Coronary Artery Disease Nursing Care Plan & Management

EXPLANATION

✔Correct answer:

A sensation of tightness, pressure, or squeezing. Anginal pain is typically described as a sensation of tightness, pressure, or squeezing in the chest. This discomfort arises from myocardial ischemia, where the oxygen supply to the heart muscle is insufficient to meet its demand. The pain is often diffuse, poorly localized, and may radiate to the neck, jaw, shoulders, or arms (most commonly the left arm). Anginal pain is usually triggered by exertion, emotional stress, or other activities that increase myocardial oxygen demand and subsides with rest or nitroglycerin use.

Angina occurs when coronary blood flow is inadequate due to conditions such as atherosclerosis, leading to transient ischemia without causing permanent damage to the myocardial tissue. The buildup of lactic acid and other metabolites during ischemia contributes to the pain sensation.

Think of anginal pain like a rubber band being stretched too tightly around your chest, creating a feeling of pressure or squeezing. When you stop stretching the band (rest or take nitroglycerin), the pressure eases, and the discomfort goes away.

Identifying the characteristics of chest pain is crucial in distinguishing anginal pain from other causes of chest discomfort. This helps guide appropriate interventions and diagnostics.

• Ask about the onset, duration, intensity, and radiation of the chest pain, as well as precipitating and relieving factors.
• Assess for associated symptoms, such as shortness of breath, diaphoresis, nausea, or fatigue, which often accompany anginal pain.
• Administer prescribed medications like nitroglycerin to relieve the pain and improve myocardial oxygen supply.
• Educate the patient on recognizing angina triggers and using nitroglycerin promptly when symptoms occur.
• Distinguish anginal pain from other types of chest pain, such as pleuritic pain (sharp and worsens with breathing) or musculoskeletal pain (localized and reproducible with palpation).

✘Incorrect answer options:

A shooting pain. Shooting pain is more commonly associated with nerve-related conditions, such as neuropathic pain, rather than cardiac ischemia.

A sharp pain. Sharp pain is not characteristic of angina. It is more typical of pleuritic pain (e.g., from pulmonary embolism or pleuritis) or musculoskeletal pain (e.g., costochondritis).

A knifelike pain. Knifelike or stabbing pain is not consistent with anginal pain. This type of pain is more commonly associated with conditions such as pericarditis or aortic dissection.

EXPLANATION

✔Correct answer:

The kidneys excreting both sodium and water. The kidneys help regulate blood pressure by excreting both sodium and water, a process known as natriuresis and diuresis. By increasing the excretion of sodium, the kidneys reduce the osmotic pull for water retention, causing water to follow sodium out of the body through urine. This reduces blood volume and subsequently decreases blood pressure. When blood pressure rises above normal, the kidneys sense the increased blood volume and pressure, which stimulates mechanisms to enhance sodium and water excretion, thereby helping restore blood pressure to normal levels.

The kidneys play a critical role in blood pressure regulation through the renin-angiotensin-aldosterone system (RAAS) and their ability to manage extracellular fluid volume. When blood pressure is high, reduced activation of the RAAS allows for increased excretion of sodium and water, reducing circulating volume and vascular resistance. This response is an essential part of maintaining blood pressure homeostasis.

Imagine your blood vessels as a garden hose. If the hose is overfilled with water (high blood volume), the pressure increases. The kidneys act like a drain valve, releasing both water and dissolved salts (sodium) to reduce the water level in the hose, lowering the pressure to normal.

Nurses should educate patients about how the kidneys contribute to blood pressure regulation and encourage behaviors that support kidney health and appropriate sodium balance.

• Teach patients to reduce sodium intake in their diet, as high sodium levels can increase water retention and raise blood pressure.
• Monitor patients with hypertension for signs of fluid overload, such as edema or weight gain, which may indicate impaired kidney function.
• Administer diuretic medications as prescribed to enhance sodium and water excretion, helping control blood pressure.
• Encourage adequate hydration to support kidney function and maintain normal fluid balance.
• Assess kidney function regularly through lab values (e.g., serum creatinine, blood urea nitrogen, and glomerular filtration rate) in hypertensive patients, as impaired kidneys may exacerbate hypertension.

✘Incorrect answer options:

The kidneys retaining both sodium and water. Retaining sodium and water increases blood volume, which raises blood pressure rather than lowering it. This response typically occurs when the body senses low blood pressure or blood volume (e.g., due to dehydration or shock).

The kidneys excreting sodium while retaining water. Excreting sodium while retaining water is not a physiological response to high blood pressure. Water retention without sodium loss can lead to hyponatremia and fluid overload, further exacerbating high blood pressure.

The kidneys excreting sodium only. Sodium excretion without accompanying water loss is not a natural response of the kidneys. Sodium and water are excreted together to effectively decrease blood volume and pressure. Sodium loss alone would not sufficiently lower blood pressure.

EXPLANATION

✔Correct answer:

Myocardial infarction. Elevated myoglobin levels are indicative of myocardial infarction (MI) or other types of muscle injury. Myoglobin is a protein found in cardiac and skeletal muscle that is released into the bloodstream when muscle tissue is damaged. In the context of chest pain and suspected myocardial infarction, an elevated myoglobin level is one of the early markers of cardiac muscle injury.

While troponin is the most specific and sensitive biomarker for myocardial infarction, myoglobin is an early marker that rises within 2–3 hours after the onset of cardiac injury, peaks at about 8–12 hours, and returns to baseline within 24 hours. However, myoglobin is not specific to cardiac muscle damage alone, as it is also released in cases of skeletal muscle injury. This lack of specificity means it is typically interpreted alongside other cardiac biomarkers like troponin and CK-MB for a definitive diagnosis of MI.

Imagine myoglobin as a smoke detector. It goes off whenever there’s a fire (muscle injury), but it doesn’t tell you whether the fire is in the kitchen (heart) or somewhere else (other muscle). Additional tools, like troponin levels, help pinpoint the source of the fire.

When myoglobin levels are elevated, the nurse must act promptly to support the patient and facilitate additional diagnostics or interventions. Key actions include:

• Correlate myoglobin levels with clinical presentation, ECG findings, and other cardiac biomarkers like troponin and CK-MB.
• Notify the physician immediately, as elevated myoglobin may indicate an evolving myocardial infarction that requires urgent intervention, such as thrombolytics or percutaneous coronary intervention (PCI).
• Continue to monitor cardiac enzymes serially to evaluate trends and confirm the diagnosis.
• Provide oxygen therapy as needed to optimize tissue perfusion and reduce myocardial oxygen demand.
• Educate the patient and family about the significance of cardiac biomarkers and the need for rapid intervention to prevent complications.

✘Incorrect answer options:

Hepatic dysfunction: Myoglobin is not a marker of liver damage or hepatic dysfunction. Liver function tests, such as ALT, AST, and bilirubin, are used to evaluate hepatic issues.

Malignancy: Elevated myoglobin levels are not associated with malignancies. Specific tumor markers (e.g., CEA, CA-125, PSA) are used to detect cancers.

Essential hypertension: Hypertension does not cause elevated myoglobin levels. Instead, complications of chronic hypertension, such as left ventricular hypertrophy or heart failure, may be assessed through imaging or echocardiography rather than myoglobin.

EXPLANATION

✔Correct answer:

Preload. Preload refers to the degree of myocardial fiber stretch at the end of diastole, just before the heart contracts (systole). It is determined by the volume of blood filling the ventricles during diastole, also known as end-diastolic volume (EDV). The more the myocardial fibers are stretched due to the incoming blood, the stronger the subsequent contraction will be, up to a certain point. This relationship between fiber stretch and contraction strength is described by the Frank-Starling Law of the Heart, which helps optimize stroke volume to meet the body's needs. However, excessive preload (e.g., in heart failure) can overstretch the myocardial fibers, reducing the heart’s efficiency and output.

Preload depends on venous return, blood volume, and ventricular compliance. Increased preload (e.g., due to fluid overload) can result in increased cardiac output, while decreased preload (e.g., due to dehydration or blood loss) can lead to reduced cardiac output.

Think of the heart as a balloon. The more you fill it with air (blood during diastole), the more the walls stretch, and the stronger the recoil (contraction) when you let go. Preload is like the amount of air filling the balloon before it is released.

Nurses must understand preload when managing patients with conditions that affect fluid volume and cardiac function, such as heart failure or dehydration.

• Monitor fluid balance closely, as increased fluid volume can lead to excessive preload and worsen heart failure symptoms.
• Administer diuretics as prescribed to reduce preload in conditions like pulmonary edema or heart failure.
• Encourage adequate hydration in cases of hypovolemia to restore preload and improve cardiac output.
• Assess for signs of fluid overload (e.g., jugular vein distension, crackles in lungs) or fluid deficit (e.g., hypotension, poor skin turgor).
• Educate patients about sodium restriction to prevent fluid retention and reduce excessive preload in heart failure.

✘Incorrect answer options:

Cardiac index. Cardiac index is the cardiac output adjusted for body surface area (BSA), providing a more individualized measure of cardiac function. It does not describe myocardial fiber stretch or preload.

Cardiac output. Cardiac output is the total volume of blood pumped by the heart per minute, calculated as stroke volume multiplied by heart rate. While preload influences stroke volume and thus cardiac output, the term itself does not describe myocardial fiber stretch.

Afterload. Afterload refers to the resistance the ventricles must overcome to eject blood during systole. It is determined by systemic vascular resistance and aortic pressure, not the degree of myocardial fiber stretch at the end of diastole.

EXPLANATION

✔Correct answer:

An acute cerebrovascular accident. Uncontrolled and untreated hypertension is a major risk factor for the development of an acute cerebrovascular accident (CVA), commonly known as a stroke. Hypertension exerts excessive pressure on blood vessel walls over time, leading to damage and weakening of the vascular endothelium. This can result in:

• Ischemic stroke: Caused by a blood clot or plaque obstructing blood flow to the brain.
• Hemorrhagic stroke: Caused by rupture of a weakened blood vessel in the brain, often due to chronic hypertension.

Hypertension is often called the "silent killer" because it frequently has no symptoms until it causes significant damage, such as a stroke. Strokes are life-threatening emergencies that can result in long-term disability, such as paralysis, speech impairment, or cognitive deficits, highlighting the importance of regular blood pressure monitoring and early management.

Imagine high blood pressure as water flowing at extreme pressure through an old, fragile pipe (blood vessel). Over time, the pipe might burst (causing a hemorrhagic stroke) or get clogged with debris (causing an ischemic stroke). Regular maintenance, like controlling blood pressure, prevents these catastrophes.

Nurse Davis can highlight the following points to educate attendees on stroke prevention and the importance of hypertension management:

• Emphasize the importance of regular blood pressure checks, especially for individuals with risk factors such as age, family history, obesity, or smoking.
• Discuss the link between hypertension and strokes, explaining that controlling blood pressure significantly reduces the risk of a stroke.
• Educate on the warning signs of a stroke using the FAST mnemonic:
  • F: Facial drooping.
  • A: Arm weakness.
  • S: Speech difficulty.
  • T: Time to call emergency services immediately.
• Promote lifestyle changes such as a low-sodium diet (e.g., the DASH diet), regular exercise, stress management, and smoking cessation to manage hypertension.
• Encourage medication adherence for those already diagnosed with hypertension, explaining that proper treatment is key to preventing complications.

✘Incorrect answer options:

Acute myocardial infarction: While hypertension is a major risk factor for myocardial infarction (heart attack), the question asks for a severe health event that Nurse Davis should emphasize during a community education session. Strokes (CVA) are more directly linked to uncontrolled hypertension, especially in educational outreach about its consequences. However, myocardial infarction remains an important complication of hypertension.

An acute episode of liver disease: Hypertension is not directly linked to liver disease. Conditions such as cirrhosis or hepatitis are more commonly associated with liver dysfunction, not blood pressure issues.

