10. Thoracic Anatomy

The central airway is the anatomic spine of the chest CT, and reading it well begins with the trachea, a fibromuscular tube whose anterior and lateral walls are supported by 16 to 20 incomplete (C-shaped) hyaline cartilage rings while its posterior wall is a membranous sheet of trachealis smooth muscle abutting the esophagus. On axial CT the normal tracheal lumen is rounded to ovoid and air-attenuating ($\approx -1000$ HU), the cartilaginous wall is a thin $1\text{--}3\,\mathrm{mm}$ soft-tissue density that may calcify with age (a normal finding, often more conspicuous in women), and the posterior membrane is flat or slightly concave anteriorly. The coronal dimension averages $\sim 13\text{--}25\,\mathrm{mm}$ in men and slightly less in women; a sagittal/coronal aspect ratio that flattens the trachea into a lunate (sabre-sheath) configuration with coronal narrowing and sagittal widening is the signature of chronic obstructive disease, whereas a posteriorly bowed, scalloped membrane that collapses by more than 50% of luminal area on dynamic expiratory imaging defines tracheobronchomalacia. The trachea descends slightly rightward and posteriorly, deviated normally by the aortic arch, before bifurcating at the carina at roughly the level of the sternal angle (T4–T5). The carinal angle and the subcarinal space are high-yield review areas: subcarinal (station 7) nodes sit immediately below the bifurcation, and a splayed carina signals subcarinal mass or left atrial enlargement.

Distal to the carina the bronchial tree is best understood as a set of bronchovascular bundles, each bronchus paired with and roughly matched in caliber to its accompanying pulmonary artery—the basis of the bronchoarterial ratio, normally near 0.65–0.70, whose elevation defines bronchiectasis (the signet-ring sign on axial images where the dilated bronchus dwarfs its artery). The right main bronchus is shorter, wider, and more vertical than the left—the reason aspirated material and malpositioned tubes preferentially enter it—and it gives off the right upper lobe bronchus as an eparterial bronchus (arising above the right pulmonary artery), a unique relationship that the trained eye uses to confirm side and lobe. Below it the bronchus intermedius runs as a smooth tube with the posterior wall outlined by lung; thickening or nodularity of the posterior wall of the bronchus intermedius is a classic early sign of endobronchial or nodal disease. The bronchus intermedius then divides into the middle and lower lobe bronchi. On the left there is no eparterial bronchus; the left main bronchus passes under the aortic arch and divides into upper-lobe (with its lingular division, the embryologic homologue of the right middle lobe) and lower-lobe bronchi. Clinically important variants are the tracheal (“pig”) bronchus arising directly from the right tracheal wall and the accessory cardiac bronchus, both readily missed unless the airway is tracked systematically. The expert search pattern tracks each bronchus from the carina to the subsegmental level on thin-section axial and reconstructs in the coronal plane to display the airway in its long axis; the dominant pitfall is satisfaction of search—accepting the obvious lobar finding while overlooking a subtle endobronchial lesion or a thickened bronchus intermedius wall on the very next image.

The lungs are organized at three nested scales, and fluent CT interpretation requires moving among all of them. At the gross scale the right lung has three lobes—upper, middle, lower—separated by the major (oblique) and minor (horizontal) fissures, while the left lung has two lobes separated by a single oblique fissure, with the lingula serving as the left-sided counterpart of the right middle lobe. The oblique fissures run obliquely from approximately the T4–T5 level posteriorly to the diaphragm anteriorly; on axial images the major fissure migrates anteriorly as one scrolls caudally, and recognizing its expected position lets the reader assign a peripheral opacity to the correct lobe and predict which structures it abuts. The minor fissure lies near-horizontal and is therefore poorly seen on axial CT (it parallels the scan plane and is blurred by partial-volume averaging), appearing instead as a triangular avascular region or a faint line; coronal and sagittal reformats display it far better, a practical reason to reformat before localizing right-sided disease.

