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Section 2: Angina & Myocardial Infarction

Myocardial perfusion: ischemia to infarction cascade.

Cell Factory Focus: The Cardiomyocyte Under Oxygen Starvation

20 NCLEX-Style Questions • 80% Required to Advance • NGN Clinical Judgment Framework

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🔗 CASCADE BRIDGE: How Section 1 Leads to Section 2

The disease cascade: Liver overproduces LDL → Endothelial damage → Plaque narrows artery → Cardiomyocyte oxygen starvation → ANGINA (reversible) or MI (irreversible cell death).

🏭 The Cardiomyocyte Factory Running Low on Fuel

When coronary arteries narrow from atherosclerosis, the cardiomyocyte factories don't get enough O₂ delivered. The mitochondria (power plants inside each factory) can't produce enough ATP (energy currency). The factory workers slow down. The patient feels this as chest PAIN — the factory's distress signal!

Angina is caused by an imbalance between oxygen supply and demand. The goal of treatment is to provide relief of the acute attack, correct the imbalance, and prevent progression to MI.

🔬 Inside the Cardiomyocyte: Normal vs. Oxygen-Starved

LEFT: Healthy cardiomyocyte with abundant O₂, ATP, and normal contraction. RIGHT: Ischemic cardiomyocyte — low O₂, failing mitochondria, lactic acid buildup causing PAIN, and if cell dies, troponin/CK-MB leak into blood.

💔 Types of Angina — Factory Stress Levels

💔 Four Types of Angina — Visual Comparison

Four types of angina compared: Stable (predictable, exercise-related), Unstable (EMERGENCY — unpredictable, may not respond to NTG), Variant (vasospasm, no plaque), Intractable (chronic, nothing helps).

✅ Stable (Exertional) Angina

Factory analogy: The factory can keep up at rest but fails during heavy production.

Occurs with exertion or emotional stress
Relieved by rest or nitroglycerin
Predictable pattern of onset, duration, severity
Usually lasts < 5 minutes (up to 15-20 min)
ECG: ST depression and/or T-wave inversion during episode
Cardiac enzymes: NORMAL

⚠ Unstable (Pre-infarction) Angina

Factory analogy: Factory struggling even at low production levels!

Unpredictable — occurs at rest!
Increases in occurrence, duration, severity
Pain may NOT be relieved by NTG
THIS IS AN EMERGENCY!
Signals progression toward MI

💔 Angina vs. Myocardial Infarction — HEAVILY TESTED ON NCLEX!

Feature	✅ Angina	💔 Myocardial Infarction
Onset	Can develop slowly or quickly	Often sudden, without cause, primarily early AM
Pain Level	Mild to moderate	CRUSHING, severe
Location	Substernal, may radiate to shoulders, arms, jaw, neck, back	Substernal, radiates to jaw, back, LEFT arm
Duration	< 5 min (up to 15-20 min)	30+ minutes
Relief	REST or Nitroglycerin	NOT relieved by rest or NTG! Only OPIOIDS (morphine)
ECG	ST depression / T-wave inversion during episode; normal at rest	ST ELEVATION (STEMI) or T-wave inversion (NSTEMI); Q-wave may appear
Cardiac Enzymes	NORMAL	ELEVATED — Troponin rises within 3 hrs
Cell Factory	Factory slowed but alive (reversible)	Factory workers DYING (irreversible necrosis)

💔 Myocardial Infarction — Factory Workers DYING

MI occurs when myocardial tissue is abruptly and severely deprived of oxygen. At the cellular level:

No O₂ → No ATP → Cell membrane breaks down → Troponin + CK-MB leak into blood → CELL DEATH → Scar tissue replaces working muscle

Scar tissue CANNOT contract! The heart is permanently weaker after MI. This is why heart failure can develop after MI (Section 3).

💔 STEMI vs. NSTEMI — Know the Difference!

STEMI

ST ↑ Elevation

COMPLETE coronary blockage

Large area of heart affected

More serious — rapid treatment critical

Factory: Entire department shut down!

NSTEMI

No ST Elevation

PARTIAL coronary blockage

T-wave inversion present

Women often present with NSTEMI

Factory: Department on reduced power

⚠ BOTH are MEDICAL EMERGENCIES! ⚠

💔 MI Location by Coronary Artery Blockage

LAD = Anterior/Septal MI ("Widow Maker"). Circumflex = Posterior/Lateral MI. RCA = Inferior MI (may also affect SA/AV nodes causing bradycardia).

📈 Cardiac Enzyme Timeline After MI

Myoglobin rises first (2h) but is not cardiac-specific. CK-MB peaks at 18h and normalizes by 48-72h. Troponin is the GOLD STANDARD — rises within 3 hours and stays elevated 7-10 days.

