learndrugs
Cardiovascular

Coronary Artery Disease & Stable Angina

CAD High-yield Verified · Sep 2026

Coronary artery disease is the buildup of atherosclerotic plaque within the coronary artery lumen that impedes blood flow and reduces oxygen delivery to the heart muscle — the most common type of heart disease in the US and the leading cause of death for both men and women.

The disorder behind the most common type of heart disease and the classic nitroglycerin protocol: supply–demand mismatch, the stable-vs-unstable line every nurse must recognize, and the risk-factor teaching that actually changes outcomes.

What’s going wrong in the body

The normal physiology, where it fails, and why the body’s compensation backfires.

01 Decades of silent plaque

Atherosclerosis begins with endothelial injury. Monocytes migrate into the subendothelial space, become macrophages, and engulf oxidized LDL until they are bloated foam cells — the fatty streak. T-cell activation and cytokines keep the lesion inflamed, and growth factors recruit smooth-muscle cells (which also take up oxidized LDL). If the plaque stabilizes, a fibrous cap forms over it and the lesion calcifies over time.

This process starts in childhood and advances silently over decades. Symptoms — if any appear at all — begin only once the obstruction reaches roughly 50% of the lumen, which is also the threshold that defines "obstructive" CAD. Most patients spend most of the disease completely asymptomatic.

The atherosclerosis cascade: from endothelial injury to foam cells to a calcified, capped plaque — silent until the lumen is about half blocked.

02 Supply–demand mismatch — why the pain is exertional

A fixed stenosis — the mechanism in more than 90% of stable angina — leaves resting coronary flow normal. The problem is the ceiling: the narrowed segment caps how much flow can rise during stress (coronary flow reserve). Flow reduction begins past 50% stenosis and accelerates past 70%; exertional angina typically appears at ≥ 70% obstruction, and angina at rest when the vessel is about 90% stenosed.

Anything that raises myocardial oxygen demand — exertion, emotional stress, cold exposure, a heavy meal — pushes demand above the capped supply, and the ischemic myocardium signals with substernal pressure that eases within minutes of rest or nitroglycerin. That reproducibility is the definition of stable angina: a consistent pattern (typically ≥ 2 months for "typical" classification) of discomfort with exertion, relieved by rest.

Stable angina is a supply–demand story: the stenosis caps maximal flow, demand spikes past the cap, ischemia hurts, rest lowers demand, and the cycle waits for the next trigger.

03 The line that matters: stable vs unstable

Stable angina is a symptom to manage; unstable angina is an emergency, because its mechanism is different: a nonocclusive thrombus forming on a disrupted plaque. That clot can progress to complete occlusion — a myocardial infarction — at any time. On labs, troponin is what separates the two ACS neighbors: normal (or minimally elevated) in unstable angina, elevated in NSTEMI.

The bedside tell is the pattern, not the pain: unstable angina is new-onset pain, pain at rest, or a crescendo — more frequent, longer, more severe — with incomplete relief from rest or nitroglycerin. It no longer follows the predictable exertion-then-rest rhythm. Patient-facing red flags to treat as an emergency: chest pain at rest, pain lasting more than 15–20 minutes, or pain not relieved by nitrates.

The "when to worry" line: a predictable exertion-relieved pattern is stable; new-onset, rest, or crescendo pain is unstable angina — ACS territory.

04 The variants: vasospasm and small vessels

Not all angina is fixed plaque. Prinzmetal (vasospastic) angina is a transient, reversible spasm of the epicardial coronary arteries without fixed obstruction — driven by endothelial dysfunction (reduced nitric-oxide vasodilation), smooth-muscle hyperreactivity, and oxidative stress. Episodes strike at rest, most often between midnight and early morning, last 5–15 minutes, and respond promptly to nitrates; the classic ECG shows transient ST elevation that resolves after the episode. Triggers include smoking (the strongest association), cocaine and amphetamines, cold, emotional stress, and alcohol.

The CAD spectrum also includes nonobstructive disease (< 50% narrowing) and coronary microvascular disease, which affects the small vessels and is more common in women — women present with non-obstructive CAD in 57% of cases. This matters clinically: a "clean" large-vessel picture does not mean no ischemia.

Causes & risk factors

Modifiable factors are teaching targets — the patient can act on them.

