Identify whether each item would increase or decrease stroke volume.
Increase stroke volume
Decrease stroke volume
\table[[-= ?Increased venous return,-= ?Decreased preload,? ?Decreased venous return,-= ?Systemic vasodilation],[,Positive inotropic agent,-= ?Negative inotropic ager,]]
The correct answer and explanation is:
Here’s the table with correct answers and explanations for each item related to stroke volume:
Table: Effects on Stroke Volume
| Factor | Effect on Stroke Volume |
|---|---|
| Increased venous return | Increase |
| Decreased preload | Decrease |
| Decreased venous return | Decrease |
| Systemic vasodilation | Increase |
| Positive inotropic agent | Increase |
| Negative inotropic agent | Decrease |
Explanations:
- Increased venous return
Effect: Increase
Venous return refers to the amount of blood returning to the heart. Increased venous return enhances end-diastolic volume (EDV), leading to greater stretch of the ventricular walls. According to the Frank-Starling mechanism, a higher EDV increases the force of contraction, thereby boosting stroke volume. - Decreased preload
Effect: Decrease
Preload is the degree of stretch in the ventricular myocardium at the end of diastole, largely determined by EDV. A decrease in preload reduces the stretch of myocardial fibers, weakening contraction strength and lowering stroke volume. - Decreased venous return
Effect: Decrease
A reduction in venous return leads to a lower EDV, which diminishes preload and the force of contraction, consequently decreasing stroke volume. - Systemic vasodilation
Effect: Increase
Vasodilation decreases systemic vascular resistance (afterload). With lower afterload, the heart can eject blood more efficiently, increasing stroke volume. - Positive inotropic agent
Effect: Increase
Positive inotropic agents (e.g., norepinephrine, digoxin) enhance myocardial contractility by increasing intracellular calcium availability. This strengthens contractions, leading to an elevated stroke volume. - Negative inotropic agent
Effect: Decrease
Negative inotropic agents (e.g., beta-blockers, calcium channel blockers) reduce myocardial contractility by limiting calcium availability or altering signaling pathways. This diminishes contraction strength and lowers stroke volume.