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Pulmonary circulation

Pulmonary circulation is the portion of the cardiovascular system that transports deoxygenated blood from the right ventricle of the heart to the lungs for gas exchange and returns oxygenated blood to the left atrium and ventricle.^[1] This low-pressure, high-flow circuit receives the entire cardiac output from the right heart and functions primarily to facilitate the oxygenation of blood and removal of carbon dioxide through diffusion in the pulmonary capillaries.^[2] Unlike the systemic circulation, which operates under higher pressure to supply oxygen and nutrients to body tissues, pulmonary circulation is characterized by thin-walled vessels and a parallel arrangement of capillaries that maximize surface area for efficient gas exchange.^[3] The anatomical structure of pulmonary circulation begins with the main pulmonary artery, which arises from the right ventricle and bifurcates into the right and left pulmonary arteries (the main trunk about 5 cm long), supplying the respective lungs.^[2] These arteries branch into smaller pulmonary arterioles and eventually form an extensive capillary network surrounding the alveoli, where gas exchange occurs.^[2] Oxygenated blood then collects in pulmonary venules, which converge into four pulmonary veins (two from each lung) that drain directly into the left atrium.^[1] The pulmonary arteries are thinner and more compliant than their systemic counterparts, with walls approximately one-third as thick, allowing them to accommodate the full cardiac output at low pressures (typically 25/8 mmHg in the pulmonary artery).^[2] Additionally, a separate bronchial circulation, derived from the systemic aorta, provides oxygenated blood to the lung parenchyma and airways, accounting for about 1% of cardiac output and draining partly into the pulmonary veins.^[2] Physiologically, pulmonary circulation operates as a low-resistance system with high vascular compliance, enabling it to handle large blood volumes without significant pressure elevation.^[2] Blood flow distribution is influenced by gravity and lung zones: Zone 1 (alveolar pressure exceeds arterial, minimal flow), Zone 2 (intermittent flow during systole), and Zone 3 (continuous flow, predominant in dependent lung regions).^[2] The circuit's efficiency is maintained by lymphatic drainage, which removes excess fluid from the interstitium to keep alveoli dry, with lymphatics originating near terminal bronchioles and draining via bronchomediastinal trunks into the thoracic duct and right lymphatic duct.^[2]^[4] In the fetus, pulmonary circulation is bypassed via shunts like the ductus arteriosus and foramen ovale, which close postnatally to establish the mature pathway.^[1] This system ensures that deoxygenated blood from the body, entering the right atrium via the venae cavae, is rapidly processed in the lungs before distribution to the systemic circulation.^[3]

Anatomy

Pulmonary Arteries

The pulmonary arteries originate from the right ventricle of the heart via the pulmonary trunk, a short vessel approximately 5 cm in length that arises at the base of the ventricle just distal to the pulmonary valve and ascends anteriorly before bifurcating into the left and right main pulmonary arteries at the level of the second costal cartilage.^[5] The pulmonary trunk has a diameter of about 2.5 to 3 cm in adults, facilitating the transport of deoxygenated blood to the lungs under low pressure.^[6] The main pulmonary arteries follow the branching pattern of the bronchial tree, dividing first into lobar arteries—typically two per lung (upper and lower for the right lung, and upper and lower for the left, with the left upper often including the lingula)—and then into segmental arteries that supply the bronchopulmonary segments.^[7] Each lung contains 8 to 10 bronchopulmonary segments, resulting in approximately 18 to 20 segments total across both lungs, with further subdivision into subsegmental arteries that penetrate the lung parenchyma.^[8] This hierarchical branching ensures even distribution of blood flow to match regional ventilation. The walls of the pulmonary arteries are thin and distensible, consisting of three layers (intima, media, and adventitia) but with significantly less smooth muscle and elastic tissue compared to systemic arteries of similar size, which accommodates the low-pressure, high-compliance environment of the pulmonary circulation.^[9] This composition allows for easy distension during systole and minimal resistance to flow, with wall thickness typically less than 5% of the external diameter in muscular branches.^[10] Anatomical variations in the pulmonary arteries include asymmetry between the left and right main branches, where the right pulmonary artery is longer and courses horizontally beneath the aortic arch, while the left is shorter and passes superior to the left main bronchus.^[5] Trifurcation of the pulmonary trunk, where it divides into three branches instead of two, occurs rarely and is often associated with other congenital anomalies.^[11] Within the lungs, variations such as absent or accessory lobar arteries (e.g., to the middle lobe) are noted in up to 20-30% of individuals, influencing surgical planning.^[12] The pulmonary arteries enter the lungs at the hilum, traveling alongside the bronchi within bronchovascular bundles that also include nerves and lymphatics, ensuring coordinated delivery of blood to ventilated regions.^[13] This close anatomical relationship facilitates the matching of perfusion to ventilation throughout the pulmonary tree.^[14]

