PN / LVN Focused

Cardiovascular Medications

Antihypertensives, anticoagulants, heart failure drugs, antiarrhythmics, diuretics, and cholesterol medications — the single most tested drug category on the LPN/LVN exit exam, broken down by class.

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01

ACE Inhibitors (-pril)

The "frill sisters" — first-line for HTN, heart failure, and diabetic nephropathy.

Suffix: -pril. Examples: lisinopril, enalapril, captopril, ramipril, benazepril

How They Work

Block the conversion of angiotensin I → angiotensin II → less vasoconstriction → less aldosterone release → lower BP and reduced cardiac workload.

Key Nursing Considerations

  • Dry, persistent cough — the #1 side effect and reason patients switch to an ARB. Caused by bradykinin accumulation.
  • Angioedema — swelling of face, lips, tongue, throat. This is a MEDICAL EMERGENCY — stop the drug, maintain airway, give epinephrine.
  • Hyperkalemia — ACE inhibitors retain potassium. Monitor K⁺ levels. Do NOT give with potassium supplements or potassium-sparing diuretics without careful monitoring.
  • Hypotension — especially first dose ("first-dose hypotension"). Monitor BP. Rise slowly.
  • Monitor renal function — BUN/Cr. Renoprotective in diabetic patients but can worsen renal impairment.
  • Contraindicated in pregnancy — teratogenic (causes fetal renal damage, especially 2nd/3rd trimester)
Exam Tip

If a question says "patient on lisinopril develops a persistent dry cough" → the answer is notify the provider; the medication will likely be changed to an ARB (-sartan), which works similarly but does NOT cause cough. If the patient develops facial/tongue swelling → stop the drug immediately (angioedema).

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02

ARBs (-sartan)

The ACE inhibitor alternative — same benefits, no cough.

Suffix: -sartan. Examples: losartan, valsartan, irbesartan, candesartan

How They Work

Block angiotensin II at the receptor level. Same endpoint as ACE inhibitors — lower BP, reduce cardiac workload — but through a different mechanism.

Key Points

  • No dry cough — this is the main advantage over ACE inhibitors
  • Still causes hyperkalemia — monitor K⁺
  • Still contraindicated in pregnancy
  • Still monitor renal function and BP
  • First-dose hypotension can still occur
ACE vs ARB — Quick Comparison

Both lower BP, protect kidneys, treat HF. Both cause hyperkalemia and are contraindicated in pregnancy. The difference: ACE inhibitors cause dry cough and angioedema risk. ARBs do NOT. If a patient can't tolerate an ACE inhibitor → switch to an ARB.

03

Beta-Blockers (-olol)

Slow the heart, lower the pressure — but check that HR first.

Suffix: -olol. Examples: metoprolol (Lopressor), atenolol (Tenormin), propranolol (Inderal), carvedilol (Coreg)

How They Work

Block beta-adrenergic receptors → decrease heart rate, decrease contractility, decrease BP, decrease cardiac workload. Used for HTN, heart failure, angina, arrhythmias, and MI.

Key Nursing Considerations

  • Check HR and BP before every dose — hold per the ordered parameters (commonly HR <60 bpm or a low/symptomatic BP). Notify provider.
  • NEVER stop abruptly — can cause rebound tachycardia, hypertension, angina, or even MI. Must taper over 1–2 weeks.
  • Masks hypoglycemia in diabetic patients — beta-blockers suppress tachycardia (which is normally an early warning sign of low blood sugar). Teach diabetic patients to monitor glucose closely.
  • Contraindicated in: severe bradycardia, heart block, uncompensated heart failure, asthma (can cause bronchospasm — especially non-selective like propranolol)
  • Side effects: fatigue, dizziness, depression, sexual dysfunction, cold extremities
  • Cardioselective (beta-1 only): metoprolol, atenolol — safer for patients with mild respiratory disease
  • Non-selective (beta-1 + beta-2): propranolol — avoid in asthma/COPD (blocks beta-2 in lungs)
#1 Beta-Blocker Rule

NEVER stop abruptly. If a patient tells you they ran out of their metoprolol and just stopped taking it → this is a safety concern. Abrupt discontinuation can trigger rebound hypertension, tachycardia, angina, or MI. Contact the provider immediately.

