A 65-year-old woman comes to the emergency department due to a 24-hour history of chest pain. She describes substernal chest pain accompanied by diaphoresis that began yesterday, persisted all night long, and started to clear only in the morning. Her son insisted that she go to the emergency department despite the fact that the pain is now "almost gone." The patient has a history of hypertension and diet-controlled diabetes mellitus. She is poorly compliant with her antihypertensive regimen. In the emergency department, her ECG shows sinus rhythm with ST-segment elevation in leads II, III, and aVF. Cardiac catheterization shows total occlusion of the proximal right coronary artery; intervention is deferred due to the patient's delayed presentation. On the third day of hospitalization, she suddenly develops severe shortness of breath and hypotension. On examination, she is diaphoretic and tachypneic. Bibasilar crackles are present. A short, soft systolic murmur is heard at the apex. Which of the following is the most likely cause of this patient's current symptoms?

Question

A 65-year-old woman comes to the emergency department due to a 24-hour history of chest pain.  She describes substernal chest pain accompanied by diaphoresis that began yesterday, persisted all night long, and started to clear only in the morning.  Her son insisted that she go to the emergency department despite the fact that the pain is now "almost gone."  The patient has a history of hypertension and diet-controlled diabetes mellitus.  She is poorly compliant with her antihypertensive regimen.  In the emergency department, her ECG shows sinus rhythm with ST-segment elevation in leads II, III, and aVF.  Cardiac catheterization shows total occlusion of the proximal right coronary artery; intervention is deferred due to the patient's delayed presentation.  On the third day of hospitalization, she suddenly develops severe shortness of breath and hypotension.  On examination, she is diaphoretic and tachypneic.  Bibasilar crackles are present.  A short, soft systolic murmur is heard at the apex.  Which of the following is the most likely cause of this patient's current symptoms?

Quizplus · Accepted Answer

11ec25c8_d873_8909_bc81_1de50f791722_MD0003_00 The development of hemodynamic compromise in the first few days following a myocardial infarction (MI) raises suspicion for mechanical complications of MI, as this is the point during the healing process in which the infarcted myocardium is softest and most prone to rupture. The 3 major mechanical complications of MI include mitral regurgitation (MR) due to papillary muscle rupture, left ventricle free wall rupture, and interventricular septum rupture. This patient's clinical features - inferior wall MI with delayed presentation, sudden onset of hypotension, dyspnea and tachypnea, pulmonary edema, and a soft systolic murmur - are consistent with acute MR due to posteromedial papillary muscle rupture, a life-threatening complication that usually occurs 3-5 days after MI. Patients commonly have a dramatic presentation with sudden onset of pulmonary edema, a mid-to-late systolic murmur consistent with MR, and possible cardiogenic shock. In up to 50% of the cases, patients may have a soft or no audible murmur (silent MR) if the MR is severe enough to cause early equalization of left atrial and left ventricular pressures. Diagnosis is typically confirmed by transthoracic or transesophageal echocardiography. Interventricular septal rupture can cause hypotension, heart failure, and a pansystolic murmur; however, the murmur is often best heard at the left sternal border, frequently has an accompanying thrill, and is less likely to radiate to the axilla. (Choice A) Aortic dissection typically presents with sudden onset of tearing chest/back pain and differential blood pressure in the upper extremities, and it can cause acute aortic regurgitation (early diastolic murmur). This patient's systolic murmur and pulmonary edema are not consistent with aortic dissection. (Choice B) Spontaneous coronary artery dissection is a rare cause of MI that would present with chest pain and would not explain this patient's murmur. (Choices C and E) Rupture of the left ventricular free wall is another post-MI complication that can cause hemopericardium and pericardial tamponade (hypotension, jugular venous distension, distant heart sounds). Patients rapidly progress to pulseless electrical activity and death. The majority of the cases occur after anterior MI (left anterior descending artery occlusion) rather than inferior MI. (Choice F) Acute pulmonary embolism can cause sudden onset of dyspnea, hypotension, right heart failure, and syncope. Patients typically do not develop acute MR or pulmonary edema. Educational objective: Papillary muscle rupture leading to acute mitral regurgitation and cardiogenic shock is a mechanical complication of acute myocardial infarction and usually occurs 3-5 days after the infarct. References: Acute valvular regurgitation. (http://www.ncbi.nlm.nih.gov/pubmed/19564568)

A 65-Year-Old Woman Comes to the Emergency Department Due to a 24-Hour