Dobutamine and its haemodynamic effects in pleural effusion

Editor, The recent report by Wemmelund et al.1 addressing the haemodynamic effects of dobutamine in a porcine model of pleural effusion outlines a very curious interpretation of their findings. They stated that dobutamine ‘aggravates haemodynamic deterioration induced by pleural effusion’ suggesting that it may be an inappropriate and potentially harmful treatment in patients with pleural effusion. In stark contrast, we believe the data show that the net effects of dobutamine are highly beneficial in treating of the haemodynamic changes associated with pleural effusions. This apparently negative view espoused by Wemmelund et al. seems to be predicated on the finding of their primary isolated endpoint of left ventricular (LV) pre-load [defined as the LV end-diastolic area (LVEDA)], that was reduced with increasing doses of this commonly used inotropic agent. Indeed, this is a very curious interpretation as almost every other haemodynamic parameter reported demonstrated significant improvement with increases in fractional area of contraction, blood pressure and mixed venous oxygen saturation (SvO2), along with decreases in LV end-systolic area and central venous pressure (CVP) – indicating that the net haemodynamic effect of dobutamine was significantly beneficial. Furthermore, it is predictable that CVP decreases with incremental doses of dobutamine, especially when the right ventricle (RV) is responsive to inotropy (as would be expected in this model). This measured CVP represents the intersection of the RV Frank-Starling and the Guytonian venous return curves. Dobutamine, through its beta-2 effects, reduces both the mean systemic filling pressure and resistance to venous return, whereas also moving the RV Frank–Starling curve leftward [due to increased contractility and increased heart rate (HR)];2 cardiac output (CO) will increase significantly, whereas CVP may be unchanged or decrease. Similarly on the left heart side, the LVEDA is predictably decreased, with the left heart dealing with the increased flow from the right heart with a high HR and increased inotropy. Importantly, dobutamine has many haemodynamic effects, not all of which were reported in this study. For example, it is clear that the overall CO and perfusion status was increased, as evidenced by large increases in increased SvO2. Furthermore, although the pulmonary artery pressures were initially increased by the pleural effusion, pulmonary pressures were not significantly reduced by the subsequent infusion of dobutamine. However, the pulmonary vascular resistance (PVR) was undoubtedly reduced, as the higher CO coupled with lower PVR, resulted in a net unchanged pulmonary pressure. In addition, other specific indices of RV function were not measured. Pleural effusions, by mechanical compression of lung and resulting reductions in functional residual capacity, increase PVR.3 Accordingly, a more complete understanding of the haemodynamic effects might have been facilitated with a more comprehensive assessment of RV function. Dobutamine, in addition to other important manoeuvers,4 is often a very effective drug in the treating RV dysfunction.5 Though choosing a single primary end point and reporting its results primarily is clearly the correct manner by which to proceed with study reporting, the global patterns seen should take precedence and drive the overall interpretation of the results. Accordingly, we suggest that despite the LVEDA being reduced by dobutamine (in isolation indicating a decrease in preload which might have negative consequences in certain clinical situations), the overall net effect suggests an amelioration of the haemodynamic deterioration induced from pleural effusion as opposed to an aggravation. Acknowledgements relating to this article Assistance with the letter: none. Financial support and sponsorship: none. Conflicts of interest: none.

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