What Is The Frank Starling Law Of The Heart?

What Is The Frank Starling Law Of The Heart
Frank-Starling Law of the Heart – The Frank-Starling law, also known as Starling’s law, or Frank-Starling law of the heart, is a physiological theory which states that, ‘the strength of the heart’s systolic contraction is directly proportional to its diastolic expansion, with the result that under normal physiological conditions the heart pumps out of the right atrium all the blood returned to it without letting any back up in the veins.’ This law is named after two physiologists, Otto Frank and Earnest Starling, who were the first to give a detailed description about the cardiac phenomenon.

What is the Frank-Starling’s law of the heart explain?

The Cardiovascular System Can Be Simplified for Analysis – In Chapter 5.8, we learned about the Frank–Starling Law of the Heart: increased filling pressure stretches the heart and increases its force of contraction. Increasing the force of contraction expels more blood from the left ventricle, so that cardiac output increases when the preload increases. What Is The Frank Starling Law Of The Heart Figure 5.12.2, The cardiac function curve. The graph shows the output of the left ventricle when it is pumping against a constant arterial pressure and when right atrial pressure is varied. The cardiac function curve was determined in isolated heart–lung preparations, which contains both sides of the heart and the intervening pulmonary circulation.

In these experiments, the outflow pressure was held constant while the input pressure was varied. Thus, the cardiac function curve describes the heart without the attached systemic circulation. In this isolated heart–lung preparation, flow out of the right heart must match flow into the left heart, or else fluid would accumulate or be drawn out of the lungs.

The Frank–Starling law of the heart indicates that the increased filling pressure of the right heart results in increased cardiac output. Any increase in output of the right heart is quickly communicated to the left heart as an increased filling pressure.

Thus, increased output of the right heart is matched to increased output of the left heart. Because of this tight coupling, we can collapse the heart and lungs to a single equivalent pumping mechanism. Similarly, we can lump the systemic circulation into a single equivalent set of vessels in series. This lumping follows the rules of combination of parallel or series resistances.

Figure 5.12.3 shows this situation. What Is The Frank Starling Law Of The Heart Figure 5.12.3, Simplified cardiovascular system. Because right and left heart outputs are tightly coupled, we collapse these two sides of the heart and its intervening pulmonary circulation into a single pump. Also, the arteries and arterioles, consisting of both series and parallel arrangements, can be combined to a single aggregate.

What does the Frank-Starling law suggest?

Frank-Starlings Law Explained – EMTprep.com

Frank-Starling Law The Frank-Starling Law is the description of cardiac hemodynamics as it relates to myocyte stretch and contractility. The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction.

What best describes the Frank-Starling law of the heart quizlet?

What best describes the Frank-Starling law? The Frank-Starling law states that the more the ventricular muscle cells are stretched, the more forcefully they contract. Sometimes health care providers will elect not to treat conditions such as atrial fibrillation in which there is no functional atrial contraction.

How does Frank-Starling increase cardiac output?

The Cardiovascular System Can Be Simplified for Analysis – In Chapter 5.8, we learned about the Frank–Starling Law of the Heart: increased filling pressure stretches the heart and increases its force of contraction. Increasing the force of contraction expels more blood from the left ventricle, so that cardiac output increases when the preload increases. Figure 5.12.2, The cardiac function curve. The graph shows the output of the left ventricle when it is pumping against a constant arterial pressure and when right atrial pressure is varied. The cardiac function curve was determined in isolated heart–lung preparations, which contains both sides of the heart and the intervening pulmonary circulation.

In these experiments, the outflow pressure was held constant while the input pressure was varied.
Thus, the cardiac function curve describes the heart without the attached systemic circulation.
In this isolated heart–lung preparation, flow out of the right heart must match flow into the left heart, or else fluid would accumulate or be drawn out of the lungs.

Thus, increased output of the right heart is matched to increased output of the left heart. Because of this tight coupling, we can collapse the heart and lungs to a single equivalent pumping mechanism. Similarly, we can lump the systemic circulation into a single equivalent set of vessels in series. This lumping follows the rules of combination of parallel or series resistances.

Does the Frank-Starling mechanism increase heart rate?

Physiology, Frank Starling Law The Frank-Starling relationship is based on the link between the initial length of myocardial fibers and the force generated by contraction. There is a predictable relationship between the length between sarcomeres and the tension of the muscle fibers.

There is an optimal length between sarcomeres at which the tension in the muscle fiber is greatest, resulting in the greatest force of contraction.
If sarcomeres are closer together or further apart compared to this optimal length, there will be a decrease in contraction tension and strength.
The greater the ventricular diastolic volume, the more the myocardial fibers are stretched during diastole.

