Forget time for a moment. A pressure–volume loop plots left-ventricular pressure (y-axis, mmHg) against left-ventricular volume (x-axis, mL) across a single heartbeat.
Because both pressure and volume change continuously, one beat traces out a closed loop. The loop runs counter-clockwise.
", "action": { "label": "Open the normal loop", "preset": "normal" } }, { "t": "Width is stroke volume", "h": "The loop’s width is the volume ejected each beat, the stroke volume. Its right edge is end-diastolic volume (EDV, the fullest point); its left edge is end-systolic volume (ESV, the emptiest).
Ejection fraction is simply SV ÷ EDV. Everything else on the loop explains why that width is what it is.
" }, { "t": "Area is work", "h": "The area enclosed by the loop is stroke work, the mechanical work the ventricle does on the blood each beat. A tall, wide loop does more work than a small one.
Turn on the stroke-work fill to see the enclosed area shaded.
", "action": { "label": "Shade stroke work", "preset": "normal", "overlays": { "sw": true } } } ], "check": [ "I can point to stroke volume and ejection fraction on the loop", "I know the loop runs counter-clockwise" ] }, { "n": 2, "eyebrow": "Mechanics", "title": "The four phases", "dek": "Two valves, opening and closing in sequence, carve the loop into four sides.", "steps": [ { "t": "Follow one beat", "h": "Start at the bottom-right corner (end-diastole, mitral valve just closed) and go counter-clockwise:
1 · Isovolumetric contraction: both valves shut, pressure rises straight up, volume fixed. 2 · Ejection: the aortic valve opens, blood leaves, volume falls. 3 · Isovolumetric relaxation: the aortic valve shuts, pressure drops straight down. 4 · Filling: the mitral valve opens, the ventricle refills along the bottom.
", "action": { "label": "Animate the four phases", "preset": "normal", "overlays": { "labels": true } } }, { "t": "The corners are valve events", "h": "Each corner is a valve opening or closing: ① MV closes (start of contraction), ② AV opens (start of ejection), ③ AV closes (end-systole), ④ MV opens (start of filling).
The two vertical sides are isovolumetric: all valves are closed, so volume can’t change. Keep this in mind: several diseases are defined by which vertical side is missing.
" }, { "t": "Why counter-clockwise?", "h": "Because the ventricle fills at low pressure (bottom), then generates high pressure to eject (top), then relaxes. Energy flows in during systole and the loop closes as it relaxes and refills.
", "quiz": { "q": "In mitral regurgitation, blood leaks back into the atrium the instant pressure rises, before the aortic valve opens. Which phase disappears?", "a": "Isovolumetric contraction. With a hole into the low-pressure atrium, volume starts falling as soon as pressure rises, so the left vertical wall of the loop is lost." } } ], "check": [ "I can name the four phases in order", "I know which sides are isovolumetric" ] }, { "n": 3, "eyebrow": "Boundaries", "title": "The three lines", "dek": "A loop lives inside a frame of three lines. Learn the frame and every disease becomes readable.", "steps": [ { "t": "ESPVR: contractility", "h": "The end-systolic pressure–volume relationship is the ceiling the loop’s top-left corner rides on. Its slope is Ees, a load-independent measure of contractility.
Steeper ESPVR = stronger heart = the ventricle empties to a smaller volume against the same pressure. Slide contractility and watch the top-left corner track the green line.
", "action": { "label": "Show ESPVR", "preset": "normal", "overlays": { "espvr": true, "edpvr": false, "ea": false } } }, { "t": "EDPVR: compliance", "h": "The end-diastolic pressure–volume relationship is the curved floor. It is passive: how stiff the ventricle is when it fills. A stiff ventricle (HFpEF, restrictive, hypertrophy) climbs this curve steeply: small volume, high filling pressure.
", "action": { "label": "Compare a stiff ventricle", "preset": "hfpef", "overlays": { "edpvr": true } } }, { "t": "Ea: the load", "h": "The effective arterial elastance line is the diagonal from EDV on the x-axis to the end-systolic corner. It summarises everything the ventricle ejects against (resistance + stiffness of the arterial tree) as one number, Ea = ESP / SV.
Where ESPVR (Ees) meets Ea sets the operating point. Their ratio, Ea/Ees, is ventriculo-arterial coupling, which is optimal near 0.6–1.2.
