Summary : This figure illustrates the left atrial (LA) pressure-volume relationship during the cardiac cycle, showing both time-course traces and a pressure-volume loop, with key phases of atrial function annotated and correlated with the ECG. line plot and loop diagram: # Panel A: LA Pressure and Volume Traces • Top trace: LA Pressure (y-axis, arbitrary units) over time. • Middle trace: LA Volume (y-axis, arbitrary units) over time. • Bottom trace: ECG waveform for temporal reference. • X-axis: Cardiac cycle phases, with systole and diastole labeled; diastole further subdivided into E, D, and A phases. • Five phases are color-coded and numbered: – (1) Atrial filling (red) – (2) Passive emptying (green) – (3) Diastasis (black) – (4) Active emptying (blue) – (5) Atrial relaxation (gray) • Vertical dashed lines demarcate transitions between phases. # Panel B: LA Pressure-Volume Loop • X-axis: LA Volume (arbitrary units). • Y-axis: LA Pressure (arbitrary units). • The loop is traced in a counterclockwise direction, with arrows indicating the sequence. • The same five phases (1–5) are color-coded as in Panel A. • The loop is divided into two segments: A-Loop (phases 1, 3, 4, 5) and V-Loop (phase 2). # Design Encodings : • Distinct colors for each phase (red, green, black, blue, gray). • Arrows on the loop indicate the direction of the cardiac cycle. • ECG trace provides timing reference for the pressure and volume changes. # Analysis : • The LA pressure and volume traces show cyclical changes corresponding to atrial filling, emptying, and relaxation. • The pressure-volume loop visually summarizes the dynamic relationship between LA pressure and volume, with distinct segments for passive and active phases. • The figure highlights the temporal coordination between atrial events and the ECG, emphasizing the mechanical and electrical coupling in the cardiac cycle.

Summary : This figure shows a pressure–volume loop for the left ventricle, illustrating how ventricular volume and pressure change during the cardiac cycle, with key phases and valve events annotated. The isovolumetric relaxation and contraction periods are highlighted, and systolic/diastolic blood pressures are marked. pressure–volume loop diagram: # Title & Axes : • No explicit title on the figure, but the legend describes it as a "Pressure–volume loop demonstrating changes in ventricular volume during filling and ejection with corresponding changes in intracavity pressure." • X-axis: "Left ventricular volume (mL)" with tick marks at 0, 20, 40, 60, 80, 100, 120, 140, 160. • Y-axis: "Left ventricular pressure (mmHg)" with tick marks at 0, 20, 40, 60, 80, 100, 120, 140. • Additional axis labels: "Left ventricular end-diastolic pressure" (blue, left), "End-diastolic volume" (blue, bottom right), "Stroke volume" (black, bottom center). # Phases & Events : • Isovolumetric relaxation: vertical line at low volume, pressure drops, labeled. • Diastolic filling: horizontal line at low pressure, volume increases, labeled. • Isovolumetric contraction: vertical line at high volume, pressure rises, labeled. • Ventricular ejection: curved line, volume decreases as pressure peaks and falls, labeled. • Valve events: – Mitral valve opens (bottom left corner, low pressure/volume). – Mitral valve closes (bottom right corner, high volume/low pressure). – Aortic valve opens (top right corner, high volume/high pressure). – Aortic valve closes (top left corner, low volume/high pressure). # Blood Pressure Markers : • Systolic BP: horizontal dashed blue line at ~120 mmHg. • Diastolic BP: horizontal dashed blue line at ~80 mmHg. # Design Encodings : • Black solid lines for the loop. • Blue dashed lines for blood pressure markers. • Blue text for end-diastolic volume/pressure. • Labeled arrows for direction of phases and valve events. # Analysis : • The loop traces the cardiac cycle, starting at low pressure/volume (end-systolic), filling during diastole, rising sharply during isovolumetric contraction, ejecting blood during ventricular ejection, and dropping pressure during isovolumetric relaxation. • Systolic and diastolic blood pressures are marked, showing the pressure range during ejection. • The width of the loop (horizontal distance) represents stroke volume. • The figure clearly distinguishes the four main phases and the timing of valve openings/closings, providing a comprehensive view of ventricular mechanics during a heartbeat.

