MSN Exam for Coronary Artery Disease 1

EXPLANATION

✔Correct answer:

Taking a blood pressure within 15 minutes after nicotine or caffeine ingestion. Nurse Garcia should avoid taking a blood pressure measurement within 15 minutes after the patient has ingested nicotine or caffeine, as both substances can temporarily elevate blood pressure. Nicotine causes vasoconstriction, increasing vascular resistance, while caffeine acts as a stimulant, potentially raising blood pressure by increasing heart rate and vascular tone. To ensure an accurate reading, the patient should avoid these substances for at least 30 minutes before blood pressure is measured.

Accurate blood pressure readings are critical in the management of primary hypertension to avoid unnecessary treatment or misdiagnosis. The nurse must eliminate factors that can artificially influence the measurement, such as recent physical activity, emotional stress, or stimulants like nicotine or caffeine.

Nicotine and caffeine stimulate the sympathetic nervous system. Nicotine causes a release of catecholamines, such as epinephrine, leading to vasoconstriction and increased heart rate. Similarly, caffeine blocks adenosine receptors, increasing circulating catecholamines, which raises blood pressure temporarily. These effects can lead to falsely elevated readings that do not accurately reflect the patient’s resting blood pressure.

Imagine measuring the water pressure in a pipe right after you’ve just turned on an extra pump to increase flow. The pressure reading will be artificially high due to the pump’s effect. Similarly, nicotine or caffeine acts like a pump, temporarily increasing blood pressure, leading to inaccurate results.

To ensure accurate blood pressure readings, nurses should follow proper procedure and avoid potential errors. Key considerations include:

• Instruct the patient to avoid nicotine, caffeine, or heavy meals for at least 30 minutes before the measurement.
• Ensure the patient is seated quietly for at least 5 minutes before taking the reading, with legs uncrossed and feet flat on the floor.
• Use a properly sized cuff, ensuring the bladder encircles at least 80% of the arm.
• Position the patient’s arm at heart level, supported, and ensure it is not covered by clothing.
• Take multiple readings if needed, at least 1–2 minutes apart, and average the readings for accuracy.

✘Incorrect answer options:

Using a cuff with a bladder that encircles at least 80% of the limb: This is the correct technique for ensuring an accurate blood pressure measurement. Using an incorrectly sized cuff, such as one that is too small, could lead to a falsely elevated reading. Nurse Garcia should always use a properly sized cuff.

Measuring the blood pressure after the patient has been seated quietly for 5 minutes: This is also a correct and necessary step for accurate readings. Blood pressure should always be measured after the patient has been resting quietly to avoid the effects of recent activity or stress.

Positioning the patient seated with their arm bare, supported, and at heart level: This is proper technique. If the arm is not at heart level, or if it is unsupported, it can lead to inaccurate measurements. For example, if the arm is below heart level, readings may be falsely elevated.

EXPLANATION

✔Correct answer:

Allowing bathroom privileges and self-care activities. For a patient recovering from a myocardial infarction (MI) who has been transferred from the coronary care unit to a general medical unit, allowing bathroom privileges and self-care activities is the most appropriate activity level at this stage. This level of activity promotes gradual mobilization while still ensuring the patient does not overexert themselves, as cardiac workload must be carefully monitored during early recovery. Patients post-MI often begin with light activities such as sitting up in a chair, walking short distances, and performing self-care tasks to encourage physical recovery and prevent complications like deconditioning, thromboembolism, or orthostatic hypotension.

After an MI, the myocardium is at risk for further ischemic injury due to the damaged area. Gradual progression of activity minimizes myocardial oxygen demand and allows time for healing while ensuring adequate circulation. Early mobilization under supervision helps reduce the risk of immobility-related complications without overburdening the heart.

Think of the heart as an injured athlete. Just like an athlete who needs to start with light exercises to avoid worsening the injury, the heart after an MI must start with light, low-stress activities to gradually rebuild strength without overexertion.

Nurses play a crucial role in planning and progressing activity levels for post-MI patients. Key nursing actions include:

• Monitor for signs of cardiac intolerance to activity, such as chest pain, shortness of breath, fatigue, or changes in blood pressure or heart rate.
• Educate the patient on recognizing symptoms of overexertion and the importance of pacing activities.
• Encourage self-care tasks like bathing, grooming, or using the bathroom, as these are low-intensity activities that promote independence.
• Collaborate with physical therapy or cardiac rehabilitation programs to ensure structured and safe activity progression.
• Maintain telemetry monitoring to observe for arrhythmias or other cardiac changes during activity.

✘Incorrect answer options:

Unrestricted activity due to continuous monitoring: While telemetry monitoring provides a safety net, unrestricted activity is inappropriate for a patient recovering from an MI, as it may lead to overexertion and cardiac complications. Activity must be gradually progressed under supervision.

Unsupervised ambulation in the hallway for distances less than 200 feet: Ambulation is an important goal for recovery, but it must be supervised, especially in the early stages post-MI. Patients may still experience fatigue, dizziness, or arrhythmias that require prompt intervention.

Strict bed rest for 24 hours post-transfer: Strict bed rest is not recommended for post-MI patients unless there are specific complications. Prolonged immobility can lead to deconditioning, thromboembolism, and respiratory issues. Early mobilization is encouraged once the patient is stable.

EXPLANATION

✔Correct answer:

Apnea. Patients with chronic obstructive pulmonary disease (COPD) often rely on a hypoxic drive to regulate their breathing. In individuals with normal respiratory function, the primary drive to breathe is triggered by rising levels of carbon dioxide (CO₂) in the blood, known as the hypercapnic drive. However, in patients with chronic CO₂ retention (as seen in COPD), the body becomes desensitized to elevated CO₂ levels, and the drive to breathe shifts to being regulated by low oxygen levels (hypoxia).

If a high concentration of oxygen is administered to such a patient, it can suppress the hypoxic drive, resulting in decreased respiratory effort or apnea (temporary cessation of breathing). High oxygen levels can also exacerbate CO₂ retention, leading to worsening hypercapnia and respiratory acidosis. This is why oxygen therapy in COPD patients must be carefully titrated to achieve target oxygen saturation levels (typically 88–92%) without suppressing their respiratory drive.

Pathophysiology of Oxygen-Induced Apnea:

1. High concentrations of oxygen increase arterial oxygen levels.
2. The elevated oxygen reduces the stimulation of the peripheral chemoreceptors that drive respiration in hypoxic patients.
3. This leads to hypoventilation or apnea, further exacerbating CO₂ retention and respiratory depression.

Imagine a campfire that relies on just the right amount of air (oxygen) to keep burning steadily. In a COPD patient, their body has adapted to low oxygen levels to "fan the flames" of their breathing. If you suddenly dump an excessive amount of air (oxygen) onto the fire, it can overwhelm and extinguish the flames, causing the fire (their respiratory drive) to go out. This is why careful oxygen control is critical in these patients.

Nurse Miller must closely monitor Mr. Davis's respiratory status and oxygen therapy to prevent complications related to excessive oxygen delivery.

• Titrate oxygen carefully: Maintain oxygen saturation between 88–92%, as per clinical guidelines for COPD patients.
• Monitor respiratory rate and effort: Watch for signs of respiratory depression, such as shallow breathing, decreased respiratory rate, or lethargy.
• Assess for hypercapnia: Monitor arterial blood gases (ABGs) if the patient shows signs of CO₂ retention, such as confusion, headache, or drowsiness.
• Educate the patient: Teach Mr. Davis about the importance of adhering to prescribed oxygen flow rates and avoiding self-adjustments.
• Consider non-invasive ventilation (NIV): If Mr. Davis's respiratory status worsens, discuss options like BiPAP or CPAP with the healthcare team to provide ventilatory support.

✘Incorrect answer options:

Increased anginal pain. While oxygen may indirectly improve myocardial oxygenation in patients with coronary artery disease, there is no evidence that high-concentration oxygen causes anginal pain. In fact, oxygen is sometimes administered during acute coronary syndromes to improve oxygen supply to the heart, though recent guidelines recommend oxygen only for hypoxemic patients.

Respiratory alkalosis. Respiratory alkalosis is caused by hyperventilation (excessive breathing), which "blows off" too much CO₂, leading to an increased blood pH. However, in COPD patients receiving excess oxygen, the concern is hypoventilation, not hyperventilation, which would cause respiratory acidosis instead.

Metabolic acidosis. Metabolic acidosis is a condition caused by non-respiratory factors, such as lactic acid accumulation, diabetic ketoacidosis, or renal dysfunction. It is not directly related to oxygen administration. In COPD, the risk is respiratory acidosis due to CO₂ retention, not metabolic acidosis.

EXPLANATION

✔Correct answer:

Inferior wall. The right coronary artery (RCA) supplies blood to the inferior wall of the left ventricle in most individuals, as well as portions of the right ventricle, the atrioventricular (AV) node, the sinoatrial (SA) node (in about 55% of people), and the posterior part of the interventricular septum. When a blockage occurs in the RCA, it leads to ischemia or infarction in the areas it supplies, most commonly the inferior wall of the heart.

Electrocardiogram (ECG) Findings in Inferior Wall Myocardial Infarction (MI): Inferior wall MI typically shows ST-segment elevations in leads II, III, and aVF on an ECG, as these leads correspond to the inferior portion of the heart. Symptoms can include chest pain, bradycardia (due to RCA involvement with the SA or AV node), nausea, and diaphoresis.

Imagine the heart as a building with different walls, and the coronary arteries are water pipes supplying those walls. If the right coronary artery is blocked, it’s like cutting off the water to the inferior wall, leading to damage (infarction) in that area.

Nurse Ramirez should monitor for complications associated with inferior wall MI, such as conduction abnormalities and right ventricular involvement.

• Monitor for bradycardia or heart block, as inferior MI can affect the AV or SA node.
• Assess for right ventricular involvement, which may present as hypotension, jugular venous distention (JVD), and clear lung sounds; avoid excessive fluid administration unless specified.
• Administer oxygen, nitroglycerin, and morphine as prescribed to reduce myocardial oxygen demand and alleviate symptoms.
• Educate the patient on the importance of lifestyle modifications to prevent future cardiac events, including smoking cessation, dietary changes, and medication adherence.
• Prepare the patient for potential interventions such as cardiac catheterization or percutaneous coronary intervention (PCI).