04

Calcium Channel Blockers (-dipine)

Two types: dihydropyridines (vessels) and non-dihydropyridines (heart).

Suffix: -dipine (for dihydropyridines). Examples: amlodipine, nifedipine

Non-dihydropyridines: diltiazem, verapamil (no shared suffix — memorize these two)

How They Work

Block calcium influx into cardiac and smooth muscle cells → vasodilation (lower BP) and/or decreased heart rate and contractility.

Dihydropyridines (-dipine)Amlodipine, nifedipine
Vasodilation (peripheral). Used for HTN. Minimal effect on heart rate.
Non-dihydropyridinesDiltiazem, verapamil
Slow HR + vasodilation. Used for HTN, angina, arrhythmias (A-fib rate control).

Key Nursing Considerations

  • Peripheral edema — especially with dihydropyridines (amlodipine). Teach patient to elevate legs.
  • No grapefruit juice — grapefruit increases drug levels (especially with verapamil) → risk of severe hypotension and cardiac arrest
  • Constipation (especially verapamil)
  • Monitor HR and BP — hold for bradycardia (non-dihydropyridines)
  • Flushing, headache, dizziness from vasodilation
  • Verapamil + beta-blocker = dangerous combination (both lower HR → severe bradycardia, heart block)
Memory Trick

"A-Dip-ine = dips the vessels" — dihydropyridines (-dipine) primarily work on blood vessels (vasodilation). Diltiazem and verapamil work on the heart AND vessels (slow HR too). No grapefruit with any CCB.

05

Diuretics

Three types — and potassium is the key difference between them.

Loop-semide · Furosemide, bumetanide
LOSES K⁺ (hypokalemia). Most potent. Monitor K⁺, daily weights, I&O. Ototoxic at high doses. Give in AM (avoids nocturia).
Thiazide-thiazide · HCTZ, chlorthalidone
LOSES K⁺ (hypokalemia). First-line for HTN. Can increase blood glucose and uric acid. Photosensitivity. Less potent than loops.
Potassium-SparingSpironolactone, triamterene, amiloride
SAVES K⁺ (hyperkalemia risk). Do NOT give K⁺ supplements. Monitor K⁺. Spironolactone: may cause gynecomastia.

Universal Diuretic Nursing Care

  • Daily weights — same time, same scale, same clothing. 1 kg = 1 liter of fluid.
  • Strict I&O monitoring
  • Monitor electrolytes (especially potassium)
  • Monitor for dehydration: dry mucous membranes, poor skin turgor, tachycardia, hypotension
  • Give in the morning (avoids nocturia/sleep disruption)
  • Monitor BP — risk for orthostatic hypotension
The Potassium Rule — Memorize This

Loop and thiazide diuretics = LOSE potassium → give K⁺-rich foods (bananas, oranges, potatoes) or supplements. Monitor for hypokalemia (weakness, leg cramps, irregular heartbeat). Potassium-sparing diuretics = SAVE potassium → AVOID extra K⁺. Monitor for hyperkalemia (peaked T waves, bradycardia). NEVER combine potassium supplements with potassium-sparing diuretics.

Digoxin + Diuretic = Watch Potassium

Hypokalemia (from loop/thiazide diuretics) INCREASES the risk of digoxin toxicity. Potassium and digoxin compete for the same binding sites. Low K⁺ → more digoxin binds → toxicity. Always check K⁺ when a patient is on both drugs.

06

Anticoagulants & Antiplatelets

The most tested drug comparison in nursing — heparin vs warfarin.

HeparinIV/SubQ
Onset: Immediate (IV). Lab: aPTT (1.5–2.5× normal). Antidote: Protamine sulfate. Special concern: HIT (Heparin-Induced Thrombocytopenia) — monitor platelets.
Enoxaparin / LovenoxSubQ
Onset: 3–5 hours. Lab: Usually none (anti-Xa if needed). Antidote: Protamine sulfate (partial). SubQ in abdomen. No aspiration, no massage.
Warfarin / CoumadinPO
Onset: 3–5 days for full effect. Lab: PT/INR (therapeutic: 2.0–3.0). Antidote: Vitamin K (phytonadione). Many food/drug interactions. Consistent vitamin K intake. Avoid leafy green fluctuations.