Within a normal physiologic range, the more the myocardial fibers are stretched, the greater the tension in the muscle fibers and the greater force of contraction of the ventricle when stimulated. The Frank-Starling relationship is the observation that ventricular output increases as preload (end-diastolic pressure) increases.

The left ventricular performance (Frank-Starling) curves relate preload, measured as left ventricular end-diastolic volume (EDV) or pressure, to cardiac performance, measured as ventricular stroke volume or cardiac output.
On the curve of a normally functioning heart, cardiac performance increases continuously as preload increases.

During states of increased left ventricular contractility, for example, due to norepinephrine infusion, there is a greater cardiac performance for a given preload. This is represented graphically as an upward shift of the normal curve. Conversely, during states of decreased left ventricular contractility associated with systolic heart failure, there is decreased cardiac performance for a given preload as compared to the normal curve.

This is represented by a downward shift of the normal curve. Decreased contractility also can result from a loss of myocardium as with myocardial infarction, beta-blockers (acutely), non-dihydropyridine Ca++ channel blockers, and dilated cardiomyopathy. Changes in afterload, which is the force of resistance that the ventricle must overcome to empty contents at the beginning of systole, will also shift the Frank-Starling curve.

A decrease in afterload will cause an upward shift of the ventricular performance curve in a similar fashion to an increase in inotropy. Conversely, an increase in afterload will cause a downward shift of the curve in a similar fashion to a decrease in inotropy.

An increase in catecholamines, such as norepinephrine, during exercise, will result in an upward shift of the Frank-Starling curve.
Catecholamines achieve this increase by binding to a myocyte beta1-adrenergic receptor, a G protein-coupled receptor, ultimately resulting in increased Ca++ channel release from the sarcoplasmic reticulum, which enhances the force of contraction.

The Frank-Starling mechanism plays a role in the compensation of systolic heart failure, buffering the fall in cardiac output to help preserve sufficient blood pressure to perfuse the vital organs. Heart failure caused by the impaired contractile function of the left ventricle causes a downward shift of the left ventricular performance curve.

At any given preload, the stroke volume will be decreased as compared to normal. This reduced stroke volume leads to incomplete left ventricular emptying. Consequently, the volume of blood that accumulates in the left ventricle during diastole is greater than normal. The amplified residual volume increases the stretch of the myocardial fibers and induces a greater stroke volume with the next contraction via the Frank-Starling mechanism.

This allows for better emptying of the enlarged left ventricle and preserves cardiac output. The benefit of the Frank-Starling mechanism in the compensation of systolic heart failure is limited. In severe heart failure with a greater cardiac contractility malfunction, the ventricular performance curve may be nearly flat at higher diastolic volumes, reducing the increased cardiac output with increases in chamber filling.

In this circumstance, a severe elevation at the EDV and left ventricular EDP may result in pulmonary congestion.
The Frank-Starling mechanism also plays a compensatory role in patients with dilated cardiomyopathy.
There is commonly dilation of both the right and left ventricles with decreased contractile function in dilated cardiomyopathy.

As impaired myocyte contractility results in depression of ventricular stroke volume and cardiac output, the Frank-Starling mechanism has compensatory effects. As the elevated ventricular diastolic volume increases the stretch on the myocardial fibers, there will be a subsequent increase in stroke volume.

Along with the Frank-Starling mechanism, neurohormonal activation mediated by the sympathetic nervous system also compensates for dilated cardiomyopathy by increasing heart rate and contractility, helping to buffer the decreased cardiac output.
These compensatory mechanisms may lead to a lack of symptoms during the early stages of ventricular dysfunction.

With progressive myocyte degeneration and volume overload, clinical symptoms of systolic heart failure will develop. In patients with impaired myocardial systolic failure, clinicians use inotropic drugs to increase the force of ventricular contraction.

Pharmacologic inotropic agents include cardiac glycosides, such as digitalis; sympathomimetic amines such as dopamine and epinephrine; and phosphodiesterase-3 inhibitors, such as milrinone. They all work through different mechanisms to enhance cardiac contraction by increasing the intracellular calcium concentration, enhancing actin and myosin interaction.

This will have the hemodynamic effect of shifting a depressed ventricular performance (Frank-Starling) curve in an upward direction toward normal. At a given preload (left ventricular EDP), the stroke volume and cardiac output are increased. With the progressive loss of ventricular contractility, increased preload (pressure) in the left ventricle will surpass the hydrostatic forces of the pulmonary venous system, resulting in pulmonary congestion.

In a patient suffering from systolic heart failure with reduced ejection fraction and resultant pulmonary congestion, treatment with a diuretic, such as furosemide or hydrochlorothiazide, or a pure venous vasodilator, such as nitrates, reduces the preload without much change in stroke volume. This is because the Frank-Starling curve is almost horizontal at higher preload levels in a patient whose curve is shifted downward due to systolic contractile dysfunction.