Pulmonary Capillaries

The pulmonary capillaries form a dense microvascular network surrounding the alveoli, creating a sheet-like bed that facilitates gas exchange across an extensive surface area estimated at 70-80 m² in humans.^[15] This network comprises approximately 280 billion capillaries associated with around 300 million alveoli, enabling efficient diffusion of oxygen and carbon dioxide between blood and air.^[15] The capillaries originate from the terminal branches of pulmonary arterioles, branching into interconnected segments embedded within the alveolar walls.^[16] Structurally, pulmonary capillaries feature thin endothelial walls, typically 0.2-0.5 μm thick, composed of flattened squamous endothelial cells that minimize the diffusion barrier.^[17] These capillaries lack fenestrations, relying instead on continuous non-fenestrated endothelium connected by tight junctions to maintain barrier integrity while allowing selective transcellular transport.^[16] The endothelial layer is supported by a thin basement membrane shared with adjacent alveolar epithelial cells, contributing to the overall blood-air barrier thickness of about 0.3-1 μm.^[16] In terms of distribution, the capillaries are primarily located within the alveolar septa, forming three morphological types: corner vessels at alveolar junctions, plate-like sheets spanning septal flats, and intricate networks in denser regions.^[18] This arrangement allows for dynamic adaptation, with capillary recruitment—opening of previously closed vessels—and distension—expansion of open vessels—occurring in response to increased pulmonary artery pressure or lung inflation.^[15] At rest, the capillary bed holds about 70 mL of blood, which can increase to 200 mL during exercise through these mechanisms, enhancing gas exchange capacity.^[15] Compared to systemic capillaries, pulmonary capillaries exhibit shorter path lengths, with individual segments averaging 8-10 μm, resulting in red blood cell transit times of approximately 0.75 seconds at rest—shorter than the typical 1-2 seconds in systemic beds—to support rapid oxygenation without compromising efficiency.^[19]^[20] This anatomical design prioritizes a vast, low-resistance network optimized for the high-flow, low-pressure pulmonary circuit.^[16]

Pulmonary Veins

The pulmonary veins are the primary vessels responsible for draining oxygenated blood from the lungs to the left atrium of the heart. Typically, there are four main pulmonary veins: two from each lung, consisting of a superior and an inferior vein per lung. The right superior pulmonary vein drains the right upper and middle lobes, while the right inferior pulmonary vein drains the right lower lobe. On the left side, the superior pulmonary vein drains the upper lobe and lingula, and the inferior pulmonary vein drains the lower lobe. These veins converge at the left atrium, forming separate ostia in the majority of cases, and play a crucial role in completing the low-pressure pulmonary circuit by returning blood to the systemic circulation.^[21]^[7] The branching pattern of the pulmonary veins begins at the subsegmental level, where smaller venules collect blood from the pulmonary capillaries and coalesce into larger segmental veins. Unlike the pulmonary arteries and bronchi, which travel together in bronchovascular bundles, the pulmonary veins course independently, often running through the interlobular septa that separate the lung lobules. This arrangement allows the veins to drain blood from multiple segments without direct anatomical alignment to the airway or arterial structures, facilitating efficient collection across the lung parenchyma.^[22]^[23] The walls of the pulmonary veins are notably thin, even compared to those of the pulmonary arteries, featuring a minimal amount of elastic tissue and lacking valves, which distinguishes them from many systemic veins. This structure supports their function in a low-pressure environment, with the thin endothelium and sparse connective tissue enabling distensibility while minimizing resistance to flow. Anatomical variations are common, including a shared common ostium for the two left pulmonary veins in approximately 20-30% of individuals, and accessory veins that drain specific regions such as the right middle lobe or left lingula, occurring in up to 26% of cases for the middle lobe variant. These variations can affect surgical planning but do not typically impair normal function.^[24]^[25]^[26] Pulmonary veins also maintain a close spatial relationship with the lung's lymphatic system, accompanying lymphatic vessels that drain from the alveolar regions through the interlobular septa and toward the hilum. This association aids in the coordinated clearance of interstitial fluid and immune cells alongside venous return, with lymphatics often positioned adjacent to venous segments in the connective tissue framework.^[27]^[28]^[29]

Physiology

Dual Pulmonary and Bronchial Circulations

The lungs are supplied by two parallel vascular systems: the pulmonary circulation, which facilitates gas exchange, and the bronchial circulation, which provides nutritional support to the lung parenchyma and supporting structures. These dual circulations operate under distinct pressure gradients and flow rates, ensuring both oxygenation of systemic blood and maintenance of lung tissue viability. Although anatomically interconnected through anastomoses, their separation allows specialized functions without significant interference under normal conditions.^[18] The pulmonary circulation is a low-pressure system that receives the entire cardiac output from the right ventricle, approximately 5 L/min in adults at rest, directing deoxygenated blood through the pulmonary arteries to the alveolar capillaries for gas exchange. Operating at mean pressures of about 15 mmHg (systolic ~25 mmHg, diastolic ~10 mmHg), this circuit minimizes the workload on the right ventricle while maximizing oxygen uptake and carbon dioxide removal across a thin blood-gas barrier. Its high compliance and low resistance enable it to handle increased flow during exercise without substantial pressure rises.^[2]^[30] In contrast, the bronchial circulation arises as a high-pressure systemic branch from the thoracic aorta via the bronchial arteries, delivering oxygenated blood to nourish the tracheobronchial tree, visceral pleura, lymph nodes, and pulmonary vessel walls. This circuit accounts for only 1-2% of cardiac output, equivalent to 50-150 mL/min, reflecting its role in metabolic support rather than bulk transport. Bronchial arteries typically originate as two left (from the descending thoracic aorta) and one right (from the first right intercostal or upper thoracic aorta), branching to follow the airways and extend to the lung periphery.^[2]^[18]^[31] Anatomically, the two systems remain largely separated, with bronchial arteries paralleling the bronchi and bronchioles to reach extrapulmonary and intrapulmonary tissues, while pulmonary arteries distribute to the gas-exchanging regions. Bronchial veins form a dual drainage pattern: superficial veins accompany the bronchi and empty into the azygos or hemiazygos system toward the superior vena cava, whereas deep bronchial veins anastomose extensively with pulmonary veins, directing up to 70-80% of bronchial flow into the left atrium and creating a small physiological right-to-left shunt. These anastomoses prevent isolated failure of either system but can lead to pathological shunting, such as desaturated blood mixing in pulmonary hypertension or bronchial artery hypertrophy.^[18]^[31] Functionally, the pulmonary circulation optimizes ventilation-perfusion matching to support systemic oxygenation, with its endothelium regulating vasomotor tone in response to local hypoxia. The bronchial circulation, despite its modest volume, serves as the primary nutritional conduit, supplying over 90% of the oxygenated blood required for lung tissue metabolism, immune defense, and airway thermoregulation, as the pulmonary circuit's deoxygenated blood contributes minimally to parenchymal nutrition. In pathological states, such as chronic obstructive pulmonary disease or pulmonary embolism, inter-system shunts expand, allowing the bronchial circulation to compensate by increasing flow up to several-fold, though this risks complications like hemoptysis.^[18]^[2]

