PULMONARY VASCULAR IMPEDANCE ANALYSIS OF ADAPTATION TO CHRONICALLY ELEVATED BLOOD-FLOW IN THE AWAKE DOG

Pulsatile pulmonary hemodynamics were analyzed in a chronic awake canine high flow model. Standard mean flow and pulsatile flow hemodynamics were measured and alterations in the proximal pulmonary vascular physical properties were quantified by the characteristic impedance (Z0). Pulmonary vascular resistance (PVR), which assesses arteriolar-capillary recruitment of perfusing radius and measures a more distal pulmonary vascular response to changing flows, also was calculated. Twelve control dogs were studied and had mean Q(pa) (pulmonary blood flow)=2.02±0.15 liters/min, Z0=193±20 dyne sec cm-5 and PVR=416±32 dyne sec-5. Ten dogs were studied awake 20 weeks after creation of bilateral arteriovenous fistulae. Five of these shunted dogs, designated group A, developed Q(pa)=3-4 liters/min (mean=3.80±0.09, P<0.001 different from control group); the other five dogs (group B) developed Q(pa)=4-8 liters/min (mean=5.87±0.16, P<0.001). In group A, Z0=143±8 (P<0.05) and PVR=249±6 (P<0.10). In group B, Z0=90±5 (P<0.005) and PVR=126±14 (P<0.01). The total input power (potential and kinetic) was 125% above the controls for group A (P<0.001) and 264% for group B (P<0.001), but the mean energy components increased significantly more than did the pulsatile components. These data demonstrate a lower impedance to pulsatile flow during chronically elevated total flow which effects a reduction in both the work load of the right ventricle and the transmission of energy to the precapillary bed. Analysis of the alterations in characteristic impedance suggests a distinct proximal pulmonary vascular mechanisms of decreased vessel stiffness (decreased elastic moduli) for adaptation to chronically elevated flow loads which is in addition to the two geometric alterations of proximal arterial dilation and distal vascular channel recruitment.