Blood pressure phenylephrine effects

Correct answer = D. Reserpine blocks the uptake of norepinephrine into intracellular storage vesicles, resulting in depletion of norepinephrine and gradual decline in blood pressure. Phenylephrine is a pure vasoconstrictor and raises systolic and diastolic blood pressures. Dopamine raises systolic and diastolic blood pressures by stimulating the heart and (at high doses) causing vasoconstriction. Ephedrine raises systolic and diastolic blood pressures by vasoconstriction and cardiac stimulation. Norepinephrine has a pressor effect. 

A large number of diugs interfere with the smooth muscle contraction. These compounds lower blood pressure and are referred to as antihypertensive. In this section, only those coumpounds will be mentioned that have a direct effect on smooth muscle tone. Phenylephrine is an agonist on most smooth muscles and activates ax adrenoceptors. Carbachol is an agonist on some smooth muscles and activates contraction through muscarinic receptors. Blockers of the ax-adrenoceptors such as prazosin and urapidil are competitive inhibitors of the ax-receptor in vascular and bladder smooth muscle. Phenoxybenzamine is an ineversible blocker of ax receptors and phentol-amine blocks ax and a2 receptors. Ca2+ channel blockers such as the dihydropyiidines, phenylalkyla-mines and benzothiazepines lower smooth muscle tone by blocking the L-type calcium channel. 

Carvedilol also (1) attenuates the pressor effects of phenylephrine, (2) causes vasodilation, and (3) reduces peripheral vascular resistance. These effects contribute to the reduction of blood pressure and usually are seen within 30 minutes of drug administration. 

Alpha receptors are widely expressed in vascular beds, and their activation leads to arterial and venoconstriction. Their direct effect on cardiac function is of relatively less importance. A relatively pure agonist such as phenylephrine increases peripheral arterial resistance and decreases venous capacitance. The enhanced arterial resistance usually leads to a dose-dependent rise in blood pressure (Figure 9-... 

Effects of an -selective (phenylephrine), 13-selective (isoproterenol), and nonselective (epinephrine) sympathomimetic, given as an intravenous bolus injection to a dog. Reflexes are blunted but not eliminated in this anesthetized animal. BP, blood pressure HR, heart rate. 

Effects of autonomic blockade on the response to phenylephrine (Phe) in a human subject. Left The cardiovascular effect of the selective K-agonist phenylephrine when given as an intravenous bolus to a subject with intact autonomic baroreflex function. Note that the increase in blood pressure (BP) is associated with a baroreflex-mediated compensatory decrease in heart rate (HR). Right The response in the same subject after autonomic reflexes were abolished by the ganglionic blocker trimethaphan. Note that resting blood pressure is decreased and heart rate is increased by trimethaphan because of sympathetic and parasympathetic withdrawal. In the absence of baroreflex buffering, approximately a tenfold lower dose of phenylephrine is required to produce a similar increase in blood pressure. Note also the lack of compensatory decrease in heart rate. 

Phenylephrine was discussed previously when describing the actions of a relatively pure 04 agonist (Table 9-2). Because it is not a catechol derivative (Figure 9-4), it is not inactivated by COMT and has a longer duration of action than the catecholamines. It is an effective mydriatic and decongestant and can be used to raise the blood pressure (Figure 9-6). 

Figure 10.6. Effects of adrenergic agonists on the heart rate (A) and the systolic (0) and diastolic ( ) blood pressure in an anesthe-sizeddog. a Absolute values after application of phenylephrine b, c, d, differences relative to time zero after application of the respective drags.

Thyroid Disease. Elevated blood pressure or other adverse cardiovascular effects can result when patients with Graves disease receive adrenergic agonists with vasopressor activity. This is due to the increased catecholamine activity associated with hyperthyroidism. The primary agent to be avoided or used cautiously is topically applied phenylephrine for pupillary dilation. 

The effects of 2.5% phenylephrine on systemic blood pressure and pulse have also been investigated. No significant change was observed in systolic and diastolic blood pressures in 252 patients ranging in age from 3 to 92 years. In another study, two cases of acute systemic hypertension were reported after instillation of 2.5% phenylephrine. Both patients, who were 69 and 71 years of age, were scheduled for surgery, and each received multiple... 

Jennings BJ, Sullivan DE. The effect of topical 2.5% phenylephrine and 1% tropicamide on systemic blood pressure and pulse. J Am Optom Assoc 1986 57 382-389. 

