The Frank-Starling mechanism is the autonomic regulation of the heart‘s internal ejection and filling capacity that compensates for short-term fluctuations in pressure and volume. This vital regulation plays a role primarily during changes in body position. The mechanism can no longer compensate for larger changes in pressure.
What is the Frank-Starling mechanism?
Schematic anatomical representation of the heart showing the ventricles. The autonomic control circuit of the heart regulates the ejection and filling output of the vital organ. The regulation adjusts the cardiac output to short-term changes in pressure and volume, allowing both chambers of the heart to eject the same stroke volume. This regulatory circuit is called the Frank-Starling mechanism. The mechanism was named after the German physiologist Otto Frank and the British physiologist Ernest Henry Starling, who first described the control loop at the beginning of the 20th century on the isolated heart and later on the heart-lung preparation. The German physiologist Hermann Straub was also involved in the initial description. For this reason, the control loop is sometimes referred to as the Frank-Straub-Starling mechanism. The mechanism is one of several vital regulations in the human organism. In its basic features, the Frank-Starling mechanism describes that volume of blood that passes through the heart during diastole and systole. The smaller the volume inflow during diastole, the smaller the volume of blood ejected during systole.
Function and purpose
The Frank-Starling mechanism consists of preload and afterload. When the atria fill, we are talking about preload. When preload increases, the ventricles also fill progressively. At a constant heart rate, the stroke volume of the heart increases. The end-systolic volume increases only slightly. When the preload is increased, there is an increased pressure-volume work in the heart. This principle corresponds to the preload of the Frank-Starling mechanism. This preload is followed by an afterload. The outflow of blood from the heart is called the afterload. When the blood outflow occurs against increased resistance, the pumping action of the heart increases to higher pressure and in this way carries the same volume of blood as before at the same heart rate. A gradual adaptation takes place. Towards the end of systole, due to the increased afterload, a particularly large amount of blood remains in the heart chambers. A backpressure occurs. In diastole, this backpressure causes the chambers to fill all the more. Myocardial cell strength is ever dependent on preload, and so is based on its preload before the actual onset of contraction. The greater the elongation of the sarcomeres in the muscle cells, the higher it is. Because the volume in the Frank-Starling mechanism increases end-diastolically, the myosin and actin filaments overlap optimally and change from a sarcomere length of previously 1.9 µm to a sarcomere length of about 2.2 µm. Thus, at optimal overlap, the maximum force is between 2.2 and 2.6 µm. Exceeding these values causes the maximum force to decrease. The optimal overlap causes a so-called calcium sensitization in the myofibrils, which makes the contractile apparatus more receptive to calcium. In this way, the conventional calcium influx during an action potential elicits an all the stronger response in the myofibrils. The blood volume of the preload is subject to certain fluctuations depending on physical activity and body position. The Frank-Starling mechanism ensures cardiac function and the adjustment of the individual ejection volumes in the right and left parts of the heart. When the volume shifts, for example, during a change in body position, the mechanism is particularly relevant. Ventricular activities are automatically adjusted by the control circuit to pressure and volume fluctuations and the associated changes in preload and afterload. As a result, both ventricles always pump the same stroke volume.
Diseases and medical conditions
When one of the loads of the Frank-Starling mechanism goes out of balance, so does the other. Preload is referred to in medical practice as end-diastolic volume or end-diastolic pressure, both of which can be measured. In heart disease, such as systolic heart failure, there is an increased end-diastolic volume. This also increases the filling pressure. The preload is therefore increased.As a consequence, fluid from the vascular system is deposited in the body tissues. This is how edema such as pulmonary edema forms. Pulmonary edema can cause, for example, shortness of breath, rales, or frothy sputum from the lungs. Decreased ventricular elasticity also presents problems with the Frank-Starling mechanism. Decreased ventricular elasticity is present, for example, in diastolic heart failure. The stiffer the ventricle, the worse the diastolic filling. This causes blood to back up in the veins. To reduce preload, the physician administers ACE inhibitors or nitrates to the patient. Hypertension or valve stenosis can just as easily increase the afterload of the heart, causing problems in the Frank-Starling mechanism. The ventricular muscles may hypertrophy due to increased night load, thus lowering wall stress. Such ventricular hypertrophy can result in heart failure. Stretching of the ventricular muscle fibers gives them greater tension, and the increased stretch allows blood to be ejected with greater force. When the Frank-Starling mechanism fails, the heart can no longer easily perform everyday pressure fluctuations and volume changes. The mechanism can compensate for a slightly increased pressure and preload in healthy individuals. However, even the regulatory mechanism is not equipped to deal with larger pressure fluctuations or load variations. For this reason, larger fluctuations may have life-threatening consequences.
