268.1 🎓 醫孞生版

268.1.0.1 📌 䞀頁重點

268.1.0.1.1 Definition
  • Clinical syndrome with symptoms (dyspnea, fatigue) + signs (peripheral edema, elevated JVP, crackles) due to structural / functional cardiac abnormality
  • Inability of heart to meet metabolic demands of tissues at normal filling pressures
  • 2022 Universal HF Definition (Lancet): symptoms + signs + objective evidence (BNP/NT-proBNP elevated OR objective cardiac dysfunction by imaging)
268.1.0.1.2 Classification by Ejection Fraction (EF)
  • HFrEF (Reduced EF): EF ≀ 40% (formerly “systolic HF”)
  • HFmrEF (Mildly Reduced EF): EF 41-49% (newer category 2021+)
  • HFpEF (Preserved EF): EF ≥ 50% (formerly “diastolic HF”)
  • HFimpEF (Improved EF): previously HFrEF → now > 40% (newer category 2022)
268.1.0.1.3 Stages (ACC/AHA)
  • A (At Risk): risk factors (HTN, DM, obesity, CKD, etc.) without structural heart disease
  • B (Pre-HF): structural heart disease without symptoms (e.g., LV hypertrophy, low EF)
  • C (HF): structural heart disease + current or prior HF symptoms
  • D (Advanced HF): refractory; requires advanced therapies (LVAD, transplant, palliative)
268.1.0.1.4 NYHA Functional Classification
  • I: no limitation; ordinary activity asymptomatic
  • II: slight limitation; ordinary activity → symptoms
  • III: marked limitation; less than ordinary → symptoms
  • IV: symptoms at rest; severe limitation
268.1.0.1.5 Pathophysiology
268.1.0.1.5.1 Neurohormonal Activation
  • RAAS (renin-angiotensin-aldosterone system) — sodium + water retention + vasoconstriction + remodeling
  • Sympathetic nervous system — initially compensatory but maladaptive long-term
  • Natriuretic peptides (BNP, ANP) — physiologic counter-regulation
  • Endothelin — vasoconstriction
  • Multiple chronic activation leads to maladaptive cardiac remodeling
268.1.0.1.5.2 Cardiac Remodeling
  • Pressure overload (HTN, AS): concentric hypertrophy
  • Volume overload (MR, AR): eccentric dilation + hypertrophy
  • Ischemia + necrosis (MI): patchy fibrosis + reduced LV function
  • Toxic / drug (anthracycline, alcohol, cocaine, COVID-19 myocarditis): direct injury
268.1.0.1.5.3 Cellular Dysfunction
  • Mitochondrial dysfunction
  • Energy depletion
  • Calcium handling abnormalities
  • Apoptosis + necrosis
  • Inflammation
  • Fibrosis (TGF-β, galectin-3)
268.1.0.1.6 HFrEF — Etiologies
  • Ischemic Cardiomyopathy (most common — post-MI; LV dysfunction)
  • Dilated Cardiomyopathy (DCM):
    • Idiopathic
    • Familial / genetic (titin, lamin, others)
    • Inflammatory (viral myocarditis, autoimmune)
    • Toxic (alcohol, cocaine, anthracycline, trastuzumab)
    • Endocrine (hyper/hypothyroidism, pheochromocytoma, acromegaly)
    • Peripartum cardiomyopathy
    • Tachycardia-induced
    • Infiltrative (amyloid, sarcoid, hemochromatosis — although HFpEF/restrictive often)
  • Valvular heart disease (severe)
  • Congenital
  • Pulmonary HTN (right HF)
268.1.0.1.7 HFpEF — Etiologies
  • Hypertensive heart disease (most common — concentric LVH + diastolic dysfunction)
  • Aging (intrinsic myocardial stiffening)
  • Obesity + metabolic syndrome
  • Diabetes
  • Coronary artery disease
  • CKD
  • Atrial fibrillation (often)
  • Restrictive cardiomyopathy (amyloid, sarcoid)
  • Hypertrophic cardiomyopathy (HCM)
  • Pulmonary hypertension
268.1.0.1.8 Symptoms
  • Dyspnea (exertional, orthopnea, paroxysmal nocturnal dyspnea)
  • Fatigue
  • Decreased exercise tolerance
  • Peripheral edema
  • Weight gain
  • Cough (sometimes)
  • Abdominal distention (ascites in advanced)
  • Anorexia (especially advanced)
  • Acute pulmonary edema (severe — life-threatening)
268.1.0.1.9 Signs
  • Elevated JVP (volume overload)
  • Hepatojugular reflux
