This educational graphic provides a side-by-side comparison of cardiac anatomy and sonographic representation in a subcostal transthoracic echocardiogram (TTE) view. On the left, an anatomical diagram illustrates a four-chamber view of the heart in cross-section, showing the left and right ventricles separated by the interventricular septum, along with the corresponding atria and atrioventricular valves. On the right, a corresponding grayscale echocardiogram (sonogram) in a sector scan format displays the heart from the subcostal acoustic window. The image highlights clinical landmarks including the hyperechoic (bright) ventricular walls and valves against the anechoic (dark) blood-filled chambers. This comparison is intended for medical trainees to correlate simplified anatomical models with real-time diagnostic imaging, specifically focusing on identifying cardiac chambers and orientation in the subcostal four-chamber view often used in emergency or critical care ultrasonography.

Summary : This figure presents six schematic diagrams of standard echocardiographic views used to visualize the heart chambers and valves, specifically focusing on the right ventricle (RV) and its relationship to other cardiac structures. illustration: # Views Presented : • Parasternal Long-Axis view: Shows RV, Ao (aorta), and LA (left atrium) in a longitudinal section. • Parasternal Long-Axis of the RV outflow view: Displays RVOT (right ventricular outflow tract), PA (pulmonary artery), and LV (left ventricle). • Parasternal Short-Axis of basal RV view (at MV level): Cross-sectional view at the mitral valve (MV) level, showing RV and MV. • Parasternal Short-Axis of mid RV view (at LV papillary muscle level): Cross-sectional view at the level of the LV papillary muscles, showing RV, LV, and papillary muscles (PM). • Modified Apical 4-chamber view: Displays RA (right atrium), RV, LA, and LV in a four-chamber perspective. • RA-focused apical 4-chamber view: Focuses on RA, RV, LA, and LV, emphasizing the right atrium. # Labels & Orientation : • Each diagram is labeled with anatomical structures (RV, LV, LA, RA, Ao, PA, MV, PM). • Orientation markers such as "Anterior," "Lateral," and "Septal" are provided for spatial reference. # Design Encodings : • Simple black-and-white line drawings. • Chamber walls and valves are outlined; no colour or shading. • Each view is titled below the corresponding diagram. # Analysis : • The figure systematically compares different echocardiographic views, highlighting how the right ventricle and associated structures appear in each orientation. • The progression from long-axis to short-axis and apical views demonstrates the versatility of echocardiography in assessing cardiac anatomy and function. • The inclusion of both standard and modified views allows for comprehensive visualization of the right heart.

This composite educational graphic illustrates cardiac anatomy segmentation for radiotherapy planning. Section A presents three-dimensional surface renderings comparing manual contours and automatic segmentations across three tiers: cardiac chambers and great vessels (LA, LV, RA, RV, AA, SVC, PA), cardiac valves (AV, MV, PV, TV), and coronary arteries (LAD, LCX, LMCA, RCA). Each rendering highlights spatial relationships between chambers and vessels, with human figure icons indicating anatomical orientation. Section B displays axial computed tomography (CT) slices demonstrating the application of automatic segmentation algorithms in diverse clinical scenarios: 'Typical anatomy', 'Tumour close to heart', 'Severe image artefacts', and 'Contrast CT (arms raised)'. The segmentations delineate the heart, atria, ventricles, and coronary vessels, showing the model's robustness to anatomical variations and imaging challenges common in thoracic oncology. This visualization highlights the clinical utility of deep learning and multi-atlas mapping for accurate cardiac substructure identification in dose-response studies and cardiac-sparing radiotherapy.

This clinical photograph captures an intraoperative view of a pericardiectomy procedure in a patient with chronic fibrous constrictive pericarditis. The primary image displays a median sternotomy with the heart exposed; the visceral and parietal layers of the pericardium appear significantly thickened, opaque, and whitish-tan in color, demonstrating loss of normal translucency. Surgical retractors and forceps are positioned to elevate the adherent, fibrous tissue from the epicardial surface. An inset image shows a gross pathological specimen of the excised pericardium. The specimen is predominantly reddish due to hypervascularization and surgical hemorrhage, featuring an irregular, roughened texture and marked thickening. The visual findings illustrate the physiological basis for ventricular constriction, where a rigid, non-compliant pericardial sac restricts cardiac filling. This content is representative of advanced cardiothoracic surgical pathology often associated with chronic inflammatory conditions such as tuberculosis.