An episode of pulmonary disease: Hypertension does not cause primary pulmonary disease. However, pulmonary hypertension (a separate condition) is associated with right-sided heart failure, which is distinct from systemic hypertension’s primary complications, such as stroke or heart attack.

EXPLANATION

✔Correct answer:

Propranolol blocks beta-adrenergic stimulation, resulting in decreased heart rate, myocardial contractility, and conduction. Propranolol hydrochloride is a non-selective beta-adrenergic blocker (beta-blocker) that works by blocking the effects of norepinephrine and epinephrine (stress hormones) on beta-adrenergic receptors. By doing so, it reduces beta-1 receptor activity (primarily found in the heart), leading to:

• Decreased heart rate (negative chronotropic effect).
• Decreased myocardial contractility (negative inotropic effect), which reduces the heart’s oxygen demand.
• Decreased conduction velocity through the atrioventricular (AV) node (negative dromotropic effect), which can help control arrhythmias.

By also blocking beta-2 receptors (found in the lungs and vascular smooth muscle), propranolol can cause bronchoconstriction, which is why it should be used cautiously in patients with asthma or chronic obstructive pulmonary disease (COPD).

The overall effects of propranolol make it effective for treating a variety of cardiovascular conditions, such as hypertension, angina, arrhythmias, and prevention of myocardial infarction. It is also used for conditions like anxiety and migraine prophylaxis due to its ability to modulate sympathetic nervous system activity.

Think of propranolol as a "brake" for the heart and sympathetic nervous system. Just like pressing the brake slows down a car to reduce strain, propranolol slows the heart and decreases its workload, protecting it from overexertion.

When educating patients about propranolol, nurses should include the following key points:

• Inform the patient that propranolol lowers blood pressure and heart rate, so they may feel less energetic initially, but their body will adjust over time.
• Advise the patient to check their pulse daily and report if it is below 50 beats per minute, as bradycardia is a potential side effect.
• Instruct the patient to avoid abrupt discontinuation of propranolol, as this can lead to rebound tachycardia or hypertension.
• Caution the patient about potential side effects, such as dizziness or fatigue, especially when standing quickly (orthostatic hypotension).
• Inform patients with asthma or COPD to notify their provider immediately if they experience shortness of breath or wheezing, as propranolol can worsen bronchoconstriction.

✘Incorrect answer options:

Propranolol is an angiotensin-converting enzyme (ACE) inhibitor that lowers blood pressure by preventing the conversion of angiotensin I to angiotensin II: This describes the mechanism of ACE inhibitors, not beta-blockers. ACE inhibitors, such as lisinopril, work by inhibiting the renin-angiotensin-aldosterone system (RAAS), reducing vasoconstriction and lowering blood pressure.

Propranolol is a strong vasodilator affecting both arteries and veins, reducing peripheral vascular resistance and lowering blood pressure: This describes drugs like nitroglycerin (a nitrate) or hydralazine. Propranolol does not directly cause vasodilation; instead, it reduces cardiac output and sympathetic stimulation, which indirectly lowers blood pressure.

Propranolol increases norepinephrine release, leading to decreased blood pressure and heart rate: This is incorrect because propranolol blocks norepinephrine’s effects on beta receptors, rather than increasing its release.

EXPLANATION

✔Correct answer:

To determine the degree and location of arterial blockage within the coronary arteries. The primary purpose of performing a cardiac catheterization for a patient with unstable angina is to assess the coronary arteries for the degree and location of arterial blockage. Unstable angina is caused by an imbalance between myocardial oxygen supply and demand, typically due to partial or transient blockage of a coronary artery by a ruptured plaque or thrombus. Cardiac catheterization, often coupled with coronary angiography, provides detailed imaging of the coronary arteries to identify:

• The presence of stenosis or blockages.
• The severity of the obstruction.
• The exact location of the affected artery.

This information is crucial for determining the most appropriate treatment plan, such as medical management, percutaneous coronary intervention (PCI, such as stent placement), or coronary artery bypass grafting (CABG).

For patients with unstable angina, cardiac catheterization is typically done on an urgent or semi-urgent basis to prevent progression to myocardial infarction (MI). It allows clinicians to quickly evaluate the coronary anatomy and decide on intervention strategies to restore blood flow.

Cardiac catheterization is like sending a small camera into a blocked pipe (the coronary arteries) to figure out where the clog is and how severe it is. Only after knowing this can plumbers (cardiologists) decide whether to clear it, replace it, or take other actions.

When preparing Mr. Jones for cardiac catheterization, Nurse Evans should provide the following education and interventions:

• Explain the procedure, including that a catheter will be inserted through a blood vessel (usually the femoral or radial artery) and guided to the coronary arteries to take images of the heart.
• Instruct the patient to remain NPO (nothing by mouth) for 6–8 hours prior to the procedure, as per hospital policy.
• Ensure the patient understands the risks, such as bleeding, infection, or contrast dye reaction, and that informed consent is obtained.
• Assess for allergies, particularly to contrast dye, iodine, or shellfish, and ensure the patient’s renal function is adequate to handle contrast dye excretion.
• After the procedure, monitor for complications such as bleeding at the insertion site, hematoma, or signs of vascular compromise (e.g., diminished pulses).
• Encourage the patient to report any chest pain during or after the procedure, as this could indicate ongoing ischemia or a complication.

✘Incorrect answer options:

To evaluate the functional capacity of the heart valves and myocardium: This is not the primary purpose of cardiac catheterization for unstable angina. While catheterization can provide some information about myocardial function (e.g., left ventricular function) and valve integrity, these assessments are secondary in this context. Echocardiography is typically used to evaluate heart valve function more specifically.

To surgically bypass obstructed coronary vessels: Cardiac catheterization itself is a diagnostic procedure. It is not a surgical procedure like coronary artery bypass grafting (CABG). However, the findings from catheterization may lead to a decision for CABG if multiple severe blockages are present.

To perform a percutaneous intervention to open and dilate narrowed coronary arteries: While cardiac catheterization can lead to immediate intervention, such as percutaneous coronary intervention (PCI) with balloon angioplasty or stent placement, its primary purpose is diagnostic: to locate and evaluate the extent of blockages. If PCI is needed, it is typically performed after the catheterization findings are reviewed, often during the same session.

EXPLANATION

✔Correct answer:

"Avoid using salt substitutes." Spironolactone is a potassium-sparing diuretic that blocks aldosterone receptors, reducing sodium reabsorption and increasing potassium retention in the kidneys. Because spironolactone causes potassium retention, the risk of hyperkalemia (high potassium levels) is significant, especially when potassium intake is excessive. Many salt substitutes contain potassium chloride, which can further increase serum potassium levels. Therefore, Nurse Patel should emphasize avoiding salt substitutes to prevent hyperkalemia, a potentially life-threatening condition that can lead to cardiac arrhythmias.

Spironolactone works by antagonizing aldosterone at the distal renal tubule. This reduces the excretion of potassium while promoting the excretion of sodium and water. While this helps manage hypertension and fluid retention, the potassium-sparing effect can cause dangerously high potassium levels if the patient consumes excess potassium.

Imagine spironolactone as a "gatekeeper" that prevents potassium from leaving your body. Adding salt substitutes (loaded with potassium) is like piling up more potassium behind the gate, increasing the risk of an overflow (hyperkalemia) that could disrupt the body's electrical systems.

Monitoring potassium levels and providing appropriate dietary education are critical for patients on spironolactone.

• Teach patients to avoid potassium-rich foods (e.g., bananas, oranges, avocados) and potassium-containing supplements unless instructed otherwise by their healthcare provider.
• Monitor serum potassium levels regularly to detect early signs of hyperkalemia.
• Educate patients to recognize symptoms of hyperkalemia, such as muscle weakness, fatigue, palpitations, or irregular heartbeat, and report them immediately.
• Reinforce adherence to prescribed sodium restrictions, as reducing sodium intake is still important for blood pressure management.
• Collaborate with the dietitian to provide individualized dietary guidance based on the patient’s needs and lab results.

✘Incorrect answer options:

"Consume foods with high potassium content." This advice is incorrect because spironolactone already causes potassium retention. Increasing potassium intake could lead to hyperkalemia, increasing the risk of life-threatening cardiac arrhythmias.

"Discontinue any sodium restrictions." Sodium restrictions remain essential for managing hypertension and fluid retention, even when taking spironolactone. Discontinuing sodium restrictions can lead to increased blood pressure and fluid retention, worsening the patient’s condition.

"Take daily potassium supplements as prescribed." Potassium supplements are not appropriate for patients taking potassium-sparing diuretics unless specifically indicated for other conditions, such as severe hypokalemia due to additional medications or diseases. In most cases, adding potassium supplements while on spironolactone increases the risk of hyperkalemia.

EXPLANATION

✔Correct answer:

Fluctuations in blood pressure. Baroreceptors are specialized mechanoreceptors located in the walls of the carotid arteries (at the carotid sinus) and the aortic arch. These receptors primarily respond to changes in blood pressure by detecting the degree of stretch in the arterial walls. When blood pressure rises, the arterial walls stretch more, triggering the baroreceptors to send signals to the medulla oblongata (in the brainstem) to initiate compensatory mechanisms, such as vasodilation and a reduction in heart rate, to lower blood pressure. Conversely, if blood pressure drops, the reduced stretch leads to signals that activate mechanisms like vasoconstriction and an increase in heart rate to restore blood pressure to normal levels.

Baroreceptors are part of a negative feedback system that regulates blood pressure. Their signals are transmitted via the glossopharyngeal nerve (cranial nerve IX) for the carotid sinus and the vagus nerve (cranial nerve X) for the aortic arch. The medulla oblongata interprets these signals and adjusts sympathetic and parasympathetic output to influence vascular tone and cardiac activity.

Imagine a car’s speedometer detecting how fast the car is going. If the car is moving too fast (high blood pressure), the driver (medulla oblongata) applies the brakes (reduces heart rate and causes vasodilation). If the car is going too slow (low blood pressure), the driver steps on the gas (increases heart rate and causes vasoconstriction).

Nurses play a critical role in understanding and supporting the body's blood pressure regulation. Key interventions related to baroreceptor activity include the following:

• Monitor and assess patients’ blood pressure regularly, especially in those with conditions like hypertension or hypotension.
• Educate patients about how lifestyle factors (e.g., posture changes, dehydration) can affect baroreceptor response and blood pressure regulation.
• Ensure patients with orthostatic hypotension rise slowly to prevent dizziness or falls due to delayed baroreceptor response.
• Support pharmacologic management, as medications like beta-blockers or vasodilators can alter baroreceptor-mediated regulation of blood pressure.

✘Incorrect answer options:

Variations in arterial oxygen tension (PaO2). Baroreceptors do not respond to oxygen levels. Instead, chemoreceptors located in the carotid and aortic bodies are responsible for detecting changes in oxygen levels (PaO2) and stimulating respiratory adjustments accordingly.

Alterations in heart rate. While baroreceptors can influence heart rate as part of blood pressure regulation (e.g., via the baroreflex), they do not directly respond to heart rate itself. Heart rate changes are a downstream effect of baroreceptor activity, not the primary stimulus.

Shifts in arterial carbon dioxide tension (PaCO2). Like oxygen levels, carbon dioxide levels are monitored by chemoreceptors, not baroreceptors. Chemoreceptors help regulate respiratory rate to maintain proper gas exchange, but they are not involved in blood pressure regulation directly.

EXPLANATION

✔Correct answer:

Creatine kinase (CK or CPK).  Creatine kinase (CK or CPK) is an enzyme released into the bloodstream when muscle tissue, including the myocardium (heart muscle), is damaged. In the context of a myocardial infarction (MI), the CK-MB isoenzyme (a cardiac-specific form of CK) begins to rise within 3 to 8 hours after the onset of myocardial injury, peaks around 12 to 24 hours, and returns to baseline within 2 to 3 days. This makes CK-MB a useful early marker for diagnosing acute MI, especially in combination with other cardiac enzymes like troponin, which is more specific to myocardial tissue.

