A. Prominent V waves in the pulmonary artery capillary wedge pressure tracing
B. Increased right heart pressures and decreased left heart pressures with inspiration
C. Elevation and equalization of cardiac pressures
D. An oxygen step-up from the right atrium to the pulmonary artery
E. Prominent V waves in the right atrial pressure tracing
F. Both B and C
Choice A describes the findings in acute mitral valve regurgitation which can occur as a complication of an inferior myocardial infarction from papillary muscle rupture. When a large pressure is forced into the left atrium during systole from the mitral regurgitant volume, a large pressure wave is created which is the V wave. Normal V waves are small, however it becomes quite large with severe mitral regurgitation. Likewise, choice E describes severe tricuspid regurgitation which has similar hemodynamics, only translated to the right heart.
Acute severe mitral regurgitation is a life-threatening disorder. Papillary muscle rupture after acute myocardial infarction can occur as a complication of an inferior MI (right coronary artery supply) since the posteromedial papillary muscle is the most likely to rupture.
There are two papillary muscles that comprise part of the complex anatomy of the mitral valve. The anterolateral papillary muscle receives dual blood supply from the left anterior descending coronary artery and the left circumflex coronary artery in most individuals while the posteromedial papillary muscle receives its sole blood supply from the right coronary artery. Complete infarction of the posteromedial papillary muscle can occur during an inferior MI while only partial or no damage will be done to the anterolateral papillary muscle during an anterior (left anterior descending) or lateral (circumflex) infarction since there is dual blood supply to this papillary muscle. Thus, the posteromedial papillary muscle is the most likely to rupture.
Emergent surgical repair or replacement of the mitral valve is indicated. Mortality approaches 100% if not surgically fixed.
A left ventricular free wall rupture causes sudden accumulation of blood in the pericardium and cardiac tamponade which can be rapidly fatal. Choice B and C describe ventricular interdependence that occurs during cardiac tamponade or constrictive pericarditis. Normally, the pericardium can expand as the heart fills, however with cardiac tamponade from a large pericardial effusion or constrictive pericarditis, this is not able to occur. As a person inspires, venous return is increased to the right heart and the interventricular septum bulges to the left impairing left ventricular filling, reducing left heart cardiac output and thus decreasing systemic pressure (increasing the “pulsus paradoxus”). As a person exhales, right ventricular filling decreases and the left heart fills causing the interventricular septum to bulge to the right impairing right ventricular filling. The diastolic pressures are elevated and equal since every cardiac chamber pressure influences the other considering the heart is not able to expand as mentioned above.
Choice D describes an acute ventricular septal defect, right heart catheterization will show an “oxygen step-up” between the right atrium and right ventricle or pulmonary artery (since oxygenated blood will be present in the right ventricle or pulmonary artery). When infarction of the interventricular septum occurs, this area can thin with the remodeling process and on occasion, a complete defect between the right and left ventricles can develop. This results in left to right shunting of blood and can be life-threatening when acute. A holosystolic murmur at the left lower sternal border occurs.