Gross pathology specimen illustrating chronic constrictive pericarditis. Modality: gross pathological examination of a fixed cardiac specimen. Technique: transverse cross-section through the pericardial sac surrounding the ventricles; surrounding mediastinal fat is variably reduced. Notable features: markedly thickened, fibrotic pericardium with calcific rim encasing an incompletely compliant heart. Visceral and parietal pericardial layers are adherent; the pericardial cavity is reduced or obliterated in several regions. The epicardial surface may show mild inflammatory change with preserved myocardial architecture. The myocardium itself demonstrates normal color and architecture but appears constrained by the stiff envelope, with limited diastolic excursion simulated by manual manipulation. Calcific nodules along the pericardial leaflets give a gritty texture on palpation. Collectively, these findings reflect the pathophysiology of constrictive physiology: restricted ventricular filling, reduced stroke volume, and equalization of diastolic pressures. The macroscopic diagnosis is constrictive pericarditis with calcification, often secondary to chronic inflammation from infection (tuberculosis), prior cardiac surgery, or idiopathic causes. Clinically, pericardiectomy removing both visceral and parietal layers is the definitive treatment. The image corroborates surgical planning by demonstrating the extent and distribution of calcification and dense fibrous tissue. Noninvasive imaging (echocardiography, CT, MRI) provides complementary assessment of hemodynamics and pericardial thickness.

This medical illustration comprises projection confocal images and corresponding line-profile graphs analyzing the spatial distribution of Connexin 43 (Cx43) at cardiac intercalated discs across different ages. Panel A displays two confocal micrographs of atrial myocyte intercalated discs labeled for Cx43. The 1-month-old specimen shows a dense, heterogeneous distribution of Cx43 'hot spots' across the entire area of the disc (approx. 8 μm width). In contrast, the 38-month-old specimen exhibits a larger intercalated disc (approx. 12 μm width) with Cx43 restricted primarily to the outer rim, indicating age-related spatial remodeling and lateralization. Panels B and C provide quantitative intensity profiles (label intensity in arbitrary units vs. distance in μm) corresponding to the dashed lines in Panel A. The 1-month profile (B) demonstrates multiple high-intensity peaks across the disc, while the 38-month profile (C) shows two distinct peaks at the periphery with a significant signal loss in the central region. This visual evidence supports concepts of cellular aging, gap junction remodeling, and potential impacts on atrial conduction velocity.

Histology of cardiac tissue demonstrating AL (light-chain) amyloid depositions with associated myocardial atrophy. Prepared as a hematoxylin and eosin stained section, viewed under bright-field microscopy, the myocardium shows extensive extracellular, eosinophilic, amorphous material within the interstitium surrounding relics of cardiac myocytes. The deposits are pale pink, homogeneous, and nonfibrillar by routine light microscopy, consistent with amyloid neuropathologic patterns and typical of AL amyloidosis. Cardiac myocytes exhibit variable atrophy with preserved nuclei in the interstitial milieu; there is sparse inflammatory infiltrate and disruption of normal architecture, contributing to stiff, diastolic-restrictive physiology. The diagnosis is supported by clinical context: a patient with multiple myeloma and lambda light chain clonal plasma cells, whose dyspnea reflects progressive restrictive cardiomyopathy due to myocardial amyloid infiltration. In histopathology terms, extracellular matrix expansion by amyloid coincides with deposition within vessel walls and perimysial spaces, potentially impairing coronary perfusion and contractile function. Clinically, this pattern signals poor prognosis if cardiac involvement is substantial, guiding oncologic therapy and cardiac supportive care. Differential considerations include transthyretin-type amyloid deposition and senile amyloidosis, but the light-chain profile and marrow findings make AL amyloidosis the favored etiology in this case. This slide illustrates characteristic cardiomyopathic changes with light-chain amyloid and myocyte attrition.

