Cardiac output (CO) is stroke volume (SV) × heart rate (HR), and at rest ∼5 L/min; during strenuous exercise this can rise to >25 L/min. SV is influenced by the filling pressure (preload), cardiac muscle force, and pressure against which the heart has to pump (afterload), which are all modulated by the autonomic nervous system (ANS) (Figure 17a). The heart and vasculature are in series and interdependent; except for transient differences venous return must equal CO.
Ventricular Function Curves
The volume of blood in the ventricle at the start of systole (end-diastolic volume, EDV) depends on the end-diastolic pressure (EDP) and compliance of the ventricular wall (how easy it is to inflate). Right ventricular (RV) EDP is dependent on right atrial and thus central venous pressure (CVP). If EDP (and so EDV) is increased, the force of the following contraction, and thus SV, increases (Figure 17b). This is known as the Frank–Starling relationship, and the graph relating SV to EDP is the ventricular function curve. The force of contraction is dependent on muscle stretch, and Starling’s law of the heart states ‘The energy released during contraction depends on the initial fibre length.’
As muscle is stretched, more myosin crossbridges can form, increasing force. Cardiac muscle has a steeper relationship between stretch and force than skeletal muscle, because in the heart stretch also increases Ca2+ binding to troponin C (see Chapter 12). The function curve is therefore steep, so small changes in EDP can lead to large increases in SV and CO (Figure 17b).
Role of Starling’s Law
The most important consequence of Starling’s law is that output is matched between right and left ventricles
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