Smoking — the number-one cause of cardiovascular disease (~2× risk; secondhand exposure raises risk 25–30%) modifiable Hypertension modifiable Diabetes (~2.5× heart-disease rate) modifiable Dyslipidemia modifiable Obesity modifiable Physical inactivity (12.2% population-attributable risk for MI) modifiable Diet high in salt, fat, and trans fat modifiable Psychosocial stress modifiable Age (lifetime risk after 40: 49% of men, 32% of women) Male sex Family history of premature CAD (father/brother before 55; mother/sister before 65) Ethnicity (higher risk in Black, Hispanic/Latino, and Southeast Asian populations)

Signs & symptoms

Each finding tied to the mechanism that produces it — and the triage it calls for.

No symptoms at all — often for decades early Expected
Why: Atherosclerosis begins in childhood and progresses silently; symptoms appear, if ever, only once obstruction reaches about 50% of the lumen.
Substernal pressure, heaviness, squeezing, or tightness with exertion or emotional stress, relieved within minutes by rest or nitroglycerin early Expected
Why: The fixed stenosis caps maximal coronary flow; when demand exceeds the cap, the myocardium becomes ischemic — and when rest lowers demand, the pain resolves.
Radiation to the left arm, neck, jaw, teeth, ear, or shoulder Expected
Why: The classic anginal referral pattern. Typical anginal pain lasts minutes — not seconds and not hours.
Predictable precipitants — uphill walking, stair climbing, cold exposure, emotional stress, heavy meals Expected
Why: Each raises myocardial oxygen demand against a supply that cannot rise past the stenosis — the supply–demand mismatch in daily life.
Anginal equivalents — exertional dyspnea or unusual fatigue instead of chest pain Expected
Why: Ischemia does not always announce itself as pain; dyspnea and fatigue on exertion can be the angina.
Atypical presentations in women, the elderly, and diabetics — shortness of breath, easy fatigability, back or epigastric pain Hold & notify
Why: These groups often lack the classic substernal story. Atypical pain leads to less accurate diagnosis and carries roughly 3× the mortality of classic angina — take it seriously.
Angina at progressively lower workloads Hold & notify
Why: The Canadian Cardiovascular Society grades this: class I (only strenuous exertion) through class III (walking 1–2 blocks) to class IV (any activity). A falling threshold means flow reserve is shrinking — the disease is worsening.
Rest angina between midnight and early morning, easing promptly with nitroglycerin Hold & notify
Why: The Prinzmetal (vasospastic) pattern — transient coronary spasm during parasympathetic predominance, lasting 5–15 minutes, with transient ST elevation during the episode.
New-onset angina, angina at rest, or a crescendo pattern (more frequent, longer, more severe) Report immediately
Why: The pattern has broken: a nonocclusive thrombus on a disrupted plaque — unstable angina, which can progress to complete occlusion.
Pain lasting more than 15–20 minutes or not relieved by rest or nitrates late Report immediately
Why: These are the patient-facing red flags that separate "angina" from "possible infarction in progress."
Pain that returns after nitroglycerin initially helped Report immediately
Why: Relief that doesn’t hold is not relief — pain that keeps coming back despite nitroglycerin may be unstable angina, a medical emergency.
Chest discomfort with diaphoresis, nausea, shortness of breath, dizziness, or palpitations Report immediately
Why: The accompaniments of unstable angina. Any pain, pressure, tightness, or discomfort in the chest, neck, arms, shoulders, upper abdomen, or back counts.

