Diagram of the physiological relationship between the Frank-Starling law of the heart and venous back pressure and volume. Contribution by Finne HA (public domain) As described elsewhere, cardiac output increases or decreases in response to changes in heart rate or stroke volume. For example, when a person stands up, cardiac output decreases because a drop in central venous pressure leads to a decrease in stroke volume. Another example is the movement of the limbs (muscle pump) during exercise improves venous return to the heart, which leads to an increase in stroke volume. What mechanisms do changes in venous return change stroke volume? The Frank-Starling mechanism plays a role in compensating for systolic heart failure and dampens the drop in cardiac output to maintain adequate blood pressure to supply blood to vital organs. Heart failure, which is caused by impaired contractile function of the left ventricle, causes a downward shift in the left ventricular performance curve. At a given preload, the displacement is reduced compared to normal. This reduction in stroke volume results in incomplete left ventricular emptying. As a result, the volume of blood that accumulates in the left ventricle during diastole is higher than normal. The reinforced residual volume increases the stretching of the myocardial fibers and induces a greater running volume at the next contraction via the Frank-Starling mechanism. This allows better emptying of the enlarged left ventricle and preserves cardiac output.
[9] The Frank-Starling law of the heart states that under normal circumstances, the heart is able to increase its stroke volume based on venous return. Understanding the factors influencing preload and postload may suggest therapeutic strategies for cardiogenic shock. The Frank-Starling mechanism is an inherent feature of the adult heart that varies the contractile force in response to acute hemodynamic stress. However, the imposition of chronic hemodynamic overload of the heart of adult mammals induces a hypertrophic response of individual cardiomyocytes to maintain ventricular function. Hypertrophy of cardiomyocytes is characterized by a selective increase in cell size, due to de novo synthesis of sarcomeres. The sarcomere is the basic contractile unit of individual cardiomyocytes consisting of thin filaments of actin and thick filaments of myosin. Depending on the type of hemodynamic load (pathological or physiological), important qualitative differences in the arrangement of sarcomeres are frequent and lead to different models of cardiac geometry. Important qualitative differences also exist in gene expression, which further distinguishes pathological and physiological hypertrophy. Cochrane Collaboration on the Frank-Starling Law of the Heart In the human heart, maximum force is generated with an initial sarcomere length of 2.2 μm, a length rarely exceeded in the normal heart. Initial lengths longer or shorter than this optimal value reduce the strength that the muscle can achieve. With longer sarcomere lengths, there is less overlap of thin and thick filaments, and with shorter sarcomere lengths, myofilaments show reduced sensitivity to calcium.According to the Frank-Starling mechanism, the left ventricle is able to increase its contractile strength and therefore its running volume in response to an increase in venous return and thus preload (2,4) (Figure 37.2). Disturbances in afterload or inotropy move the Frank-Starling curve up or down. In HF, the Frank-Starling curve is shifted downward (flattened), so back venous pressure and filling is required to increase the contractility and volume of the stroke. This change in the Frank-Starling curve helps explain why increased water retention occurs when cardiac dysfunction worsens in HF. More and more preload is needed to increase displacement with decreasing inotropy. Finally, stroke volume in end-stage HF becomes much more dependent on afterload, so reducing afterload has a greater impact on cardiac output than normal hearts (4). Due to the intrinsic property of the myocardium, which is responsible for the Frank-Starling mechanism, the heart can automatically absorb an increase in venous reflux at any heart rate. [1] [10] The mechanism is of functional importance because it is used to match left ventricular flow to right ventricular performance. [3] If this mechanism did not exist and the right and left cardiac outputs were not equivalent, blood would accumulate in the pulmonary circulation (if the right ventricle produced more power than the left) or in the systemic circulation (if the left ventricle produced more power than the right). [1] [14] The Frank-Starling mechanism also plays a compensatory role in patients with dilated cardiomyopathy.
In dilated cardiomyopathy, dilation of the right and left ventricles often occurs with reduced contractile function. Since impaired myocytic contractility leads to depression of ventricular stroke volume and cardiac output, the Frank-Starling mechanism has compensatory effects. Since the increase in ventricular diastolic volume increases the stretching of myocardial fibers, there is a subsequent increase in the volume of stroke. With the Frank-Starling mechanism, neurohormonal activation mediated by the sympathetic nervous system also compensates for dilated cardiomyopathy by increasing heart rate and contractility and helping to cushion the decrease in cardiac output. These compensatory mechanisms can lead to an absence of symptoms in the early stages of ventricular dysfunction. With progressive myocyte degeneration and volume overload, clinical symptoms of systolic heart failure develop. Clinical evidence of myocardial dysfunction during hypovolemic shock is scarce.46,56,162 Nevertheless, it is conceivable that severe hypotension reduces the balance between oxygen supply and cardiac needs, as many patients with hypovolemic shock may be elderly and have coronary artery disease, impairing coronary vasodilation.