Heart failure Study Guide

📖 Core Concepts Heart Failure (HF) – syndrome where the heart cannot fill or pump blood adequately, leading to congestion (edema, pulmonary fluid) and reduced tissue perfusion. Cardiac Output (CO) – volume of blood the heart pumps per minute; ↓CO → high filling pressures → congestion. Frank–Starling Law – in a normal heart, more filling → stronger contraction; in HF the ventricle is overstretched, so contractility falls. Ejection Fraction (EF) – % of blood ejected each beat; normal 50‑75 %. HFrEF: EF < 40 % (reduced systolic function) HFmrEF: EF 41‑49 % (mildly reduced) HFpEF: EF ≥ 50 % with impaired diastolic relaxation (stiff ventricle) Neurohormonal Activation – chronic RAAS and sympathetic drive → fibrosis, dilation, ventricular shape change (elliptical → spherical). NYHA Functional Classes – I (none) → IV (symptoms at rest). ACC/AHA Stages – A (risk) → D (advanced, needing advanced therapies). 📌 Must Remember Prevalence: 40‑64 million worldwide; >10 % > 70 yrs. Key lab: ↑BNP/NT‑proBNP; hyponatremia signals severe neurohormonal activation. Four‑pillar (quadruple) therapy for HFrEF: ARNI (sacubitril/valsartan) or ACE‑I/ARB β‑blocker (carvedilol, bisoprolol, metoprolol succinate) Mineralocorticoid receptor antagonist (spironolactone, eplerenone) SGLT2 inhibitor (dapagliflozin, empagliflozin) Loop diuretic – symptomatic relief of congestion; does not improve survival. Device indications: ICD – EF ≤ 35 % + NYHA II‑III, primary/secondary prevention. CRT – LBBB or QRS ≥ 150 ms + EF ≤ 35 % + NYHA II‑IV. Acute decompensation: give vasodilators (nitroglycerin), oxygen only if SpO₂ < 90 %, consider non‑invasive ventilation. Low‑risk ADHERE rule: BUN < 43 mg/dL and SBP ≥ 115 mmHg → <10 % in‑hospital death/complications. VO₂ max < 12–14 mL·kg⁻¹·min⁻¹ → consider transplant; < 10 mL·kg⁻¹·min⁻¹ = very poor prognosis. 🔄 Key Processes Diagnostic Work‑up History + physical → suspect HF. BNP/NT‑proBNP → confirm neurohormonal activation. Echocardiography → measure EF, chamber size, valvular disease, filling pressures. Add Chest X‑ray, ECG, labs (electrolytes, renal, liver, thyroid) as needed. Initiating Quadruple Therapy (HFrEF) Start ARNI (after 36 h washout if switching from ACE‑I). Titrate β‑blocker to target dose (monitor HR, BP). Add MRA (watch K⁺, renal function). Introduce SGLT2‑i (no dose titration needed). Adjust loop diuretic for euvolemia. Acute Decompensation Management Verify airway, breathing, circulation. Give IV vasodilator (nitroglycerin) to lower preload/afterload. Provide oxygen if SpO₂ < 90 %; avoid hyperoxia. Initiate non‑invasive positive‑pressure ventilation for severe pulmonary edema. Optimize diuretics; consider inotropes only if cardiogenic shock. 🔍 Key Comparisons HFrEF vs HFpEF EF: < 40 % vs ≥ 50 % Pathophysiology: systolic contractile failure vs diastolic stiffening Therapy: quadruple neurohormonal blockade (HFrEF) vs blood pressure/volume control + SGLT2‑i (HFpEF) ARNI vs ACE‑I/ARB ARNI: adds neprilysin inhibition → more natriuretic peptide effect, superior mortality benefit. ACE‑I: risk of cough; requires washout before ARNI. Hydralazine + Isosorbide dinitrate vs ACE‑I Used when ACE‑I/ARB intolerant; mortality benefit especially in Black patients. ICD vs CRT ICD: prevents sudden death, no need for QRS prolongation. CRT: corrects dyssynchrony; requires wide QRS (≥150 ms) and