Heart Failure

Prepared for Pass the Shift (owner: Kristina, RN). Always follow your facility’s protocols, provider orders, and current drug references.

1. Overview and Pathophysiology

Heart failure (HF) is a clinical syndrome, not one disease. A structural or functional problem keeps the ventricles from filling well, pumping well, or both. The result is low forward flow (poor tissue perfusion) and backward congestion (fluid backing up into the lungs or body).

Compensation that turns harmful. When cardiac output falls, the body tries to protect blood pressure:

• Sympathetic nervous system: faster heart rate and vasoconstriction. Oxygen demand goes up.
• RAAS (renin-angiotensin-aldosterone system): sodium and water retention plus vasoconstriction. Preload and Afterload go up.
• Ventricular remodeling: over time the heart dilates or thickens and works less efficiently.

Most HF drugs work by blocking these loops. That is why they lower mortality instead of just easing symptoms.

Left-sided vs. right-sided HF

• Left-sided: the left ventricle cannot move blood forward into the aorta, so pressure backs up into the pulmonary veins and lungs. Expect respiratory signs.
• Right-sided: the right ventricle cannot push blood into the pulmonary artery, so blood backs up into the venous system (neck veins, liver, gut, legs). The most common cause of right-sided HF is left-sided HF. Isolated right HF (“cor pulmonale”) comes from lung disease or pulmonary hypertension.

Classification by ejection fraction (EF) (2022 AHA/ACC/HFSA):

Type	LVEF	Key idea
HFrEF (reduced EF; “systolic”)	≤ 40%	Weak, often dilated ventricle that can’t squeeze
HFmrEF (mildly reduced)	41–49%	In-between group
HFpEF (preserved EF; “diastolic”)	≥ 50%	Stiff, thick ventricle that can’t relax and fill; common in older adults with hypertension, obesity, and diabetes
HFimpEF (improved EF)	Previously ≤ 40%, now > 40%	Keep up guideline therapy

Staging: ACC/AHA Stages A–D track how the disease progresses (A = at risk, B = structural disease without symptoms, C = symptoms, D = advanced). Stages only move forward. NYHA Class I–IV describes symptoms with activity (I = no limits; IV = symptoms at rest) and can improve or worsen.

2. Causes and Risk Factors

• Most common causes: coronary artery disease or prior MI, and long-standing hypertension
• Other causes: cardiomyopathies (genetic, alcohol, stimulants, chemotherapy such as anthracyclines), valve disease, arrhythmias (e.g., atrial fibrillation), myocarditis, congenital disease, thyroid disease
• Risk factors: age ≥ 65, diabetes, obesity, smoking, chronic kidney disease, sleep apnea, family history
• Common triggers of acute decompensation: missed medications, high-sodium meals or excess fluid, infection, new arrhythmia, uncontrolled BP, ischemia, and fluid-retaining drugs (NSAIDs, thiazolidinediones, non-dihydropyridine calcium channel blockers in HFrEF)

3. Signs and Symptoms

Left-sided (think Lungs)	Right-sided (think Rest of body)
Dyspnea on exertion, then at rest	Dependent edema (ankles, sacrum if in bed)
Orthopnea; paroxysmal nocturnal dyspnea	Jugular venous distension (JVD)
Crackles; cough; pink, frothy sputum (pulmonary edema)	Rapid weight gain from fluid
Low SpO₂, tachypnea	Hepatomegaly, RUQ discomfort, ascites
S3 gallop (HFrEF); S4 can occur (stiff ventricle)	Anorexia, nausea, abdominal bloating
Fatigue, weakness, cool or pale skin	Hepatojugular reflux
Confusion or restlessness (low cerebral perfusion), especially in older adults	Nocturia (fluid shifts back when legs are elevated)
Oliguria in low-output states	Weight gain often appears before visible edema

Both sides: fatigue, activity intolerance, tachycardia.

4. Diagnostics and Labs

Lab reference ranges vary by laboratory. Always use your facility’s ranges.

