A 66-year-old man is evaluated for recurrent syncope. He has had 3 episodes of dizziness and palpitations followed by brief loss of consciousness over the last 6 months. He has no chest pain or dyspnea. The patient has a history of hypertension and hyperlipidemia. There is no family history of sudden death. Initial evaluation shows normal ECG and echocardiogram. A cardiac electrophysiologic study is performed. During the study, intravenous infusion of a medication is administered and produces the responses shown below. Which of the following medications was most likely administered to this patient?

Question

A 66-year-old man is evaluated for recurrent syncope.  He has had 3 episodes of dizziness and palpitations followed by brief loss of consciousness over the last 6 months.  He has no chest pain or dyspnea.  The patient has a history of hypertension and hyperlipidemia.  There is no family history of sudden death.  Initial evaluation shows normal ECG and echocardiogram.  A cardiac electrophysiologic study is performed.  During the study, intravenous infusion of a medication is administered and produces the responses shown below.  Which of the following medications was most likely administered to this patient?

Quizplus · Accepted Answer

11ec160b_3ba0_11eb_9249_ef6454b507b5_MD0001_00 The effects seen in the graphs above are most similar to those elicited by isoproterenol, a nonselective β adrenergic agonist. Isoproterenol increases cardiac contractility (positive inotropic effect) by acting on myocardial β-1 adrenergic receptors. It also binds to β-2 adrenergic receptors and causes vasodilation by relaxation of vascular smooth muscle, leading to decreased vascular resistance and mean arterial blood pressure. Isoproterenol has negligible effects on α-1 adrenergic receptors. (Choice A) Acetylcholine binds to M₂ muscarinic receptors in the heart and M₃ receptors in the vasculature and causes decreased heart rate and conduction velocity and vasodilation (indirectly mediated by endothelial nitric oxide release). Acetylcholine has no significant effect on ventricular contractility. (Choice B) Adenosine acts on A1 receptors on cardiac cells and activates potassium channels, increasing potassium conductance. This leads to transient conduction delay through the atrioventricular node. Adenosine can also cause peripheral vasodilation, but it attenuates the adrenergic-mediated increase in myocardial contractility. (Choice C) Clonidine stimulates α₂ adrenoceptors in the brainstem, resulting in reduced sympathetic outflow from the central nervous system, leading to a decrease in peripheral vascular resistance, heart rate, and blood pressure. It has no effect on cardiac contractility. (Choice D) Esmolol is a selective β-1 adrenergic blocking agent with negative inotropic and chronotropic effects. It would cause a decrease in cardiac contractility. (Choice F) Norepinephrine acts on α-1 receptors, causing vasoconstriction and an increase in systemic vascular resistance. Norepinephrine also acts as a weak agonist at β-1 receptors, with a modest increase in myocardial contractility. (Choice G) Phenylephrine is a sympathomimetic drug with pure α adrenergic agonist activity. Infusion of this drug causes vasoconstriction with an increase in systemic vascular resistance. Educational objective: Isoproterenol is a β-1 and β-2 adrenergic receptor agonist that causes increased myocardial contractility and decreased systemic vascular resistance.

A 66-Year-Old Man Is Evaluated for Recurrent Syncope