GI Joe Medical Boards

Heart Failure

I. Overview of Heart Failure
Heart failure (HF) is a complex clinical syndrome resulting from structural or functional impairment in blood ejection or ventricular filling. It manifests with signs of fluid overload and/or decreased cardiac output.
Key Characteristics:
  • Fluid overload symptoms: Dyspnea (shortness of breath), paroxysmal nocturnal dyspnea (PND), orthopnea (difficulty breathing when lying flat), peripheral edema, crackles in lungs, elevated central venous pressure, and an S3 heart sound.
  • Decreased cardiac output symptoms: Hypotension, low pulse pressure, cool extremities, reduced cognition, and worsening kidney or liver function.
Types of Heart Failure based on Left Ventricular Ejection Fraction (LVEF):
  • Heart failure with reduced ejection fraction (HFrEF): LVEF of 40% or less.
  • Common Causes: Coronary artery disease (CAD), hypertension, obesity, diabetes mellitus, and valvular heart disease.
  • Pathophysiology: Reduced LVEF triggers neurohormonal system activation (Renin-Angiotensin-Aldosterone System (RAAS) and sympathetic nervous system). Initially adaptive, this becomes "chronic and maladaptive in the long term," leading to vasoconstriction, fluid overload, and "ventricular remodeling" (structural and functional changes in myocytes that worsen LV function).
  • Heart failure with preserved ejection fraction (HFpEF): LVEF of 50% or greater.
  • Common Causes: Hypertension (most common), aging, obesity, diabetes mellitus, atrial fibrillation, and CAD. Amyloid deposits are found in over 10% of HFpEF patients.
  • Heart failure with mildly reduced ejection fraction (HFmEF): LVEF between 40% and 50%. This category includes "up to 25% of all patients with heart failure" and often receives similar treatment to HFrEF.
II. Screening and Diagnosis
A. Screening for Asymptomatic Patients at Risk:
  • Pooled Cohort Equation to Prevent Heart Failure risk score: Can identify asymptomatic patients at increased risk, though the inclusion of race as a variable "is likely a flawed approach and limits the utility."
  • Natriuretic Peptide Biomarker-based Screening: Useful in patients at risk (e.g., hypertension, diabetes, vascular disease). Elevated B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels may prompt team-based care to prevent LV dysfunction. However, "there is no agreed-on standard for such screening and no certainty as to its cost-effectiveness."
B. Clinical Evaluation and Diagnosis:
  • Comprehensive History and Physical Examination: Focus on risk factors and assessment of fluid and perfusion status.
  • Initial Diagnostic Testing:ECG: Evaluates for myocardial infarction, tachyarrhythmia, or LV hypertrophy.
  • Chest Radiography: May show cardiomegaly, vascular congestion, Kerley B lines, or pleural effusion; can also rule out pulmonary causes of dyspnea.
  • Natriuretic Peptides (BNP/NT-proBNP): Crucial for differentiating cardiac from pulmonary causes of dyspnea. "BNP levels are elevated in patients with increased filling pressures and heart failure (typically >400 pg/mL)," while low in pulmonary disease (typically <100 pg/mL). High sensitivity and negative predictive value for HF. Note: BNP levels can be influenced by kidney failure, age, sepsis, ARNI therapy, female sex, and are typically reduced in elevated BMI.
  • Laboratory Assessment: Complete blood count, serum electrolytes, kidney and liver function tests, glucose, lipid levels, and thyroid-stimulating hormone (TSH).
  • Echocardiography: "The primary diagnostic modality for evaluation of heart failure." Provides information on chamber size, thickness, systolic/diastolic function, valvular pathology, and clues to underlying causes (e.g., regional wall motion abnormalities for CAD, myocardial changes for amyloidosis).
  • Cardiac Magnetic Resonance (CMR) Imaging: Used for myocarditis and infiltrative processes (e.g., hemochromatosis, sarcoidosis, amyloidosis). Not routinely recommended; used only "in the search for a specific diagnosis."
  • H2FPEF Risk Score: Assesses the likelihood of HFpEF to discriminate cardiac versus noncardiac dyspnea. Variables include obesity, atrial fibrillation, age >60, multiple antihypertensive drugs, and specific echocardiographic findings (E/e′ ratio >9, estimated pulmonary artery systolic pressure >35 mm Hg).
