A 59-year-old man presents to the emergency department with a 4-hour history of “crushing” chest…

A 59-year-old man presents to the emergency department with
a 4-hour history of “crushing” chest pain. His cardiac examination is normal
with no murmurs and normal heart sounds. An ECG reveals ST segment elevation in
the lateral precordial leads, and cardiac enzymes show evidence of myocardial
injury. He undergoes emergent cardiac catheterization that shows a thrombus in
the left circumflex artery. He undergoes successful angioplasty, and a stent is
placed. He is monitored in the cardiac intensive care unit. He does well until
the next day, when he develops sudden shortness of breath and
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A 59-year-old man presents to the emergency department with
a 4-hour history of “crushing” chest pain. His cardiac examination is normal
with no murmurs and normal heart sounds. An ECG reveals ST segment elevation in
the lateral precordial leads, and cardiac enzymes show evidence of myocardial
injury. He undergoes emergent cardiac catheterization that shows a thrombus in
the left circumflex artery. He undergoes successful angioplasty, and a stent is
placed. He is monitored in the cardiac intensive care unit. He does well until
the next day, when he develops sudden shortness of breath and decreasing oxygen
saturations. Physical examination now reveals jugular venous distention, rales
at both lung bases, and a blowing holosystolic murmur loudest at the apex, radiating
into the axilla.

Questions

A. What likely accounts for this patient’s sudden
decompensation?

B. What is the main pathophysiologic derangement in this
condition?

C. What changes in the heart take place if this condition
develops slowly rather than suddenly?

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