⏱ Timeline of Cellular Death After MI

6 Hours

Blue & swollen

Cells dying, filling with fluid

48 Hours

Gray + yellow streaks

Neutrophils invade (cleanup crew)

8-10 Days

Granulation tissue

Body starts repair process

2-3 Months

SCAR TISSUE

Permanent! Cannot contract! → HF risk

⚠ Atypical MI Presentations — NCLEX LOVES THIS!

♀ Women

Atypical discomfort (not classic crushing pain)
Shortness of breath
Fatigue
Often present with NSTEMI
T-wave inversion rather than ST elevation

👴 Older Adults

Shortness of breath
Pulmonary edema
Dizziness
Altered mental status
Dysrhythmia

👥 LPN Data Collection for MI — COLLECT DATA and REPORT!

⚠ LPNs COLLECT DATA and REPORT! RNs ASSESS and DIAGNOSE!

Pain (PQRST: Provocation, Quality, Region/Radiation, Severity, Timing)
Nausea and vomiting
Diaphoresis (sweating)
Dyspnea (difficulty breathing)
Dysrhythmia (on cardiac monitor)
Feelings of fear and anxiety
Pallor, cyanosis, and coolness of extremities

⚠ Complications of MI

Dysrhythmia

Most common! Especially first few hours

Heart Failure

Dead muscle weakens the pump (→ S3!)

Pulmonary Edema

LV fails → lungs flood

Cardiogenic Shock

>40% LV necrosis → pump failure

Dressler's Syndrome

Pericarditis + effusion weeks-months later

Other

Thrombophlebitis, valve damage, ventricular rupture

💡 Immediate MI Interventions — Priority Actions

Obtain description of chest discomfort (PQRST)
Administer oxygen by nasal cannula as prescribed
Administer nitroglycerin and morphine sulfate as prescribed
Monitor VS and cardiac rhythm continuously
Assess breath sounds for crackles/wheezes (HF signs)
Bed rest, semi-Fowler's position, stay with client
Establish IV access, obtain 12-lead ECG
Assist with thrombolytic therapy if prescribed (within 6 hours!)
Monitor lab values, administer beta-blockers as prescribed
Monitor for dysrhythmias (especially first few hours)

💡 Memory Trick: M-O-N-A for MI

Morphine

Reduces pain, anxiety, preload

Oxygen

↑ O₂ to starving factories

Nitroglycerin

Dilates coronary arteries

Aspirin

Stops platelet aggregation

Note: Actual priority order may vary by facility protocol. Always follow prescriber's orders.

💊 Nitroglycerin Protocol — HEAVILY TESTED!

Step 1

Take 1 NTG sublingual

Place under tongue, let dissolve

Step 2

Wait 5 min

If not better → 2nd dose
If worse → Call 911!

Step 3

Wait 5 min

If not better → 3rd dose
If worse → Call 911!

MAX 3!

No relief?

CALL 911 IMMEDIATELY!

✅ Burning/tingling under tongue = drug is still potent

✅ Headache is EXPECTED (vasodilation) — treat with acetaminophen

🔴 Store in dark glass bottle, replace every 6 months

🔴 NEVER with Viagra/Cialis! → Life-threatening hypotension!

🚨 CRITICAL DRUG INTERACTION: NTG + PDE-5 Inhibitors

Nitroglycerin + Sildenafil (Viagra) / Tadalafil (Cialis) = LIFE-THREATENING HYPOTENSION!

Both drugs cause vasodilation. Together → catastrophic BP drop!
Must wait at least 24-48 hours between these drugs.

👥 LPN Action: ALWAYS ask male patients about erectile dysfunction medications before giving NTG!

🔗 CASCADE BRIDGE: How MI Leads to Heart Failure (Section 3)

MI → Scar tissue → Compensation → Compensation fails → LV fails → Lungs flood → HEART FAILURE (Section 3)

🎯 NCLEX Test-Taking Strategy: Angina vs. MI Questions

When NCLEX asks about chest pain → first determine: angina or MI?
Key differentiators: Duration (<15 min = angina, >30 min = MI), Relief (NTG helps angina, NOT MI), Enzymes (normal vs. elevated)
For priority questions → ABCs (Airway, Breathing, Circulation) FIRST
For Recognize Cues (NGN) → identify the abnormal finding requiring immediate action
"Which finding should the nurse report immediately?" → Look for signs of complications
Drug suffixes: -pril = ACE inhibitor, -sartan = ARB, -olol = Beta-blocker
NTG rule: Burning/tingling = potent. No relief after 3 doses = call 911

📝 Quiz 2: Angina & Myocardial Infarction

20 Questions • 80% Required to Advance • Detailed Rationales for Every Question

Question 1 of 20

A client reports substernal chest pain that occurs with exercise and is relieved by rest. This pain has a predictable pattern. The LPN recognizes these cues as which type of angina?