✘Incorrect answer options:

Lateral wall. The lateral wall of the left ventricle is primarily supplied by the left circumflex artery (LCX). Blockage in the LCX would result in a lateral wall infarction, not an inferior wall infarction.

Anterior wall. The anterior wall of the left ventricle is supplied by the left anterior descending artery (LAD). An occlusion in the LAD typically leads to an anterior wall MI, characterized by ST-segment elevations in leads V1–V4 on an ECG.

Apex. The apex of the heart is typically supplied by the distal portion of the LAD. Blockages in the LAD can lead to anterior or apical infarction, but this is not related to the RCA.

EXPLANATION

✔Correct answer:

Assess the patient's condition and verify proper lead placement. A flat line on the cardiac monitor (asystole) is a critical finding that requires immediate intervention. However, before assuming that the patient has no cardiac activity, Nurse Evans must assess the patient and verify the accuracy of the reading. A flat line could be caused by a technical issue, such as loose or disconnected ECG leads, rather than true asystole. The nurse should first check for responsiveness, pulse, and breathing to confirm the patient’s actual clinical status, and then ensure that all ECG leads are correctly attached and functioning. This step prevents unnecessary interventions if the flat line is due to a monitoring artifact or equipment issue.

If true asystole is confirmed (no pulse, unresponsiveness, and proper lead placement), immediate initiation of advanced life support measures (e.g., initiating a code blue, starting CPR) is required. However, verifying the patient’s condition and lead placement is the priority initial action because it differentiates between a real emergency and a technical issue.

Asystole is the absence of electrical and mechanical cardiac activity, meaning the heart has completely stopped. It is a life-threatening condition requiring rapid action. However, cardiac monitors are susceptible to artifacts, loose leads, and equipment malfunctions, which can mimic asystole. Assessing the patient ensures that interventions are based on accurate data.

Imagine your phone suddenly shows "no signal," but before assuming that the network is down, you would first check if your phone is properly connected, turned on, or if the problem is just a loose SIM card. Similarly, before treating a flat line on a cardiac monitor, the nurse must confirm if the “no signal” is due to a true emergency (asystole) or just a technical issue like a loose lead.

The nurse must act promptly to verify the situation and respond appropriately. Key steps include:

• Immediately assess the patient for responsiveness, pulse, and breathing.
• Verify that all ECG leads are properly attached to the patient and the cardiac monitor.
• Check for signs of life, such as spontaneous movement or respirations.
• If true asystole is confirmed:
  • Activate the emergency response team (code blue).
  • Begin CPR immediately, following Advanced Cardiovascular Life Support (ACLS) guidelines.
  • Administer epinephrine as directed by the code team.
• If a technical issue is identified (e.g., disconnected lead), correct the issue and continue monitoring the patient’s cardiac status.

✘Incorrect answer options:

Initiate a code blue: While a code blue should be initiated if true asystole is confirmed, the nurse’s first action must be to verify the accuracy of the flat line reading by assessing the patient and ensuring proper lead placement. Jumping to initiate a code blue without confirming asystole risks unnecessary disruption and resource use.

Activate the recording function on the electrocardiogram machine: Recording the ECG may be useful for documentation or further analysis, but it is not the priority when a flat line appears. Immediate assessment of the patient’s condition takes precedence.

Contact the attending physician: Although the physician should be notified if asystole is confirmed, contacting the physician is not the priority when responding to a potential emergency. The nurse must first verify the patient’s status and initiate appropriate interventions if required.

EXPLANATION

✔Correct answer:

Atherosclerosis. The most common cause of coronary artery disease (CAD) is atherosclerosis, a progressive disease characterized by the accumulation of fatty deposits, cholesterol, and other substances in the inner lining of the coronary arteries. Over time, this buildup forms plaques that narrow the arterial lumen, restricting blood flow to the myocardium (heart muscle). Atherosclerosis also contributes to plaque rupture, which can result in the formation of a thrombus (blood clot) and lead to acute coronary syndromes such as myocardial infarction (MI).

The process of atherosclerosis begins with damage to the endothelium, triggered by risk factors such as hypertension, hyperlipidemia, smoking, and diabetes mellitus. The damaged endothelium allows low-density lipoproteins (LDL cholesterol) to penetrate the arterial wall, promoting an inflammatory response. Macrophages engulf the LDL, forming foam cells that contribute to fatty streaks and plaque development. As plaques grow, they stiffen the arterial walls, reduce blood flow, and increase the risk of ischemia and infarction.

Think of coronary arteries as pipes carrying water (blood) to a garden (the heart). Atherosclerosis is like rust and debris building up inside the pipes, reducing the flow of water and starving the garden of what it needs to thrive. Over time, the pipe can become completely clogged, causing severe damage to the garden.

Nurse Peterson should emphasize the importance of addressing modifiable risk factors to slow or prevent the progression of atherosclerosis and CAD.

• Promote a heart-healthy diet low in saturated fats, cholesterol, and trans fats to reduce LDL cholesterol levels and plaque formation.
• Encourage regular physical activity to improve circulation, reduce weight, and manage blood pressure and blood sugar levels.
• Educate about the importance of smoking cessation, as smoking accelerates endothelial damage and atherosclerosis.
• Highlight the importance of managing chronic conditions like diabetes and hypertension to minimize endothelial injury and slow disease progression.
• Stress the need for routine health screenings, including lipid panels, to monitor cholesterol levels and identify risk factors early.

✘Incorrect answer options:

Myocardial infarction (MI). While an MI is a potential consequence of CAD, it is not the underlying cause. MI occurs when atherosclerotic plaque ruptures and triggers the formation of a thrombus, resulting in the complete blockage of coronary blood flow to a portion of the myocardium.

Diabetes mellitus (DM). Diabetes mellitus is a major risk factor for atherosclerosis and CAD due to its association with chronic hyperglycemia, endothelial dysfunction, and increased LDL cholesterol oxidation. However, DM itself is not the direct cause of CAD—it contributes to its development via atherosclerosis.

Renal failure. Renal failure is not a direct cause of CAD but is often a complicating condition. Chronic kidney disease (CKD) can worsen atherosclerosis and CAD due to its association with hypertension, hyperlipidemia, and systemic inflammation. However, it is not the primary etiology of CAD.

EXPLANATION

✔Correct answer:

Warfarin prevents the liver from producing certain clotting factors, and it takes about 3-4 days for this effect to become significant. Warfarin works by inhibiting the action of vitamin K in the liver, which is essential for synthesizing certain clotting factors (II, VII, IX, and X). These clotting factors already exist in the bloodstream when warfarin therapy begins, so it takes approximately 3-4 days for those factors to degrade naturally and for warfarin's anticoagulant effects to become significant. During this time, heparin (a fast-acting anticoagulant) is continued to provide immediate protection against clot formation until warfarin reaches therapeutic levels. This overlap is necessary to prevent thromboembolic events while transitioning between the two medications.

Heparin works quickly by activating antithrombin III, which inhibits clotting factors IIa (thrombin) and Xa, thereby immediately reducing clot formation. In contrast, warfarin indirectly reduces clotting by decreasing the synthesis of vitamin K-dependent clotting factors. Warfarin’s effect depends on the half-life of these clotting factors, which is why it takes a few days to become effective. For example, factor VII has a half-life of about 6 hours, while factor II (thrombin) has a half-life of 50 hours, contributing to the delayed onset of action.

Think of heparin as a fast-acting umbrella that protects you immediately from the rain, while warfarin is like slowly building a roof over your head. It takes time for the roof to be fully constructed (warfarin to take effect), so you need the umbrella (heparin) for protection in the meantime.

Nurses play a vital role in educating patients about the rationale for combined anticoagulant therapy and ensuring safe medication use. Key actions include:

• Explain to the patient that warfarin takes several days to achieve its full anticoagulant effect, necessitating the use of heparin for immediate clot prevention.
• Monitor laboratory values closely, including:
  • Prothrombin Time (PT) and International Normalized Ratio (INR): To assess warfarin effectiveness, with a target INR of 2.0–3.0 for most conditions.
  • Activated Partial Thromboplastin Time (aPTT): To monitor heparin therapy until it is discontinued.
• Watch for signs of bleeding, such as bruising, nosebleeds, or blood in the urine or stool, and educate the patient to report these symptoms immediately.
• Reinforce dietary precautions, particularly the importance of consistent vitamin K intake (e.g., leafy green vegetables), as large changes in dietary vitamin K can interfere with warfarin's effectiveness.
• Ensure the patient understands the importance of medication adherence and routine INR monitoring to maintain safe and effective anticoagulation.

✘Incorrect answer options:

Warfarin works in the same way as heparin, and the overlap is necessary to allow warfarin to reach therapeutic levels in the blood: Warfarin and heparin have different mechanisms of action. Heparin works by inhibiting clotting factors already in the blood, while warfarin prevents the liver from synthesizing new clotting factors. The overlap in therapy is due to warfarin's delayed onset, not because the two drugs work the same way.

Warfarin stimulates the body to produce its own clot-dissolving substances, but this process takes 2-4 days to begin: Warfarin does not stimulate clot breakdown; it prevents the formation of new clots by inhibiting clotting factor synthesis. The body's fibrinolytic system, which breaks down clots, is independent of warfarin's action.

Warfarin increases the breakdown of specific clotting factors in the liver, with noticeable anticoagulant effects starting in 2-3 days: Warfarin does not increase clotting factor breakdown. Instead, it inhibits the synthesis of vitamin K-dependent clotting factors, leading to their gradual depletion over several days.

EXPLANATION

✔Correct answer:

The medication will dissolve any existing blood clots. Thrombolytic therapy, also known as fibrinolytic therapy, is specifically designed to dissolve blood clots (thrombi) that obstruct blood flow in the coronary arteries during a myocardial infarction (MI). These medications, such as alteplase (tPA), work by activating plasminogen to form plasmin, an enzyme that breaks down fibrin, which is a key structural component of blood clots. The dissolution of clots restores blood flow to the ischemic myocardium, minimizing tissue damage and reducing the risk of complications such as heart failure or death.

