Phenylephrine Tricyclic antidepressants

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... 

Patients taking medications with pressor effects, such as MAO inhibitors, tricyclic antidepressants, and anticholinergic agents, should be monitored closely if phenylephrine is used (SEDA-16, 542). 

Affective and Mental Disorders. Anxiety and emotional instability can be associated with psychogenic reactions, such as vasovagal syncope, that may appear to be drug related. Medications used to treat these disorders may potentiate the activity of ophthalmic medications. The use of monoamine oxidase inhibitors or tricyclic antidepressants can enhance the systemic effects of topically applied phenylephrine and a2-adrenergic agonists. 

Patients taking certain systemic medications are also more sensitive to the pressor effects of phenylephrine. In individuals taking atropine, the pressor effect of phenylephrine is augmented, and tachycardia can occur. Tricyclic antidepressants and monoamine oxidase (MAO) inhibitors also potentiate the cardiovascular effects of topical phenylephrine. The concomitant use of phenylephrine is contraindicated with these agents, even up to 21 days after cessation of MAO inhibitor therapy. Similarly, patients taking reserpine, guanethidine, or methyldopa are at increased risk for adverse pressor effects from topical phenylephrine because of denervation hypersensitivity accompanying the chemical sympathectomy. 

Clinically important, potentially hazardous interactions with albuterol, alpha-blockers, amitriptyline, amoxapine, atenolol, beta-blockers, carteolol, chlorpromazine, clomipramine, cocaine, desipramine, doxepin, ephedra, ergotamine, furazolidone, halothane, imipramine, insulin detemir, MAO inhibitors, metoprolol, nadolol, nortriptyline, oxprenolol, penbutolol, phenelzine, phenoxybenzamine, phenylephrine, pindolol, prazosin, propranolol, protriptyline, sympathomimetics, terbutaline, thioridazine, timolol, tranylcypromine, tricyclic antidepressants, trimipramine, vasopressors... 

Clinically important, potentially hazardous interactions with amitriptyline, amoxapine, amphetamines, bupropion, citalopram, clomipramine, cyproheptadine, desipramine, dextroamphetamine, dextromethorphan, diethylpropion, dopamine, doxepin, entacapone, ephedra, ephedrine, epinephrine, fluoxetine, fluvoxamine, ginseng, imipramine, levodopa, mazindol, meperidine, methamphetamine, nefazodone, nortriptyline, paroxetine, phendimetrazine, phentermine, phenylephrine, pizotifen, propoxyphene, protriptyline, pseudoephedrine, rizatriptan, sertraline, sibutramine, sumatriptan, sympathomimetics, tramadol, tricyclic antidepressants, trimipramine, tryptophan, venlafaxine, zolmitriptan... 

Patients taking tricyclic antidepressants show a grossly exa er-ated response (hypertension, cardiac arrhythmias, etc.) to parenteral noradrenaline (norepinephrine), adrenaline (epinephrine) and to a lesser extent to phenylephrine. Case reports suggest that this interaction only occurs rarely with local anaesthetics containing these vasoconstrictors. 

Doxepin in doses of less than 150 to 200 mg daily blocks neuronal uptake much less than other tricyclic antidepressants and so is unlikely to show this interaction to the same degree, but in larger doses it will interact like other tricyclics. > It does not seem to have been established whether the response to oral doses or nasal drops containing phenylephrine is enhanced by the presence of a tricyclic, but there seem to be no reports of problems. 

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