CK is found in various tissues, including the heart (CK-MB), skeletal muscle (CK-MM), and brain (CK-BB). During an MI, myocardial cells are deprived of oxygen, leading to cell membrane rupture and the release of CK-MB into the bloodstream. The timing of CK-MB elevation helps detect early myocardial injury and can confirm MI when paired with clinical symptoms and ECG findings.

Think of CK-MB as a “signal flare” released from the heart when it’s under attack (an MI). This flare appears quickly (within 3 to 8 hours), peaks after some time (12–24 hours), and then fades away (returns to normal after 2–3 days).

Monitoring cardiac enzyme levels is essential for diagnosing and managing MI.

• Collect serial cardiac enzyme tests as ordered (e.g., every 6–8 hours for the first 24 hours) to track changes in CK-MB levels over time and confirm the diagnosis of MI.
• Monitor other cardiac biomarkers, especially troponin, as it is more specific to myocardial damage and remains elevated for a longer period (up to 7–10 days).
• Assess for clinical symptoms of MI, such as chest pain, diaphoresis, nausea, and epigastric discomfort, and correlate these findings with laboratory and ECG results.
• Provide prompt interventions, such as oxygen therapy, nitroglycerin, and pain management, while preparing the patient for additional diagnostic or therapeutic procedures (e.g., coronary angiography or thrombolytic therapy).
• Educate the patient and family about the importance of monitoring cardiac enzymes to assess the extent of myocardial injury and guide treatment decisions.

✘Incorrect answer options:

Lactic dehydrogenase (LDH): LDH is a nonspecific enzyme found in various tissues, including the heart, liver, and kidneys. It becomes elevated later in the course of an MI, typically rising 24 to 48 hours after myocardial injury and peaking at 48 to 72 hours. Because LDH lacks specificity for myocardial tissue, it is not as useful for diagnosing acute MI compared to CK-MB and troponin.

LDH-2: LDH-2 is a subtype of LDH found predominantly in the reticuloendothelial system and is not specific to the myocardium. After an MI, LDH-1 (heart-specific subtype) rises and becomes higher than LDH-2, a phenomenon called a "flipped LDH ratio," but this occurs much later (24–48 hours) and is not useful for early diagnosis.

LDH-1: LDH-1 is a heart-specific isoenzyme that rises during an MI, but it does so later than CK-MB, typically beginning to elevate at 24 hours and peaking at 48–72 hours. It is no longer commonly used for diagnosing MI due to the availability of more specific and timely markers, such as troponin and CK-MB.

EXPLANATION

✔Correct answer:

Atrial depolarization and conduction through the AV node. The P-R interval on an ECG represents the time it takes for the electrical impulse to travel from the atria (atrial depolarization) through the atrioventricular (AV) node and into the ventricles. Specifically, it includes the time for the impulse to pass through the sinoatrial (SA) node, atria, AV node, and the His-Purkinje system. The normal P-R interval is 0.12 to 0.20 seconds (3 to 5 small ECG boxes). Prolongation of the P-R interval suggests a delay in conduction, such as in first-degree AV block, whereas a shortened interval may indicate pre-excitation syndromes like Wolff-Parkinson-White syndrome.

The P wave on an ECG reflects atrial depolarization, and the PR segment (the flat line after the P wave) represents the delay of the impulse at the AV node. This delay ensures that the ventricles have adequate time to fill with blood before they contract. The entire P-R interval reflects both atrial depolarization and conduction through the AV node into the ventricles.

Think of the heart as a relay race. The P-R interval is like the handoff zone where the baton (electrical impulse) moves from the atria (first runner) to the ventricles (second runner). A delay or problem in the handoff zone (AV node) slows the race and affects overall performance (cardiac output).

Understanding the P-R interval is essential for identifying conduction abnormalities and managing cardiac conditions.

• Assess the P-R interval duration on the ECG to determine if it is within the normal range (0.12–0.20 seconds).
• Monitor for conditions like first-degree AV block (prolonged P-R interval) or other heart blocks, which may require further evaluation or intervention.
• Observe for associated symptoms, such as dizziness, syncope, or fatigue, which may indicate impaired cardiac conduction and output.
• Collaborate with the healthcare provider to evaluate medications (e.g., beta-blockers or calcium channel blockers) that may prolong the P-R interval by slowing AV node conduction.
• Educate the patient about the importance of follow-up care and routine ECG monitoring if conduction abnormalities are present.

✘Incorrect answer options:

Ventricular depolarization. Ventricular depolarization is represented by the QRS complex, not the P-R interval. The QRS complex reflects the electrical activation of the ventricles.

Ventricular repolarization. Ventricular repolarization is represented by the T wave, which occurs after the QRS complex. The P-R interval does not include ventricular repolarization.

Atrial contraction and relaxation. The P wave reflects atrial depolarization, but the P-R interval extends beyond the P wave to include conduction through the AV node and into the ventricles. Atrial relaxation (repolarization) is not visible on an ECG, as it is masked by the QRS complex.

EXPLANATION

✔Correct answer:

Pulmonic valve. The pulmonic valve is auscultated at the second left intercostal space along the left sternal border. This is the designated landmark for listening to blood flow through the pulmonic valve, which controls blood flow from the right ventricle into the pulmonary artery. Murmurs heard in this area are typically associated with conditions affecting the pulmonic valve, such as pulmonic stenosis or pulmonic regurgitation. The specific location is part of the systematic approach to cardiac auscultation, where heart sounds are assessed at specific landmarks corresponding to each valve.

Murmurs in the pulmonic area may indicate abnormal blood flow through the pulmonic valve or nearby structures, often caused by congenital defects, pressure overload in the right heart, or other cardiac abnormalities. For example, pulmonic stenosis produces a systolic murmur due to the narrowing of the valve, creating turbulent blood flow during systole.

Imagine the heart as a building with four doors (valves), each leading to a different area. The pulmonic valve is like the door on the left side of the second floor, leading to the rooftop garden (the pulmonary artery). If there's a problem with this door—like it's squeaky or stuck—you’d hear the noise (murmur) when standing right outside it, at the second left intercostal space, because that’s where this specific door is located.

When auscultating for murmurs, it is important to follow a systematic approach to identify which valve or cardiac area is affected. Nurses should also consider the timing (systolic or diastolic), quality, and intensity of the murmur.

• Ensure a quiet environment and use both the diaphragm and the bell of the stethoscope to capture high- and low-pitched murmurs.
• Document the timing (e.g., systolic or diastolic), grade, and location of the murmur accurately for physician follow-up.
• Monitor for associated signs and symptoms, such as cyanosis, fatigue, or shortness of breath, which may indicate right-sided heart issues.
• Encourage follow-up diagnostics such as echocardiography to confirm the presence and cause of the murmur.

✘Incorrect answer options:

Aortic valve. The aortic valve is auscultated at the second right intercostal space along the right sternal border. This valve is responsible for blood flow from the left ventricle into the aorta and is not associated with the second left intercostal space.

Mitral valve. The mitral valve is auscultated at the fifth intercostal space at the midclavicular line on the left side of the chest. It is associated with blood flow between the left atrium and left ventricle.

Tricuspid valve. The tricuspid valve is auscultated at the fourth or fifth intercostal space along the left sternal border. It controls blood flow between the right atrium and right ventricle.

EXPLANATION

✔Correct answer:

During diastole (ventricular relaxation). The coronary arteries primarily receive blood flow during diastole, the phase of the cardiac cycle when the ventricles relax. During systole (ventricular contraction), the coronary arteries are compressed by the contracting myocardium, particularly in the left ventricle, which reduces blood flow. When the heart relaxes during diastole, the compression is relieved, and the coronary arteries are perfused with blood. Adequate coronary perfusion during diastole is crucial for delivering oxygen and nutrients to the heart muscle, particularly to the left ventricle, which has a high oxygen demand.

Coronary artery perfusion depends on diastolic pressure and duration. Conditions that shorten diastole, such as tachycardia, can reduce coronary artery perfusion and increase the risk of myocardial ischemia, particularly in patients with coronary artery disease. This is why controlling heart rate is important in these patients to ensure optimal coronary blood flow.

Imagine filling a water balloon through a hose. If someone is stepping on the hose (systole), very little water gets through. When the pressure is removed from the hose (diastole), the water flows freely and fills the balloon. Similarly, during diastole, blood flows more freely into the coronary arteries to "fill" the heart muscle with oxygen and nutrients.

Nurses should focus on educating patients about the importance of heart rate control and measures to improve coronary perfusion.

• Teach patients with coronary artery disease to recognize symptoms of inadequate coronary perfusion, such as chest pain or fatigue, especially during physical activity.
• Administer medications such as beta-blockers or calcium channel blockers, as prescribed, to slow the heart rate and prolong diastole, improving coronary perfusion.
• Encourage lifestyle modifications, such as regular exercise, a heart-healthy diet, and stress management, to optimize cardiovascular health and reduce oxygen demand on the heart.
• Monitor for complications in patients with tachycardia or atrial fibrillation, as these conditions can reduce diastolic time and compromise coronary artery perfusion.
• Provide education on the importance of controlling conditions like hypertension, as elevated blood pressure can increase the heart's workload and reduce perfusion efficiency.

✘Incorrect answer options:

During the expiratory phase of respiration. Coronary artery perfusion is not significantly affected by the phases of respiration. While respiration influences venous return and cardiac output, it does not dictate when coronary arteries are perfused.

During the inspiratory phase of respiration. Like expiration, inspiration has no direct impact on the timing of coronary artery perfusion. Coronary blood flow is determined by the cardiac cycle phases (diastole and systole), not respiration.

During systole (ventricular contraction). During systole, the contracting heart muscle compresses the coronary arteries, especially in the left ventricle, significantly reducing coronary blood flow. This is why coronary artery perfusion predominantly occurs during diastole, when the myocardium relaxes and coronary vessels are no longer compressed.

EXPLANATION

✔Correct answer:

Instructing her to take a nitroglycerin tablet prophylactically before climbing the stairs. For a patient with stable angina, prophylactic use of nitroglycerin is the most effective intervention to prevent exertion-related chest pain, such as the pain Ms. Johnson experiences when climbing stairs. Nitroglycerin is a nitrate that acts by dilating coronary arteries and systemic veins, reducing myocardial oxygen demand by decreasing preload and afterload. By taking nitroglycerin before engaging in an activity that triggers angina (e.g., climbing stairs), Ms. Johnson can reduce the risk of ischemia and chest pain.

Stable angina occurs when there is a temporary mismatch between myocardial oxygen supply and demand, usually triggered by physical exertion or emotional stress. Prophylactic nitroglycerin is a well-established intervention for managing such predictable episodes of angina.

Think of nitroglycerin as a "shortcut" for the heart, allowing it to work less hard during an uphill climb (like climbing stairs). By taking it beforehand, Ms. Johnson prepares her heart to manage the added workload more efficiently, reducing the risk of chest pain.

Nurses can provide the following guidance to ensure safe and effective management of stable angina for Ms. Johnson:

• Teach the patient how to use nitroglycerin correctly, including taking it 5–10 minutes before exertion and placing the tablet under the tongue to dissolve.
• Instruct the patient to sit down while taking nitroglycerin to avoid dizziness or hypotension.
• Explain that prophylactic nitroglycerin use is safe for predictable exertion-related activities and does not increase dependency on the medication.
• Encourage Ms. Johnson to keep nitroglycerin readily available and check the expiration date regularly, as expired nitroglycerin loses potency.
• Advise the patient to report any new or worsening chest pain (e.g., pain at rest, pain unrelieved by nitroglycerin) as it may indicate progression to unstable angina or acute coronary syndrome (ACS).
• Promote a heart-healthy lifestyle, including regular physical activity as tolerated, smoking cessation, and a low-sodium, low-cholesterol diet.

