Acute, but massive pulmonary thromboembolytic event, likely secondary to an isol
ID: 34276 • Letter: A
Question
Acute, but massive pulmonary thromboembolytic event, likely secondary to an isolated, deep vein thrombosis; this event initially caused transmural left ventricular myocardial infarction due to liberation of vasoconstrictive mediators from the thrombus acting at the left anterior ventricular branch of the coronary artery. the thrombus also led to a large increase in physiological dead space. in the intervening three days the secondary complication of right ventricular dilation caused by pulmonary hypertension brought on by both left ventricular failure and constriction of pulmonary flow from eh thrombus exacerbated both the pulmonary and left ventricular pathologies as follows: pulmonary pathology was worsened by edema caused by pulmonary hypertension (which clearly exaggerated the already hypoxemic condition), while left ventricular function was severely hampered by septal deviation toward the left secondary to overwork of (and thus, elevated pressure within) the right ventricle. This, in turn, decreased left ventricular filling and, further, exaggerated the ischemic, hypoxemic state.
Describe this in terms that an introductory bio major would understand.
Explanation / Answer
Deep vein thrombosis, or deep venous thrombosis, (DVT) is the formation of a blood clot (thrombus) within a deep vein, predominantly in the legs.Pulmonary embolism, a potentially life-threatening complication, is caused by the detachment (embolization) of a clot that travels to the lungs.The beginning of venous thrombosis is thought to be caused by tissue factor, which leads to conversion of prothrombin to thrombin, followed by fibrin deposition.when the embolus lodges in heart vessels it leads to MI of the region and when in pulonary vessels it leads to pulmonary hypertension and increased ead space due to lackk of exchange of gases distal to blocked vessel.
Pulmonary htn leads to decrease in clearance of transudate by the lymphatics leading to pulmonary oedema and thus dyspnoea.Pulmonary htn leads to right ventricular overload leading to hypertrophy and deviation of septum to left.this decreases left ventricular volume.thus decreasing the cardiac output.decreased cardiac output leads to less supply of blood to peripheries and thus ischemia.
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