The pump is broken. But HOW it's broken changes everything you do about it. HFrEF vs HFpEF, NYHA staging, the GDMT algorithm boards loves, and when a patient's "shortness of breath" means five different things.
Heart failure isn't one disease. It's a syndrome with two fundamentally different mechanisms. Board questions ALWAYS give you the EF and expect you to know what follows from it.
The heart can fail in two ways:
| HFrEF (Systolic) | HFpEF (Diastolic) | |
|---|---|---|
| The Problem | Weak squeeze — ventricle dilates, can't pump enough out | Stiff wall — ventricle can't relax, can't fill properly |
| EF | ≤ 40% | ≥ 50% |
| Ventricle | Dilated, thin walls | Normal size, thickened walls |
| Classic Cause | Post-MI, dilated cardiomyopathy, valvular regurgitation | Long-standing HTN, HCM, restrictive cardiomyopathy |
| Who Gets It | Men, younger, post-MI patients | Elderly women, obese, HTN, diabetes |
| Drug Therapy | Tons of options — GDMT works here | Fewer proven options — treat the underlying cause + SGLT2i |
| S3 Gallop | S3 — blood sloshing into a floppy ventricle | S4 — atria pushing against a stiff wall |
Boards gives you a patient and expects you to classify them. NYHA is functional — it's about what they can do, not what the echo shows.
Class I: Heart failure exists on echo, but the patient is living normally. They climb stairs, exercise, carry groceries. No shortness of breath beyond what's expected. Board question: "Asymptomatic patient found to have EF 35% on screening echo."
These patients STILL need GDMTGuideline-Directed Medical Therapy — the 4-pillar drug regimen for HFrEF. These drugs have mortality benefit, so you start them even when the patient feels fine. Waiting for symptoms means missing the window to prevent remodeling.. Just because they feel fine doesn't mean the ventricle isn't remodeling.
Class II: "I get winded walking up a flight of stairs" or "I can't keep up with my grandkids anymore." Ordinary activities cause symptoms. They're comfortable at rest. This is where most HF patients live on boards.
Treatment: Full GDMT. Consider cardiac rehab. The goal is keeping them HERE and not letting them progress.
Class III: "I get short of breath walking to the bathroom." Less-than-ordinary activity triggers symptoms. They're limited but still comfortable sitting. Getting dressed is an effort.
Treatment: Optimize GDMT, consider ICDImplantable Cardioverter-Defibrillator — placed for primary prevention in HFrEF (EF ≤35%) despite ≥3 months of optimal GDMT. These patients are at high risk for sudden cardiac death from ventricular arrhythmias. The ICD doesn't fix the heart — it catches fatal rhythms. if EF ≤ 35%, evaluate for CRTCardiac Resynchronization Therapy (biventricular pacing) — for HFrEF patients with EF ≤35% AND wide QRS (≥150ms, especially LBBB). The dyssynchronous squeeze wastes energy. CRT re-coordinates the ventricles. Actual mortality benefit in the right patients. if QRS wide.
Class IV: Symptomatic at rest. Can't get out of bed without dyspnea. These patients are in and out of the hospital. This is end-stage.
Treatment: IV inotropes, LVADLeft Ventricular Assist Device — a mechanical pump surgically implanted to help the failing LV. Used as bridge-to-transplant or destination therapy. The patient carries a battery pack. Complications: driveline infections, pump thrombosis, GI bleeding from the continuous flow shearing vWF multimers., transplant evaluation. Advanced HF center referral. These patients are dying without escalation.
NYHA class and ACC/AHA stage are different systems. NYHA fluctuates (patient can improve from III to II with treatment). ACC/AHA stages (A-D) only go forward — once you're Stage C, you never go back to B. Boards loves asking which classification system allows regression. Answer: NYHA.
Heart failure symptoms depend on WHICH side failed. Blood backs up behind the broken pump.
| Left Heart Failure | Right Heart Failure | |
|---|---|---|
| Blood backs into | Pulmonary veins → lungs | Systemic veins → body |
| Dyspnea | Yes — exertional, orthopnea, PND | Usually only if biventricular |
| Crackles | Bilateral basilar crackles (fluid in alveoli) | Clear lungs |
| Edema | Pulmonary edema | Peripheral pitting edema, ascites |
| JVD | Only if right side also fails | JVD + hepatojugular reflux |
| Liver | Usually spared | Hepatomegaly, "nutmeg liver," elevated LFTs |
| S3/S4 | S3 (HFrEF) or S4 (HFpEF) | Right-sided S3 (louder with inspiration) |
| Most Common Cause of Right HF | Left heart failure. It's almost always secondary. Increased pulmonary pressures from LHF → RV has to pump against higher resistance → RV fails. | |
Two things confirm heart failure: the clinical picture + objective evidence. Boards always gives you labs and imaging and expects you to know what to order and what it means.
