FIG 65.2 Left, Temporal changes in the volume of the left ventricle (LV), the pressures within the left atrium (LA), and the left ventricle and aorta during the cardiac cycle The onset of the isovolumic contraction time begins at I, when the pressure in the ventricle exceeds that within the atrium This period ends at II, with the onset of ejection as the pressure within the ventricle exceeds that in the aorta The period of isovolumic relaxation begins at III, when the pressure in the left ventricle falls below that in the aorta Filling of the ventricle begins at IV, when ventricular pressure falls below that in the atrium Right, Instantaneous relationship between the pressure and volume in the ventricle, with the time points represented as I to IV corresponding to the same events as those at left Diastole is traditionally assumed to begin with closure of the aortic valve; however, the decay in ventricular pressure (relaxation) begins before this event After aortic valve closure, ventricular pressure continues to decay rapidly―an energy-requiring mechanism―together with the passive release of myocardial elastic forces generated during contraction As the ventricular pressure continues to decay, the mitral valve initially remains closed The period of relaxation during which ventricular volume remains constant is termed isovolumic relaxation When ventricular pressure falls below atrial pressure, the mitral valve opens and ventricular filling begins During the early period of ventricular filling, the ventricle's pressure falls This anomalous relationship between pressure and volume is thought to result from restorative forces, which attempt to restore the shape of the ventricle to that at end-diastole After this time, both pressure and volume increase in the ventricle, which exhibits elastic behavior Later in diastole the rate of ventricular filling is further augmented by atrial contraction Examination of Cardiac Function With the Pressure-Volume Loop Up to this point, we have considered the temporal changes in left ventricular pressure and volume; however, the essence of the pressure-volume analysis is to consider the relationship between ventricular pressure and volume, represented by the pressure-volume loop The latter has four characteristic phases Beginning at the bottom right hand corner (I to II in Fig 65.2), an initial upstroke represents the rapid increase in ventricular pressure, with little volume change; this is isovolumic contraction There is then a rapid fall in ventricular volume as ventricular ejection proceeds to the end-systolic point (II to III) Ventricular pressure then rapidly falls, with little volume change, as the ventricle enters the isovolumic relaxation phase (III to IV) Finally, ventricular volume increases to its end-diastolic level, reflecting ventricular filling (IV to I) Suga noted that at a constant inotropic state, alterations in ventricular load resulted in a population of pressure-volume loops in which, at any time in the cardiac cycle, the pressure-volume points follow a straight line It was proposed, therefore, that cardiac contraction could be modeled as a time-varying elastance, with maximal elastance occurring at end-systole (end-systolic elastance),9 represented by the upper left-hand corner of the pressure-volume loop (Fig 65.3) FIG 65.3 Left, Changes in left ventricular (LV) pressure, volume, and rate of change of pressure (dP/dt) recorded with a conductance catheter during caval occlusion Right, Series of pressure-volume loops is generated, with a linear relationship between pressure and volume at end-systole While the end-systolic pressure-volume relationship has been considered the definitive measure of ventricular contractility, the importance of other indices should not be underestimated It is important to emphasize that there is no single gold-standard measure, which will encompass the complex physiologic processes that determine myocardial contractility, rather, there are a number of measures, each of which provides individual pieces of a complex jigsaw It must be appreciated that the pressure-volume relationship provides a wealth of information about cardiovascular physiology beyond end-systolic elastance The intricate coupling between the ventricle and the vasculature is an extremely important clinical determinant of cardiovascular function Although many treatments for heart failure are aimed at augmenting ventricular systolic performance, it is clear that without the ability of the vasculature to convert within itself the increased pressure work of the ventricle into flow work, these therapeutic strategies would be of little benefit One measure of the efficiency of ventriculovascular coupling, based on an examination of the pressure-volume relationship, examines the coupling between end-systolic elastance and arterial elastance12 to illustrate how the arterial response determines the physiologic