✘Incorrect answer options:

Recommending that she lie down upon reaching her friend's apartment: While lying down can help relieve angina symptoms by reducing oxygen demand, it is not a preventive measure. The goal is to prevent angina from occurring during exertion, not just manage it after it develops.

Suggesting she visit her friend earlier in the day: While timing physical activities during periods of lower stress or cooler temperatures may reduce the likelihood of angina, this approach is not a direct intervention. It does not address the exertion-related nature of Ms. Johnson's chest pain or provide a reliable way to prevent it during climbing stairs.

Advising her to rest for at least one hour before climbing the stairs: Rest can reduce the heart's workload, but it is not a sufficient preventive strategy for exertion-induced angina. Ms. Johnson will still experience increased myocardial oxygen demand while climbing stairs, regardless of prior rest.

EXPLANATION

✔Correct answer:

Poor arterial blood flow causing ischemia and tissue necrosis. Leg ulcers related to arterial insufficiency result from inadequate blood flow through the arteries, leading to ischemia (lack of oxygen) in the affected tissues. The reduced oxygen and nutrient delivery impair the body's ability to maintain tissue integrity, causing tissue death (necrosis) and the development of ulcers. These ulcers typically occur in areas where blood supply is most compromised, such as the toes, heels, lateral malleolus, or pressure points, and are often characterized by a punched-out appearance with well-defined edges, minimal drainage, and pale or necrotic wound beds. Patients with arterial insufficiency may also exhibit other signs of peripheral artery disease (PAD), such as cool extremities, diminished or absent pulses, and intermittent claudication (pain during activity relieved by rest).

Arterial ulcers are caused by atherosclerosis or other conditions that reduce blood flow, such as embolism, arterial trauma, or vasospasm. Without sufficient arterial blood flow, tissues are deprived of oxygen and nutrients, which are essential for cellular metabolism and wound healing. Prolonged ischemia leads to tissue breakdown and ulcer formation.

Think of tissues in the legs like a garden. If the water supply (arterial blood flow) to the garden is blocked, the plants (tissues) dry up and eventually die, creating barren patches (ulcers) where growth is no longer possible.

Addressing arterial insufficiency ulcers focuses on improving blood flow, preventing further ischemia, and promoting wound healing.

• Assess vascular status: Evaluate peripheral pulses, capillary refill, skin temperature, and color to assess the degree of arterial insufficiency.
• Promote blood flow: Position the legs to encourage arterial circulation (e.g., keeping the legs below the level of the heart) and avoid tight clothing or crossing the legs, which can reduce blood flow.
• Educate the patient: Encourage smoking cessation, which improves circulation, and emphasize the importance of managing comorbidities like hypertension, diabetes, and hyperlipidemia.
• Provide wound care: Use non-occlusive dressings and sterile techniques to protect the ulcer from infection while minimizing further trauma to the area.
• Collaborate with the healthcare team: Work with vascular specialists to assess for surgical or interventional options, such as angioplasty or bypass grafting, to restore blood flow to the affected area.

✘Incorrect answer options:

Increased venous pressure leading to fluid leakage and tissue damage. This description applies to venous insufficiency ulcers, not arterial ulcers. Venous ulcers occur due to high venous pressure and incompetent valves, leading to pooling of blood, fluid leakage, and tissue damage. Venous ulcers are typically found on the medial malleolus (inner ankle) and are associated with edema, brownish skin discoloration, and irregular wound borders.

Trauma to areas with adequate arterial blood supply. Trauma can contribute to ulcer formation in some cases, but ulcers due to arterial insufficiency occur in areas of inadequate blood supply rather than areas with sufficient blood flow. Even minor trauma in ischemic tissues can lead to ulceration because the tissues lack the oxygen needed for proper healing.

Infection spreading from surrounding tissues to the ulcer site. While infection can develop in an arterial ulcer as a secondary complication, it is not the primary cause. The primary cause of arterial ulcers is ischemia and tissue necrosis due to poor blood flow.

EXPLANATION

✔Correct answer:

Heart rate increases. Direct-acting vasodilators (e.g., hydralazine, minoxidil, or nitroprusside) cause arterial vasodilation, leading to a reduction in systemic vascular resistance and a subsequent drop in blood pressure. This sudden decrease in blood pressure activates the baroreceptor reflex, which stimulates the sympathetic nervous system to compensate for the hypotension by increasing the heart rate (reflex tachycardia). Reflex tachycardia occurs as the body attempts to maintain adequate cardiac output and perfusion in response to the drop in vascular resistance caused by the medication.

Direct-acting vasodilators work by relaxing the smooth muscle in the walls of blood vessels, primarily the arterioles, reducing afterload (the resistance the heart must pump against). However, this vasodilation is detected by baroreceptors in the carotid sinus and aortic arch as a decrease in blood pressure, triggering an autonomic response that increases heart rate to compensate for the reduced vascular tone.

Imagine your blood vessels as garden hoses delivering water (blood) to your plants (organs). Direct-acting vasodilators make the hoses wider, reducing water pressure (blood pressure). However, the water pump (your heart) notices the drop in pressure and starts working faster (increasing heart rate) to ensure the plants still get enough water. This is your body's way of compensating for the sudden drop in pressure caused by the medication.

Nurses should monitor heart rate and blood pressure closely in patients taking direct-acting vasodilators to identify reflex tachycardia and other hemodynamic changes.

• Monitor vital signs: Check heart rate and blood pressure regularly to detect tachycardia or excessive hypotension, which could lead to dizziness, syncope, or inadequate perfusion.
• Administer beta-blockers as prescribed: To mitigate reflex tachycardia, patients may be prescribed beta-blockers alongside vasodilators to counteract the increase in heart rate while maintaining the antihypertensive effect.
• Educate the patient: Teach the patient to recognize symptoms of tachycardia, such as palpitations or lightheadedness, and to report them promptly. Advise against abrupt position changes to reduce the risk of orthostatic hypotension.
• Assess for fluid retention: Reflex tachycardia may lead to activation of the renin-angiotensin-aldosterone system (RAAS), causing fluid retention. Diuretics may be prescribed to manage this effect.
• Monitor for other side effects: Be aware of additional adverse effects, such as headache, flushing, or edema, that are common with vasodilators.

✘Incorrect answer options:

Heart rate remains significantly unchanged. This is incorrect because the baroreceptor reflex is activated in response to the drop in blood pressure caused by direct vasodilation, leading to an increase in heart rate (reflex tachycardia).

Heart rate becomes irregular. While direct-acting vasodilators can cause reflex tachycardia, they do not typically lead to irregular heart rhythms. Irregular rhythms, such as arrhythmias, are more commonly associated with electrolyte imbalances or underlying cardiac conditions, not direct vasodilator use.

Heart rate decreases. This is incorrect because the body compensates for the drop in blood pressure caused by vasodilation by increasing, not decreasing, the heart rate. Reflex bradycardia is uncommon with direct-acting vasodilators.

EXPLANATION

✔Correct answer:

“Apply the nitroglycerin patch for 12-14 hours each day and then remove it for a 10-12 hour period, typically at night.”  This is the correct instruction because a 10-12 hour nitrate-free period each day is necessary to minimize the risk of developing tolerance to nitroglycerin. Tolerance occurs when the body becomes less responsive to the effects of the medication after continuous exposure, reducing its effectiveness in preventing angina. Removing the patch for a specific duration allows the body to "reset" its sensitivity to nitroglycerin, ensuring that the medication remains effective during the active hours of the day when the patient is more likely to experience angina. Typically, patients wear the patch during waking hours (e.g., 8 AM to 10 PM) and remove it at night when angina is less likely to occur due to reduced activity levels.

Continuous exposure to nitroglycerin leads to depletion of sulfhydryl groups in vascular smooth muscle, which are needed to produce nitric oxide (the active metabolite of nitroglycerin). This results in reduced vasodilation and a diminished anti-anginal effect. Implementing a nitrate-free interval restores the body's ability to respond to nitroglycerin.

Think of nitroglycerin as a light switch for relaxing blood vessels. If the switch is always "on," it wears out over time and becomes less effective. Turning it "off" for a while (nitrate-free period) helps reset the switch so it works again the next day.

Proper education on nitroglycerin use is essential to ensure safety, prevent tolerance, and maximize the therapeutic effect.

• Instruct on timing: Advise the patient to apply the patch at the same time each day and remove it for a nitrate-free interval, typically overnight.
• Monitor for side effects: Educate the patient about potential side effects, such as headaches, dizziness, or skin irritation at the application site, and how to manage them.
• Avoid abrupt discontinuation: Stress the importance of following the prescribed schedule and not abruptly stopping nitroglycerin use, as this can lead to rebound angina.
• Warn about drug interactions: Counsel the patient to avoid medications that may interact with nitroglycerin, such as phosphodiesterase inhibitors (e.g., sildenafil/Viagra), which can cause severe hypotension.
• Encourage compliance: Reinforce the importance of adhering to the prescribed regimen and not extending the wear time of the patch to prevent tolerance.

✘Incorrect answer options:

“Switch to sublingual nitroglycerin when his systolic blood pressure rises above 140 mm Hg.” This is incorrect. Sublingual nitroglycerin is used for acute episodes of angina, not for managing high blood pressure or preventing tolerance to transdermal patches. Nitroglycerin patches and sublingual nitroglycerin serve different purposes and should not be interchanged without medical guidance.

“Apply the nitroglycerin patch every other day.” This is incorrect. Nitroglycerin patches are intended to be used daily, with a nitrate-free interval of 10-12 hours each day. Skipping entire days would reduce the effectiveness of the medication in preventing angina.

“Use the nitroglycerin patch only for acute episodes of angina.” This is incorrect. Transdermal nitroglycerin patches are designed for prophylaxis (prevention) of angina, not for treating acute episodes. Acute angina is best treated with sublingual nitroglycerin or fast-acting nitrate formulations.

EXPLANATION

✔Correct answer:

Systemic vascular resistance. Diastolic blood pressure (DBP) is primarily determined by systemic vascular resistance (SVR), which refers to the resistance offered by the small arteries and arterioles to blood flow. During diastole, the heart is in the relaxation phase, and the pressure in the arteries reflects the resistance created by the tone of the systemic vasculature. When the arterioles constrict (increased SVR), diastolic blood pressure rises; when they dilate (decreased SVR), diastolic pressure falls. This makes SVR the main determinant of diastolic blood pressure, as it reflects the balance between vasoconstriction and vasodilation throughout the body.

The arterial walls and tone of the arterioles maintain pressure in the vascular system during diastole, even when the heart is not actively pumping. Conditions such as increased sympathetic nervous system activity or hormonal influences (e.g., from angiotensin II or norepinephrine) can increase SVR, leading to elevated DBP. Conversely, vasodilators or a loss of vascular tone (e.g., in septic shock) reduce SVR, causing a drop in DBP.

Think of your blood vessels as garden hoses. When the hoses are narrow (high resistance), the water pressure remains higher even when the faucet is off (diastole). When the hoses are wide (low resistance), the pressure drops quickly once the faucet is turned off. Similarly, systemic vascular resistance controls the pressure in your arteries when the heart is at rest.

Understanding the factors that influence systemic vascular resistance and diastolic blood pressure is crucial for managing patients with hypertension or other cardiovascular conditions.

• Monitor diastolic blood pressure in patients at risk for vascular complications, such as those with hypertension, diabetes, or atherosclerosis.
• Educate patients about lifestyle factors that influence vascular tone, such as stress, smoking, and dietary sodium, which can increase systemic vascular resistance.
• Administer prescribed antihypertensive medications, such as vasodilators, calcium channel blockers, or ACE inhibitors, to reduce vascular resistance and control DBP.
• Evaluate for signs of increased SVR, such as cool, pale extremities due to peripheral vasoconstriction.
• Reassure patients that maintaining vascular health (e.g., through regular exercise and a healthy diet) can improve systemic vascular resistance and support normal blood pressure regulation.