DOACs (Direct Oral Anticoagulants) — Newer Agents

Examples: rivaroxaban (Xarelto), apixaban (Eliquis), dabigatran (Pradaxa)

  • Oral, fixed dose, fewer monitoring requirements (no routine INR/aPTT)
  • Fewer food interactions than warfarin
  • Antidotes: idarucizumab (Praxbind) for dabigatran; andexanet alfa (Andexxa) for rivaroxaban/apixaban
  • Still monitor for bleeding
  • Renal function must be adequate (excreted by kidneys)

Antiplatelets

  • Aspirin — chew 325 mg during MI (antiplatelet effect). Low-dose (81 mg) daily for prevention. GI irritation, bleeding risk.
  • Clopidogrel (Plavix) — used after stent placement, MI, stroke. Takes 5–7 days to clear. Hold before surgery.

Bleeding Precautions for ALL Anticoagulants

  • Soft-bristle toothbrush, electric razor
  • Avoid contact sports and activities that could cause injury
  • Report: bleeding gums, nosebleeds, blood in urine/stool, excessive bruising, dark/tarry stools
  • Wear a medical alert bracelet
  • Avoid aspirin/NSAIDs (unless ordered) — increases bleeding risk
Exam Tip

If a question asks "which lab monitors heparin?" → aPTT. "Which lab monitors warfarin?" → INR. If the INR is 5.0 → hold warfarin, notify provider (bleeding risk). If a patient on heparin has a sudden drop in platelets → think HIT → stop heparin immediately and notify the provider.

? A patient on warfarin reports eating large amounts of spinach every day this week. Why is this a concern?
Spinach is high in vitamin K, which reverses the anticoagulant effect of warfarin. A sudden increase in vitamin K intake can reduce the INR below therapeutic range, increasing clot risk. Patients should keep vitamin K intake consistent — not eliminate it, just avoid large swings.
07

Nitroglycerin

The angina drug — know the administration protocol and the #1 drug interaction.

How It Works

Vasodilator — relaxes vascular smooth muscle → dilates coronary arteries (improves blood flow to the heart) and veins (decreases preload). Relieves chest pain.

Administration Protocol (Sublingual)

1
Take 1 tablet SL at onset of chest pain. Sit or lie down (prevents hypotension/dizziness).
2
If no relief (or pain worsens) 5 minutes after the first dose → call 911 immediately (possible MI)
3
While waiting for EMS, may take a 2nd tablet, then a 3rd 5 minutes later (3 tablets total)

Key Teaching Points

  • Headache is the most common side effect (vasodilation) — expected, not dangerous
  • Tablet should tingle/burn under the tongue — if it doesn't, the medication may have lost potency
  • Store in a dark, glass container — light degrades the drug. Replace every 6 months.
  • Keep away from heat and moisture
  • Hold per the ordered parameters (commonly HR <60 or a low/symptomatic BP)
  • Transdermal patches: apply to hairless area, rotate sites, remove old patch before applying new one. Remove patch at night for 10–12 hours (prevents tolerance — "nitrate-free interval").
Nitroglycerin + PDE-5 Inhibitors (Viagra/Cialis) = DO NOT COMBINE

Both cause vasodilation. Together they can cause severe, life-threatening hypotension. Do NOT give nitroglycerin if the patient has taken sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra) within the past 24–48 hours. This is one of the most commonly tested drug interactions on the exam.

08

Digoxin (Lanoxin)

Ranges vary by lab, facility, and textbook — for exams, use the range given in the question. See the full NCLEX-PN lab-value reference & sources →

The drug with more exam questions than any other single medication.

How It Works

Cardiac glycoside — increases the force of cardiac contraction (positive inotrope) and slows heart rate (negative chronotrope). Used for heart failure and atrial fibrillation.

Critical Nursing Actions

  • Check apical pulse for 1 FULL MINUTE before every dose — hold if HR <60 bpm (adult), <70 (child), <90 (infant). Notify provider.
  • Therapeutic level: 0.5–2.0 ng/mL — VERY narrow therapeutic window
  • Monitor potassium — hypokalemia INCREASES digoxin toxicity risk (K⁺ and digoxin compete for the same binding sites). Always check K⁺.

Toxicity Signs (Must Know!)