The intermediate and most diagnostically powerful scale is the bronchopulmonary segment—ten on the right (three upper, two middle, five lower) and eight to ten on the left (the apicoposterior and anteromedial fusions reducing the count)—each a pyramidal unit ventilated by a segmental bronchus and perfused by a segmental pulmonary artery at its core, with the segmental pulmonary veins running in the intersegmental planes. Because each segment is a surgically and functionally semi-independent unit fed by a central bronchus and artery, localizing a nodule, an area of consolidation, or an endobronchial obstruction to a named segment (using the segmental bronchus as the landmark) directly informs the differential, the biopsy approach, and the resectability question. The smallest scale, and the true unit of radiologic pattern recognition, is the secondary pulmonary lobule: a $1\text{--}2.5\,\mathrm{cm}$ polyhedral parcel of lung supplied at its center by a lobular bronchiole and pulmonary arteriole (the centrilobular structures, the arteriole visible as a tiny dot a few millimeters inside the lobule) and bounded by interlobular septa that carry the pulmonary veins and lymphatics. This architecture predicts disease distribution: processes spread along the airways are centrilobular (tree-in-bud infection, hypersensitivity pneumonitis, respiratory bronchiolitis); processes that travel the lymphatics are perilymphatic, beading the septa, fissures, and bronchovascular bundles (sarcoidosis, lymphangitic carcinomatosis, silicosis); and hematogenous processes are random (miliary tuberculosis, hematogenous metastases). Assigning a micronodular pattern to one of these three compartments is frequently the single most discriminating step in the thoracic differential.

Variants matter clinically. The azygos lobe, created when the azygos vein migrates abnormally through the apex of the right upper lobe trailing a four-layered mesentery (the azygos fissure), is present in roughly 1% of people and must not be mistaken for a bulla, scar, or pathologic fissure. Accessory fissures (inferior accessory, superior accessory, left minor) can trap fluid or wall off disease and simulate masses. The expert search pattern interrogates the lungs at two windows—a lung window ($\mathrm{WW}\approx1500$, $\mathrm{WL}\approx-600$) for parenchyma and a soft-tissue/mediastinal window for the hila and nodes—reads the periphery and the apices and lung bases deliberately (the lower-lobe “corner” behind the dome of the diaphragm is a notorious miss site), and confirms any subtle nodule on a second plane to exclude partial-volume mimicry. The cognitive trap is anchoring on the lung window alone and failing to corroborate a peripheral opacity against the fissures and the secondary-lobular framework that would have explained its distribution.

The pleura is a single continuous serosal sac invaginated by the lung, and almost every pleural diagnosis follows from understanding that geometry. The visceral pleura intimately invests the lung surface, dips into the fissures, and is innervated by autonomic fibers (hence insensate to pain), while the parietal pleura lines the inner chest wall, mediastinum, and diaphragm and carries somatic innervation from the intercostal and phrenic nerves—the reason parietal, not visceral, irritation produces sharp, localized, breath-dependent pain referred to the chest wall or, via the phrenic nerve, the shoulder. Between the two layers lies a capillary film of physiologic fluid (a few milliliters) that couples lung to chest wall. On CT the normal pleura is imperceptible; the only normally visible structure in the pleural region is the $1\text{--}2\,\mathrm{mm}$ stripe formed by visceral pleura, a thin extrapleural fat layer, parietal pleura, and the innermost intercostal muscle between adjacent ribs. Any soft-tissue density appreciably exceeding this, or any nodular contour, is abnormal.

