In preparation for cardiac surgery, a patient was taught about measures to prevent venous thromboembolism.
Which statement indicates that the patient clearly understood this education?

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.

Choice A rationale:

Increased afterload refers to the resistance against which the heart must pump to eject blood into the aorta. While increased afterload can contribute to chest pain in certain conditions like aortic stenosis, it's not the primary cause of angina.

Angina is typically triggered by exertion or emotional stress, which increase myocardial oxygen demand. Increased afterload doesn't directly cause this imbalance in oxygen supply and demand, making it less likely to be the primary driver of angina pain.

Choice B rationale:

Inadequate myocardial oxygenation is a key concept in understanding angina, but it's not the most precise answer to the patient's question about the cause of their pain.

It's important to explain the underlying reason for the inadequate oxygenation, which is coronary artery disease.

Choice C rationale:

Coronary artery disease (CAD) is the most common cause of angina. It's characterized by narrowing or blockage of the coronary arteries, which supply oxygen-rich blood to the heart muscle.

When the heart's demand for oxygen exceeds the supply available through the narrowed arteries, it experiences ischemia (lack of oxygen), leading to the characteristic chest pain of angina.

This explanation directly addresses the patient's question about the cause of their pain, linking the symptom to the underlying disease process. Choice D rationale:

Increased preload refers to the amount of blood filling the ventricles before they contract. While increased preload can contribute to heart failure and pulmonary edema, it's not typically a direct cause of angina.