A 38-year-old man is brought to the emergency department due to sudden-onset shortness of breath and diaphoresis. He has no fever, chills, cough, or abdominal pain. The patient has no other medical problems and takes no medications. He had surgery for bilateral inguinal hernias at age 16. The patient does not use tobacco, alcohol, or illicit drugs. Blood pressure is 95/60 mm Hg, pulse is 116/min and regular, and respirations are 28/min. He is in marked respiratory distress. Pallor and diaphoresis are noted. His skin is velvety and has many atrophic scars. The apical impulse is hyperdynamic. Cardiac auscultation reveals a soft, early-systolic decrescendo murmur at the cardiac apex. S1 is barely audible; S2 is normal. Lung examination reveals bibasilar crackles. Jugular venous distension is present. The abdomen is soft, nontender, and nondistended. Neurologic examination shows no abnormalities. ECG shows sinus tachycardia with occasional premature ventricular complexes. Chest x-ray reveals no cardiomegaly, but bilateral alveolar infiltrates and hilar prominence are present.
Which of the following is the most likely cause of this patient's condition?

Question

A 38-year-old man is brought to the emergency department due to sudden-onset shortness of breath and diaphoresis.  He has no fever, chills, cough, or abdominal pain.  The patient has no other medical problems and takes no medications.  He had surgery for bilateral inguinal hernias at age 16.  The patient does not use tobacco, alcohol, or illicit drugs.  Blood pressure is 95/60 mm Hg, pulse is 116/min and regular, and respirations are 28/min.  He is in marked respiratory distress.  Pallor and diaphoresis are noted.  His skin is velvety and has many atrophic scars.  The apical impulse is hyperdynamic.  Cardiac auscultation reveals a soft, early-systolic decrescendo murmur at the cardiac apex.  S1 is barely audible; S2 is normal.  Lung examination reveals bibasilar crackles.  Jugular venous distension is present.  The abdomen is soft, nontender, and nondistended.  Neurologic examination shows no abnormalities.  ECG shows sinus tachycardia with occasional premature ventricular complexes.  Chest x-ray reveals no cardiomegaly, but bilateral alveolar infiltrates and hilar prominence are present. 
Which of the following is the most likely cause of this patient's condition?

Quizplus · Accepted Answer

Explanation: 11ec2b69_c11a_9d59_8f63_33e9f66a0df6_MD0005_00 This patient has acute heart failure due to acute mitral valve regurgitation (MR). Acute MR can occur due to papillary muscle rupture, typically in the setting of myocardial infarction (MI), or due to rupture of the mitral chordae tendineae. Patients with mitral valve prolapse, especially when it is related to underlying connective tissue disease (eg, Marfan syndrome, Ehlers-Danlos syndrome), are at risk for mitral chordae tendineae rupture, leading to a flail leaflet and acute MR. Patients with acute MR typically have a dramatic presentation (due to lack of time for left heart adaptation) compared to those with chronic MR. They often present with sudden-onset hypotension and can rapidly progress to cardiogenic shock with poor tissue perfusion and peripheral vasoconstriction. Cardiac examination reveals a hyperdynamic precordium and a decrescendo holosystolic murmur at the cardiac apex. Patients with acute, severe MR have early equalization of left atrial and left ventricular pressures, and up to 50% (especially with ischemic MR) may have no audible murmur (silent MR). The diagnosis is typically confirmed by rapid bedside echocardiography. (Choices A and C) Papillary muscle rupture with acute, severe MR can occur as a life-threatening mechanical complication of acute MI, typically 3-5 days after the infarct. This patient's presentation and ECG findings do not show evidence of ischemia or recent MI. Spontaneous papillary muscle rupture in young patients without any symptoms suggestive of recent MI is uncommon. (Choice B) Infective endocarditis involving the mitral valve can lead to acute MR due to inadequate leaflet coaptation, leaflet perforation, or papillary muscle involvement. This patient's absence of preceding fever combined with his velvety skin with scar formation and previous bilateral hernias (suggestive of underlying connective tissue disease) make mitral chordae tendineae rupture more likely. (Choice D) Massive, acute pulmonary embolism can cause sudden-onset dyspnea, hypotension, right heart failure, and syncope. However, patients do not typically develop acute pulmonary edema. Educational objective: Patients with underlying connective tissue disease are at risk for acute mitral valve regurgitation (MR) due to chordae tendineae rupture. Typical presentation is with sudden-onset pulmonary edema, hypotension, and a hyperdynamic precordium with a holosystolic murmur; however, the murmur may be absent in up to 50% of patients with acute, severe MR. References: Acute mitral regurgitation requiring urgent surgery because of chordae ruptures after extreme physical exercise: case report. (http://www.ncbi.nlm.nih.gov/pubmed/18782707) Simultaneous onset of mitral regurgitation requiring surgery due to primary chordal rupture in middle-aged identical twins. (http://www.ncbi.nlm.nih.gov/pubmed/16080985) Incidence of ruptured chordae tendineae in the mitral valvular prolapse syndrome: an echocardiographic study. (http://www.ncbi.nlm.nih.gov/pubmed/421575)

A 38-Year-Old Man Is Brought to the Emergency Department Due