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Respiratory depression, drug-induced

Fatigue, drowsiness, as adjunct in analgesic formulation, respiratory depression Drug-induced postanesthesia, drug-induced respiratory depression, acute respiratory insufficiency superimposed on COPD Narcolepsy... [Pg.248]

Doxapram is used to treat drug-induced respiratory depression and to temporarily treat respiratory depression in patients with chronic pulmonary disease This drug also may be used during the postanesthesia period when respiratory depression is caused by anesthesia It also is used to stimulate deep breathingin patients after anesthesia... [Pg.247]

The history of this class of analgesics might have stopped there were it not for the manifold ancillary activities shown by that molecule. Although still one of the most widely used agents for treatment of severe pain, morphine is a drug that must be used with caution. Side effects include respiratory depression, induction of constipation, and sometimes marked sedation. The one property that most severely limits use of this drug is its propensity to induce physical dependence in patients subjected to more than casual exposure. [Pg.315]

Reversal of opioid effects Complete or partial reversal of opioid drug effects, including respiratory depression, induced by either natural or synthetic opioids. Opioid overdose Management of known or suspected opioid overdose. [Pg.379]

A stands for provision of airway B stands for breathing and ventilation C stands for circulation support D stands for drug-induced depression (central nervous and respiratory system) and E for electrolyte and metabolic abnormalities and... [Pg.278]

There are some clinically important pharmacodynamic drug-drug interactions to be mentioned. Antipsychotics will potentiate the central depressant effects of sedatives and of alcohol. They will also increase the risk of respiratory-depressant effects of opiates. Inducers of drug metabolic enzymes like for example rifampicin and several antiepileptics, may increase the elimination rate of antipsychotic agents and thus decrease their efficacy. [Pg.350]

GNS depressants are drugs that decrease brain activity, resulting in both behavioral and physiological changes. The effects of alcohol on coordination, speech, and cognitive functions are familiar to most people. The effects of barbiturates are similar to alcohol. In low doses, barbiturates act as sedatives increased doses have a hypnotic or sleep-inducing effect and stiU larger doses have anticonvulsant and anesthetic activity, and can lead to respiratory depression, coma, and death. Barbiturate addicts... [Pg.85]

Like other sedative-hypnotic drugs, alcohol is a CNS depressant. At high blood concentrations, it induces coma, respiratory depression, and death. [Pg.494]

The respiratory depression induced by morphine can add to that of alcohol, barbiturates, benzodiazepines (such as Valium), and even with antihistamines taken for allergies. Combined effects of these drugs with morphine can dangerously compromise breathing. Tricyclic antidepressants can hamper the metabolism of morphine. [Pg.360]

Any new hypnotic should induce and maintain natural sleep without producing residual sedative effects during the day it should not cause dependence or interact adversely with other sedatives, including alcohol. The ideal hypnotic should not cause respiratory depression or precipitate cardiovascular collapse when taken in overdose. So far no drug fulfils all these criteria. [Pg.251]

GHB is gaining popularity in France and Italy as an aid in childbirth because it induces remarkable hypotonia, or muscle relaxation.40 GHB has been reported to cause spectacular action on the dilation of the cervix, decreased anxiety, greater intensity and frequency of uterine contractions, and increased sensitivity to drugs used to induce contractions. It also produces a lack of respiratory depression in the fetus, and protection against fetal cardiac anoxia (lack of oxygen to the heart, especially in cases where the umbilical cord wraps around the fetus s neck).41... [Pg.44]

Alcohol-induced CNS and respiratory depression is enhanced by neuroleptic drugs (623), but enhancement can be slight if both are used in reasonable amounts (624). [Pg.233]

Neuroleptic drugs increase sedative- and hypnotic-induced sleep time and respiratory depression. Lower dosages of barbiturates or other hypnotics should be used, at least initially, in patients receiving neuroleptic drugs (622). [Pg.235]

In a retrospective study of the case notes of patients who had been admitted to hospital with acute attacks of asthma, there was a high prevalence of heroin use—15 % had used only heroin and another 16% had used both heroin and cocaine (9). Heroin users had been intubated more often than non-drug users (17% versus 2.3%). Similarly, more heroin users were admitted to ICU than non-users (21% versus 12%). However, they did not spend more time receiving mechanical ventilation or being in hospital. These findings suggest that heroin induced some degree of bronchoconstriction and respiratory depression, which worsened the initial presentation of asthma. [Pg.542]


See other pages where Respiratory depression, drug-induced is mentioned: [Pg.147]    [Pg.338]    [Pg.346]    [Pg.78]    [Pg.248]    [Pg.470]    [Pg.162]    [Pg.20]    [Pg.253]    [Pg.259]    [Pg.806]    [Pg.352]    [Pg.348]    [Pg.55]    [Pg.153]    [Pg.481]    [Pg.696]    [Pg.1249]    [Pg.462]    [Pg.51]    [Pg.192]    [Pg.194]    [Pg.101]    [Pg.520]    [Pg.1398]    [Pg.301]    [Pg.158]    [Pg.148]    [Pg.715]    [Pg.263]    [Pg.78]    [Pg.297]   


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