  • Pulmonary crackles (rales — bilateral)
  • S3 gallop (HFrEF particularly)
  • S4 gallop (HFpEF + LVH)
  • Peripheral edema (pitting)
  • Cool peripheral extremities (low CO)
  • Sinus tachycardia (compensatory)
  • Hepatomegaly (right HF or biventricular)
  • Ascites + JVD + edema (severe)
  • Pulsus alternans (severe LV dysfunction)
  • Cheyne-Stokes respiration (advanced HF)
268.1.0.1.10 Diagnosis
268.1.0.1.10.1 Initial Tests
  • ECG: rhythm, ischemia, prior MI, conduction (BBB, LVH)
  • CXR: cardiomegaly, pulmonary congestion (Kerley B lines, alveolar edema), pleural effusion
  • Echocardiogram: EF, chamber sizes, valvular function, diastolic function, RV function
  • BNP / NT-proBNP: elevated supports HF; helps differentiate HF from non-cardiac dyspnea
  • CMP: renal function, sodium, potassium, glucose, hepatic enzymes
  • CBC: anemia
  • Thyroid function
  • Lipid panel
  • HbA1c
  • Iron studies (especially HFpEF + HFrEF — iron deficiency common)
268.1.0.1.10.2 BNP / NT-proBNP
  • BNP: < 100 = unlikely HF; > 400 = HF likely; 100-400 = consider HF
  • NT-proBNP: < 300 = unlikely HF; cutoffs vary with age (older = higher)
  • Affected by: age (rises), obesity (lower BNP), renal function (rises), AF (rises), pulmonary HTN
268.1.0.1.10.3 Echocardiogram Findings
  • EF + chamber sizes
  • Wall motion abnormalities (post-MI, ischemic CM)
  • LV hypertrophy (HTN, HCM, amyloid)
  • Diastolic function (E/A, E/e’, LA size)
  • Valvular disease (especially significant MR, AR, AS)
  • Right heart function + PASP
  • Pericardial disease
268.1.0.1.10.4 Cardiac MRI
  • Tissue characterization (LGE patterns — Ch 261)
  • Quantitative chamber sizes + function
  • Cardiomyopathy etiology workup
268.1.0.1.10.5 Coronary Angiography
  • For ischemic etiology workup
  • Especially in HFrEF + chest pain or risk factors
268.1.0.1.10.6 Right Heart Catheterization
  • For:
    • Severe HF (advanced therapies workup)
    • Pulmonary HTN assessment
    • Constrictive vs restrictive
    • Pre-heart transplant
    • Cardiogenic shock evaluation
268.1.0.1.11 Acute Decompensated Heart Failure (ADHF)
268.1.0.1.11.1 Clinical Profiles
268.1.0.1.11.2 “Wet” + “Warm” (Volume Overload)
  • Peripheral edema + crackles + elevated JVP
  • Adequate perfusion
  • IV diuretics + nitrates
268.1.0.1.11.3 “Wet” + “Cold” (Cardiogenic Shock)
  • Volume overload + poor perfusion
  • Cold extremities, hypotension, oliguria
  • IV inotrope (dobutamine) + diuretic + consider mechanical support
268.1.0.1.11.4 “Dry” + “Cold” (Low-Output)
  • Poor perfusion without volume overload
  • Cold extremities, hypotension
  • Inotrope + cautious fluid administration
268.1.0.1.11.5 “Dry” + “Warm” (Compensated)
  • No volume overload, good perfusion
  • Optimize chronic therapy
268.1.0.1.11.6 Acute Management
  • IV loop diuretic (furosemide 1-2 × home dose typically)
  • Oxygen if hypoxemic
  • Vasodilator (nitroglycerin) for elevated BP / pulmonary edema
  • Non-invasive ventilation (CPAP/BiPAP) for severe pulmonary edema
  • Inotropes (dobutamine, milrinone) for low-output
  • Vasopressors (norepinephrine) for cardiogenic shock
  • Mechanical support if refractory (IABP, Impella, VA-ECMO)
268.1.0.1.12 Worsening HF / Triggers
  • Medication non-adherence
  • Dietary indiscretion (sodium, fluid)
  • Atrial fibrillation (loss of atrial kick)
  • Ischemia / MI
  • Infection
  • Pulmonary embolism
  • Anemia
  • Hyperthyroidism
  • Renal failure
  • NSAID use
268.1.0.1.13 Prognosis
  • 5-year mortality: 50% post-diagnosis (decreasing with modern therapy)
  • Worsening prognosis with advanced symptoms, decreasing EF, comorbidities, BNP elevation
  • Modern therapies improve outcomes significantly (HFrEF — Ch 268)

