What is Frank-Starling law regarding cardiac output activity?

From the Guidelines

Frank-Starling's law is a critical mechanism by which the heart increases its cardiac output in response to increased venous return, but its effectiveness can be compromised in heart failure states where increased central venous pressure and right ventricular dilation lead to decreased cardiac output. The law describes how the heart naturally increases its cardiac output in response to increased venous return, with the heart muscle contracting more strongly when stretched during filling (preload), resulting in greater stroke volume 1. This occurs because as cardiac muscle fibers are stretched to an optimal length, there is increased overlap between actin and myosin filaments, allowing for more cross-bridge formation and a stronger contraction. However, in heart failure, the direct effect of over-dilation causes decreased ventricular contractility (Frank–Starling relationship) 1, and dilation of the right ventricle impairs LV filling by increasing LV extramural pressure, reducing LV functional volume and reducing preload (the reverse Bernheim phenomenon) 1. Key points to consider regarding Frank-Starling's law and cardiac output activity include:

• The law allows the heart to automatically adjust its output based on the body's needs without requiring nervous system input
• Fluid administration can improve cardiac output in hypovolemic patients, while excessive fluid can overstretch the heart beyond optimal fiber length, potentially reducing contractility
• The Frank-Starling mechanism is fundamental to understanding how the heart maintains equal output between the right and left ventricles despite varying conditions
• In clinical settings, understanding Frank-Starling's law is crucial for managing patients with heart failure, where decreased cardiac output can lead to reduced renal perfusion and impaired renal function 1.

From the Research

Frank-Starling Law and Cardiac Output

• The Frank-Starling law of the heart is a filling-force mechanism, which describes the positive relationship between the distension of a ventricular chamber and its force of ejection 2.
• This mechanism plays a crucial role in stabilizing the short-term variations in the working of the cardiovascular system, and is found across all studied vertebrate lineages 2.
• The Frank-Starling law allows for rapid changes in cardiac output, smooths out perturbations in volumes, and decreases the demands of a central controlling system over the circulatory system 2.

Cardiac Output and Heart Failure

• In heart failure, the inability of the heart to eject a sufficient amount of blood is thought to result from molecular changes in cardiac cells, causing decreased active force and impaired relaxation, as well as a greater stiffness of the remodelled ventricular wall 3.
• The failure to generate a forceful contraction is in part a consequence of derailment of the processes in the failing cardiac cells to manipulate calcium ions, despite the increased stimulus from nervous and hormone systems to enhance cardiac performance 3.
• Arterial dilators, such as hydralazine, can decrease afterload and improve cardiac output in patients with heart failure 4.

Treatment of Heart Failure

• Diuretics, direct vasodilators, and angiotensin-converting enzyme (ACE) inhibitors can be used to reduce symptoms, prolong life, or both, in patients with congestive heart failure 4.
• ACE inhibitors can cause hemodynamic and neurohormonal changes that lead to a reduction of preload and afterload, decreasing symptoms of heart failure, and significantly decreasing congestive heart failure mortality 4.
• The combination of hydralazine and isosorbide dinitrate provides balanced vasodilation, improves survival, but is associated with a relatively high frequency of side effects necessitating discontinuation of one or both agents 4.