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Heart Failure: Management

Chapter 265 | Part 6: Disorders of the Cardiovascular System

KEY CLINICAL POINTS

  • HFrEF management includes RAAS antagonists (ACEIs, ARBs, ARNIs), beta-blockers, mineralocorticoid receptor antagonists, and SGLT-2 inhibitors as cornerstone therapies.
  • HFpEF treatment focuses on lifestyle modifications, control of comorbidities, and emerging therapies like SGLT-2 inhibitors and GLP-1 agonists.
  • ADHF management prioritizes diuresis, vasodilators, and inotropic agents, with sacubitril-valsartan showing benefit in reducing HF hospitalizations.
  • Mineralocorticoid receptor antagonists (e.g., spironolactone) are recommended for HFrEF but require monitoring for hyperkalemia and renal function.
  • Cardiac resynchronization therapy (CRT) and implantable cardioverter-defibrillators (ICDs) are indicated for specific HFrEF patients with QRS duration >149 ms and reduced LVEF.

1. DEFINITION & OVERVIEW

Heart failure (HF) is a clinical syndrome characterized by impaired cardiac pump function. Classification is based on ejection fraction (EF): HFrEF (EF ≤ 40%), HFmrEF (EF 41–49%), and HFpEF (EF ≥ 50%). Management varies by HF phenotype, with HFrEF benefiting from neurohormonal antagonists and HFpEF requiring comorbidity-focused strategies.

Table 265-1: Vasoactive Therapy in Acute Decompensated Heart Failure

DRUG CLASS GENERIC DRUG USUAL DOSING SPECIAL CAUTION COMMENTS
Inotropic therapy Dobutamine 2–20 mg/kg per min Increased myocardial oxygen demand, arrhythmia Short acting, variable efficacy in presence of beta blockers
Inotropic therapy Milrinone 0.375–0.75 mg/kg per min Hypotension, arrhythmia Decrease dose in renal insufficiency; effectiveness retained with beta blockers
Inotropic therapy Levosimendan 0.1 mg/kg per min; range, 0.05–0.2 mg/kg per min Hypotension, arrhythmia Long acting; similar effectiveness as dobutamine
Vasodilators Nitroglycerin 10–20 mg/min, increase up to 200 mg/min Headache, flushing, tolerance Most common vasodilator but often underdosed
Vasodilators Nesiritide Bolus 2 mg/kg and infusion at 0.01 mg/kg per min Hypotension Decrease in blood pressure may reduce renal perfusion
DRUG CLASS GENERIC DRUG USUAL DOSING SPECIAL CAUTION COMMENTS
Vasodilators Nitroprusside 0.3 mg/kg per min titrated to 5 mg/kg per min Thiocyanate toxicity in renal insufficiency (>72 h) Requires arterial line placement for titration
Diuretics Furosemide 20–240 mg daily Monitor for electrolyte loss In severe congestion, use intravenously and consider continuous infusion
Diuretics Torsemide 10–100 mg daily Monitor for electrolyte loss High bioavailability; anecdotally more effective in advanced heart failure
Diuretics Bumetanide 0.5–5 mg daily Monitor for electrolyte loss Can be used orally; intermediate bioavailability

1.1 Ejection Fraction Classification

HFrEF (EF ≤ 40%): Treated with RAAS inhibitors, beta-blockers, and SGLT-2 inhibitors. HFmrEF (EF 41–49%): Similar to HFrEF but with less evidence. HFpEF (EF ≥ 50%): Managed with lifestyle changes, comorbidity control, and emerging therapies like SGLT-2 inhibitors.

1.2 Acute Decompensated Heart Failure (ADHF)

ADHF is a heterogeneous syndrome requiring urgent decongestion, hemodynamic optimization, and targeted therapy. Management includes diuretics, vasodilators, and inotropes, with sacubitril-valsartan showing potential benefits in reducing hospitalizations.

