Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ventilatory response to CO2 was measured before and after two different benzodiazepine hypnotics in both chronic bronchitics and patients without chest disease. Flurazepam, but not nitrazepam, produced a significant decrease in CO2 sensitivity, although there was no significant change in FEV1 or mixed venous PCO2. This is the first unequivocal evidence of central depression of respiration by a benzodiazepine and may be the mechanism by which benzodiazepines cause deterioration in patients with respiratory failure.
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PMID:Effect of nitrazepam and flurazepam on the ventilatory response to carbon dioxide. 1 71

The anesthesiologist uses a wide spectrum of drugs, including inhalational general anesthetics, barbiturates, benzodiazepines, narcotics analgesics and their antagonists, and neuromuscular blocking drugs. All of these drugs in sufficient dose impair the ventilatory response to chemical stimuli, and may cause inadequate gas exchange. The effect of depression of ventilatory control depends on the magnitude of depression and the coexistence of functional abnormalities in the respiratory system. The functional abnormalities are the result of preexistent pulmonary disease or other disease processes that impair respiratory function, the anticipated effects of major surgery (e.g., pulmonary resection), and the complications of anesthesia and surgery. From a functional viewpoint, the mechanisms of the effects of these disease processes on ventilatory control are: (1) interference with the neurophysiological control of automatic ventilation; (2) impairment of peripheral or central chemoreceptor function; (3) impairment of respiratory muscle function; (4) increase in the mechanical load to breathing as a result of increased resistance or decreased compliance of the respiratory system; and (5) increase in the ventilatory requirements as a result of ventilation/blood flow maldistribution, metabolic acidosis, or increased metabolic rate. As a result of current trends in the use of multiple drugs and controlled ventilation during anesthesia, the patient is at greatest risk during the early postoperative period in the recovery room. In addition to the functional abnormalities described above, the probability of impaired gas exchange and respiratory failure is increased as a result of impaired metabolism and elimination of drugs as a result of hepatic and renal insufficiency, and acute changes in acidbase status, which alter the ionization and distribution of drugs.
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PMID:The effects of anesthetic drugs and disease on the chemical regulation of ventilation. 1 49

Two patients with clinically mild congenital myopathies presented with chronic respiratory failure. Muscle weakness alone could not account for the respiratory insufficiency since static respiratory pressures were not markedly impaired, ventilation during exercise was normal, and daytime ventilation was normal if ventilatory assistance was provided at night. The ventilatory responses to inhaled carbon dioxide were very low, suggesting that impairment of the central nervous respiratory chemoreceptor contributed to hypoventilation. These patients and others described in the literature suggest that central depression of ventilation may occur more frequently than previously recognized in patients with muscular disorders. Patients with chronic respiratory failure due to central depression of respiratory drive can be effectively managed by assisted ventilation at night.
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PMID:Blunted respiratory drive in congenital myopathy. 1 71

In a 66-year-old patient with chronic obstructive pulmonary disease (COPD) complicated by arterial hypoxemia and repeated episodes of respiratory and right ventricular failure, a satisfactory level of oxygenation could not be maintained despite controlled oxygen therapy. To enable oxygen to be administered without depression ventilation, artificial respiration by means of phrenic nerve stimulation (diaphragm pacing) has been employed. Evidence of clinical improvement since pacing was begun 32 months ago include fewer episodes of respiratory failure and better control of congestive heart failure despite a gradual worsening of pulmonary function.
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PMID:Diaphragm pacing. Application to a patient with chronic obstructive pulmonary disease. 30 48

Serial measurements of CH50, C3, C4, and factor B were performed on three newborn infants with group B streptococcal sepsis. Two of the septic infants had a colonized but noninfected identical twin. All three infants with group B streptococcal sepsis had hypotension, prolonged coagulation times, neutropenia, and respiratory failure. During the course of the sepsis, factor B was depressed 30% to 35%, C3 was depressed 40% to 60%, and CH50 was depressed by 100% when compared to their cord blood levels. Two of the infants also had a 50% to 70% depression of C4. In contrast, no significant decrease in complement levels occurred in the siblings of the twins or in two additional control infants. These data are characteristic of older patients with Gram-negative sepsis and strongly suggest that the group B Streptococcus has endotoxin-like properties.
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PMID:Complement activation and group B streptococcal infection in the newborn: similarities to endotoxin shock. 34 Oct 69