Diagnostics

Test In this disorder Normal
Resting 12-lead ECG Cheap, fast, and not user-dependent — the first test during any chest-pain episode. It detects active ischemia, so a normal tracing while pain-free does not exclude CAD ST-segment/T-wave changes with active ischemia; may show evidence of prior MI —
Exercise (treadmill) stress test Know the abort criteria: exertional hypotension, BP > 200/110 mm Hg, ST elevation or depression, or ventricular/supraventricular arrhythmias ST-segment depression ≥ 1 mm indicates ischemia; patient exercises to 85% of age-predicted maximal heart rate StatPearls —
Troponin Drawn during acute chest pain to rule out MI Normal (or minimally elevated) in unstable angina; elevated in NSTEMI — the lab that separates the two StatPearls —
Lipid panel Prognostic and a teaching anchor — an LDL above goal on a statin is a follow-up finding, not background noise The key chronic-setting lab. LDL-C goal < 70 mg/dL for stable ischemic heart disease (< 55 mg/dL for the highest-risk patients) StatPearls —
Coronary artery calcium (CAC) score Recommended for intermediate-risk patients (10-year ASCVD risk 7.5% to < 20%) and selected borderline-risk patients A score of 0 in symptomatic patients excludes obstructive CAD in 98.2% of cases StatPearls —
Coronary angiography (cardiac catheterization) Done under moderate sedation; watch for the complications — severe allergic reactions and kidney injury The gold standard — the most accurate modality for evaluating ischemic CAD; FFR ≤ 0.80 or iFR ≤ 0.89 marks a hemodynamically significant intermediate (40–70%) stenosis StatPearls —

Complications

Warning: Unstable angina — the plaque has disrupted Report immediately
A nonocclusive thrombus forms on a disrupted plaque; the predictable pattern breaks into new-onset, rest, or crescendo pain that rest and nitroglycerin no longer fully relieve.
The heralding cue is a change in the established pattern — stronger, more frequent, longer, at rest, or no longer relieved. The nurse’s move: treat it as ACS — stop activity, emergency evaluation, 12-lead ECG, troponin. This clot can complete the occlusion at any time.
Warning: Myocardial infarction Report immediately
A blood clot on the plaque blocks flow completely. Even well-managed stable angina carries an annual MI risk of about 1–3% per year.
MI survivors carry an annual mortality 5–6× higher than people without CAD — which is why the unglamorous work of aspirin, statins, and risk-factor control is the treatment. Chest pain at rest, pain > 15–20 minutes, or pain unrelieved by nitrates gets 911, not observation.
Warning: Arrhythmias & sudden cardiac death Report immediately
Both sit on the downstream path of CAD alongside infarction — ischemic myocardium is electrically unreliable.
This is why acute chest pain gets a continuous cardiac monitor: the point is to catch arrhythmias and ischemic changes while they are still catchable. New palpitations or an irregular rhythm during an episode is a report-immediately finding.
Caution: Ischemic heart failure Hold & notify
Chronic ischemia and infarction remodel the left ventricle until the pump itself fails — heart failure is a listed downstream event of CAD.
During chest-pain episodes, auscultate for rales — detecting pulmonary edema early is part of the standard acute assessment. See the heart failure page for where this road leads.

Medications for this condition

Why each class is prescribed here — every card links to its full pharmacology page.

Nitrates First-line
Cardiovascular · nitroglycerin

The acute rescue and the exam favorite: venodilation pools blood in the veins — preload falls, wall stress falls, oxygen demand falls (higher doses also dilate coronaries toward ischemic areas). Sublingual NTG is the therapy of choice for acute episodes (onset 1–3 minutes); long-acting forms prevent episodes but need a 10–12 hour nitrate-free interval daily to avoid tolerance. Absolute contraindication with PDE-5 inhibitors (sildenafil, vardenafil, tadalafil) — combined vasodilation can cause severe hypotension.
Statins First-line
Cardiovascular · atorvastatin

Statins "remain the first-line therapy for dyslipidemia" in chronic coronary disease (StatPearls). Recommended for all CAD patients if tolerated: high-intensity therapy (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) targeting ≥ 50% LDL-C reduction and an LDL < 70 mg/dL. If the goal isn’t reached, ezetimibe is added first, then a PCSK9 inhibitor.
Antiplatelets First-line
Cardiovascular · clopidogrel

The anti-thrombus insurance: aspirin irreversibly blocks platelet cyclooxygenase → less thromboxane A₂ → less aggregation on the plaque. Low dose (81–162 mg) daily, indefinitely, in established CAD — this is secondary prevention; routine primary prevention is out (no significant event reduction, more bleeding). Clopidogrel 75 mg daily substitutes when aspirin can’t be used.
Beta-Blockers First-line
Cardiovascular · metoprolol

Lower heart rate, contractility, and BP — oxygen demand falls. Beta-blockers are first-line for angina symptom control, with calcium channel blockers used when a beta-blocker is contraindicated, not tolerated, or insufficient. Titrate to a resting HR of 55–60 if symptoms persist; avoid in vasospastic (Prinzmetal) angina, where CCBs are first-line and beta-blockers can worsen spasm.

