The systolic pressure gradually increases until it reaches its maximum at the optimal preload. However, if diastolic filling continues beyond this point, the pressure development during systole will no longer increase. In fact, at very high filling pressures, peak pressure development in systole is actually reduced.

When the preload is constant, a higher systolic pressure can be achieved during ventricular contractions by increasing the afterload. This can be done by increasing the aortic pressure and restricting the runoff of arterial blood to the periphery. Incremental increases in afterload result in progressively higher peak systolic pressures. However, if the afterload continues to increase, the ventricle will be unable to generate enough force to open the aortic valve. This leads to a state of ventricular systole where no blood is ejected and no change in ventricular volume occurs. The maximum pressure that the left ventricle can generate under these conditions is the maximal isometric force at a given preload. It is important to note that at preloads below the optimal filling volume, an increase in preload can result in greater maximal isometric force.

Preload and afterload are influenced by various characteristics of the vascular system and the behavior of the heart. Factors such as venomotor tone and peripheral resistance affect preload and afterload. Additionally, changes in heart rate or stroke volume can also alter these parameters. Therefore, cardiac and vascular factors interact with each other to affect preload and afterload.

Contractility refers to the cardiac performance at a specific preload and afterload. It determines the change in peak isometric force (isovolumic pressure) at a given initial fiber length (end-diastolic volume). Contractility can be enhanced by drugs like norepinephrine or digitalis, or by increasing contraction frequency (tachycardia). These interventions result in incremental increases in the force developed and the velocity of contraction, indicating a positive inotropic effect.

A reliable index of myocardial contractility can be obtained from the contour of ventricular pressure curves. A hypodynamic heart is characterized by elevated end-diastolic pressure, slowly rising ventricular pressure, and a somewhat reduced ejection phase. On the other hand, a hyperdynamic heart is characterized by reduced end-diastolic pressure, fast-rising ventricular pressure, and a brief ejection phase. The slope of the ascending limb of the ventricular pressure curve indicates the maximum rate of force development by the ventricle. The maximal rate of change in pressure with time, known as maximum dP/dt, can be determined by the tangents to the steepest portion of the ascending limbs of the ventricular pressure curves. The slope of the ascending limb is highest during the isovolumic phase of systole and serves as an index of the initial contraction velocity and contractility.

Similarly, the contractile state of the myocardium can be calculated from the initial velocity of blood flow in the ascending aorta during the cardiac cycle.
Fig. 16.36 ). Systolic pressure increases until a maximal systolic pressure is reached at the optimal preload (see
Fig. 16.36 ). If diastolic filling continues beyond this point, the pressure developed will no longer increase. At very high filling pressures, peak pressure development in systole is actually reduced.
At a constant preload, higher systolic pressure can be reached during ventricular contractions by an increase in the afterload (e.g., increasing aortic pressure by restricting the runoff of arterial blood to the periphery). Incremental increases in afterload produce progressively higher peak systolic pressures. However, if the afterload continues to increase, it becomes so great that the ventricle can no longer generate enough force to open the aortic valve. At this point, ventricular systole is totally isometric (i.e., there is no ejection of blood), and thus no change occurs in ventricular volume during systole. The maximal pressure developed by the left ventricle under these conditions is the maximal isometric force that the ventricle is capable of generating at a given preload. At preloads below the optimal filling volume, an increase in preload can yield greater maximal isometric force (see
Fig. 16.36
Preload and afterload depend on certain characteristics of the vascular system and the behavior of the heart. With regard to the vasculature, the degree of venomotor tone and peripheral resistance influences preload and afterload. With regard to the heart, a change in rate or stroke volume can also alter preload and afterload. Hence, cardiac and •Fig. 16.37 Preload and Afterload in a Papillary Muscle. A, Restingstage(noload)intheintactheartjustbeforeopeningoftheAVvalves.B, Preload(PL)intheintactheartattheendofventricularfilling.C, Supportedpreloadplusafterload(AL)intheintactheartjustbeforeopeningoftheaorticvalve.D, Liftingpreloadplusafterloadintheintactheartduringventricularejection,withadecreaseinventricularvolume.PL+ AL,totalload.
vascular factors interact with each other to affect preload and afterload (see
Contractility defines cardiac performance at a given preload and afterload. Contractility determines the change in peak isometric force (isovolumic pressure) at a given initial fiber length (end-diastolic volume). Contractility can be augmented by drugs, such as norepinephrine or digitalis, or by an increase in contraction frequency (tachycardia). The increase in contractility (positive inotropic effect) produced by these interventions is reflected by incremental increases in the force developed and in the velocity of contraction.
Indices of Contractility
A reasonable index of myocardial contractility can be derived from the contour of ventricular pressure curves (
Fig. 16.38 ). A hypodynamic heart is characterized by elevated end-diastolic pressure, slowly rising ventricular pressure, and a somewhat reduced ejection phase (curve C in
Fig. 16.38 ). A hyperdynamic heart (curve B in
Fig.
16.38 ) is characterized by reduced end-diastolic pressure, fast-rising ventricular pressure, and a brief ejection phase. The slope of the ascending limb of the ventricular pressure curve indicates the maximal rate of force development by the ventricle. The maximal rate of change in pressure with time—that is, the maximum dP/dt—is illustrated by the tangents to the steepest portion of the ascending limbs of the ventricular pressure curves in
Fig. 16.38 . The slope of the ascending limb is maximal during the isovolumic phase of systole (see
Fig. 16.38 ). At any given degree of ventricular filling, the slope provides an index of the initial contraction velocity and hence an index of contractility.
Similarly, the contractile state of the myocardium can be calculated from the velocity of blood flow that occurs initially in the ascending aorta during the cardiac cycle (
Fig.