In a recent review article in the journal, Professor Magder and colleagues invite us to abandon some of the most entrenched words in our hemodynamic vocabulary.1 Rather than explaining cardiac preload, afterload, and contractility with ever more precise definitions, they argue that these terms are fundamentally misleading when applied to the ejecting ventricle. The convincing arguments come from the fact that the classical descriptions of these vital indices come from the physiology of skeletal muscles. The heart, and especially both ventricles, is not a muscle whose function is to shorten in a manner controlled by the central nervous system to provide intermittent, and sometimes prolonged, effort, but a pump that must pressurize its cavity intermittently. The alternative proposed by the authors is a model built explicitly on time-varying elastance: contractility becomes end-systolic elastance (EES), stroke volume is governed by end-diastolic volume, and “afterload” is replaced by an ejection threshold load corresponding to aortic or pulmonary diastolic pressure.1 This review is well worth reading. First, because the senior authors share their extensive expertise, honed over time. Second, by presenting their perspective, the authors remind us of the animal and clinical studies that have shaped the history of cardiovascular physiology. And finally, because this changes the way we view the effect of the most common therapeutic interventions we perform every day. The clinical implications in shock resuscitation are substantial. Fluids should be judged by their effect on stroke volume, because they can only exert an ultimate benefit on tissue perfusion if they have increased cardiac output. Yet, one should bear in mind that rising right atrial pressure with minimal output gain signals that the right ventricle has reached its filling limit. Central venous pressure must be a safety variable we consider when building our fluid strategy. Vasopressors must be titrated with an explicit awareness that increasing diastolic pressure raises the threshold load, i.e., it shortens the time available for ejection on the elastance trajectory, and can thus decrease stroke volume, particularly when EES is depressed. Inotropes are best understood as agents that steepen EES, increasing the maximal pressure attainable for a given end-diastolic volume, rather than nonspecific boosters of “contractility.” Perhaps most importantly, by reframing cardiac output as fundamentally constrained by right-ventricular EES, end-diastolic volume, and pulmonary artery diastolic pressure, the authors offer a coherent physiological lens through which to interpret echocardiography and invasive monitoring in the sickest shock patients. Conflicts of interest Prof. Xavier MONNET has received honoraria for consultancy from Pulsion Medical Systems (Getinge), BD, Masimo and Baxter Healthcare. He has received honoraria for giving lectures from AOP health, Pulsion Medical Systems (Getinge), Edwards Lifesciences, BD, Philips, Masimo and Baxter Healthcare.
Xavier Monnet (Sun,) studied this question.