights sleep. This approach consists of three steps, each one of major importance. (1) Correct diagnosis based on detailed anamnesis of the patient, of the spouse or of the caregiver; a one week recording on a symptom diary (log) by the patient or the caregiver; excluding co morbidities. Then choosing the most appropriate sleep test, if necessary: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), actigraphy or video-PSG. This first step allows the diagnosis of one of the above mentioned sleep-arousal disturbances. (2) The non-specific therapeutic approach consists of: (a) checking the sleep effect on motor performance: beneficial, worse or neutral. (b) Dopaminergic adjustment is necessary due to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals which alter the normal modulator mechanisms of motor centers in LPD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and non-REM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates LPD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. L-Dopa has also an arousal effect on Non-REM sleep, repeatedly awakening the patient and enhancing the fragmentation due to the involuntary movements. (c) Socio-physical assistance. (3) The specific therapy consists of: LFS-Sinemet CR, Tolcapone, Intranasal Desmopressin, Domperidon, Cisapride and neurosurgery; SRBD-CPAP, UPPP, nasal interventions, losing weight; RLS-PLM-Benzodiazepine (Clonazepam), Opioid, Apomorphine infusion; RBD-Clonazepam and dopaminergic agonists; SRH-Clozapine, Risperidone; SRPD-Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual LPD patient.
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PMID:Approaching disturbed sleep in late Parkinson's Disease: first step toward a proposal for a revised UPDRS. 1148 77

The present article is meant to suggest an approach to the guidelines for the therapy of sleep disturbances in Parkinson's Disease (PD) patients.The factors affecting the quality of life in PD patients are depression, sleep disturbances and dependence. A large review of the literature on sleep disturbances in PD patients, provided the basis for the following classification of the sleep-arousal disturbances in PD patients. We suggest a model based on 3 steps in the treatment of sleep disturbances in PD patients. This model allowing the patient, the spouse or the caregiver a quiet sleep at night, may postpone the retirement and the institutionalization of the PD patient. I. Correct diagnosis of sleep disorders based on detailed anamnesis of the patient and of the spouse or of the caregiver. One week recording on a symptom diary (log) by the patient or the caregiver. Correct diagnosis of sleep disorders co morbidities. Selection of the most appropriate sleep test among: polysomnography (PSG), multiple sleep latency test (MSLT), multiple wake latency test (MWLT), Epworth Sleepiness Scale, actigraphy or video-PSG. II. The nonspecific therapeutic approach consists in: a) Checking the sleep effect on motor performance, is it beneficial, worse or neutral. b) Psycho-physical assistance. c) Dopaminergic adjustment is necessary owing to the progression of the nigrostriatal degeneration and the increased sensitivity of the terminals, which alter the normal modulator mechanisms of the motor centers in PD patients. Among the many neurotransmitters of the nigro-striatal pathway one can distinguish two with a major influence on REM and NonREM sleep. REM sleep corresponds to an increased cholinergic receptor activity and a decreased dopaminergic activity. This is the reason why REM sleep deprivation by suppressing cholinergic receptor activity ameliorates PD motor symptoms. L-Dopa and its agonists by suppressing cholinergic receptors suppress REM sleep. The permanent adjustment according to the progression of the degenerative process of the disease will diminishe aggravation. The following types of sleep-arousal disturbances have to be considered in PD patients: - Sleep Disturbances, Light Fragmented Sleep (LFS), Abnormal Motor Activity During Sleep (AMADS), REM Behavior Disorders (RBD), Sleep Related Breathing Disorders (SRBD), Sleep Related Hallucinations (SRH), Sleep Related Psychotic Behavior (SRPB). - Arousal Disturbances, Sleep Attacks (SA), Excessive Daytime Sleepiness (EDS), Each syndrome has to receive a score according to its severity. III. The specific therapy consists in: LFS: Benzodiazepines & Nondiazepines. AMADS: Clonazepam, Opioid, Apomorphine infusion; RBD: Clonazepam and dopaminergic agonists; SRBD: CPAP, UPPP, nasal interventions, losing weight; SRH: Clozapine, Risperidone; SRPD: Nortriptyline, Clozapine, Olanzepine; SA-adjustment; EDS-arousing drugs. Each therapeutic approach must be tailored to the individual PD patient.
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PMID:Sleep disturbances in Parkinsonism. 1258 74

Although clinical experience has suggested for more than two decades that OSA is associated with impairment of cognition, emotional state, and quality of life and that treatment with nasal CPAP produces significant improvements in these areas, sound empirical evidence to support this view, especially regarding treatment outcome, has been lacking. More recent investigations have begun to provide this support from randomized, adequately controlled studies. These assessments suggest that some degree of cognitive dysfunction is associated with OSA. The effects are most apparent in the severe cases, whereas results in mild cases are more equivocal. Reported impairments include global intellectual dysfunction and deficits in vigilance, alertness, concentration, short- and long-term memory, and executive and motor function. Considerable discrepancy exists across studies with respect to type and degree of dysfunction, however. Disturbances in general intellectual function and executive function show strongest correlations with measures of hypoxemia. Not unexpectedly, alterations in vigilance, alertness, and, to some extent, memory seem to correlate more with measures of sleep disruption. Although many inadequately controlled investigations have demonstrated reversibility of most or all of these deficits with effective treatment, more recent placebo-controlled studies have raised doubts regarding whether the observed changes are truly a function of treatment. This issue requires further systematic exploration with adequate controls and step-wise analysis of treatment duration effects. A similar set of considerations exists with respect to the relationship between psychological disturbance, primarily depression, and OSA. Although several studies suggest significant depression in these patients, the results are mixed. Placebo-controlled treatment trials fail to demonstrate consistently a difference in mood improvement between active treatment groups and controls, although several methodologic considerations suggest that these results should be interpreted with caution. Numerous investigations leave little doubt about the issue of quality of life impairment among persons with OSA. Further characterization of impairment, particularly in areas specific to this population, will provide clearer understanding of the problem. Preliminary investigations of treatment response in controlled studies indicate significantly greater improvement of quality of life in response to CPAP. Although patients with OSA commonly report disturbances in cognitive and psychological function and general quality of life, the increased rates of obesity, hypertension, diabetes, cardiovascular disease, medication use, and related psychosocial complications present a host of potential etiologies that might explain the impairments noted. There can be little doubt that these covariants do, in some cases, contribute to neuropsychological dysfunctions. It is essential that future studies continue to define those disturbances that are specific to OSA, the relationship between levels of severity and impairment, the role of treatment in reversing these dysfunctions, and the correlation between test results and significant day-to-day social and occupational functional impairment.
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PMID:Neuropsychological impairment and quality of life in obstructive sleep apnea. 1280 Jul 82

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