Frank-Starling

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. 

The sympathetic system also innervates vascular smooth muscle and regulates the radius of the blood vessels. All types of blood vessels except capillaries are innervated however, the most densely innervated vessels include arterioles and veins. An increase in sympathetic stimulation of vascular smooth muscle causes vasoconstriction and a decrease in stimulation causes vasodilation. Constriction of arterioles causes an increase in TPR and therefore MAP. Constriction of veins causes an increase in venous return (VR) which increases end-diastolic volume (EDV), SV (Frank-Starling law of the heart), CO, and MAP. 

In other words, the increase in cardiac output occurs by extrinsic (sympathetic stimulation) and intrinsic (increased VR and the Frank-Starling law of the heart) mechanisms. Venous return is also markedly increased by the compression of blood vessels in the working muscles. TTie increase in CO causes an increase in MAP, and the increase in MAP contributes to an increase in muscle blood flow. 

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. 

Cardiac dilatation and hypertrophy — taking advantage of the Frank-Starling relationship to utilize more contractile elements. 

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... 

Ventricular function (Frank-Starling) curves, which plot any function of preload versus any function of cardiac work, reveal that compensatory mechanisms in untreated heart failure (mostly deleterious) may shift such curves upward and to the left. Compensation in heart failure is offset by specific drugs that can ... 

Figure 13-2. Ventricular function (Frank-Starling) curves. The abscissa can be any measure of preload—fiber length, filling pressure, pulmonary capillary wedge pressure, etc. The ordinate is a measure of useful external cardiac work—stroke volume, cardiac output, etc. In congestive heart failure, output is reduced at all fiber lengths and the heart expands because ejection fraction is decreased. As a result, the heart moves from point A to point B. Compensatory sympathetic discharge or effective treatment allows the heart to eject more blood, and the heart moves to point C on the middle curve.

FIGURE 10.7 The Frank-Starling law of the heart 3-D of Sagawa s [1967] left-ventricle equation for a 10-kg dog CO, cardiac output MAP, mean arterial pressure MLAP, mean left arterial pressure. 

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... 

Moss, R.L., Fitzsimons, D.P. (2002). Frank-starling relationship long on importance, short on mechanism. Circ. Res. 90 11-13. 

The circulatory fluid is ejected by an electropneumatically driven ventricular pump. Downstream of the pump, an aortic valve assembly is located two different models have been built in order to offer lateral or frontal view of the prosthesis movements. Suitable stent adapters allow to test prostheses of different type and size. The aorta is a variable compliance rubber tube. Through a rigid conduit the fluid is conveyed to the laminar flow assembly which controls peripheral resistances. Aortic compliance and peripheral resistances are hydropneumatically controlled. The fluid, passing through a venous reservoir open to atmospheric pressure, reaches the left atrium. This is a rigid wall chamber in which a hydropneumatic system relates cardiac output to venous return, reproducing Frank--Starling s Law. Between atrium and ventricle there is another valve test assembly which allows to test mitral valves. 

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