Question 1
VT-PHA-013
A 9-year-old Cavalier King Charles Spaniel with Stage B2 myxomatous mitral valve disease (MMVD) and echocardiographic evidence of cardiomegaly is prescribed pimobendan. The owner asks how this medication differs from the digoxin their previous dog received for heart failure. What is the key mechanistic difference between pimobendan and digoxin in how they increase cardiac contractility?
- APimobendan increases calcium release from intracellular storage sites, while digoxin increases calcium binding to contractile elements
- BPimobendan increases calcium binding to contractile elements, while digoxin increases calcium release from intracellular storage sites
- CPimobendan inhibits the sodium-potassium-ATPase pump, while digoxin directly stimulates beta-1 adrenergic receptors
- DPimobendan is a pure vasodilator with no inotropic effect, while digoxin is a pure positive inotrope with no vasodilator effect
Show answer
The answer is B.
Why B is right
- Pimobendan increases the sensitivity of the contractile elements (troponin C) to calcium, enhancing calcium binding.
- Digoxin inhibits the sodium-potassium-ATPase pump; intracellular sodium accumulates and displaces calcium from its storage sites.
Why the others are wrong
- A: reverses the mechanisms.
- C: misattributes digoxin's mechanism to pimobendan.
- D: false; pimobendan has both inotropic and vasodilator effects.
Full explanation
Pimobendan is an inodilator, meaning it acts as both a positive inotrope and a vasodilator. Its positive inotropic mechanism is unique: unlike catecholamines (dobutamine) or digoxin, pimobendan does not increase the release of calcium from intracellular storage sites. Instead, it increases the sensitivity of the contractile elements (troponin C) to calcium, enhancing calcium binding and producing a more effective contraction without raising intracellular calcium concentration. Digoxin, by contrast, inhibits the sodium-potassium-ATPase pump, causing intracellular sodium to accumulate, which displaces calcium from its storage sites and increases calcium availability for contraction. This elevated intracellular calcium is thought to contribute to digoxin's arrhythmogenic risk and reduced long-term survival compared to pimobendan.
Option A reverses the mechanisms.
Option C misattributes digoxin's mechanism to pimobendan and invents a beta-1 mechanism for digoxin.
Option D is false because pimobendan has both inotropic and vasodilator effects.
Bill's Clinical Pharmacology and Therapeutics for Veterinary Technicians
Anderson, 5th edition — chapter 5, page 122