Certified Medical-Surgical Registered Nurse Practice Exam

The primary purpose of administering an ACE inhibitor to a patient with an acute myocardial infarction is to reduce preload and afterload. ACE inhibitors help to decrease the blood volume returning to the heart (reducing preload) and lower peripheral vascular resistance (reducing afterload). This overall reduction in workload on the heart can lead to improved hemodynamics, reducing the strain on a damaged cardiac muscle.

In this context, lowering preload diminishes the fluid returning to the heart, which is particularly important after a myocardial infarction, as the heart may be compromised in its ability to handle increased volume. Additionally, by reducing the afterload, the heart can pump more efficiently, leading to better perfusion and potentially minimizing further ischemic damage.

Other options, while they may seem relevant, do not play the primary role in the context of administering ACE inhibitors post-MI. For instance, minimizing platelet aggregation is typically managed through antiplatelet therapy rather than ACE inhibitors. Although myocardial oxygen consumption and demand are critical considerations in managing an infarction, the direct impacts of ACE inhibitors are most significantly attributed to their effects on preload and afterload, which facilitate enhanced cardiac performance during recovery.