Central venous pressure, pulmonary artery occlusion pressure, intrathoracic blood volume, and right ventricular end-diastolic volume as indicators of cardiac preload

Abstract

Purpose: Central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and right ventricular end-diastolic volume (RVEDV) are often regarded as indicators of both circulating blood volume and cardiac preload. To evaluate these relationships, the response of each variable to induced volume shifts was tested. The relationships between these variables and cardiac index (CI) and stroke volume index (SVI) was also recorded to assess the utility of each variable as an indicator of cardiac preload. The responses of the new variable intrathoracic blood volume (ITBV) to the same maneuvers was also tested. To examine the effects of changes in cardiac output alone on ITBV, the effects of infusing dobutamine were studied. Materials and Methods: Ten anesthetized piglets were studied during conditions of normovolemia, hypovolemia, and hypervolemia. The effects of an infusion of dobutamine were examined under normovolemia and hypovolemia. Cardiac output was measured by thermodilution, and ITBV was measured by double-indicator dilution. Results: CI was correlated to CVP with r 2 = .42 ( P ≤ .01), to PAOP with r 2 = .43 ( P ≤ 5.01), to RVEDV index with r 2 = .21 ( P ≤ .01), and to ITBV with r 2 = .78 ( P ≤ .01) (pooled absolute values). Bias (mean difference of the percent changes with normovolemia = 100%) ± 1 SD; for SVI - ITBV index was 1 ± 22%, for SVI — CVP it was −128 ± 214%; for SVI — PAOP it was −36 ± 46%; and for SVI -RVEDV index it was 1 ± 29%. Dobutamine infusion increased heart rate (to about 190 × min −1) and CI by 30% in normovolemia and hypovolemia, while ITBV remained basically unchanged. Conclusions: Under the experimental conditions choosen neither CVP, PAOP, nor RVEDV reliably indicated changes in circulating blood volume, nor were they linearly and tightly correlated to the resulting changes in SVI. ITBV reflected both changes in volume status and the resulting alteration in cardiac output. The possibility that ITBV might be cardiac output-dependent was not supported. ITBV, therefore, shows potential as a clinically useful indicator of overall cardiac preload.