Peripheral Venous Pressure as an Indicator of Preload Responsiveness During Volume Resuscitation from Hemorrhage.
Fluid resuscitation of hypovolemia presumes that peripheral venous pressure (PVP) increases more than right atrial pressure (RAP), so the net pressure gradient for venous return (PVP-RAP) rises. However, the heart and peripheral venous system function under different compliances that could affect their respective pressures during fluid infusion. In a porcine model of hemorrhage resuscitation, we examined whether RAP increases more than PVP, thereby reducing the venous return pressure gradient and blood flow.



Anesthetized pigs (n = 8) were bled to a mean arterial blood pressure of 40 mm Hg and resuscitated with stored blood and albumin for pulmonary artery occlusion pressures (PAOPs) of 5, 10, 15, and 20 mm Hg. Venous pressures, inferior vena cava blood flow (ultrasonic flowprobe), and left ventricular diastolic compliance (Doppler echocardiography) were measured. Stroke volume variability was calculated.



With volume resuscitation, the slope of RAP exceeded PVP (P ≤ 0.0001) when PAOP is 10 to 20 mm Hg, causing the pressure gradient for venous return to progressively decrease. Inferior vena cava blood flow did not further increase after PAOP > 10 mm Hg. The E/e' ratio increased (P = 0.001) during resuscitation indicating reduced diastolic compliance. A significant curvilinear relationship was found between PVP and stroke volume variability (R = 0.62; P < 0.001), where fluid responders had PVP < 15 mm Hg.



Fluid resuscitation above a PAOP 10 mm Hg reduces myocardial compliance and reduces the venous return pressure gradient. The hemodynamic response to fluid resuscitation becomes limited by diastolic properties of the heart. PVP measurement during hemorrhage resuscitation may predict fluid responsiveness and nonresponsiveness.
From the *Department of Anesthesiology, The University of Texas Medical Branch at Galveston, Galveston, Texas; †Department of Anesthesiology and Perioperative Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California; ‡Department of Respiratory Care and §Department of Biostatistics, The University of Texas Medical Branch at Galveston, Galveston, Texas; and ‖Baylor Scott & White Healthcare, Texas A&M University School of Medicine, Temple, Texas.
Michael
M
Kinsky
Nicole
N
Ribeiro
Maxime
M
Cannesson
Donald
D
Deyo
George
G
Kramer
Michael
M
Salter
Muzna
M
Khan
Hyunsu
H
Ju
William E
WE
Johnston
D000818:Animals; D062186:Arterial Pressure; D016280:Atrial Function, Right; D062185:Atrial Pressure; D001810:Blood Volume; D003971:Diastole; D004195:Disease Models, Animal; D005260:Female; D005440:Fluid Therapy; D020896:Hypovolemia / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy*; D011237:Predictive Value of Tests; D011651:Pulmonary Artery / Q000503:physiopathology; D012151:Resuscitation / Q000379:methods*; D012771:Shock, Hemorrhagic / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy*; D034421:Sus scrofa; D013997:Time Factors; D014690:Venous Pressure; D016277:Ventricular Function, Left