Anesthesia Pharmacology Chapter
6: Autonomic (ANS) Pharmacology
Practice Questions
Click on the correct answer.
1 / 10
Major mechanism of antihypertensive effects associated with alpha-2-selective adrenergic agonists:
- competitive inhibition of vascular alpha receptors
- reduced sympathetic outflow
Alpha-2-selective adrenergic agonists: examples
- isoproterenol (Isuprel)
- metaraminol (Aramine)
- dopamine (Intropin)
- dobutamine (Dobutrex)
- guanabenz (Wytensin)
Adverse effects associated with clonidine (Catapres):
- dry mouth
- sedation
- sexual dysfunction
- all of the above
Clinical uses for sympathomimetic drugs:
- hypovolemic shock caused by dehydration or blood loss
- cardiogenic shock (pump failure)
- cardiac output obstruction
- loss of peripheral vascular tone
- all of the above
Primary objective sympathomimetic drug use for management of shock:
- increase myocardial contractility
- decreased peripheral resistance
- promote better renal perfusion
- ensure adequate CNS perfusion
- improve coronary perfusion
Most likely to reduce myocardial performance in a damaged heart by increasing afterload:
- isoproterenol (Isuprel)
- phenylephrine (Neo-Synephrine)
- low-dose dopamine (Intropin)
- low-dose epinephrine
Receptor system most likely responsible for improved myocardial contractility when dopamine is administered at low concentrations:
- muscarinic cholinergic receptors
- alpha adrenergic receptors
- beta adrenergic receptors
- dopamine receptors (D1)
- leukotriene receptors
Reasonable intervention(s) to reverse cardiogenic shock caused by acute myocardial infarction
- supplemental oxygen
- IV nitroglycerin
- intra-aortic balloon pump
- revascularization
- all of the above
Phosphodiesterase inhibitor(s) which have positive inotropic actions; might be used in management of cardiogenic shock
- phentolamine (Regitine)
- nitroglycerin
- amrinone (Inocor)
- clonidine (Catapres)
- caffeine
Mechanism by a which methoxamine might terminate paroxysmal supraventricular tachycardia:
- direct action at the AV node
- increases SA nodal rates -- overdrives the ectopic focus
- blocks beta-1-receptors
- causes increased vagal tone through reflex activation -- secondary to increase blood pressure
- directly inhibit sodium channel conductance