Because of the premature infent s small body mass and less mature cardiovascular and cerebrovascular status, prudence dictates using the lowest concentration yet the most effective combination of mydriatics for pupillary dilation. A combination of 2.5% phenylephrine and 0.5% to 1.0% tropicamide provides sufficient mydriasis without adverse cardiovascular effects in preterm infents.The use of tropicamide alone, however, does not generally produce a sufficient mydriasis in premature infants. Adding cyclopentolate to the tropicamide regimen improves mydriasis but may contribute to elevated blood pressure and heart rate. Moreover, because of possible gastric secretory inhibition in preterm infants, the concentration of cyclopentolate should be limited to 0.25%. A commercially available combination of 1% phenylephrine and... 

In newborn infants the benefit of accurate assessment of gestational age by examination of the anterior vascular capsule of the lens and the value of funduscopic examination in ill premature babies must be weighed against the possible risks of the associated increase in blood pressure produced by the pupillary dilators. Since there is no increase in mydriatic effect with repeated instillation or increasing concentration, and their small body mass places premature neonates at increased risk of phenylephrine overdose, it is prudent to use the lowest possible concentration, as well as the most effective combination of mydriatics for indirect ophthalmoscopy in premature infants when such examination is absolutely necessary. The hypertensive effect is likely to be maximal at some time within the first 20 minutes, and whenever possible (or when risk factors are present) the blood pressure should be monitored. 

Clinicians have used both vasoconstrictors and vasodilators in the treatment of priapism. Vasoconstrictors, such as phenylephrine or epinephrine, are thought to work by forcing blood out of the corpus cavernosum into the venous return. Epinephrine use has been associated with increases in heart rate and blood pressure. In one prospective nonrandomized unblinded study, aspiration followed by intrapenile irrigation with epinephrine was effective and well tolerated. In that study, as much blood as possible was aspirated from the corpus cavernosum, and the area was irrigated with a 1 1,000,000 solution of epinephrine. The priapism resolved in 37 of the 39 occasions in which it was nsed. The therapy was well tolerated with no serious immediate or long-term side effects. On two occasions, a small intrapenile hematoma formed after treatment. 

Agents commonly considered for vasopressor or inotropic support include dopamine, dobutamine, norepinephrine, phenylephrine, and epinephrine (Table 117 ). Dopamine, an a- and -adrenergic agent with dopaminergic activity, appears to increase MAP effectively in patients who remain hypotensive with reduced cardiac function after aggressive fluid resuscitation. Thus it is often the initial choice in sepsis because of combined vasopressor and inotropic effects. While low-dose dopamine (1 to 5 mcg/kg per minute) is effective in maintaining renal perfnsion, higher doses (>5 mcg/kg per minute) exhibit a and f) activity and are used frequently to support blood pressure and to improve cardiac function such as an increase in cardiac index (Cl). 

Phenylephrine, a selective a i-agonist, has a rapid onset, short duration, and primary vascular effects, making it an attractive agent in the management of hypotension associated with septic shock. The limited available information suggests that it can increase blood pressure in fluid-resuscitated patients, and it does not appear to impair cardiac or renal function. Phenylephrine appears useful when tachycardia limits the use of other vasopressors. 

As is the case with trifluoperazine, concomitant use of triflupromazine with sympathomimetics, including epinephrine, phenylephrine, phenylpropanolamine, ephedrine (often found in nasal sprays), and appetite snppressants may decrease their stimulatory and pressor effects. Using epinephrine as a pressor agent in patients taking triflupromazine may result in epinephrine reversal or further lowering of blood pressure. 

Epinephrine reversal is a predictable result of the use of this agonist in a patient who has received an alpha-blocker. The term refers to a reversal in the blood pressure effect of moderate to large doses of epinephrine, from a pressor response (mediated by alpha-receptors) to a depressor response (mediated by pj-receptors) (Figure 10-2). The effect is not observed with phenylephrine or norepinephrine because these drugs lack p effects. 

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.

Reflex changes in heart rate involve ganglionic transmission. Activation of alphaj receptors on blood vessels by phenylephrine elicits a reflex bradycardia since mean blood pressure is increased. One of the characteristic effects of tubocurarine is its block of autonomic ganglia—this action can interfere with reflex changes in heart rate. Tubocurarine would not prevent bradycardia due to neostigmine (an inhibitor of acetylcholinesterase) since this occurs via stimulation by acetylcholine of cardiac muscarinic receptors. 

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. 

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