When the ventricle ejects, it generates a pressure and flow wave that propagates along the pulmonary or arterial tree. Pressure and flow do not transmit instantaneously through the circulation but travel at finite speed in the form of waves. Spatial variations in vessel diameter, wall stiffness, branching patterns, and distal terminations create a distributed, time-dependent load on the ventricle. The heart therefore experiences the superposition of a forward-traveling wave from the inlet and backward-traveling waves generated by downstream changes. The amplitude and timing of these returning waves determine the instantaneous afterload and the work of ejection.
Three constitutive elements shape this behavior. Inertia resists rapid changes in velocity due to the mass of the moving fluid column. Compliance reflects the ability of the vessel wall to store and release elastic energy as volume changes with pressure, thereby smoothing pulsatility while shifting events in time. Resistance represents viscous dissipation, which reduces mean flow for a given mean pressure and attenuates pulsatile amplitude with distance.
Impedance is not an independent component but rather the frequency-dependent opposition to pulsatile flow that arises from inertia, compliance, resistance, and vessel geometry. Two forms are most useful. Characteristic impedance is a local property of a uniform segment and describes the pressure–flow relation for a purely forward wave, excluding reflections by definition. Input impedance is the pressure–flow relation measured at an inlet and incorporates the effects of wave travel, reflections, and distal boundary conditions. At high frequencies, input impedance approaches the local characteristic impedance because short wavelengths do not sample distant reflections within a cycle.
In lumped-parameter models such as the Windkessel, impedance reflects only the combined effects of resistance, compliance, and inertia. These models do not include distances or explicit wave travel, and therefore cannot assign reflections to specific sites or predict their arrival times. Geometry becomes essential in distributed or transmission-line models, where vessel length, diameter, and branching create propagation delays, location-dependent reflections, and resonance phenomena that shape the full impedance spectrum.
A change in impedance along the path creates a reflection. An increase in impedance produces a positive pressure reflection, raising inlet pressure for a given flow. A decrease in impedance produces a negative pressure reflection, lowering inlet pressure relative to flow. The arrival time of any reflection is determined by propagation distance and local wave speed. Early positive reflections elevate peak ventricular pressure. Late positive reflections extend the systolic pressure tail and may prolong ejection. Late negative reflections reduce ventricular load during mid- to late systole.
Together, these mechanisms define how wave travel and reflections shape ventricular afterload and the hemodynamic profile of ejection.
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