Vascular Compliance and Capacity

The pulmonary vasculature exhibits high compliance, defined as the change in blood volume per unit change in transmural pressure (C = \Delta V / \Delta P), enabling it to distend readily in response to pressure variations while maintaining low overall resistance. This property arises primarily from the thin walls of pulmonary arteries and veins, which are approximately one-third the thickness of comparable systemic vessels, allowing for greater elasticity. In healthy adults, arterial compliance averages about 7 mL/mmHg, contributing to the system's ability to handle pulsatile flow from the right ventricle with minimal pressure elevation.^[2] The total pulmonary vascular compliance is estimated at approximately 20 mL/mmHg, reflecting the combined elastic properties of arteries, capillaries, and veins across the entire vascular bed. This value is derived from physiological models and measurements emphasizing the distensibility of the pulmonary circuit, which contrasts with the stiffer systemic arteries. The large total cross-sectional area of the pulmonary vascular bed—roughly 10 times that of the systemic circulation—further enhances compliance by distributing pressure over an extensive network of thin-walled vessels.^[32]^[33] As a capacitance vessel, the pulmonary circulation functions as a dynamic reservoir, normally containing 500–900 mL of blood, or about 9–12% of the total circulating volume. This capacity varies with posture, increasing in the supine position due to reduced gravitational pooling in the lower extremities and decreasing by up to one-third when upright. The reservoir role accommodates fluctuations in cardiac output, such as during exercise, by recruiting additional capillaries and distending existing ones without substantial pressure rises.^[34]^[35] Physiologically, the high compliance and capacity buffer systolic pressure peaks from the right ventricle, damping pulsations to protect the thin alveolar-capillary membrane and prevent interstitial edema. This damping effect ensures stable low mean pulmonary artery pressures (typically 15 mmHg), facilitating efficient gas exchange. In pathological conditions like pulmonary fibrosis, compliance declines due to vessel stiffening and remodeling, elevating pressures and impairing this buffering function.^[36]^[37]

Hemodynamics: Flow, Pressure, and Resistance

Pulmonary circulation operates under low-pressure conditions compared to systemic circulation, with normal mean pulmonary artery pressure (mPAP) of approximately 15 mmHg.^[38] Systolic pulmonary artery pressure typically measures around 25 mmHg, while diastolic pressure ranges from 8 to 10 mmHg.^[39] These values reflect the efficient, low-resistance pathway that facilitates gas exchange without excessive strain on the right ventricle. Blood flow through the pulmonary circulation equals the cardiac output, averaging 5 to 6 L/min at rest in healthy adults.^[38] Pulmonary vascular resistance (PVR) quantifies the opposition to this flow and is calculated as PVR = (mPAP - left atrial pressure) / cardiac output, with normal values ranging from approximately 1 to 2 Wood units.^[38] Left atrial pressure, often 2 to 12 mmHg, serves as the downstream reference, ensuring a minimal transpulmonary pressure gradient of about 10 mmHg under resting conditions.^[39] Gravity significantly influences regional blood flow distribution in the upright lung, creating a hydrostatic gradient of 0.77 mmHg per cm of vertical height.^[40] This results in lower perfusion at the lung apices compared to the bases, where pressure is higher due to the column of blood. The zonal model, proposed by West and colleagues, divides the lung into three zones based on the interplay of pulmonary arterial (Pa), venous (Pv), and alveolar (PA) pressures.^[41] In Zone 1 (typically apical regions under low flow conditions), PA exceeds both Pa and Pv, leading to high ventilation but low or absent perfusion as capillaries collapse. Zone 2 (intermediate regions) features intermittent flow where Pa > PA > Pv, resembling a Starling resistor with flow dependent on the arterial-alveolar pressure difference. Zone 3 (basal regions) predominates under normal conditions, where Pa and Pv both exceed PA, allowing continuous perfusion driven by the arterial-venous gradient. During exercise, pulmonary blood flow increases 3- to 5-fold to match elevated cardiac output, yet mean pulmonary artery pressure rises only minimally, often to 30-40 mmHg at maximal effort.^[42] This accommodation occurs primarily through recruitment of previously underperfused capillaries, particularly in apical zones, and distension of existing vessels, which reduces PVR by up to 50%.^[42] Such passive mechanisms maintain efficient flow without substantial pressure elevation in healthy individuals.

