Question 1
VT-ECC-056
A dog with a severe infection has developed a systemic inflammatory response and is now in shock, with hypotension and weak femoral pulses. Which mechanism best accounts for the fall in stroke volume and cardiac output in this patient?
- AMediators released by the infection are depressing myocardial contractility, so the ventricle empties less completely with each beat.
- BThe infection has driven the heart rate so high that the ventricle has too little time to fill, lowering end-diastolic volume.
- CVasodilatory mediators have expanded the vascular compartment, so blood is displaced away from the central circulation and preload falls.
- DFluid losses caused by the infection have reduced the total blood volume, so less blood is returning to the heart to fill it.
Show answer
The answer is C.
Why C is right
- Sepsis produces distributive shock: the vascular compartment itself expands.
- Vessel tone is lost through a decrease in sympathetic control, vasodilatory mediators, or both.
- A normal volume of blood is then insufficient to fill the dilated compartment.
- Blood is displaced from the central circulation, preload is diminished, and stroke volume and cardiac output fall.
Why the others are wrong
- A and B: forms of cardiac dysfunction (a weak pump, too little time to fill), not what sepsis does.
- D: in distributive shock there is no total decrease in blood volume; the blood is in the wrong place rather than gone.
Full explanation
Sepsis is the systemic inflammatory response to an infection, and the form of shock it produces is distributive shock. In distributive shock the vascular compartment itself expands. Vessel tone is lost - through a decrease in sympathetic control of vasomotor tone, through the release of vasodilatory mediators, or both - and a normal volume of blood is then insufficient to fill the dilated compartment. Blood is displaced away from the heart and the central circulation, preload is diminished, and stroke volume and cardiac output fall as a result. In sepsis specifically, various mediators are released that affect capillary permeability and the distribution of blood flow to the tissues and organs; prostaglandin is one example of a mediator that causes vasodilation. Sepsis, anaphylaxis and neurogenic states all reach shock by this route.
Option D is the tempting one, because the end result - poor preload, poor cardiac output - looks identical at the cage side. The distinction is that in distributive shock there is no total decrease in blood volume; the blood is in the wrong place rather than gone, which is why the category exists as something separate from hypovolemic shock.
Options A and B describe real mechanisms of poor cardiac output, but both are forms of cardiac dysfunction rather than what sepsis does. Reduced contractility means the pump is weak, and a tachyarrhythmia lowers end-diastolic volume by denying the heart enough time to fill - each will drop stroke volume and cardiac output, but neither depends on the vascular compartment having enlarged.
Small Animal Emergency and Critical Care for Veterinary Technicians
Battaglia, Steele, 4th edition — chapter 14, page 483