Thrombolytic therapy is most effective when administered as early as possible, ideally within the first 6 hours of symptom onset. Early restoration of coronary blood flow significantly reduces myocardial damage, improving patient outcomes.

Imagine a thrombus as a traffic jam on a highway (the coronary artery). Thrombolytic therapy acts like a tow truck that removes the cars (the clot) blocking the road, allowing traffic (blood flow) to resume to its destination (the heart muscle).

Nurses play a critical role in monitoring patients receiving thrombolytic therapy. Key interventions include:

• Monitor for signs of bleeding, as thrombolytic therapy increases the risk of hemorrhage, especially at invasive procedure sites.
• Assess vital signs and cardiac rhythm regularly to detect signs of reperfusion or complications such as arrhythmias.
• Monitor for resolution of ischemic symptoms (e.g., decreased chest pain or improved ST-segment elevation on ECG).
• Educate the patient about the purpose of thrombolytic therapy and the importance of reporting any unusual bleeding or changes in condition.
• Collaborate with the healthcare team to prepare for additional interventions, such as percutaneous coronary intervention (PCI), if necessary.

✘Incorrect answer options:

The medication will prevent kidney failure: Thrombolytic therapy is not aimed at preventing kidney failure. While kidney injury may occur as a complication of MI or treatment (e.g., contrast-induced nephropathy during diagnostic or interventional procedures), thrombolytics do not directly address renal issues.

The medication will help maintain proper hydration: Maintaining hydration is important during MI management to support perfusion and prevent complications, but thrombolytics do not have any direct effect on hydration status. Fluid balance is typically managed through IV fluids or oral intake under close monitoring.

The medication will treat potential heart rhythm abnormalities: Thrombolytics do not directly treat arrhythmias. However, restoring blood flow with thrombolytics may indirectly reduce ischemia-related arrhythmias by reestablishing oxygen and nutrient supply to the myocardium. Specific antiarrhythmic drugs or interventions, such as defibrillation, are used to manage heart rhythm abnormalities.

EXPLANATION

✔Correct answer:

All of the choices. Coronary artery disease (CAD) is diagnosed using a combination of tests and procedures designed to evaluate blood flow to the heart, assess for ischemia, and identify structural or functional abnormalities in the coronary arteries. Each of the options listed—treadmill exercise stress test, cardiac catheterization, and electrocardiogram (ECG)—plays an important role in the diagnostic process for CAD. Therefore, the correct answer is that all of these options are used to diagnose CAD.

1. Treadmill Exercise Stress Test: This test evaluates how the heart responds to physical activity. It can reveal signs of ischemia (reduced blood flow to the heart) by identifying abnormal changes in heart rate, blood pressure, or the ECG during exercise. It is often used as a preliminary screening tool for CAD, particularly in patients with stable angina.
2. Cardiac Catheterization: This invasive procedure involves the insertion of a catheter into a coronary artery, typically via the femoral or radial artery. A contrast dye is injected, and X-ray imaging is used to identify blockages or narrowing in the coronary arteries. It is considered the gold standard for diagnosing CAD because it provides direct visualization of the coronary arteries.
3. Electrocardiogram (ECG): This non-invasive test records the electrical activity of the heart and is used to detect abnormalities such as ischemia, myocardial infarction, or arrhythmias. While a resting ECG may appear normal in some patients with CAD, it is an essential diagnostic tool, especially in emergency settings or when combined with stress testing.

Together, these tests provide a comprehensive approach to diagnosing CAD by identifying both structural and functional abnormalities.

Coronary artery disease is caused by atherosclerosis, where plaques made of cholesterol, fatty substances, and inflammatory cells build up in the walls of the coronary arteries. This process restricts blood flow, leading to myocardial ischemia. Diagnostic tests like stress tests and ECGs help identify ischemic changes, while cardiac catheterization directly visualizes the extent of arterial blockage.

Imagine the coronary arteries as water pipes supplying your house. If the water pressure drops or you notice other issues, you might test the system by turning on multiple faucets (stress test), using a camera to check inside the pipes for clogs (cardiac catheterization), or monitoring the flow meter for irregular patterns (ECG). Each method provides valuable insights about the state of the pipes, just as these tests assess heart function and blood flow.

During the diagnostic process, nurses play a critical role in preparing and educating the patient for the various tests, ensuring safety during procedures, and providing emotional support. Key nursing interventions include:

• Explain the purpose and process of each diagnostic test to alleviate patient anxiety and gain informed consent where applicable.
• For the treadmill exercise stress test:
  • Ensure the patient understands the need to avoid caffeine or certain medications before the test.
  • Monitor for signs of chest pain, shortness of breath, or ECG abnormalities during the test.
• For cardiac catheterization:
  • Assess for allergies to contrast dye and premedicate if necessary.
  • Monitor for signs of bleeding or hematoma at the catheter insertion site after the procedure.
• For ECG:
  • Ensure proper placement of electrodes to obtain accurate readings.
  • Interpret the results or communicate findings to the healthcare provider promptly.
• Educate the patient on lifestyle modifications and treatment options following diagnosis to manage CAD.

✘Incorrect answer options:

Each of the other individual options is correct but incomplete when considered alone. None of these tests provides a complete diagnosis of CAD by itself. Instead, they are complementary and often used together to confirm the diagnosis and guide treatment decisions. Therefore, selecting only one option would overlook the comprehensive approach needed for CAD evaluation.

EXPLANATION

✔Correct answer:

Inquiry about allergies to iodine or shellfish. Before a cardiac catheterization, it is critical to assess for allergies to iodine or shellfish because the contrast dye used in the procedure often contains iodine. If the patient has a known allergy to iodine or shellfish, they may be at increased risk of experiencing an allergic reaction to the dye, which can range from mild (itching or rash) to severe (anaphylaxis). Early identification of this risk allows the healthcare team to implement preventive measures, such as premedication with corticosteroids and antihistamines, or choosing an alternative dye if possible.

Contrast dye reactions are a serious concern in cardiac catheterization, making allergy assessment the most important pre-procedure evaluation to ensure patient safety. This aligns with the nursing priority of risk prevention and is considered a standard practice in pre-procedure care for invasive diagnostics involving contrast agents.

Contrast media, particularly iodine-based contrast, can trigger hypersensitivity reactions in some patients. This is due to either direct mast cell activation or an IgE-mediated immune response. Shellfish allergy is commonly used as an indicator due to its association with iodine, although recent studies suggest that the link between shellfish allergy and iodine is less direct than previously thought.

Imagine preparing a car for a wash at an automated carwash that sprays a specific cleaning solution. Before starting, you need to check if the car has any special coatings or materials that might react poorly to the solution—like checking for a wax finish that might strip away. Similarly, before using contrast dye in cardiac catheterization, nurses must check if the patient has a "sensitivity coating" (allergy to iodine or shellfish) that could trigger a harmful reaction, ensuring the procedure is safe and effective.

Key nursing actions before a cardiac catheterization include thorough assessment and preparation. Specific interventions related to contrast dye use are as follows:

• Inquire about allergies to iodine, shellfish, or previous reactions to contrast dyes and document findings.
• If allergies are identified, notify the healthcare provider immediately to consider premedication (e.g., corticosteroids or antihistamines) or alternative contrast agents.
• Ensure the patient is adequately hydrated to reduce the risk of contrast-induced nephropathy (kidney damage from the dye).
• Educate the patient about potential side effects of the contrast dye, such as a warm or flushed sensation during injection.
• Verify that consent for the procedure has been obtained, and review any additional pre-procedure orders (e.g., fasting).

✘Incorrect answer options:

Measurement of height and weight: While height and weight are often measured as part of general assessments or medication dosing calculations, they are not the most critical pre-procedure consideration for cardiac catheterization.

Assessment of baseline peripheral pulses: Peripheral pulse assessment is an important pre-procedure step to document circulation in the extremity that will be accessed for catheter insertion (e.g., radial or femoral artery). However, it is a secondary priority compared to identifying an allergy to contrast dye, which could cause an immediate life-threatening reaction.

Monitoring of intake and output: While monitoring intake and output is vital post-procedure to assess kidney function and fluid status (especially after contrast dye use), it is not the most urgent pre-procedure assessment.

EXPLANATION

✔Correct answer:

Recurring pain or discomfort in the chest, arms, or jaw. The hallmark symptom of coronary artery disease (CAD) is angina pectoris, which manifests as recurring pain or discomfort in the chest. This pain can radiate to other areas, such as the arms, jaw, neck, shoulder, or back. Angina occurs when the heart muscle does not receive enough oxygenated blood, often due to narrowed coronary arteries caused by atherosclerosis. Angina is typically triggered by physical exertion, emotional stress, or heavy meals, and it may be relieved by rest or nitroglycerin.

Other associated symptoms of CAD include shortness of breath, fatigue, nausea, dizziness, or diaphoresis, particularly in women, who may experience more atypical presentations (e.g., fatigue or jaw discomfort without chest pain). Recognizing these symptoms is critical, as they can indicate underlying myocardial ischemia and a risk for more serious events such as myocardial infarction.

Imagine the coronary arteries as pipes supplying blood (fuel) to the heart (engine). If the pipes are narrowed, the engine struggles and sends out warning signals like chest discomfort or pain radiating to other areas, alerting us to address the problem before a breakdown (heart attack) occurs.

Nurse Brown should prioritize assessing Ms. Johnson’s description of her symptoms to determine if they are consistent with angina or another cardiac condition and act promptly to ensure further evaluation.

• Assess the quality, duration, and intensity of the discomfort, and determine if it is relieved by rest or nitroglycerin.
• Ask about associated symptoms, such as shortness of breath, dizziness, nausea, or fatigue, to identify possible myocardial ischemia or atypical presentations.
• Obtain a detailed history of CAD risk factors, such as hypertension, diabetes, smoking, hyperlipidemia, and family history of cardiovascular disease.
• Ensure prompt referral for diagnostic tests, such as an electrocardiogram (ECG), stress testing, or cardiac biomarkers, to evaluate for myocardial ischemia or infarction.
• Educate the patient about recognizing early warning signs of worsening CAD and when to seek emergency care (e.g., symptoms unrelieved by rest or nitroglycerin).

