Intravascular imaging puts a tiny camera inside the coronary artery — either ultrasound (IVUS) or light (OCT) — to see the vessel wall in cross-section. A standard angiogram is only a 2-D silhouette of the lumen; this shows what that silhouette can't.

Each cross-section shows the lumen (the open channel), the vessel wall, and the external elastic membrane (EEM) that marks the outer border — together they define the plaque burden. IVUS penetrates deep and shows the whole wall and calcium arc (ideal for sizing and the left main). OCT has ~10× finer resolution near the lumen — best for thin caps, dissection, thrombus, and stent-strut apposition — but shallow penetration, and it needs a contrast flush to clear blood.

The classic uses: size the vessel before stenting, characterize the plaque (calcium changes the strategy), and confirm afterward that the stent is fully expanded and apposed.

A pressure–volume loop plots left-ventricular pressure against its volume across one beat, so a single closed loop captures the whole mechanical performance of the ventricle. Read it counter-clockwise: filling along the bottom, isovolumic contraction up the right side, ejection across the top, isovolumic relaxation down the left.

Three properties set its shape. Preload is how full the ventricle is before it contracts (the right-hand end-diastolic corner). Afterload is the pressure it must overcome to eject (roughly the loop's height). Contractility is the intrinsic squeeze, captured by the slope of the end-systolic pressure–volume relationship. The width of the loop is the stroke volume; its area is the stroke work.

Every disease state moves the loop in a recognizable way — tall and narrow with high afterload, wide and short in a failing ventricle, small and left-shifted when preload is low.

The cardiac cycle is the sequence of electrical, pressure, and volume events in a single heartbeat. The Wiggers diagram stacks them on one time axis so you can see how they line up — and once you know it, almost every hemodynamic finding becomes "a departure from this."

Follow one beat: the ECG fires first (P wave = atrial contraction, QRS = ventricular contraction). The ventricle then contracts with all valves shut (isovolumic contraction) until its pressure exceeds the aorta and the aortic valve opens — blood ejects and volume falls. When the ventricle relaxes below aortic pressure the aortic valve closes (the dicrotic notch), then the mitral valve opens and filling begins again.

The heart sounds mark the valve closures: S1 at mitral closure (start of systole), S2 at aortic closure (end of systole).

A right heart catheterization floats a balloon-tipped catheter (a Swan–Ganz) from a vein through the right atrium → right ventricle → pulmonary artery, out to the wedge position. You never see the tip directly — you know where it is from the pressure waveform it shows and the oxygen saturation you sample there.

As the catheter advances, the waveform changes in recognizable ways: the low a/v waves of the right atrium; a sudden tall systolic wave as you cross into the right ventricle ("ventricularization"); a step-up in the diastolic pressure with a dicrotic notch as you enter the pulmonary artery; and finally the damped a/v waves of the wedge, which reflect left-atrial filling pressure. Those transitions are how you navigate.

Saturations matter too: an unexpected jump in oxygen saturation between two chambers (a "step-up") signals a left-to-right shunt.

Breathing changes the pressures inside the heart, and the pattern of that change is diagnostic. The key idea is ventricular interdependence: the two ventricles share a septum and, in some diseases, a fixed space — so when one fills more, the other must fill less.

Normally, inspiration slightly increases right-heart filling and slightly decreases left-heart filling — a small effect. Disease exaggerates it in specific ways. In constrictive pericarditis a rigid pericardium forces the ventricles to compete, so on inspiration RV pressure rises while LV pressure falls (discordance). In cardiac tamponade the same competition produces an exaggerated inspiratory fall in systemic pressure — pulsus paradoxus over 10 mmHg. In restrictive cardiomyopathy, with no pericardial constraint, the two pressures fall together (concordance) — which is how you separate it from constriction.

CathSim cases are plain data. Paste a case in the schema below and it becomes a fully playable branching case — a way for your division to author its own teaching cases without touching code.

A pressure waveform is just the pressure inside a chamber or vessel plotted against time, traced out as the catheter tip sits there. Every site has a characteristic shape, and learning to recognize those shapes — and how disease distorts them — is one of the core skills of invasive cardiology.

The low-pressure chambers (the atria and the wedge position that mirrors the left atrium) show a repeating set of small waves and descents: the a wave (atrial contraction), the v wave (atrial filling against a closed valve), and the x and y descents between them. Ventricles show a tall systolic peak dropping to a low diastolic baseline. Arteries show a brisk upstroke, a dicrotic notch (valve closure), then a gradual runoff.

Disease shifts these predictably — a giant v wave in mitral regurgitation, a blunted y descent in tamponade, a dip-and-plateau ("square-root sign") in constriction. Reading a tracing is really about spotting the departure from normal.