Tricyclic antidepressants anesthetics

Carboplatin/Etoposide Ethacrynic acid Inhalation anesthetics Phenytoin Tricyclic antidepressants... 

Jandhyala B, Steenberg M, Perel J, et al. Effects of several tricyclic antidepressants on the hemodynamics and myocardial contractility of the anesthetized dogs. Eur J Pharmacol 1977 42 403-410. 

Since local anesthetics have membrane-stabilizing effects, both parenteral (eg, intravenous lidocaine) and oral (eg, mexiletine, tocainide) formulations of local anesthetics have been used to treat patients with neuropathic pain syndromes because these syndromes are thought to involve uncontrolled, rapid, sensory fiber firing. Systemic local anesthetic drugs are commonly used as adjuvants to the combination of a tricyclic antidepressant (eg, amitriptyline) and an anticonvulsant (eg, carbamazepine) in chronic pain patients who fail to respond to the combination of antidepressant and anticonvulsant. 

Toxicants may have three effects on pulse rate bradycardia (decreased rate), tachycardia (increased rate), and arrhythmia (irregular pulse). Alcohols may cause either bradycardia or tachycardia. Amphetamines, belladonna alkaloids, cocaine, and tricyclic antidepressants (see imi-primine hydrochloride in Figure 6.12) may cause either tachycardia or arrhythmia. Toxic doses of digitalis may result in bradycardia or arrhythmia. The pulse rate is decreased by toxic exposure to carbamates, organophosphates, local anesthetics, barbiturates, clonidine, muscaric mushroom toxins, and opiates. In addition to the substances mentioned above, those that cause arrhythmia are arsenic, caffeine, belladonna alkaloids, phenothizine, theophylline, and some kinds of solvents. 

Drugs and chemicals are known to cause activated interaction. The depressant action of opioid drugs is enhanced by drugs acting on the central nervous system (CNS) such as alcohol, anesthetics, anxiolytics, hypnotics, tricyclic antidepressants, and antipsychotics. Concomitant administration of opioid analgesics and monoamine oxidase inhibitors (MAOIs) should be avoided, or extra care should be taken if such a therapy is inevitable. Fatal reactions are reported when treated along with selegiline. Interactions also are reported with cyclizine, cimetidine, mexiletine, cisapride, metoclopramide, or domperidone. 

Anesthetics, antihistamines, barbiturates, benzodiazepines, chloral hydrate, meprobamate, narcotics, phenothiazines, tricyclic antidepressants Phenothiazines Diazepam... 

Tricyclic antidepressants act on both presynaptic and postsynaptic neurons, as well as on alpha- and beta-adrenoceptors. Because their principal action is to block the re-uptake of noradrenaline at the presynaptic neuron, they potentiate the hypertensive effects of both directly acting and indirectly acting amines (158,159). The hypertensive effects of phenylephrine are increased by a factor of 2-3, and of noradrenaline by a factor of 4-8. Even the administration of local anesthetics containing noradrenaline as a vasoconstrictor has proven fatal. The types of... 

Tricyclic antidepressants inhibit the uptake of catecholamines, such as adrenaline, into sympathetic neurons and can enhance the cardiovascular effects, so that even the small amounts of adrenaline present as additives in some local anesthetics can have a marked effect on the cardiovascular system. 

Clinically important, potentially hazardous interactions with acyclovir, alcohol, amphetamines, barbiturates, CNS depressants, fluoxetine, furazolidone, general anesthetics, glycopyrrolate, glycopyrronium, isocarboxazid, linezolid, lithium, MAO inhibitors, moclobemide, phenelzine, phenobarbital, phenothiazines, rasagiline, ritonavir, selegiline, sibutramine, SSRIs, tranquilizers, tranylcypromine, tricyclic antidepressants, val acyclovir... 

Use it cautiously and in rednced dosage with alcohol, barbiturates, and other sedatives, narcotics, dextromethorphan, and tricyclic antidepressants. Cocaine and vasoconstrictors in local anesthetics may precipitate a hypertensive response (see also Figure 80). 

Numerous CNS drugs including narcotics, analgesics, general anesthetics, antihistamines, phenothiazines, barbiturates, benzodiazepines, sedative-hypnotics, tricyclic antidepressants, alcohol, and muscle relaxants, potentiate the respiratory and CNS depression, sedation, and hypotensive effects of levorphanol. 

The antihypertensive effects of guanethidine may be partially or totally reversed by the mixed-acting sympathomi-metics. Halogenated hydrocarbon anesthetics may sensitize the myocardium to the effects of catecholamines. Use of vasopressors may lead to serious arrhythmias. MAO inhibitors, such as tranylcypromine, increase the pressor response to mixed-acting vasopressors. Possible hypertensive crisis and intracranial hemorrhage may occur. This interaction may also occur with furazolidone, an antimicrobial with MAO inhibitor activity. In obstetrics, if vasopressor drugs are used either to correct hypotension or are added to the local anesthetic solution, some oxytocics may cause severe persistent hypertension in the presence of mephenteramine. The pressor response of mephenteramine may be attenuated by tricyclic antidepressants, which block the uptake of norepinephrine. 

Drug interactions The most important drug interactions involving opioid analgesics are additive CNS depression with ethanol, sedative-hypnotics, anesthetics, antipsychotic drugs, tricyclic antidepressants, and antihistamines. Concomitant use of certain opioids (eg, meperidine) with MAO inhibitors increases the incidence of hyperpyrexic coma. Meperidine has also been implicated in the serotonin syndrome when used together with selective serotonin rcuptake inhibitors. 

Hydromorphone should be used with caution if other central nervous system depressants are given concomitantly. These drugs are other opioids, general anesthetics, phenothiazine, tricyclic antidepressants, sedative-hypnotics, and other central nervous system depressants (including ethanol). 

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