✘Incorrect answer options:

Difficulty falling asleep and staying asleep. While insomnia and sleep disturbances can occur in people with chronic illnesses, they are not specific symptoms of CAD. Sleep disturbances may indirectly exacerbate CAD by increasing stress or contributing to poor management of other risk factors, but they are not direct indicators of the disease.

Frequent episodes of diarrhea. Diarrhea is not associated with CAD. This symptom is more commonly linked to gastrointestinal disorders, infections, or medication side effects and has no direct connection to myocardial ischemia.

Persistent headaches. Headaches are not a typical symptom of CAD. They may be caused by tension, migraines, or other unrelated conditions. While certain cardiac medications (e.g., nitroglycerin) can cause headaches as a side effect, headaches alone are not indicative of CAD.

EXPLANATION

✔Correct answer:

Daily use of antiplatelet medications like aspirin. The daily use of antiplatelet medications, such as aspirin, is a key component of the medical treatment for coronary artery disease (CAD). Antiplatelet medications help to reduce the risk of blood clot formation by preventing platelets from sticking together, which can lower the risk of heart attacks and other complications in CAD patients. Aspirin, in particular, is widely used for secondary prevention in patients with known atherosclerosis or CAD.

Aspirin irreversibly inhibits cyclooxygenase-1 (COX-1), an enzyme involved in the production of thromboxane A2, which promotes platelet aggregation and vasoconstriction. By reducing thromboxane A2 levels, aspirin prevents clot formation, reducing the likelihood of arterial blockages and improving blood flow to the heart.

Think of platelets in the blood as bricks in a construction site that might accidentally block a pipe. Aspirin acts like a safety inspector, ensuring the bricks (platelets) don’t stick together and block the flow of water (blood) through the pipe (artery).

Nurse Davis should educate Mr. Johnson about the proper use of antiplatelet medications, along with their benefits and potential side effects.

• Teach the patient the importance of adherence to prescribed medications to prevent heart attack and stroke.
• Explain common side effects of aspirin, such as gastrointestinal upset or bleeding, and advise reporting any unusual symptoms like black, tarry stools.
• Ensure that the patient does not take aspirin concurrently with other blood-thinning agents (e.g., warfarin) unless specifically directed by the healthcare provider.
• Highlight the need for regular follow-ups to monitor cardiovascular health and adjust treatment as needed.
• Combine medication education with lifestyle modifications such as a heart-healthy diet, weight management, and smoking cessation.

✘Incorrect answer options:

Applying warm compresses to the chest daily. Warm compresses are not a treatment for CAD. While warmth can occasionally provide comfort for muscular or soft tissue pain, it has no effect on reducing arterial plaque, improving blood flow, or managing CAD.

High-intensity aerobic exercise without prior medical clearance. Exercise is an important part of CAD management, but it must be medically supervised, especially for patients with known coronary artery blockages. High-intensity exercise without medical clearance can increase the risk of angina, arrhythmias, or even a heart attack, making this option unsafe.

Regular consumption of herbal teas to clear arterial plaques. While certain herbal teas may have general health benefits (e.g., antioxidant properties), there is no clinical evidence to suggest that herbal teas can "clear" arterial plaques. Treating CAD requires evidence-based interventions, such as medications, lifestyle changes, and sometimes surgical procedures.

EXPLANATION

✔Correct answer:

Protamine sulfate. When initiating intravenous heparin therapy, protamine sulfate must be readily available as it is the specific antidote for heparin. Protamine sulfate binds to heparin, neutralizing its anticoagulant effects, and is used in cases of heparin overdose or excessive bleeding caused by heparin therapy. Ensuring the availability of protamine sulfate is a key safety precaution, as heparin increases the risk of bleeding complications, including hemorrhage.

Heparin works by activating antithrombin III, which inhibits clotting factors IIa (thrombin) and Xa, reducing clot formation. While effective in preventing or treating thrombosis, excessive heparin activity can lead to dangerous bleeding. Protamine sulfate, when administered intravenously, counteracts this effect by forming a stable complex with heparin, rendering it inactive.

Heparin's anticoagulant properties are critical in conditions such as deep vein thrombosis, pulmonary embolism, or myocardial infarction. However, its effects must be carefully monitored using parameters like activated partial thromboplastin time (aPTT). If bleeding occurs or lab values indicate overdose, protamine sulfate provides rapid reversal, minimizing the risk of life-threatening complications.

Imagine heparin as a chemical that melts ice (clots), but too much of it could also damage nearby plants (cause bleeding). Protamine sulfate works like a neutralizer that stops the melting effect, protecting the surrounding area. Similarly, it stops heparin from "overdoing" its job.

Nurse Patel must take several precautions to ensure safe administration of heparin and appropriate use of protamine sulfate if needed:

• Monitor activated partial thromboplastin time (aPTT) to assess the therapeutic effect of heparin and identify potential overdose.
• Observe the patient for signs of bleeding, such as hematuria, melena, ecchymosis, or epistaxis.
• Have protamine sulfate readily available as the antidote in case of heparin-induced bleeding or overdose.
• Administer protamine sulfate cautiously and as prescribed, as rapid administration may cause adverse effects such as hypotension or bradycardia.
• Educate the patient about the signs and symptoms of bleeding and the importance of notifying the healthcare team immediately if they occur.

✘Incorrect answer options:

Vitamin K: Vitamin K is the antidote for warfarin, not heparin. It reverses the anticoagulant effects of warfarin by promoting the synthesis of clotting factors II, VII, IX, and X in the liver.

Potassium chloride: Potassium chloride is used to correct hypokalemia, not as an antidote for anticoagulants. It has no role in heparin therapy.

Aminocaproic acid: Aminocaproic acid is an antifibrinolytic agent used to treat bleeding caused by hyperfibrinolysis. It is not used to reverse the effects of heparin.

EXPLANATION

✔Correct answer:

Obstruction of the artery by plaque accumulation. Atherosclerosis is a progressive disease characterized by the buildup of plaques composed of cholesterol, fatty substances, calcium, and cellular debris within the arterial walls. This process primarily affects the arteries, not veins, because arteries are exposed to higher pressures and turbulent blood flow that promote plaque formation.

Atherosclerosis begins with damage to the endothelium (inner lining of the artery), often caused by risk factors such as high cholesterol, hypertension, smoking, or diabetes. This damage triggers an inflammatory response, allowing low-density lipoproteins (LDL) to penetrate the arterial wall. Over time, immune cells like macrophages engulf the LDL, forming foam cells that contribute to fatty streaks. These fatty streaks develop into plaques, which narrow the arterial lumen, impede blood flow, and reduce oxygen delivery to tissues like the heart muscle.

As the plaque enlarges, it can rupture, leading to the formation of a thrombus (blood clot), which can completely occlude the artery and result in an acute coronary syndrome, such as a myocardial infarction (heart attack).

Imagine an artery as a water pipe and blood as the water flowing through it. Atherosclerosis is like a buildup of rust and debris inside the pipe. Over time, the rust narrows the pipe, making it harder for water (blood) to flow freely. In severe cases, the pipe can become completely blocked.

Nurse Riley should emphasize the importance of managing modifiable risk factors to prevent or slow the progression of atherosclerosis. Patient education should focus on recognizing the symptoms of reduced blood flow (e.g., angina) and understanding the importance of early intervention.

• Educate patients about a heart-healthy diet low in saturated fats, trans fats, and cholesterol to reduce plaque buildup.
• Encourage regular physical activity to improve circulation and lower cholesterol levels.
• Discuss the importance of smoking cessation, as smoking damages the endothelium and accelerates atherosclerosis.
• Explain the role of medications, such as statins, to reduce cholesterol and slow plaque progression.
• Teach patients to monitor and control blood pressure and blood sugar levels, which are critical in reducing endothelial damage.

✘Incorrect answer options:

Formation of blood clots external to the vessel wall. Blood clots (thrombi) associated with atherosclerosis form within the vessel at the site of plaque rupture, not external to the vessel wall. Thrombi may completely block blood flow, but they are a secondary complication of plaque rupture, not the primary mechanism by which blood flow is impeded.

Obstruction of the vein by plaque accumulation. Atherosclerosis occurs in arteries, not veins. Veins operate under low pressure and do not experience the same turbulent flow as arteries, which makes them less prone to plaque formation.

Dilation of hardened vessels to facilitate blood passage. In atherosclerosis, vessels do not dilate; rather, they lose elasticity and become narrowed due to plaque buildup. This narrowing reduces blood flow to tissues, leading to ischemia and potentially serious complications.

EXPLANATION

✔Correct answer:

"Does the pain worsen when you take a deep breath?" Asking if the pain worsens with deep breathing helps Nurse Davis differentiate between cardiac and non-cardiac causes of chest pain. Pain that intensifies with deep breathing is often associated with pleuritic (lung-related) conditions, such as pleurisy, pulmonary embolism, or pneumonia, which are non-cardiac in origin. In contrast, cardiac-related chest pain, such as angina or pain from a myocardial infarction (MI), is typically not affected by breathing but is often described as a heavy, squeezing, or pressure-like sensation. This question directly targets a hallmark characteristic of non-cardiac chest pain, making it an effective tool for initial differentiation.

Non-cardiac chest pain related to respiratory causes often stems from inflammation of the pleura (the membrane surrounding the lungs), which becomes more painful with movement, such as deep inhalation. On the other hand, cardiac chest pain results from myocardial ischemia and is not directly influenced by respiratory mechanics.

Think of a sore muscle in your chest that hurts more when you stretch it (similar to pleuritic pain with deep breathing). In contrast, if the discomfort were coming from the heart, stretching wouldn’t affect the pain because the source is internal and unrelated to movement.

When differentiating chest pain causes, nurses should focus on a detailed assessment of the pain’s characteristics and associated symptoms to guide further evaluation and interventions.

• Ask about pain characteristics, including location, quality, intensity, and duration.
• Identify exacerbating and relieving factors (e.g., deep breathing, movement, rest, or exertion).
• Assess associated symptoms such as shortness of breath, fever, cough, nausea, or diaphoresis, which can help differentiate between cardiac and non-cardiac origins.
• Monitor vital signs and oxygen saturation to identify respiratory or circulatory distress.
• Be prepared to perform an electrocardiogram (ECG) and obtain cardiac enzymes if a cardiac cause is suspected.