✘Incorrect answer options:

Cardiac output. While cardiac output (CO) is a major determinant of systolic blood pressure, it has less influence on diastolic blood pressure. CO represents the amount of blood pumped by the heart per minute and primarily affects the pressure generated during systole.

Renal function. Renal function indirectly affects blood pressure regulation through fluid volume control and the renin-angiotensin-aldosterone system (RAAS). While it plays a role in long-term blood pressure regulation, it is not the primary determinant of diastolic blood pressure.

Baroreceptor activity. Baroreceptors help regulate blood pressure by detecting changes in arterial wall stretch and triggering compensatory mechanisms, such as altering heart rate or vascular tone. However, they are not the direct determinant of diastolic blood pressure; their role is modulatory rather than primary.

EXPLANATION

✔Correct answer:

The left anterior descending artery. The left anterior descending artery (LAD) is the primary blood supply to the anterior wall of the heart. It is a branch of the left coronary artery and runs along the anterior interventricular groove. The LAD supplies oxygenated blood to the anterior portion of the left ventricle, the interventricular septum, and part of the right ventricle. This artery is critically important because the left ventricle is responsible for pumping oxygenated blood to the systemic circulation. Blockage of the LAD can lead to significant myocardial damage and is often referred to as the "widow-maker" due to its association with fatal anterior wall myocardial infarctions (MIs).

Adequate blood supply to the anterior wall of the heart is crucial because the left ventricle must maintain sufficient contractility to supply blood to the entire body. Occlusion of the LAD leads to ischemia or infarction of the anterior wall, which can compromise cardiac output and cause life-threatening complications.

Think of the LAD as a "main highway" delivering supplies to the most heavily loaded section of the heart—the anterior wall of the left ventricle. If this highway becomes blocked, traffic (blood flow) cannot reach the heart's essential structures, leading to a shutdown (heart attack).

Nurses should understand the importance of the LAD when assessing cardiac function and educating patients about coronary artery disease.

• Monitor for signs of anterior wall myocardial infarction, including chest pain, ST-elevation in anterior ECG leads (V1–V4), and reduced cardiac output.
• Educate patients about risk factors for coronary artery disease, such as smoking, hypertension, hyperlipidemia, and diabetes, which can increase the likelihood of LAD blockage.
• Administer prescribed medications, such as nitroglycerin or beta-blockers, to reduce myocardial oxygen demand and improve perfusion.
• Reinforce the importance of emergency care if symptoms of MI occur, as LAD blockages require rapid intervention.

✘Incorrect answer options:

The internal mammary artery. The internal mammary artery is primarily used as a graft during coronary artery bypass surgery. While it can supply blood to coronary vessels after bypass, it is not the primary blood supply to the anterior wall of the heart.

The circumflex artery. The circumflex artery is another branch of the left coronary artery, but it supplies blood to the lateral and posterior walls of the left ventricle, not the anterior wall.

The right coronary artery. The right coronary artery supplies blood to the right atrium, right ventricle, and parts of the posterior heart. It does not primarily supply the anterior wall of the heart.

EXPLANATION

✔Correct answer:

“Apply the patch to a non-hairy, non-fatty area of the upper torso or arms.”  This instruction is correct because transdermal nitroglycerin patches are most effective when applied to clean, dry, non-hairy, and non-fatty areas of the skin, such as the upper torso or arms. These areas allow for optimal absorption of the medication through the skin into the bloodstream. Hairy or fatty areas can interfere with adhesion and absorption, reducing the effectiveness of the medication. Additionally, the skin site should be rotated daily to prevent irritation and skin breakdown.

Nitroglycerin is a vasodilator that works by relaxing the smooth muscles in blood vessel walls, reducing myocardial oxygen demand by decreasing both preload and afterload. Transdermal nitroglycerin provides a steady release of the medication over a prolonged period to prevent episodes of angina (chest pain).

Think of the skin as a doorway for medication. A smooth, clean doorway (non-hairy, non-fatty skin) allows the medicine to enter quickly and effectively, while a blocked doorway (hairy or fatty skin) slows the process.

Nurses should provide detailed instructions on the proper use of transdermal nitroglycerin patches to ensure safety and effectiveness.

• Educate about skin preparation: Clean the area with soap and water, dry it thoroughly, and avoid using lotions or powders, which can interfere with absorption.
• Rotate application sites: Advise the patient to apply the patch to a different site each day to prevent skin irritation or sensitization. Avoid broken or irritated skin.
• Instruct on patch timing: Teach the patient to wear the patch as prescribed, often for 12–14 hours, followed by a nitrate-free period of 10–12 hours to reduce the risk of tolerance.
• Manage side effects: Inform the patient that headaches are a common side effect and can be managed with over-the-counter analgesics (e.g., acetaminophen). Do not remove the patch unless instructed by a physician.
• Emergency precautions: Advise the patient not to use the patch to treat acute chest pain. Instead, they should follow their physician’s instructions for using sublingual nitroglycerin during acute angina episodes.

✘Incorrect answer options:

“If you experience a headache, remove the patch for 4 hours and then reapply it.” This is incorrect. While headaches are a common side effect of nitroglycerin due to vasodilation, removing the patch prematurely can reduce its effectiveness. Instead, patients should manage headaches with analgesics (e.g., acetaminophen) and discuss persistent or severe symptoms with their healthcare provider.

“Apply the patch to the same site each day to maintain consistent drug absorption.” This is incorrect. Reapplying the patch to the same site daily can lead to skin irritation, sensitization, and reduced absorption over time. The application site should be rotated to maintain healthy skin and effective drug delivery.

“If you experience chest pain, apply a second patch directly next to the first one.” This is incorrect. Transdermal nitroglycerin patches are used for prophylaxis (prevention) of angina, not for treating acute chest pain. For acute angina, patients should use sublingual nitroglycerin tablets or sprays as prescribed. Applying additional patches is unsafe and can lead to overdose or severe hypotension.

EXPLANATION

✔Correct answer:

Distal to the catheter insertion site. After a cardiac catheterization, assessing the vascular status distal to the catheter insertion site is essential to evaluate adequate blood flow to the affected extremity. Cardiac catheterization typically involves arterial access (commonly the femoral or radial artery), and complications such as arterial occlusion, hematoma formation, or thrombosis can compromise distal circulation. By palpating the pulse distal to the insertion site (e.g., the dorsalis pedis pulse for femoral access or radial pulse for brachial access), Nurse Rodriguez can determine if there is adequate perfusion and identify any vascular complications early.

In addition to palpating pulses, Nurse Rodriguez should assess for other signs of compromised blood flow, such as pallor, coolness, pain, diminished capillary refill, and paresthesia (the 5 P’s of neurovascular assessment: pain, pallor, pulselessness, paresthesia, and paralysis).

Imagine the insertion site as a faucet connected to a hose. Checking the pulse distal to the site is like making sure water is flowing freely to the far end of the hose, indicating no blockages or leaks along the way.

Assessing vascular status is critical post-procedure to ensure timely identification of complications and maintain perfusion.

• Palpate distal pulses to assess for changes in strength or presence compared to baseline findings documented before the procedure.
• Inspect the insertion site for signs of bleeding, hematoma, or swelling, which could indicate vascular injury or compression of the artery.
• Assess the limb for skin temperature, color, and sensation to identify early signs of ischemia or compromised circulation.
• Monitor vital signs and check for hypotension or tachycardia, which could indicate bleeding or arterial dissection.
• Provide patient education about reporting symptoms such as numbness, pain, or coldness in the limb, which may signal complications requiring immediate attention.

✘Incorrect answer options:

Proximal to the catheter insertion site. Assessing pulses proximal to the catheter insertion site is not a priority in this situation. Pulses proximal to the insertion site (e.g., femoral artery in the groin for femoral access or brachial artery for radial access) are less likely to be affected by vascular complications caused by the procedure.

Directly at the insertion site. It is not appropriate to palpate directly at the insertion site because this can disrupt the clot or seal that forms at the access site, increasing the risk of bleeding or hematoma. Instead, the site should be visually inspected for signs of complications.

In all extremities. While assessing pulses in all extremities might be necessary during a general cardiovascular assessment, it is not specific to evaluating perfusion after a cardiac catheterization. The focus should be on the limb distal to the catheter insertion site, as this is where perfusion is most at risk.

EXPLANATION

✔Correct answer:

Headache. Nitroglycerin commonly causes headaches as a side effect, which occurs due to the vasodilation it induces. Nitroglycerin relaxes and dilates blood vessels, including those in the brain. This vasodilation increases blood flow to the brain and can cause a throbbing headache, especially when starting the medication. Headaches associated with nitroglycerin are often mild to moderate in severity and usually diminish with continued use as the body adjusts to the drug.

Nitroglycerin is a nitrate that releases nitric oxide, leading to vasodilation by relaxing smooth muscle in the vessel walls. This vasodilation lowers blood pressure and reduces myocardial oxygen demand, but the widened cerebral vessels can stimulate pain receptors, resulting in a headache.

Think of nitroglycerin as opening a valve to release pressure in a plumbing system. While the overall pressure decreases, the sudden change in flow can create turbulence in certain areas (like blood vessels in the brain), causing temporary discomfort, such as a headache.

Patients should be informed that headaches are a common and expected side effect of nitroglycerin, not an indication of a serious problem. Nurses can provide tips for management and reassurance.

• Explain to the patient that headaches are a normal response to nitroglycerin and tend to decrease with continued use as the body acclimates to the medication.
• Advise the patient to use over-the-counter pain relievers (e.g., acetaminophen) if the headache is bothersome, as recommended by their healthcare provider.
• Monitor the patient for other signs of excessive vasodilation, such as dizziness or hypotension, which may also occur as side effects.
• Reassure the patient that headaches caused by nitroglycerin do not typically indicate a serious condition and are temporary in nature.

✘Incorrect answer options:

Elevated blood pressure. Nitroglycerin does not elevate blood pressure; it lowers it due to its vasodilatory effects. In fact, hypotension (low blood pressure) is a potential side effect, especially in cases of overdose or improper use.

Dyspnea (shortness of breath). Dyspnea is not a common side effect of nitroglycerin. On the contrary, nitroglycerin may improve symptoms of dyspnea in patients with heart failure or angina by reducing cardiac workload and improving circulation.

Abdominal cramping. Abdominal cramping is not typically associated with nitroglycerin. This side effect is more commonly linked to gastrointestinal disorders or certain medications that directly affect the digestive system.

EXPLANATION

✔Correct answer:

“Cardiac rehabilitation is not a cure but can help restore you to many of your former activities.”  This response by Nurse Evans is the most appropriate because it validates Mr. Davis's concerns while offering a realistic and positive perspective on the benefits of cardiac rehabilitation. Cardiac rehabilitation does not reverse coronary artery disease (CAD), but it is designed to improve quality of life, restore physical function, and reduce the risk of future cardiac events by addressing modifiable risk factors such as diet, physical activity, and stress management. By emphasizing that cardiac rehabilitation can help him regain many of his former activities, Nurse Evans provides a hopeful yet realistic view, empowering Mr. Davis to participate actively in the program.

Cardiac rehabilitation programs aim to optimize physical, psychological, and social functioning for patients with cardiac disease. They include supervised exercise, education about heart-healthy behaviors, and psychosocial support to improve long-term outcomes. Patients often regain confidence, physical stamina, and emotional well-being through structured programs.

Think of cardiac rehabilitation as a "tune-up" program for the heart. While it doesn’t replace a worn-out engine (irreversible heart disease), it helps improve the engine's performance and ensures smoother functioning for daily activities.

It is critical for nurses to address misconceptions about cardiac rehabilitation and motivate patients to participate actively in their care.

