Systolic dysfunction

Systolic dysfunction

Description, Causes and Risk Factors:

Systolic dysfunction refers to impaired ventricular contraction. In chronic heart failure, this is most likely due to changes in the signal transduction mechanisms regulating cardiac excitation-contraction coupling. The loss of cardiac inotropy (i.e., decreased contractility) causes a downward shift in the Frank-Starling curve. These results in a decrease in stroke volume and a compensatory rise in preload (often measured as ventricular end-diastolic pressure or pulmonary capillary wedge pressure). The rise in preload is considered compensatory because it activates the Frank-Starling mechanism to help maintain stroke volume despite the loss of inotropy. If preload did not rise, the decline in stroke volume would be even greater for a given loss of inotropy. Depending upon the precipitating cause of the heart failure, there will be ventricular hypertrophy, dilation, or a combination of the two.

The effects of a loss of intrinsic inotropy on stroke volume, and end-diastolic and end-systolic volumes, are best depicted using ventricular pressure-volume loops. Loss of intrinsic inotropy decreases the slope of the end-systolic pressure-volume relationship (ESPVR). This leads to an increase in end-systolic volume. There is also an increase in end-diastolic volume (compensatory increase in preload), but this increase is not as great as the increase in end-systolic volume.

The force-velocity relationship provides insight as to why a loss of contractility causes a reduction in stroke volume. Briefly, at any given preload and afterload, a loss of inotropy results in a decrease in the shortening velocity of cardiac fibers. Because there is only a finite period of time available for ejection, a reduced velocity of ejection results in less blood ejected per stroke. The residual volume of blood within the ventricle is increased (increased end-systolic volume) because less blood is ejected.

The reason for preload rising as inotropy declines is that the increased end-systolic volume is added to the normal venous return filling the ventricle. For example, if end-systolic volume is normally 50 ml of blood and it is increased to 80 ml in failure, this extra residual volume is added to the incoming venous return leading to an increase in end-diastolic volume and pressure.

An important and deleterious consequence of systolic dysfunction is the rise in end-diastolic pressure. If the left ventricle is involved, then left atrial and pulmonary venous pressures will also rise. This can lead to pulmonary congestion and edema. If the right ventricle is in systolic failure, the increase in end-diastolic pressure will be reflected back into the right atrium and systemic venous vasculature. This can lead to peripheral edema and ascites.


Symptoms may include:


  • Palpitation.

  • Dyspnea.

  • Angina pectoris.


Many options exist to diagnose systolic dysfunction. Electrocardiography (ECG) is the most common and reliable method. A doctor is able to measure heart function and gauge whether the heart is ejecting an adequate amount of blood with every pump. The doctor most likely will be able to determine the cause of the dysfunction at the same time. In some cases, though, a biopsy of heart tissue is necessary to check for bacterial infection.


Treatment for systolic dysfunction involves the use of inotropic drugs, afterload reducing drugs, venous dilators, and diuretics. Inotropic drugs include digitalis (commonly used in chronic heart failure) and drugs that stimulate the heart via beta-adrenoceptor activation or inhibition of cAMP-dependent phosphodiesterase (used in acute failure). Afterload reducing drugs (e.g., arterial vasodilators) augment ventricular ejection by increasing the velocity of fiber shortening (see force-velocity relationship). Venous dilators and diuretics are used to reduce ventricular preload and venous pressures (pulmonary and systemic) rather than augmenting systolic function directly.

For those whose systolic dysfunction is caused by a heart attack, a change is diet is essential for better health. Reducing salt intake and eating a low-fat, fiber-rich diet will help a patient lose weight and lower blood pressure. Quitting smoking and severely reducing alcohol intake is an absolute necessity. A doctor might suggest this course even if the dysfunction has a different cause, because lifestyle changes allow certain heart medications to act much more effectively.

NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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