Beyond medications

  • Smoking cessation — the single biggest modifiable lever: CAD risk falls back to never-smoker levels within 4–10 years of quitting.
  • Exercise — about 150 minutes/week of moderate-intensity aerobic activity (50–70% of maximum heart rate) or 75 minutes vigorous; add 2–3 resistance-training sessions per week. The most active people carry 35–40% lower CAD risk.
  • Diet & weight — DASH lowers systolic BP by ~11.5 mm Hg and CAD risk by 21%; Mediterranean eating cuts CV risk ~20–25%; every 2% of calories from trans fat raises CAD risk 23%. Even a 5% weight loss yields clinically significant benefit.
  • Cardiac rehabilitation — a supervised cardiac rehab program is recommended for patients with frequent angina.
  • Revascularization (PCI or CABG) for lifestyle-limiting angina despite optimal medical therapy: improves symptoms; improves survival for left-main, three-vessel, or two-vessel disease involving the proximal LAD. CABG is favored over PCI for complex anatomy, LV dysfunction, and diabetes.

Nursing considerations

The RN-specific layer — each action paired with the reason it matters.

Assessment & monitoring
Assess every angina episode against the patient’s established pattern: trigger, duration, severity, what relieved it.
Why: A change in the pattern — stronger, more frequent, longer, at rest, or no longer relieved — is the heralding cue that stable disease is becoming unstable.
During any episode, get a 12-lead ECG and keep the patient on a continuous cardiac monitor.
Why: The ECG catches active ischemia (or STEMI); the monitor catches the arrhythmias and ischemic changes that ride along with it.
Screen the medication list for PDE-5 inhibitors (sildenafil, vardenafil, tadalafil) before any nitrate is given.
Why: Nitrate + PDE-5 inhibitor is absolutely contraindicated — both vasodilate, and together they can cause severe hypotension.
Report immediately: hypotension, unrelenting chest pain, arrhythmias, tachycardia, tachypnea, dyspnea, altered mental status, declining urine output.
Why: These are the report-now findings of the nursing references — each one signals the ischemia is no longer contained.
Track the lipid panel against goal (LDL-C < 70 mg/dL) and ask about statin adherence at every touchpoint.
Why: The LDL number is prognostic in chronic CAD, and an above-goal value on paper is often a skipped-doses story in person.
During an acute chest-pain episode
Stop all activity and put the patient on bed rest; raise the head of bed to 45°.
Why: Rest cuts cardiac workload — the demand side of the mismatch — and semi-Fowler’s reduces the work of breathing and the heart.
Apply supplemental O₂ via nasal cannula and take frequent vital signs.
Why: Oxygen supports myocardial oxygenation and perfusion; serial vitals track hemodynamic stability while the episode evolves.
Give sublingual nitroglycerin as ordered and reassess the pain after each dose; watch for hypotension and headache.
Why: Pain assessment is the effectiveness measure. Headache is expected (> 10% — it can even signal the drug is working); syncope is the dangerous one — it causes falls.
Draw troponin as ordered and anticipate aspirin 162–325 mg PO.
Why: Troponin rules an MI in or out — it separates unstable angina from NSTEMI — and aspirin keeps the platelet plug from growing.
Auscultate the lungs for rales.
Why: Ischemia can push the left ventricle into failure; crackles mean pulmonary edema is developing behind it.
Patient teaching
Teach the nitroglycerin protocol: sit down, place one tablet under the tongue and let it dissolve (don’t swallow); one more tablet may follow every 5 minutes — no more than 3 in 15 minutes. Call 911 if the pain continues after a second dose, and right away if the pain feels different from your usual angina or you can’t tell angina from a heart attack.
Why: Unrelieved pain may be unstable angina or an MI — a medical emergency that is never waited out, which is why the call comes after the second dose. Sitting first matters too — nitroglycerin can cause dizziness and fainting from low blood pressure, and fainting means falls.
Teach nitroglycerin handling: keep tablets in the original glass container, tightly capped after each use, at room temperature; a tablet 5–10 minutes before an activity that usually brings on angina can prevent the episode; headache and dizziness are expected side effects.
Why: An open or transferred container lets the tablets lose potency, and dosing before a predictable trigger prevents the episode instead of chasing it.
Never stop the antianginal or antiplatelet medicines without talking to the provider first.
Why: Abrupt withdrawal is a classic exacerbator.
Work the risk-factor list: stop smoking (household members too), LDL-C ≤ 70 mg/dL, blood-pressure control, diabetes management, low-fat diet, regular exercise.
Why: The nursing references call household smoking cessation mandatory to prevent recurrent events. On blood pressure, guideline targets have shifted between editions — the hypertension page owns the number; teach "controlled, per your provider’s target."
Teach pacing: learn how much exertion triggers the angina so you can stop and rest before the pain starts; avoid very hot or cold conditions, eat smaller meals if large meals bring on pain, and ask the provider what level of activity is right before starting a new program.
Why: Staying under the personal exertion threshold keeps demand below the capped coronary supply; temperature extremes and heavy meals raise demand too.
Sexual activity: most people with stable angina can continue normal activities, including sex — but ask the provider whether it is safe; unstable or poorly controlled angina means no sexual activity until it is under control. No ED drugs with nitroglycerin without checking with the provider.
Why: Sex is exertion like any other activity, so the same personal threshold applies — and raising it answers the question patients are afraid to ask. The PDE-5 rule is an absolute one.