• Educate the patient: Explain the goals and components of cardiac rehabilitation, emphasizing that it improves overall quality of life, stamina, and emotional well-being rather than curing the underlying disease.
• Address emotional concerns: Explore the patient’s feelings of hopelessness and confusion to provide emotional support and motivate engagement in rehabilitation.
• Encourage goal setting: Collaborate with the patient to set achievable goals for physical activity and lifestyle changes, focusing on improving functional capacity.
• Monitor progress: Evaluate the patient’s physical and psychological progress throughout the rehabilitation program and adjust interventions as necessary.
• Provide psychosocial support: Encourage participation in group sessions where the patient can meet others with similar conditions, helping reduce feelings of isolation.

✘Incorrect answer options:

“Do you feel that you will have to make some changes in your life now?” This response shifts the focus to lifestyle changes without addressing Mr. Davis's immediate concerns about the purpose and benefits of cardiac rehabilitation. It may come across as dismissive of his emotional distress and confusion.

“Here we teach you to gradually change your lifestyle to accommodate your heart disease.” While this statement is factual, it lacks empathy and does not directly address Mr. Davis’s belief that rehabilitation cannot help him. Patients often need encouragement and reassurance to feel motivated to participate in rehabilitation.

“You are probably right, but we can gradually increase your activities so that you can live a more active life.” This response is inappropriate because it reinforces the patient’s pessimistic outlook (“You are probably right”), which may further discourage him from engaging in the rehabilitation program. It also downplays the potential benefits of rehabilitation.

EXPLANATION

✔Correct answer:

Afterload. Afterload refers to the resistance the left ventricle must overcome to pump blood into the systemic circulation. It is primarily determined by systemic vascular resistance (SVR) and the condition of the aortic valve. High afterload means the heart has to work harder to eject blood, which can increase myocardial oxygen demand and contribute to heart failure progression. Conditions like hypertension, aortic stenosis, or increased systemic vascular resistance elevate afterload, making it more difficult for the left ventricle to effectively pump blood.

Afterload is influenced by factors such as vascular tone (vasoconstriction or vasodilation) and blood pressure. When afterload is high, the heart must generate greater force during systole to open the aortic valve and maintain cardiac output. Over time, increased afterload can lead to left ventricular hypertrophy, as the heart compensates for the increased workload.

Imagine the left ventricle as a balloon and the blood vessels as a narrow straw. Afterload is like the resistance you feel when trying to push air out of the balloon through the straw. If the straw is narrowed (high afterload), it takes more effort to push the air out. If the straw is wide (low afterload), it’s much easier to release the air.

Managing afterload is critical for patients with heart failure, as reducing afterload can improve cardiac output and reduce the workload of the heart.

• Monitor blood pressure regularly, as elevated systemic blood pressure directly increases afterload.
• Administer prescribed vasodilators (e.g., ACE inhibitors, ARBs, or hydralazine) to reduce systemic vascular resistance and lower afterload.
• Educate the patient on the importance of managing hypertension, as it is a significant contributor to increased afterload.
• Assess for signs of worsening heart failure, such as dyspnea, fatigue, or edema, which may indicate the heart is struggling with increased afterload.
• Promote a low-sodium diet to help reduce blood pressure and vascular resistance.

✘Incorrect answer options:

Overload. "Overload" is not a specific physiological term used to describe cardiac workload. It is a nonspecific term that does not refer to the resistance the heart faces during ejection.

Preload. Preload refers to the amount of blood in the ventricles at the end of diastole, just before systole. It represents the volume of blood returning to the heart and the degree of ventricular stretch prior to contraction. While preload affects stroke volume, it does not describe the resistance the heart must overcome to pump blood.

Cardiac output. Cardiac output is the total volume of blood pumped by the heart per minute, calculated as stroke volume multiplied by heart rate. While it reflects overall heart performance, it does not describe the resistance against which the heart must pump.

EXPLANATION

✔Correct answer:

Implementing continuous cardiac monitoring. The priority action for Nurse Williams is to implement continuous cardiac monitoring to detect and respond to life-threatening arrhythmias, which are a common complication of myocardial infarction (MI), even in the absence of initial ECG abnormalities. Continuous cardiac monitoring ensures that any subtle changes in cardiac rhythm or conduction—such as ventricular fibrillation, ventricular tachycardia, or heart blocks—are identified and treated immediately. Prompt recognition of arrhythmias is crucial because they can lead to cardiac arrest or worsening myocardial injury.

In the early phase of a suspected MI, ischemic changes in the myocardium may not yet be apparent on the ECG, particularly if the infarct is small or in its early stages. However, the risk of complications such as arrhythmias remains high, necessitating close cardiac monitoring to protect the patient from sudden cardiac events.

Continuous cardiac monitoring is like having a smoke detector in a house. Even if there are no visible flames (normal ECG), the detector can sense subtle changes (arrhythmias) early, giving you time to act before a serious fire (cardiac arrest) develops.

Ensuring effective cardiac monitoring and addressing the patient's physiological needs are critical in this scenario.

• Place the patient on continuous telemetry immediately upon admission to monitor for any arrhythmias or ischemic changes in real time.
• Maintain emergency equipment (e.g., defibrillator, code cart) readily available in case life-threatening arrhythmias, such as ventricular fibrillation, occur.
• Assess for chest pain characteristics and associated symptoms, such as diaphoresis, nausea, and shortness of breath, and report changes promptly.
• Prepare for further diagnostic testing, including serial ECGs and cardiac enzyme measurements (e.g., troponin), to confirm or rule out myocardial infarction.
• Provide emotional support to alleviate anxiety, which can increase myocardial oxygen demand and worsen symptoms.

✘Incorrect answer options:

Performing a comprehensive physical assessment. While performing a physical assessment is important to evaluate Ms. Johnson's overall condition and identify clinical signs of MI (e.g., diaphoresis, pallor, or jugular vein distention), it is not the immediate priority. Monitoring cardiac rhythm is more urgent to detect potentially fatal arrhythmias in real time.

Establishing and maintaining at least one intravenous (IV) access site. IV access is necessary for administering medications, such as nitroglycerin, morphine, or thrombolytics, and for drawing blood for diagnostic tests. However, it is not the top priority. Continuous cardiac monitoring takes precedence to ensure immediate detection and treatment of life-threatening arrhythmias.

Monitoring vital signs at regular intervals. Monitoring vital signs is important to assess the patient's hemodynamic stability, but it is performed intermittently and cannot replace the real-time detection of arrhythmias provided by cardiac monitoring.

EXPLANATION

✔Correct answer:

This combination promotes diuresis while mitigating the risk of hypokalemia. Spironolactone (Aldactone) and furosemide (Lasix) are often prescribed together because their mechanisms of action complement one another, achieving effective diuresis while minimizing the risk of hypokalemia (low potassium levels). Furosemide is a loop diuretic that works by inhibiting sodium, chloride, and water reabsorption in the ascending loop of Henle, resulting in significant potassium excretion. Spironolactone, on the other hand, is a potassium-sparing diuretic that acts on the distal tubules to block aldosterone, promoting sodium and water excretion but retaining potassium. When used together, spironolactone helps counteract the potassium loss caused by furosemide, creating a balance that promotes diuresis while maintaining normal potassium levels.

Furosemide is highly effective for reducing fluid overload, as seen in heart failure, liver cirrhosis, or edema. However, the excessive loss of potassium that accompanies its use can cause serious complications, such as arrhythmias or muscle weakness. Spironolactone’s potassium-sparing effects mitigate this risk while also addressing fluid retention. By combining these diuretics, healthcare providers maximize the therapeutic benefits of each drug while minimizing side effects.

Think of furosemide as a "strong broom" sweeping out excess fluid and electrolytes, including potassium, from the body. Spironolactone acts as a "safety net," catching potassium before it is completely swept away, helping maintain balance while still removing the excess fluid.

When managing patients on a combination of furosemide and spironolactone, nurses must carefully monitor for both desired effects and potential complications.

• Monitor potassium levels: Regularly check serum potassium levels to ensure that they remain within the normal range (3.5–5.0 mEq/L) and to detect signs of hyperkalemia or hypokalemia.
• Assess for signs of electrolyte imbalances: Observe for symptoms of hypokalemia (e.g., muscle weakness, cramps, arrhythmias) or hyperkalemia (e.g., fatigue, irregular heartbeat, muscle twitching).
• Monitor fluid status: Assess for signs of fluid overload (e.g., edema, crackles in the lungs) or dehydration (e.g., hypotension, dry mucous membranes) to evaluate the diuretics' effectiveness and avoid over-diuresis.
• Provide dietary education: Educate the patient to avoid excessive potassium intake (e.g., bananas, oranges) while on spironolactone to prevent hyperkalemia. However, if potassium levels are low due to furosemide, dietary potassium sources may still be encouraged.
• Monitor blood pressure: Both diuretics can lower blood pressure, so regular blood pressure monitoring is important to detect hypotension or orthostatic changes.
• Educate the patient about timing: Advise the patient to take diuretics in the morning to avoid nocturia and to follow their prescribed schedule for optimal effectiveness.

✘Incorrect answer options:

“Moderate doses of two different types of diuretics are more effective than a large dose of one type.” While this may be true in certain cases, it is not the primary reason for combining furosemide and spironolactone. The primary rationale is to counteract potassium loss caused by furosemide while promoting effective diuresis.

“This combination prevents dehydration and hypovolemia.” This is incorrect because both furosemide and spironolactone promote fluid loss, which can lead to dehydration or hypovolemia if not carefully monitored. The combination does not specifically prevent these conditions but rather requires close management to avoid them.

“Using two drugs increases plasma osmolality and the glomerular filtration rate.” This is incorrect. Diuretics reduce plasma volume, which can decrease renal perfusion and glomerular filtration rate (GFR) if used excessively. The combination of these drugs is aimed at balancing electrolyte levels and promoting diuresis, not increasing osmolality or GFR.

EXPLANATION

✔Correct answer:

Myocardial scarring and perfusion. The primary purpose of a thallium scan during nuclear cardiography is to assess myocardial perfusion (blood flow to the heart muscle) and identify areas of scarring or damage caused by previous myocardial infarctions. Thallium is a radioisotope that behaves like potassium and is taken up by healthy myocardial cells with adequate blood supply. Regions of the heart that do not take up thallium, referred to as cold spots, indicate areas of decreased perfusion, which may be due to ischemia (reversible) or infarction (irreversible scarring). This test is particularly useful for detecting coronary artery disease (CAD) and evaluating myocardial viability.

Thallium is injected intravenously during exercise or pharmacologic stress (e.g., using adenosine or dipyridamole) to assess the heart’s ability to receive adequate blood flow under stress. The scan can also be repeated at rest to differentiate between ischemia (temporary reduction in blood flow) and infarction (permanent damage).

Think of a thallium scan as a GPS heat map of a city (the heart). The injected thallium acts like tiny sensors lighting up areas where blood (traffic) is flowing smoothly. Bright areas on the map indicate well-perfused, healthy heart tissue, while dim or "cold" spots show areas where blood flow is reduced (ischemia) or blocked entirely (scarring from previous damage). By comparing maps during stress and rest, doctors can identify areas that may be temporarily under-supplied (reversible ischemia) versus permanently damaged (infarcted tissue).

Nurse Nguyen should ensure that Mr. Lee understands the procedure and provide necessary education to prepare him for the scan.

• Explain the procedure: Tell the patient that the scan involves injecting a small amount of radioactive material (thallium) and taking images of the heart to evaluate blood flow and identify any damage.
• Prepare for stress testing: If the test involves exercise, instruct the patient to wear comfortable clothing and refrain from eating, drinking caffeine, or smoking for several hours prior to the test. If pharmacologic stress is used, explain that a medication will be given to mimic the effects of exercise.
• Reassure about safety: Assure the patient that the radioisotope used is safe and that exposure to radiation is minimal and well within medical guidelines.
• Assess for contraindications: Confirm that the patient does not have allergies to the radioisotope or contraindications to stress testing, such as uncontrolled arrhythmias or recent myocardial infarction.
• Post-test instructions: Advise the patient to drink plenty of fluids after the scan to help flush the radioactive material out of their system.