A. Unstable angina
B. Stable (exertional) angina
C. Variant (Prinzmetal's) angina
D. Intractable angina

Correct: B. Stable angina occurs with exertion or emotional stress, is relieved by rest or nitroglycerin, and has a predictable, stable pattern. At the factory level, the heart can keep up at rest but fails during heavy production demands. Unstable angina is unpredictable and may NOT be relieved by NTG. Variant occurs at rest from coronary spasm. Intractable is unresponsive to all treatment. Recognize Cues: "predictable pattern" + "relieved by rest" = stable angina.

Question 2 of 20

A client has crushing substernal chest pain that has lasted 45 minutes and is not relieved by nitroglycerin. The LPN suspects which condition?

A. Stable angina
B. Variant angina
C. Myocardial infarction
D. Pericarditis

Correct: C. MI presents with crushing substernal pain lasting 30+ minutes that is NOT relieved by rest or nitroglycerin — only opioids provide relief. The factory cells are DYING, not just running low on oxygen. Angina pain typically lasts <15-20 minutes and IS relieved by NTG. Pericarditis pain is grating and worsens with breathing. Recognize Cues: "45 minutes" + "not relieved by NTG" = MI.

Question 3 of 20

Which type of angina occurs at rest, often in the early morning, and is caused by coronary artery spasm rather than plaque?

A. Stable angina
B. Unstable angina
C. Variant (Prinzmetal's) angina
D. Intractable angina

Correct: C. Variant (Prinzmetal's) angina results from coronary artery spasm, NOT plaque. It occurs at rest, often early morning, and shows ST elevation on ECG. Factory analogy: the supply highway goes into sudden spasm, temporarily cutting off the factory even though there's no physical obstruction. Treated with calcium channel blockers. Recognize Cues: "at rest" + "early morning" + "spasm" = Variant/Prinzmetal's.

Question 4 of 20

Using the Cell Factory model, why do cardiac enzymes (troponin, CK-MB) become elevated after a myocardial infarction?

A. The liver releases them in response to pain signals
B. Cardiomyocyte cell membranes break down, and intracellular proteins leak into the blood
C. The coronary arteries produce them as part of inflammation
D. The kidneys cannot filter them during low blood pressure

Correct: B. When cardiomyocyte factories die from lack of oxygen, their cell membranes break down. The proteins that were INSIDE the cell (troponin, CK-MB) leak out into the bloodstream — like factory workers' tools spilling out when the factory walls collapse. This is why elevated cardiac enzymes are diagnostic of myocardial damage. Troponin is the gold standard, rising within 3 hours and staying elevated for 7-10 days.

Question 5 of 20

Obstruction of the right coronary artery (RCA) would result in which type of MI?

A. Anterior wall MI
B. Inferior wall MI
C. Lateral wall MI
D. Septal MI

Correct: B. RCA obstruction = inferior wall MI. The RCA supplies the inferior wall of the left ventricle plus the SA and AV nodes. This is why RCA blockage can also cause bradycardia. LAD obstruction = anterior/septal MI. Circumflex obstruction = posterior/lateral wall MI. Memory: RCA = iRferior (bottom).

Question 6 of 20

A client experiencing chest pain takes one sublingual nitroglycerin tablet. After 5 minutes, the pain continues. What should the LPN instruct the client to do?

A. Wait 15 more minutes before taking another dose
B. Take a second NTG tablet and call 911 if symptoms do not improve or worsen
C. Chew and swallow the next tablet for faster absorption
D. Apply a nitroglycerin patch to the chest immediately

Correct: B. The NTG protocol is: Take 1 tablet → wait 5 min → if not relieved, take 2nd → wait 5 min → 3rd dose. If symptoms do not improve or worsen after any dose, CALL 911. Maximum 3 doses in 15 minutes. NTG is sublingual only (never chew or swallow — stomach acid destroys it). Patches are for prevention, not acute attacks.

Question 7 of 20

Which diagnostic finding is the GOLD STANDARD marker for diagnosing myocardial infarction?