The fissures are the visceral pleura folded on itself, and their CT appearance is governed by their orientation to the scan plane: the obliquely oriented major fissures are crossed by axial images and appear as thin avascular lines or, on thicker sections, as lucent bands sparse of vessels, whereas the horizontally oriented minor fissure is poorly resolved axially and far better shown on coronal and sagittal reformats. Knowing a fissure’s position is diagnostically load-bearing: fluid tracking into a fissure produces a lenticular pseudotumor, the position of a pneumothorax or effusion relative to the fissure localizes disease to a lobe, and a peripheral mass that abuts but does not cross a fissure is constrained by it. The pleural recesses are the potential spaces where parietal pleura reflects from one surface to another and where lung does not fully reach in quiet respiration; the posterior costophrenic recess is the deepest and most dependent, the first place a small effusion collects and the corner most often under-scrutinized at the lung bases, while the anterior costomediastinal recesses and the retrocrural and posterior junction lines are the analogous reflections seen mediastinally. Pleural fluid layers dependently and, being water-attenuation ($0$ to $20$ HU when simple), forms a meniscus posteriorly in the supine patient; higher attenuation suggests hemothorax or empyema, and locules that do not shift with position imply adhesions. The distinction of pleural from parenchymal or extrapleural disease rests on the obtuse-versus-acute angle the lesion makes with the chest wall (pleural and extrapleural lesions form obtuse angles and displace the extrapleural fat; parenchymal lesions form acute angles), on the smooth lenticular shape of pleural collections, and on whether the lesion moves with the lung or the chest wall across respiratory phases. The expert reviews the pleura on both lung and soft-tissue windows, deliberately inspecting the dependent posterior recesses and the diaphragmatic surface, and resists the anchoring error of dismissing dependent posterior opacity as atelectasis without excluding a layering effusion—one of the highest-frequency, lowest-drama misses in body CT.

The mediastinum is the soft-tissue core of the chest between the pleural sacs, and the most useful contemporary framework for CT is the three-compartment ITMIG model defined on the lateral/sagittal projection and applied at the workstation: a prevascular (anterior) compartment in front of the heart and great vessels, a visceral (middle) compartment containing the heart, pericardium, great vessels, trachea, esophagus, and the bulk of the lymph nodes, and a paravertebral (posterior) compartment hugging the spine. This compartmental thinking is not academic—it is the engine of the mediastinal-mass differential, because the normal contents of each compartment dictate what can arise there. The prevascular compartment is home to the thymus (a normally fatty, arrowhead-shaped structure in adults that should not be mistaken for a mass; in young patients it retains soft-tissue density and a bilobed quadrilateral shape), prevascular nodes, and fat, so its classic masses are the “four T’s”—thymoma and other thymic epithelial tumors, teratoma and germ-cell tumors, (terrible) lymphoma, and thyroid extension—plus intrathoracic goiter dipping in from the neck. The visceral compartment’s masses are dominated by lymphadenopathy, foregut duplication and bronchogenic cysts (well-defined, water- to high-attenuation depending on proteinaceous content), and esophageal and tracheal lesions. The paravertebral compartment, by contrast, is the province of neurogenic tumors arising from the sympathetic chain and intercostal nerves (schwannoma, neurofibroma, ganglioneuroma), extramedullary hematopoiesis, and spinal/discitis processes; a mass here with rib or neural-foraminal remodeling is neurogenic until proven otherwise.

Within the visceral compartment the lymph-node stations follow the IASLC map that drives lung-cancer staging, and the physician must be able to localize them on axial CT: station 2 (upper paratracheal) and station 4 (lower paratracheal, the most clinically pivotal, with the right 4R nodes bounded by the trachea and the azygos arch), station 5 (the aortopulmonary window, beneath the arch and lateral to the ligamentum arteriosum) and station 6 (para-aortic), station 7 (subcarinal, directly below the carina), and the hilar (10) and interlobar (11) stations. Nodal short-axis diameter above $10\,\mathrm{mm}$ is the conventional size criterion for enlargement, but size is an imperfect surrogate—micrometastases inhabit normal-sized nodes and reactive nodes enlarge benignly—so PET and tissue sampling refine what CT can only flag. Several normal mediastinal lines and stripes encode three-dimensional anatomy onto the axial image and serve as sensitive tripwires for disease: the right paratracheal stripe (thickened by nodal or tracheal disease), the azygoesophageal recess (a normally concave interface that bulges with subcarinal nodes, a large left atrium, or a hiatal hernia), and the anterior and posterior junction lines where the lungs approximate behind the sternum and in front of the spine. The expert search pattern reads the mediastinum on a dedicated soft-tissue/mediastinal window ($\mathrm{WW}\approx350$, $\mathrm{WL}\approx50$) and ideally with intravenous contrast to separate nodes and masses from vessels, marches through each nodal station and interface in turn, and treats the prevascular thymic bed, the aortopulmonary window, and the retrocrural and cardiophrenic-angle nodes as deliberate review areas. The governing cognitive risk is anchoring on a striking lung mass and under-reading the mediastinum, thereby missing the nodal disease that determines stage and operability.

