We appreciate the interest of Grocott and Jacobsohn1 and their comments regarding our experimental study in which we report on the basic physiological effects of dobutamine administration after induction of pleural effusion.2 Grocott and Jacobsohn provide further explanation of the haemodynamic effects of dobutamine, with which we completely agree, and the overall increase in many factors of global haemodynamic parameters cannot be disputed. However, we find the distinction between ‘global haemodynamic effects’ and the ‘underlying physiological determinants’ essential, especially when dealing with healthy, well functioning myocardiums as in our experimental study. Left ventricular (LV) pre-load is such a physiological determinant, which has had our interest since we introduced focused transthoracic echocardiography (FATE) in the hands of non-cardiologists in the late 1980s. The first thing we noticed was that many patients had inotropes running on well functioning but ‘empty’ hearts, and we termed it ‘iatrogenic inotropic intoxication syndrome’. Over the years, we have received similar feedback from many ICU physicians after implementation of FATE in their daily clinical practice. Thus, our message is that haemodynamic optimisation should start with an analysis of the basic physiological determinants and strive to normalise these, instead of focussing on the easily available parameters of global circulation as the latter strategy carries a substantial risk of aggravating, for example, pre-load depletion.
Pleural effusion induces increased right-sided pressures, and, if the pleural effusion is sufficiently large,2–5 decreases in both systemic blood pressure and cardiac output. This may prompt suspicion of cardiac failure and administration of dobutamine. This approach may normalise or even augment the mentioned parameters of pressure and flow (happy physician), but subjects the recipient to a considerable risk due to the vastly increased inotropic state, as exemplified by the increase in heart rate (myocardial energy consumption) and increase in LV fractional area change despite unchanged stroke volume. Providing inotropes to empty hearts is, in our opinion, dangerous for the reasons mentioned above and it furthers LV unloading, and this remains the key message of our experimental study.2
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1. Grocott HP, Jacobsohn E. Dobutamine and its haemodynamic effects in pleural effusion. Eur J Anaesthesiol
2. Wemmelund KB, Sorensen AH, Ringgard VK, et al. Dobutamine aggravates haemodynamic deterioration induced by pleural effusion: a randomised controlled porcine study. Eur J Anaesthesiol
3. Sloth E. Inotropic support with little physiological rationale. Acta Anaesthesiol Scand
4. Jensen MB, Sloth E, Larsen KM, et al. Transthoracic echocardiography for cardiopulmonary monitoring in intensive care. Eur J Anaesthesiol
5. Wemmelund KB, Lie RH, Juhl-Olsen P, et al. Pleural effusion decreases left ventricular preload and causes haemodynamic compromise: an experimental porcine study. Acta Anaesthesiol Scand