Antianginal therapy is usually nitrates and/or beta blockers (fa18 p 312). Nitrates cause vasodilation and reflex TACHYcardia, the pt has bradycardia, suggesting beta blocker.
B1 receptor causes incr HR and contractility, suggesting the drug was antagonist of this (b1 selective antagonists = A-M olol's, FA18 p 241).
Isoproterenol is a B1=B2 sympathomimetic (FA18 p 238) so would agonize the blocked receptors, increasing HR.
An irreversible drug (like aspirin as irrev cox inhibitor) would take longer to overcome (must wait for synthesis of new cells or enzymes). The fact that the patient took 4x the normal dose and had severe effects suggests dose dependent response.
submitted by โcheesetouch(250)
Antianginal therapy is usually nitrates and/or beta blockers (fa18 p 312). Nitrates cause vasodilation and reflex TACHYcardia, the pt has bradycardia, suggesting beta blocker.
B1 receptor causes incr HR and contractility, suggesting the drug was antagonist of this (b1 selective antagonists = A-M olol's, FA18 p 241).
Isoproterenol is a B1=B2 sympathomimetic (FA18 p 238) so would agonize the blocked receptors, increasing HR.
An irreversible drug (like aspirin as irrev cox inhibitor) would take longer to overcome (must wait for synthesis of new cells or enzymes). The fact that the patient took 4x the normal dose and had severe effects suggests dose dependent response.