Cardiac output is the product of stroke volume and heart rate. Both are under the control of the sympathetic nervous system. Stroke volume is also affected by changes in preload, contractility and afterload, and their interaction. This chapter will deal with preload and afterload only. For the effect of contractility on cardiac performance, see chapter Cardiac cycle: pressure–volume relationships. Venous return (preload) depends on blood volume, posture and venous tone. Venous tone is under the control of the sympathetic nervous system. Sympathetic output changes in response to the peripheral metabolic need.

Figure 90 shows the Frank–Starling relationship between the left ventricular end-diastolic pressure (LVEDP) and stroke volume (SV). The Frank–Starling curve mechanism allows a ventricle to match its output (stroke volume) to the volume of blood that enters it (the preload).

On the x-axis, end diastolic pressure is substituted for fibre length, and on the y-axis stroke volume is substituted for force of contraction (fibre length and force of contraction were the variables used in the original research on isolated muscle fibre). In practice, we use surrogate parameters that can be directly measured and make assumptions which are valid under normal physiological conditions, the assumption being that LVEDV (left ventricular end diastolic volume) ∼ LVEDP = LAP (left atrial pressure) = PAOP (pulmonary artery occlusion pressure). The relationship between LVEDP and SV is linear up to a certain unphysiological point. After that, the mechanism fails (in the original research this happened because of fibre disruption).