1 In cats anaesthetized with pentobarbitone, saxitoxin and, on a few occasions, tetrodotoxin were injected into a lateral cerebral ventricle or into the subarachnoid space of the lower brain stem. Observations were made on frequency and tidal volume of breathing, on CO(2) responsiveness and on electrical responsiveness of the respiratory centre. Effects on the blood pressure were observed simultaneously.2 A single large dose of toxin, e.g., 250 ng, produced within minutes apneustic breathing and a rise in blood pressure which were converted rapidly to respiratory failure and hypotension. In contrast, repeated small doses, e.g., 25 ng, yielded only progressive slowing of the respiration together with circulatory hypotension. Bulbar depression was produced as effectively by subarachnoid injection as by intraventricular injection of the toxins. Onset of action was detectable within seconds.3 Slowing of the respiration occurred independently of change in tidal volume and whether or not the vagus nerves were cut. The reduction in breathing frequency is attributed to direct toxin-induced depression of the central respiratory oscillator.4 Steady-state measurements of tidal volume at controlled levels of alveolar CO(2) pressure in intermediate stages of respiratory depression showed that the toxins produced an increase in CO(2) stimulation threshold as well as a reduction in gain of CO(2) responsiveness, whether or not the vagus nerves were cut. Carotid arterial chemoreceptor reactivity to O(2) was demonstrable when central sensitivity to CO(2) was depressed. These effects are attributed to a direct influence of the toxins upon the brainstem CO(2)-tidal volume controller.5 Responsiveness of the medullary inspiratory centre to electrical stimulation persisted after the failure of spontaneous breathing was caused by the toxins. Conversely, restitution of electrical responsiveness preceded the reappearance of spontaneous respiratory activity in the recovery phase of toxic depression. Circulatory effects paralleled the changes in respiratory behaviour.6 On the basis of the relatively prompt and discrete alterations in the central respiratory and circulatory control mechanisms produced by saxitoxin and tetrodotoxin placed in the cerebrospinal fluid, it is concluded that the agents rapidly penetrated to deep target loci in the lower brain stem.
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PMID:Respiratory and circulatory effects of saxitoxin in the cerebrospinal fluid. 59 70

Two patients are presented with respiratory depression for which no cause was apparent. Both had ingested narcotics without the parents' knowledge. Narcotic ingestion should be suspected if signs of respiratory failure with constricted pupils are present, and a diagnostic test with naloxone should be performed.
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PMID:Respiratory depression due to unsuspected narcotic ingestion treated with naloxone. 68 79

Indirect measures of left ventricular function were studied in seven patients with respiratory failure secondary to chronic obstructive pulmonary disease to determine if there were a relationship between left ventricular function and treatment of the pulmonary disease. All patients were studied during acute episodes while in respiratory failure having arterial Pco2 (Paco2) values greater than 49 torr with no clinical evidence of left ventricular failure. Indirect methods to evaluate left ventricular function included the use of the Swan-Ganz catheter for pulmonary capillary wedge pressure measurement, systolic time intervals, and cardiac output. There was improvement in left ventricular function with treatment of the respiratory failure manifested by decreases in the wedge pressure and pre-ejection period/left ventricular ejection time ratio, and an increase in the dp/dt/pulmonary capillary wedge pressure with treatment of the chronic obstructive pulmonary disease. The improvement in left ventricular function suggests that there is a depression of left ventricular function in respiratory failure. The depressed function improved with therapy of the lung disease without additional medication directed at cardiac function.
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PMID:Left ventricular function during respiratory failure. 87 4

An unusual neuropsychiatric disorder inherited in autosomal dominant fashion occurred in three successive generations of a family. Symptoms commenced late in the fifth decade in six affected patients and led to death in four to six years. The earliest and most prominent symptom was mental depression not responsive to antidepressant drugs or electroconvulsive therapy. This was accompanied by exhaustion, sleep disturbances, and marked weight loss. Later in the disease, symptoms of parkinsonism appeared, and respiratory failure occured terminally. The most recently affected family member was investigated biochemically late in his illness. Concentrations of taurine were greatly diminished in plasma and cerebrospinal fluid, and at autopsy, all regions of brain examined had a markedly reduced taurine content. Since taurine is a putative inhibitory synaptic transmitter, deficiency of brain taurine may possibly have caused the psychiatric and neurological manifestations of this disorder.
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PMID:Hereditary mental depression and Parkinsonism with taurine deficiency. 112 73

Apart from the usual hazards of local anesthesia (toxic reaction due to overdose or intravasal administration, allergic reaction, reaction to the vasoconstrictor), a further risk which should be borne in mind in local anesthesia of the neck region is inadvertent epidural or intrathecal administration of the local anesthetic agent. Depression of respiration or total respiratory failure may occur due to blockade of the superficially located medullary chemoreceptors in the form of a high or total spinal block. The pathogenesis of these incidents is investigated. Respiratory failure is usually reversible and requires immediate and effective therapy (artificial respiration, oxygen administration). The indications for neck anesthesia and their relativity within the entire therapeutic program should be given careful consideration. If (radicular) pain occurs during the injection, or if cerebrospinal fluid is aspirated, the procedure should be interrupted immediately and some time allowed to elapse. In fatal cases the injection channel must be dissected layer-wise in local anemia down to the dural sac. The possible pathway of toxic administration (epidural, subdural, intravasal) must be demonstrated chemically.
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PMID:[Clinical and experimental contribution concerning the pathogenesis of acute life-threatening complications during neck anaesthesia]. 117 98


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