How a real nurse thinks

The clinical-judgment loop, worked for a typical presentation — reasoning, not reference.

  1. 1
    Recognize cues

    The cues that matter are all in the history, not the vitals: angina at one block instead of two flights, an episode at rest, lasting ~10 minutes, needing a second nitroglycerin dose — plus an LDL of 88 on (sometimes-skipped) atorvastatin and active smoking. The normal vitals and clean pain-free ECG are the noise: a resting ECG detects active ischemia, and he isn’t having an episode right now.

  2. 2
    Analyze cues

    Put the pattern changes together — lower workload, longer episodes, rest pain, incomplete first-dose relief — and this is the crescendo picture of unstable angina: a nonocclusive thrombus on a disrupted plaque, no longer the fixed-stenosis supply–demand story his last 3 years followed. The mechanism can progress to complete occlusion, which is exactly why the pattern change — not today’s comfortable appearance — is the finding.

  3. 3
    Prioritize

    A suspected unstable pattern outranks everything else on the visit checklist. The LDL gap and the smoking are real problems — for later. Sequence: get this history to the provider now, before the patient leaves the building; risk-factor teaching follows once he is safe.

  4. 4
    Generate solutions

    Notify the provider immediately with the pattern change spelled out; anticipate emergency evaluation — serial 12-lead ECGs and troponin (normal in unstable angina, elevated in NSTEMI). Keep him at rest and monitored, not walking to the parking lot. Plan the discharge-level teaching — 911 protocol, medication adherence, smoking cessation — for after disposition is settled.

  5. 5
    Take action

    Report: "Established stable angina, pattern changed this week — angina at one block, a 10-minute rest episode overnight requiring two NTG doses. Currently pain-free, vitals stable, pain-free ECG unchanged. Requesting evaluation for unstable angina." Reinforce the current protocol before anything else: if pain starts — sit down, one SL tablet, repeat every 5 minutes up to 3 in 15 minutes, and call 911 if the pain continues after the second dose. The trap is treating this as a stable-angina medication-adjustment visit because he looks well right now.

  6. 6
    Evaluate

    Short-term success: he is evaluated emergently with troponins and serial ECGs rather than sent home with a tweaked prescription, and he can teach back the sit, dose, repeat-every-5-minutes, 911-if-pain-continues-after-the-second-dose rule. Long-term success looks like a pattern that is predictable again, a statin taken daily with LDL falling toward < 70 mg/dL, and a real smoking-cessation plan — for the whole household.

Scenario — you’re the nurse

Work each question before revealing the answer. Rationales explain the wrong options too.

Cardiology clinic · routine follow-up, nurse intake

A 64-year-old man with CAD and stable angina diagnosed 3 years ago. Home meds: aspirin 81 mg, atorvastatin 80 mg, metoprolol, and sublingual nitroglycerin PRN. He still smokes half a pack per day and admits he "sometimes skips the statin."

