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* Cardiac output is a function of the interplay of multiple physiologic parameters. Stroke volume is influenced in a predictable order: 1. Preload first influences contractility. 2. The combined effect of preload and contractility then influences the afterload response. 3. Only after the stroke volume is established does the heart rate respond to adjust the final cardiac output. * Preload can be simply stated as the volume stretching the ventricular muscle prior to ejection. Afterload is the resistance to flow from the circulatory system. * Implications of Starling’s Law: The heart is a demand pump: within limits, it pumps whatever volume of blood is delivered to it. The heart normally functions on the ascending limb of the Frank-Starling relationship. So there is an enough cardiac reserve. There is no drop limb, indicating the difference from skeletal muscle. The high tension resists further extending of the sareomere----connectin or titin Mechanism: The increased force of contraction is probably caused by the fact that the actin and myosin filaments are brought to a more nearly optimal degree of interdigitation for achieving contraction. The tension of the cardiac muscle at the optimal length ( 2.0-2.2μm ) of sarcomere is higher than that of the skeletal muscle. The high tension resists further extending of the sareomere. So the force of muscle contraction can not be decreased, hence no drop limb of the curve. The affinity of the troponin for calcium are length-depended Factors determining the preload (LVEDP) Period of the ventricle diastole (filling) – heart rate Speed of the venous return (difference between the venous pressure and atrial pressure) Importance of the heterometeric regulation In general, heterometric regulation plays only a short-time role, such as during the body posture change, artery pressure increase, and unbalance of ventricular outputs. In other conditions, such as exercise, cardiac output is mainly regulated by ho
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