How does angiotensin II increase the workload of the heart?

Angiotensin II plays a critical role in the regulation of blood pressure and fluid balance, primarily by acting as a potent vasoconstrictor. When angiotensin II increases peripheral vascular resistance, it narrows blood vessels, leading to elevated blood pressure. This increase in resistance forces the heart to pump harder to maintain adequate blood flow and pressure throughout the body.

As the heart works against this heightened resistance, the workload significantly increases. This can be particularly detrimental in the context of acute coronary syndrome, where the heart may already be compromised. Consequently, the workload on the heart is a crucial factor that can exacerbate existing issues such as ischemia or heart failure.

The other options would not directly explain the increased workload of the heart. Angiotensin II does not directly cause dysrhythmias; while electrolyte imbalances can have this effect, it is not the primary mechanism through which angiotensin II impacts heart workload. Additionally, angiotensin II is known to enhance contractility, not reduce it, which contradicts the third option. Finally, although angiotensin II does stimulate the sympathetic nervous system, this pathway contributes to the overall cardiovascular response rather than being a direct cause of increased workload tied exclusively to resistance.