  • Evaluation for Ischemia: CAD is the "leading cause of heart failure in the United States (>50% of patients)." Stress testing or coronary angiography may be considered based on symptoms, risk factors, and ECG/echocardiogram findings.
  • Diagnosis Confirmation: HFrEF and HFpEF are diagnosed by appropriate LVEF combined with increased left ventricular filling pressures, documented by elevated natriuretic peptides, echocardiographic criteria, or invasive hemodynamic assessment.
C. Classification of Heart Failure Severity:
  • New York Heart Association (NYHA) Functional Classification: Categorizes symptom severity (Class I: no limitations to Class IV: unable to perform any physical activity without symptoms). Patients can move between classes.
  • American College of Cardiology (ACC)/American Heart Association (AHA) Stages of Heart Failure:Stage A: At Risk for HF: Risk factors present, but no symptoms, structural heart disease, or cardiac biomarkers.
  • Stage B: Pre-HF: No symptoms, but evidence of structural heart disease, reduced ventricular function, increased filling pressures, or elevated biomarkers.
  • Stage C: Symptomatic HF: Structural heart disease with current or previous HF symptoms.
  • Stage D: Advanced HF: Marked HF symptoms that interfere with daily life and recurrent hospitalizations despite optimized guideline-directed medical therapy (GDMT). Patients can only progress in these stages.
III. Management of Heart Failure
A. General Principles:
  • Multidisciplinary Team Management: Essential for optimal treatment due to the complexity and high comorbidity burden (e.g., hypertension, diabetes, CKD, COPD, dementia, malignancy, depression). Involves primary care, cardiology, and other specialists.
  • Patient Education and Adherence: Repeated patient education, nonjudgmental assessment of adherence, and addressing obstacles are crucial for medication, diet, activity, and weight monitoring. Avoiding over-the-counter NSAIDs is advised.
  • Primary Care Prevention: Focus on modifying risk factors like hypertension (goal <130/80 mm Hg) and diabetes (metformin, SGLT2 inhibitors). Weight loss and smoking cessation also prevent CAD, a major HF cause. Routine vaccinations (pneumonia, influenza) are important.
  • Lifestyle Modification: Sodium restriction (1.5-2 g/day) and fluid restriction (1.5-2 L/day) are commonly advised. "Exercise training is recommended for all patients," improving functional capacity and quality of life.
  • Sleep-Disordered Breathing: Common and underdiagnosed. Guideline-directed medical therapy for HF is the initial treatment. Persistent sleep-disordered breathing despite HF therapy should be treated with CPAP for obstructive sleep apnea. Adaptive servoventilation for central sleep apnea is associated with increased mortality in patients with LVEF <45% and is not recommended.
  • Echocardiography in Chronic HF: Repeat assessment of LV function after optimizing medical therapy for new-onset HF is suggested. Routine surveillance echocardiography is not recommended in stable patients.
B. Medical Therapy for HFrEF:
  • Foundational Therapies (Stage B HFrEF): RAAS inhibition (ACE inhibitor, ARB, or ARNI) and β-blockade.
  • Stage C (Symptomatic) HFrEF:ACE Inhibitors/ARBs: Reduce morbidity and mortality in HFrEF. ACE inhibitors are first-line; ARBs are used for ACE inhibitor-induced cough or angioedema. Monitor for hypotension, kidney dysfunction, and hyperkalemia.
  • Angiotensin Receptor–Neprilysin Inhibitor (ARNI) (Valsartan-Sacubitril): Combines ARB with neprilysin inhibitor, increasing natriuretic peptides. "Reduced mortality and heart failure hospitalization by 20% compared with enalapril" in symptomatic HFrEF. Recommended to replace ACEI/ARB in chronic symptomatic HFrEF or initiate in new-onset HFrEF. Caution in hypotension, contraindicated within 36 hours of ACEI.
  • β-Blockers (Bisoprolol, Carvedilol, Metoprolol Succinate): Reduce morbidity and mortality. Start low and titrate slowly. Contraindicated in acute decompensation, cardiogenic shock, and higher-grade AV block.
  • Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitors (Empagliflozin, Dapagliflozin, Canagliflozin): "Significant reductions in cardiovascular events" and "reduce the risk for heart failure hospitalization by 35%." Recommended for HFrEF (NYHA class II-IV) with or without type 2 diabetes, in addition to GDMT.