However, excessive diuresis or venous vasodilation can result in an unwanted fall in stroke volume, resulting in hypotension. Arteriolar vasodilation therapy, like hydralazine, also has value when treating systolic heart failure with pulmonary congestion.

Arteriolar vasodilators result in a decrease in afterload, allowing for an increase in stroke volume—the improved left ventricular emptying results in a decreased preload and improvement of pulmonary symptoms.
There is the potential added benefit of combining treatment with a vasodilator and a positive inotropic agent, allowing for a larger increase in stroke volume than would be seen with monotherapy.

Even with combination therapy with a vasodilator and inotropic agent, the Frank-Starling curve will not improve to the performance level of a normal ventricle.

How does the heart alter stroke volume?

Preload and afterload – Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank–Starling law of the heart, will increase stroke volume.

Decreased venous return has the opposite effect, causing a reduction in stroke volume.
Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume.
It usually does not affect stroke volume in healthy individuals, but increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume.

Increased afterload may be found in aortic stenosis and arterial hypertension,

How the Starling’s law of the heart is involved in the maintenance of the blood pressure?

Starling’s Law – Starling’s Law states that the heart will eject a greater stroke volume if it is filled to a greater volume at the end of diastole. The volume of the heart at end diastole is related to the filling pressure of the heart (preload) which is determined by the left atrial pressure (LAP).

What happens during cardiac drift?

Abstract – Cardiovascular drift, the progressive increase in heart rate and decrease in stroke volume that begins after approximately 10 min of prolonged moderate-intensity exercise, is associated with decreased maximal oxygen uptake, particularly during heat stress.

What happens to stroke volume during exercise?

Stroke volume – Stroke volume refers to the volume of blood ejected per beat from the left or right ventricle and increases from approximately 1000 mL (2–2.5 mL/kg) at rest up to 1700 mL (3–4 mL/kg) or higher at maximal exercise ( Table 31.6 ).12,60,61,63,73 If a maximum heart rate of 225 beats/min is assumed for Secretariat, his stroke volume would have been well in excess of 2000 mL/beat.

Typically, stroke volume increases sharply at exercise onset up to around 40% consequent to increased blood volume, venous return, and filling pressures according to the Frank–Starling mechanism.30,77 What is particularly remarkable is that ventricular filling (and thus stroke volume) does not appear to be compromised at maximal exercise despite heart rates of 4 beats/s.

Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780702047718000314

How does the Frank-Starling mechanism work during exercise?

Abstract – To determine the effects of β blockade on hemodynamics during increasing levels of treadmill exercise, 10 healthy volunteers were studied after 1 week of placebo, and then after 1 week of treatment with oral propranolol, 80 mg twice daily, or dilevalol, 400 mg once daily. The study was randomized and double-blind, with a crossover sequence. Hemodynamics were measured by CO 2 rebreathing at rest and at 25, 50, 75 and 100% of V̇O 2 max. After placebo, cardiac output increased from 5.8 ± 2.1 (rest), to 19.4 ± 6.4 liters/min (100% V̇O 2 max), mainly due to an increase in heart rate from 84 ± 6 to 169 ± 15 beats/min. Stroke volume increased from 70 ± 27 (rest), to 137 ± 65 ml (25% V̇O 2 max), and then leveled off to 116 ± 41 at 100% V̇O 2 max. After both β blockers, exercise cardiac output was maintained at 100% V̇O 2 max: 20.1 ± 9.3 liters/min with propranolol and 19.1 ± 8.6 with dilevalol. However, a significant reduction versus placebo values was observed for cardiac output at 25% V̇O 2 max, from 13.7 ± 5.9 during placebo, to 9.4 ± 2.5 during propranolol, and to 9.6 ± 2.3 during dilevalol (both p <0.01 vs placebo). Maintenance of cardiac output with both β blockers at higher levels of exercise came from an increased stroke volume (p <0.05 vs placebo), while heart rate (in beats/min) was greatly reduced (propranolol 61.6 ± 9.4 rest, 90.1 ± 10.7 at 100% V̇O 2 max; dilevalol 70.8 ± 6.4 rest, 99.2 ± 11.8 at 100% V̇O 2 max, p <0.01 vs placebo for each). All subjects were able to exercise up to maximal control level during β-blocker treatment. The decrease in total peripheral resistances was already evident at 25% V̇O 2 max and was not counteracted by β blockade. Thus, in normal volunteers, β blockers do not reduce exercise cardiac output, even at doses that greatly reduce heart rate. At low levels of exercise, a transient blunting of cardiac output increase probably reflects a delay in sympathetic activation. At higher exercise levels, an increase in stroke volume, that is an effective Frank-Starling mechanism, allows maintained oxygen supply to the exercising muscles. To read this article in full you will need to make a payment