✘Incorrect answer options:

Normal versus abnormal tissue characteristics. While the thallium scan can detect abnormal areas of the myocardium, it is specifically designed to assess perfusion and scarring, not general tissue characteristics. Techniques like MRI or CT scans are better suited for identifying structural abnormalities or specific tissue characteristics.

Areas of damage within the heart muscle. Although the thallium scan can identify areas of myocardial infarction (irreversible damage), its primary purpose is to assess perfusion, which may also reveal areas of reversible ischemia. Other diagnostic tools, such as echocardiography, may also detect damage to the myocardium.

Ventricular function. Ventricular function is typically evaluated using an echocardiogram, ventriculography, or radionuclide ventriculography (MUGA scan). While a thallium scan may provide some information about the effects of ischemia on ventricular performance, it is not its primary purpose.

EXPLANATION

✔Correct answer:

Maintain blood pressure within the normal range consistently. The most crucial long-term objective for a patient with hypertension is to consistently maintain blood pressure within the normal range. The primary goal of managing hypertension is to prevent complications such as stroke, myocardial infarction, kidney damage, heart failure, and other conditions caused by prolonged elevated blood pressure. According to current guidelines, normal blood pressure is less than 120/80 mmHg. For patients with hypertension, individualized target ranges may be set, but consistent control is essential for reducing long-term health risks.

This long-term objective encompasses all other goals, such as reducing sodium intake, exercising, and achieving weight loss, as they are supportive interventions aimed at helping the patient achieve and sustain blood pressure control. Maintaining normal blood pressure is the ultimate measure of success in managing hypertension.

Think of hypertension management like keeping a car’s engine running at the right temperature. All actions, such as adding coolant (reducing sodium), checking the oil (exercising), and performing maintenance (weight loss), work together to ensure the engine operates smoothly. Similarly, these measures all contribute to achieving the goal of normal blood pressure.

To help the patient achieve consistent blood pressure control, Nurse Jones should focus on the following key interventions:

• Educate the patient on the target blood pressure range and the risks of uncontrolled hypertension, such as heart attack, stroke, and kidney disease.
• Encourage regular monitoring of blood pressure at home, ensuring the patient knows how to use a blood pressure monitor correctly and interpret their readings.
• Promote adherence to prescribed antihypertensive medications by providing education on their purpose, side effects, and importance of taking them consistently.
• Support lifestyle modifications, including:
  • Following the DASH diet, which emphasizes low sodium, high potassium, fruits, vegetables, and whole grains.
  • Exercising regularly (e.g., at least 30 minutes of moderate activity 5 days per week).
  • Maintaining a healthy weight or achieving gradual weight loss if overweight.
  • Reducing alcohol consumption and avoiding smoking.
• Encourage regular follow-up appointments to evaluate blood pressure trends and adjust treatment plans as needed.

✘Incorrect answer options:

Reduce dietary sodium intake to less than 4,000 mg per day: While reducing sodium is a critical intervention for managing hypertension, the goal of sodium reduction (typically to less than 2,300 mg/day per guidelines) is secondary to the larger objective of maintaining normal blood pressure. Sodium reduction is a means to achieve blood pressure control, not the ultimate goal.

Exercise at least once per week for 30 minutes: While physical activity is beneficial for hypertension management, exercising once per week is insufficient to achieve significant, lasting blood pressure control. Current recommendations suggest at least 150 minutes of moderate-intensity exercise per week for optimal cardiovascular health. Regular exercise supports blood pressure control but is not the primary objective.

Achieve a weight loss of 5 pounds within the next month: Weight loss is an important goal, especially for overweight patients, as it can significantly lower blood pressure. However, a short-term goal like losing 5 pounds in one month is a specific step in a larger care plan and does not address the overarching long-term goal of maintaining normal blood pressure.

EXPLANATION

✔Correct answer:

Question the physician about the medication order. Propranolol (Inderal) is a non-selective beta-blocker that blocks both beta-1 (cardiac) and beta-2 (bronchial) receptors. While it is effective in managing hypertension and other cardiovascular conditions, it is contraindicated or used with extreme caution in patients with a history of asthma. Blocking beta-2 receptors can lead to bronchoconstriction, which may trigger or worsen asthma symptoms, potentially causing severe respiratory distress. For Mr. Henderson, a patient with a history of asthma, Nurse Emily's priority should be to clarify the propranolol order with the prescribing physician to ensure that it is appropriate. Cardioselective beta-blockers (e.g., atenolol or metoprolol) that primarily block beta-1 receptors may be safer alternatives for managing his hypertension without affecting the bronchial airways.

Beta-2 receptors in the bronchial smooth muscle mediate relaxation and dilation of the airways. By blocking these receptors, propranolol can lead to bronchial constriction, increasing airway resistance and exacerbating asthma. For patients with asthma, non-selective beta-blockers like propranolol are generally avoided unless there is no suitable alternative.

Imagine beta-2 receptors as "relaxation switches" in the lungs that keep the airways open. Propranolol blocks these switches, which is dangerous for someone with asthma because their airways are already prone to tightening. Nurse Emily needs to ensure the right "switch" (medication) is chosen to avoid worsening the patient’s condition.

Ensuring safe administration of medications, particularly in patients with contraindications or underlying conditions, is essential.

• Review the patient’s medical history for asthma or other respiratory conditions before administering beta-blockers.
• Communicate with the prescribing physician to confirm whether a cardioselective beta-blocker would be a safer option.
• Monitor for signs of bronchospasm, such as wheezing, shortness of breath, or respiratory distress, if a non-selective beta-blocker is administered.
• Provide patient education on the potential side effects of propranolol, including the risk of respiratory issues in patients with asthma.
• Ensure the patient understands the importance of reporting respiratory symptoms immediately if they occur after taking the medication.

✘Incorrect answer options:

Instruct the patient to take the medication with food. While propranolol can be taken with food to reduce gastrointestinal upset, this action is not the most crucial initial step. The priority in this situation is ensuring the medication is safe for a patient with asthma.

Caution the patient to rise slowly when standing. Beta-blockers can cause orthostatic hypotension, so advising the patient to rise slowly is an important nursing consideration. However, it is not the priority action in this scenario, as the patient’s asthma history presents a more immediate concern.

Monitor the patient’s apical pulse rate. Beta-blockers can decrease heart rate (bradycardia), so monitoring the apical pulse rate is a necessary nursing intervention before administration. However, the potential risk of bronchospasm due to the patient’s asthma history is a more urgent concern that must be addressed first by questioning the order.

EXPLANATION

✔Correct answer:

Dilation of the peripheral blood vessels. Nitroglycerin primarily works by dilating peripheral blood vessels, including veins and arteries, which reduces the workload on the heart and helps relieve angina symptoms. By causing venous dilation, nitroglycerin reduces venous return to the heart (preload), thereby decreasing the volume of blood the heart has to pump. Additionally, it dilates systemic arteries, reducing systemic vascular resistance (afterload), which decreases the pressure against which the heart must pump. Both effects lower myocardial oxygen demand, which alleviates chest pain caused by ischemia in patients with angina.

Angina occurs due to an imbalance between myocardial oxygen supply and demand, often caused by coronary artery disease or arterial spasms. By decreasing both preload and afterload, nitroglycerin reduces the oxygen demand of the heart, allowing better perfusion of the myocardium with the limited oxygen available.

Think of the heart as a factory that pumps blood (its "product") through pipes (blood vessels) to supply the body. When the pipes are narrow or clogged, the factory works harder, using more energy (oxygen) to push the blood through. Nitroglycerin acts like a pipe lubricant and expander, relaxing and widening the pipes. This reduces the pressure and effort needed to pump the blood, allowing the factory (heart) to conserve energy and prevent overexertion, effectively relieving the chest pain (angina).

Sublingual nitroglycerin is a critical medication for angina management. Nurses should educate the patient on proper administration and monitor for common side effects.

• Instruct the patient to place the nitroglycerin tablet under their tongue and allow it to dissolve completely without swallowing, ensuring rapid absorption.
• Warn about possible side effects, such as headaches, dizziness, or hypotension, and advise the patient to sit or lie down when taking the medication.
• Monitor blood pressure before and after administration, as nitroglycerin can cause significant hypotension.
• Teach the patient to take nitroglycerin at the onset of angina and to repeat doses every 5 minutes (up to 3 doses) if pain persists, seeking emergency medical attention if the pain does not subside after 3 doses.
• Store nitroglycerin tablets in a dark, airtight container to maintain potency, and advise the patient to check expiration dates regularly.

✘Incorrect answer options:

Increasing the myocardial oxygen demand. Increasing myocardial oxygen demand would worsen angina, as the condition arises from an insufficient oxygen supply to meet the heart's needs. Nitroglycerin reduces, rather than increases, myocardial oxygen demand.

Relaxing the pericardium through an antispasmodic action. The pericardium is a fibrous sac surrounding the heart and does not play a direct role in angina or its relief. Nitroglycerin works on blood vessels, not the pericardium.

Enhancing electrical conduction within the myocardium. Electrical conduction refers to the propagation of impulses that trigger heart contractions. Nitroglycerin does not affect myocardial conduction; its action is primarily vascular and metabolic.

EXPLANATION

✔Correct answer:

The heart compensates for lowered arterial oxygen tension by pumping faster to meet the body's oxygen demands. Tachycardia is often a compensatory mechanism in response to lowered arterial oxygen tension (hypoxemia) or increased oxygen demand. When arterial oxygen levels are reduced, as in conditions like anemia, hypovolemia, or respiratory dysfunction, the body attempts to maintain adequate oxygen delivery to tissues by increasing cardiac output. Since cardiac output is the product of heart rate and stroke volume, the heart compensates by pumping faster (tachycardia) to ensure that sufficient oxygen reaches the tissues. This is particularly important when oxygen transport is compromised.

Hypoxemia triggers baroreceptors and chemoreceptors in the carotid arteries and aortic arch, which activate the sympathetic nervous system. Sympathetic stimulation increases the heart rate and strength of contraction to improve oxygen delivery. However, sustained tachycardia can strain the heart and reduce diastolic filling time, potentially worsening oxygen delivery over time.

Imagine your heart as a delivery truck carrying oxygen to your body’s tissues. If there’s a shortage of oxygen (like fewer packages to deliver), the truck speeds up (tachycardia) to ensure all deliveries are made on time, even though the load is reduced.

Addressing the underlying cause of tachycardia is critical in managing this compensatory mechanism.

• Assess for hypoxemia: Monitor oxygen saturation levels using pulse oximetry, and if necessary, administer supplemental oxygen as prescribed to improve arterial oxygen tension.
• Monitor hemodynamic stability: Continuously evaluate the patient’s heart rate, blood pressure, and respiratory rate to detect signs of decompensation (e.g., worsening hypoxia or shock).
• Identify and treat the underlying cause: Determine whether the tachycardia is due to hypoxemia, dehydration, fever, anemia, or other factors, and intervene appropriately (e.g., administering IV fluids or treating an infection).
• Prevent excessive cardiac workload: Collaborate with the healthcare team to reduce myocardial oxygen demand by addressing pain, anxiety, or fever, which can exacerbate tachycardia.
• Educate the patient: Teach the patient about lifestyle measures, such as avoiding stimulants (e.g., caffeine) and managing stress, which can also contribute to an increased heart rate.

✘Incorrect answer options:

Respirations are labored, contributing to the increased heart rate. While labored respirations often occur alongside tachycardia in response to hypoxemia, they are not the direct cause of the increased heart rate. Rather, both tachycardia and labored breathing are compensatory mechanisms triggered by hypoxemia or increased oxygen demand.

The demand for oxygen is decreased due to pleural involvement, triggering tachycardia. This statement is incorrect because pleural involvement (e.g., pleural effusion or pneumothorax) typically increases oxygen demand or impairs oxygen delivery. Tachycardia is triggered when the body detects increased oxygen demand or decreased oxygen availability, not a reduction in oxygen demand.

