How heart failure is tested on Step 1

Vignettes describe dyspnea, edema, and an extra heart sound and ask for the type of failure, a histologic finding, a lab such as BNP, or a drug and its mechanism.

workspace_premium Symptom relief vs survival

Diuretics and digoxin relieve symptoms. Drugs that block neurohormonal activation — ACE inhibitors or ARNI, β blockers, spironolactone, SGLT2 inhibitors — reduce mortality.

HFrEF vs HFpEF

Ejection fraction separates two mechanisms that look similar at the bedside.

HFrEF (systolic)EF ≤ 40%Dilated, thin-walled ventricleEccentric remodelingS3Causes: ischemic heart disease, dilatedcardiomyopathy, myocarditisHFpEF (diastolic)EF ≥ 50%Thick, stiff ventricleConcentric remodelingS4Causes: hypertension, aging, obesity,diabetes, restrictive diseasevs
HFrEF vs HFpEF. EF 41–49% is "mildly reduced" and is often treated like HFrEF.
lowmidhighlowmidhighPreload (LV end-diastolic volume)Stroke volumeNormalSystolic failureCongestion
Frank-Starling curve. In systolic failure the curve flattens: higher filling pressures add little stroke volume and back up into the lungs. Positive inotropes shift the curve up; diuretics move along it to the left.

Neurohormonal activation

Low cardiac output looks like low blood volume to the kidneys and baroreceptors.

↓ CardiacoutputFailing pumpSympathetic↑↑ HR,vasoconstrictionRAAS ↑Aldosterone,angiotensinIINa⁺,waterretainedADH ↑ tooRemodelingFibrosis,dilation
Self-perpetuating cycle. Natriuretic peptides (BNP) rise from ventricular stretch; neprilysin inhibitors (sacubitril) prolong their effect.

Left vs right failure, and the drugs that change survival

Symptoms follow the direction of congestion; treatment targets both the congestion and the neurohormonal drive behind it.

FeatureLeft heart failureRight heart failure
CongestionPulmonarySystemic venous
SymptomsDyspnea, orthopnea, paroxysmal nocturnal dyspneaEdema, abdominal fullness
SignsCrackles, S3, pleural effusionsJVD, hepatomegaly, ascites, pitting edema
HistologyHemosiderin-laden macrophages ("heart failure cells") in alveoliCentrilobular congestion — nutmeg liver
Common causesIschemia, hypertension, valve diseaseLeft heart failure, cor pulmonale (lung disease)

Orthopnea occurs because lying flat returns more blood to an overloaded heart.

DrugMechanismEffect on survival in HFrEF
ACE inhibitor / ARB / sacubitril-valsartanBlock RAAS (ARNI also raises natriuretic peptides)↓ Mortality
Metoprolol succinate, carvedilol, bisoprololBlock sympathetic toxicity↓ Mortality
Spironolactone, eplerenoneBlock aldosterone (antifibrotic)↓ Mortality
SGLT2 inhibitors (dapagliflozin, empagliflozin)Natriuresis; metabolic and renal effects↓ Mortality and hospitalization
Hydralazine + isosorbide dinitrateArteriolar + venous dilation↓ Mortality in Black patients
Loop diureticsRemove volumeSymptoms only
DigoxinNa⁺/K⁺-ATPase inhibition → ↑ contractilitySymptoms and hospitalizations only

Ivabradine (If channel blocker) lowers heart rate when β blockers are maximized.

Clinical application

Match the drug to the problem.

functions Worked example — symptom relief vs survival

A 66-year-old with ischemic cardiomyopathy (EF 25%) is admitted with leg edema and orthopnea. He improves with IV furosemide. At discharge, which drugs should he take to reduce mortality?

  1. Furosemide relieves congestion but does not change survival.
  2. Mortality falls with blockade of the neurohormonal systems that drive remodeling.
  3. Four pillars: ARNI (or ACE inhibitor/ARB), an evidence-based β blocker, a mineralocorticoid antagonist, and an SGLT2 inhibitor.
  4. Monitor potassium and creatinine with RAAS blockers and spironolactone.

Answer. Sacubitril-valsartan (or an ACE inhibitor/ARB), metoprolol succinate or carvedilol, spironolactone, and dapagliflozin or empagliflozin, with furosemide as needed for volume.