An ECG has been ordered for a newly admitted patient.
What should the nurse do prior to electrode placement?

Choice A rationale:

Antipyretic action refers to the ability to reduce fever. While aspirin does have antipyretic properties, this is not the primary reason it is administered during an MI. Fever is not a characteristic symptom of MI, and reducing fever would not directly address the underlying cause of the MI, which is the formation of a blood clot in a coronary artery.

Choice B rationale:

Antiplatelet action is the ability to prevent platelets from clumping together and forming blood clots. This is the crucial mechanism by which aspirin helps in the setting of an MI.

During an MI, a blood clot forms in a coronary artery, blocking blood flow to the heart muscle. This blockage can cause severe damage to the heart muscle, leading to chest pain, shortness of breath, and potentially life-threatening complications.

Aspirin irreversibly inhibits the enzyme cyclooxygenase (COX), which is essential for platelet aggregation. By blocking COX, aspirin prevents platelets from sticking together and forming new clots. This can help to:

Limit the size of the existing clot in the coronary artery.

Prevent the formation of additional clots that could further block blood flow.

Allow for better blood flow to the heart muscle, reducing damage and improving outcomes.

Choice C rationale:

Analgesic action refers to the ability to relieve pain. While aspirin does have analgesic properties, this is not the primary reason it is administered during an MI. Pain relief is an important aspect of managing MI symptoms, but it does not directly address the underlying cause of the MI, which is the blood clot.

Choice D rationale:

Antithrombotic action is a broader term that encompasses any action that prevents or reduces blood clot formation. Aspirin's antiplatelet action is a specific type of antithrombotic action. However, it's important to note that aspirin does not directly dissolve existing clots; it primarily prevents new clots from forming.

Choice A rationale:

Blocking impulse transmission to the AV node is not the primary function of an ICD. This is typically achieved through medications such as beta blockers or calcium channel blockers, or through a procedure called AV node ablation.

While ICDs can sometimes have a secondary effect of slowing AV node conduction, their primary purpose is to actively monitor heart rhythm and deliver electrical shocks when necessary to restore normal rhythm.

Choice B rationale:

Assuming the function of the SA node is not the primary function of an ICD. The SA node, located in the right atrium, is the natural pacemaker of the heart, responsible for initiating electrical impulses that trigger each heartbeat.

While ICDs can sometimes pace the heart if the SA node is not functioning properly, their primary purpose is to intervene when life-threatening arrhythmias occur, rather than to continuously regulate heart rate.

Choice C rationale:

Triggering electrical impulses to the heart is the core function of an ICD. It continuously monitors heart rhythm and can deliver electrical shocks to restore normal rhythm when it detects potentially dangerous arrhythmias, such as ventricular tachycardia or ventricular fibrillation.

These shocks are designed to interrupt chaotic electrical activity in the heart and allow the natural pacemaker to regain control, preventing cardiac arrest and sudden cardiac death.

Choice D rationale:

Increasing ventricular conduction is not the primary function of an ICD. In fact, in some cases, ICDs may actually slow down ventricular conduction to prevent certain types of arrhythmias.

Medications or procedures such as cardiac resynchronization therapy (CRT) are specifically designed to improve ventricular conduction in patients with heart failure.