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Pressure overload may affect any of the four chambers of the heart, though the term is most commonly applied to one of the two ventricles. Chronic pressure overload leads to concentric hypertrophy of the cardiac muscle, which can in turn lead to heart failure , myocardial ischaemia or, in extreme cases, outflow obstruction.
Right ventricular hypertrophy is the intermediate stage between increased right ventricular pressure (in the early stages) and right ventricle failure (in the later stages). [11] As such, management of right ventricular hypertrophy is about either preventing the development of right ventricular hypertrophy in the first place, or preventing the ...
Rhythmicity and contractility of the heart may be normal, but the stiff walls of the heart chambers (atria and ventricles) keep them from adequately filling, reducing preload and end-diastolic volume. Thus, blood flow is reduced, and blood volume that would normally enter the heart is backed up in the circulatory system.
The rising central venous pressure is evidenced by distended jugular veins while in a non-supine position. It is caused by reduced diastolic filling of the right ventricle, due to pressure from the adjacent expanding pericardial sac. This results in a backup of fluid into the veins draining into the heart, most notably, the jugular veins.
When pulmonic stenosis (PS) is present, resistance to blood flow causes right ventricular hypertrophy. If right ventricular failure develops, right atrial pressure will increase, and this may result in a persistent opening of the foramen ovale, shunting of unoxygenated blood from the right atrium into the left atrium, and systemic cyanosis.
The pathophysiology of pulmonary heart disease (cor pulmonale) has always indicated that an increase in right ventricular afterload causes RV failure (pulmonary vasoconstriction, anatomic disruption/pulmonary vascular bed and increased blood viscosity are usually involved [1]), however most of the time, the right ventricle adjusts to an overload in chronic pressure.
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