![]() A failure in this process sometimes leads to persistent pulmonary hypertension, causing respiratory distress in the newborn. The pulmonary vessels remain closed under high pressure, and it is only after birth as the newborn takes its first breaths that the pulmonary artery pressures fall, shunts existing in the fetal life close, and blood begins to enter the lungs for exchange of gases for the fetus is no longer dependent on the placental circulation. The blood from the right atrium makes its way to the systemic circulation without actually reaching the lungs. The fetal circulation is designed to shunt blood across the liver and lungs during fetal life via the ductus venosus, foramen ovale, and the ductus arteriosus. The growing fetus receives its nutrients and excretes metabolic waste products via the placental vessels that connect the umbilical veins, which in turn drain into the inferior vena cava and then into the right atrium. The fetal circulation begins to form as early as 15 days after conception in the form of immature placental vessels and slowly grows to form a fully functional four-chambered heart, beating independently from the maternal circulation by the fourth week of gestation. This manifests as pleuritic chest pain and respiratory distress. Pleural effusion: A disturbance in the starling forces (see below, pathophysiology) of the pleural circulation can lead to accumulation of fluid in the pleural space, a phenomenon known as pleural effusion. If prolonged, it can lead to right ventricular stain and right heart failure, a phenomenon known as cor-pulmonale. It leads to impaired gas exchange and commonly manifests as exertional dyspnea. Pulmonary hypertension: An increase in the mean pulmonary artery pressure beyond 25 mmHg is known as pulmonary arterial hypertension. It is important to note that the peripheral parenchyma is more prone to infarcation as it is purely reliant on the pulmonary circulation for oxygenation (see below, function). Pulmonary embolism: A dislodged clot from a distant source (most commonly a deep venous thrombus) can embolize to the pulmonary circuit and lead to ischemia and, if prolonged, infarction of the lung parenchyma as well as severely impaired gaseous exchange. inflammation), and decreased surfactant (i.e. lymphedema), increased vessel permeability (i.e. low albumin), decreased lymphatic clearance (i.e. Causes include elevated hydrostatic pressure (i.e heart failure), decreased serum oncotic pressure (i.e. Pulmonary edema can either be cardiogenic or non-cardiogenic. ![]() Pulmonary edema: Any disturbance in the starling forces (see below, pathophysiology) operating in the pulmonary circulation can lead to an accumulation of fluid in the alveoli, impairing gas exchange, and causing respiratory distress. Some of the common pathologies of the pulmonary circuit include but are not limited to the following: Any compromise can have grave consequences and lead to tissue dysfunction secondary to hypoxia. Pulmonary circulation is essential for the body to ensure a continuous supply of oxygenated blood. ![]() However, its venous return to the left heart is minimal (0-0.5% of cardiac output) and does not affect cardiac output to any significant degree as volumes between right and left ventricles are nearly identicle. As a result, the deep bronchial system effectively functions as an arteriovenous shunt. However, the deep circulation drains into the pulmonary vein and thus left ventricle. The superficial system drains into the hemiazygos and azygos veins, which ultimately drain into the right heart with the systemic venous return. The bronchial circulation has superifical and deep systems. In addition to the pulmonary circulation, the lung parenchyma receives oxygenated blood via the bronchial circulation (accounting for about ~1% of the cardiac output) which arises from the aorta, and thus left ventricle. The large negative pleural pressure (approximately -4 to -7 mmHg) exists because of an efficient efferent venous and lymphatic system that keeps the alveoli closely tethered to the visceral pleura and prevents them from collapsing inwards. ![]() It is appropriate to mention that a similar system of lymphatics and vessels exists between the parietal and visceral pleurae, draining the pleural fluid which plays an important role in providing a viscous medium for expansion of lungs during their respiratory excursion. They can be found close to the terminal bronchioles and drain the mediastinal lymphatics before emptying into the right lymphatic duct. Lymphatics play a crucial role in maintaining a dry alveolar membrane and preventing accumulation of tissue fluid around the pulmonary circulation. ![]()
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