Bradycardia phenylephrine

A) Methacholine-induced tachycardia Nicotine-induced hypertension Norepinephrine-induced bradycardia Phenylephrine-induced mydriasis Pilocarpine-induced miosis... 

Phenylephrine. Phenylephrine hydrochloride is an a -adrenoceptor agonist. Phenylephrine produces powerful vasoconstrictor and hypertensive responses. This results in baroreceptor activation of a reflex bradycardia and thus is useful in the treatment of supraventricular tachyarrhythmias. Unlike epinephrine [51-43-4] the actions of which are relatively transient, phenylephrine responses are more sustained (20 min after iv dosing and 50 min after subcutaneous dosing) (86). 

Phenylephrine 10-1000 pg/minute Seconds Bradycardia, coronary vasoconstriction, decreased renal perfusion, metabolic acidosis Alpha-1, increased cardiac output (CO), decreased systemic vascular resistance (SVR)... 

Phenylephrine, Nasal (Neo-Synephrine Nasal) (OTC) [Vasopressor/Decongestant] Uses Can be used prior to nasal intubation and NG tube insCTtion to reduce bleeding Action a-Adren gic agonist Dose Adults Feds. 1—2 sprays/nostril q4h (usual 0.25%).Caution [C, +/—] HTN, acute pancreatitis, H, coronary Dz, NAG, h5 pCTth5Toidism Contra Bradycardia, arrhythmias Disp Nasal soln (0.125-0.25%) SE Arrh5rthmias, HTN, nasal irritation, dryness, sneezing, HA Interactions May -1- effects OF nitrates EMS Ocular instillation may dilate pupil... 

The clinical uses of these drugs are associated with their potent vasoconstrictor action. They are used to restore or maintain blood pressure during spinal anesthesia and certain other hypotensive states. The reflex bradycardia induced by their rapid intravenous injection has been used to terminate attacks of paroxysmal atrial tachycardia. Phenylephrine is commonly used as a nasal decongestant, although occasional nasal mucosal... 

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. 

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. 

Cardiovascular Disease. Patients with systemic hypertension, arteriosclerosis, and other cardiovascular diseases may be at risk when high concentrations of topically administered adrenergic agonists such as phenylephrine are used. Repeated topical doses or soaked cotton pledgets placed in the conjunctival sac have been associated with adverse cardiovascular effects. Likewise, P-blockers should be avoided or used cautiously in patients with congestive heart disease, severe bradycardia, and high-grade atrioventricular block. Topical P-blockers, however, may be used safely in patients with cardiac pacemakers. 

A 38-year-old white man with a history of coronary artery disease, myocardial infarction, coronary artery by-pass, alcoholism, and depression took a combined massive overdose of diltiazem and atenolol (24). He underwent cardiopulmonary resuscitation because of cardiac arrest bradycardia, hypotension, and oliguria followed and were resistant to intravenous pacing and multiple pharmacological interventions, including intravenous fluids, calcium, dopamine, dobutamine, adrenaline, prenalterol, and glucagon. Adequate mean arterial pressure and urine output were restored only after the addition of phenylephrine and transvenous pacing. He survived despite myocardial infarction and pneumonia. 

Example Hexamethonium will block the reflex bradycardia that occurs when phenylephrine (an alpha-adrenoceptor agonist) causes vasoconstriction, but it will not block a bradycardia that results from the direct activation by ACh of M receptors in the heart. 

The major dired-ading adrenoceptor agonist drugs are described. The alpha agonist phenylephrine increases mean BP, has no effed on pulse pressure, and elicits a reflex bradycardia. Isoproterenol, a beta agonist, decreases mean BP, increases pulse pressure, and causes marked tachycardia. Cardiovascular effects of norepinephrine (NE) are similar to phenylephrine, but it is also a cardiac (i, adrenoceptor j activator. The cardiovascular effects of epinephrine (E) are betalike at low doses and alphalike at high j doses. 

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). 

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). 

The predominant actions of phenylephrine are on the cardiovascular system. Parenteral administration causes a rise in systolic and diastolic pressures due to peripheral vasoconstriction. Accompanying the pressor response to phenylephrine is a marked reflex bradycardia that can be blocked by atropine after atropine, large doses of the peripheral resistance is considerably increased. Circulation time is slightly prolonged, and venous pressure is slightly increased venous constriction is not marked. Most vascular beds are constricted renal, splanchnic, cutaneous, and limb blood flows are reduced, but coronary blood flow is increased. Pulmonary vessels are constricted, and pulmonary arterial pressure is raised. 

The drug is a powerful vasoconstrictor with properties very similar to those of norepinephrine but almost completely lacking the chronotropic and inotropic actions on the heart. Cardiac irregularities are seen only very rarely, even with large doses. In contrast to epinephrine and ephe-drine, phenylephrine produces longer-lasting vasoconstriction, a reflex bradycardia, and increases the stroke output, producing no disturbance in the rhythm of the pulse. 

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