Each time the heart pumps, it ejects a certain volume of blood, termed the stroke volume (SV). Since it is simple to assess the heart rate (HR), physiologists have defined a measurement called “”cardiac output”” (CO) that takes into account both of these factors in the equation:
CO = SV x HR
Heart rate is controlled by the sinoatrial (SA) node, an electrical pacemaker located in the back of wall of the right atrium. The primary input to the SA node is the vagus nerve, a carrier of parasympathetic nerve fibers that, when stimulated, acts to slow the heart rate. There are also sympathetic nerves and receptors that respond to the sympathetic nervous system or to circulating catecholamines (e.g. epinephrine/adrenaline) that can act to increase the heart rate.
Systole refers to the time during which the heart is contracting. Diastole refers to the time at which the heart is at rest. SV is determined by calculating the end diastolic volume (EDV, the volume at the end of diastole, just before systole) and subtracting the end systolic volume (ESV, the volume left after contraction). Or:
SV = EDV – ESV
There are three main factors that determine SV.
1. Preload – the initial stretching of heart muscle (myocytes) prior to contraction. Myocytes of the ventricles will stretch when they fill with blood, so anything that increases ventricular filling will increase preload. Increasing preload increases EDV.
2. Afterload – the pressure that the left ventricle must overcome to pump blood out the aorta. For instance, high blood pressure will increase afterload, which will increase ESV (and decrease SV).
3. Contractility – if the heart muscle physically pushes harder, it will pump more blood per beat, decreasing ESV. Contractility (or inotropy) increases with sympathetic activation, and it is also proportional to calcium concentration.
Note that increasing HR increases CO, but decreases SV. The relationship between the three is shown below (the Y-axis shows relative magnitude as an arbitrary percent):
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