2. EPIDEMIOLOGY

HF is a leading cause of hospitalization and mortality. HFrEF is more common in men, while HFpEF is prevalent in women and older adults. Prevalence increases with age, and comorbidities like diabetes, hypertension, and obesity are major risk factors.

2.1 Risk Factors

Hypertension, diabetes, obesity, coronary artery disease, and atrial fibrillation are key risk factors. HFpEF is associated with obesity, sleep apnea, and metabolic syndrome.

2.2 Demographics

HFrEF is more common in men, while HFpEF predominates in women and older adults. Prevalence rises with age, with significant racial disparities in outcomes.

3. ETIOLOGY & PATHOPHYSIOLOGY

HF results from impaired cardiac function due to myocardial damage, neurohormonal activation, and comorbidities. HFrEF involves systolic dysfunction, while HFpEF is linked to diastolic stiffness and microvascular dysfunction.

3.1 HFrEF Pathophysiology

Myocardial remodeling, neurohormonal activation (RAAS, SNS), and ventricular dysfunction drive HFrEF. SGLT-2 inhibitors and ARNIs target these pathways.

3.2 HFpEF Pathophysiology

Diastolic dysfunction, microvascular inflammation, and endothelial dysfunction are central. Obesity, sleep apnea, and metabolic syndrome contribute to impaired myocardial relaxation.

4. CLINICAL FEATURES

Symptoms include dyspnea, fatigue, and fluid retention. Signs include jugular venous distension, pulmonary rales, and peripheral edema. Complications include arrhythmias, renal failure, and sudden cardiac death.

4.1 Symptomatology

Dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and reduced exercise tolerance are hallmark symptoms.

4.2 Physical Findings

Jugular venous distension, pulmonary rales, peripheral edema, and hepatomegaly are common. Cardiac enlargement and S3 gallop may be present.

5. DIFFERENTIAL DIAGNOSIS

Differential diagnoses include pulmonary hypertension, valvular heart disease, and myocardial infarction. Echocardiography and biomarkers (BNP/NT-proBNP) aid in differentiation.

5.1 Non-Cardiac Causes

Pulmonary embolism, anemia, and thyroid dysfunction can mimic HF. Sleep apnea and obesity hypoventilation syndrome are common comorbidities.

5.2 Cardiac Causes

Valvular disease, hypertrophic cardiomyopathy, and arrhythmias must be excluded. Echocardiography is critical for assessing ventricular function.

6. INVESTIGATIONS & DIAGNOSIS

Diagnosis involves clinical evaluation, biomarkers (BNP/NT-proBNP), echocardiography, and imaging. Electrocardiography and chest X-ray are essential for assessing cardiac size and rhythm.

6.1 Biomarkers

Elevated BNP/NT-proBNP levels correlate with HF severity. Levels normalize with effective treatment but may persist in chronic cases.

6.2 Imaging

Echocardiography assesses EF, ventricular size, and valvular function. Cardiac MRI may identify myocardial scar in ischemic cardiomyopathy.

7. MANAGEMENT & TREATMENT

Guideline-directed medical therapy (GDMT) includes RAAS inhibitors, beta-blockers, and SGLT-2 inhibitors. ADHF requires aggressive diuresis, vasodilators, and inotropes. CRT and ICDs are indicated for specific patients.