", "action": { "label": "Show all three lines", "preset": "normal", "overlays": { "espvr": true, "edpvr": true, "ea": true } } } ], "check": [ "ESPVR slope = contractility (Ees)", "EDPVR = passive stiffness", "Ea = load; Ea/Ees = coupling" ] }, { "n": 4, "eyebrow": "Levers", "title": "Preload, afterload, contractility", "dek": "Three independent levers move the loop. Change one at a time and watch.", "steps": [ { "t": "Preload", "h": "Preload is how full the ventricle is before it contracts (EDV). Add preload and the loop’s right edge slides right: more stretch, more stroke volume (the Frank–Starling mechanism), same ESPVR corner.
", "action": { "label": "Raise preload", "preset": "normal", "overlays": { "espvr": true, "ea": true } } }, { "t": "Afterload", "h": "Afterload is the pressure the ventricle must beat against. Raise it and the aortic valve opens later and higher: the loop grows taller and narrower, stroke volume falls, end-systolic volume rises.
", "action": { "label": "Raise afterload", "preset": "vasocon" } }, { "t": "Contractility", "h": "Contractility rotates the ESPVR ceiling upward. A stronger heart empties further for the same load: end-systolic volume falls, stroke volume and EF rise. This is the one lever that is truly intrinsic to the muscle.
", "action": { "label": "Add contractility (dobutamine)", "preset": "dobut", "overlays": { "espvr": true } } }, { "t": "Isolate them", "h": "The determinant sliders on the simulator move each lever independently, which you cannot do at the bedside. Return to normal, then push one slider at a time and predict the loop before it redraws.
", "quiz": { "q": "You raise afterload but stroke volume barely changes and EF stays high. What does that tell you about the ESPVR?", "a": "The ventricle has strong contractility (steep ESPVR / large contractile reserve). A steep ESPVR is relatively afterload-insensitive; a flat one (failing heart) is exquisitely afterload-sensitive." } } ], "check": [ "Preload → width via Frank–Starling", "Afterload → taller, narrower", "Contractility → rotates ESPVR" ] }, { "n": 5, "eyebrow": "Energetics", "title": "Work, oxygen and efficiency", "dek": "The loop is also an energy diagram, and oxygen is the currency.", "steps": [ { "t": "PVA predicts MVO₂", "h": "The pressure–volume area (PVA) is stroke work plus the potential energy stored in the contracted muscle. Suga showed PVA is linearly related to myocardial oxygen consumption, so the loop predicts how much O₂ the beat costs.
", "action": { "label": "Shade PVA energy", "preset": "normal", "overlays": { "pe": true, "sw": true } } }, { "t": "Efficiency and coupling", "h": "Efficiency is the fraction of that energy that becomes useful work: SW / PVA. It peaks when Ea/Ees is near 0.6–1.0. A failing heart (flat ESPVR, high Ea) is uncoupled: it spends oxygen on pressure it can’t convert to output.
", "action": { "label": "See an uncoupled heart", "preset": "hf", "overlays": { "espvr": true, "ea": true, "pe": true } } }, { "t": "Why unloading helps", "h": "Anything that lowers PVA lowers oxygen demand: reducing afterload, reducing volume, or mechanically unloading the ventricle. This is the logic behind afterload reduction in HF and behind Impella in cardiogenic shock: shrink the loop, spend less oxygen.
" } ], "check": [ "PVA ≈ myocardial oxygen consumption", "Efficiency = SW/PVA, best when coupled" ] }, { "n": 6, "eyebrow": "Failure", "title": "HFrEF vs HFpEF", "dek": "Two heart failures, two different lines break.", "steps": [ { "t": "HFrEF: the ceiling falls", "h": "In heart failure with reduced EF, contractility collapses: the ESPVR flattens. The ventricle can’t empty, so it dilates to preserve output (Frank–Starling). The loop shifts right, EF falls, and Ea/Ees uncouples.
", "action": { "label": "Load HFrEF", "preset": "hf", "overlays": { "espvr": true, "ea": true } } }, { "t": "HFpEF: the floor rises", "h": "In HF with preserved EF the systolic line is fine. The problem is the EDPVR. A stiff ventricle climbs the diastolic curve steeply: normal EF, but high filling pressure at a small volume. That pressure backs up into the lungs.
