Cecily Zamora
Eccentric hypertrophy is a condition in which the ventricular chamber becomes dilated, causing a relative thinning of the heart wall. This is distinct from concentric hypertrophy, which is associated with chronic pressure overload states and results in thicker heart walls and a smaller chamber size. Eccentric hypertrophy is characterised by a progressive increase in cardiac diameter, while the wall thickness remains relatively constant. According to the Law of Laplace, ventricular wall stress is directly proportional to ventricular pressure and radius, and inversely proportional to ventricular wall thickness. Therefore, eccentric hypertrophy, by increasing the chamber size, helps to accommodate increased blood volume, normalise stroke volume and improve cardiac output.
| Characteristics | Values |
|---|---|
| Law of Laplace | Wall stress (T) is directly proportional to transmural pressure (P) and cavitary radius (r) and inversely proportional to wall thickness (W) |
| Eccentric hypertrophy | Progressive increase in cardiac diameter with relatively constant wall thickness |
| Concentric hypertrophy | Thickening of walls, decrease in ventricular compliance, increase in diastolic ventricular wall thickness |
| Eccentric hypertrophy and Law of Laplace | As cavity radius increases and wall thickness remains constant, wall stress increases |
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What You'll Learn
Law of Laplace and ventricular wall stress
The Law of Laplace is a law in physics that states that the wall tension of a hollow sphere or cylinder is proportional to the pressure of its contents and its radius. In the context of the left ventricle of the heart, the law of Laplace can be applied to understand ventricular wall stress.
The formula for ventricular wall stress according to Laplace's law is: wall stress = P x r / 2w, where P is pressure, r is the total radius, and w is wall thickness. This formula demonstrates that wall stress is directly proportional to pressure and radius, and inversely proportional to wall thickness.
Ventricular wall stress is an important hemodynamic parameter that represents myocardial oxygen demand and ventricular workload. It plays a crucial role in understanding the development and progression of left ventricular remodelling. Assessing ventricular wall stress is important in clinical settings, especially in the context of hypertrophic responses and ventricular remodelling.
In the case of eccentric hypertrophy, there is a dilated ventricular chamber with relative wall thinning. This increase in ventricular chamber size helps to normalise wall stress and improve stroke volume and cardiac output. On the other hand, concentric hypertrophy is characterised by an increased left ventricular wall thickness and a relatively unchanged cavitary radius, which can lead to diastolic dysfunction and ventricular failure.
Therefore, the Law of Laplace helps explain the relationship between ventricular wall stress and hypertrophy. By understanding the impact of pressure, radius, and wall thickness on ventricular wall stress, we can comprehend the compensatory mechanisms that occur in eccentric and concentric hypertrophy.
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Ventricular dilation and overload
Chronic volume overload, such as that stimulated by ventricular failure or renal failure, can lead to eccentric hypertrophy and increased left ventricular chamber size. This helps to normalise stroke volume and cardiac output. The hypertrophied ventricle is prone to ischemia, which leads to fibrosis and an increase in collagen content, which in turn interferes with diastolic filling, decreasing preload and SV. This results in both systolic and diastolic dysfunction.
Concentric hypertrophy, on the other hand, is a hypertrophic growth of a hollow organ without overall enlargement, resulting in thickened walls and a diminished capacity or volume. This is associated with chronic pressure overload states like hypertension or aortic stenosis. In the case of the left ventricle, the ventricular wall thickness increases markedly, while the cavitary radius remains relatively unchanged. This leads to a decrease in ventricular compliance and diastolic dysfunction, which can eventually result in ventricular failure and systolic dysfunction.
The geometric response of the heart to arterial hypertension can follow one of four patterns, with approximately half of all patients exhibiting a normal LV geometry. These patterns are influenced by preload, blood volume, venous compliance, and LV dilation due to the growing inadequacy of (concentric) hypertrophy to compensate for increased afterload.
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Pressure overload and left ventricle hypertrophy
Pressure overload refers to the pathological state of the cardiac muscle in which it has to contract while experiencing an excessive afterload. This overload can affect any of the four chambers of the heart, but the term is most commonly used to refer to one of the two ventricles.
Left ventricular hypertrophy (LVH) is a condition in which there is an increase in left ventricular mass, either due to an increase in wall thickness or left ventricular cavity enlargement, or both. The increase in wall thickness is a compensatory mechanism to maintain normal wall stress. However, the benefits of increased wall thickness are offset by a significant increase in the stiffness of the hypertrophied walls, which leads to diastolic dysfunction and puts the patient at a significant risk of heart failure.
Left ventricular hypertrophy is commonly caused by pressure overload-induced by arteriolar vasoconstriction, which occurs in chronic hypertension or aortic stenosis. In these conditions, the heart contracts against an elevated afterload. Hypertension is the most common cause of LVH, and it can be diagnosed by sphygmomanometry. A forceful apex beat indicates left ventricular pressure overload.
