Adrenergic drugs – Flashcards

effects perfusions which leads to effecting blood pressure

Alpha-adrenergic receptors Beta-adrenergic receptors Dopaminergic receptors: respond only to dopamine

Located on postsynaptic effector cells (the cell, muscle, or organ that the nerve stimulates

Vasoconstriction CNS stimulation - effects if muscle stretched or dialates - effects GI and urine spinchters

All are located on postsynaptic effector cells Beta1-adrenergic receptors—located primarily in the heart - heart - epinehphrine and nor epi - going to be increased Beta2-adrenergic receptors—located in smooth muscle of the bronchioles, arterioles, and visceral organs - lungs - decrease - smooth muscle, GI tract, urinary bladderw, skeletal muscle, and some coronary verssles

Bronchial, GI, and uterine smooth muscle relaxation Glycogenolysis Cardiac stimulation B1 & B2 determines where stimulatuion occurs

Causes dilation of the following blood vessels, resulting in increased blood flow Renal Mesenteric Coronary Cerebral

Effects are similar or mimic the effect of the sympathetic nervous system (SNS) neurotransmitte

Endogenous Norepinephrine (NE), Epinephrine (EPI), Dopamine Synthetic - Dobutamine, phenylephrine

Phenylephrine, metaproterenol (asthma), and albuterol (relax airway smooth muscle) Longer duration of action than either the endogenous or synthetic catecholamines

Selective (only affect one receptor subtype): phenylephrine and clonidine Nonselective agonists act at both alpha and beta receptors -Epinephrine and norepinephrine

Adrenergic drugs stimulate alpha1 adrenergic receptor sites located on smooth muscles, vasoconstriction usually occurs Binding to these alpha1 receptors can also cause: Relaxation of GI smooth muscle (decreased motility) Contraction of the uterus Constriction of the bladder sphincter Male ejaculation Contraction of pupillary muscles of eye (dilated pupils) Beta1-adrenergic receptors on myocardium & conduction system of the heart, including the SA & AV node Stimulation with adrenergic drugs causes 3 things: Increased force of contraction (positive inotropic effect) Increased heart rate (positive chronotropic effect) Increased conduction through AV node (positive dromotropic effect) Bronchodilation (relaxation of the bronchi) Stimulation of beta2-adrenergic receptors on the airways results in Other effects of beta2-adrenergic stimulation Uterine relaxation Glycogenolysis in the liver

Used in the treatment of a wide variety of illnesses and conditions Their selectivity for either alpha or beta-adrenergic receptors & affinity for certain tissues/organs determine the settings in which they are most commonly used

Bronchodilators are adrenergic drugs that tend to stimulate the beta2-adrenergic receptors and cause bronchodilation Beta2 agonists are helpful in treating conditions such a asthma and bronchitis Common bronchodilators classified as beta2-selective adrenergic drugs include Albuterol Ephedrine Formoterol Terbutaline: used to stop premature labor—causes relaxation of uterine smooth muscle

Intranasal application of certain adrenergics can cause constriction of dilated arterioles and reduction in nasal blood flow - which decreases congestion These drugs work by stimulating alpha1-adrenergic receptors & have little or no effect on beta-adrenergic receptors examples: Ephedrin Naphazoline Phenylephrine

Stimulate alpha-adrenergic receptors located on small arterioles in the eye Temporarily relieve conjunctival congestion by causing arteriolar vasoconstriction Can also be used to decrease intraocular pressure - useful in treatment of open-angle glaucoma Can dilate the pupils (mydriasis) which is useful for eye exams

Adrenergic drugs are also used to support the cardiovascular system during cardiac failure & shock These drugs have a variety of effects on various alpha and beta-adrenergic receptors These drugs are referred to as - vasoactive sympathomimetics - vasoconstrictive drugs (also known as vasopressive drugs, pressor drugs, or pressors) - Inotropes - Cardioselective sympathomimetics

Dopamine Ephedrine Epinephrine: medication error w/ neo bc the close name Fenoldopam, Midodrine Norepinephrine (Levophed) Phenylephrine (Neo-Synephrine): medication error bc the names are close together

CNS - Headache, restlessness, excitement, insomnia, euphoria Cardiovascular - Palpitations (dysrhythmias), tachycardia, vasoconstriction, hypertension Other - Loss of appetite, dry mouth, nausea, vomiting, taste changes (rare)

CNS Mild tremors, headache, nervousness, dizziness Cardiovascular Increased heart rate (positive chronotrophy), palpitations (dysrhythmias), fluctuations in BP Other Sweating, nausea, vomiting, muscle cramps

The toxic effects of adrenergic drugs are an extension of their common adverse effects Seizures from excessive CNS stimulation Hypotension or hypertension Dysrhythmias Palpitations Nervousness Dizziness Fatigue Malaise Insomnia If having this problem just turn the drug off bc it has a short half life. Hopefully you can stop this before it happens.

