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Benzodiazepines respiratory

Although rare, benzodiazepine toxicity may occur from an overdose of the drug. Benzodiazepine toxicity causes sedation, respiratory depression, and coma. Flumazenil (Romazicon) is an antidote (antagonist) for benzodiazepine toxicity and acts to reverse die sedation, respiratory depression, and coma within 6 to 10 minutes after intravenous administration. The dosage is individualized based on the patient s response, widi most patients responding to doses of 0.6 to 1 mg. However, die drug s action is short, and additional doses may be needed. Adverse reactions of flumazenil include agitation, confusion, seizures, and in some cases, symptoms of benzodiazepine withdrawal. Adverse reactions of flumazenil related to the symptoms of benzodiazepine withdrawal are relieved by die administration of die benzodiazepine. [Pg.279]

Benzodiazepines, especially lorazepam, are used to prevent and treat CINV.5,10 Lorazepam is thought to prevent input from the cerebral cortex and limbic system from reaching the central vomiting center in the brain stem.10 Sedation and amnesia are common side effects. Respiratory depression can occur with high doses or when other central depressants such as alcohol are combined with benzodiazepines. [Pg.301]

Benzodiazepines are the evidence-based treatment of choice for uncomplicated alcohol withdrawal.17 Barbiturates are not recommended because of their low therapeutic index due to respiratory depression. Some of the anticonvulsants have also been used to treat uncomplicated withdrawal (particularly car-bamazepine and sodium valproate). Although anticonvulsants provide an alternative to benzodiazepines, they are not as well studied and are less commonly used. The most commonly employed benzodiazepines are chlordiazepoxide, diazepam, lorazepam, and oxazepam. They differ in three major ways (1) their pharmacokinetic properties, (2) the available routes for their administration, and (3) the rapidity of their onset of action due to the rate of gastrointestinal absorption and rate of crossing the blood-brain barrier. [Pg.535]

These differences may become particularly germane if co-prescribing with some antipsychotics is undertaken. For example, in certain individuals, combinations of clozapine with benzodiazepines may lead to unexpected adverse events, including delirium and augmented respiratory depression (Jackson, Markowitz Brewer-ton, 1995 Grohmann et al, 1989). Presumably if there are additive or synergistic effects of ethnicity on clearance of one or both substances, adverse events may be enhanced. Similar interactions are theoretically possible with olanzapine, as adverse interactions have been described between olanzapine and benzodiazepines, at least in the elderly (Kryzhanovskaya etal, 2006). [Pg.47]

Secobarbital exhibits the same pharmacologic properties as other members of the barbiturate class. Most nonmedical use is with short-acting barbiturates, such as secobarbital. Although there may be considerable tolerance to the sedative and intoxicating effects of the drug, the lethal dose is not much greater in addicted than in normal persons. Tolerance does not develop to the respiratory effect. The combination of alcohol and barbiturates may lead to fatalities because of their combined respiratory depressive effects. Similar outcomes may occur with the benzodiazepines. Severe withdrawal symptoms in epileptic patients may include grand mal seizures and delirium. [Pg.166]

The underlying cause of acute acidosis should be treated aggressively (e.g., administration of bronchodilators for bronchospasm or discontinuation of respiratory depressants such as narcotics and benzodiazepines). Bicarbonate administration is rarely necessary and is potentially harmful. [Pg.860]

Following acute exposure to cyclodiene organochlorine pesticides, seizures and respiratory depression may occur (Ellenhom 1988 Proctor et al. 1988). Benzodiazepines (e.g., diazepam or lorazepam) or other anticonvulsant medications (e.g., phenobarbital) have been commonly used to control seizures (Ford 1993). Organochlorines may sensitize the myocardium to the proarrhythmic effects of adrenergic amines, potentially resulting in initiation of ventricular fibrillation (TOMES 1994). [Pg.87]

Side effects of benzodiazepines include sedation, dizziness, poor coordination, and, at higher doses, amnesia. Benzodiazepines also increase the effects of alcohol therefore, alcohol use should be avoided or markedly curtailed. Benzodiazepines can also exacerbate the breathing problems of patients with sleep apnea and other respiratory disorders such as emphysema. Like the barbiturates, long-term use of benzodiazepines can lead to physical dependence, and abrupt discontinuation can produce an unpleasant, or even dangerous, withdrawal syndrome. [Pg.132]

Side effects of benzodiazepines include drowsiness and reduced respiratory function. In patients who are severely medically ill, especially those with lung disease, this side effect can be problematic. However, benzodiazepines are much safer in this regard than their predecessors, the barbiturates, and untreated delirium tremens, the most severe form of alcohol withdrawal, can be fatal. [Pg.194]

Unlike barbiturates, benzodiazepine derivatives administered orally lack a general anesthetic action cerebral activity is not globally inhibited (respiratory paralysis is virtually impossible) and autonomic functions, such as blood pressure, heart rate, or body temperature, are unimpaired. Thus, benzodiazepines possess a therapeutic margin considerably wider than that of barbiturates. [Pg.222]

Since GABA-ergic synapses are confined to neural tissues, specific inhibition of central nervous functions can be achieved for instance, there is little change in blood pressure, heart rate, and body temperature. The therapeutic index of benzodiazepines, calculated with reference to the toxic dose producing respiratory depression, is greater than 100 and thus exceeds that of barbiturates and other sedative-hypnotics by more than tenfold. Benzodiazepine intoxication can be treated with a specific antidote (see below). [Pg.226]

