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Major factors influencing cardiac output – heart rate and stroke volume, both of which are variable. [1]In cardiac physiology, cardiac output (CO), also known as heart output and often denoted by the symbols , ˙, or ˙, [2] is the volumetric flow rate of the heart's pumping output: that is, the volume of blood being pumped by a single ventricle of the heart, per unit time (usually measured ...
Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.
The transportation of large amounts of blood to and from the lungs to reach all bodily tissues depends on a high cardiac output and sufficient levels of total body hemoglobin. Hemoglobin is the oxygen carrying protein within blood cells that transports oxygen from the lungs to other bodily tissues via the circulatory system . [ 9 ]
The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, [2] without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality. [1] [3]
In a normal circulatory system, the volume of blood returning to the heart each minute is approximately equal to the volume that is pumped out each minute (the cardiac output). [12] Because of this, the velocity of blood flow across each level of the circulatory system is primarily determined by the total cross-sectional area of that level.
The cardiovascular system responds to changing demands on the body by adjusting cardiac output, blood flow, and blood pressure. Cardiac output is defined as the product of heart rate and stroke volume which represents the volume of blood being pumped by the heart each minute. Cardiac output increases during physical activity due to an increase ...
This leads to a decrease in stroke volume by the Frank–Starling mechanism and a fall in cardiac output and aortic pressure. This reduction in afterload (in particular, aortic diastolic pressure) enables the end-systolic volume to decrease slightly but not enough to overcome the decline in end-diastolic volume.
Note that, for cardiac function curve, "central venous pressure" is the independent variable and "systemic flow" is the dependent variable; for vascular function curve, the opposite is true. It shows a steep relationship at relatively low filling pressures and a plateau, where further stretch is not possible and so increases in pressure have ...