  • GI: nausea, vomiting, anorexia (often the FIRST signs)
  • Visual: blurred vision, yellow-green halos around lights, photophobia
  • Cardiac: bradycardia, heart block, dysrhythmias
  • Neuro: fatigue, weakness, confusion

Antidote: Digibind (Digoxin Immune Fab)

Used for severe, life-threatening digoxin toxicity (lethal arrhythmias, K⁺ >5 mEq/L with digoxin toxicity).

The Digoxin Triple-Check

Before giving digoxin, ask yourself 3 things: 1) Is the apical HR ≥60? 2) Is the potassium level normal (3.5–5.0)? 3) Is the digoxin level <2.0 ng/mL? If ANY answer is no → hold and notify the provider.

09

Antiarrhythmics

Know the big three: amiodarone, adenosine, and atropine.

Amiodarone (Cordarone)A-Fib, V-Tach, V-Fib
Very effective but VERY toxic. Monitor: pulmonary toxicity (CXR, lung function), thyroid dysfunction (hypo or hyper), liver toxicity (LFTs), corneal deposits (eye exams), photosensitivity (sunscreen, protective clothing). Turns skin blue-gray with long-term use. Multiple drug interactions.
Adenosine (Adenocard)SVT
Given rapid IV push followed by NS flush. Causes brief asystole (3–6 seconds) — warn the patient they may feel a "thud" or chest tightness. Monitor with continuous telemetry. Have crash cart available.
AtropineSymptomatic bradycardia
Increases heart rate by blocking vagal (parasympathetic) stimulation. Anticholinergic side effects: dry mouth, urinary retention, constipation, blurred vision. Also used as antidote for organophosphate poisoning.
LidocaineVentricular arrhythmias
Given IV during cardiac emergencies (V-Tach). Monitor for CNS toxicity: tinnitus, confusion, tremors, seizures. Also used as a local anesthetic.
Amiodarone — The Multi-Organ Toxin

If a question mentions a patient on amiodarone with new-onset shortness of breath → think pulmonary toxicity. New thyroid symptoms → thyroid dysfunction. Elevated LFTs → hepatotoxicity. Corneal deposits → blurred vision. This drug affects almost every organ system — that's why it requires extensive monitoring.

10

Statins & Cholesterol Drugs

Suffix: -statin. Take at bedtime, and always ask about muscle pain.

Suffix: -statin. Examples: atorvastatin (Lipitor), simvastatin (Zocor), rosuvastatin (Crestor), pravastatin

How They Work

Inhibit HMG-CoA reductase → decrease cholesterol production in the liver → lower LDL ("bad" cholesterol), raise HDL ("good" cholesterol), lower triglycerides.

Key Nursing Considerations

  • Take at bedtime — cholesterol synthesis peaks at night (though atorvastatin and rosuvastatin can be taken any time due to long half-lives)
  • Report muscle pain immediately — can indicate rhabdomyolysis (breakdown of muscle tissue → myoglobin release → kidney damage). Check CK levels if suspected.
  • Monitor liver function (LFTs) — hepatotoxicity risk. Baseline and periodic monitoring.
  • Avoid excessive alcohol (additive liver damage)
  • Avoid grapefruit juice (increases drug levels with certain statins)
  • Contraindicated in pregnancy (teratogenic)

Target Cholesterol Values

Total cholesterol
<200 mg/dL
LDL ("bad")
<100 mg/dL (optimal)
HDL ("good")
>40 mg/dL (male), >50 mg/dL (female)
Triglycerides
<150 mg/dL
Memory Trick

LDL = "Lousy" cholesterol (you want it LOW). HDL = "Happy/Healthy" cholesterol (you want it HIGH). Statins primarily lower LDL. Diet + exercise help raise HDL.

11

Heart Failure Drug Regimen

The standard drug combination for HF — know why each one is used.

Heart failure management typically involves a combination of drug classes. Each targets a different mechanism to reduce symptoms, improve cardiac output, and prolong life.

