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.

A 12-lead electrocardiogram (ECG) showing a sinus rhythm with a prolonged PR interval (238 ms) and a wide QRS complex (126 ms), characteristic of a first-degree atrioventricular (AV) block and an intraventricular conduction delay or borderline left bundle branch block (LBBB). In the limb leads (I, II, III, aVR, aVL, aVF), the P waves are upright in the inferior leads and inverted in aVR. The precordial leads (V1-V6) demonstrate deep S-waves in V1-V3 and tall R-waves in V4-V6, typical of LBBB morphology. There is noticeable ST-segment depression and T-wave flattening in leads V1-V3, while leads V4-V6 show more prominent upright T-waves and slight ST-elevation. This image represents the post-treatment state following calcium chloride administration for hyperkalemia, illustrating the narrowing of the QRS complex and stabilization of the cardiac membrane compared to earlier findings. Key educational concepts include ECG recognition of electrolyte imbalances, conduction abnormalities, and the therapeutic effect of calcium in emergency medicine.

This pathophysiology diagram presents electrophysiological traces and calcium transients from a cardiac cellular model, comparing Wild Type (WT) in grey and the T309I mutation (WT/T309I) in red under beta-adrenergic stimulation and a shortened cycle length (CL 500 ms). The top-left panel illustrates the intracellular calcium concentration at the end of diastole ([Ca2+]i,end), showing a sudden onset of oscillations in the mutant line starting at 540 seconds, labeled as the 'start of DADs' (delayed afterdepolarizations). The subsequent Vm (membrane voltage) plots show that while WT maintains stable action potentials, the WT/T309I variant exhibits abnormal voltage oscillations and triggers spontaneous activity, marked by red asterisks. The bottom panels provide a high-resolution view of cytosolic calcium ([Ca2+]i) and Vm between 550 and 560 seconds, demonstrating the temporal coupling between erratic calcium handling and membrane potential instability. This visual data illustrates the cellular mechanism of arrhythmia, specifically how increased calcium load under sympathetic stimulation leads to triggered activity and potential ventricular tachycardia in the context of T309I-related channelopathy.

Two-panel axial CT scan of the abdomen in the arterial (a) and venous (b) phases, demonstrating a post-radiofrequency ablation (RFA) assessment in a patient with cirrhosis. Image (a) shows a hyperattenuating, arterial-enhancing nodule located at the periphery of a hypodense, well-defined rounded ablation zone in the liver. Image (b) shows the same nodule in the portal venous phase, characterized by contrast 'washout,' where the nodule becomes hypoattenuating relative to the surrounding liver parenchyma. The ablation zone itself remains non-enhancing and relatively homogeneous in both phases. This dynamic contrast enhancement pattern—arterial hyperenhancement followed by venous washout—is the hallmark of recurrent or residual hepatocellular carcinoma (HCC). The image illustrates the clinical application of CT in monitoring locoregional therapy response and identifying residual tumor at the treatment margins.

Contrast-enhanced axial computed tomography (CT) images of the abdomen displaying a comparison between the arterial phase (top row, a-c) and the venous/portal phase (bottom row, d-f). The images demonstrate hallmark features of liver cirrhosis and portal hypertension. Key findings include an irregular liver contour with surface undulations (white arrows) and significant ascites (arrowheads) manifesting as low-attenuation fluid in the perihepatic and perisplenic spaces. In the portal phase (d-f), there is a prominent, dilated, and tortuous ectopic venous varix located in the third section of the duodenum (empty arrows). High-attenuation contrast leakage (star) within the duodenal lumen in the portal phase indicates active intraluminal bleeding. The images effectively contrast the differential enhancement of hepatic parenchyma and the progressive visualization of venous structures and hemorrhage between phases. This clinical imaging set is highly relevant for medical education on the complications of portal hypertension and the diagnostic utility of multi-phase CT in identifying ectopic variceal bleeding.

This diagnostic image is a triple-phase axial computed tomography (CT) scan of the lower abdomen, demonstrating a vascular malformation in the small bowel. The image is divided into three panels representing different contrast phases: (A) non-contrast (NCCT), (B) arterial phase, and (C) portal venous phase. Each panel shows the central lumbar vertebral body, paraspinal musculature, and abdominal cavity containing loops of bowel. White arrows in each phase point to a specific bowel loop in the left quadrant. In the non-contrast phase (A), the target loop is isodense to surrounding soft tissue. In the arterial phase (B), there is subtle hyperattenuation indicating early filling of a vascular lesion. In the portal venous phase (C), the enhancement becomes significantly more pronounced and radio-dense, characteristic of a slow-flow vascular malformation or hemangioma that fills over time. This sequence illustrates the importance of multiphase imaging in identifying mucosal vascular ectasias and angioectasias, which are key clinical considerations in patients presenting with obscure gastrointestinal bleeding or melena.