Test	Typical reference / target	Nursing relevance
BNP	< 100 pg/mL makes acute HF unlikely	Released when ventricles are stretched; higher usually means more severe. Sacubitril/valsartan raises BNP, so NT-proBNP is preferred for monitoring those patients
NT-proBNP	< 300 pg/mL makes acute HF unlikely; cutoffs for “likely” HF rise with age	Not affected by sacubitril. Both peptides read falsely low in obesity and can rise with kidney disease, older age, AF, and PE
Potassium (K⁺)	3.5–5.0 mEq/L	Low with loop/thiazide diuretics (raises digoxin toxicity risk); high (Hyperkalemia) with ACEi/ARB/ARNI/MRA and CKD
Sodium (Na⁺)	135–145 mEq/L	Hyponatremia from dilution means advanced HF and a worse prognosis
Magnesium	~1.7–2.2 mg/dL	Low Mg worsens arrhythmias and digoxin toxicity
BUN / Creatinine	~7–20 mg/dL / ~0.6–1.2 mg/dL	Low perfusion (“cardiorenal”) or overdiuresis; drug dosing
Digoxin level	Common therapeutic range 0.5–2.0 ng/mL; HF target is lower (~0.5–0.9)	Draw a trough (≥ 6–8 h after dose); toxicity can occur even at “normal” levels if K⁺ is low
CBC, iron studies, TSH, LFTs, A1c, lipids, troponin	Per lab	Anemia/iron deficiency, thyroid causes, hepatic congestion, ischemia
Echocardiogram	Normal LVEF ≈ 50–70%	Key test to classify HF type (EF), plus valves, wall motion, chamber size
Chest X-ray	—	Cardiomegaly, vascular congestion, Kerley B lines, pleural effusions
12-lead ECG	—	Ischemia, prior MI, AF, LVH, QRS width (affects device decisions)
ABG / SpO₂	SpO₂ usually ≥ 94% unless a lower target is ordered	Hypoxemia in pulmonary edema

5. Priority Nursing Assessments

1. Airway, breathing, oxygenation: RR, work of breathing, SpO₂, lung sounds (crackles rising from the bases), orthopnea (how many pillows?), frothy sputum
2. Fluid status: daily weight (same scale, same time, after voiding, before breakfast, similar clothing), strict I&O, edema grading, JVD. 1 kg of weight ≈ 1 L of fluid.
3. Perfusion: BP, HR and rhythm (telemetry), cap refill, skin temperature and color, mental status, urine output (report < 0.5 mL/kg/hr or per protocol)
4. Labs: K⁺, Na⁺, Mg²⁺, BUN/Cr, BNP or NT-proBNP trends, digoxin level if prescribed
5. Pre-medication checks: apical pulse (1 full minute) before digoxin; HR/BP before beta blockers and vasodilators; K⁺ before diuretics, ACEi/ARB/ARNI, and MRAs
6. Activity tolerance: dyspnea, fatigue, HR/BP response to activity
7. Psychosocial: anxiety, depression, health literacy, ability to afford meds, home support

6. Priority Nursing Interventions

• Position: high Fowler’s or semi-Fowler’s; let legs dangle in severe dyspnea to reduce venous return
• Oxygen as ordered to keep SpO₂ at target. Have noninvasive ventilation (CPAP/BiPAP) available
• Give diuretics and GDMT as ordered. Watch for over-diuresis (hypotension, dizziness, rising creatinine, low K⁺)
• Sodium and fluid limits as prescribed. Fluid restriction (often ~1.5–2 L/day) is usually for advanced HF or hyponatremia. Spread allowed fluids across the day and give ice chips and mouth care
• Daily weights and strict I&O; report sudden gains
• Cluster care and pace activity to balance rest and gradual mobility. Prevent VTE
• Skin care for edematous tissue (turn, pad heels and sacrum)
• Telemetry for dysrhythmias, especially with electrolyte shifts or digoxin
• Medication reconciliation: flag NSAIDs, decongestants, and other drugs that make HF worse
• Discharge planning: follow-up within ~7 days, teach-back, cardiac rehab referral, palliative care discussion in advanced HF

7. Medications

GDMT for HFrEF, the “four pillars”: (1) ARNI (or ACEi/ARB), (2) an evidence-based beta blocker, (3) an MRA, and (4) an SGLT2 inhibitor. Diuretics relieve congestion but have not been shown to lower mortality. Typical “hold” parameters (e.g., HR < 60, SBP < 90) vary, so follow the specific order.