Regulation of Blood Flow

Pulmonary blood flow is primarily regulated through local intrinsic mechanisms rather than extrinsic neural control, ensuring efficient gas exchange by matching perfusion to ventilation. The pulmonary vasculature maintains low resistance under normal conditions but can dynamically adjust to physiological demands, such as changes in oxygen levels or pressure, via specialized responses that differ markedly from systemic circulation.^[18] A key regulatory mechanism is hypoxic pulmonary vasoconstriction (HPV), a local response in which low alveolar oxygen tension (PO₂ below approximately 60 mmHg) triggers vasoconstriction in affected pulmonary arterioles to redirect blood flow away from poorly oxygenated regions. This process involves contraction of pulmonary arterial smooth muscle cells, mediated by endothelial-derived factors and ion channel activity, including inhibition of voltage-gated potassium channels and influx of calcium through voltage-dependent channels. HPV is biphasic, with an initial rapid phase occurring within seconds and a slower sustained phase peaking after several minutes, and it is abolished under general anesthesia, which can impair ventilation-perfusion matching during surgery.^[43]^[44]^[45]^[46] Autoregulation in the pulmonary circulation involves an intrinsic myogenic response to transmural pressure changes, where increased pressure stretches vascular smooth muscle, leading to depolarization and contraction that helps maintain relatively constant blood flow despite fluctuations in cardiac output. This response is present in adult pulmonary arteries, as demonstrated in isolated vessel studies where pressure elevation elicits force generation in 70% of adult cat pulmonary arteries. Modulation occurs through potassium (K⁺) channels, such as KCNQ (Kv7) channels, which regulate membrane potential, and nitric oxide (NO), which promotes vasodilation to counteract excessive constriction and preserve low pulmonary vascular resistance.^[47]^[45]^[18] Neural influences on pulmonary blood flow are minimal under basal conditions, with sparse sympathetic innervation providing limited vasoconstrictive tone via alpha-adrenergic receptors and norepinephrine release, while parasympathetic effects are negligible. Humoral factors play a more prominent role: vasoconstrictors like angiotensin II and endothelin-1 elevate vascular tone by activating G-protein-coupled receptors and promoting smooth muscle contraction, whereas vasodilators such as prostacyclin and NO, produced by endothelial cells, relax vessels through cyclic nucleotide pathways to maintain low resistance.^[18]^[48]^[18] By redistributing blood flow from hypoxic to well-ventilated alveoli, HPV optimizes the ventilation-perfusion (V/Q) ratio, minimizing shunting and enhancing overall oxygenation efficiency. In pathological states like chronic obstructive pulmonary disease (COPD), sustained or heterogeneous HPV contributes to pulmonary hypertension by increasing overall pulmonary vascular resistance.^[49]^[50]

Pulmonary Blood Volume

The total pulmonary blood volume in resting adults is approximately 500 mL, constituting about 10% of the total circulating blood volume of around 5 L.^[15] This volume can increase to 900–1000 mL under conditions such as exercise or changes in posture, representing up to 15–20% of circulating volume.^[51] At rest, the distribution of this volume is uneven across the pulmonary vasculature, with approximately 30-40% in the arteries, 15-20% in the capillaries, and 40-50% in the veins.^[52] During exercise, pulmonary blood flow rises significantly, leading to recruitment and distension of previously underperfused capillaries, which shifts a greater proportion of the blood volume into the capillary bed to enhance gas exchange efficiency.^[53] This redistribution can increase capillary blood volume by up to 50–100% from resting levels, depending on exercise intensity.^[54] Postural changes also affect volume dynamics; transitioning from upright to supine position increases pulmonary blood volume by approximately 50–80% (or about 400 mL) due to gravitational pooling of blood in the thoracic vasculature.^[55] Pulmonary blood volume is measured using indicator dilution techniques, such as injecting Evans blue dye into the pulmonary artery and sampling from the left atrium to quantify the dilution curve, providing an estimate of central pulmonary volume.^[56] Modern noninvasive methods include contrast-enhanced computed tomography (CT) or magnetic resonance imaging (MRI) to assess vascular volumes directly.^[57] Physiological variations influence this volume; hypovolemia, as in dehydration or hemorrhage, reduces pulmonary blood volume by decreasing overall circulating volume, while hypervolemia from fluid overload expands it, potentially impairing vascular compliance.^[58] The mean transit time of blood through the pulmonary circulation, which reflects perfusion efficiency, is given by the equation:

\text{Transit time} = \frac{\text{Pulmonary blood volume}}{\text{Pulmonary blood flow}}

where pulmonary blood flow approximates cardiac output at rest (about 5 L/min), yielding a typical transit time of approximately 6-8 seconds.^[54]^[59] In clinical contexts, elevated pulmonary blood volume, often exceeding 700–800 mL, is observed in left-sided heart failure, where backward pressure transmission leads to vascular engorgement and interstitial congestion, increasing the risk of dyspnea and impaired oxygenation.^[57] This volume expansion highlights the pulmonary circulation's role as a compliant reservoir, but excessive accumulation strains its low-resistance design.^[2]