A. Myoglobin level
B. CK-MB level
C. Troponin level
D. White blood cell count

Correct: C. Troponin is the GOLD STANDARD for MI diagnosis. It rises within 3 hours and remains elevated for 7-10 days, making it useful for diagnosis even days after the event. A troponin value >0.50 ng/mL indicates a strong probability of acute MI. CK-MB is useful but peaks at 18 hours and normalizes by 48-72 hours. Myoglobin rises earliest (2 hours) but is not cardiac-specific. WBC elevation is nonspecific.

Question 8 of 20 — Select All That Apply

The LPN is collecting data on a client suspected of having an MI. Which findings should be reported to the RN? (Select ALL that apply)

A. Diaphoresis (sweating) B. Nausea and vomiting C. Pallor and cyanosis of extremities D. Feelings of fear and anxiety E. Dysrhythmia on cardiac monitor

Correct: A, B, C, D, E — ALL are correct! ALL of these are data collection findings associated with MI that must be reported: diaphoresis, nausea/vomiting, pallor/cyanosis, anxiety/fear, and dysrhythmia. As an LPN, you COLLECT DATA and REPORT all findings to the RN or PHCP. The dying cardiomyocyte factories trigger a massive sympathetic response (sweating, pallor, anxiety) while reduced cardiac output causes nausea and cyanosis.

Question 9 of 20

A client taking sublingual nitroglycerin reports, "I feel a burning and tingling under my tongue." What is the LPN's best response?

A. "That means the medication is still potent and working."
B. "You should spit out the tablet immediately."
C. "The tablet tastes sweet."
D. "That indicates an allergic reaction."

Correct: A. Burning and tingling under the tongue indicates the nitroglycerin is still potent. NTG must be stored in a dark glass bottle and replaced every 6 months. If there is no burning/tingling, the drug may have lost potency. Headache is also expected from vasodilation — treat with acetaminophen.

Question 10 of 20

A female client age 72 presents with sudden fatigue, shortness of breath, and mild nausea. No classic chest pain is reported. The LPN should recognize these cues as potentially indicating:

A. Anxiety disorder
B. Stable angina
C. Gastric reflux
D. Atypical myocardial infarction

Correct: D. Not all clients experience classic MI symptoms. Women may present with atypical discomfort, shortness of breath, or fatigue and often have NSTEMI. Older adults may experience shortness of breath, dizziness, or altered mental status. This 72-year-old woman has TWO atypical risk factors (female + elderly). The LPN must recognize these atypical cues and report immediately! Recognize Cues: Female + elderly + fatigue/SOB/nausea without classic pain = suspect atypical MI.

Question 11 of 20

The LPN is caring for a client 24 hours after an MI. Which complication should the LPN monitor for FIRST during this critical period?

A. Dysrhythmia
B. Dressler's syndrome
C. Ventricular rupture
D. Thrombophlebitis

Correct: A. Dysrhythmia is the most common complication of MI, especially during the first 24-48 hours. The damaged cardiomyocytes create unstable electrical pathways. Dressler's syndrome occurs weeks to months later. Ventricular rupture is rare and occurs later. Thrombophlebitis relates to immobility. Priority: Continuous cardiac monitoring is essential in the first 24-48 hours post-MI.

Question 12 of 20

Which ECG finding differentiates STEMI from NSTEMI?

A. Presence of P waves
B. ST segment elevation
C. Normal QRS complex
D. Shortened PR interval

Correct: B. STEMI = ST Elevation MI (coronary artery completely blocked, larger area of damage). NSTEMI = Non-ST Elevation MI (partially blocked, may show T-wave inversion). The ST segment elevation on ECG is what differentiates them. Both are emergencies, but STEMI is more serious and requires urgent reperfusion. Hours to days after MI, ST changes return to normal, but Q-wave changes usually remain permanently.

Question 13 of 20 — Fill in the Blank

Explain, using the Cell Factory model, the cascade of events that occurs when a coronary artery becomes completely blocked during an MI. Include what happens to the cardiomyocyte's mitochondria, ATP production, cell membrane, and what substances leak into the blood.

0 / 500 minimum characters

Model Answer: When a coronary artery is completely blocked (usually from plaque rupture + thrombus), oxygen delivery to the cardiomyocyte factories stops completely. Without O₂, the mitochondria (power plants) cannot perform aerobic respiration, so ATP production drops drastically. The cell switches to anaerobic metabolism, producing lactic acid (which causes pain). Without adequate ATP, the sodium-potassium pumps fail, causing the cell to swell. The cell membrane breaks down, and intracellular proteins — specifically troponin and CK-MB — leak into the bloodstream. These become the diagnostic markers for MI. The cell dies and is eventually replaced by scar tissue that cannot contract, permanently weakening the heart.

Question 14 of 20

The LPN is reinforcing discharge teaching to a client prescribed sublingual nitroglycerin. Which statement by the client requires further teaching?

