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Quick Review: Hemodynamics

机译：快速回顾：血液动力学

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Before discussing basic hemodynamics, we should remind ourselves of the systemic circuit: 1. Cardiac Anatomy2. Circulatory PathwaysThis brief review discusses the basics of hemodynamics. Cardiac Anatomy The Heart: 2 Separate Volume Pumps !The in-series nature of these two systems implies that the output of the Right Heart becomes the input of the Left Heart, and therefore, the output of the Left Heart becomes the input of the Right Heart Flow via Series: Demonstrated by William Harvey, 1628 Desaturated Blood returns from the Systemic Vessels via the SVC & IVC Saturated Blood is then returned to the Left Atrium via the Pulmonary Veins ! Myocardial Perfusion occurs primarily during Diastole Myocardial Blood Flow: Myocyte Contraction At the cellular level, electrical depolarization of the myocardial cell membrane allows ionized calcium flux into the cytoplasm - leading to hydrolysis of ATP by Myosin.This leads to a conformational change in the Actin-Myosin Cross Bridge producing sliding of myosin filaments relative to actin & overall shortening of the sarcomere [Sliding Filament Theory] Calcium is then removed from the cell by Active Transport in the Sarcoplasmic Reticulum - allowing Relaxation, while ATP is regenerated by Metabolic Processes Over the physiologic range of sarcomere length (1.6 - 2.0 um), the amount of metabolic energy converted to mechanical work is dependent on the available Surface Area of Cross-Bridge Interactions !Work is directly proportional to End-Diastolic Sarcomere LengthThis “Length Dependency” is the fundamental basis for the Frank-Starling Law ! Otto Frank, 1885 (Frog Heart Preparations): “the output of a normal heart is influenced primarily by the volume of blood in the ventricle at the end of diastole”
机译：在讨论基本的血液动力学之前，我们应该提醒自己全身循环：1.心脏解剖2。循环通路这篇简短的评论讨论了血液动力学的基本原理。心脏解剖心脏：2个独立的容积泵！这两个系统的串联性质意味着右心的输出成为左心的输入，因此，左心的输出成为右心的输入经系列的心流：由威廉·哈维（William Harvey）演示，1628饱和血通过SVC和IVC从全身血管返回，然后，饱和血通过肺静脉回流到左心房！心肌灌注主要发生在舒张期心肌血流过程中：心肌细胞收缩在细胞水平，心肌细胞膜的电去极化使离子钙流进入细胞质，导致肌球蛋白水解ATP，从而导致肌动蛋白构象改变。肌球蛋白跨桥产生肌球蛋白丝相对于肌动蛋白的滑动以及肌节的整体缩短[滑动丝理论]然后通过肌浆网中的主动转运从细胞中除去钙-允许松弛，而ATP通过生理过程中的代谢过程再生肌节长度的范围（1.6-2.0 um），转换为机械功的代谢能的量取决于跨桥相互作用的可用表面积！功与舒张末期肌节长度直接成比例此“长度依赖性”是基础弗兰克-史达琳法的基础！奥托·弗兰克（Otto Frank），1885年（青蛙心脏准备）：“正常心脏的输出主要受舒张末期心室中血液量的影响”

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