✘Incorrect answer options:

"Can you describe the pain to me?" While understanding the pain's characteristics is essential, this question is too broad to specifically differentiate between cardiac and non-cardiac causes. Further targeted questions are needed for clarification.

"Can you rate the pain on a scale of 1 to 10, with 10 being the worst?" The intensity of pain alone does not help determine whether it is cardiac or non-cardiac in origin, as both can vary widely in severity.

"Have you ever experienced this type of pain before?" While this question might provide insight into the patient’s history, it does not help differentiate the nature of the pain during this acute episode.

EXPLANATION

✔Correct answer:

Women with lower socioeconomic status are more likely to develop CAD due to limited access to healthcare and higher stress levels. Socioeconomic status (SES) plays a significant role in the risk and progression of coronary artery disease (CAD), especially in women. Women with lower SES are disproportionately affected due to factors such as limited access to healthcare services, inability to afford medications or preventive care, higher prevalence of modifiable risk factors (e.g., smoking, obesity, and hypertension), and exposure to chronic stress. Chronic stress, often linked to financial insecurity and poor working conditions, activates the hypothalamic-pituitary-adrenal (HPA) axis and promotes inflammatory and cardiovascular changes, increasing CAD risk. Additionally, lower SES is associated with reduced health literacy and fewer opportunities to adopt heart-healthy behaviors, such as regular physical activity and a balanced diet.

Women with lower SES are often underdiagnosed or receive delayed diagnosis of CAD due to differences in symptom presentation (e.g., atypical symptoms like fatigue or nausea) and inequities in healthcare systems. These factors compound the challenges faced by this population in managing CAD effectively.

Think of SES as a ladder. Women at the lower rungs face more obstacles to accessing preventive care, making it harder to maintain heart health, while those on higher rungs have fewer barriers and more resources to stay healthy.

Nurse Edwards should highlight ways to address these disparities in her presentation by advocating for equitable care and emphasizing the importance of community outreach.

• Promote accessible community health programs offering free or low-cost screenings for blood pressure, cholesterol, and glucose levels.
• Educate women in underserved populations about heart disease symptoms and the importance of early intervention.
• Advocate for policies that improve access to affordable healthcare, including medications and cardiac rehabilitation programs.
• Encourage stress management techniques, such as mindfulness, and provide referrals to social support resources, like counseling or financial assistance programs.
• Collaborate with local organizations to improve access to nutritious foods and safe spaces for physical activity.

✘Incorrect answer options:

Women with higher socioeconomic status have the same risk of CAD as women with lower socioeconomic status due to genetic factors. This statement is incorrect because socioeconomic factors significantly influence CAD risk, independent of genetic predisposition. Women with higher SES generally have better access to healthcare, healthier lifestyle options, and lower stress levels, which reduce their overall CAD risk compared to women with lower SES.

Socioeconomic status has little to no effect on CAD risk because lifestyle choices are the primary determinant. This is incorrect because SES heavily influences lifestyle choices. For example, individuals with lower SES may face barriers to making healthier choices, such as living in food deserts, lacking access to fitness facilities, or experiencing chronic financial stress that affects their ability to prioritize health.

Women of all socioeconomic statuses have an equal risk of CAD when their diets are similar. While diet is an important risk factor, CAD risk is multifactorial and cannot be equalized solely based on similar diets. Other SES-related factors, such as stress, access to healthcare, and environmental influences, play critical roles in determining CAD risk.

EXPLANATION

✔Correct answer:

The PT is within the therapeutic range, indicating effective anticoagulation. Ms. Chen's prothrombin time (PT) of 20 seconds, with a control value of 11 seconds, is within the expected therapeutic range for a patient receiving warfarin (Coumadin). The therapeutic range for anticoagulation therapy typically involves a PT that is 1.5 to 2 times the control value. In this case, the therapeutic range would be 16.5 to 22 seconds (11 × 1.5 to 11 × 2). Since Ms. Chen’s PT is 20 seconds, it falls within this range, indicating that her warfarin dose is effectively thinning her blood without significantly increasing the risk of bleeding.

Warfarin works by inhibiting the synthesis of vitamin K–dependent clotting factors (II, VII, IX, and X), prolonging clotting time as measured by PT. By extending PT into the therapeutic range, warfarin reduces the risk of thromboembolic events, such as pulmonary embolism, while minimizing the risk of excessive anticoagulation and bleeding complications.

It is also important to consider the International Normalized Ratio (INR), which standardizes PT values to account for differences in lab methods. For most conditions requiring warfarin, the target INR is 2.0–3.0. However, based on the PT provided, Ms. Chen's result is therapeutic.

Think of the PT range like the recommended speed limit on a highway: going too slow (low PT) might cause accidents (blood clots), while speeding excessively (high PT) increases the risk of losing control and crashing (bleeding). Ms. Chen’s PT is like driving at the perfect speed within the safe range.

Nurses monitoring patients on warfarin should focus on maintaining effective anticoagulation while minimizing the risk of bleeding. Key nursing interventions include:

• Monitor PT and INR levels regularly to ensure the patient remains in the therapeutic range.
• Assess for signs of bleeding, such as bruising, gum bleeding, hematuria, melena, or excessive menstrual flow.
• Educate the patient to avoid excessive intake of vitamin K–rich foods (e.g., leafy greens), as they can reduce warfarin's effectiveness.
• Ensure the patient understands the importance of taking warfarin at the same time each day and not skipping doses.
• Advise the patient to avoid activities that increase the risk of trauma or injury and to notify healthcare providers before starting new medications, including over-the-counter drugs or supplements, as these can interact with warfarin.

✘Incorrect answer options:

The PT is too low, suggesting the need for a higher dose of warfarin: A PT of 20 seconds, in the context of a control value of 11 seconds, is therapeutic. It does not suggest under-anticoagulation, so no increase in the dose is necessary.

The PT is too high, indicating an increased risk of bleeding: While an excessively prolonged PT (>2 times the control value or beyond therapeutic INR range) would indicate a bleeding risk, Ms. Chen’s PT of 20 seconds is well within the therapeutic range for anticoagulation therapy.

The PT result is unreliable and needs to be retaken: There is no indication that the PT result is unreliable. The reported PT is consistent with therapeutic anticoagulation for warfarin therapy.

EXPLANATION

✔Correct answer:

Review the intake and output records for the last two days. Observing bilateral lower extremity edema in a patient who recently suffered a myocardial infarction is a significant finding that may indicate fluid retention, potentially due to heart failure, impaired renal function, or excessive fluid intake. Reviewing the intake and output (I&O) records over the past two days is the most appropriate next step to determine if there is a positive fluid balance (intake exceeding output), which would explain the edema. This information is crucial for guiding further interventions, such as adjusting diuretic therapy or fluid restrictions.

Nurse Riley’s assessment must focus on determining whether the patient's fluid status is being appropriately managed post-MI. Fluid overload can worsen myocardial workload, leading to complications like pulmonary congestion or worsening heart failure. By examining I&O, the nurse can identify trends in fluid balance and discuss findings with the healthcare provider to implement appropriate interventions.

After an MI, the heart may be less effective at pumping blood, leading to fluid backup and increased hydrostatic pressure in the capillaries. This pressure can cause fluid to leak into the interstitial spaces, manifesting as edema. Accurate tracking of fluid intake and output is a cornerstone of monitoring for early signs of heart failure or fluid overload in post-MI patients.

Imagine you’re watering a garden with a hose and notice that the soil is soggy and water is pooling around the plants. Before deciding what to do next—like turning off the water or digging trenches—you’d first check how much water you’ve already added and whether the hose is draining properly. Similarly, when a patient develops edema, reviewing their intake and output records is like checking how much "water" (fluid) has gone in versus how much has drained (urine output) to identify if the system is overloaded and guide the next steps.

Managing edema in post-MI patients requires comprehensive assessment and collaboration with the healthcare team. Key actions include:

• Accurately document I&O to identify fluid retention trends.
• Monitor daily weights as an ongoing assessment of fluid balance, with 1 kg of weight gain equaling approximately 1 liter of fluid retention.
• Assess for other signs of fluid overload, such as lung crackles, shortness of breath, jugular vein distension, or elevated blood pressure.
• Notify the healthcare provider if findings suggest worsening fluid retention, so adjustments can be made to diuretics, fluid restrictions, or other therapies.
• Educate the patient about sodium and fluid restrictions if prescribed, to prevent further fluid accumulation.

✘Incorrect answer options:

Request a sodium restriction of 1 g/day from the physician: While reducing sodium intake is an important long-term intervention for fluid management in heart failure or post-MI patients, this is not the most immediate step. Sodium restriction should be based on the physician's assessment of fluid status and dietary needs.

Change the time of diuretic administration from morning to evening: Diuretics are generally given in the morning to prevent nocturia (frequent urination during the night) and promote patient comfort. Changing the administration time to evening is unlikely to address the underlying cause of edema and could disrupt the patient's sleep pattern.

Order daily weights starting the following morning: Daily weights are an excellent tool for tracking fluid retention, but they provide information on future trends. Reviewing I&O records offers a more immediate understanding of the patient’s current fluid balance and is the priority in this situation.

EXPLANATION

✔Correct answer:

It indicates the electrical impulse originating from the AV node.The P wave on an electrocardiogram (ECG) represents atrial depolarization, which is the electrical activation of the atrial muscles as the impulse spreads from the sinoatrial (SA) node through the atria. The SA node is the primary pacemaker of the heart, located in the right atrium. The impulse then travels to the atrioventricular (AV) node; however, the AV node is not responsible for the initiation of the electrical activity reflected by the P wave. Therefore, stating that the P wave originates from the AV node is inaccurate.

The P wave is typically characterized by the following:

• Duration: It is normally 0.11 seconds or less (i.e., less than three small squares on the ECG paper).
• Amplitude: It is typically 2.5 mm or less.
• Morphology: The P wave is smooth and rounded in a normal ECG.

