For each risk factor, click to specify whether the risk factor is a modifiable or non-modifiable risk factor for coronary artery disease.

• Smoking cigarettes: Smoking promotes endothelial damage, increases platelet aggregation, and raises blood viscosity, all of which contribute to clot formation. Nicotine also causes vasoconstriction, reducing normal blood flow. These changes support Virchow’s triad of hypercoagulability and vessel injury. As a result, smoking significantly increases DVT risk.

• Taking a walk every day: Regular ambulation promotes calf muscle contraction, which enhances venous return to the heart. Improved circulation reduces blood pooling in the lower extremities. Physical activity counteracts venous stasis, one component of Virchow’s triad. Daily walking therefore lowers DVT risk.

• Drinking water frequently: Adequate hydration prevents hemoconcentration and reduces blood viscosity. Thinner blood flows more easily through veins, decreasing clot formation risk. Proper hydration also supports overall circulatory efficiency. Maintaining fluid balance helps reduce DVT development.

• Undergoing orthopedic surgery: Orthopedic procedures, especially involving the hip or knee, increase venous stasis due to immobility and tissue trauma. Surgical manipulation of large bones can release procoagulant substances into circulation. Postoperative immobility further slows venous return. These factors substantially elevate DVT risk.

• Flying on a 12-hour flight: Prolonged sitting restricts calf muscle contraction, decreasing venous return from the lower extremities. Venous stasis allows blood to pool, increasing the likelihood of clot formation. Dehydration during long flights can further thicken blood. Extended immobility is a well-established DVT risk factor.

A. The heart stops working to pump blood to the body:Cardiac arrest may occur as a complication of a myocardial infarction, but it does not precede the event. Before an MI, the heart continues to pump, although its tissue may be ischemic.

B. The blood is too thin:Thin blood, or decreased viscosity, is not a typical precursor to myocardial infarction. MI is primarily caused by blockage of coronary arteries, not changes in blood thickness.

C. The hemoglobin count is low:Low hemoglobin can reduce oxygen delivery to tissues but is not the direct cause of a myocardial infarction. An MI results from sudden obstruction of blood flow rather than anemia.

D. The blood supply to the heart is suddenly cut off:A myocardial infarction occurs when a coronary artery becomes blocked, often due to plaque rupture and thrombosis, resulting in sudden cessation of oxygen-rich blood to a portion of the heart muscle. This ischemia triggers myocardial cell injury and death, which defines the infarction.