A 64-year-old woman presents on postoperative day 7 following total hip arthroplasty with sudden onset severe dyspnea, pleuritic chest pain, near-syncope, and hypotension (BP 78/50). On examination she is tachypneic, tachycardic with cool extremities, loud P2, and elevated JVP. Bedside echocardiogram shows a dilated, hypokinetic right ventricle with septal flattening and McConnell's sign. CT pulmonary angiogram demonstrates the structure marked **A** in the diagram. Which of the following best describes the pathophysiological consequence of this finding?
A. Gradual pulmonary vascular remodeling with chronic RV hypertrophy and eventual cor pulmonale development over weeks to months
B. Localized alveolar hemorrhage with pulmonary infarction confined to a single lobe due to bronchial circulation insufficiency
C. Acute left ventricular failure secondary to mitral valve obstruction from thrombus embolization into the left heart chambers
D. Sudden mechanical obstruction of pulmonary blood flow leading to acute right ventricular afterload increase, RV dilation, interventricular septal flattening, and obstructive shock
Explanation
Why "Sudden mechanical obstruction of pulmonary blood flow leading to acute right ventricular afterload increase, RV dilation, interventricular septal flattening, and obstructive shock" is right
The structure marked A — a saddle thromboembolus straddling the bifurcation of the main pulmonary artery — causes immediate mechanical obstruction of pulmonary blood flow. This sudden increase in RV afterload forces the right ventricle to dilate acutely, causing interventricular septal flattening (D-shaped LV in short axis on echo) and decreased LV preload, culminating in obstructive shock. The patient's hemodynamic collapse (BP 78/50), tachycardia, cool extremities, elevated JVP, and echocardiographic findings of RV dilation with septal flattening and McConnell's sign are all direct consequences of this acute mechanical obstruction. This is the defining pathophysiology of massive (high-risk) pulmonary embolism as per ESC Guidelines 2019 and AHA 2011 criteria.
Why each distractor is wrong
Gradual pulmonary vascular remodeling with chronic RV hypertrophy and eventual cor pulmonale development over weeks to months: This describes chronic pulmonary hypertension or chronic thromboembolic disease, not the acute presentation of massive PE. The patient's acute shock state and immediate hemodynamic collapse rule out a gradual process.
Localized alveolar hemorrhage with pulmonary infarction confined to a single lobe due to bronchial circulation insufficiency: While pulmonary infarction can occur in PE, it is typically peripheral and occurs only when bronchial circulation is compromised. A saddle embolus at the PA bifurcation causes massive bilateral obstruction, not localized infarction, and the primary pathophysiology is mechanical obstruction, not infarction.
Acute left ventricular failure secondary to mitral valve obstruction from thrombus embolization into the left heart chambers: Thrombi do not typically cross the pulmonary circulation to obstruct the mitral valve. The left ventricular dysfunction in massive PE is secondary to decreased preload and septal flattening from RV dilation, not from direct valve obstruction.
High-YieldNEET PG
Massive PE = saddle embolus at PA bifurcation → acute RV afterload surge → RV dilation + septal flattening + obstructive shock; mortality 25–65% without thrombolysis.
ESC Guidelines on PE 2019; AHA Massive PE 2011
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