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Papillary muscle rupture pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Overview

Overview

The vascularization of the papillary muscles shows many individual variations and depends in part on coronary artery anatomy and dominance. However, the posterior papillary muscle is vascularized by posterior left ventricular branches that may have origin in the right, left or both coronary arteries. The anterior papillary muscle is vascularized by branches from diagonal, circumflex or even acute marginal branches of the left coronary artery. Papillary muscle ischemia occurs along with ischemia of the adjacent ventricular wall.

  • Acute mitral regurgitation (as may occur due to the sudden rupture of a chordae tendineae or papillary muscle) causes a sudden volume overload of both the left atrium and the left ventricle.
  • The left ventricle develops volume overload because with every contraction it now has to pump out not only the volume of blood that goes into the aorta (the forward cardiac output or forward stroke volume), but also the additional blood that regurgitated into the left atrium (the regurgitant volume).
  • The combination of the forward stroke volume and the regurgitant volume is known as the total stroke volume of the left ventricle.
  • In the acute setting, the total stroke volume (i.e. the forward plus the regurgitant volume) is increased, but the forward cardiac output into the aorta is decreased because a proportion of the blood is going backward into the left atrium. The mechanism by which the total stroke volume is increased as a result of increased left ventricular filling is known as the Frank-Starling mechanism.

The regurgitant volume causes acute volume overload and pressure overload of the left atrium as shown in the figure below. The sudden increase in pressure in the left atrium is transmitted backward into the pulmonary vein which in turn reduces drainage of blood from the lungs via the pulmonary veins and raises the pulmonary capillary sedge pressure. This causes pulmonary congestion.

Microscopic Pathology

Microscopic Pathology

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission. © PEIR, University of Alabama at Birmingham, Department of Pathology

References

References


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