Cardiology

Heart Failure

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.

Opening Quiz
A 68-year-old man with HTN and diabetes presents with progressive dyspnea, bilateral crackles, and JVD. Echo shows EF 30%. Quick · which type of heart failure is this?
↓ scroll to begin ↓

CLINICAL IMAGES

Chest X-ray showing congestive heart failure
📷 CHF chest X-ray · cardiomegaly
Pulmonary edema alveolar infiltrates
📷 Pulmonary edema · bilateral infiltrates
Jugular venous distension
📷 JVD · right heart failure sign
Pitting edema lower extremity
📷 Pitting edema · bilateral leg swelling
Echocardiogram dilated cardiomyopathy
📷 Echo · dilated cardiomyopathy HFrEF
1
First · What Broke?

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
💡 There's also HFmrEF (EF 41-49%) · the "gray zone." Boards rarely tests it directly, but treatment generally follows HFrEF guidelines. Think of it as HFrEF's less committed sibling.
🔑rEF = reduced squeeze. pEF = preserved squeeze but can't pull blood in.

Split-Screen Compare · Tap a Side to Light It Up

Two failures, same syndrome. Tap each ventricle to reveal how its profile differs.

HFrEF

Reduced EF · systolic failure
Ejection fraction40% or less
GeometryDilated, eccentric, thin
Heart soundS3 gallop
DefectWeak contraction
Classic patientPost-MI, dilated CMP
Drugs that save livesAll four pillars

HFpEF

Preserved EF · diastolic failure
Ejection fraction50% or more
GeometryConcentric, thick, stiff
Heart soundS4 gallop
DefectImpaired relaxation/filling
Classic patientElderly, HTN, diabetes, obese
Drugs that save livesSGLT2 inhibitor
⚡HFmrEF (EF 41 to 49%) is the bridge between the two. Modern guidance treats it like HFrEF, so when the EF lands in that gray band, reach for the four pillars.

Failure Archetypes · Tap to Flip

Four presentations boards throws at you. Front = the clues. Back = the board locks.

SYSTOLIC
💔
HFrEF
Heart failure with reduced EF
EF≤ 40%
ProblemWeak squeeze, dilated LV
SoundS3 gallop
Classic causePost-MI, dilated CMP
4 GDMT pillars all work here
tap to flip
HFrEF: Board Locks
Why EF drops
Myocyte loss (MI, myocarditis, alcohol, peripartum) or chronic pressure/volume overload → eccentric remodeling → dilated, thin-walled LV that can't generate enough pressure to push blood out.
The 4 pillars
ARNI (sacubitril/valsartan), beta-blocker (carvedilol, metoprolol succinate, bisoprolol), MRA (spironolactone), SGLT2i (dapagliflozin or empagliflozin). All have mortality benefit.
Device threshold
EF ≤35% after 3+ months GDMT → ICD. Add CRT if LBBB + QRS ≥150ms.
Board trap
Never uptitrate beta-blockers during acute decompensation. Metoprolol TARTRATE has no HFrEF mortality data. Only succinate.
DIASTOLIC
🥟
HFpEF
Heart failure with preserved EF
EF≥ 50%
ProblemStiff wall, can't relax/fill
SoundS4 gallop
Classic causeElderly woman, HTN, obesity
SGLT2i is the one drug with clear benefit
tap to flip
HFpEF: Board Locks
Why EF stays normal
The ventricle squeezes fine. The problem is relaxation (diastolic dysfunction). Long-standing HTN → LVH → stiff, non-compliant walls. Blood can't fill properly → low stroke volume despite preserved ejection.
Treatment (limited)
Empagliflozin (EMPEROR-Preserved). Diuretics for volume (careful: preload-sensitive). BP control. Rate control if AFib. Weight loss if obese. ARNI/BB/MRA lack proven mortality benefit here.
Diagnosis clue
Classic boards patient: 70s woman, obese, diabetic, HTN x20 years, exertional dyspnea, EF 58%, grade II diastolic dysfunction on echo. BNP mildly elevated.
Board trap
Don't give HFrEF drugs and expect HFpEF outcomes. Only SGLT2i crosses over reliably. Give the drug class that works, not the class that sounds right.
RIGHT-SIDED
🌊
Right HF
RV can't pump to lungs
Blood backs intoSystemic veins
SignsJVD, edema, hepatomegaly
LungsCLEAR
Most common causeLeft heart failure
Clear lungs + JVD + edema = right side
tap to flip
Right HF: Board Locks
Trace It
RV fails → blood backs up into systemic veins → increased venous pressure → JVD, peripheral pitting edema, ascites, hepatic congestion. No fluid in the lungs because the problem is BEFORE the lungs (right side doesn't pump there).
Causes
#1: Left heart failure (backpressure). Others: COPD/cor pulmonale, pulmonary HTN, RV infarct (RCA occlusion), tricuspid regurgitation, PE.
RV infarct trap
Inferior MI (RCA) + hypotension + clear lungs + JVD → suspect RV infarct. Check right-sided V4R lead for ST elevation. NO nitrates or diuretics (preload-dependent RV will crash). Give fluids instead.
Kussmaul sign
JVD that increases with inspiration (opposite of normal). Seen in RV infarct, constrictive pericarditis, tamponade. Classic boards physical exam finding.
COR PULMONALE
💨
Cor Pulmonale
Right HF from lung disease
CauseCOPD, pulmonary HTN, PE
Trace ItHigh pulm. pressure → RV fails
EKGRAD, P pulmonale, RVH
LungsAbnormal (the cause)
COPD + JVD = cor pulmonale until proven otherwise
tap to flip
Cor Pulmonale: Board Locks
Trace It
Chronic hypoxia or lung destruction → pulmonary vasoconstriction → elevated pulmonary vascular resistance → RV hypertrophy → RV dilation and failure. The lungs are killing the right heart.
EKG findings
Right axis deviation, P pulmonale (peaked P >2.5mm in II), RVH (tall R in V1). Also: low voltage in limb leads from hyperinflated lung tissue between heart and electrode.
Treatment
Treat the underlying lung disease. O2 therapy (reduces hypoxic vasoconstriction). Diuretics for volume. Avoid agents that drop pulmonary BP too fast. Heart transplant alone won't fix it if lungs are still the problem.
vs Primary Pulm HTN
Cor pulmonale = secondary to known lung/vascular disease. Primary (idiopathic) pulmonary HTN = no underlying cause. Young women. Treated with endothelin antagonists (bosentan), PDE-5 inhibitors (sildenafil), prostacyclins.
2
NYHA Classification · How Bad Is It?