On a contrast-enhanced or ECG-gated chest CT the heart is read chamber by chamber, and orientation begins with the recognition that the cardiac axis is oblique—the right-sided chambers are anterior and the left-sided chambers posterior, so the right ventricle sits immediately behind the sternum and the left atrium is the most posterior chamber, abutting the esophagus and the descending aorta. The right atrium forms the right heart border on the frontal projection and receives the superior and inferior venae cavae and the coronary sinus; its appendage is broad-based and pyramidal. The right ventricle, the most anterior chamber, is coarsely trabeculated, carries the moderator band across its apex, and tapers into the conus toward the pulmonary valve; its free wall is thin ($\approx 3\text{--}5\,\mathrm{mm}$) compared with the left ventricle. The left atrium lies posteriorly and superiorly, receiving four pulmonary veins (a high-yield site for variant anatomy and for the pre-ablation evaluation of atrial fibrillation), and its narrow, finger-like appendage is the dominant source of cardioembolic thrombus—filling defects there must be distinguished from slow-flow pseudo-defects on properly timed imaging. The left ventricle is the thick-walled ($\approx 6\text{--}10\,\mathrm{mm}$) conical pump whose myocardium is partitioned, for reporting, into the standardized 17-segment model that maps directly onto coronary territories. The four valves lie in the fibrous skeleton along the plane of the atrioventricular and ventriculoarterial junctions; valvular and annular calcification is well shown on CT, and mitral annular calcification is a common, benign-appearing but clinically meaningful incidental finding.

The pericardium is a two-layered sac—a visceral epicardial layer and a fibrous parietal layer—seen on CT as a thin ($\le 2\,\mathrm{mm}$) curvilinear soft-tissue line separated from the myocardium and chest wall by epicardial and mediastinal fat; it is most reliably identified anterior to the right ventricle where fat brackets it on both sides. The pericardial recesses (notably the superior pericardial recess wrapping around the ascending aorta) are fluid-filled normal spaces that are routinely mistaken for lymphadenopathy or aortic dissection by the unwary, a classic anchoring trap resolved by recognizing their characteristic location and water attenuation. Pericardial thickening above $4\,\mathrm{mm}$, especially with calcification and a tubular/conical deformation of the ventricles, points to constrictive physiology.

The coronary anatomy is the highest-stakes content of cardiac CT. The left main coronary artery arises from the left coronary sinus and bifurcates (or trifurcates, adding a ramus intermedius) into the left anterior descending artery, which runs in the anterior interventricular groove giving diagonal and septal branches and perfusing the anterior wall, anterior septum, and apex, and the circumflex artery, which courses in the left atrioventricular groove to supply the lateral wall. The right coronary artery arises from the right coronary sinus, runs in the right atrioventricular groove, and supplies the right ventricle and—in the 85% of people with right dominance—the inferior wall and posterior septum via the posterior descending artery and the AV nodal branch; in left dominance the circumflex supplies that territory, and codominance is intermediate. Dominance is therefore not a curiosity but the determinant of which vessel feeds the inferior wall and the conduction system. The conduction system itself—sinoatrial node at the superior cavoatrial junction, atrioventricular node in the triangle of Koch near the coronary sinus ostium—is supplied by small branches whose occlusion produces predictable rhythm disturbance. Anomalous coronary origins, particularly a vessel arising from the opposite sinus and taking an interarterial course between the aorta and pulmonary trunk, are a recognized cause of sudden cardiac death and a deliberate search target on every gated study. The expert reads the coronaries on thin gated reconstructions with multiplanar and curved reformats, scores calcium, and traces each vessel to its territory; the dominant pitfalls are motion-blurring of the mid right coronary and circumflex (which can fabricate or efface stenosis) and satisfaction of search after a single obvious lesion.