ACE InhibitorLisinopril
Reduces afterload (vasodilation) and prevents remodeling. Monitor: BP, K⁺, renal function, cough.
Beta-BlockerCarvedilol, metoprolol succinate
Reduces HR and cardiac workload, prevents remodeling. Monitor: HR (>60), BP (>90 systolic). Start low, go slow.
Loop DiureticFurosemide
Removes excess fluid (reduces preload and edema). Monitor: daily weights, K⁺, I&O, dehydration signs.
Digoxin
Increases contractility, slows HR. Monitor: apical pulse ×1 min, K⁺, dig level (0.5–2.0).
Aldosterone AntagonistSpironolactone
Mild diuretic, blocks aldosterone, saves K⁺. Monitor: K⁺ (hyperkalemia risk), renal function.
Vasodilator (PRN)Hydralazine + Isosorbide dinitrate
Alternative if ACE/ARB not tolerated. Reduces preload and afterload. Monitor: BP, headache, reflex tachycardia.
Key Teaching for HF Patients

Daily weights (report 2 lbs/day or 5 lbs/week gain), low-sodium diet (≤2,000 mg), fluid restriction (1.5–2 L/day), take meds consistently, avoid NSAIDs (fluid retention, worsens HF), elevate HOB for breathing, and activity as tolerated with rest periods.

12

Frequently Asked Questions

Common student questions on this topic.

What is the difference between ACE inhibitors and ARBs?
Both treat hypertension and heart failure by blocking the renin-angiotensin system. ACE inhibitors (-pril family: lisinopril, enalapril, captopril) block the conversion of angiotensin I to II. Common side effect: dry cough. ARBs (-sartan family: losartan, valsartan) block the angiotensin II receptor directly — used when ACE inhibitor cough is intolerable. Both: risk of hyperkalemia, angioedema, hypotension, fetal harm (Category D). Monitor potassium and renal function.
How are beta blockers different from calcium channel blockers?
Both lower BP and slow the heart. Beta blockers (-olol family: metoprolol, atenolol, propranolol) block beta-1 receptors in the heart — slow HR, reduce contractility. Hold per the ordered parameters — commonly for HR < 60 or a low/symptomatic BP. Calcium channel blockers (-dipine family + verapamil, diltiazem) block calcium influx — relax smooth muscle (lower BP), slow conduction (verapamil, diltiazem only). Both can cause hypotension and bradycardia. Grapefruit juice increases CCB levels — avoid.
Why should you hold digoxin if the apical pulse is low?
Digoxin slows the heart and strengthens contraction by inhibiting Na/K ATPase. The therapeutic margin is narrow. Hold the dose if apical pulse < 60 in adults (< 70 in children, < 90 in infants) and notify the provider. Toxicity signs: nausea, vomiting, anorexia, confusion, visual disturbances (yellow halos), bradycardia, dysrhythmias. Hypokalemia increases digoxin toxicity risk — monitor potassium and serum dig levels (therapeutic: 0.5–2.0 ng/mL).
What is the difference between heparin and warfarin?
Heparin: IV/SQ, fast onset (immediate IV, 1–2 hours SQ), short half-life. Monitor with aPTT (therapeutic 1.5–2.5× normal, ~46–70 sec). Antidote: protamine sulfate. Warfarin (Coumadin): oral, slow onset (3–5 days), long half-life. Monitor with INR (therapeutic 2–3 for most indications). Antidote: vitamin K. Teach to keep vitamin K intake consistent (don't binge on leafy greens). Many drug interactions.
What are the signs of digoxin toxicity?
Therapeutic dig level: 0.5–2.0 ng/mL. Toxicity signs: nausea, vomiting, anorexia, abdominal pain (GI symptoms often first), visual disturbances (yellow-green halos, blurred vision), bradycardia and dysrhythmias (any rhythm is possible), confusion, fatigue. Risk factors: hypokalemia, hypomagnesemia, hypercalcemia, kidney impairment. Treatment: stop the drug, correct electrolytes, digoxin immune Fab (Digibind) for severe toxicity.
How do statins work and what side effect should I monitor for?
Statins (-statin family: atorvastatin, simvastatin, rosuvastatin) lower LDL cholesterol by inhibiting HMG-CoA reductase. Take in the evening (most cholesterol synthesis at night), except atorvastatin and rosuvastatin (long half-life, any time). Most serious side effects: rhabdomyolysis (severe muscle pain/weakness — report immediately; can cause acute kidney injury) and hepatotoxicity (monitor LFTs). Avoid grapefruit juice with most statins.
13

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Cardiovascular Medications Cheatsheet

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