Stroke volume increases as cardiac filling increases.

"Cardiac filling" refers to the process of the heart (specifically the ventricles) filling with blood during diastole (the relaxation phase of the cardiac cycle).

Cardiac filling determines end-diastolic volume, which is a major determinant of stroke volume. More filling (to a physiological point) leads to a greater stroke volume, enhancing cardiac output.

Better cardiac filling → higher EDV → higher stroke volume, assuming ESV remains constant.

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The stroke volume is determined by three parameters: (1) contractility, (2) preload, and (3) afterload.

Contractility is the amount of force exerted at a given muscle fiber length.

Preload is defined as the ventricular wall tension at the end of diastole and is quantified by the left ventricular end-diastolic pressure (LVEDP).

Afterload is the ventricular wall tension during systole and is determined by the mean arterial pressure. 

🔍 Key Concepts:

1. Preload:

   • Refers to the degree of stretch of the heart muscle before contraction, which is directly related to cardiac filling.

   • Higher preload (better filling) enhances stroke volume via the Frank-Starling mechanism.

2. Diastolic Function:

   • Efficient filling requires good diastolic relaxation.

   • In diastolic dysfunction (e.g., in stiff ventricles), filling is impaired, potentially lowering stroke volume even if systolic function is preserved.

3. Venous Return:

   • The amount of blood returning to the heart impacts filling.

   • Low venous return (e.g., hypovolemia) decreases filling and stroke volume.

Figure 3–4A illustrates how increasing muscle preload will increase the extent of shortening during a subsequent contraction with a fixed total load.

Recall from the nature of the resting length–tension relationship that an increased preload is necessarily accompanied by increased initial muscle fiber length.

When a muscle starts from a greater length, it has more distance to shorten before it reaches the length at which its tension-generating capability is no longer greater than the load on it. The same behavior is exhibited by cardiac muscle cells when they are actually operating in the ventricular wall. Increased ventricular preload (i.e., diastolic filling) increases both end-diastolic volume and stroke volume almost equally, as illustrated in Figure 3–4B.

The precise relationship between cardiac diastolic filling pressure and end-diastolic volume has especially important physiological and clinical consequences. Although the actual relationship is somewhat curvilinear, especially at very high filling pressures, it is nearly linear over the normal operating range of the normal heart. The low slope of this relationship indicates the substantial compliance of the normal ventricle during diastole (e.g., a change in filling pressure of only 1 mm Hg normally will change end-diastolic volume by approximately 25 mL). As will be discussed in Chapter 11, one major form of cardiac failure is called “diastolic failure” and is characterized by a low ventricular compliance and a decidedly abnormal relationship between cardiac filling pressure and end-diastolic volume. 4

It should be noted in Figure 3–4A that increasing preload increases initial muscle length without significantly changing the final length to which the muscle shortens against a constant total load. Thus, increasing ventricular filling pressure increases stroke volume, primarily by increasing end-diastolic volume. As shown in Figure 3–4B, this is not accompanied by a significant alteration in end-systolic volume.

Effect of Changes in Ventricular Afterload

As stated previously, systemic arterial pressure is usually taken to be the left ventricular “afterload.” A slight complication is that arterial pressure varies between a diastolic value and a systolic value during each cardiac ejection. Usually, however, we are interested in mean ventricular afterload and take this to be mean arterial pressure.

 Figure 3–5A shows how increased afterload, at constant preload, has a negative effect on cardiac muscle cell shortening. Again, this is simply a consequence of the fact that muscle cannot shorten beyond the length at which its peak isometric tension-generating potential equals the total load on it. Thus, shortening must stop at a greater muscle length when afterload is increased.

Normally, mean ventricular afterload is quite constant because mean arterial pressure is held within tight limits by the cardiovascular control mechanisms described later. In many pathological situations such as hypertension and aortic valve obstruction, however, ventricular function is adversely influenced by abnormally high ventricular afterload. When this occurs, stroke volume may be decreased, as shown by the changes in the pressure–volume loop in Figure 3–5B. Under these conditions, note that stroke volume is decreased because end-systolic volume is increased.

The relationship between end-systolic pressure and end-systolic volume obtained at a constant preload but different afterloads is indicated by the dotted line in Figure 3–5B. In a normally functioning heart, the effect of changes in afterload on end-systolic volume (and therefore stroke volume) is quite small (approximately 0.5 mL/mm Hg). However, in what is termed “systolic cardiac failure,” the effect of changes in afterload on end-systolic volume is greatly exaggerated such that a small increase in arterial pressure can significantly reduce stroke volume. Thus, the slope of this line can be used clinically to assess the systolic function of the heart, as discussed further in Chapter 11.

Effect of Changes in Cardiac Muscle Contractility

Recall that activation of the sympathetic nervous system results in release of norepinephrine from cardiac sympathetic nerves, which increases contractility of the individual cardiac muscle cells. This results in an upward shift of the peak isometric length–tension curve. As shown in Figure 3–6A, such a shift will result in an increase in the shortening of a muscle contracting with constant preload and total load. Thus, as shown in Figure 3–6B, the norepinephrine released by sympathetic nerve stimulation will increase ventricular stroke volume by decreasing the end-systolic volume, without directly influencing the end-diastolic volume.

The term ejection fraction is a clinically useful variable used to assess cardiac muscle contractility. It is the fraction of the blood in the ventricle at the end of diastole that is ejected during systole. It is defined as the ratio of stroke volume (SV) to end-diastolic volume (EDV):

Because increased myocardial contractility causes an increase in ventricular ejection fraction, measurements of ejection fraction are often used clinically to assess the state of myocardial contractility. 5

In addition to this change in the extent of myocyte shortening, an increase in contractility will also cause an increase in the rates of myocyte tension development and of shortening. This will result in an increase in the rate of isovolumetric pressure development and the rate of ejection during systole.

SUMMARY OF DETERMINANTS OF CARDIAC OUTPUT