The AV node plays a critical role in delaying the conduction of the electrical impulse after the P wave, allowing time for the ventricles to fill with blood before they contract. However, it does not generate the electrical activity that causes the P wave.

Think of the SA node as a light switch that turns on a light bulb (the atrial muscles). The P wave is like the glow of the bulb, showing the light is on. The AV node is more like a checkpoint or a traffic signal for the electrical impulse but doesn’t "turn on" the light.

When interpreting the P wave in an ECG, nurses should consider the following:

• Evaluate the shape, size, and duration of the P wave for any abnormalities, such as peaked or notched P waves, which may indicate atrial enlargement.
• Check whether a P wave is present before each QRS complex, which reflects normal sinus rhythm.
• Monitor for abnormal rhythms such as atrial fibrillation (no identifiable P waves) or atrial flutter (sawtooth-like P waves).
• Correlate the patient's symptoms with ECG findings to guide appropriate interventions.
• Ensure accurate lead placement during ECG monitoring to avoid waveform distortions.

✘Incorrect answer options:

Its duration is typically 0.11 seconds or less: This statement is accurate. A normal P wave duration is ≤0.11 seconds (less than three small squares on ECG paper), reflecting the time it takes for atrial depolarization.

It reflects the electrical impulse originating from the SA node: This statement is correct. The SA node is the natural pacemaker of the heart and is responsible for initiating the electrical impulse that creates the P wave.

It represents atrial muscle depolarization: This is also correct. The P wave directly represents the depolarization (activation) of the atrial muscles as the electrical impulse spreads through the atria.

EXPLANATION

✔Correct answer:

Genetic predisposition. A non-modifiable risk factor is one that cannot be altered or controlled through lifestyle changes or medical intervention. Genetic predisposition, or family history of coronary artery disease (CAD), is a non-modifiable risk factor because it is determined by inherited traits and cannot be changed. Individuals with a family history of premature CAD (e.g., first-degree relatives with CAD diagnosed before age 55 in men or 65 in women) are at a higher risk of developing the condition themselves due to genetic and hereditary influences.

Genetic factors contribute to CAD by influencing cholesterol metabolism, endothelial function, inflammatory responses, and blood pressure regulation. For example, inherited conditions like familial hypercholesterolemia (a genetic disorder affecting LDL metabolism) significantly increase the risk of CAD.

Think of genetic predisposition as a blueprint you inherit from your family. While you can change the way you live (modifiable risk factors), you cannot alter the blueprint itself (non-modifiable risk factors like genetics).

Nurse Patel should emphasize that while non-modifiable risk factors cannot be changed, understanding and acknowledging these risks allows patients to focus on modifying other risk factors to reduce their overall likelihood of developing CAD.

• Encourage patients with a strong family history of CAD to undergo regular cardiovascular screenings (e.g., cholesterol levels, blood pressure, and glucose levels).
• Educate patients about the importance of aggressive management of modifiable risk factors, such as controlling blood pressure, blood sugar, and cholesterol levels, as well as maintaining a healthy lifestyle.
• Reassure patients that family history is only one part of the risk equation, and adopting a heart-healthy lifestyle can significantly mitigate overall risk.
• Encourage open communication with healthcare providers about family history so personalized prevention plans can be developed.

✘Incorrect answer options:

Diabetes mellitus. Diabetes is a major risk factor for CAD, but it is considered modifiable because blood sugar levels can be managed through lifestyle changes (e.g., diet, exercise, and weight management) and medical treatment (e.g., insulin or oral antidiabetic agents). Proper control of diabetes significantly reduces the risk of CAD.

Cigarette smoking. Smoking is a well-known modifiable risk factor for CAD. Quitting smoking can dramatically reduce cardiovascular risk by improving vascular health and reducing oxidative stress and inflammation. Smoking cessation programs and nicotine replacement therapies are effective interventions.

Hypertension. Hypertension, or high blood pressure, is another modifiable risk factor. It can be controlled through lifestyle modifications (e.g., a low-sodium diet, regular physical activity, and weight management) and medications (e.g., antihypertensives). Proper blood pressure control lowers the risk of CAD and other cardiovascular complications.

EXPLANATION

✔Correct answers:

Obesity, Elevated serum cholesterol levels, and Cigarette smoking. Nurse Rodriguez should emphasize obesity, elevated serum cholesterol levels, and cigarette smoking as modifiable risk factors for coronary artery disease (CAD). These are preventable contributors to the development and progression of CAD and can be targeted through lifestyle and behavioral changes.

1. Obesity: Obesity is strongly linked to an increased risk of CAD. Excess weight contributes to other risk factors, including hypertension, type 2 diabetes, and dyslipidemia. Modifiable through diet, physical activity, and behavioral interventions, reducing obesity can significantly decrease the risk of CAD.
2. Elevated serum cholesterol levels: High levels of low-density lipoprotein (LDL, "bad" cholesterol) and low levels of high-density lipoprotein (HDL, "good" cholesterol) promote plaque buildup in the coronary arteries, leading to atherosclerosis. Managing cholesterol through a healthy diet, medications (e.g., statins), and regular exercise can help prevent CAD.
3. Cigarette smoking: Smoking is a major modifiable risk factor for CAD. It damages the endothelium of blood vessels, promotes atherosclerosis, and decreases oxygen delivery to the heart. Smoking cessation is one of the most effective ways to lower CAD risk.

Imagine your coronary arteries as a highway. Obesity, high cholesterol, and smoking are like adding traffic jams and potholes to the highway. By addressing these factors, you help maintain smooth and safe traffic flow (healthy blood flow).

Coronary artery disease occurs when atherosclerotic plaques develop in the coronary arteries, leading to reduced blood flow to the heart muscle. Modifiable risk factors like obesity, hyperlipidemia, and smoking directly contribute to the formation of these plaques. Over time, reduced coronary blood flow can lead to angina, myocardial infarction, or heart failure. Addressing modifiable risk factors early can significantly reduce disease progression and improve cardiovascular outcomes.

Nurses play a key role in educating patients and the community about CAD prevention. The following interventions should be emphasized:

• Promote a heart-healthy diet, such as the Mediterranean diet, which is low in saturated fats and high in fruits, vegetables, and whole grains.
• Encourage regular physical activity, aiming for at least 150 minutes of moderate aerobic exercise per week.
• Educate about the dangers of smoking and provide resources for smoking cessation programs, such as nicotine replacement therapy or counseling.
• Discuss the importance of regular cholesterol screenings and adhering to prescribed medications for dyslipidemia management.
• Address weight management strategies and provide referrals to dietitians or structured weight loss programs if needed.

✘Incorrect answer options:

Consistent use of personal protective equipment (PPE): While PPE is important for infection control and occupational safety, it is unrelated to the prevention of CAD. CAD prevention focuses on modifiable lifestyle factors, not protective measures designed for workplace safety.

Exposure to polyacrylamide: Polyacrylamide exposure is not recognized as a risk factor for coronary artery disease. While certain environmental toxins, such as air pollution, can contribute to cardiovascular risk, polyacrylamide is not specifically implicated in CAD development.

EXPLANATION

✔Correct answer:

Inflation of a small balloon within the narrowed artery. Coronary angioplasty, also known as percutaneous transluminal coronary angioplasty (PTCA), is a minimally invasive procedure used to treat coronary artery disease (CAD). The primary mechanism involves inserting a catheter with a small inflatable balloon into the narrowed or blocked coronary artery. Once positioned at the site of the blockage, the balloon is inflated, compressing the plaque against the arterial walls and widening the lumen of the artery. This restores blood flow to the myocardium, relieving symptoms such as chest pain (angina) and reducing the risk of myocardial infarction (heart attack).

In most cases, a stent (a wire mesh tube) is placed during the procedure to keep the artery open after the balloon is deflated and removed. Stents may be either bare-metal or drug-eluting, the latter being coated with medication to prevent restenosis (re-narrowing of the artery).

Think of a clogged artery as a squished garden hose that restricts water flow. The balloon acts like a tool that temporarily inflates the hose from the inside, reopening it so water (blood) can flow freely again.

Nurse Sanchez should ensure Mr. Rodriguez understands the procedure and its purpose, as well as provide education on pre- and post-procedure care.

• Explain the steps of the angioplasty procedure, including the insertion of a catheter through the femoral or radial artery and the use of X-ray imaging to guide the catheter to the coronary arteries.
• Reassure the patient that the procedure is typically done under local anesthesia and conscious sedation, and he will likely remain awake but comfortable.
• Instruct the patient to report any chest discomfort or pain during the procedure, as this could indicate complications such as artery spasm or reocclusion.
• Review pre-procedure requirements, such as fasting for 6–8 hours and withholding certain medications (e.g., anticoagulants) if directed by the provider.
• Post-procedure, educate the patient on monitoring for complications such as bleeding, infection at the catheter insertion site, or symptoms of re-occlusion (e.g., chest pain or shortness of breath).

✘Incorrect answer options:

Administration of medication to dilate the artery. While medications like nitrates, calcium channel blockers, or antiplatelet drugs are used to treat CAD and prevent complications, coronary angioplasty specifically relies on mechanical widening of the artery using a balloon and does not involve administering medication to directly dilate the artery.

Surgical replacement of the obstructed arterial segment with a graft. This describes coronary artery bypass grafting (CABG), a surgical procedure in which a healthy blood vessel (graft) is taken from another part of the body (e.g., leg vein, chest artery) and used to bypass a blocked coronary artery. CABG is different from angioplasty and is typically reserved for more severe or diffuse coronary blockages.

None of the provided options. This is incorrect because one of the options provided—"Inflation of a small balloon within the narrowed artery"—accurately describes the primary mechanism of coronary angioplasty.

EXPLANATION

✔Correct answer:

Improving myocardial oxygen supply. Chest pain, shortness of breath, and diaphoresis are hallmark symptoms of acute coronary syndrome (ACS), which can be caused by myocardial ischemia. The priority nursing intervention in this scenario is to improve the myocardial oxygen supply, as the heart muscle may not be receiving adequate oxygen due to decreased blood flow from narrowed or blocked coronary arteries. This intervention aligns with the Airway, Breathing, Circulation (ABC) framework, prioritizing the heart's oxygenation needs to prevent further ischemic damage and potentially life-threatening complications such as myocardial infarction.