This composite educational graphic details the pathophysiology of myocardial perfusion and coronary hemodynamics. Panel A features a pathophysiology diagram illustrating the extravascular forces and intraluminal pressures affecting the myocardial layers during the cardiac cycle. It compares diastole and systole, highlighting the differences in intramural pressure (PINTRAMURAL), left ventricular lumen pressure (PLUMEN), and pericardial space pressure (PPERICARDIUM). The diagram shows the subendocardial plexus and epicardial artery, emphasizing greater subendocardial compression and reduced vascular volume during systole. Panel B presents a cardiac perfusion quantification map from a patient with aortic stenosis (AS). The map is organized in a grid: rows represent basal, mid, and apical short-axis slices of the left ventricle; columns demonstrate stress perfusion, rest perfusion, and myocardial perfusion reserve (MPR). The color-coded mapping shows regional perfusion distribution, with the MPR column specifically highlighting global limitations in perfusion reserve. This visual is designed for medical education focusing on cardiovascular hemodynamics, coronary microcirculation, and the physiological impact of valvular heart disease on myocardial blood flow.

This diagnostic trace image displays eight simultaneous monophasic action potential (MAP) recordings, labeled MAP1 through MAP8, used in cardiac electrophysiology research. The primary focus is the determination of effective refractory periods (ERP) at a basic cycle length of 500 ms. The traces exhibit characteristic cardiac action potential morphology with rapid depolarization and subsequent repolarization phases. Throughout the 2-second time interval (indicated by the scale bar), regular pacing stimuli are followed by short-coupled extrastimuli (S2/S3) to test ventricular vulnerability and refractory periods. Variations in amplitude and morphology are visible across the different MAP traces, with a voltage scale of 7.5 mV provided for reference. Notable features include the presence of premature beats and varying repolarization kinetics (APD90/APD50) across different anatomical recording sites. This recording is representative of programmed electrical stimulation protocols used to assess spatial dispersion of repolarization and the propensity for arrhythmias such as ventricular tachycardia or torsade de pointes.

This Comparison Chart illustrates cardiac optical mapping data obtained from two different camera systems: the iDS (left column) and MiCAM (right column). Panels A and B display still frames of a Langendorff-perfused mouse heart, stained with a voltage-sensitive dye (Di-4-ANEPPS). Three color-coded pixels (blue, orange, and green) are marked on the ventricular surface of each heart image, indicating specific regions of interest. Panels C through H present the corresponding action potential (AP) waveforms recorded from these marked locations. The x-axis represents time in milliseconds (0–200 ms) and the y-axis shows normalized signal amplitude. The AP waveforms demonstrate characteristic cardiac electrophysiological phases, including rapid depolarization and subsequent repolarization. Visually, the iDS system images (A) appear brighter with a clearer anatomical outline but show higher high-frequency noise in the raw AP traces (C, E, G). In contrast, the state-of-the-art MiCAM system (B) produces traces with a higher signal-to-noise ratio (D, F, H), resulting in smoother AP curves. This comparison is used in cardiovascular research to validate the efficacy of lower-cost imaging systems for measuring cardiac activation sequences and action potential duration (APD).

Summary : This figure illustrates the relationship between the surface electrocardiogram (ECG) waveform and the myocardial action potential, highlighting the corresponding ion channels responsible for different phases of cardiac electrical activity. line diagram: # Panel A: Surface Electrocardiogram (ECG) Waveform : • Shows a typical ECG trace with labeled points: P, Q, R, S, T, and U. • The waveform represents the electrical activity of the heart during a cardiac cycle. • P wave: atrial depolarization. • QRS complex: ventricular depolarization. • T wave: ventricular repolarization. • U wave: sometimes seen, origin not fully understood. # Panel B: Myocardial Action Potential : • Plots membrane potential (mV) on the y-axis (ranging from -90 mV to above 0 mV) against time (msec) on the x-axis. • Shows the phases of the cardiac action potential: – Rapid upstroke (depolarization) due to I_Na (sodium current). – Early repolarization (I_to, transient outward potassium current). – Plateau phase (I_Ca-L, L-type calcium current). – Repolarization phase (I_Kr and I_Ks, rapid and slow delayed rectifier potassium currents). – Resting potential maintained by I_K1 (inward rectifier potassium current). # Ion Channels & Phases : • I_Na: Responsible for the initial rapid depolarization. • I_to: Contributes to early repolarization. • I_Ca-L: Maintains the plateau phase. • I_Kr and I_Ks: Mediate repolarization. • I_K1: Maintains the resting membrane potential. # Design Encodings : • Simple black line traces for both ECG and action potential. • Ion channel names are annotated above the relevant phases of the action potential. # Analysis : • The figure visually links the phases of the ECG waveform to the underlying myocardial action potential and the specific ion channels involved. • The QRS complex corresponds to the rapid depolarization (I_Na), while the T wave aligns with repolarization (I_Kr, I_Ks). • The plateau phase (I_Ca-L) is crucial for the duration of the QT interval, which is clinically significant for arrhythmia risk. • The diagram provides a clear educational overview of how surface ECG features relate to cellular electrophysiology.

