© 2003 European Society of Cardiology
Ventriculo–arterial function curves—a new dimension in characterising acute heart failure
Academic Unit of Molecular Vascular Medicine, Martin Wing University of Leeds, Leeds General Infirmary, Leeds LS1 3EX, UK
Starling's law of the heart was formulated at the beginning of the 20th century and formally stated in his famous lecture in 1915 [1]. It did not produce any clinical impact until the middle of the 20th century when Sarnoff and Berglund [2] introduced the concept of ‘ventricular function curves’. In these graphs, each of the curves not only relates changes in ventricular performance to preload, but through a family of similar curves also depict changes in myocardial ‘contractility’ [3]. This framework has remained the mainstay of haemodynamic evaluation and management of acute circulatory failure in coronary and intensive care units worldwide. Its versatility allows the clinician to use their individual preferred parameters to represent the variables on the two axes, such that nowadays, the x-axis is usually represented by pulmonary artery wedge pressure while the y-axis by stroke work index, cardiac output or index, or stroke volume. In practice, it is relatively inconsequential which combinations of parameters are used.
Cardiac physiological research then took a very different path, as the ventricular function curves gave rise to a notion that there might be an ‘index of contractility’ that was totally independent of ventricular loading conditions, especially preload and afterload, but intrinsically indicative of myocardial contractility. This index would then obviate the need to think in terms of two-dimensional graphs depicting the family of curves. The utopian aim was that clinicians would only need to handle a one-dimensional variable, instead of having to work out where the prevailing cardiac functional state of the patient was in relation to a family of known ‘ventricular function curves’ in a two-dimensional graph. Though laudable as a wishful ideal, these attempts to search for such an ideal ‘index of contractility’ were misguided and clinically ineffectual. Perhaps because of this wrong turn in physiological history, it has taken a further half century for the concept of ventricular function curves to be extended to involve not just the preload, but also the afterload. The paper by Cotter et al. in this issue (pages xx–xx) exemplifies the need for such a consideration, especially in the management of acute heart failure [4].
If it were possible to fine-tune and fix the various ‘settings’ of ventricular performance at a certain constant state—at a predetermined chronotropic, inotropic, lusitropic, dromotropic state, as if dealing with an isolated heart (with fixed-rate pacing and absent autonomic influences), which is still connected to the vasculature that is also devoid of autonomic influences—then as the preload is altered, the performance of the heart will be described by a line depicted by one of the curves in the Starling's ‘ventricular function curves’ [2]. At a different ‘setting’, such as after lowering contractility, the performance will be along a lower curve, and similarly along a higher curve if the contractility is augmented.
When the preload is held constant instead, and the afterload is varied, the performance of the heart will be described by a line in a different family of curves, which we can refer to as ‘ventriculo–arterial function curves’ (VAFCs). The axes on this graph are represented by an indicator of ventricular performance along the y-axis and systemic vascular impedance along the x-axis. In this case, which variable should be selected to represent ventricular performance is of crucial importance. It will have to comply with one important criterion, and that is, at infinite impedance (e.g. ascending aorta clamped during surgery) and zero impedance (heart ejecting into air), when there is no effective perfusion of blood into the vasculature, the parameter representing cardiac performance will have to indicate zero. This effectively rules out cardiac output, stroke volume and any of the so-called ‘indices of contractility’ because they attain peak values at zero impedance. An obvious variable would be one that is a mathematical function containing the product of cardiac flow output and arterial perfusion pressure. Such a term will be zero at both infinite and zero vascular impedance. In other words, the variable should contain the term hydraulic energy output of the heart either expressed per unit time (e.g. per second in ‘power output’ [5,6] or per minute as in ‘minute-work’ [7]), or per heart beat as in ‘stroke work index’ [8,9].
Representation of the x-axis is more straightforward. Aortic input impedance is the best representation of systemic afterload to cardiac pump as a whole [10]. However, since impedance is a complex mathematical term (with real and imaginary components) and since the resistive (real) term usually predominates, in everyday cardiological practice, it is sufficient to approximate and use vascular resistance to represent the x-axis. The family of VAFCs would appear as shown in Fig. 1. Wilcken et al. [11] were the first to show that a normal left ventricle normally functions at the operating point which is at the zenith of the normal VAFC. During exercise, as positive chronotropic and inotropic effects are activated, the heart functions along higher VAFCs.
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Put in this context, the results of Cotter et al. [4] not only provide a way of categorising the subclasses of acute heart failure patients, but also a deeper understanding of the pathophysiological processes involved, which therefore would lead to a more rational approach to treatment. Once the body surface areas of individual patients are available, the operating points of their patients’ hearts in Cotter's Figure 5 can then be superimposed on the VAFCs in Fig. 1. It is immediately apparent that the operating points of the subgroups of Cotter's patients cluster in different regions of the families of VAFCs. The normal control subjects tend to be in the region of Wilcken's optimal operating points for normal circulations [11]. As suggested from animal experiments [12,13] and consistent with previous descriptions in humans [14,15], patients with heart failure tend to have operating points in regions with higher systemic vascular resistances than in normals, with some cardiogenic shock patients having the most vasoconstricted systemic arterial system (Fig. 1B). The cardiogenic shock patients, more than the chronic heart failure population, have cardiac function in the more depressed VAFCs. The septicaemic shock patients operate in the region of low systemic resistances whereas the hypertensive crisis and pulmonary oedema patients in vasoconstrictive states and all of them with augmented cardiac performances (Fig. 1C). One objective of treatment becomes apparent, and that is to optimise the systemic vascular resistances, and in doing so, the cardiac performances can actually be moved away from disadvantageous vascular tones towards more optimal loading conditions to effect greater hydraulic power output into the circulation [14]. More research in this area is required and will no doubt lead to enhanced management of heart failure patients.
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