Cardiac adaptation to changes in heart rate also involves alterations in ventricular volume. For instance, during bradycardia, the extended duration of diastole permits greater ventricular filling, leading to an increase in stroke volume. As a result, the decrease in heart rate can be fully compensated by the rise in stroke volume, thereby maintaining constant cardiac output.

When the heart compensates through ventricular dilation, it is important to consider the impact of the increased ventricle size on intraventricular pressure generation. According to Laplace's relationship, if the ventricle enlarges, each myocardial fiber must exert a significantly greater force to produce a specific intraventricular systolic pressure compared to fibers in a normal-sized ventricle. Consequently, a dilated heart requires more energy to perform the same amount of external work as a heart of normal size. Therefore, when calculating afterload on contracting myocardial fibers in the ventricular walls, both ventricular dimensions and intraventricular (and aortic) pressure must be taken into account.

The relatively inflexible pericardium, which encloses the heart, determines the pressure-volume relationship at high pressure and volume levels. Even under normal conditions when an individual is at rest with a slow heart rate, the pericardium limits heart volume. However, in patients with chronic congestive heart failure, the sustained cardiac dilation and hypertrophy can significantly stretch the pericardium. Consequently, the pericardial limitation on cardiac filling is exerted at different pressures and volumes compared to those in normal individuals.

To evaluate changes in ventricular performance, the Frank-Starling mechanism is often represented by a family of ventricular function curves. For instance, a control ventricular function curve is constructed by altering blood volume across a range of values and measuring stroke work (i.e., stroke volume × mean arterial pressure) and end-diastolic ventricular pressure at each step. Similar observations are then made during the desired experimental intervention. For example, the ventricular function curve obtained during the infusion of norepinephrine is positioned above and to the left of the control ventricular function curve (Fig. 18.12). Clearly, for a given level of left ventricular end-diastolic pressure (an index of preload), the left ventricle performs more work during the norepinephrine infusion compared to control conditions. Thus, the upward and leftward shift of the ventricular function curve indicates improved ventricular contractility. Conversely, a downward and rightward shift signifies impaired contractility and a tendency towards cardiac failure.

The Frank-Starling mechanism is well-suited for matching cardiac output to venous return. If one ventricle suddenly produces excessive output, it soon results in an increase in venous return to the other ventricle. This leads to an augmentation in diastolic fiber length in the second ventricle, matching its output to that of the first ventricle. In this manner, the Frank-Starling mechanism maintains a precise balance between the outputs of the right and left ventricles. If the two ventricles were not arranged in series in a closed circuit, even a small but sustained imbalance in their outputs would have catastrophic consequences.

The curves that illustrate the relationship between cardiac output and mean atrial pressure for the two ventricles do not coincide; the curve for the left ventricle typically lies below that for the right ventricle (Fig. 18.13). When right and left atrial pressures are equal.
Cardiac adaptation to alterations in heart rate also involves changes in ventricular volume. During bradycardia, for example, the increased duration of diastole allows greater ventricular filling. The consequent increase in myocardial fiber length increases stroke volume. Therefore, the reduction in heart rate may be fully compensated by the increase in stroke volume, and cardiac output may therefore remain constant.
When cardiac compensation involves ventricular dilation, the effect of the increased size of the ventricle on the generation of intraventricular pressure must be considered. According to Laplace’s relationship (see
Chapter 17), if the ventricle enlarges, the force required by each myocardial fiber to generate a given intraventricular systolic pressure must be appreciably greater than that developed by the fibers in a ventricle of normal size. Thus more energy is required for a dilated heart to perform a given amount of external work than for a normal-sized heart to do so. Hence, computation of afterload on contracting myocardial fibers in the walls of the ventricles must account for ventricular dimensions along with intraventricular (and aortic) pressure.
The relatively rigid pericardium that encloses the heart determines the pressure-volume relationship at high levels of pressure and volume. The pericardium limits heart volume even under normal conditions, when an individual is at rest and the heart rate is slow. In patients with chronic congestive heart failure, the sustained cardiac dilation and hypertrophy may stretch the pericardium considerably. In such patients, the pericardial limitation of cardiac filling is exerted at pressures and volumes entirely different from those in normal individuals.
To assess changes in ventricular performance, the Frank-Starling mechanism is often represented by a family of ventricular function curves. To construct a control ventricular function curve, for example, blood volume is altered over a range of values, and stroke work (i.e., stroke volume × mean arterial pressure) and end-diastolic ventricular pressure are measured at each step. Similar observations are then made during the desired experimental intervention. For example, the ventricular function curve obtained during infusion of norepinephrine lies above and to the left of the control ventricular function curve (
Fig. 18.12). Clearly, for a given level of left ventricular end-diastolic pressure (an index of preload), the left ventricle performs more work during the norepinephrine infusion than during control conditions. Hence, the upward and leftward shift of the ventricular function curve signifies improved ventricular contractility. Conversely, a shift downward and to the right indicates impaired contractility and a tendency toward cardiac failure.
The Frank-Starling mechanism is well suited to match cardiac output to venous return. Any sudden, excessive output by one ventricle soon causes an increase in venous return to the second ventricle. The consequent increase in diastolic fiber length in the second ventricle augments the output of that ventricle to correspond to the output of its mate. In this way, the Frank-Starling mechanism maintains a precise balance between the output of the right and left ventricles. If the two ventricles were not arranged in series in a closed circuit, any small but maintained imbalance in output of the two ventricles would be catastrophic.
•Fig. 18.12 Aconstantinfusionofnorepinephrineshiftstheventricu-larfunctioncurveupandtotheleft.Thisshiftsignifiesanenhancementinventricularcontractility.(RedrawnfromSarnoffSJ,etal.Circ Res. 1960;8:1108.)0 5 10 15 20 25 30 35 40 Norepinephrine Control 0 10 20 30 40 50 60 Left ventricular end-diastolic pressure (cm H2O) Left ventricular stroke work (g•m)
The curves that relate cardiac output to mean atrial pressure for the two ventricles do not coincide; the curve for the left ventricle usually lies below that for the right ventricle (
Fig. 18.13). At equal right and left atrial pressures