LaCombe Philip, Tariq Muhammad Ali, Lappin Sarah L.
SUNY Upstate Medical University
Tower Health
The systolic performance of the heart is determined by 3 factors: preload, afterload, and contractility. The direct relationship between preload and cardiac output was formulated in the early 1900s based on the work of Otto Frank and Ernest Starling. It led to the well-known Frank-Starling curves. Gordon et al. helped to elucidate the underlying mechanism for this phenomenon in their 1966 experiments involving sarcomere length-tension relationships. During this same period, extensive research demonstrated an inverse relationship between afterload and systolic performance, which is accepted today. This means that cardiac output decreases as the afterload on the heart increases and vice versa. Despite this simple concept, there has been substantial controversy over the best way to represent cardiac afterload. The afterload of any contracting muscle is defined as the total force that opposes sarcomere shortening minus the stretching force that existed before contraction. Applying this definition to the heart, afterload can be most easily described as the "load" against which the heart ejects blood. The load on individual fibers can be expressed as left ventricular wall stress, which is proportional to [(LV Pressure x LV Radius)/ LV wall thickness], or [(P x r)/h]. However, the true equation is complex because it depends on the shape of the cardiac chamber, which is affected by several factors that are changing over time. Therefore, afterload cannot be represented by a single numerical value or described only regarding pressure. Arterial pressure (diastolic, mean, or systolic) is frequently used as a surrogate measure, but perhaps the best available techniques involve measuring systemic arterial resistance by various invasive and noninvasive methods. Several mathematical models have been developed using arterial impedance and pressure-flow relationships to characterize afterload better, but these are complex and less often utilized in practice. The inverse relationship between afterload and cardiac output is important in understanding the pathophysiology and treatment of several diseases, including aortic stenosis, systemic hypertension, and congestive heart failure.
前负荷、后负荷和心肌收缩力。基于奥托·弗兰克和欧内斯特·斯塔林的研究成果，20世纪初确立了前负荷与心输出量之间的直接关系。这一关系形成了著名的弗兰克 - 斯塔林曲线。1966年，戈登等人通过涉及肌节长度 - 张力关系的实验，帮助阐明了这一现象的潜在机制。同一时期，大量研究表明后负荷与收缩功能呈反比关系，这一关系如今已被广泛接受。这意味着随着心脏后负荷增加，心输出量减少，反之亦然。尽管这一概念简单，但对于表示心脏后负荷的最佳方法仍存在大量争议。任何收缩肌肉的后负荷定义为对抗肌节缩短的总力减去收缩前存在的拉伸力。将此定义应用于心脏，后负荷最容易被描述为心脏射血时所对抗的“负荷”。单个纤维上的负荷可以表示为左心室壁应力，它与[(左心室压力×左心室半径)/左心室壁厚度]，即[(P×r)/h]成正比。然而，实际公式很复杂，因为它取决于心腔的形状，而心腔形状受多种随时间变化的因素影响。因此，后负荷不能用单一数值表示，也不能仅从压力方面来描述。动脉压（舒张压、平均压或收缩压）常被用作替代指标，但或许现有的最佳技术是通过各种有创和无创方法测量体循环动脉阻力。已经开发了几种利用动脉阻抗和压力 - 流量关系来更好地表征后负荷的数学模型，但这些模型很复杂，在实践中较少使用。后负荷与心输出量之间的反比关系对于理解包括主动脉瓣狭窄、系统性高血压和充血性心力衰竭在内的多种疾病的病理生理学和治疗方法很重要。