Development

Embryonic Formation

The embryonic formation of the pulmonary circulation begins around the fourth week of gestation, with the pulmonary arteries originating from the ventral segments of the sixth pair of aortic arches. These arches develop from the aortic sac and contribute to the proximal portions of the main pulmonary arteries, while the pulmonary trunk forms from the bulbus cordis, a component of the primitive heart tube derived from splanchnic mesoderm. This early vascular framework establishes the outflow tract connection between the right ventricle and the developing lungs, ensuring initial blood flow routing during cardiogenesis.^[60] The angiogenic process is driven primarily by vascular endothelial growth factor (VEGF), which promotes sprouting angiogenesis from pre-existing systemic vessels toward the lung buds, inducing arterial patterning that aligns with bronchial branching. Lung buds secrete VEGF to attract endothelial progenitors, facilitating the integration of vascular networks with the respiratory epithelium. Between weeks 5 and 6, proximal pulmonary arteries elongate and branch in parallel with the tracheobronchial tree during the pseudoglandular stage, while weeks 7 to 8 mark the onset of distal vascularization through vasculogenesis, where a primitive capillary plexus forms de novo around the lung buds via aggregation of angioblasts.^[61] Genetic regulation involves Hox genes, particularly groups 3 through 6, which pattern the proximal-distal axis of lung development and influence vascular smooth muscle recruitment to arterial walls; disruptions in Hox expression, such as in Hoxa3 mutants, lead to tracheobronchial malformations that secondarily affect vascular alignment. Fibroblast growth factor (FGF) signaling, especially FGF10, coordinates mesenchymal-epithelial interactions to guide branching morphogenesis, thereby dictating the spatial organization of the pulmonary vasculature; FGF defects result in hypoplastic lungs and associated vascular anomalies like persistent truncus arteriosus.^[62] The pulmonary veins initially form a plexus that drains into systemic veins connected to the right atrium via cardinal and vitelline systems, but by week 8, a common pulmonary vein canalizes from splanchnic mesoderm and incorporates into the left atrial wall through remodeling, severing right-sided connections to establish direct left atrial drainage.^[63]^[64]^[21]

Fetal and Neonatal Transitions

In fetal circulation, pulmonary vascular resistance (PVR) is approximately 10 times higher than in adults, primarily due to hypoxic vasoconstriction, low pulmonary blood flow, and the fluid-filled state of the lungs, which limits vascular recruitment and distension.^[65] This high resistance results in pulmonary blood flow constituting only about 10% of the combined ventricular cardiac output, with the majority of right ventricular output shunted away from the lungs via the ductus arteriosus to the descending aorta, bypassing the non-functional pulmonary vasculature.^[66] The ductus arteriosus remains patent due to low oxygen tension and circulating prostaglandins, ensuring oxygenated blood from the placenta reaches systemic circulation efficiently.^[65] At birth, the transition to neonatal circulation begins with the first breath, which dramatically reduces PVR by about 50% within minutes through lung expansion and the onset of oxygenation.^[65] This initial drop facilitates a rapid increase in pulmonary blood flow, redirecting it to the now-aerated lungs for gas exchange. The ductus arteriosus typically closes functionally within 24 to 72 hours postnatally, driven by rising oxygen levels and falling prostaglandin concentrations, which eliminates the right-to-left shunt.^[67] Similarly, the foramen ovale closes functionally at birth as left atrial pressure exceeds right atrial pressure due to increased pulmonary venous return, though anatomical closure occurs later, often within the first year.^[68] Multiple mechanisms orchestrate this transition: mechanical factors, such as lung aeration, increase vascular compliance by recruiting previously collapsed vessels and stretching the pulmonary capillary bed; chemical mediators, including rising oxygen tension and falling carbon dioxide levels, inhibit hypoxic vasoconstriction and stimulate endothelium-derived nitric oxide (NO) production for vasodilation; and hormonal signals, like the release of bradykinin from the lungs upon initial ventilation, further promote pulmonary vasodilation by enhancing prostacyclin synthesis and NO pathways.^[69]^[65] In the neonatal period, PVR continues to decline gradually, reaching adult levels by around 2 weeks of age through ongoing vascular remodeling, including thinning of arterial walls and maturation of endothelial function.^[70] This adaptation ensures stable pulmonary hemodynamics, but delays in the transition can lead to persistent pulmonary hypertension of the newborn (PPHN), characterized by sustained high PVR and right-to-left shunting, affecting approximately 2 per 1,000 live births.^[65]

