How does angiotensin II increase the workload of the heart after a myocardial infarction (MI)?

A. Bradycardia: Bradycardia, which is a slower than normal heart rate, is not a typical clinical manifestation of pleural effusion with empyema. In fact, fever and infection usually lead to tachycardia (an increased heart rate) as the body attempts to respond to infection.

B. Pleural pain: Pleural pain is a common symptom associated with pleural effusion and empyema, resulting from irritation of the pleura due to inflammation or infection.

C. Cough: A cough can occur with pleural effusion and empyema, often as a response to irritation or pressure in the thoracic cavity. It may also be associated with underlying lung conditions contributing to the effusion.

D. Fever: Fever is a typical clinical manifestation of empyema, indicating an infectious process. The presence of infection in the pleural space often results in systemic signs of infection, such as fever.

A. By causing dysrhythmias as a result of hyperkalemia: Angiotensin II does not directly cause dysrhythmias through hyperkalemia. While hyperkalemia can lead to dysrhythmias, angiotensin II primarily acts as a vasoconstrictor and does not directly influence potassium levels.

B. By increasing peripheral vasoconstriction: Angiotensin II increases peripheral vascular resistance through vasoconstriction, which raises blood pressure. This increased resistance requires the heart to work harder to pump blood, thereby increasing the workload on the heart following a myocardial infarction.

C. By stimulating the sympathetic nervous system: Angiotensin II does stimulate the sympathetic nervous system, which can increase heart rate and contractility; however, the direct effect on increasing workload is more prominently due to peripheral vasoconstriction.

D. By reducing the contractility of the myocardium: Angiotensin II does not reduce contractility; in fact, it can enhance contractility in some contexts. It primarily increases the workload of the heart through vasoconstriction and increased afterload rather than reducing contractility.