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.

I
No symptoms
II
Symptoms with ordinary activity
III
Symptoms with less-than-ordinary activity
IV
Symptoms at rest

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.

Board Trap

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.

3
The Clinical Picture · Left vs Right

Heart failure symptoms depend on WHICH side failed. Blood backs up behind the broken pump.

A patient has bilateral pitting edema, JVD, and hepatomegaly but clear lungs. Which side failed?
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.
💡 OrthopneaDyspnea when lying flat. Gravity redistributes blood from legs to lungs. With a failing left ventricle, that extra preload overwhelms the pump → pulmonary congestion → "I need 3 pillows to sleep." The number of pillows IS the severity. = left side. PNDParoxysmal Nocturnal Dyspnea · waking up 1-2 hours after falling asleep, gasping for air. Same mechanism as orthopnea but delayed · interstitial fluid slowly redistributes back into the vascular space while supine. Classic board buzzword for left HF. = left side. JVD alone = right side. Both = biventricular (the most common presentation by the time patients reach the hospital).
🔑Left = Lungs. Right = the Rest of the body.
4
How You Diagnose It

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
Board Trap

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.

Board Trap

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.

5
The GDMT Algorithm · HFrEF Treatment

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.

Which of these is NOT one of the four pillars of GDMT for HFrEF?

The Four Pillars of HFrEF (EF ≤ 40%)

Pillar 1 · RAAS Inhibition
ARNIAngiotensin Receptor-Neprilysin Inhibitor · sacubitril/valsartan (Entresto). Sacubitril blocks neprilysin → increases natriuretic peptides → vasodilation + diuresis + reduced fibrosis. Valsartan blocks AT1 receptors. PARADIGM-HF showed 20% mortality reduction vs enalapril. Must wash out ACEi for 36 hours before starting (risk of angioedema). (sacubitril/valsartan) preferred over ACEi/ARB
Reduces mortality 20% vs ACEi alone (PARADIGM-HF). If can't afford ARNI → use ACEi. If cough on ACEi → use ARB. Never combine ACEi + ARB.
Pillar 2 · Beta-Blocker
Carvedilol, metoprolol succinate, or bisoprolol · only these three
Reduces mortality ~35%. Blocks sympathetic overdrive that's remodeling the ventricle. Start LOW, titrate SLOW. Only these three have HF mortality data · metoprolol tartrate doesn't count.
Pillar 3 · MRA
SpironolactoneMineralocorticoid Receptor Antagonist · blocks aldosterone → reduces sodium retention, fibrosis, and potassium wasting. RALES trial showed 30% mortality reduction in severe HF. Watch for hyperkalemia (especially with ACEi/ARB) and gynecomastia (use eplerenone instead if this happens). or eplerenone
30% mortality reduction (RALES). Blocks aldosterone-driven fibrosis. Watch K+ · these patients are already on ACEi/ARB. Contraindicated if K+ > 5.0 or CrCl < 30.
Pillar 4 · SGLT2 Inhibitor
Dapagliflozin or empagliflozinOriginally diabetes drugs. DAPA-HF and EMPEROR-Reduced showed mortality + hospitalization benefit in HFrEF regardless of diabetes status. Mechanism in HF is still being clarified · likely involves osmotic diuresis, reduced preload, improved cardiac energetics, and anti-fibrotic effects. One of the biggest cardiology breakthroughs of the decade.
Works even WITHOUT diabetes. Reduces HF hospitalization and CV death. Newest pillar · added after DAPA-HF and EMPEROR-Reduced trials. This is the one most commonly missed on newer exams.