Clinical Significance

Pathophysiological Disorders

Pulmonary circulation can be disrupted by various pathophysiological disorders that impair blood flow, increase vascular resistance, and lead to right heart strain. These conditions often result from endothelial injury, thrombosis, or increased permeability, compromising gas exchange and cardiac output. Major disorders include pulmonary hypertension, embolism, edema, and cor pulmonale, each with distinct mechanisms and hemodynamic consequences. Pulmonary hypertension (PH) is characterized by elevated mean pulmonary artery pressure (mPAP) exceeding 20 mmHg at rest, as measured by right heart catheterization.^[71] The World Health Organization (WHO) classifies PH into five groups based on underlying etiology: Group 1 encompasses pulmonary arterial hypertension (PAH) due to endothelial dysfunction and vascular remodeling; Group 2 arises from left heart disease; Group 3 from lung diseases and/or hypoxia; Group 4 from chronic thromboembolic disease; and Group 5 from multifactorial or unclear mechanisms.^[72] In Group 1 PAH, progressive endothelial dysfunction leads to imbalanced vasoconstrictors and vasodilators, causing intimal proliferation, medial hypertrophy, and plexiform lesions that narrow pulmonary arteries.^[73] Pulmonary embolism (PE) occurs when a thrombus, typically originating from deep vein thrombosis, obstructs pulmonary arteries, acutely increasing pulmonary vascular resistance (PVR) and right ventricular afterload.^[74] This obstruction reduces perfusion to lung segments, potentially causing ventilation-perfusion mismatch and hypoxemia. Risk factors align with Virchow's triad: venous stasis, endothelial injury, and hypercoagulability, which promote thrombus formation and embolization.^[75] Pulmonary edema manifests as fluid accumulation in the alveolar and interstitial spaces, disrupting gas exchange and leading to respiratory distress. It is classified as cardiogenic, resulting from left heart failure that elevates pulmonary capillary wedge pressure above 18 mmHg and forces fluid into the interstitium via hydrostatic forces, or non-cardiogenic, as in acute respiratory distress syndrome (ARDS), where increased vascular permeability from inflammatory injury allows protein-rich fluid leakage despite normal wedge pressures.^[76] Cor pulmonale refers to right ventricular hypertrophy and eventual failure secondary to chronic PH, where sustained elevation in pulmonary vascular resistance imposes excessive afterload on the right ventricle, leading to dilation, contractile dysfunction, and reduced cardiac output.^[77] In the post-2020 era, severe COVID-19 infection has been linked to acute PH through widespread pulmonary microthrombi formation, driven by endothelial inflammation and coagulopathy.^[78] These microthrombi exacerbate PVR and contribute to right heart strain, often detectable via echocardiography in affected cases.^[79]

Diagnostic and Imaging Techniques

Diagnostic and imaging techniques for pulmonary circulation are essential for evaluating structure and function, particularly in conditions like pulmonary hypertension (PH) and pulmonary embolism (PE), where early detection guides management. These methods range from non-invasive imaging modalities that provide anatomical and functional insights to invasive procedures that offer precise hemodynamic measurements. A multimodal approach, integrating clinical assessment with multiple imaging tools, is recommended to enhance diagnostic accuracy and tailor evaluations to suspected pathophysiology. Echocardiography serves as the initial non-invasive screening tool for assessing pulmonary circulation, estimating pulmonary artery systolic pressure (PASP) through the tricuspid regurgitant (TR) jet velocity using the simplified Bernoulli equation, \Delta P = 4v^2, where \Delta P is the pressure gradient and v is the peak velocity of the TR jet.^[80] This estimate, combined with right atrial pressure (often assumed at 5-10 mmHg), yields right ventricular systolic pressure (RVSP), which approximates PASP in the absence of pulmonic stenosis.^[81] Additionally, echocardiography evaluates right ventricular (RV) function via parameters such as tricuspid annular plane systolic excursion (TAPSE) and RV fractional area change, identifying RV dilation or dysfunction indicative of elevated pulmonary pressures.^[82] Its widespread availability and lack of radiation make it ideal for initial PH suspicion, though it has limitations in accuracy for mild cases or poor acoustic windows.^[83] Right heart catheterization (RHC) remains the gold standard for definitive diagnosis of PH and direct measurement of pulmonary vascular resistance (PVR), calculated as (mean pulmonary artery pressure - pulmonary artery wedge pressure) / cardiac output.^[84] Performed via femoral or jugular access, RHC provides invasive hemodynamic data, including pulmonary artery pressures, cardiac output via thermodilution or Fick method, and PVR in Wood units, essential for confirming pre-capillary PH (mean PAP ≥20 mmHg, PVR >2 Wood units, wedge pressure ≤15 mmHg).^[85] It also enables vasoreactivity testing with agents like inhaled nitric oxide to guide therapy in select patients.^[86] Despite risks such as arrhythmias or vascular injury, RHC's precision justifies its role in ambiguous non-invasive findings.^[87] Computed tomography pulmonary angiography (CTPA) is the preferred modality for detecting acute PE, visualizing intraluminal filling defects in pulmonary arteries with high resolution, often centrally located in acute cases.^[88] Dual-energy CTPA further identifies parenchymal perfusion defects by assessing iodine distribution, distinguishing embolic from non-embolic causes without additional radiation.^[89] For functional assessment, ventilation-perfusion (V/Q) single-photon emission computed tomography (SPECT) detects mismatch between ventilated and perfused lung regions, with sensitivity of approximately 96% and specificity of 90% for PE diagnosis.^[90] This is particularly useful in chronic thromboembolic PH, where it outperforms planar scans.^[91] Magnetic resonance imaging (MRI) offers radiation-free evaluation of pulmonary circulation, quantifying blood flow in pulmonary arteries using phase-contrast techniques to measure velocity and volume, with high reproducibility for pulmonary venous return.^[92] Four-dimensional (4D) flow MRI visualizes vortical flow patterns and collateral vessels in the main pulmonary artery, aiding in congenital or chronic vascular assessments.^[93] It also delineates vessel anatomy, such as branch pulmonary arteries, supporting diagnosis in patients with contraindications to CT or echocardiography.^[94] The 2022 European Society of Cardiology (ESC)/European Respiratory Society (ERS) guidelines advocate a multimodal diagnostic strategy for PH, starting with echocardiography for screening, followed by V/Q scanning or CTPA for thromboembolic evaluation, MRI for functional insights, and confirmatory RHC, to streamline detection and reduce diagnostic delays.^[95]