  • Aldosterone Antagonists (Spironolactone, Eplerenone): Reduce mortality and hospitalizations in symptomatic HFrEF. Monitor for hyperkalemia and kidney dysfunction. Not a diuretic.
  • Isosorbide Dinitrate–Hydralazine: Recommended as an add-on in Black patients with NYHA class III-IV symptoms who remain symptomatic on maximal foundational therapies. May also be considered for ACEI/ARB-intolerant patients, especially with CKD.
  • Diuretics (Loop diuretics: Furosemide, Torsemide, Bumetanide): Primary therapy for volume overload. Use lowest effective dose; monitor electrolytes.
  • Ivabradine: Sinoatrial node modulator. Reduces heart rate without negative inotropic effects. Indicated for HFrEF (LVEF ≤35%) and NYHA class II-III symptoms, in sinus rhythm with heart rate ≥70/min and on maximally tolerated β-blocker. Reduces hospitalizations.
  • Digoxin: Reduces heart failure hospitalization but not mortality. Used for rate control in concomitant atrial fibrillation or refractory symptoms. Monitor levels due to toxicity risk.
  • Calcium Channel Blockers (non-dihydropyridine): Verapamil and diltiazem are detrimental in HFrEF and "should not be used." Amlodipine and felodipine show no benefit or harm.
  • Statins: No routine benefit in HFrEF unless there is "another accepted indication." Moderate-intensity statin therapy can be considered for HFrEF due to ischemic heart disease if life expectancy is reasonable.
  • Iron Therapy: All patients should be evaluated for anemia and iron deficiency. Intravenous iron therapy is suggested for iron deficiency to improve functional capacity and quality of life.
C. Device Therapies:
  • Implantable Cardioverter-Defibrillator (ICD): Improves survival for primary and secondary prevention of sudden cardiac death. Recommended for patients with LVEF ≤35% and NYHA class II or III symptoms on GDMT. Reassess LVEF and symptoms after GDMT optimization (40 days post-MI, 3 months others) as improvement may negate need. Wearable cardioverter-defibrillator is an option as a bridge to ICD.
  • Cardiac Resynchronization Therapy (CRT): Improves LVEF, reduces symptoms and mortality in patients with dyssynchrony (prolonged QRS or LBBB). Indicated for LVEF ≤35%, NYHA class II-IV symptoms, sinus rhythm, and LBBB with QRS ≥150 ms (Class 1). Can be useful for LBBB with QRS 120-149 ms or non-LBBB with QRS >150 ms (Class 2a).
D. Management of HFpEF:
  • Primary Therapies: Diuretics for volume overload and antihypertensive agents (systolic BP <130 mm Hg).
  • SGLT2 Inhibitors: "Class 2a recommendation" (may be beneficial). Reduce risk for worsening HF, particularly hospitalizations, in HFpEF with or without diabetes.
  • Aldosterone Antagonists: "May be considered to decrease hospitalizations" in selected patients with elevated BNP or recent hospitalization. Caution for hyperkalemia.
  • ARNIs and ARBs: Weak recommendation (Class 2b). FDA expanded valsartan-sacubitril indication to all HF patients based on apparent benefit in LVEF 45-55%.
E. Acute Decompensated Heart Failure:
  • Initial Management: Identify cause, assess physiologic state, remove fluid, optimize medical therapy.
  • Common Causes: Nonadherence (diet, fluids, salt), recurrent ischemia, progression of LV dysfunction, arrhythmias.
  • Volume Status and Perfusion Assessment: Symptoms of volume overload (orthopnea, PND, edema, weight gain, dyspnea). Signs of inadequate perfusion ("cold" patients): cool extremities, narrow pulse pressure, poor mentation, worsening kidney function.
  • Diuresis: Loop diuretics are principal therapy. Higher doses or adding thiazides may be needed if inadequate diuresis. Withholding ACE inhibitors and aldosterone antagonists may be reasonable if kidney function worsens; withholding diuretics for 1 day may allow fluid redistribution.
  • Medication Management: Maintain or restart standard HF therapy (ACEI/ARB, β-blockers, aldosterone antagonists) before discharge. β-blockers should not be reinitiated if low cardiac output.
  • Noninvasive Positive Pressure Ventilation: May reduce need for intubation in respiratory distress.