268.1.0.2 1⃣ HFrEF Pathophysiology Detail

268.1.0.2.1 Key Components
268.1.0.2.1.1 LV Dysfunction
  • Decreased contractility → reduced cardiac output
  • Increased LV filling pressures
  • Decreased EF
268.1.0.2.1.2 Neurohormonal Activation (Maladaptive)
268.1.0.2.1.3 RAAS
  • Renin from juxtaglomerular cells
  • → Angiotensin I → Angiotensin II (potent vasoconstrictor + sodium retention + aldosterone)
  • → Aldosterone (sodium + water retention)
  • Long-term harmful (remodeling, fibrosis)
268.1.0.2.1.4 Sympathetic Nervous System
  • Initial compensation (increases HR + contractility)
  • Long-term harmful (downregulation of β-receptors, increased afterload, arrhythmia)
268.1.0.2.1.5 Natriuretic Peptides
  • BNP + ANP from cardiac myocytes
  • Counter-regulatory (vasodilation, natriuresis, antifibrotic)
  • Elevated in HF
268.1.0.2.1.6 Cardiac Remodeling
  • LV dilation
  • LV hypertrophy
  • Interstitial fibrosis
  • Myocyte death / apoptosis
  • Functional + structural deterioration
268.1.0.2.2 Pharmacologic Targets
  • RAAS: ACEi/ARB, ARNI (sacubitril/valsartan), MRA (spironolactone)
  • Sympathetic: β-blocker (metoprolol succinate, carvedilol, bisoprolol)
  • Volume: loop diuretic, MRA
  • SGLT2i: dapagliflozin, empagliflozin (mechanism includes inflammation + remodeling reduction)
  • Other: ivabradine, hydralazine/nitrates, digoxin

268.1.0.3 2⃣ HFpEF Pathophysiology

268.1.0.3.1 Mechanisms
  • Concentric LV hypertrophy (often from HTN)
  • Diastolic dysfunction (impaired LV relaxation + increased stiffness)
  • Increased LV filling pressures
  • Pulmonary venous congestion
  • RV dysfunction (in advanced)
  • Systemic inflammation (obesity, DM, metabolic syndrome)
  • Microvascular dysfunction
268.1.0.3.2 Comorbidities (Major Contributors)
  • Hypertension (#1)
  • Obesity (especially metabolic obesity)
  • Type 2 diabetes
  • Coronary artery disease
  • Aging
  • Atrial fibrillation
268.1.0.3.3 Diagnostic Criteria (HFA-PEFF Score)
  • Functional: E/e’ ratio, septal e’, LA volume index, TR velocity
  • Morphologic: LA size, LV mass, LVH
  • Biomarker: BNP/NT-proBNP elevated
  • Plus clinical HF symptoms + EF ≥ 50%
268.1.0.3.4 Specific Subtypes
268.1.0.3.4.1 “Garden Variety” HFpEF
  • HTN + age + obesity + metabolic syndrome
268.1.0.3.4.2 Cardiac Amyloidosis (HFpEF Phenotype)
  • ATTR vs AL
  • Subendocardial circumferential LGE
  • Apical sparing on echo strain
  • Bilateral CTS
  • Low voltage ECG with LVH echo
268.1.0.3.4.3 HCM (Hypertrophic Cardiomyopathy)
  • Asymmetric septal hypertrophy
  • LVOT obstruction with SAM
  • Family history
268.1.0.3.4.4 Constrictive Pericarditis
  • Equalization of diastolic pressures
  • Pericardial calcification
  • Differentiate from restrictive cardiomyopathy
268.1.0.3.5 Treatment (Ch 268)
  • SGLT2i (dapagliflozin, empagliflozin) — DELIVER, EMPEROR-Preserved trials
  • Diuretics for symptoms
  • Optimal comorbidity management (HTN, DM, AF)
  • No mortality benefit shown for most HFrEF medications in pure HFpEF (except SGLT2i; tirzepatide STEP-HFpEF)
  • GLP-1 RA (semaglutide) for HFpEF + obesity (STEP-HFpEF trial)