Table 265-2: Guideline-Directed Pharmacologic Therapy and Target Doses in HFrEF

DRUG CLASS GENERIC DRUG MEAN DAILY DOSE IN CLINICAL TRIALS (mg) INITIATION (mg) TARGET DOSE (mg)
Angiotensin-Converti ng Enzyme Inhibitors Lisinopril 4.5–33 2.5–5 qd 20–35 qd
Angiotensin-Converti ng Enzyme Inhibitors Enalapril 17 2.5 bid 10–20 bid
Angiotensin-Converti ng Enzyme Inhibitors Captopril 123 6.25 tid 50 tid
Angiotensin-Converti ng Enzyme Inhibitors Trandolapril N/A 0.5–1 qd 4 qd
Angiotensin Receptor Blockers Losartan 129 50 qd 150 qd
Angiotensin Receptor Blockers Valsartan 254 40 bid 160 bid
Angiotensin Receptor Blockers Candesartan 24 4–8 qd 32 qd
Aldosterone Antagonists Eplerenone 42.6 25 qd 50 qd
Aldosterone Antagonists Spironolactone 26 12.5–25 qd 25–50 qd
Beta Blockers Metoprolol succinate CR/XL 159 12.5–25 qd 200 qd
Beta Blockers Carvedilol 37 3.125 bid 25–50 bid
Beta Blockers Bisoprolol 8.6 1.25 qd 10 qd
Arteriovenous Vasodilators Hydralazine isosorbide dinitrate 270/136 37.5/20 tid 75/40 tid
Arteriovenous Vasodilators Fixed-dose hydralazi ne/isosorbide dinitrate 143/76 37.5/20 qid 75/40 qid
Angiotensin Receptor-Neprilysin Inhibitor Sacubitril-valsartan 375 100 bid 200 bid
SGLT-2 Inhibitor Dapagliflozin 10 10 qd 10 qd
SGLT-2 Inhibitor Empagliflozin 10 10 qd 10 qd
SGLT-2 Inhibitor Sotagliflozin 200 200 qd 200 qd
Novel Therapies Vericiguat (sGC stimulator) 9.2 2.5 qd 10 qd
Novel Therapies Omecamtiv mecarbil (myosin activator) Not reported 25 bid Up to 50 mg bid

7.1 HFrEF Treatment

RAAS antagonists (ACEIs, ARBs, ARNIs), beta-blockers (carvedilol, bisoprolol), mineralocorticoid receptor antagonists, and SGLT-2 inhibitors are first-line. Sacubitril-valsartan reduces hospitalizations and mortality.

7.2 ADHF Management

Diuretics (loop, thiazide), vasodilators (nitroglycerin, nitroprusside), and inotropes (dobutamine) are used. Sacubitril-valsartan may reduce hospitalizations in ADHF.

7.3 CRT & ICD

CRT is indicated for QRS >149 ms and LVEF ≤ 35%. ICDs are used for primary prevention in patients with EF ≤ 35% and high risk of sudden death.

8. PROGNOSIS & COMPLICATIONS

HF is associated with high mortality and morbidity. Complications include arrhythmias, renal failure, and sudden cardiac death. Prognosis is worse in HFpEF and advanced stages.

8.1 Mortality

Annual mortality in HFrEF is ~5–10%. HFpEF has higher mortality due to comorbidities and limited therapeutic options.

8.2 Complications

Worsening heart failure, acute decompensation, and arrhythmias are common. Renal dysfunction and thromboembolism are significant risks.

9. SPECIAL CONSIDERATIONS

Management varies by age, gender, and comorbidities. Pregnancy requires careful monitoring, while elderly patients may need dose adjustments. Sleep apnea and obesity are critical comorbidities in HFpEF.

9.1 Pregnancy

Beta-blockers and ACEIs are contraindicated. Spironolactone is preferred for mineralocorticoid antagonism. Close monitoring for decompensation is essential.

9.2 Obesity and Sleep Apnea

Weight loss and CPAP therapy are critical in HFpEF. Obesity is a major risk factor for HF and worsens outcomes.

10. KEY POINTS & CLINICAL PEARLS

  1. HFrEF management includes RAAS antagonists, beta-blockers, and SGLT-2 inhibitors. 2. HFpEF requires comorbidity control and lifestyle modifications. 3. ADHF is managed with diuresis, vasodilators, and inotropes. 4. CRT and ICDs improve outcomes in specific HFrEF patients. 5. Early postdischarge follow-up reduces readmissions and improves outcomes.