", "action": { "label": "Load HFpEF", "preset": "hfpef", "overlays": { "edpvr": true } } }, { "t": "Same syndrome, opposite loops", "h": "Side by side, HFrEF is a wide, short, right-shifted loop; HFpEF is a narrow, tall loop crammed against a steep diastolic curve. Both raise filling pressure, by different mechanics.
", "quiz": { "q": "Which line would you target with a positive inotrope, and which is essentially inotrope-proof?", "a": "Inotropes steepen the ESPVR, which helps in HFrEF. HFpEF’s problem is the passive EDPVR, which inotropes don’t fix; that’s why HFpEF has been so hard to treat pharmacologically." } } ], "check": [ "HFrEF = flat ESPVR, dilated", "HFpEF = steep EDPVR, preserved EF" ] }, { "n": 7, "eyebrow": "Valves", "title": "Reading valve disease", "dek": "One question unlocks every valve lesion: which phase or line is broken?", "steps": [ { "t": "A framework, not a list", "h": "Stenosis = obstruction to forward flow. Regurgitation = backward leak that erases an isovolumetric phase. Where the lesion sits (aortic vs mitral) decides which corner moves.
" }, { "t": "Aortic stenosis", "h": "The ventricle must generate huge pressure to force blood through a narrow valve, so peak LV pressure rises far above aortic pressure. That gap is the gradient. Turn on the peak-LVP line to see LV and aorta diverge.
", "action": { "label": "Aortic stenosis", "preset": "as", "overlays": { "lvp": true, "bp": true } } }, { "t": "Aortic vs mitral regurgitation", "h": "AR fills the ventricle in diastole (aortic leak): no true isovolumetric relaxation, wide loop, low diastolic BP. MR empties into the atrium in systole: no true isovolumetric contraction, the left wall of the loop vanishes.
", "action": { "label": "Mitral regurgitation", "preset": "amr", "overlays": { "labels": true } } }, { "t": "Acute vs chronic", "h": "Chronicity changes the EDPVR. Chronic volume overload remodels eccentrically into a compliant, dilated chamber that tolerates the volume. An acute lesion hits a normal-sized, stiff ventricle: filling pressure rises sharply. Compare chronic vs acute MR to see the same leak on two different floors.
", "action": { "label": "Acute MR", "preset": "acutemr", "overlays": { "edpvr": true } } }, { "q": "", "t": "Test yourself", "h": "", "quiz": { "q": "A loop has lost its left vertical wall and sits shifted left with a low peak pressure. Which lesion?", "a": "Mitral regurgitation. The systolic leak into the atrium erases isovolumetric contraction and unloads the ventricle, lowering peak pressure." } } ], "check": [ "AS → LV–aortic gradient", "AR erases IVR; MR erases IVC", "Acute lesions hit a stiff floor" ] }, { "n": 8, "eyebrow": "Support & repair", "title": "Devices and interventions", "dek": "How mechanical support and valve/lead procedures reshape the loop.", "steps": [ { "t": "IABP vs Impella", "h": "The balloon pump nudges: it lowers afterload and improves coronary flow, modestly shrinking the loop. Impella actively drains the ventricle. The loop shrinks and triangularises, PVA (oxygen demand) drops sharply. Layer each device onto cardiogenic shock and watch.
", "action": { "label": "Impella on shock", "preset": "shock", "device": "impella", "overlays": { "pe": true } } }, { "t": "The VA-ECMO paradox", "h": "VA-ECMO rescues the circulation but punishes the ventricle: retrograde aortic flow raises afterload, so the loop is pushed up and right and PVA rises. Adding an Impella to vent the LV (ECPELLA) pulls it back down. This is the rationale for LV venting.
", "action": { "label": "VA-ECMO, then compare", "preset": "shock", "device": "ecmo", "ref": "unsupported", "overlays": { "pe": true } } }, { "t": "TAVR, MVR, CRT", "h": "Interventions are best read as before → after pairs. TAVR abolishes the aortic gradient (loop widens, peak LVP drops to aortic). MVR restores isovolumetric contraction and unmasks true EF. CRT re-coordinates a dyssynchronous ventricle so the loop lifts and narrows.
", "action": { "label": "Pre-TAVR (then pick Post)", "preset": "pre_tavr", "overlays": { "lvp": true } } } ], "check": [ "Impella unloads; ECMO can distend", "LV venting lowers PVA on ECMO", "Interventions read as before→after" ] } ]