Class / examples	How it helps	Key nursing considerations
ARNI: sacubitril/valsartan	Blocks angiotensin II and boosts natriuretic peptides; preferred RAAS agent in HFrEF	Wait 36 hours after the last ACE inhibitor dose (Angioedema risk); never combine with an ACEi. Watch for hypotension, hyperkalemia, and creatinine rise. Contraindicated in pregnancy
ACE inhibitors (“-pril”: lisinopril, enalapril)	Lower afterload/preload; slow remodeling	Dry cough (switch to ARB); angioedema (stop drug, airway emergency); first-dose hypotension; hyperkalemia; rising creatinine. Avoid in pregnancy
ARBs (“-sartan”: losartan, valsartan, candesartan)	Same pathway; usually no cough	Hyperkalemia, hypotension, renal monitoring. Avoid in pregnancy
Beta blockers (carvedilol, metoprolol succinate, bisoprolol)	Slow HR, reduce sympathetic stress, improve EF over time	Check apical HR and BP. “Start low, go slow.” Fatigue may worsen briefly. Don’t stop abruptly. Can mask hypoglycemia signs. Usually not started while the patient is unstable or “wet”
MRAs (spironolactone, eplerenone)	Block aldosterone; reduce mortality	Hyperkalemia (monitor K⁺ and renal function; avoid K⁺ supplements and salt substitutes unless ordered); gynecomastia with spironolactone
SGLT2 inhibitors (dapagliflozin, empagliflozin)	Benefit in HFrEF and HFpEF, with or without diabetes	Genital yeast infections, UTI, volume depletion, euglycemic DKA (nausea, vomiting, abdominal pain with near-normal glucose). Usually held ~3+ days before surgery and on “sick days” per prescriber
Loop diuretics (furosemide, bumetanide, torsemide)	Rapid fluid removal; symptom relief	Hypokalemia, hypomagnesemia, hyponatremia, hypotension, dehydration, AKI. Ototoxicity with fast IV push or high doses. Give early in the day. Monitor weight, I&O, K⁺
Thiazides (metolazone, HCTZ)	Added to loops for resistant edema	Profound electrolyte loss when combined with a loop diuretic
Digoxin	Positive Inotrope; slows AV conduction; reduces HF hospitalizations (no mortality benefit)	Apical pulse 1 full minute; usual hold if < 60/min in adults or per order. Toxicity: anorexia, nausea/vomiting, visual changes (blurred, yellow-green halos), confusion, any new dysrhythmia (bradycardia, heart block, PVCs). Hypokalemia, hypomagnesemia, hypercalcemia, renal impairment, and older age raise risk. Antidote: digoxin immune fab
Hydralazine + isosorbide dinitrate	Vasodilation; recommended for self-identified African American patients with NYHA III–IV on optimal therapy, or when ACEi/ARB/ARNI can’t be used	Headache, hypotension, dizziness. No PDE-5 inhibitors (e.g., sildenafil) with nitrates
Ivabradine	Slows sinus rate when HR stays ≥ 70 despite a beta blocker	Bradycardia, luminous visual phenomena, fetal toxicity; requires sinus rhythm
IV vasodilators/inotropes (nitroglycerin, nitroprusside, dobutamine, milrinone)	Acute or advanced HF	Continuous BP, ECG, and often hemodynamic monitoring; titrate per protocol

8. Patient Education

• Weigh daily at the same time on the same scale. Commonly taught: call your provider for a gain of 2–3 lb (≈1 kg) in a day or 5 lb (≈2.3 kg) in a week, or as your care team instructs
• Limit sodium as prescribed. Read labels (canned soups, deli meats, frozen meals, fast food). Ask before using salt substitutes, which often contain potassium
• Follow any fluid limit, and remember soups, ice cream, gelatin, and ice count as fluids
• Take medications every day, even when you feel well. Don’t stop beta blockers suddenly. Bring a list to every visit
• Avoid NSAIDs (ibuprofen, naproxen) and check with a pharmacist before OTC cold or decongestant products
• Know the warning signs: worse shortness of breath, needing more pillows, waking up breathless, new swelling, a cough that won’t quit, dizziness or fainting. Call 911 for severe breathing trouble or chest pain
• Change positions slowly (orthostatic hypotension). Limit alcohol, quit smoking, get vaccines (influenza, pneumococcal, COVID-19), and join cardiac rehab or stay active as advised
• SGLT2 inhibitor users: genital hygiene, and “sick-day” guidance (call the provider if unable to eat or drink, or if vomiting)

9. Complications

Acute pulmonary edema is a medical emergency: sudden severe dyspnea, anxiety, tachypnea, coarse crackles or wheezes, pink frothy sputum, hypoxemia, diaphoresis, and cool skin.

Emergency nursing steps (team-based; follow protocol and orders):

1. Stay with the patient and call for help (rapid response team)
2. Sit the patient upright (high Fowler’s, legs dependent)
3. Give oxygen. Prepare for CPAP/BiPAP, and for intubation if the patient is tiring or has altered mental status
4. Establish IV access; connect continuous ECG and SpO₂ monitoring
5. Give an IV loop diuretic as ordered. Expect brisk diuresis (consider a urinary catheter or urinal, strict I&O)
6. Vasodilator (e.g., nitroglycerin) as ordered if BP allows. Morphine is no longer routine because it can depress breathing
7. Monitor BP, lung sounds, SpO₂, urine output, K⁺, and mental status closely. Stay calm and reassure the patient

Other complications: cardiogenic shock, dysrhythmias (AF, ventricular tachycardia, sudden cardiac death), thromboembolism (stroke, DVT/PE), cardiorenal syndrome, hepatic congestion or cardiac cirrhosis, pleural effusion, electrolyte imbalance, cardiac cachexia.

