A 42-year-old man comes to the emergency department due to acute-onset shortness of breath. He has no medical conditions and does not use alcohol, tobacco, or illicit drugs. The patient works as a box handler at a warehouse and has excellent exercise tolerance. Family history is insignificant. Blood pressure is 98/60 mm Hg and pulse is 112/min and regular. A short systolic murmur is heard at the apex. Bilateral crackles are present on lung auscultation. Bedside echocardiography reveals a flail posterior mitral leaflet due to chordal rupture and severe mitral regurgitation. Which of the following best reflects this patient's left ventricular hemodynamics compared to the normal heart?

Question

A 42-year-old man comes to the emergency department due to acute-onset shortness of breath.  He has no medical conditions and does not use alcohol, tobacco, or illicit drugs.  The patient works as a box handler at a warehouse and has excellent exercise tolerance.  Family history is insignificant.  Blood pressure is 98/60 mm Hg and pulse is 112/min and regular.  A short systolic murmur is heard at the apex.  Bilateral crackles are present on lung auscultation.  Bedside echocardiography reveals a flail posterior mitral leaflet due to chordal rupture and severe mitral regurgitation.  Which of the following best reflects this patient's left ventricular hemodynamics compared to the normal heart?

Quizplus · Accepted Answer

11ec160b_3a93_35b0_9249_69d07ab3e06d_MD0001_00 This patient has acute mitral regurgitation (MR) due to a spontaneous chordae tendineae rupture. In acute MR, the left atrium (LA) is of normal size and compliance and is suddenly exposed to a large volume of regurgitant blood from the left ventricle (LV). This leads to very high LA pressures and subsequent pulmonary edema. In addition, because the LV must accommodate the regurgitant blood volume along with normal pulmonary venous return, there is increased LV end-diastolic volume (preload). Meanwhile, the incompetent mitral valve forms a low-resistance regurgitant pathway for blood to flow into the LA during ventricular systole, decreasing LV afterload. The decreased afterload leads to increased LV ejection fraction (via increased stroke volume); however, much of the stroke volume is lost to regurgitation into the LA, resulting in overall decreased forward stroke volume and reduced cardiac output (manifesting as hypotension and cardiogenic shock). In chronic MR, compensatory LA enlargement allows the LA to receive the regurgitant volume at lower filling pressures, preventing pulmonary edema from developing. Chronic volume overload also causes the LV to undergo substantial enlargement due to eccentric hypertrophy. Early on, the larger ventricular volume helps maintain forward stroke volume even in the setting of substantial regurgitant flow. However, with prolonged hemodynamic overload, progressive eccentric remodeling of the LV becomes maladaptive, resulting in an overwhelming increase in wall stress with eventual contractile dysfunction. The impaired contractility culminates in decompensation of chronic MR with reduced forward stroke volume (decreased cardiac output) and increased left-sided filling pressures (pulmonary edema). Educational objective: Regurgitant flow into the left atrium in acute mitral regurgitation leads to increased left atrial pressure and increased left ventricular end-diastolic volume (preload). The low-resistance regurgitant pathway also decreases left ventricular afterload with a resulting increase in ejection fraction but overall decrease in forward stroke volume. Increased left atrial pressure and decreased cardiac output result in pulmonary edema and severe hypotension, respectively. __________ References: Left ventricular response to mitral regurgitation: implications for management. (http://www.ncbi.nlm.nih.gov/pubmed/19029478)

A 42-Year-Old Man Comes to the Emergency Department Due to Acute-Onset