Heart failure is not a single disease but a syndrome defined by a mismatch between what the heart can deliver and what the body demands. Cardiac output is insufficient for metabolic demand, or it can only be sustained by abnormally high filling pressures. The pump can fail through two distinct mechanisms.
In systolic failure, contractility is reduced. The ventricle cannot generate enough force to eject blood effectively, so stroke volume falls and end-systolic volume rises. Because the ventricle empties poorly, ejection fraction — the fraction of end-diastolic volume ejected as stroke volume — drops below the normal 55–70%, typically below 40%. The ventricle dilates to accommodate the residual volume.
In diastolic failure, contractility is preserved and ejection fraction remains normal or even supranormal, but the ventricle cannot relax and fill properly. The myocardium is stiff, so a normal filling pressure produces a smaller end-diastolic volume. Stroke volume falls because there is less blood to eject, not because the muscle is weak. The ventricle is often hypertrophied and thick-walled rather than dilated.
The distinction matters because it determines the hemodynamic profile. In systolic failure, the dilated, weakly contracting ventricle raises filling pressures on both sides. In diastolic failure, the stiff ventricle transmits high pressures backward despite normal contraction. In both cases, the elevated filling pressures are what produce congestion — the clinical hallmark of heart failure.