10. Memory Aids

• “Left = Lungs, Right = Rest of body.” Left-sided HF shows up in breathing; right-sided HF shows up in neck veins, liver, gut, and legs
• “Four pillars, ABMS: All Bodies Make Salt water.” ARNI/ACEi/ARB, Beta blocker, MRA, SGLT2 inhibitor
• Potassium direction: “Loops Lose K⁺; RAAS blockers Retain K⁺”
• Digoxin toxicity, “Gut, Eyes, Brain, Beat”: nausea/anorexia, yellow-green halos, confusion, dysrhythmias. And low K⁺ makes digoxin more toxic
• “A liter a kilo”: 1 kg of overnight weight gain ≈ 1 L of retained fluid
• “36 hours, no ACE”: washout from an ACE inhibitor before starting sacubitril/valsartan
• Pulmonary edema, “SIT, BLOW, DRAIN, DILATE”: sit upright, oxygen/NIPPV, IV loop diuretic, vasodilator if BP allows

11. NCLEX-Style Practice Questions

1. A client with HFrEF takes digoxin and furosemide. The client reports nausea and “yellowish halos around lights.” Apical pulse is 52/min; K⁺ is 3.1 mEq/L. Which action should the nurse take first?

A. Give the digoxin with food to reduce nausea
B. Hold the digoxin and notify the provider
C. Give the scheduled furosemide
D. Encourage the client to drink more fluids

Answer: B. Nausea, visual changes, bradycardia, and hypokalemia together point to digoxin toxicity. Hold the drug and report findings (a digoxin level, K⁺ replacement, and possibly digoxin immune fab may follow). Giving digoxin (A) worsens toxicity. More furosemide (C) would drop K⁺ further. Extra fluids (D) don’t address the problem and may worsen HF.

2. Which findings support right-sided heart failure? Select all that apply.

A. Jugular venous distension
B. Pink, frothy sputum
C. Dependent ankle edema
D. Hepatomegaly with RUQ tenderness
E. Orthopnea
F. Anorexia and abdominal bloating

Answer: A, C, D, F. Right-sided failure backs blood up into the systemic veins, causing JVD, dependent edema, liver congestion, and GI congestion. Frothy sputum (B) and orthopnea (E) are pulmonary (left-sided) findings.

3. A client with HF suddenly becomes extremely anxious, has RR 34/min, SpO₂ 84%, coarse crackles throughout, and pink frothy sputum. What is the nurse’s priority action?

A. Draw a STAT BNP level
B. Place the client in high Fowler’s position and apply oxygen
C. Insert an indwelling urinary catheter
D. Obtain a chest X-ray

Answer: B. This is acute pulmonary edema, an airway and breathing emergency. Sitting the client upright cuts venous return and helps breathing, and oxygen treats hypoxemia. Call for help and expect an IV loop diuretic and possibly CPAP/BiPAP. Labs, imaging, and a catheter (A, C, D) come after you stabilize oxygenation.

4. A client is being switched from lisinopril to sacubitril/valsartan. Which client statement shows correct understanding?

A. “I’ll take my last lisinopril tonight and start the new pill tomorrow morning.”
B. “I need to wait at least 36 hours after my last lisinopril before starting the new pill.”
C. “I can take both pills together for a week to be safe.”
D. “This new pill will make me cough more than lisinopril did.”

Answer: B. Combining or overlapping an ACE inhibitor with sacubitril sharply raises the risk of angioedema, so a 36-hour washout is required. A is too short, and C is dangerous. Cough is less likely without an ACE inhibitor (D).

5. A client with HF on spironolactone and lisinopril has a morning K⁺ of 5.9 mEq/L. Which action is most appropriate?

A. Give both medications and recheck K⁺ tomorrow
B. Encourage a potassium-based salt substitute
C. Hold the spironolactone, place the client on a cardiac monitor, and notify the provider
D. Offer a banana with breakfast

Answer: C. Both drugs retain potassium. A K⁺ of 5.9 risks dangerous dysrhythmias, so hold the potassium-raising drug(s) per order or protocol, monitor the ECG, and report promptly. A delays treatment, and B and D add potassium.

References

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MedlinePlus. (n.d.). Heart failure. National Library of Medicine. Retrieved October 14, 2026, from https://medlineplus.gov/heartfailure.html

MedlinePlus. (n.d.). Natriuretic peptide tests (BNP, NT-proBNP). National Library of Medicine. Retrieved October 14, 2026, from https://medlineplus.gov/lab-tests/natriuretic-peptide-tests-bnp-nt-probnp/

National Council of State Boards of Nursing. (2026). 2026 NCLEX-RN test plan. https://www.nclex.com/test-plans.page

Regina, A. C., & Hai, O. (2025). Cardiac glycoside and digoxin toxicity. In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK459165/

Shams, P., Malik, A., & Chhabra, L. (2025). Heart failure (congestive heart failure). In StatPearls. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK430873/