Intake vitals — HR 76 · BP 128/78 · RR 16 · SpO₂ 98% on room air · currently pain-free
Established pattern — substernal pressure after two flights of stairs, relieved within minutes by rest; unchanged for 3 years
This week — episodes now after one level block; last night an episode at rest lasting ~10 minutes, easing only after a second nitroglycerin dose
Labs (last week) — LDL-C 88 mg/dL
12-lead ECG in clinic (pain-free) — no ST-segment or T-wave changes
Q1 Select all that apply
Which findings from the intake require follow-up? Select all that apply.
  1. A. Angina now occurring after one block instead of two flights of stairs
  2. B. An episode of chest pain at rest lasting about 10 minutes
  3. C. Heart rate 76 with blood pressure 128/78
  4. D. LDL-C of 88 mg/dL while prescribed atorvastatin
  5. E. No ST-segment or T-wave changes on the pain-free clinic ECG
  6. F. He still smokes half a pack of cigarettes per day
Reveal answer & rationale
Answer: A, B, D, F
The falling exertion threshold and the rest episode are the pattern change that defines unstable angina — the emergency-level cues. The LDL of 88 is above the < 70 mg/dL goal for established disease (and he skips doses), and smoking is the number-one cause of cardiovascular disease — both are follow-up teaching targets. The vitals (C) are normal, and a clean pain-free ECG (E) is expected — the resting ECG detects active ischemia, so it neither reassures nor requires action here.
Q2 Multiple choice
The change in this patient’s angina — lower workload, longer episodes, pain at rest, incomplete relief from the first nitroglycerin dose — most likely represents:
  1. A. Expected progression of stable angina that PRN nitroglycerin will continue to manage
  2. B. Unstable angina — a nonocclusive thrombus on a disrupted plaque that can progress to complete occlusion
  3. C. Prinzmetal (vasospastic) angina, since one episode occurred at night
  4. D. Noncardiac chest pain, since the clinic ECG is normal
Reveal answer & rationale
Answer: B
New-onset, rest, or crescendo pain with incomplete relief is the definition of unstable angina, and its mechanism — thrombus on a disrupted plaque — is why it is an emergency (B). "Expected progression" (A) is the trap: a changed pattern is never expected; it is the heralding cue of worsening disease. Vasospastic angina (C) classically strikes at rest between midnight and early morning and responds promptly to nitrates — it doesn’t explain a falling exertional threshold in established fixed-plaque disease. A normal pain-free ECG (D) excludes nothing: the resting ECG detects active ischemia.
Q3 Multiple choice
Based on this history, the nurse’s best next action is to:
  1. A. Schedule a treadmill stress test at the next available appointment
  2. B. Notify the provider now and anticipate emergency evaluation with serial ECGs and troponin
  3. C. Reinforce the nitroglycerin protocol and have him return if the episodes worsen
  4. D. Teach him to take a nitroglycerin dose prophylactically before all activity
Reveal answer & rationale
Answer: B
A suspected unstable pattern is an emergency, and troponin is what separates unstable angina (normal) from NSTEMI (elevated) — the provider needs this history before the patient leaves (B). Scheduling routine testing weeks out (A) treats an emergency on a clinic timeline. Teaching-and-release (C) sends home a patient whose plaque may be actively thrombosing — the episodes have already worsened. Prophylactic pre-activity dosing (D) is legitimate stable-angina teaching (5–10 minutes before known triggers), which is exactly why it’s a plausible wrong answer: it manages the old pattern instead of responding to the new one.
Q4 Put in order
The nurse reinforces what to do if chest pain begins at home. Place the steps in the correct order:
  1. A. If the pain continues, take a second tablet — and call 911 if it continues after that second dose
  2. B. Sit down and stop all activity
  3. C. Place one nitroglycerin tablet under the tongue and let it dissolve — do not swallow it
  4. D. Wait 5 minutes
Reveal answer & rationale
Correct order: B → C → D → A
Sit first — resting cuts cardiac workload, and sitting protects against the falls that nitroglycerin-induced dizziness and low blood pressure can cause. Then one sublingual tablet, dissolved (swallowing defeats the sublingual route that bypasses first-pass metabolism), then the 5-minute wait; if pain continues, a second tablet — and 911 if it continues after that second dose (NHLBI), or at once if the pain is different from the usual angina. The label caps use at 3 tablets in 15 minutes; "keep dosing until it works" was never the rule.
Q5 Multiple choice
The patient mentions a friend offered him sildenafil for erectile dysfunction. The nurse’s best response is:
  1. A. "That is safe as long as you separate it from your nitroglycerin by 24 hours."
  2. B. "ED medicines must never be combined with your nitroglycerin — together they can cause severe hypotension. Don’t take any ED drug or herbal supplement without checking with your provider."
  3. C. "Since you only use nitroglycerin as needed, occasional sildenafil is fine."
  4. D. "Only the herbal versions are dangerous — prescription sildenafil is safe with nitrates."
Reveal answer & rationale
Answer: B
Nitrate + PDE-5 inhibitor is an absolute contraindication — both vasodilate, and the combination can cause severe hypotension; the patient-facing rule is that people who take nitrates "should not take medicines for erectile dysfunction without checking with their provider first" (B). The 24-hour rule (A) is the trap: the drug label simply contraindicates the combination, and even acute-care practice holds nitrates for 48 hours after a PDE inhibitor (see acute coronary syndrome) — for the patient, the rule is contraindication plus provider consultation, not a countdown. "PRN nitro makes it fine" (C) fails because his rescue drug is a nitrate — the interaction risk travels with him. (D) has it backwards: the warning covers prescription PDE-5 inhibitors and herbal ED supplements alike.