Improving oxygen supply can include actions such as administering supplemental oxygen (if hypoxemia is present), ensuring a patent airway, and collaborating with the healthcare provider for interventions like initiating intravenous (IV) access for medications that can enhance oxygen delivery to the myocardium.

Myocardial ischemia occurs when the oxygen demand of the heart exceeds its supply due to partial or complete occlusion of coronary arteries. If oxygen delivery is not promptly restored, ischemia may progress to infarction (permanent damage to the heart muscle). Interventions aimed at improving oxygenation help restore balance between oxygen demand and supply, minimizing cardiac damage.

Think of the heart as an engine that requires fuel (oxygen) to keep running. If the fuel line is partially blocked, the engine will sputter and struggle. The first priority is to restore the flow of fuel to the engine so it can function properly. Similarly, the heart needs an adequate oxygen supply to maintain its function.

To improve myocardial oxygen supply, nurses should act promptly and strategically. Below are key interventions for this patient:

• Administer supplemental oxygen if oxygen saturation levels are below 90% or if the patient shows signs of hypoxemia.
• Position the patient in a semi-Fowler’s position to facilitate breathing and reduce cardiac workload.
• Monitor vital signs and cardiac rhythm continuously to detect signs of worsening ischemia or arrhythmias.
• Prepare for diagnostic procedures such as an electrocardiogram (ECG) to assess the presence of myocardial ischemia or infarction.
• Collaborate with the healthcare team for timely administration of medications such as nitroglycerin or morphine if prescribed.

✘Incorrect answer options:

Providing education about the presenting symptoms. While patient education is essential for long-term management of coronary artery disease, it is not the priority during an acute episode. The immediate goal is to stabilize the patient and address the myocardial oxygen deficit.

Administering sublingual nitroglycerin. Although nitroglycerin is often used to relieve chest pain by dilating coronary arteries, it is not the first priority in this scenario. Nitroglycerin administration must be done after assessing the patient’s blood pressure to prevent hypotension, and it is part of the broader intervention plan to improve myocardial oxygen supply.

Reducing patient anxiety. Anxiety reduction is an important nursing intervention as it can decrease the patient’s oxygen demand by lowering sympathetic nervous system activity. However, it is a secondary intervention that should only be addressed after oxygen supply has been optimized.

EXPLANATION

✔Correct answer:

Electrocardiogram (ECG). An electrocardiogram (ECG) is the primary diagnostic tool used to determine the specific location of myocardial damage during a suspected myocardial infarction (MI). The ECG provides a detailed record of the heart's electrical activity, and specific changes in the ST segment, T waves, or Q waves in particular leads can indicate the affected region of the myocardium. For example:

• Leads II, III, and aVF correspond to the inferior wall of the heart (supplied by the right coronary artery).
• Leads V1-V4 represent the anterior wall (supplied by the left anterior descending artery).
• Leads I, aVL, V5, and V6 indicate the lateral wall (supplied by the left circumflex artery).
• Leads V1 and V2 may show reciprocal changes or evidence of posterior wall involvement.

The ECG is crucial not only for identifying the location of ischemia or infarction but also for determining the severity and type of MI (e.g., STEMI or NSTEMI).

Think of an ECG like a GPS that pinpoints the location of a traffic jam (myocardial damage) in a city's road network (the heart). By looking at specific areas of the city map (leads), you can identify where the blockage (ischemia or infarction) is occurring.

Nurse Garcia should ensure that the ECG is performed promptly, as the test is time-sensitive in identifying myocardial damage and guiding treatment.

• Prepare Mr. Thompson by ensuring electrodes are placed correctly and explaining the procedure to reduce anxiety.
• Monitor for changes in the ECG and report findings, such as ST-segment elevation or T-wave inversion, to the healthcare provider immediately.
• Assist in serial ECGs to track the progression or resolution of ischemia or infarction over time.
• Collaborate with the team to initiate treatments like thrombolytic therapy or percutaneous coronary intervention (PCI) based on the ECG findings.
• Educate Mr. Thompson about the purpose of the ECG and the importance of timely intervention to minimize heart muscle damage.

✘Incorrect answer options:

Echocardiogram. An echocardiogram uses ultrasound to visualize the structure and function of the heart. While it is useful for assessing wall motion abnormalities, ejection fraction, and valve function, it does not pinpoint the specific location of ischemic damage during an acute MI.

Cardiac catheterization. Cardiac catheterization is a procedure used to directly visualize the coronary arteries for blockages and assess blood flow. While it identifies the cause of myocardial damage (e.g., a blocked coronary artery), it does not determine the specific myocardial region affected without correlating with ECG findings.

Cardiac enzyme analysis. Cardiac enzyme analysis measures biomarkers like troponin and CK-MB to confirm myocardial damage, but it cannot identify the specific location of the damage. Elevated enzymes indicate that myocardial injury has occurred, but they do not provide spatial information.

EXPLANATION

✔Correct answer:

200 mg/dL. A total serum cholesterol level of 200 mg/dL or higher is considered a threshold value that significantly elevates the risk for coronary artery disease (CAD). According to guidelines from the American Heart Association (AHA) and National Cholesterol Education Program (NCEP), total cholesterol levels are categorized as follows:

• Desirable: Less than 200 mg/dL
• Borderline high: 200–239 mg/dL
• High: 240 mg/dL or higher

When total cholesterol levels reach or exceed 200 mg/dL, the individual is at increased risk of atherosclerosis, where fatty plaques accumulate on arterial walls, narrowing the arteries and reducing blood flow to the heart. Over time, this process can lead to CAD, increasing the likelihood of angina, myocardial infarction, or stroke. Nurse Brown should educate patients with borderline or high cholesterol levels on lifestyle modifications, such as diet and exercise, and recommend medical follow-up for further management.

Elevated cholesterol, particularly low-density lipoprotein (LDL) cholesterol, contributes to endothelial injury and the formation of atheromatous plaques. These plaques cause inflammation and vascular remodeling, eventually leading to arterial stenosis. High cholesterol levels can also reduce the elasticity of arteries, making them less responsive to changes in blood flow demands, further increasing CAD risk.

Think of cholesterol as grease in a pipe. A small amount is necessary to keep the pipe (arteries) functioning smoothly, but too much grease can clog the pipe over time, reducing water flow (blood flow). At 200 mg/dL or more, the "grease" becomes excessive, creating a significant risk of blockage.

For patients with cholesterol levels ≥200 mg/dL, it is important to provide targeted health education and support. Key nursing actions include:

• Educate the patient on the role of cholesterol in cardiovascular health and its contribution to CAD.
• Encourage dietary modifications, such as reducing saturated fats, trans fats, and cholesterol intake while increasing fiber and healthy fats (e.g., omega-3 fatty acids).
• Promote physical activity, recommending at least 150 minutes of moderate-intensity aerobic exercise per week.
• Discuss the potential need for lipid-lowering medications, such as statins, if lifestyle changes are insufficient or if the patient has additional risk factors.
• Monitor the patient’s lipid profile regularly to assess progress and compliance with interventions.

✘Incorrect answer options:

100 mg/dL: A cholesterol level of 100 mg/dL is well within the desirable range and poses no increased risk for CAD. It is considered optimal.

150 mg/dL: A cholesterol level of 150 mg/dL is also within the desirable range and is not associated with an elevated risk for CAD.

175 mg/dL: While slightly higher, a cholesterol level of 175 mg/dL remains below the 200 mg/dL threshold and is still considered desirable. It does not significantly elevate the risk for CAD but warrants continued monitoring to ensure it does not rise further.

EXPLANATION

✔Correct answer:

Obesity. Obesity is considered a modifiable risk factor for coronary artery disease (CAD) because it can be managed or reduced through lifestyle changes such as diet, exercise, and medical interventions. Obesity contributes to CAD by promoting conditions like hypertension, dyslipidemia (elevated LDL cholesterol and low HDL cholesterol), and insulin resistance, which increase the risk of atherosclerosis (plaque buildup in the arteries).

Excess body weight places additional strain on the heart and blood vessels. Adipose tissue, particularly visceral fat, is metabolically active and releases inflammatory substances, contributing to chronic low-grade inflammation and endothelial damage. These factors accelerate the progression of CAD.

Think of the heart and blood vessels as a highway system. Obesity is like adding extra traffic and debris to the road, increasing wear and tear on the system. By "clearing the road" (losing excess weight), the traffic (blood flow) improves, reducing the risk of blockages (plaque buildup).

Nurse Kelly should help the patient understand the role of obesity in CAD and provide tailored recommendations to support weight management.

• Encourage the patient to adopt a heart-healthy diet, such as the DASH diet or Mediterranean diet, focusing on whole grains, lean proteins, fruits, and vegetables.
• Promote regular physical activity, recommending at least 150 minutes of moderate-intensity aerobic exercise per week, per American Heart Association (AHA) guidelines.
• Discuss behavioral changes and provide resources, such as nutritional counseling or weight-loss support groups, to foster sustainable lifestyle changes.
• Collaborate with the healthcare team to determine if medical interventions (e.g., medications, bariatric surgery) are appropriate for the patient.
• Monitor and address comorbid conditions like hypertension, diabetes, or dyslipidemia that may complicate weight management efforts.

✘Incorrect answer options:

Biological sex. Biological sex is a non-modifiable risk factor for CAD. Men are at a higher risk of developing CAD earlier in life, while women’s risk increases after menopause due to a decline in protective estrogen levels. This risk is determined by hormonal and biological differences that cannot be altered.

Genetic predisposition. A family history of CAD is a non-modifiable risk factor. While a genetic predisposition cannot be changed, individuals with a strong family history can reduce their overall risk by addressing modifiable factors like diet, smoking, and physical activity.

Chronological age. Age is a non-modifiable risk factor for CAD. As individuals age, their risk of developing CAD increases due to cumulative vascular wear and tear, as well as age-related changes in cholesterol metabolism and arterial stiffness.

