CNS-depressants

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. 

As a therapeutic class, hypnotics are nonselective CNS depressants that eflcit drowsiness and a natural sleep state from which the individual can be aroused. The effects of hypnotics are generally dose-dependent. 

Pyridine Acute Toxicology. Pyridine causes gastrointestinal upset and central nervous system (CNS) depression at high levels of exposure. The odor of pyridine can be detected at extremely low concentrations (12 ppb). The LD q (oral, rats) is 891 mg/kg, the LC q (inhalation, rats) is 4000/4 (ppm/h), and the TLV is 15 mg/nP (79,80). 

Benzodiazepiaes have largely replaced barbiturates and barbiturate-like agents for use as anxiolytics and sedative—hypnotics. Because benzodiazepiaes rarely produce levels of CNS depression that require therapeutic iatervention, the need for analeptics has decreased considerably. 

Acute benzene poisoning results in CNS depression and is characterized by an initial euphoria followed by staggered gait, stupor, coma, and convulsions. Exposure to approximately 4000 ppm benzene results in complete loss of consciousness. Insomnia, agitation, headache, nausea, and drowsiness may persist for weeks after exposure (126). Continued inhalation of benzene to the point of euphoria has caused irreversible encephalopathy with tremulousness, emotional lability, and diffuse cerebral atrophy (125). In deaths arising from acute exposure, respiratory tract infection, hypo- and hyperplasia of sternal bone marrow, congested kidneys, and cerebral edema have been found at autopsy. 

Benzyl chloride is a severely irritating Hquid and causes damage to the eyes, skin, and respiratory tract including pulmonary edema. Other possible effects of overexposure to benzyl chloride are CNS depression, Hver, and heart damage. Table 3 Hsts some exposure limits. 

In addition, various pyridopyridazines have been claimed to have activity as antibacterials and antiseptics, antitubercular agents, analgesics, anti-inflammatories, antiallergics, tranquillizers, CNS depressants and muscle relaxants. 

Fused isoxazoles (631) were prepared as GABA analogs (75MI41604) and some exhibited CNS depression effects (74JAP(K)7480062) or were effective as minor tranquilizers, muscle relaxants and/or sleep inducers (76USP3966748, 79USP4163057). 

CNS DEPRESSANT Substanccs, e.g. anaesthetics and narcotics, which depress the activity of the central nervous system. Symptoms following exposure include headache, dizziness, loss of consciousness, respiratory or cardiac depression, death. 

Synthesis of the CNS depressant/tranquil izer tioperidone (59) begins by alkylation of piperazine derivative with 4-chlorobutyronitrile to give Lithium aluminum hydride... 

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

Opiate overdose is a medical emergency that can result in respiratory and CNS depression. The opioid receptor antagonist naloxone immediately reverses cardiorespiratory depression. However, repeated naloxone administration is required, since the effects of naloxone last for 30 min, while opioid agonists can remain at potentially lethal blood levels for several hours. 

The term pasaon flower is used to denote many of the approximately 400 species of the herb. F saon flower has been used in medicine to treat pain, anxiety, and insomnia. Some herbalists use the herb to treat symptoms of parkinsonism. F saon flower is often used in combination with other herbs , such a valerian, chamomile, and hops, for promoting relaxation, rest and sleep. Although no adverse reactions have been reported, large doses may cause CNS depression. The use of passion flower is contraindicated in pregnancy and in patientstaking the monoamine oxidase inhibitors (MAOIs). Fission flower contains coumarin, and the risk of bleeding may be increased when used in patientstaking warfarin and pasaon flower. 

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. 

All barbiturates have essentially die same mode of action. Depending on the dose given, tiiese drags are capable of producing central nervous system (CNS) depression and mood alteration ranging from mild excitation to mild sedation, hypnosis (sleep), and deep coma These drugs also are respiratory depressants the degree of depression... 

Somnolence, agitation, confusion, ataxia, vertigo, CNS depression, nightmares, nausea, constipation, bradycardia, hypotension, respiratory depression Same as amobarbital sodium... 

CNS—somnolence, agitation, confusion, CNS depression, ataxia, nightmares, lethargy, residual... 

Because narcoticanalgesicsdepressthe CNS(see Chap. 19), the nurse should not administer a barbiturate or miscellaneous sedativesand hypnoticsapproximately 2 hoursbefore or after administration of a narcoticanalgesic or other CNS depressant. If the time interval between administration of a narcotic analgesic and a sedative or hypnotic is less than 2 hours the patient may experien ce severe respiratory depres-son, bradycardia, and unresponsiveness. 

If the patient lias an order for a PRN narcotic analgesic or odier CNS depressant and a hypnotic, die nurse should consult die primary healdi care provider regarding die time interval between administration of tiiese drugp. Usually at least 2 hours should elapse between administration of a hypnotic and any odier CNS depressant, but this interval may vary, depending on factors such as die patient s age and diagnosis. 

Use With Alcohol. Alcohol is a CNS depressant, as are the sedatives and hypnotics. When alcohol and a sedative or hypnotic are taken together, there is an additive effect and an increase in CNS depression, which has, on occasion, resulted in death. The nurse must emphasize tiie importance of not drinking alcohol while taking this drug and stress that the use of alcohol and any one of these drains can result in serious effects. 

Administration of trimethadione (Tridione) may result in hematologic changes, such as pancytopenia (decrease in all the cellular components of the blood), leukopenia, aplastic anemia, and thrombocytopenia Also reported are various types of skin rashes, diplopia (double vision), vomiting, changes in blood pressure, CNS depression, photosensitivity, and fatal nephrosis. Because these dm have been associated with serious adverse reactions and fetal malformations, they should be used only when other less toxic dm are not effective in controlling seizures. The oxazolidinediones may precipitate a tonic-clonic seizure... 

The barbiturates are contraindicated in patients with known hypersensitivity to the drugs. The barbiturates are used cautiously in patients with liver or kidney disease and those with neurological disorders. The barbiturates (eg, phenobarbital) are used with caution in patients with pulmonary disease and in hyperactive children. When barbiturates are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. See Chapter 26 for additional information on the barbiturates. 

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