Common questions

What causes coronary artery disease & stable angina?
Common causes and risk factors include smoking — the number-one cause of cardiovascular disease (~2× risk; secondhand exposure raises risk 25–30%), hypertension, diabetes (~2.5× heart-disease rate), dyslipidemia, obesity, and others.
What are the early signs of coronary artery disease & stable angina?
Early findings include No symptoms at all — often for decades, Substernal pressure, heaviness, squeezing, or tightness with exertion or emotional stress, relieved within minutes by rest or nitroglycerin.
Which findings should a nurse report immediately in coronary artery disease & stable angina?
Report immediately: New-onset angina, angina at rest, or a crescendo pattern (more frequent, longer, more severe), Pain lasting more than 15–20 minutes or not relieved by rest or nitrates, Pain that returns after nitroglycerin initially helped, Chest discomfort with diaphoresis, nausea, shortness of breath, dizziness, or palpitations, Unstable angina — the plaque has disrupted, and others. These signal deterioration that needs rapid intervention.
Is it 3 nitroglycerin doses before calling 911, or call after the first dose?
Sit down and put one tablet under the tongue; another may follow every 5 minutes, but no more than 3 in 15 minutes (drug label). Call 9-1-1 if the pain continues after a second dose (NHLBI) — and immediately if the pain feels different from your usual angina or you can’t tell angina from a heart attack. Follow your provider’s specific plan; never wait out unrelieved chest pain.
What is the difference between stable and unstable angina?
Stable angina is predictable: a fixed stenosis caps coronary flow, so exertion brings on the pain and rest or nitroglycerin relieves it within minutes, in a pattern consistent over time. Unstable angina is a different mechanism — a nonocclusive thrombus on a disrupted plaque — and shows up as new-onset pain, pain at rest, or a crescendo pattern with incomplete relief. It can progress to complete occlusion (MI), so it is an emergency. On labs, troponin is normal in unstable angina and elevated in NSTEMI.
Is sexual activity safe with coronary artery disease?
For most people with stable angina, yes — NHLBI lists sexual activity among the normal activities most can continue, but ask your provider whether it is safe for you. People with unstable angina, or angina that does not respond well to treatment, should hold off until it is under control. Men who take nitrates, including nitroglycerin, must not take erectile-dysfunction medicines without checking with their provider first.

Sources

Reviewed by Hae Suk Lee, RN

Educational summary for nursing students. Scenarios are fictional teaching cases. Always verify against current guidelines and your institution's protocols before acting in practice. Not medical advice.

Bookmark LearnDrugs.com?

Your saved pages are kept in this browser. Add LearnDrugs.com to your browser’s bookmarks to get back to them in one click.

Drag this link to your bookmarks bar: LearnDrugs.com

Or press Ctrl + D to bookmark the page you’re on.