Heart Failure

Clinical Orientation

A 74-year-old woman with known systolic heart failure (EF 25%) is admitted with worsening dyspnea. She has gained 4 kg in 5 days. She sleeps sitting up. Her JVD is elevated to the angle of her jaw. Crackles are present halfway up both lung fields. An S3 gallop is audible. Her BNP is 2,400. This is acute decompensated heart failure. This chapter answers: What mechanism links heart failure to bedside findings, tests, red flags, and nursing priorities?

What Is Normal?

Ventricular function: The heart pumps by coordinated contraction (systole) and relaxation/filling (diastole). Left ventricular ejection fraction (EF) is the percentage of end-diastolic volume ejected: normal ≥55%. However, a normal EF does NOT exclude heart failure — heart failure with preserved EF (HFpEF, EF ≥50%) accounts for ~50% of cases.

Frank-Starling mechanism: Within limits, increased ventricular filling (preload) → increased stretch → stronger contraction → increased stroke volume. In heart failure, the curve is flattened and depressed — increased filling produces minimal increase in output while raising filling pressures.

Neurohormonal regulation: When CO falls, baroreceptors detect decreased stretch → SNS activation (increased HR, contractility, vasoconstriction) + RAAS activation (sodium/water retention, vasoconstriction) + ADH release (water retention). These compensatory mechanisms initially maintain perfusion but ultimately worsen heart failure: increased afterload, increased blood volume, increased myocardial oxygen demand, direct myocardial toxicity (angiotensin II, aldosterone, norepinephrine), and pathologic remodeling.

What Goes Wrong?

Heart failure classification:

• HFrEF (reduced EF, ≤40%): Impaired contractility → cannot eject adequate blood. Most commonly from MI, dilated cardiomyopathy. Treatment: guideline-directed medical therapy (GDMT) including ACEi/ARB/ARNI, beta-blockers, MRAs, SGLT2i.
• HFpEF (preserved EF, ≥50%): Impaired relaxation → stiff ventricle cannot fill adequately at normal pressures → elevated filling pressures → pulmonary congestion. Most commonly from hypertension, aging, diabetes, obesity.
• HFmrEF (mid-range EF, 41-49%): Intermediate.

Forward vs backward failure:

• Forward: Decreased CO → fatigue, weakness, confusion, oliguria, cool extremities.
• Backward: Increased filling pressures → pulmonary congestion (left-sided) → dyspnea, orthopnea, PND, crackles. Systemic congestion (right-sided) → JVD, hepatomegaly, ascites, edema.

Compensatory mechanisms that become maladaptive:

Decreased CO → SNS activation → increased HR, contractility, vasoconstriction
→ increased myocardial O2 demand, arrhythmias, direct myocyte toxicity
Decreased renal perfusion → RAAS → sodium/water retention, vasoconstriction
→ increased preload and afterload, pathologic remodeling, fibrosis
→ natriuretic peptides (BNP, ANP) released — beneficial (vasodilation, natriuresis) but overwhelmed

Heart Failure Signs — Left vs Right

What the Nurse May See

Compensated vs decompensated:

• Compensated: Stable on medications, minimal symptoms with normal activity. May have mild JVD, trace edema.
• Decompensated: Worsening dyspnea, orthopnea, PND, weight gain, increasing edema, crackles, S3, hypotension or hypertension, tachycardia, hypoxia, oliguria despite fluid overload.

Key assessment: Daily weights (most reliable fluid status indicator). Strict I&O. Lung sounds. JVD measurement. Edema grading. Abdominal girth (ascites). Mental status. Perfusion assessment (cap refill, skin temperature, urine output).

Tests and Monitoring

• BNP/NT-proBNP: Released from ventricular myocytes in response to stretch. BNP >100 pg/mL (or NT-proBNP >300 pg/mL) supports HF diagnosis. Levels correlate with severity. Trend is useful — falling BNP with treatment = improving. Low BNP effectively excludes HF.
• Echocardiogram: EF, chamber sizes, wall thickness, valvular function, diastolic function.
• BMP: Renal function (cardiorenal syndrome — worsening HF reduces renal perfusion, worsening renal function worsens fluid overload). Potassium (diuretic effects).
• Chest X-ray: Cardiomegaly, pulmonary vascular congestion, pleural effusions.

Nursing Priorities

1. Respiratory assessment and support: Position upright (High Fowler's). Oxygen if hypoxemic. Monitor for worsening crackles or respiratory fatigue (may need BiPAP or intubation).

1. Fluid management: Strict I&O, daily weights. Administer diuretics as ordered — monitor response (urine output, weight loss, lung clearance). Monitor potassium and renal function. If the patient is diuretic-resistant, notify provider.

1. Hemodynamic monitoring: BP, HR trends. Narrowing pulse pressure suggests falling SV. Hypotension with worsening HF = cardiogenic shock pattern.

1. Medication administration: IV diuretics for acute decompensation. Continue/initiate GDMT as tolerated (ACEi/ARB/ARNI, beta-blockers, MRA, SGLT2i). Monitor for hypotension, hyperkalemia, worsening renal function.

1. Patient education: Daily weights — same scale, same time, call for 2-3 lb gain in 1 day or 5 lb in 1 week. Sodium restriction (typically <2000-3000 mg/day). Fluid restriction (typically 1.5-2 L/day if hyponatremic or severe). Medication adherence. Symptom recognition.

Red Flags

Common Student Mistakes

1. Treating BP instead of perfusion: A HF patient with BP 88/54 may be adequately perfused if alert, warm, and making urine. Don't reflexively give fluids — they'll worsen pulmonary congestion.
2. Stopping beta-blockers during acute decompensation: Beta-blockers should generally be continued unless the patient is in cardiogenic shock or severely hypotensive. Abrupt withdrawal can cause rebound tachycardia and ischemia.