In some patients, fetal circulation shunts remain patent after delivery. Usually, patients with an open fetal shunt are asymptomatic and may only have a cardiac murmur upon auscultation. A patent foramen ovale connects the right and left atria and is usually found as an incidental finding on echocardiogram or after a cryptogenic stroke. In patients with a patent foramen ovale, there is a possibility that a thrombus from the lower extremity may bypass the lungs. This can be accomplished when the blood enters the right atrium, flows through the foramen ovale, and empties into the left atrium.[2] The thrombus would be able to travel from the left atrium into systemic circulation where it can, unfortunately, be delivered to the brain causing a thromboembolic cerebrovascular accident (CVA).

The most worrisome complication of pulmonary circulation dysfunction is a pulmonary embolism which usually arises as a deep venous thrombosis (DVT) of the lower extremity. Rarely do DVTs occur without satisfying at least one of the three components of Virchow’s triad: hypercoagulability, endothelial damage, and venous stasis.[5] Certain genetic disorders like factor V Leiden, protein C deficiency, and protein S deficiency along with more common conditions like pregnancy and cancer are related to states of hypercoagulability.[6] Endothelial damage can occur from trauma or surgery, and venous stasis is commonly associated with periods of immobility either from traveling and disability. If the deep venous thrombus is dislodged from the lower extremity, it is pushed by deoxygenated blood back into the heart and then into the lungs where it can lodge into a small pulmonary vessel. If large enough, the clot can cause hemodynamic compromise to areas proceeding it. Automatically, pulmonary vessels in the area of the thrombus vasoconstrict which causes shunting of blood to non-occluded portions of the lung.[5]

Classically, a patient with a pulmonary embolism (PE) due to a DVT presents with symptoms of crushing, pleuritic chest pain, chest pressure, or dyspnea with a history of a swollen, painful lower extremity. Upon physical exam, tachycardia is almost always present. In most cases, the chest x-ray is unremarkable, but occasionally, one or both of the classic chest x-ray findings are visible. Westermark's sign is a sharp delineation between the area of perfusion and hypo-perfusion within a vessel indicating an embolism is blocking flow, and Hampton's hump presents as a wedge-shaped, focal opacity in the periphery of the lung.[5]

When clots form in the body, they are continually being reconstructed. Clotting factor XIII is responsible for cross-linking fibrin into a mesh. Upon degradation, plasmin lyses the fibrin bonds and releases the fibrin degradation products called D-dimers. In some cases of suspected pulmonary embolisms, physicians may order blood samples to test a D-dimer. An elevated D-dimer level has high sensitivity but low specificity for a pulmonary embolism. A D-dimer can be elevated in the setting of any hypercoagulable state such as pregnancy, congestive heart failure, systemic lupus erythematosus (SLE), and other chronic diseases, this test is most useful when a pulmonary embolism is suspected in a younger patient with no co-morbidities. The gold standard of diagnosing a PE is computed tomography (CT) angiography. The contrast is given intravenously and will indicate areas of hypoperfusion caused by a thrombus. However, in instances when there is a contraindication to this imaging study such as in the setting of renal failure when contrast dye cannot be given, a pulmonary ventilation/perfusion (V/Q) scan can be performed.[5]

Another potential complication of pulmonary circulation is pulmonary arterial hypertension. Pulmonary arterial hypertension is defined by a mean pulmonary artery pressure of greater than twenty-five millimeters of mercury and pulmonary vascular resistance greater than three millimeters of mercury which is measured via right heart catheterization. Interestingly, pulmonary arterial hypertension can be caused by a variety of circumstances such as obstruction of the pulmonary arteries and arterioles, increased pulmonary vascular resistance, luminal thickening, vascular remodeling, and chronic inflammation.[4]

In pulmonary arterial hypertension, there is an increase in pulmonary vascular resistance which can be caused by the destruction of the pulmonary vasculature, chronic vasoconstriction, endothelial thickening, arteriole smooth muscle hypertrophy, and endothelial wall remodeling. Thromboxane and endothelin-1 are believed to have increased activity which causes enhanced vasoconstriction while prostacyclin and nitric oxide which both function as vasodilators, have decreased efficiency. Because of these, blood vessels are narrowed which causes higher flow rates and thus pressure in the vasculature. However, these cause increased pulmonary vascular resistance which decreases endothelial integrity. The body naturally attempts to heal endothelial damage by sending coagulation factors to the intimal surface of the vessel.[7]

Left-sided heart failure commonly causes pulmonary venous hypertension. The left side of the heart has difficulty maintaining function. Therefore, blood is forced back into the lungs leading to increased pressure in the pulmonary vein. In the case of left-sided heart failure due to valve failure, decreased ejection fraction, or volume overload, blood that should be ejected into systemic circulation backs up into the left ventricle, left atrium, and finally, the pulmonary veins. Increased pulmonary venous pressure can lead to capillary remodeling and elevated capillary permeability causing fluid leakage into the lung bases. The most common cause of this is congestive heart failure due to left heart dysfunction and volume overload.[4]