The inflammatory process causes the body to demand more oxygen, which the heart attempts to meet by increasing its rate. Although inflammation can increase metabolic demand and oxygen consumption (e.g., in fever or infection), tachycardia is primarily triggered by oxygen availability (hypoxemia) or volume-related factors, not just inflammation itself.

EXPLANATION

✔Correct answer:

Hypokalemia. Hypokalemia is a common electrolyte disturbance associated with the use of loop diuretics like furosemide (Lasix), which promote the excretion of potassium, sodium, and water. Low potassium levels disrupt the electrical activity of the heart, increasing the risk of arrhythmias such as ventricular tachycardia (VT). Potassium is crucial for maintaining normal cardiac conduction and repolarization. When potassium levels fall, the myocardial cells become hyperexcitable, predisposing the patient to life-threatening arrhythmias.

Furosemide acts on the loop of Henle in the kidneys to inhibit sodium and chloride reabsorption, leading to significant potassium loss in the urine. This can result in hypokalemia, especially if potassium replacement is inadequate or if the patient is already predisposed to electrolyte imbalances. Hypokalemia prolongs repolarization (visible as a flattened T wave or the presence of U waves on an ECG) and can lead to arrhythmias like ventricular tachycardia.

Think of potassium as a “key” that helps unlock proper electrical signals in the heart. When potassium levels are too low, the key doesn’t fit correctly, leading to erratic signals (arrhythmias) like ventricular tachycardia.

Monitoring and managing electrolyte levels are critical after administering loop diuretics to prevent complications like hypokalemia and arrhythmias.

• Monitor serum potassium levels regularly, particularly in patients receiving diuretics such as furosemide.
• Assess the patient’s ECG for changes suggestive of hypokalemia, such as flattened T waves, the presence of U waves, or ventricular ectopy.
• Administer potassium supplements as prescribed to correct hypokalemia and prevent arrhythmias.
• Encourage a potassium-rich diet (e.g., bananas, oranges, spinach) for patients at risk of hypokalemia, unless contraindicated by other conditions (e.g., kidney disease).
• Monitor for other signs of hypokalemia, such as muscle weakness, fatigue, or cramps, which may indicate severe potassium depletion.

✘Incorrect answer options:

Hypermagnesemia. Hypermagnesemia is not a likely result of furosemide administration. In fact, furosemide increases magnesium excretion and can cause hypomagnesemia, which may also lead to arrhythmias, but it is less common compared to hypokalemia. Symptoms of hypermagnesemia typically include reduced deep tendon reflexes, bradycardia, and hypotension, not ventricular tachycardia.

Hypernatremia. Hypernatremia (high sodium levels) is not typically caused by furosemide, as the diuretic promotes sodium excretion. Sodium imbalances generally affect fluid status rather than directly causing arrhythmias like ventricular tachycardia.

Hypocalcemia. Hypocalcemia is not directly associated with furosemide-induced arrhythmias. While furosemide can increase calcium excretion, calcium disturbances more commonly cause neuromuscular symptoms (e.g., tetany) rather than ventricular tachycardia. Calcium imbalances are more often implicated in other conditions, such as parathyroid disorders.

EXPLANATION

✔Correct answer:

A noticeable alteration in the established pattern of her chest pain. In patients with unstable angina, any noticeable alteration in the established pattern of chest pain is a red flag that requires immediate medical attention. Changes that warrant concern include:

• Chest pain that occurs at rest or becomes more frequent, severe, or prolonged.
• Pain that is not relieved by rest or nitroglycerin.
• New symptoms, such as nausea, diaphoresis (sweating), or shortness of breath accompanying the chest pain.

Unstable angina indicates that the heart's demand for oxygen is exceeding supply, typically due to partial occlusion of a coronary artery by atherosclerotic plaque or clot formation. This condition increases the risk of myocardial infarction (MI). Thus, changes in the pattern of angina suggest worsening ischemia or progression to an acute coronary syndrome (ACS), requiring immediate medical evaluation.

Stable angina is predictable and typically occurs with exertion or stress, but unstable angina lacks predictability and occurs even at rest. Any shift from a patient's "normal" angina pattern is a significant warning sign of potential cardiac events, such as an MI.

Imagine chest pain like an engine warning light in a car. Stable angina is a consistent, predictable warning that the engine is under strain (e.g., when driving uphill). However, a sudden, unpredictable warning light flashing (unstable angina) means something more serious is happening, and immediate attention is required before the engine fails completely.

Nurse Riley should ensure that Mrs. Smith understands the warning signs of unstable angina and the importance of early intervention to prevent complications. Key teaching points include:

• Educate the patient about the symptoms of worsening angina and emphasize the need to report changes immediately to a healthcare provider.
• Encourage the patient to seek medical attention if chest pain occurs at rest, lasts longer than usual, or becomes more severe despite nitroglycerin use.
• Advise Mrs. Smith to take prescribed nitroglycerin as instructed and to call 911 if chest pain persists 5 minutes after the first dose of nitroglycerin.
• Stress the importance of adherence to medications, such as antiplatelets (e.g., aspirin, clopidogrel) and beta-blockers, to reduce the risk of plaque rupture or further ischemia.
• Encourage lifestyle changes to minimize cardiac risk factors, such as smoking cessation, stress management, and dietary modifications (e.g., low-sodium, low-cholesterol diet).
• Schedule regular follow-ups with her healthcare provider to monitor for changes in her angina and adjust her treatment plan as needed.

✘Incorrect answer options:

Chest pain experienced during sexual activity: While exertion, including sexual activity, can trigger chest pain in patients with stable or unstable angina, this symptom alone does not necessarily indicate an emergency unless it represents a change in the established pattern or is unrelieved by nitroglycerin. This situation is typically associated with stable angina, not unstable angina.

Chest pain occurring during an argument with her husband: Emotional stress is a common trigger for stable angina, as it increases sympathetic nervous system activity and myocardial oxygen demand. However, this does not indicate worsening angina unless it deviates from her established pattern (e.g., lasting longer, occurring at rest, or not responding to nitroglycerin).

Chest pain occurring during or after physical exertion, such as lawn mowing: Physical exertion can trigger stable angina because it increases the heart's oxygen demand. This is expected and predictable in patients with stable angina. However, this situation would not necessarily indicate unstable angina unless the pain pattern has changed (e.g., occurs with less exertion than before or is unrelieved by nitroglycerin).

EXPLANATION

✔Correct answer:

Troponin I. Troponin I is the most sensitive and specific biomarker for myocardial damage. Troponins are proteins found in cardiac muscle, and they are released into the bloodstream when myocardial cells are injured, such as during a myocardial infarction (MI). Troponin I levels begin to rise within 3–6 hours of myocardial injury, peak at 12–24 hours, and remain elevated for up to 7–10 days, making it a highly specific and reliable indicator of cardiac muscle damage. Unlike other markers, such as creatine kinase, troponins are almost exclusively found in the heart muscle, making them the gold standard for diagnosing acute coronary syndromes (ACS).

When myocardial cells are deprived of oxygen due to ischemia or infarction, they undergo cell death (necrosis), which leads to the release of intracellular proteins like troponin into the bloodstream. Elevated troponin levels correlate with the extent of myocardial damage and are critical for diagnosing MI and guiding treatment decisions.

Think of the heart muscle as a sealed container of ink (troponin). If the container is damaged (heart attack), the ink leaks out into the surrounding area (bloodstream). Measuring the amount of ink (troponin levels) in the area tells us how much damage occurred and confirms the source of the problem.

Nurses play a key role in preparing the patient for laboratory testing, interpreting results, and monitoring for complications related to myocardial infarction.

• Ensure blood samples are drawn at appropriate intervals (e.g., upon admission and at 3–6-hour intervals) to track changes in troponin levels over time.
• Monitor for other signs and symptoms of myocardial infarction, such as chest pain, dyspnea, diaphoresis, and ST changes on ECG.
• Provide emotional support and education to the patient and family, explaining the importance of troponin tests and their role in diagnosis.
• Collaborate with the healthcare team to initiate timely treatments, such as oxygen therapy, nitroglycerin, or thrombolytic therapy, based on diagnostic results.

✘Incorrect answer options:

Creatine kinase (CK). While CK, specifically the CK-MB isoenzyme, can be used to diagnose myocardial damage, it is less specific than troponin because CK is also found in skeletal muscle. CK-MB levels can rise due to other conditions, such as muscle injury, reducing its specificity for myocardial infarction.

Lactate dehydrogenase (LDH). LDH is an enzyme found in many tissues throughout the body, and its elevation is not specific to myocardial injury. It is now rarely used as a diagnostic marker for MI due to the availability of more specific tests like troponin.

Complete blood count (CBC). A CBC measures general blood parameters (e.g., red and white blood cell counts, hemoglobin, and hematocrit) and is not used to diagnose myocardial infarction. While a CBC may be ordered to evaluate overall health or detect signs of infection or anemia, it is not specific to cardiac damage.

EXPLANATION

✔Correct answer:

Explain that he should take one tablet, followed by a second tablet every 5 minutes, up to a maximum of three tablets. He should then contact his physician if the pain continues after the third tablet. Nitroglycerin is a fast-acting medication that is commonly prescribed for the immediate relief of chest pain (angina). Nurse Patel should instruct Mr. Chen to take one sublingual nitroglycerin tablet as soon as he experiences chest pain. If the pain persists after 5 minutes, he should take a second tablet. If the pain continues 5 minutes after the second dose, he should take a third tablet. If the pain is not relieved after the third tablet (15 minutes total), Mr. Chen should call emergency services or seek immediate medical attention, as unresolved chest pain may indicate a myocardial infarction (heart attack).

Nitroglycerin works by dilating blood vessels, reducing myocardial oxygen demand by decreasing both preload (venous return to the heart) and afterload (arterial resistance). Its rapid onset of action makes it ideal for acute angina relief. If the pain does not subside after three doses, it is likely that the cause of the chest pain is not responding to nitroglycerin and may be due to a more serious condition, such as myocardial infarction.

Think of nitroglycerin like an emergency sprinkler system for a fire (chest pain). You activate it (take the tablet) to quickly reduce the flames. If it doesn’t work after three attempts, it means the fire is too severe to be handled with this system, and you need to call the fire department (emergency services).

Nurses should educate patients thoroughly on the proper administration of nitroglycerin and when to seek emergency medical help.

• Instruct the patient to sit or lie down before taking the medication to avoid dizziness or fainting due to a sudden drop in blood pressure.
• Emphasize the importance of waiting 5 minutes between doses to allow the medication time to work.
• Teach the patient to call emergency services (911) if chest pain is not relieved after three doses, as this may indicate a serious cardiac event.
• Ensure the patient knows how to store the medication properly (in a dark, airtight container) to maintain potency.
• Advise the patient to carry nitroglycerin with them at all times for quick access during an angina attack.

✘Incorrect answer options:

Instruct him to take one tablet every 2 to 5 minutes until the pain completely subsides. This option is incorrect because it does not specify the maximum of three doses within 15 minutes, which is critical for avoiding excessive hypotension or other adverse effects. Continuing nitroglycerin beyond three doses without medical supervision can be dangerous.

Advise him to take one tablet. If the pain persists after 5 minutes, he should take two tablets. If the pain is still present 5 minutes after taking the second dose, he should call his physician. Taking two tablets at once is not recommended, as it increases the risk of severe hypotension and other side effects. The proper approach is to take one tablet at a time, spaced 5 minutes apart.

Direct him to take one tablet and rest for 10 minutes. If the pain persists after this 10-minute rest period, he should contact his physician. Waiting 10 minutes after the first tablet delays treatment and does not follow the recommended guideline of taking additional doses every 5 minutes, up to a maximum of three doses. Prompt action is essential in managing chest pain to prevent complications.