STEPTRACKERCARDIOVASCULAR | PATHOLOGY + PHYSIOLOGY | HIGH-YIELD REVIEW

Heart Failure

The heart can't move enough blood at normal filling pressures — the body's compensations then make it worse.

FOCUS ON
Separate HFrEF (weak pump) from HFpEF (stiff pump). Separate left-sided signs (lungs) from right-sided signs (systemic veins). The vicious cycle is RAAS + sympathetic activation, and the drugs that lower mortality block it: ACEi/ARB/ARNI, β-blockers, aldosterone antagonists, SGLT2 inhibitors.
TOPIC
DETAIL
MECHANISM
CLUE
HFrEF
systolic, EF < 40%
Ischemic heart disease, dilated cardiomyopathy, myocarditis, toxins (alcohol, doxorubicin).
↓ contractility → ↓ stroke volume
Dilated ventricle; S3
HFpEF
diastolic, EF preserved
Hypertensive LVH, HCM, restrictive disease, aging.
Stiff ventricle can't fill at normal pressure
Concentric LVH; S4
Neurohormonal response
Low output activates RAAS, sympathetic system and ADH.
Na⁺/water retention + vasoconstriction → ↑ preload and afterload → remodeling
Stretched myocytes release ANP/BNP
Left HF — lungs
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, crackles, pleural effusions.
↑ pulmonary venous pressure → interstitial and alveolar edema
"Heart failure cells" — hemosiderin-laden alveolar macrophages
Left HF — forward
Fatigue, cool extremities, prerenal azotemia.
↓ renal perfusion → more RAAS activation
↑ BUN:Cr
Right HF
JVD, hepatojugular reflux, pitting edema, ascites, hepatomegaly, splenomegaly.
Most common cause is left HF; isolated = cor pulmonale (lung disease, pulmonary hypertension)
Nutmeg liver → centrilobular necrosis → cardiac cirrhosis
High-output HF
Anemia, thyrotoxicosis, AV fistula, wet beriberi, Paget disease, sepsis.
Demand exceeds even a normal heart's output
Warm extremities, bounding pulses
Diagnosis
BNP/NT-proBNP, echocardiography (EF), chest x-ray.
CXR: cardiomegaly, cephalization, Kerley B lines, effusions, "bat-wing" edema
Normal BNP makes HF unlikely in dyspnea
Treatment
Mortality benefit: ACEi/ARB or sacubitril-valsartan, β-blockers, spironolactone, SGLT2 inhibitors, hydralazine + nitrate (Black patients).
Symptoms only: loop diuretics, digoxin
Device: ICD, CRT for selected patients

Mechanism — the vicious cycle

InjuryMI, pressure, toxin
→
↓ Cardiac output
→
RAAS + SNS + ADH
→
Fluid retention, vasoconstriction
→
↑ Wall stressRemodeling
→
Worse pumpCongestion

The mortality-lowering drugs all interrupt this neurohormonal loop.

Left vs right heart failure

FEATURE
LEFT
RIGHT
Congestion
Pulmonary veins
Systemic veins
Symptoms
Dyspnea, orthopnea, PND
Leg swelling, abdominal fullness, RUQ pain
Signs
Crackles, S3, effusions
JVD, HJR, pitting edema, ascites
Organ pathology
Heart-failure cells in alveoli
Nutmeg liver
Usual cause
Ischemia, HTN, valve disease
Left HF; lung disease (cor pulmonale)

How it's tested

COMMON CONFUSIONOrthopnea happens because lying down shifts fluid from the legs back to the central circulation, which the failing left ventricle can't handle.
THE TRAP"Which drug improves symptoms but not survival?" The answer is loop diuretics, and digoxin. ACE inhibitors, β-blockers, spironolactone and SGLT2 inhibitors are the survival drugs.
YOUR APPROACHEF (reduced or preserved) → side of congestion → cause → treatment tier (mortality vs symptoms).

If you see… think…

Orthopnea + PND + basal crackles + S3 → left heart failure
Hemosiderin-laden alveolar macrophages → heart-failure cells
Liver with dark red centers and pale rims → nutmeg liver (right HF)
COPD with JVD, edema and loud P2 → cor pulmonale
Dyspnea with very high BNP → heart failure
Hypertensive with thick LV, normal EF, dyspnea → HFpEF
Hyperthyroid patient with warm skin and HF → high-output failure
Alcoholic with edema and high-output HF → wet beriberi (thiamine)
Drugs proven to cut HFrEF mortality → ACEi/ARB/ARNI, β-blocker, spironolactone, SGLT2i