A. "I will store the tablets in a dark glass bottle."
B. "I should replace the tablets every 6 months."
C. "I can take my Viagra before using the nitroglycerin."
D. "A headache after taking the tablet is expected."

Correct: C. This statement requires further teaching! NTG + PDE-5 inhibitors (sildenafil/Viagra, tadalafil/Cialis) = LIFE-THREATENING HYPOTENSION! Both drugs cause vasodilation. Together, blood pressure can drop to dangerous levels. Must wait at least 24-48 hours between these drugs. The other statements are all correct NTG education.

Question 15 of 20

The LPN is caring for a client with an acute MI. Place the following interventions in the correct PRIORITY order:

A. Administer nitroglycerin and morphine as prescribed

B. Prepare for thrombolytic therapy

C. Obtain description of chest discomfort (PQRST)

D. Monitor vital signs and establish IV access

Click items in priority order:

Correct Order: C, A, D, B. 1st: Obtain pain description (PQRST) — you must collect data before acting. 2nd: Administer NTG and morphine — pain relief is priority because pain increases O₂ demand. 3rd: Monitor VS and establish IV access — ongoing monitoring and access for medications. 4th: Prepare for thrombolytics — must be given within 6 hours but requires physician order and IV access first.

Question 16 of 20

Which memory device helps the LPN remember immediate MI medications?

A. ABCDE (Airway, Breathing, Circulation, Disability, Exposure)
B. RACE (Rescue, Alarm, Contain, Evacuate)
C. PQRST (Provocation, Quality, Region, Severity, Timing)
D. MONA (Morphine, Oxygen, Nitroglycerin, Aspirin)

Correct: D. MONA = Morphine (reduces pain/anxiety/preload), Oxygen (increases O₂ to starving factories), Nitroglycerin (dilates coronary arteries), Aspirin (prevents platelet aggregation). ABCDE is for trauma assessment. RACE is for fire safety. PQRST is for pain assessment — used WITH MONA, not instead of it.

Question 17 of 20

A client 6 weeks post-MI develops chest pain, fever, and a pericardial friction rub. The LPN recognizes these cues as consistent with:

A. A new MI
B. Stable angina returning
C. Dressler's syndrome
D. Pulmonary embolism

Correct: C. Dressler's syndrome is a combination of pericarditis, pericardial effusion, and pleural effusion that occurs several weeks to months after MI. Key cues: chest pain + fever + pericardial friction rub + timing (weeks-months post-MI). It is an autoimmune-mediated inflammatory response to the necrotic tissue. A new MI would show elevated enzymes. Stable angina has no fever or friction rub. PE presents with sudden dyspnea and pleuritic pain.

Question 18 of 20

The LAD coronary artery is nicknamed the "Widow Maker" because it:

A. Supplies blood to the SA and AV nodes
B. Supplies the anterior wall and septum of the left ventricle — a large territory
C. Is the smallest coronary artery
D. Only supplies the right ventricle

Correct: B. The LAD (Left Anterior Descending) supplies the anterior wall and septum of the left ventricle — a large, critical territory. Blockage of the LAD causes an anterior/septal MI affecting a large area of the heart's main pumping chamber. This makes it particularly dangerous and earned it the nickname "Widow Maker." The RCA supplies the inferior wall and the SA/AV nodes.

Question 19 of 20

A client with an acute MI is placed in which position to decrease cardiac workload?

A. Supine with legs elevated
B. Semi-Fowler's position
C. Left lateral (Sims') position
D. Prone position

Correct: B. Semi-Fowler's position (head of bed elevated 30-45 degrees) decreases venous return (preload), reducing the workload on the damaged heart. Bed rest is maintained, and the nurse should stay with the client. Supine with legs elevated would INCREASE venous return. For pulmonary edema, HIGH-Fowler's with legs dangling is preferred (you'll learn this in Section 3).

Question 20 of 20

The LPN recognizes that morphine sulfate is a priority medication for MI because it: (Select the BEST answer)

A. Dissolves the clot blocking the coronary artery
B. Increases blood pressure to improve perfusion
C. Relieves pain and reduces preload, decreasing the heart's oxygen demand
D. Stimulates the SA node to normalize heart rhythm

Correct: C. Morphine sulfate is a priority because pain increases oxygen demand on the already-starving cardiomyocyte factories. Morphine relieves pain (reducing sympathetic stimulation), reduces anxiety, and decreases preload (venous dilation = less blood returning to heart = less work for damaged pump). It does NOT dissolve clots (that's thrombolytics). It does NOT increase BP or stimulate the SA node.

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