Summary : This figure compares cardiac function under two conditions using two types of plots: (A) the Frank-Starling relationship between stroke volume and left ventricular filling, and (B) pressure-volume loops with end-systolic elastance (Ees) lines. line and schematic plot: # Panel A: Frank-Starling Curve : • Y-axis: Stroke Volume (no units shown). • X-axis: LVEDP or LVEDV (Left Ventricular End-Diastolic Pressure or Volume; no units shown). • Two curves are shown: – Curve 1: Higher, solid line, labeled "1". – Curve 2: Lower, dashed line, labeled "2". • Each curve has a point marked (solid dot) on it. # Panel B: Pressure-Volume Loop and End-Systolic Elastance : • Y-axis: Pressure (no units shown). • X-axis: Volume (no units shown). • Two pressure-volume loops: – Loop 1: Solid line, larger, leftward, labeled "1". – Loop 2: Dashed line, smaller, rightward, labeled "2". • Two Ees (end-systolic elastance) lines: – Ees 1: Steeper, solid line, labeled "1". – Ees 2: Less steep, dashed line, labeled "2". # Design Encodings : • Solid lines for condition 1, dashed lines for condition 2. • Dots mark specific points on the curves in panel A. • Pressure-volume loops are outlined, with loop 2 shown as a dashed outline. # Analysis : • Panel A shows that condition 1 (solid line) has a higher stroke volume for any given LVEDP/LVEDV compared to condition 2 (dashed line), indicating better cardiac function. • Panel B shows that condition 1 has a larger, leftward pressure-volume loop and a steeper Ees line, indicating greater contractility. Condition 2 has a smaller, rightward loop and a less steep Ees line, indicating reduced contractility. • The figure visually contrasts normal/enhanced versus impaired cardiac function using both stroke volume response and pressure-volume relationships.

This pathophysiology diagram illustrates the differences in regional oxygen saturation and blood flow distribution between a normal physiological state and circulatory shock. The diagram features anatomical icons of the brain, heart, and kidney, with arrows representing venous return and mixed venous output. In the 'Normal state,' the venous return from the brain is shown with a dark blue arrow (high extraction), while the return from the kidney is pale purple (low extraction), resulting in the relationship ScvO2 < SvO2. Conversely, in the 'Shock' state, the centralization of circulation is depicted: the kidney return becomes dark blue (indicating increased extraction or decreased perfusion), and the brain return becomes pale purple, leading to the inversion ScvO2 > SvO2. The comparison highlights how circulatory failure and compensatory vasoconstriction in visceral organs alter the balance between central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2), serving as a critical indicator for monitoring tissue perfusion and cardiac output adequacy in critical care settings.

This multi-panel figure illustrates the application of high-resolution micro-CT data in mathematical modeling of human cardiac anatomy and electrophysiology. Panel (a) presents a segmented 3D reconstruction of the cardiac conduction system, color-coded to show the sinus node (blue), paranodal area (turquoise), atrioventricular (AV) conduction axis (green), and the intricate right (red) and left (purple) Purkinje networks. Panel (b) overlays these segmented structures onto a semi-transparent 'ghosted' volume rendering of the whole heart, providing anatomical context within the right and left atria (RA, LA) and ventricles (RV, LV). Panel (c) provides a four-chamber cross-sectional view of cardiomyocyte orientation, using a color map to represent absolute helical angles (0° to 90°). This reveals complex transmural patterns and longitudinal alignment in the papillary muscles. Panel (d) shows a computer-generated isochrone map of cardiac depolarization (activation time in ms) seeded from the sinus node. This visualization integrates anatomically accurate geometry with electrophysiological measurements to demonstrate physiological conduction pathways across the myocardium.

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.