Phenylephrine Beta blockers

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 alcohol, amiodarone, beta-blockers, cimetidine, donidine, digoxin, diltiazem, disopyramide, ephedrine, epinephrine, ergot alkaloids, guanethidine, halothane, isoprenaline, lidocaine, noradrenaline, NSAIDs, phenylephrine, quinidine, reserpine, verapamil... 

Answer A. Although used primarily via inhalation for asthma, systemic effects of albuterol include vasodilation due to its p2 receptor activation. This can result in a decrease in PVR and mean BP, which elicits a reflex tachycardia. Methoxamine and phenylephrine are Ct-receptor activators causing vasoconstriction, which would result in reflex bradycardia. Ganglion blockers (mecamylamine) prevent autonomic reflexes, and a reflex increase in heart rate could not occur in the presence of a beta blocker (propranolol). 

Answer A. Mydriasis and fixed far vision can be due to either muscarinic receptor antagonists or ganglionic blockade. Because no M blockers are listed, the correct answer is mecamylamine. Alpha agonists (phenylephrine) have no effects on the focus of the eye. The cholinesterase inhibitor (neostigmine) and alpha blocker (phentolamine) cause miosis. Ocular effects of the beta blocker (timolol) are restricted to decreased formation of aqueous humor by the ciliary epithelium. 

Figure II-4-5 The effects of Drug U are changed by treatment with the alpha-blocker, but not by the beta-blocker. Drug U must be an alpha-activator with no beta actions—the only choice is phenylephrine.

The beta-blocker will not block the vagal slowing induced by norepinephrine hypertension. Nicotine-induced hypertension and phenylephrine-induced mydriasis are mediated by alpha receptors. Pilocarpine is a muscarinic agonist. The answer is (A). 

Effects on blood pressure and heart rate The hypertensive effects of adrenaline (epinephrine) can be markedly increased in patients taking non-selective beta blockers such as propranolol. A severe and potentially life-threatening hypertensive reaction and/or marked bradycardia can develop. Cardioselective beta blockers such as atenolol and metoprolol interact minimally. An isolated report describes a fatal hypertensive reaction in a patient given propranolol and phenylephrine, but concurrent use normally seems to be uneventful Paradoxically, marked hypotension occurred in one patient given low-dose carvedilol and dobutamine. Anaphylaxis Some evidence su ests that anaphylactic shock in... 

Adrenaline (epinephrine) stimulates alpha- and beta-receptors of the cardiovascular system, the former results in vasoconstriction (mainly alphaj) and the latter in both vasodilatation (mainly beta2) and stimulation of the heart (mainly betaj). The net result is usually a modest increase in heart rate and a small rise in blood pressure. However, if the heta-reeeptors are blocked by a non-selective beta blocker, such as propranolol or nadolol (see Table 22.1 , (p.833) for a list), the unopposed alpha vasoeonstrietion causes a marked rise in blood pressure, followed by reflex bradyeardia. Cardioselective beta blockers such as atenolol and metoprolol, whieh are more selective for betaj receptors, do not prevent the vasodilator aetion of adrenaline at beta2 receptors to the same extent, and therefore the effect of any interaction is relatively small. Consequently, adrenaline has been used to assess the degree of beta blockade produced by propranolol and other beta blockers.Phenylephrine is largely an alpha stimulator, therefore beta blockers should have a minimal effect on its action. 

No interaction between phenylephrine and the beta blockers would be expected, and apart from the single unexplained case cited above, the literature appears to support this. Concurrent use normally appears to be clinically unimportant, particularly bearing in mind the widespread use of beta blockers and the ready availability of phenylephrine in the form of non-prescription cough-and-cold remedies and nasal decongestants. 

Figure 10-2. The effects of an alpha-blocker, eg, phentolamine, on the blood pressure responses to epinephrine and phenylephrine. The epinephrine response exhibits reversal of the mean blood pressure change from a net increase (the alpha response) to a net decrease (the beta response). The response to phenylephrine is suppressed but not reversed, because phenylephrine is a pure" alpha agonist without beta action.

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