The physician prescribes 0.15 mg of digoxin IV push for a heart failure patient.

The available dose is 1 mg/1 ml. How many milliliters will the nurse administer?

Choice A rationale

While aspirin does possess analgesic properties by inhibiting the synthesis of prostaglandins in the central and peripheral nervous systems, this is not the primary reason for its prescription following a myocardial infarction. In the context of post-MI care, the dose of 325 mg is intended for its systemic vascular benefits rather than simple pain relief. Other medications or lower doses of aspirin might be used for pain, but the clinical priority here is cardiovascular protection.

Choice B rationale

Aspirin exhibits anti-inflammatory effects by blocking cyclooxygenase enzymes, which reduces the production of mediators that cause tissue swelling and pain. Although inflammation plays a significant role in the progression of atherosclerosis, the specific indication for a client with a history of myocardial infarction focuses more on the immediate prevention of acute thrombotic events. While the anti-inflammatory benefit is present, it is secondary to the critical need for maintaining patency in the coronary arteries.

Choice C rationale

The antipyretic action of aspirin involves acting on the hypothalamus to override an interleukin-induced increase in body temperature. While effective for reducing fever, this pharmacological action is irrelevant to the long-term management of a client with a history of myocardial infarction. Clients in this category are not typically suffering from chronic febrile conditions; therefore, using aspirin for its heat-reducing properties would not provide the specific secondary prevention required for their underlying cardiac pathology.

Choice D rationale

In post-myocardial infarction management, aspirin is primarily used for its antiplatelet aggregate effect. It irreversibly inhibits the cyclooxygenase-1 enzyme within platelets, preventing the formation of thromboxane A2, which is a potent inducer of platelet aggregation. By reducing the ability of platelets to clump together, aspirin decreases the risk of re-occlusion of coronary arteries and prevents subsequent ischemic events. This is the therapeutic cornerstone for long-term survival and reduction of recurrent cardiac mortality.

Choice A rationale

Dilation of coronary arteries actually facilitates increased blood flow and is a physiological response during exercise to meet metabolic demands. In coronary artery disease, the vessels are typically unable to dilate effectively due to atherosclerosis and endothelial dysfunction. Increased pressure within the vessel does not cause the typical manifestations of angina; rather, it is the obstruction and lack of flow through a narrowed lumen that leads to the clinical symptoms experienced by the client.

Choice B rationale

Coronary artery disease involves the buildup of plaque within the intimal layer of the vessel wall, a process known as atherosclerosis. This plaque accumulation progressively decreases the diameter of the artery, creating a physical obstruction. Consequently, during periods of increased myocardial oxygen demand, the restricted blood flow cannot deliver sufficient oxygen and nutrients to the myocardium. This imbalance between supply and demand results in myocardial ischemia, which is the underlying cause of anginal pain and potential infarction.

Choice C rationale

While chronic ischemia can eventually lead to weakening of the heart muscle, known as ischemic cardiomyopathy, the term weakening does not accurately describe the primary correlation in coronary artery disease. Perfusion is poor because of the physical narrowing and reduced elasticity of the coronary vessels, not because the vessels themselves are weak. Angina is specifically a symptom of oxygen deprivation caused by the arterial blockage rather than a generalized weakening of the cardiovascular structural components.

Choice D rationale

As individuals age, coronary arteries generally become less elastic and more rigid due to calcification and collagen deposition, a process termed arteriosclerosis. Increased elasticity would actually allow the vessels to better accommodate blood flow. The lack of oxygen reaching the heart in coronary artery disease is caused by the stiffening and narrowing of the lumen, which prevents the vessels from stretching or dilating to accommodate the blood flow necessary to meet the metabolic needs of the heart.