EXPLANATION

✔Correct answer:

Apnea. In patients with chronic obstructive pulmonary disease (COPD), the primary drive for breathing can shift from being controlled by elevated carbon dioxide levels (the normal "hypercapnic drive") to low oxygen levels (the "hypoxic drive"). This occurs because long-standing hypercapnia (high CO₂ levels) desensitizes the central chemoreceptors, and the body relies on peripheral chemoreceptors to detect low oxygen levels as the main stimulus to breathe. If a high concentration of oxygen is administered to a patient with COPD, it can suppress the hypoxic drive, leading to reduced respiratory effort or even apnea (a temporary cessation of breathing).

• In COPD, chronic hypoxemia and hypercapnia are common. The administration of excessive oxygen increases the blood oxygen level significantly, diminishing the hypoxic drive. This leads to hypoventilation, further retention of CO₂, and respiratory acidosis.
• Additionally, high oxygen concentrations can worsen ventilation-perfusion mismatching in the lungs. Oxygen can cause vasodilation of pulmonary blood vessels in poorly ventilated alveoli, leading to increased shunting and impaired gas exchange. This effect exacerbates hypercapnia and hypoventilation.

Imagine the brain's breathing drive as an alarm clock. In most people, the alarm is set to wake them up when CO₂ levels rise (hypercapnic drive). In patients with COPD, the alarm shifts to detect low oxygen levels (hypoxic drive). If oxygen levels become too high, the alarm stops working, and the person forgets to breathe (apnea).

Nurse Thompson must carefully titrate Mr. Evans's oxygen therapy to balance maintaining adequate oxygenation without suppressing his hypoxic drive. Regular monitoring of his respiratory status and oxygenation is essential.

• Use the lowest effective oxygen concentration to maintain target oxygen saturation levels, typically 88–92% for COPD patients, as recommended by evidence-based guidelines.
• Monitor for signs of respiratory depression, such as a decreased respiratory rate, shallow breathing, or changes in mental status.
• Assess arterial blood gases (ABGs) to detect hypercapnia and respiratory acidosis, especially if the patient's condition worsens.
• Educate patients and caregivers on the importance of appropriate oxygen use and adherence to prescribed flow rates.
• Coordinate with the healthcare team to adjust oxygen therapy as needed and consider non-invasive ventilation (e.g., CPAP or BiPAP) if respiratory failure is imminent.

✘Incorrect answer options:

Respiratory alkalosis. Respiratory alkalosis results from hyperventilation, where excessive CO₂ is "blown off," leading to elevated blood pH. In COPD patients, the concern is hypoventilation, not hyperventilation, especially when excessive oxygen suppresses the hypoxic drive.

Metabolic acidosis. Metabolic acidosis is a condition characterized by a decrease in blood pH due to non-respiratory causes, such as renal failure or lactic acidosis. While respiratory acidosis can occur in COPD patients with hypoventilation and CO₂ retention, metabolic acidosis is not directly related to oxygen therapy.

Exacerbation of anginal pain. While oxygen therapy can indirectly influence coronary blood flow, high-concentration oxygen is not known to exacerbate anginal pain. In fact, supplemental oxygen is sometimes administered during acute coronary syndromes to improve myocardial oxygenation, though current evidence suggests limiting oxygen use unless hypoxemia is present.

EXPLANATION

✔Correct answer:

Administer oxygen 4L/min via nasal cannula.In the acute management of myocardial infarction (MI), the priority is to optimize oxygenation to prevent further ischemia and minimize myocardial damage. Myocardial infarction occurs due to an obstruction in coronary blood flow, leading to oxygen deprivation of the cardiac tissue. Administering oxygen immediately increases the oxygen supply to the heart, ensuring that tissues receive adequate oxygenation while other interventions are being performed. Without prompt oxygenation, the risk of extensive myocardial injury and subsequent complications increases.

Imagine a fire breaking out in a room (representing the myocardial infarction), and oxygen is like a firefighter ensuring the room doesn't completely burn down. Administering oxygen acts as the first line of defense to contain the damage while other resources (e.g., ECG, blood work, and medications) are mobilized.

While administering oxygen is the immediate priority, other interventions should follow in a timely and systematic manner. Key steps include:

• Monitor the patient's oxygen saturation using a pulse oximeter and titrate oxygen therapy as necessary to maintain SpO₂ above 94%.
• Ensure that the oxygen delivery device (e.g., nasal cannula) is properly positioned for optimal efficiency.
• Assess the patient's respiratory effort and monitor for signs of hypoxia, such as cyanosis or restlessness.
• Coordinate with the healthcare team to prepare for additional diagnostic and therapeutic interventions.
• Document the oxygen therapy provided, including flow rate, method of administration, and the patient's response.

✘Incorrect answer options:

Administer morphine 2mg IV to relieve chest pain: While pain management is an essential component of MI care, it is not the immediate priority. Morphine is given after oxygenation and ECG to relieve pain, reduce anxiety, and lower oxygen demand on the heart. Administering oxygen takes precedence to stabilize the patient physiologically before addressing pain.

Obtain blood samples for laboratory analysis: Blood tests such as cardiac biomarkers (e.g., troponin, CK-MB) are critical for diagnosing myocardial infarction. However, these tests are not prioritized over oxygen therapy, as they do not directly impact the patient's oxygenation or cardiac perfusion in the acute phase.

Perform a 12-lead ECG to assess cardiac activity: Performing an ECG is a vital step in diagnosing and determining the extent of myocardial damage, but it does not take precedence over ensuring adequate oxygen supply. ECG findings guide treatment, but oxygen therapy addresses the underlying ischemia directly.

EXPLANATION

✔Correct answer:

Coronary artery disease (CAD). Coronary artery disease (CAD) is the leading cause of mortality in the United States for both men and women. CAD occurs when atherosclerosis leads to narrowing or blockage of the coronary arteries, reducing blood flow to the heart muscle and potentially resulting in myocardial infarction (heart attack) or sudden cardiac death. According to the Centers for Disease Control and Prevention (CDC), heart disease—including CAD—accounts for approximately 1 in every 5 deaths in the U.S., making it the number one cause of death. Major risk factors for CAD include hypertension, diabetes, high cholesterol, smoking, obesity, and a sedentary lifestyle, as well as non-modifiable factors like age, sex, and family history.

Imagine the coronary arteries as highways delivering essential supplies (oxygen and nutrients) to the heart. Over time, "traffic jams" (plaques) build up, restricting delivery. This can cause serious breakdowns (heart attacks), which explains why CAD is the leading cause of death.

Nurse Williams should emphasize prevention strategies to reduce CAD risk, especially focusing on modifiable risk factors that community members can control.

• Promote heart-healthy diets rich in fruits, vegetables, lean proteins, whole grains, and healthy fats, while limiting salt, sugar, and saturated/trans fats.
• Encourage regular physical activity, such as 150 minutes of moderate-intensity exercise per week, as recommended by the American Heart Association (AHA).
• Educate about smoking cessation programs and the risks of tobacco use in contributing to CAD.
• Discuss the importance of routine health screenings, including blood pressure, cholesterol levels, and blood glucose, to detect and manage risk factors early.
• Provide information on managing stress and prioritizing mental health, as chronic stress contributes to cardiovascular risk.

✘Incorrect answer options:

Hepatic failure. Hepatic failure, or liver failure, is not a leading cause of mortality in the U.S. While it can result from chronic liver diseases like cirrhosis or hepatitis, its prevalence and mortality rates are significantly lower than those of CAD or cancer.

Malignant neoplasms (cancer). Cancer is the second leading cause of death in the U.S., accounting for approximately 1 in 4 deaths. While it remains a major health concern, CAD surpasses cancer in mortality rates. Common cancers, such as lung, colorectal, and breast cancer, vary in prevalence and outcomes based on screening, early detection, and treatment advancements.

Renal failure. Renal failure, including end-stage renal disease (ESRD), contributes to morbidity and mortality but is not as prevalent or lethal as CAD or cancer. However, it often coexists with other chronic conditions, such as diabetes and hypertension, which are significant risk factors for CAD.

EXPLANATION

✔Correct answer:

Avoiding consumption of very large meals. Patients with coronary artery disease (CAD) should avoid eating very large meals because overeating can increase the workload on the heart. Large meals divert blood to the gastrointestinal system for digestion, which can temporarily reduce the blood supply to the heart muscle, leading to symptoms such as chest pain (angina). Additionally, large meals may contribute to postprandial (after eating) spikes in blood sugar and lipids, which can worsen CAD by promoting inflammation and atherosclerosis. Small, frequent, heart-healthy meals are generally recommended to manage energy levels and avoid placing excess strain on the cardiovascular system.

Think of the heart as an engine and digestion as a load the engine needs to carry. Overloading the engine with a large meal makes it work harder, which can cause it to overheat, just like a large meal puts stress on the heart in a CAD patient.

Nurse Smith should provide specific guidance on meal planning and portion sizes to support the patient's heart health.

• Encourage the patient to consume smaller, more frequent meals to maintain stable energy levels and reduce the cardiovascular burden.
• Recommend a heart-healthy diet, such as the Mediterranean diet, which includes plenty of fruits, vegetables, whole grains, lean proteins (e.g., fish, poultry), and healthy fats (e.g., olive oil, nuts).
• Advise limiting saturated and trans fats, as well as added sugars, to lower cholesterol levels and reduce plaque buildup in the arteries.
• Encourage avoiding heavy meals close to bedtime, as this can exacerbate reflux and place stress on the heart.
• Educate on reading food labels to manage intake of sodium, fats, and sugar effectively.

✘Incorrect answer options:

Increasing consumption of complex carbohydrates. While complex carbohydrates (e.g., whole grains, legumes, fruits, and vegetables) are part of a heart-healthy diet, this option does not specifically address the importance of avoiding very large meals. Additionally, increasing carbohydrate intake excessively can lead to weight gain, which is a risk factor for CAD.

Restricting sodium intake to 7 grams daily. This is incorrect because the recommended sodium intake for individuals with CAD or at risk for cardiovascular disease is less than 2.3 grams (2,300 mg) per day, per the American Heart Association. A daily limit of 7 grams would be far too high and could exacerbate hypertension, a major risk factor for CAD.

Consuming three balanced meals per day. While consuming balanced meals is important, the recommendation to eat three meals does not address the need to avoid very large meals. For CAD patients, smaller, frequent meals may be more beneficial in reducing cardiovascular strain.