Systemic arterial pressure wave reflections during acute hemorrhage

To determine the effects of hemorrhage on wave-reflection-induced systolic pressure augmentation in the aorta.

Randomized, controlled laboratory experiment.

University research laboratory.

Twenty-five anesthetized pigs randomized to surgical controls (n = 7), hemorrhage (n = 9, H), and hemorrhage with reinfusion (n = 9, HR).

Hemorrhage of 1 mL/kg/min over 20 mins followed by observation (H) or reinfusion (HR) of shed blood.

High-fidelity systemic arterial pressure waveforms, from ascending aorta to femoral artery, were transduced and archived digitally using intravascular semiconductor catheter-tipped pressure transducers. Wave-reflection-induced systolic pressure augmentation was determined using the augmentation index in the ascending aorta (AIaa) and distal descending aorta (AIda). Pulse wave velocity, wave travel times, and lumped pressure wave reflection sites were also calculated. AI values were positive at baseline with greater decreases in AIda compared with AIaa observed following hemorrhage, with negative values achieved for AIda alone. AI returned to control values following reinfusion. Lumped reflection site positions and pressure contour maps suggested that a single lumped reflection site (lower abdomen/pelvis) at baseline was replaced by two discrete sites (upper abdomen and pelvis) following hemorrhage, which only recovered following reinfusion. Hemorrhage was associated with hemodynamic conditions that favored late return of wave reflection from the trunk and with the absence of significant changes in systemic vascular resistance.

Hemorrhage-induced early return of pressure wave reflection from the abdominal vasculature is associated with systolic pressure augmentation in the ascending aorta and has the potential to worsen afterload conditions and decrease coronary artery perfusion and cardiac performance. Hemorrhage-induced splanchnic vasoconstriction causing pressure wave reflection may explain these loading conditions in the ascending aorta, and systolic pressure augmentation may be a more useful guide to left ventricular afterload than systemic vascular resistance.