Therapeutic Interventions

Therapeutic interventions for pulmonary circulation disorders primarily target pulmonary arterial hypertension (PAH) and pulmonary embolism (PE), aiming to reduce pulmonary vascular resistance, prevent thrombosis, and support cardiac function. In PAH, a subset of pulmonary hypertension (PH), treatments focus on vasodilation and remodeling inhibition, guided by risk stratification from diagnostic assessments such as right heart catheterization. For PE, acute management emphasizes anticoagulation to halt clot propagation, with escalation to thrombolysis in hemodynamically unstable cases. Supportive measures and advanced procedures address refractory disease, while emerging therapies like activin signaling inhibitors represent recent advancements. Pharmacological therapies for PAH target three main pathways: endothelin, nitric oxide, and prostacyclin. Endothelin receptor antagonists, such as bosentan, block endothelin-1-mediated vasoconstriction and proliferation, improving exercise capacity and delaying clinical worsening in WHO functional class II-IV patients. Phosphodiesterase-5 inhibitors like sildenafil enhance nitric oxide effects by increasing cyclic GMP, reducing pulmonary artery pressure and improving hemodynamics in PAH. Prostacyclin analogs, including intravenous epoprostenol, promote vasodilation and inhibit platelet aggregation, serving as first-line therapy for high-risk PAH patients with demonstrated survival benefits. Combination therapy, often initiating with dual or triple oral agents and escalating to parenteral prostacyclin, is recommended for most patients to optimize outcomes. For PE, anticoagulation remains the cornerstone, with low-molecular-weight heparin or unfractionated heparin initiated acutely, followed by direct oral anticoagulants (DOACs) like rivaroxaban for at least three months in non-cancer patients. DOACs offer comparable efficacy to vitamin K antagonists with lower bleeding risk, suitable for outpatient management in low-risk cases. In massive PE with hemodynamic instability, systemic thrombolysis using agents like alteplase is indicated to rapidly dissolve clots and restore right ventricular function, though it carries a 2-3% major bleeding risk. Supportive interventions include supplemental oxygen therapy, which alleviates hypoxemia-induced hypoxic pulmonary vasoconstriction (HPV), thereby reducing pulmonary vascular resistance and improving oxygenation in PH patients with PaO2 below 60 mmHg. For end-stage PH refractory to medical therapy, lung transplantation—typically bilateral—offers curative potential, with one-year survival rates exceeding 80% and significant improvements in quality of life. Interventional procedures are vital for specific etiologies, such as balloon pulmonary angioplasty (BPA) in chronic thromboembolic PH (CTEPH), where it dilates distal vascular lesions, improving mean pulmonary artery pressure by 20-30% and functional status in inoperable cases. BPA, performed in staged sessions with refined techniques to minimize reperfusion injury, has evolved as an adjunct or alternative to pulmonary endarterectomy. Recent advancements include sotatercept, an activin signaling inhibitor approved by the FDA in March 2024 for PAH (WHO Group 1), which reduces pulmonary vascular remodeling by balancing TGF-β superfamily signaling, leading to sustained improvements in six-minute walk distance and reduced clinical worsening when added to background therapy. In October 2025, the FDA updated the indication to include reduction in clinical worsening events in adults with PAH (WHO Group 1), based on results from the phase 3 ZENITH trial.^[96] Gene therapy trials targeting BMPR2 mutations, which underlie 70-80% of heritable PAH, have shown promise; for instance, lipid nanoparticle-delivered BMPR2 mRNA restores endothelial signaling in preclinical models, attenuating PAH progression.

History

Anatomical Discoveries

In ancient times, the Roman physician Galen (c. 129–216 AD) described the vessels of the lungs and proposed that venous blood from the right ventricle passed through invisible pores in the interventricular septum to the left ventricle, where it mixed with air drawn from the lungs via the pulmonary vein to form arterial blood vital for the body.^[97] This model, while recognizing a pulmonary role in blood modification, fundamentally erred by denying a complete circulatory transit through the lungs and overemphasizing septal passage.^[97] In the 13th century, the Syrian physician Ibn al-Nafis (1213–1288) provided the first known description of pulmonary circulation in his Commentary on Anatomy in Avicenna's Canon. He rejected Galen's septal pores theory, stating that blood travels from the right ventricle to the lungs via the pulmonary artery, where it is refined by air in the lungs before returning to the left ventricle through the pulmonary vein. This insight, though not widely disseminated in Europe at the time, accurately outlined the pulmonary transit of blood.^[97] During the Renaissance, Andreas Vesalius advanced anatomical accuracy through direct human dissections, illustrating the pulmonary arteries and veins with unprecedented detail in his seminal work De Humani Corporis Fabrica (1543).^[98] Vesalius corrected several of Galen's errors, such as the non-existence of interventricular pores, and clarified the origins and branching of pulmonary vessels, though he still adhered to a partial mixing theory without fully grasping systemic-pulmonary connectivity.^[99] His illustrations, based on meticulous observations, laid the groundwork for later circulatory insights by emphasizing empirical anatomy over classical doctrine.^[99] Building on these foundations, Michael Servetus (1511–1553) described the pulmonary circulation in his theological work Christianismi Restitutio (1553), proposing that blood from the right ventricle passes through the lungs to the pulmonary vein and into the left ventricle, where it mixes with air for vitalization. Independently, Realdo Colombo (1516–1559), Vesalius's successor at Padua, explicitly detailed the pulmonary transit in De re anatomica (1559), emphasizing the flow from pulmonary artery to lungs to pulmonary vein without septal passage, supported by dissections. These accounts bridged the gap toward a full circulatory model.^[97] William Harvey's Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus (1628) revolutionized understanding by demonstrating a closed circulatory system, inferring the pulmonary circuit as essential for blood to pass from the right ventricle through the lungs to the left via the pulmonary artery and vein.^[97] While Harvey's primary focus was on systemic circulation—proven through quantitative dissections showing blood volume exceeding daily production—his work implicitly required pulmonary transit to explain the heart's dual roles, rejecting Galenic consumption models.^[100] This inference bridged anatomy and emerging physiological concepts, though direct pulmonary emphasis came later.^[97] Building on Harvey, Richard Lower provided the first explicit and detailed description of pulmonary blood transit in Tractatus de Corde (1669), observing that dark venous blood pumped from the right ventricle becomes bright red upon passing through the lung's fine vessels due to aeration.^[101] Lower's experiments, including animal vivisections, highlighted the lungs' role in blood transformation without vital spirits, emphasizing structural flow from pulmonary artery to vein as a continuous circuit.^[102] His anatomical focus on the heart-lung interface clarified the mechanism of lesser circulation, resolving ambiguities in Harvey's framework.^[102] Marcello Malpighi confirmed the microstructural basis of pulmonary transit in 1661 by using early microscopes to observe capillary networks in frog and mammalian lungs, linking pulmonary arteries directly to veins through a web of minute vessels surrounding alveoli.^[103] This discovery validated Harvey's circulation by visualizing the anatomical continuity essential for blood exchange with air, marking a pivotal shift toward microscopic anatomy in understanding pulmonary function.^[103] Malpighi's observations thus transitioned anatomical discoveries toward physiological explorations of gas exchange.^[103]