low EF. ⚠️ Common Misunderstandings “Low sodium diet always improves outcomes.” Evidence for hard mortality benefit is weak; focus on fluid restriction and overall dietary pattern. “Loop diuretics improve survival.” They relieve congestion but do not reduce mortality; over‑diuresis can worsen renal function. “All HF patients need ACE‑I.” Patients intolerant (cough, angioedema) switch to ARB or ARNI; ARNI preferred when tolerated. “HFpEF is benign.” HFpEF carries similar morbidity and mortality; aggressive risk‑factor control is essential. 🧠 Mental Models / Intuition “Pump‑and‑Pipe”: Heart = pump, vasculature = pipe. HF can be pump failure (low CO) or pipe overload (high output demand). Treat pump failure with neurohormonal blockade; treat pipe overload by fixing the underlying cause (anemia, thyrotoxicosis). “Volume‑Pressure Loop”: In HF the loop shifts rightward (higher EDV) but with a flatter slope (reduced contractility). Remember: ↑EDV + ↓SV = congestion. “Four‑Pillar Checklist” – before you finish a new HFrEF patient chart, ask: ARNI? β‑blocker? MRA? SGLT2‑i? 🚩 Exceptions & Edge Cases Hypertensive HFpEF: May need calcium‑channel blocker or ARNI for BP control; β‑blocker benefit modest. Black patients: Add hydralazine + isosorbide dinitrate if ARNI/ACE‑I intolerant or as adjunct. Atrial fibrillation with HFrEF: β‑blocker mortality benefit smaller; consider rate control plus anticoagulation. Renal dysfunction: Dose‑adjust MRA; monitor K⁺ closely; consider SGLT2‑i even with eGFR ≥ 30 mL/min/1.73 m². 📍 When to Use Which ARNI vs ACE‑I/ARB – choose ARNI first‑line unless recent ACE‑I use (need 36‑h washout) or contraindication (angioedema). Hydralazine + Nitrate – reserve for ACE‑I/ARB intolerance or Black patients needing additional mortality reduction. IV Vasodilator – for acute decompensation with hypertensive presentation (SBP > 140 mmHg). Non‑invasive ventilation – severe pulmonary edema with hypoxia or respiratory distress. ICD – EF ≤ 35 % + NYHA II‑III, regardless of symptoms. CRT – LBBB or QRS ≥ 150 ms + EF ≤ 35 % + NYHA II‑IV. Ivabradine – HFrEF on maximal β‑blocker, HR > 70 bpm, sinus rhythm. 👀 Patterns to Recognize Dyspnea + orthopnea + bibasilar crackles → left‑sided HF. Elevated JVP + hepatojugular reflux + peripheral edema → right‑sided HF. BNP/NT‑proBNP > 500 pg/mL (or > 300 pg/mL in atrial fibrillation) strongly suggests HF. Low BUN & high SBP in ADHERE → low‑risk acute HF. QRS ≥150 ms + LBBB → CRT candidate. Rapid weight gain > 2 kg in 3 days → impending decompensation. 🗂️ Exam Traps “All HF patients should be on a loop diuretic.” Diuretics are for congestion; asymptomatic, euvolemic patients may not need chronic loops. “HFpEF patients cannot benefit from ARNI.” Recent trials show ARNI improves outcomes in selected HFpEF patients (especially with high natriuretic peptides). “Beta‑blockers are contraindicated in acute decompensated HF.” Initiate only after stabilization; they are essential chronic therapy. “A normal EF rules out HF.” HFpEF demonstrates normal EF with symptoms; rely on BNP and echo diastolic parameters. “Hyponatremia is a cause of HF.” It is a marker of severe neurohormonal activation, not a primary cause. --- Use this guide for quick recall before exams – focus on the bolded “must‑remember” facts, the four‑pillar checklist, and the decision trees in “When to Use Which.” Good luck!