, Benjamin Hohlfelder2 and Samuel Z. Goldhaber3
(1)
Cardiovascular Division, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA
(2)
Department of Pharmacy Services, Brigham and Women’s Hospital, Boston, Massachusetts, USA
(3)
Thrombosis Research Group, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA
Abstract
Deep vein thrombosis (DVT) and pulmonary embolism (PE) result from a combination of pathophysiological states including endothelial injury, stasis, inflammation, and hypercoagulability. The extent of the PE, the patient’s underlying cardiopulmonary reserve, and compensatory neurohumoral adaptations determine the overall hemodynamic impact. The right ventricle (RV) plays a central role in PE pathophysiology. A sudden increase in RV afterload due to PE can lead to RV dilation and hypokinesis, RV ischemia, and ultimately acute RV failure.
Keywords
Deep vein thrombosisPathophysiologyPulmonary embolismRight ventricleSelf-Assessment Questions
1.
Which of the following processes result in increased pulmonary vascular resistance and RV pressure overload in the setting of acute PE?
(a)
Direct physical obstruction of the pulmonary arterial tree, hypoxemic vasoconstriction, and decreased RV cardiac output
(b)
Direct physical obstruction of the pulmonary arterial tree, hypoxemic vasoconstriction, and release of potent pulmonary arterial vasoconstrictors
(c)
Direct physical obstruction of the pulmonary arterial tree, right-to-left shunting through a patent foramen ovale, and release of potent pulmonary arterial vasoconstrictors
(d)
Direct physical obstruction of the pulmonary arterial tree, hypoxemic vasoconstriction, and interventricular septal deviation toward the RV
2.
Hemodynamic collapse due to acute PE may occur as a result of all of the following processes except?
(a)
RV dilatation and hypokinesis
(b)
Impaired LV filling
(c)
RV ischemia and infarction
(d)
Tricuspid regurgitation
Clinical Vignette
A 41-year-old obese woman with recent hospitalization for Crohn’s Disease presented with sudden onset dyspnea and pleuritic pain. Two days prior to presentation, she noted right calf discomfort. In the Emergency Department, she was noted to be tachycardic to 110 beats per minute, hypotensive with a blood pressure of 86/52 mmHg, and hypoxemic with a room air oxygen saturation of 88 %. An electrocardiogram was significant for sinus tachycardia. A contrast-enhanced chest CT demonstrated bilateral PE (Fig. 3.1) with right ventricular (RV) enlargement (Fig. 3.2). Venous ultrasound demonstrated right popliteal DVT.
Fig. 3.1
Contrast-enhanced chest computed tomogram (CT) demonstrating bilateral pulmonary embolism (PE) (arrows) in a 41-year-old woman with dyspnea, pleuritic pain, and hypoxemia
Fig. 3.2
Contrast-enhanced chest computed tomogram (CT) demonstrating right ventricular (RV) enlargement defined as an RV diameter-to-left ventricular diameter ratio greater than 0.9 in a 41-year-old woman with dyspnea, pleuritic pain, and hypoxemia who was diagnosed with bilateral pulmonary embolism (PE)
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