Anesthetic drugs ↑ cardiac dysrhythmias Tricyclic antidepressants - Acute hypertensive crisis MAOIs - Life-threatening hypertensive crisis Antihistamines ↑ effects of adrenergic drugs Thyroid preparations - ↑ effects of adrenergic drugs Adrenergic antagonists - Will directly antagonize each other, resulting in reduced effects Includes some antihypertensives

Used to treat failing heart or shock Used to treat hypotension Wide range of effects on alpha and beta-adrenergic receptors - depending on dosage Very potent, quick-acting, injectable drugs ALL doses are titrated to the desired physiologic response All have a rapid onset (except midodrine) & effects will cease once administration is stopped

Beta1-selective vasoactive adrenergic Stimulates beta1 receptors on heart muscle Increases cardiac output by increasing contractility (positive inotrophy) Increases stroke volume especially in patients with heart failure Available only in IV form (preferably through a central line) and is a continuous infusion

Naturally occurring catecholamine neurotransmitter Potent dopaminergic, beta1 & alpha1-adrenergic receptor activity Low dosages can dilate blood vessels in the brain, heart, kidneys and mesentery High doses can improve cardiac contractility and output At the highest doses dopamine can cause vasoconstriction IV infusion only preferably through a central

Endogenous vasoactive catecholamine Acts directly on alpha and beta-adrenergic receptors Used in emergency situations Primary drug used in ACLS (cardiac arrest) Low doses - stimulates beta1 adrenergic receptors (increasing force of contraction & HR) Used to treat acute asthma attacks & anaphylactic shock because of bronchodilatory effects

Peripheral dopamine1 (D1) agonist indicated for parental use to lower blood pressure Induces arteriolar vasodilation mainly through stimulation of D1 receptors Used for severe hypertension & positive benefits on renal function due to increasing renal blood flow

Prodrug that is converted in the liver to its active form, desglymidodrine desglymidodrine is responsible for the primary action of midodrine which is alpha1 adrenergic receptor stimulation Causes constriction of arterioles and veins resulting peripheral vasoconstriction Indicated primarily for symptomatic orthostatic hypotension Last dose of day should not be given after 6 pm

Stimulates alpha-adrenergic receptors which leads to vasoconstriction Direct stimulating beta-adrenergic effects on heart (beta1-adrenergic receptors) Used for treatment of shock and hypotension Given only by continuous infusion via central line

Works exclusively on alpha-adrenergic receptors Control some dysrhythmias (SVT - supraventricular tachycardia) Produce vasoconstriction in regional anesthesia Used for short-term treatment to raise blood pressure in patients in shock Topically as ophthalmic drug Nasal decongestant

Assess for allergies, asthma, and history of hypertension, cardiac dysrhythmias, or other cardiovascular disease Assess renal, hepatic, and cardiac function before treatment Perform baseline assessment of vital signs, peripheral pulses, skin color, temperature, and capillary refill; include postural blood pressure and pulse Follow administration guidelines carefully

Intravenous administration Check IV site often for infiltration Use clear IV solutions Use an infusion pump Infuse drug slowly to avoid dangerous cardiovascular effects Monitor cardiac rhythm

Instruct patients to avoid factors that exacerbate their condition Encourage fluid intake (up to 3000 mL/day) if permitted Educate patients about proper dosing, use of equipment (metered-dose inhaler [MDI], spacer, nebulizer), and equipment care

Salmeterol is indicated for prevention of bronchospasms, not management of acute symptoms Overuse of nasal decongestants may cause rebound nasal congestion or ulcerations Avoid over-the-counter or other medications because of possible interactions Administering two adrenergic drugs together may precipitate severe cardiovascular effects such as tachycardia or hypertension

Monitor for therapeutic effects (cardiovascular uses) Decreased edema Increased urinary output Return to normal vital signs Improved skin color and temperature Increased LOC

Monitor for therapeutic effects (asthma) Return to normal respiratory rate Improved breath sounds, fewer crackles Increased air exchange Decreased cough Less dyspnea Improved blood gases Increased activity tolerance