Hypoventilation Monitor patients who have received flumazenil for the reversal of benzodiazepine effects (after conscious sedation or general anesthesia) for resedation, respiratory depression or other residual benzodiazepine effects for an appropriate period (120 minutes or less) based on the dose and duration of effect of the benzodiazepine employed, because flumazenil has not been established as an effective treatment for hypoventilation due to benzodiazepine administration. Flumazenil may not fully reverse postoperative airway problems or ventilatory insufficiency induced by benzodiazepines. In addition, even if flumazenil is initially effective, such problems may recur because the effects of flumazenil wear off before the effects of many benzodiazepines. [Pg.392]

Respiratory disease Appropriate ventilatory support is the primary treatment of patients with serious lung disease who experience serious respiratory depression due to benzodiazepines rather than the administration of flumazenil. [Pg.393]

Other adverse cardiovascular and respiratory effects Orthostatic hypotension, with or without syncope, can occur with clozapine treatment. Rarely, collapse can be profound and accompanied by respiratory and/or cardiac arrest. Orthostatic hypotension is more likely to occur during initial titration in association with rapid dose escalation. In patients who have had even a brief interval off clozapine, start treatment with 12.5 mg once or twice daily (see Warnings). Because collapse, respiratory arrest, and cardiac arrest during initial treatment have occurred in patients receiving benzodiazepines or other psychotropic drugs, caution is advised when clozapine is initiated in patients taking a benzodiazepine or any other psychotropic drug. [Pg.1092]

However, adverse effects also include dependence and thus drug abuse. Tolerance develops within 3 months for anxiety. However considerable interindividual variability exists for the development of this tolerance. Benzodiazepines have very little effect on respiration which is not seen with sedative doses. In cases involving benzodiazepine intoxication, respiratory assistance has only been needed in patients who had also taken another CNS depressants. [Pg.348]

Patients in whom haloperidol is contraindicated can be treated by intramuscular injection of benzodiazepines, but these can cause respiratory depression or respiratory arrest if given in too high a dose, are contra-indicated in patients with preexisting respiratory depression, and have no specific anti-psychotic effect. [Pg.506]

Flumazenil Romazicon) is a benzodiazepine antagonist that specifically reverses the respiratory depression and hypnosis produced by the benzodiazepine receptor agonists. Its block of the amnesic effect of the agonists is less reliable. Flumazenil is particularly useful when an overdose of benzodiazepines has occurred. It is also employed when a benzodiazepine has been used to produce conscious sedation and rapid recovery of psychomotor competency is desirable. To avoid resedation, flumazenil may require administration by intravenous infusion. [Pg.296]

One of the major reasons for the popularity of the benzodiazepines is their relative safety. Overdoses with the benzodiazepines occur commonly, but fatal toxic occurrences are rare. Fatal intoxications are more likely in children, in individuals with respiratory difficulties, and in individuals who have consumed another central nervous system depressant, such as alcohol. After an overdose, the patient begins a deep sleep that may last for 24 to 48 hours, depending on the dose. However, even with large overdoses, the patient can usually still be aroused. [Pg.360]

The acute effects of depressants can include euphoria, anxiety reduction, anticonvulsant activity, sedation, ataxia, motor incoordination, impaired judgment, anesthesia, coma, and respiratory depression resulting in death. The benzodiazepines are rarely involved in lethality, but all CNS depressants enhance the effects of other depressant drugs. The physiological effects of high-dose depressants include miosis, shallow respiration, and reduction in reflex responses. [Pg.412]

Monitor for seizures, sedation, respiratory depression, or other residual benzodiazepine effects for an appropriate period (up to 120 min) based on dose and duration of effect of the benzodiazepine employed pharmacokinetics of benzodiazepines are not altered in the presence of flumazenil... [Pg.508]

Monitor and maintain a patent airway and prepare to assist with ventilation if flumazenil does not fully reverse the respiratory depressant effects of the benzodiazepine... [Pg.508]

For the treatment of panic disorder, the starting adult dose is 0.25 mg twice a day, which may be increased by one mg daily after three days. Clonazepam s safety and effectiveness has not been determined for individuals under the age of 18. Side effects in the treatment of panic disorders are similar to many of the benzodiazepines, and include allergic reaction, inflamed sinuses or nasal passages, flu, menstrual problems, respiratory infection, speech problems, and vaginal inflammation. [Pg.26]


See other pages where Benzodiazepines respiratory is mentioned: [Pg.729]    [Pg.729]    [Pg.228]    [Pg.240]    [Pg.277]    [Pg.130]    [Pg.464]    [Pg.466]    [Pg.470]    [Pg.532]    [Pg.532]    [Pg.537]    [Pg.107]    [Pg.59]    [Pg.127]    [Pg.459]    [Pg.175]    [Pg.204]    [Pg.70]    [Pg.1127]    [Pg.362]    [Pg.510]    [Pg.296]    [Pg.334]    [Pg.408]    [Pg.680]    [Pg.681]   
See also in sourсe #XX -- [ Pg.380 ]




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Benzodiazepine respiratory effects

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