In our study, values of DcoSB calculated from the single-breath measurement of Va were also closely related to PDG (r = – 0.754, p < 0.025), but the slope of PDG on the inverse of DcoSB calculated from the single-breath measurement of Va was significantly less than the slope calculated from the rebreathing measurement of Va (p < 0.01). This implies a greater loss of microcirculation than would be predicted from the rebreathing measurement of Va or from the PDG/DcoSB relationship in ILD.
In the present study, resistance to pulmonary blood flow was evaluated from the PDG measured as the difference between the PA diastolic and mean wedge pressures. Alterations in the flow-resistive properties of the pulmonary circulation are more accurately reflected by changes in PDG than by fluctuations in calculated ohmic resistance (PVR = [mean PA-mean LA] x 80/cardiac output), especially when pressures and flow vary simultaneously, since PDG is not affected by variations in cardiac output, stroke volume, or LA pressure, whereas PVR is affected by these variables. Calculated ohmic resistance assumes constant, laminar flow through rigid vessel walls. The pulmonary vessels are more distensible than those of the systemic circulation and apparent changes in resistance may result from passive changes in vessel lumen with varying flow rates.
The present study reports only steady-state observations and, as might be expected, ohmic resistance was related to abnormalities of pulmonary function in the same fashion as PDG. Furthermore, in obstructive lung disease, where left heart pressures are usually normal, there is a high correlation between PDG and calculated resistance. In this setting, the two indices may be used interchangeably. Canadian health care mall more We chose to present observations in terms of the gradient to facilitate comparison with previous observations in patients with pulmonary hypertension reported by this laboratory.
Increased resistance to pulmonary blood flow in COPD-A has long been ascribed to anatomic restriction of the vascular bed on the basis of indirect evidence. Such conclusions have been drawn from demonstrations of the development of pulmonary hypertension during exercise in the absence of significant changes in respiratory gas exchange and of a redistribution of the normal pattern of pulmonary blood flow to apical regions of the lung under resting conditions. The present study offers evidence of increased pulmonary vascular resistance as the microcirculation is restricted by increasingly severe COPDA. Further, we show that this evolution of resistance is indistinguishable from that in patients with ILD (when vital capacity exceeds 50 percent predicted) in whom anatomic restriction of the bed is widely accepted as the cause of hemodynamic abnormalities.