Frank-Starling mechanism

In the setting of a sustained loss of myocardium, a number of mechanisms aid the heart when faced with an increased hemodynamic burden and reduced CO. They include the following the Frank-Starling mechanism, tachycardia and increased afterload, and cardiac hypertrophy and remodeling (Table 3-2).5,7... 

Frank-Starling mechanism The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. 

As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms (1) tachycardia and increased contractility through sympathetic nervous system activation (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume (3) vasoconstriction and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression. 

This can be equated to the end-diastolic volume and is described by the Frank-Starling mechanism. Clinically it is equated to the CVP when studying the RV or the PAOP when studying the LV. 

Heart rate is controlled by the autonomic nervous system. Stroke volume, or the volume of blood ejected during systole, depends on preload, afterload, and contractility. As defined by the Frank-Starling mechanism, the ability of the heart to alter the force of contraction... 

In both previously mentioned examples, a fundamental property of the myocardium, described by the Frank-Starting mechanism, comes into play. The Frank-Starling mechanism holds that the force of contraction generated by the heart is increased as the amount of blood filling the LV is increased and the myocardium is stretched (Moss and Fitzsimons, 2002 Vincent, 2008). In the example of valvular... 

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