  • Biomarkers: BNP level on admission and before discharge predicts mortality and rehospitalization. Elevated troponin predicts worse outcomes. Use in combination with clinical judgment.
F. Cardiogenic Shock:
  • Characterized by low cardiac output, hypotension, and end-organ hypoperfusion.
  • Treatment: Reversing cause (e.g., reperfusion for acute coronary syndrome). Intravenous vasoactive medications (inotropes, vasodilators, vasopressors) are used.
  • Mechanical Circulatory Support: Percutaneous devices (intra-aortic balloon pumps, ventricular assist devices, ECMO) can quickly support critically ill patients. Requires a multidisciplinary team. Consideration of long-term options (heart transplantation, LVAD) is vital.
G. Strategies to Prevent Readmission:
  • Treat reversible causes of exacerbation.
  • Discharge only when euvolemic.
  • Medication reconciliation for appropriate, mortality-reducing medications.
  • Patient education on HF physiology, medication/diet adherence, worsening symptoms, and when to contact physician.
  • Home nurse follow-up or phone call within 48 hours post-discharge.
  • Early follow-up appointment (within 7 days).
H. Advanced Refractory Heart Failure:
  • Heart Transplantation: Definitive therapy. Candidates typically younger than 65-70, no major contraindications, good social support. Many require LVAD as bridge to transplant.
  • Mechanical Circulatory Support (LVADs): "Clinical outcomes in patients with advanced heart failure have markedly improved." Provide continuous flow, "1-year survival approximating that of cardiac transplant recipients and substantial improvements in functional capacity and quality of life." Increasingly used as destination therapy. Indicated for LVEF <25% with poor exercise tolerance (NYHA III/IV) despite maximal therapy, high predicted mortality, or inotrope dependency, desiring aggressive care. Requires anticoagulation, continued HF therapy, and specialized care. Complications include stroke, infection, pump thrombosis, arrhythmias, and GI bleeding.
  • Palliative Care/Hospice: Discussed for patients ineligible for or uninterested in advanced therapies.
I. Post-Transplant Management:
  • Complications: Infection (especially CMV, managed with prophylaxis), rejection (highest in first 6 months, monitored by biopsy/gene expression profiling), hypertension, diabetes, increased malignancies (skin cancer, B-cell lymphoma).
  • Immunosuppressive Therapy: Careful attention to drug-drug interactions, particularly with CYP3A4 metabolism (e.g., cyclosporine, tacrolimus).
IV. Specific Cardiomyopathies
  • Takotsubo Cardiomyopathy (Stress-Induced Cardiomyopathy): Associated with reduced LVEF, elevated cardiac enzymes, ECG ischemia. Typically in older women, precipitated by stress. Reversible myocardial toxicity from high catecholamines. Treatment is supportive, similar to other HF causes. Most recover cardiac function within weeks to months; continue medical therapy for at least 1 year.
  • Acute Myocarditis: Acute-onset HF, often viral. Causes myocyte destruction. Diagnosis by CMR or endomyocardial biopsy (recommended for recent-onset HF with hemodynamic compromise or unexplained HF unresponsive to therapy). Standard HF therapy; anti-inflammatory agents do not benefit.
  • Giant Cell Myocarditis: Rapidly progressive, often fatal, typically in younger persons. Can cause biventricular dysfunction, high-grade AV block, ventricular arrhythmias. Requires prompt transfer to facility with mechanical support.
  • Sarcoidosis (Cardiac Sarcoidosis): Granulomatous inflammation. Manifestations include ventricular tachycardia, AV block, HFrEF. Diagnosis by noncaseating granuloma or cardiac imaging (CMR, PET) with clinical manifestations. Therapy: standard HF therapy and immunosuppressants (prednisone for acute flares).
  • Tachycardia-Mediated Cardiomyopathy: Associated with supraventricular and ventricular arrhythmias. Rate control (β-blockers) or rhythm control (catheter ablation) improves LV function. For atrial fibrillation, rate control is as efficacious as rhythm control. Ablation may be considered for frequent premature ventricular contractions.

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I'm Dr. Joseph Kumka, Gastroenterology Fellow, educator, and host of evidence-based, board-oriented medical podcasts. Whether you're a resident gearing up for the boards, a fellow diving deep into subspecialty topics, or a practicing clinician hungry for high-yield updates—you’re in the right place.