| Test | What It Tells You | Board Pearl |
|---|---|---|
| BNP / NT-proBNPBrain Natriuretic Peptide — released by ventricular myocytes when they're stretched (volume overload). Elevated BNP (>100 pg/mL) or NT-proBNP (>300 pg/mL) strongly suggests heart failure. Used to differentiate cardiac from pulmonary causes of dyspnea. Falls with treatment → good prognostic marker. | Confirms volume overload / wall stress | Best initial test to distinguish HF from other causes of dyspnea. Normal BNP essentially rules OUT HF. |
| Echocardiogram | EF, wall motion, valves, chamber size, diastolic function | Most important test — this is what classifies HFrEF vs HFpEF. Boards always gives you the EF. |
| CXR | Cardiomegaly, pulmonary congestion, effusions | Look for cephalization (upper lobe pulmonary veins distended), Kerley B lines, pleural effusions |
| EKG | Rhythm, ischemia, LVH, conduction disease | Wide QRS (esp LBBB) → consider CRT. Old Q waves → ischemic cardiomyopathy. A-fib → rate control critical |
BNP can be falsely LOW in obesity. Fat tissue has natriuretic peptide clearance receptors. An obese patient with real HF might have a "borderline" BNP. If the clinical picture screams HF, don't let a normal-ish BNP in an obese patient fool you — get the echo.
BNP is elevated by ARNI (sacubitril/valsartan) because sacubitril inhibits neprilysin, which normally degrades BNP. So BNP goes UP on treatment even as the patient gets BETTER. Use NT-proBNP (not affected by neprilysin) to track patients on ARNI.
This is the most testable part of heart failure. HFrEF has four pillars of therapy — all with mortality benefit. Boards expects you to know all four, when to start them, and what to watch for.
The Four Pillars of HFrEF (EF ≤ 40%)
Additional Therapies (not pillars, but testable)
Beta-blockers are contraindicated in acute decompensated HF. Don't start or uptitrate during an acute exacerbation — the patient needs their sympathetic drive right now. Start or resume once they're stable and euvolemic. Board question: patient admitted with acute HF, already on metoprolol → hold, don't increase.
Metoprolol succinate (extended-release) has HF mortality data. Metoprolol tartrate (immediate-release) does NOT. Same drug, different formulation, different evidence. Boards will specify. If they say "metoprolol" without specifying, the context matters.
HFpEF is frustrating because most HFrEF drugs don't work here. The ventricle squeezes fine — it just can't relax. Different problem, different approach.
| Strategy | Details |
|---|---|
| SGLT2 inhibitor | The ONE drug class with clear benefit in HFpEF (EMPEROR-Preserved). Empagliflozin reduced HF hospitalizations. This is the answer on modern board exams. |
| Diuretics | For volume management. These patients are preload-sensitive — too much diuresis drops their filling and they crash. |
| BP control | Most HFpEF is from long-standing HTN → LVH → diastolic dysfunction. Controlling the cause prevents progression. |
| Rate control | A-fib is extremely common in HFpEF. Fast rates shorten diastole → less filling time → worse symptoms. |
| Weight loss | Obesity is a major driver. Even modest weight loss improves symptoms and functional capacity. |
Patient arrives to the ED with severe dyspnea, bilateral crackles, SpO2 88%, BNP 1200. They're "wet and cold" or "wet and warm." This is the acute management question.
The Warm/Cold × Wet/Dry Matrix
This is how you triage acute HF. Two questions: Is the patient congested (wet)? Is the patient perfusing (warm)?
| Warm (adequate perfusion) | Cold (poor perfusion) | |
|---|---|---|
| Dry (no congestion) | Warm & Dry — Compensated. Adjust oral meds and send home. | Cold & Dry — Rare. May need gentle volume + inotropes. Careful. |
| Wet (congested) | Warm & Wet — Most common admission. IV diuretics. Patient is perfusing fine, just overloaded. | Cold & Wet — Cardiogenic shock territory. Inotropes + diuretics. Consider vasopressors. ICU. |
Nesiritide (IV BNP) used to be given for acute HF. It fell out of favor — no mortality benefit and possible renal harm. If boards offers it as an answer, it's almost always the wrong choice. IV diuretics are first-line.
Boards gives you an HF patient. Work through this algorithm to get the answer.
Four patients walk in. Each clue eliminates one diagnosis. Click the one that DOESN'T fit each clue.
Round 2 — Four more diagnoses. Same drill.
Six patients just showed up to your cardiology clinic. Let's see if you were paying attention.