Concentric hypertrophy is a type of LVH in which the walls of the ventricles thicken, but the overall size of the organ remains the same, resulting in a decreased ventricular capacity or volume. This form of hypertrophy is commonly associated with chronic pressure overload states like hypertension or aortic stenosis. In response to the pressure overload, the left ventricular wall thickness increases markedly, while the cavitary radius remains relatively unchanged. This increase in wall thickness reduces left ventricular radial and circumferential wall stress, benefiting the systolic function of the left ventricle.
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Eccentric hypertrophy and cardiac output
Eccentric hypertrophy is a condition that generally occurs as a healthy response to increased cardiac demand. It is often observed in athletes and pregnant individuals, and is characterised by an increase in the heart's muscle mass and pumping ability. This results in a dilated ventricular chamber with relative wall thinning, which can help improve stroke volume and cardiac output.
The Law of Laplace states that wall stress is directly proportional to intraventricular pressure and chamber radius but inversely proportional to wall thickness. In the context of eccentric hypertrophy, the increase in ventricular chamber size and wall thinning may impact wall stress, as described by Laplace's law.
Eccentric hypertrophy is typically associated with endurance training, where the volume load is a predominant factor. This is in contrast to strength training, which primarily focuses on pressure load. During endurance training, the heart responds to the increased volume load by adding new sarcomeres in series to existing sarcomeres, resulting in ventricular dilation and eccentric hypertrophy.
The cardiac output of trained endurance athletes can significantly increase during maximal exercise, which requires the heart to adapt to both volume and pressure load. This adaptation results in an increase in the left ventricular internal diameter and left ventricular wall thickness. However, eccentric hypertrophy is not limited to athletes and can also occur in pregnant individuals as a physiologic, adaptive process in response to increased blood volume.
While eccentric hypertrophy is generally considered healthy, it is important to note that it carries certain risks. For example, in athletes with a significantly increased left ventricular weight, there is an increased risk of conduction abnormalities and sudden cardiac death. Additionally, a subpopulation of pregnant individuals may progress to peripartum cardiomyopathy, which is characterised by a dilation of the left ventricle and impaired heart function.
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Diastolic dysfunction and ventricular failure
Diastolic dysfunction is a condition where the end-diastolic ventricular pressure is high. This increase in volume or pressure backs up to the left atrium and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins impairs the normal drainage of the alveoli and can cause pulmonary edema. Diastolic dysfunction is often associated with eccentric hypertrophy, which creates a dilated ventricular chamber with relative wall thinning. This can lead to ventricular failure.
Eccentric hypertrophy is a response to volume overload, where individual muscle fibres elongate due to the addition of sarcomeres in series. This results in an increase in left ventricular chamber size, which can help to normalise stroke volume and cardiac output. However, if the eccentric hypertrophy leads to a significant increase in left ventricular chamber size, it can result in diastolic dysfunction and ventricular failure.
Ventricular failure occurs when the heart fails to pump enough blood to meet the body's demands. This can be due to a reduction in the efficiency of the heart muscle, through damage or overloading. Diastolic dysfunction is one of the main causes of ventricular failure, as it impairs the filling of the ventricles and reduces the stroke volume. This can lead to a backup of blood in the left atrium and pulmonary veins, causing pulmonary congestion and edema.
The Law of Laplace states that wall stress is directly proportional to intraventricular pressure and chamber radius but inversely proportional to the wall thickness. In the context of diastolic dysfunction and ventricular failure, the Law of Laplace helps to explain the relationship between ventricular volume, pressure, and wall stress. As the ventricular volume increases during diastolic dysfunction, the wall stress also increases, which can lead to ventricular failure if the heart muscle is unable to cope with the increased workload.
Overall, diastolic dysfunction and ventricular failure are complex conditions that can have significant impacts on an individual's health. Eccentric hypertrophy can contribute to diastolic dysfunction and ventricular failure by altering the geometry and function of the heart, leading to increased wall stress and reduced cardiac output. Understanding the underlying mechanisms, including the application of the Law of Laplace, can help inform treatment and management strategies for these conditions.
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Frequently asked questions
Eccentric hypertrophy is a condition in which the ventricular chamber becomes dilated, leading to a relative thinning of the ventricular walls. This occurs as a response to volume overload, where the increase in blood volume is accommodated by an increase in chamber size, rather than an increase in wall thickness.
The Law of Laplace states that wall stress is directly proportional to intraventricular pressure and chamber radius, but inversely proportional to wall thickness. In eccentric hypertrophy, the ventricular wall stress increases as the ventricular chamber dilates and the wall thickness remains relatively constant. This results in a progressive increase in end-diastolic fibre stress and overall chamber volume.
Concentric hypertrophy is characterised by an increase in wall thickness and a decrease in chamber size, while eccentric hypertrophy involves an increase in chamber size and a relatively constant wall thickness. Concentric hypertrophy is often associated with chronic pressure overload states, such as hypertension or aortic stenosis, while eccentric hypertrophy is associated with volume overload.
Eccentric hypertrophy can lead to both systolic and diastolic dysfunction, as well as an increased risk of cardiac failure. The dilation of the ventricular chamber and the increase in ventricular wall stress can result in a reduced cardiac output and progressive heart failure.
