Test 2 Adrenergics Flashcards
Epinephrine
Low Dose: β-agonist. Increase systolic BP, HR, CO (β1); decrease diastolic BP (β2).
High Dose: adrenergic agonist. Increase TPR and CO (α1, α2, β1) leading to increased systolic (β1) and slight diastolic BP (α1, α2, w/ β2 countering).
Ind: Anaphylaxis, cardiac arrest, and bronchospasm (heart block)
Tox: Arrhythmias (Ca2+ channel activation) (cerebral hemorrhage, anxiety, cold, pulm. edema from rapid increase in BP)
Contra: Late term pregnancy (issues with fetal blood flow)
Does not cross BBB
Norepinephrine
α1, α2, β1 stimulation.
Physio: Increases CO (β1), TPR (α1, α2), and MAP; decreases HR (baroreflex)
Ind: Vasodilatory shock (too much vasoconstriction)
Tox: Ischemia
Contra: Ischemia/pre-existing vasocontriction
Dopamine
D1, D2 (low dose), β1 (med.), α1, α2 (high) stimulation
Low dose: Decrease TPR (D1); increase CO, chronotropy and ionotropy (β1).
High dose: Increase TPR and MAP (α1, α2)
Ind: Cardiogenic shock (low dose, increase CO w/o TPR and is vasodilatory in renal/mesenteric beds (renal/splanchnic vessels))
Tox: Low BP (low dose), ischemia (high dose)
Contra: (tachyarrythmias, ventricular fibrillation)
Isoproterenol
β1, β2 stimulation (β non-selective)
Physio: Decrease TPR (β2), increase CO (β1), HR (β1, β2 baroreflex), bronchodilation (β2). Slight MAP decrease (β2) w/ transient systolic increase.
Ind: Bradycardia, heart block with highTPR (avoiding baroreflex stim)
Tox: Tachyarrythmias
Contra: Angina with arrhythmias
Dobutamine
β1 agonist at low doses
Physio: Increase CO (ionotropy, little chronotropy b/c no baroreflex tachycardia)
Ind: Short-term treatment of cardiac insufficiency with chronic heart failure, cardiogenic shock, (β-blockade)
Tox: Hypotension at high doses
Terbutaline and Albuterol
β2 agonist
Physio: Bronchodilation and (uterine relaxation in pregnant uterus)
Ind: Bronchospasm, chronic treatment of obstructive airway disease
Tox: Tachycardia (β1 at high doses), tolerance, skeletal muscle tremors (pre-synaptic β2 receptors on cholinergic somatomotor neurons lead to increased NT release at NMJ)
Phenylephrine
α1 agonist
Physio: Increases TPR, MAP, decreases HR (baroreflex), pupillary dilation, decreases bronchiole and sinus secretions.
Ind: Hypotension during anesthesia (pressor for anesthetics), paroxysmal SV tachycardia, mydriatic (dilatory) agent in ophthalmic treatment, nasal congestion
Tox: Hypertension
Contra: (hypertension, ventricular tachycardia)
Not subject to degradation by COMT
Clonidine
α2 agonist
Physio: Acute BP increase (peripheral effect) followed by decreased BP (central effect)
Ind: Hypertension due to increased sympathetic drive
Tox: Dry mouth, hypertensive crisis (after acute withdrawal), (sedation, bradycardia)
α2 receptors on pre-motor neurons (provide tonic stimulus to pre-gang symp.) stimulated, decreasing their excitatory output, leading to a decreased output to the vasc. smooth muscle.
Amphetamine
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Potential for abuse because of dopamine release after crossing BBB
Resistant to degradation (not a catecholamine)
Methamphetamine
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Potential for abuse because of dopamine release after crossing BBB (esp. meth)
Resistant to degradation (not a catecholamine)
Methylphenidate
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Potential for abuse because of dopamine release after crossing BBB
Resistant to degradation (not a catecholamine)
Ephedrine
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Potential for abuse because of dopamine release after crossing BBB
Resistant to degradation (not a catecholamine)
Pseudoephedrine
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Potential for abuse because of dopamine release after crossing BBB
Resistant to degradation (not a catecholamine)
Tyramine
Indirect acting sympathomimetic. Taken up by reuptake channels, reverse the channels, releasing NE in a Ca2+ independent fashion.
Physio: Increased TPR, diastolic BP (α1, α2), +ionotropy and chronotropy (β1) and increased systolic BP. (Similar to NE)
Ind: ADD, narcolepsy, and nasal congestion
Tox: Tachycardia
Contra: MAO inhibitor within 2wks
Not a drug, but same effect if have taken and MAOi.
Resistant to degradation (not a catecholamine)
Propranolol
non-selective β-blocker. High BP. Orig, cross BBB w/ short 1/2 life.
Physio: Decrease HR, contractility, renin release, sympathetic activation, and inhibits aqueous humor production.
Ind: Hypertension, angina, early/moderate heart failure (decreased angiotensin), arrhythmias, thyrotoxicosis (excessive symp stim by thyroid), anxiety (banned by PGA)
Tox: Bronchospasm, masks symptoms of hypoglycemia, bradycardia, (insomnia, wild dreams, depression).
Contra: Bronchospasm during asthma, sinus bradycardia, 2nd/3rd degree heart block, cardiogenic shock