Physiological Advancements

The development of cardiac catheterization techniques in the mid-20th century revolutionized the measurement of pulmonary hemodynamics, enabling direct assessment of low pulmonary artery pressures distinct from systemic circulation. André F. Cournand and Dickinson W. Richards, building on Werner Forssmann's initial self-experimentation, refined right heart catheterization to sample mixed venous blood and quantify pulmonary blood flow using the Fick principle, revealing mean pulmonary artery pressures around 15 mmHg in healthy individuals.^[104]^[105] Their work, conducted primarily in the 1940s and 1950s at Bellevue Hospital, demonstrated the low-resistance, high-compliance nature of pulmonary vasculature, contrasting with higher systemic pressures and laying the groundwork for understanding pulmonary hypertension.^[106] For their contributions to cardiopulmonary diagnostics, Cournand, Richards, and Forssmann shared the 1956 Nobel Prize in Physiology or Medicine.^[104] A pivotal advancement in pulmonary vasoregulation came in 1946 when Ulf von Euler and Gunnar Liljestrand observed hypoxic pulmonary vasoconstriction (HPV) in isolated cat lungs, where alveolar hypoxia triggered localized pulmonary artery constriction to redirect blood flow from poorly ventilated regions, optimizing ventilation-perfusion matching. This mechanism, now known as the Euler-Liljestrand reflex, increases pulmonary vascular resistance in response to low oxygen tension without systemic effects, as confirmed in subsequent studies on perfused lung preparations.^[107] HPV's discovery provided a physiological basis for adaptive responses in conditions like pneumonia or high-altitude hypoxia, influencing modern interpretations of regional lung perfusion.^[108] In 1964, John B. West introduced the zonal model of pulmonary blood flow distribution, delineating three vertical zones in the upright lung based on the interplay of pulmonary arterial (Pa), venous (Pv), and alveolar (PA) pressures.^[109] Zone 1 at the apex features PA > Pa > Pv, potentially leading to collapsed capillaries and no flow in pathological states; Zone 2 (mid-lung) has Pa > PA > Pv, resulting in intermittent flow like a Starling resistor; and Zone 3 at the base shows Pa > Pv > PA, ensuring continuous perfusion.^[110] Derived from experiments in isolated, perfused dog lungs, this model explained gravity-dependent perfusion gradients, with base-to-apex flow ratios up to 4:1 in humans, and has informed imaging and ventilation strategies.^[111] Advancements in gas exchange modeling culminated in the Roughton-Forster refinement of the Krogh equation during the 1950s, quantifying pulmonary diffusing capacity (DL) for gases like carbon monoxide (CO) as the reciprocal of resistances in plasma and red blood cells:

DL = \frac{1}{\frac{1}{DM} + \frac{1}{\theta \cdot V_c}}

where DM represents membrane diffusing capacity (DLplasma), θ is the CO uptake rate by hemoglobin in red cells, and Vc is pulmonary capillary blood volume.^[112] Originally proposed by Marie Krogh in 1915 for oxygen diffusion, this equation was experimentally validated using varying oxygen tensions to isolate components, showing DLCO values around 25-30 mL/min/mmHg in healthy adults and highlighting diffusion limitations in disease.^[113] These insights advanced non-invasive assessments of gas transfer efficiency. Recent research in the 2020s has leveraged single-cell RNA sequencing (scRNA-seq) to uncover endothelial dysfunction in pulmonary hypertension (PH), identifying heterogeneous pulmonary endothelial cell (PEC) subclusters with dysregulated pathways in proliferation and inflammation.^[114] Studies on human and mouse PH lungs reveal upregulated genes like SOX17 and DDIT4 in arterial PECs, driving vascular remodeling and stiffness, while venous ECs show metabolic shifts toward glycolysis.^[115] For instance, scRNA-seq profiling has delineated PEC markers such as ECAM1 and PLVAP, linking their loss to impaired barrier function and offering targets for precision therapies in PH subtypes.^[116]

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