A posterior-anterior (PA) chest x-ray demonstrating significant pathology in the superior and middle mediastinum. The most prominent finding is a severely widened mediastinum, characterized by a large, well-defined radiopaque mass occupying the upper and middle thoracic cavity. This mass is causing a marked mass effect, resulting in the significant deviation of the trachea to the left of the midline, as indicated by the labeled red arrow. The mass displays a radiographic appearance consistent with a retrosternal goiter, extending from the cervical region into the thoracic inlet. Metallic surgical clips are visible in the upper right cervical area, suggesting previous surgery. The lung fields appear relatively clear, though the cardiac silhouette is partially obscured by the large mediastinal opacity. This diagnostic image is used to illustrate the complications of large mediastinal masses, such as airway compression and displacement, relevant for pulmonology, endocrine surgery, and critical care education.

A posterior-anterior (PA) view chest radiograph (diagnostic imaging) demonstrating a significant widening of the superior and middle mediastinum. A yellow arrow points to the left-sided expansion of the mediastinal silhouette, specifically in the region of the aortic knob and descending thoracic aorta, suggesting vascular pathology such as an aortic aneurysm or pseudo-aneurysm. The lung fields appear relatively lucent, though there is some obscured detail in the left upper lobe due to the overlying mass effect of the widened mediastinum. Notable external or iatrogenic findings include irregular, highly radiopaque objects located in the superior chest and supraclavicular regions, as well as metallic surgical clips or staples visible along the lateral ribcage and paraspinal areas. This imaging serves as an educational example for identifying mediastinal mass effects and vascular emergencies in clinical radiology.

Anatomical Diagram over a clinical photograph of a gross cardiac specimen, viewed from the atrial aspect (superior view) of the cardiac base. The image illustrates the complex anatomy of the cardiac conduction system and vestigial embryonic structures. Key landmarks include the atrioventricular (AV) node (white star with red borders) and the retroaortic node (red star with white borders). The conduction pathway is delineated by a solid red line representing the bundle of His. Supplemental embryonic and auxiliary tracts are marked with dotted lines: a green dotted line shows the 'dead-end tract' continuing from the AV conduction axis toward the outflow tract; a yellow dotted line marks the retro-aortic ring branch; and a white dotted line traces the path of the embryonic atrioventricular ring. This visual is designed for advanced medical education in cardiac electrophysiology and embryology, highlighting the anatomical basis for idiopathic ventricular arrhythmias and the clinical significance of persistent embryonic tissues within the heart's conduction framework.

This composite medical illustration demonstrates the pathophysiology of right ventricular (RV) pacing-induced left ventricular (LV) dyssynchrony. The left side features a schematic anatomical diagram of the heart showing the cardiac conduction system (Sinus node, AV node, Bundle branches, and Purkinje fibers). A red line represents a pacing lead traversing the right atrium to the RV apex (marked by a red star). Red wavefront arcs illustrate electrical activation spreading from the RV pacing site to the LV, highlighting the late activation of the LV lateral wall. The right side contains diagnostic images, including a color tissue Doppler echocardiogram and a corresponding velocity-time tracing. The Doppler tracing shows two distinct myocardial velocity curves (green) with vertical blue and red marker lines indicating the significant temporal delay between segmental contractions. A label and arrows point to both the LV basal lateral segment on the diagram and the delayed peak on the Doppler tracing, identifying the mechanical dyssynchrony resulting from the non-physiological electrical sequence of RV apical pacing.

Educational medical graphic illustrating abnormal ventricular conduction system (VCS) structure and electrophysiology in a mouse model of miR-1 overexpression. Panel A shows whole-mount P5 neonatal hearts with CCS-LacZ reporter activity; magnified views compare wild-type (WT) and transgenic (TG) atrioventricular bundles (AVB) and Purkinje fibers (PF), revealing significantly reduced PF branching in TG hearts. Panel B utilizes Irx3-LacZ staining to further demonstrate diminished PF density in the left bundle branch and right ventricle of TG mice. Panel C provides quantification, with a bar graph showing a statistically significant decrease in normalized PF density (p < 0.01). Panel D displays averaged lead aVF ECG tracings, highlighting a prolonged QRS duration in TG mice compared to WT. Panel E includes bar graphs of cardiac intervals (RR, PR, and QRS), confirming that while heart rate and AV node conduction are unchanged, VCS conduction is significantly slowed, as evidenced by increased QRS duration (p < 0.05). This composite figure demonstrates that premature miR-1 upregulation leads to Purkinje fiber hypoplasia and conduction dysfunction.