Which of the following BEST describes the primary mechanism for the termination of action of clevidipine?
- (A) Pulmonary excretion
- (B) Redistribution into tissue
- (C) Blood and tissue esterase hydrolysis
Clevidipine is a rapid-acting intravenous dihydropyridine L-type calcium channel antagonist. It has a rapid onset of two to four minutes, with an offset of action of five to 15 minutes. The rapid termination of action is due to the rapid hydrolysis by blood and tissue esterases, similar to the β blocker esmolol. Clevidipine exerts arterial-specific vasodilating effects and is associated with a lowering of afterload by decreasing systemic vascular resistance (SVR), leading to a lower mean arterial pressure (MAP). Because of the selective arterial vasodilating effects, clevidipine has little effect on left ventricular filling pressure or pulmonary capillary wedge pressure. In normotensive patients, it was found to lower pulmonary vascular resistance. In postcardiac surgery patients, clevidipine was found to be effective at lowering MAP and SVR with no effect on cardiac filling pressure, heart rate, or cardiac index.
Clevidipine is relatively insoluble in water and is, therefore, prepared as a lipid emulsion. It has an appearance very similar to propofol (Figure). Therefore, care must be taken to avoid medication errors when these two medications are used. In addition, some concern has been raised regarding the cumulative effect of concurrent infusions of these two lipid-based medications in the critical care setting, especially in patients requiring lipid-based total parenteral nutrition (TPN). At least one case report exists that demonstrated hypertriglyceridemia in the setting of concurrent administration of TPN, clevidipine, and propofol infusion. The termination of action for clevidipine is not related to redistribution or pulmonary excretion.
Answer: C
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