The great vessels are the structures whose variant anatomy most often changes a procedure, and their CT analysis is inseparable from the timing of the contrast bolus that opacifies them. The thoracic aorta is read in three segments: the ascending aorta rising from the aortic root (sinuses of Valsalva, sinotubular junction) anterior and rightward; the arch crossing right-to-left and anterior-to-posterior over the left main bronchus and pulmonary artery; and the descending aorta running in the posterior left paravertebral position. The arch gives three branches in the standard configuration—the brachiocephalic (innominate) trunk, then the left common carotid, then the left subclavian artery—but the single most common variant, the so-called bovine arch (present in $\sim 10\text{--}25\%$, more frequent in some populations), is a shared or common origin of the brachiocephalic trunk and left common carotid and must be recognized before arch intervention or great-vessel cannulation. The aberrant right subclavian artery (arteria lusoria), arising as the last arch branch and coursing behind the esophagus, is the classic cause of a posterior esophageal impression and of dysphagia lusoria, and it frequently originates from a Kommerell diverticulum. Aortic caliber is size-thresholded for aneurysm, and the normal ascending aorta measures $\le 3.5\text{--}4\,\mathrm{cm}$; measurements should be made perpendicular to the vessel’s centerline (double-oblique reformats), because axial measurements of a tortuous or obliquely oriented aorta systematically overestimate diameter—a quantitative pitfall with direct surgical consequences.

The pulmonary arteries arise from the right ventricular outflow into the main pulmonary trunk, which bifurcates into a right pulmonary artery passing anterior to the right main bronchus and bronchus intermedius and a left pulmonary artery arching over the left main bronchus. The main pulmonary artery normally measures $\le 29\,\mathrm{mm}$ and, when its diameter exceeds that of the adjacent ascending aorta, suggests pulmonary hypertension—a quick, robust visual sign on any chest CT. The pulmonary veins, four in the standard pattern (two on each side draining superiorly and inferiorly), return to the left atrium; partial anomalous pulmonary venous return, most commonly a right upper-lobe vein draining into the superior vena cava or right atrium (frequently with a sinus venosus atrial septal defect), is a readily overlooked left-to-right shunt that is increasingly relevant given pulmonary-vein imaging before atrial-fibrillation ablation. On the systemic venous side, the superior vena cava forms from the confluence of the brachiocephalic veins; a persistent left superior vena cava draining via an enlarged coronary sinus is the most common thoracic systemic venous anomaly and is recognized by the vertical vessel lateral to the aortic arch and the dilated coronary sinus it produces, a finding that complicates central-line and pacing-lead placement and can confound the unwary into calling a dissection or a nodal mass. The azygos and hemiazygos veins ascend in the paravertebral gutters and drain into the superior vena cava via the azygos arch; their enlargement signals caval obstruction or elevated right-heart pressures and provides collateral pathways that the reader should recognize rather than mistake for adenopathy. The expert evaluates the great vessels on a contrast phase appropriate to the question—an ECG-gated arterial acquisition for the aortic root and dissection, a pulmonary-arterial timing for embolism—measures the aorta on centerline-perpendicular reformats, and treats the arch-branch pattern, the pulmonary-vein drainage, and the systemic venous variants as a deliberate checklist. The principal cognitive errors are mistaking flow-related and timing artifacts (mixing artifact in the SVC, transient interruption of contrast in the pulmonary arteries) for thrombus, and anchoring on the aorta while overlooking an anomalous vein or a left SVC that changes the entire procedural plan.