268.1.0.4 3⃣ Etiology Workup

268.1.0.4.1 Ischemic vs Non-Ischemic Cardiomyopathy
  • Coronary angiography or CCTA
  • Cardiac MRI (LGE pattern: subendocardial CAD vs mid-wall DCM)
  • History (chest pain, prior MI, risk factors)
268.1.0.4.2 Specific Cardiomyopathy Workup
268.1.0.4.2.1 Familial / Genetic
  • Family history
  • Genetic testing for known mutations
  • First-degree relatives screening (echo + ECG)
268.1.0.4.2.2 Inflammatory / Myocarditis
  • Cardiac MRI (Lake Louise criteria)
  • Endomyocardial biopsy (rare)
  • Acute myocarditis workup
268.1.0.4.2.3 Toxic
  • History (alcohol, cocaine, chemotherapy)
  • Anthracycline cumulative dose
  • Trastuzumab + immune checkpoint inhibitor cardiotoxicity
268.1.0.4.2.4 Infiltrative
  • Cardiac amyloidosis:
    • Free light chains (FLC ratio) — AL
    • PYP scan — ATTR
    • Cardiac MRI (subendocardial LGE)
    • Subtype determination essential
268.1.0.4.2.5 Sarcoidosis
  • FDG-PET for active inflammation
  • Cardiac MRI for fibrosis (patchy)
  • Biopsy (endomyocardial or extracardiac)
  • Treatment: corticosteroids + ICD if indicated
268.1.0.4.2.6 Iron Overload
  • Hemochromatosis (HFE gene)
  • Cardiac iron on MRI (T2*)
  • Phlebotomy treatment
268.1.0.4.2.7 Endocrine
  • Hyperthyroidism (high-output HF possible)
  • Hypothyroidism (rare cause)
  • Acromegaly
  • Pheochromocytoma (catecholamine-induced)
  • Cushing’s
268.1.0.4.2.8 Peripartum Cardiomyopathy
  • Pregnancy / postpartum
  • Diagnosis after exclusion of other causes
  • Usually improves with treatment

268.1.0.5 4⃣ BNP / NT-proBNP

268.1.0.5.1 Mechanism
  • Released from cardiac myocytes in response to stretch / wall tension
  • Counter-regulatory: vasodilation + natriuresis
  • Increased in HF (LV dysfunction)
268.1.0.5.2 Diagnostic Cutoffs
268.1.0.5.2.1 BNP (ng/L or pg/mL)
  • < 100: unlikely HF
  • 100-400: gray zone; correlate with clinical
  • > 400: HF very likely
268.1.0.5.2.2 NT-proBNP
  • < 300: unlikely HF
  • 300-450 (age < 50): consider HF
  • 450-900 (age 50-75): HF likely
  • > 900 (age 50-75): HF very likely
  • > 1800 (age > 75): HF very likely
268.1.0.5.3 Factors Affecting
  • Increases BNP: age, female, AF, pulmonary HTN, renal failure, sepsis, pulmonary disease
  • Decreases BNP: obesity (especially BMI > 35), inferior MI
268.1.0.5.4 Use in Management
  • Diagnosis: rule in / out HF
  • Prognosis: higher = worse
  • Monitoring: trend with treatment

268.1.0.6 5⃣ ADHF (Acute Decompensated Heart Failure)

268.1.0.6.1 Triggers
  • Medication non-adherence
  • Dietary indiscretion (Na+, fluid)
  • AF (loss of atrial kick)
  • MI / ischemia
  • Infection / sepsis
  • PE
  • Anemia
  • NSAIDs
  • Hyperthyroidism
  • Pregnancy / peripartum
268.1.0.6.2 Clinical Presentation Phenotypes
Phenotype Symptoms Treatment
Wet + Warm Volume overload, normal perfusion Diuretics + nitrates
Wet + Cold Volume overload + poor perfusion Diuretics + inotrope + cautious vasodilator
Dry + Cold Poor perfusion, no volume overload Inotrope + cautious fluid; consider mechanical support
Dry + Warm Compensated; no signs of decompensation Optimize chronic therapy
268.1.0.6.3 Acute Management Approach
  1. Assess perfusion + volume status
  2. Oxygen if hypoxic
  3. NIV (CPAP/BiPAP) for severe pulmonary edema (DOSE trial supports)
  4. IV diuretics: furosemide 1-2× home dose (DOSE trial)
  5. Vasodilators (nitroglycerin) for HTN or pulmonary edema
  6. Inotropes (dobutamine, milrinone) for low-output / shock
  7. Vasopressors (norepinephrine) for cardiogenic shock
  8. Mechanical support (IABP, Impella, VA-ECMO) for refractory
  9. Monitor + adjust therapy
268.1.0.6.4 Discharge Planning
  • Optimize chronic therapy (HFrEF: GDMT — quadruple therapy)
  • Education: weight monitoring, sodium restriction, medications
  • Follow-up: within 1 week + cardiology
  • Cardiac rehabilitation
268.1.0.6.5 Hospital Discharge Criteria
  • Stable volume status
  • Stable on oral medications
  • Stable BP + HR
  • No active triggers
  • Patient + family education completed
  • Follow-up arranged