Phenylephrine blood pressure increased

Phenylephrine is a nasal decongestant that mimics the sympathetic system, thereby increasing the heart rate and blood pressure. It may aggravate conditions such as diabetes, hypertension and glaucoma. Patients with hypertension, ischaemic heart disease, hyperthyroidism, diabetes and glaucoma are therefore given topical nasal sympathomimetics rather than systemic sympathomimetics. Both topical and systemic sympathomimetics are contraindicated in patients taking monoamine oxidase inhibitors, because concurrent administration of the two products may lead to a hypertensive crisis. 

B. Phenylephrine is an aj-selective agonist. It causes an increase in peripheral vascular resistance. The major cardiovascular response to this drug is a rise in blood pressure associated with reflex bradycardia. The slowing of the heart rate is blocked by atropine. 

Phenylephrine is used to increase peripheral vascular resistance when cardiac output is maintained. It increases arterial blood pressure and this often results in reflex bradycardia. It is mainly used to correct anaesthesia-induced hypotension. It is also used to dilate the pupil (mydriasis) and as a nasal decongestant. 

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 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. 

Methoxamine acts pharmacologically like phenylephrine, since it is predominantly a direct-acting o -receptor agonist. It may cause a prolonged increase in blood pressure due to vasoconstriction it also causes a vagally mediated bradycardia. Methoxamine is available for parenteral use, but clinical applications are rare and limited to hypotensive states. 

Phenylephrine and entry 1, 30 and 10p,g/kg, respectively, were introduced into the vena femoralis through a polyethylene cannula. Compared with phenylephrine, the experimental agent exhibited a potency factor 2.73 times greater with regard to the contraction of the urethra and with a duration longer by a factor of 4.3. Moreover, the increase in blood pressure associated with entry 1 was only 1.39 times that of phenylephrine. Testing results are provided in Table 2. 

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. 

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. 

Phenylephrine is a selective ai adrenergic agonist, with a pharmacological structure similar to norepinephrine (noradrenaline), which causes peripheral vasoconstriction. Stimulation of adrenoceptors in the myocardium has an inotropic effect. However, phenylephrine produced no increase in cardiac output, increased systemic vascular resistance and mean arterial pressure and reduced muscle blood flow in anaesthetized horses (Lee et al 1998). Phenylephrine should be reserved for critical conditions where the perfusion of essential organs is compromised and inotropes are not effectively maintaining organ function. The recommended infusion rates are shown in Table 12.3. 

Phenylephrine is a pure a 1-agonist and is heheved to increase blood pressure through vasoconstriction. Given the presence of cardiac a 1-receptors, phenylephrine also may increase contractility and cardiac output. ... 

There are three clinical trials using phenylephrine in septic shock evaluating 38 patients. Phenylephrine (0.5 to 9 mcg/kg per minute), when used alone or in combination with dobutamine or low doses of dopamine, improves blood pressure and myocardial performance in fluid-resuscitated septic patients. Incremental doses of phenylephrine over 3 hours result in linear dose-related increases in MAP, SVR, heart rate, and stroke index when administered as a single agent in stable, nonhypotensive but hyperdynamic, volume-resuscitated... 

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. 

Baroreflex sensitivity (BRS) is a measure of the reflex bradycardia that follows an increase in systemic blood pressure. This reflex is mediated by arterial baroreceptors and may be measured after injection of phenylephrine or after spontaneous rises in blood pressure (64). Correlation between the two different tests is poor (69) and measures of baroreflex sensitivity are only moderately reproducible (70). Data on the ability of BRS to predict sudden death are conflicting. In the ATRAMI study in 1284 patients post-MI, HRV, and BRS were assessed at discharge (71). Depressed HRV and BRS carried a significant risk of cardiac mortality when both parameters were depressed the risk increased further. Thus, ATRAMI demonstrated that since BRS adds to the prognostic value of HRV, the two measures are complimentary rather than redundant. However, in another study of 700 post-MI patients, HRV or BRS was not predictive of SCD (60). BRS also does not appear useful for risk stratification in patients with nonischemic cardiomyopathy (63). 

Concomitant use of trimipramine with sympathomimet-ics, including epinephrine, phenylephrine, phenylpropanolamine, and ephedrine (often found in nasal sprays) may increase blood pressure. Use with warfarin may increase prothrombin time and cause bleeding. 

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. 

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