Build the Regimen · Tap Each Pillar

Each pillar you add to a 40%-or-less EF patient stacks more mortality protection. Watch the bar fill as you assemble the guideline-directed regimen.

✓
ARNI (sacubitril/valsartan)
Preferred over ACEi/ARB. Block neprilysin, boost natriuretic peptides, drop afterload. If unavailable, an ACEi or ARB still counts as this pillar. Never stack all three.
✓
Beta-blocker
Carvedilol, metoprolol succinate, or bisoprolol only. Blunts the sympathetic overdrive that remodels the ventricle. Start low, go slow.
✓
MRA (spironolactone or eplerenone)
Blocks aldosterone-driven fibrosis. Watch potassium 5.0 mEq/L (3.5 to 5.0) and creatinine, since these patients also sit on RAAS blockade.
✓
SGLT2 inhibitor (dapagliflozin/empagliflozin)
The newest pillar. Cuts hospitalizations and cardiovascular death even without diabetes. The choice most often missed on current exams.
0 of 4 pillars · start building.

Additional Therapies (not pillars, but testable)

Symptom Relief
Loop diuretics (furosemide, bumetanide) · for congestion
No mortality benefit. Pure symptom relief. "Dry" the patient out when they're volume-overloaded. Adjust dose to euvolemia.
Hydralazine + Nitrate
Hydralazine + isosorbide dinitrate
Mortality benefit specifically in Black patients with NYHA III-IV already on standard GDMT (A-HeFT trial). Also used when patient can't tolerate ACEi/ARB (renal failure, hyperkalemia).
Ivabradine
Ivabradine (Corlanor)
For patients on max beta-blocker who still have HR ≥ 70 in sinus rhythm. Blocks the funny (If) current in the SA node. Only works in sinus · useless in a-fib.
Devices
ICD if EF ≤ 35% on 3+ months of optimal GDMT. CRT if EF ≤ 35% + LBBB + QRS ≥ 150ms.
ICD prevents sudden cardiac death. CRT resynchronizes a dyssynchronous squeeze · actual mortality benefit when indicated.
End-Stage (NYHA IV)
LVAD (bridge or destination), heart transplant, inotropes (milrinone, dobutamine)
When drugs and devices aren't enough. Inotropes improve symptoms but may worsen mortality · they're for comfort or bridge to transplant.
Board Trap

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.

Board Trap

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.

6
HFpEF · The One With Fewer Answers

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.
💡 The simplest board answer for HFpEF: SGLT2i + treat the underlying cause + diuretics for symptoms. If they give you an HFpEF patient and ask "what medication?", SGLT2i is the answer (unless there's a contraindication).
7
Acute Decompensated HF · The ER Scenario

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.

What's the FIRST thing you give this patient?

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.
💡 Warm & Wet is the bread-and-butter HF admission. IV furosemide, supplemental O2, monitor I/Os, optimize GDMT once stable. Cold & Wet is the scary one · you need something to squeeze the heart harder (dobutamine, milrinone) while also decongesting.
Board Trap

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.

8
Decision Tree · What Do I Do?

Boards gives you an HF patient. Work through this algorithm to get the answer.

Answer each node before the next branch unlocks.
A 64-year-old man arrives at the emergency department with crushing dyspnea, SpO2 84% on room air, bibasilar crackles to the scapulae, JVP to the jaw, and a third heart sound. Blood pressure is 148/92 mmHg, extremities warm. What is the first move?
Step 1: Is this acute or chronic?
9
Elimination Game · Name That Failure

Four patients walk in. Each clue eliminates one diagnosis. Click the one that DOESN'T fit each clue.

HFrEF
Weak pump, EF 25%
HFpEF
Stiff wall, EF 60%
Cor Pulmonale
RV failure from lung disease
Tamponade
Fluid compressing the heart
Loading clue...

Round 2 · Four more diagnoses. Same drill.

Dilated CMP
Big floppy ventricle
HCM
Thick septum, obstruction
Restrictive CMP
Stiff walls, can't fill
Takotsubo
Stress-induced, apical ballooning
Loading clue...
10
Quiz · Don't Kill Them

Six patients just showed up to your cardiology clinic. Let's see if you were paying attention.

Board-Style Walkthrough

Board-Style Walkthrough

Original board-style vignettes. Shuffled, never-repeat until the bank exhausts. Right-click or long-press to cross out. Double-click or double-tap to highlight. Answer to make the clues glow.

Medically reviewed by Kaitlyn Cocuzzo, MD and Fatima Ali, DO · Last reviewed June 2026